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| Prozac -- the Toxic Miracle Drug Name: Michelle T Date: 2002-02-25 13:37:34 Link to this Comment: 1149 |
3) "Hedweb Good Drug Guide: the Responsible Parent's Guide to Healthy Moodboosters for All the Family",
4) College Magazine, "Numb and Number, How One Little Pill is Changing the Face of College"
5) Antipsychiatry, "Psychiatric Drugs: Cure or Quakery?"
6) "Manufacturer's Report, Eli Lilly"
7) Breggin, Peter. Talking Back to Prozac. St. Martin's Paperback's edition Sept. 1995
| Prozac -- the Toxic Miracle Drug Name: Michelle T Date: 2002-02-25 13:56:06 Link to this Comment: 1150 |
Although Prozac has been on the market since 1988, the initial trial studies that were done on Prozac in order to prove its efficacy were manipulated in order to make the drug pass FDA approval. The drug studies themselves were considerably shady. First of all,
"all FDA drug studies are constructed, supervised, and paid for by the drug companies themselves, using doctors and research teams of their own choosing... Pharmaceutical companies do everything they can to make the studies turn out right" (7). Some people may think that the federal government actually supervises the safety of all the drugs that are screened, but this is not the case. The drug manufacturers themselves do the testing and can therefore pick the doctors who would endorse the drug. These are often people with longstanding relationships with the company. In the Manufacturer's Report of June 1998, Eli Lilly claims: "the efficacy of Prozac for the treatment of patients with depression (>18 years of age) has been studied in 5 and 6 week placebo-controlled studies"(6). There are several major points that are essentially left unsaid by this statement. One might ask is this drug safe for adolescence or the elderly; what are the effects of long-term dosages on the nervous system; was this drug able to prevent suicide in at risk patients? The answer to these questions is that they don't know. The community at large is basically one big guinea pig at the moment with thousands of people on antidepressants. "86 percent of all the patients in all the studies were treated for 'three months or less'"(7). This is inadequate time to monitor the effects on one's body. It will not be surprising if, twenty years from now, someone discovers major damage is done to the liver or the brain. There has already been evidence that Prozac is addictive. In addition to the lack of long-term observations, the trials did not include a large number of people due to their age or severity of illness. "The Prozac studies as designed by Lilly excluded all patients with serious tendency toward suicide... Hospitalized psychiatric patients were also excluded... There were no children or elderly adults in the Lilly sponsored FDA studies of Prozac" (7). The trial studies were biased. What is even worse is the fact that the data from the trials was manipulated. Some data was left out while the rest was pooled together in order to have the studies show that Prozac was effective. In actuality, "the number of Prozac patients who actually completed the four-, five-, or six-week trials used as the basis for FDA approval... turned out to be 286 patients" (7). This is unlike the reported 6,000 people that Eli Lilly claimed they had tested. The FDA approval of Prozac was an atrocity. If there was sufficient investigation into the data of the studies, Prozac may not be on the market today.
Even though Prozac passed FDA approval, the drug continues to be a threat because the dangers of Prozac are extremely understated by health care professionals. Most of the populace does not comprehend the extent of adverse reactions that are linked to Prozac. "By December '95 there had already been reported 35,230 adverse reactions to Prozac - including hallucinations, aggression, hostility, assault, manslaughter, and suicide - resulting in a total of 2,394 deaths" (2). In a time span of seven years there had been over two thousand deaths caused by this antidepressant, yet patients are, most likely, only told of the minor side effects such as nausea, sleeplessness, and loss of libido. Neither is the association with fits of aggression or death indicated as warnings on prescription bottles; nor is it likely told of by the patient's doctor. Yet, indeed Prozac can elevate one's mood to a highly agitated state in which one cannot rationally evaluate the surrounding environment. This may cause the patient to behave irrationally and violently. "In some rare, but much publicized cases, patients on the drug have murdered relatives or others"(1). The fact that these extreme states can occur at all on Prozac is call for concern from at least the patients taking Prozac, if not the public at large. The lack of warnings is also significant when it comes to telling the patient that Prozac and other drugs "cause permanent brain damage at the doses customarily given" (5). These are factors that should be of substantial controversy, yet are most likely not discussed when prompting the patient to take antidepressants.
In addition to the potential harm that the patient is at risk for by simply ingesting the antidepressant, suicidal tendencies may occur due to the improper monitoring or distribution of Prozac and other such drugs. Theoretically, Prozac is administered to individuals who are undergoing therapy so as to help that person deal with certain disturbing issues. Unfortunately, this is often not the case. Many people, especially students, take Prozac as either a "quick fix" or an upper. They use the drug in a way as to continually avoid their problems or to escape from the depressing feelings. Due to the large number of people who experience depressing feelings at some point in their life, professionals may prescribe them with medication instead of therapy. Often times, an appointment with a psychiatrist only lasts twenty minutes. Is that really long enough to thoroughly assess a patient? In addition, doctors who prescribe antidepressants are not limited to psychiatrists. "Because Prozac can be prescribed by all medical doctors, many fear that understaffed and overburdened counselors may be prescribing the drug to lessen their load... The net result: a nationwide culture of collegiate pod people" (4). A detachment from emotion and an estrangement from the everyday world are experienced by some people who take Prozac. With enough people on antidepressants, the world could change drastically. Prozac "inspires a dreamily contented disengagement from the problems of the world. [It also] diminishes any drive to constructive activity" (3). This can be detrimental to society as well as to patients who may be using Prozac as a means to avoid one's issues. The further estrangement felt by a patient can make him or her feel alone and detached from the community. This causes a greater risk of one committing suicide. In fact, Prozac "was implicated in inducing suicidal ideas and behaviors" (1) - the exact conduct it is supposed to counteract. The misuse of Prozac is a direct result of individuals not being informed of the dangers associated with psychiatric drugs. Less people with minor depression would take Prozac and risk themselves to these potential threats if doctors told them of the adverse reactions, such as suicidal ideation and aggression. These drugs have become so commonplace that people consider them to be as safe as aspirin; however, this is certainly not the case.
Prozac, the wonder drug of the nineties, has proven to be both harmful and ineffective, yet it is still readily prescribed to fight depression. During the past fourteen years, one would think that the populace would have discovered this, but there are several reasons why Prozac has been so popular. First of all, the mindset of a person who seeks a psychiatrist's advice is most often desperately yearning for a change in his or her lifestyle. This alone could be the reason for one's improved mood. Attitude is a very powerful tool to becoming well. This may seem euphemistic, but "it's been repeatedly demonstrated that up to fifty percent or more of depressed patients improve on the sugar pill. In some studies, nearly 90 percent have improved on placebo" (7). The person merely thinking that the pill will have some effect on his or her mood drastically can change one's outlook. One other reason that Prozac could be considered effective is that some of the side effects could make a person happier. For example, Prozac is a stimulant, which can boost a person out of the tiredness that most depressed people feel. The positive side effects alone are not good reasons to be having a large percentage of the American society on drugs such as Prozac. There are many natural means to change one's mood such as eating well, taking one's vitamins, getting sufficient sleep, and exercising. It seems today people are more willing to putting themselves at risk by taking antidepressants than they are willing to take care of themselves naturally.
1) Peter Breggin Homepage , "Dangers of Fluoxetine"
3) "Hedweb Good Drug Guide: the Responsible Parent's Guide to Healthy Moodboosters for All the Family",
4) College Magazine, "Numb and Number, How One Little Pill is Changing the Face of College"
5) Antipsychiatry, "Psychiatric Drugs: Cure or Quakery?"
6) "Manufacturer's Report, Eli Lilly"
7) Breggin, Peter. Talking Back to Prozac. St. Martin's Paperback's edition Sept. 1995
| Progressive Supranuclear Palsy: A Neurophysiologic Name: Raquel P. Date: 2002-02-25 14:35:41 Link to this Comment: 1152 |
Progressive Supranuclear Palsy (PSP) is a rare neurodegenerative disorder categorized as a form of parkinsonism. First described in 1964 by three Canadian neurologists, PSP is sometimes referred to as Steele-Richardson-Olszewski Syndrome, or Nuchal Dystonia Dementia Syndrome (1). Progressive damage to multiple brain cells associated with deterioration of the myelin sheath that speeds up nerve impulse conduction, as well as destruction of the entire nerve (2), result in severe and irreversible problems controlling balance, eye movement, breathing, and voluntary muscle movement (3). The actor Dudley Moore has been diagnosed with PSP and presently works to improve awareness and treatment of this enigmatic disease.
Although PSP is frequently misdiagnosed as Parkinson's, the disorder progresses much more quickly, maintaining very unique and exclusive manifestations. Individuals suffering from PSP present clinically with akinetic rigid syndrome, gait ataxia, and supranuclear vertical-gaze palsy (4). Akinesia refers to the loss of control of voluntary muscle movements. This is expressed in loss of balance while walking and recurrent falls. A permanent "Mona Lisa" stare and wide-eyed expression is often described, in addition to guttural, slurred speech and swallowing difficulties (5). These facial distortions result from nerve damage controlling the facial muscles. All PSP individuals suffer from some degree of vertical-gaze palsy, in which the ability to move the eyes up-and-down is impaired (4). Muscles in the back of the neck and spine are usually severely affected, resulting in a retro-collis posture; the individual appears to perpetually look up toward the ceiling. Rigidity in the limbs is also observed, although to a lesser degree. If rigidity does exist here, it is equal on both sides of the body. In Parkinson's disease, rigidity is more prominent and pronounced in the limbs, favoring one side more that the other (6). None of the tremors characteristic of Parkinson's are observed in PSP. Personality changes and dementia are also noted, particularly later in the development of the disease.
PSP affects the brainstem, basal ganglia, and cerebellum. The brainstem controls involuntary movements such as breathing and heart rate. Three divisions of the brainstem have been delineated: the medulla oblongata, the pons, and the midbrain. In PSP, all three sections are affected. The pons controls facial nerves and eye muscles, while the midbrain is the visual center of the brain (3). The medulla (sometimes referred to as the "bulb") maintains speech and swallowing abilities. Paralysis here results in impairment of these functions. Although PSP does not involve true bulbar-palsy, the nerve cells and fibers originating from the bulb are affected, resulting in harsh, grating speech and swallowing complications. Emotional instability is also associated with this pseudobulbar-palsy (6). The basal ganglia, congregations of nerve cells located deep within the brain involved with control of emotion and voluntary movement, are additionally affected. The basal ganglia are important in cortical-subcortical loops for information processing, access to memory, and language (4). Damage here is responsible for the muscle stiffness, or spasticity, experienced by PSP individuals as well as being involved with the numerous cognitive difficulties experienced in concert with the physical complications. The cerebellum, controlling balance and muscle coordination, is likewise affected (3).
Groups of cells called "nuclei" in the brainstem control vision. In PSP, the mechanisms controlling these nuclei (not the nuclei themselves) are damaged, resulting in difficulty with voluntary eye movement (3). The mechanisms include eye movement centers superior to the nuclei in the brainstem. These locations are progressively impaired by prolonged attack, and adjacent areas are also targeted (6). PSP is initially associated with difficultly in moving the eyes downward. However, left-to-right eye movement is additionally limited as the disease progresses. Reflex eye movements remain normal until late in the course of the disease. Blinking may be reduced from the normal 20-30 per minute rate to a 3-5 per minute rate (3). Sometimes blepharo-spasm, or uncontrolled eye-lid tightening, is experienced. It becomes very difficult for the PSP individual to maintain eye contact during conversation at this stage. Individuals with PSP appear to maintain markedly decreased levels of the neurotransmitters dopamine, and dopamine's main metabolite homovanillic acid, in the striatum. The dopamine receptors also tend to degenerate; one reason why Sinemet treatment proves to be minimally effective (6).
Post-mortem examination of the PSP brain reveals moderate to marked atrophy of the brainstem and less marked atrophy of the cerebellum. Gliosis, replacement of normal nerve cells with glial cells, is also appreciated. The dying nerve cells in the brainstem develop entangled, partially crystallized fibers containing tau protein. This type of modification is referred to as neurofibrillary degeneration (6). Neurofibrillary tangles (NFT) are found to be more dense in the supragranular layers than in the infragranular layers. The opposite pattern is observed in Alzheimer's disease. NFT are also found in many of the subcortical nuclei and in the primary motor regions of the isocortex (7).
PSP is estimated to affect ~1.1/100,000 people, in addition to ~5-6 percent of those individuals initially diagnosed with Parkinson's disease. Men are slightly more affected than women (8). Median age of onset is 64 years, with a range of approximately 50-77 years (9). Scientists are unsure of the causes of PSP. There is little evidence that this is an inheritable disease, although pedigrees have been reported. No population or ethnic group is particularly favored. It has been suggested that an unknown virus implants itself into the body and causes presentation of PSP symptoms several years later, although this theory has not been confirmed. More recent genetic studies indicate that an autosomal recessive polymorphism of the tau protein gene may be responsible for some cases of PSP. Metabolic studies are investigating oxidative stress as a possible cause (8). It has been suggested that free radicals, unstable molecules constantly produced by cells in the body, may cause the cellular damage associated with PSP (4). At present, no tests for diagnosing PSP are available. As in Parkinson's disease, blood tests, CT, and MRI scans are usually normal (8).
Many of the drug therapies proven successful in treating Parkinson's disease have shown transient effectiveness in PSP individual. The common dopaminergic drug, levapoda (Sinemet), is sometimes prescribed for PSP to decrease spasicity and ease involuntary movement. The anticholinergic, trihexyphenidyl (Artane), has restored some function to the neurotransmitters. Also, anti-depressants have shown effective in speech improvement, walking, and inappropriate emotional responses (3). The drug "seligiline" has been prescribed in both PSP and Parkinson's disease, although the true effectiveness of this treatment is not presently known. Some evidence suggests that seligiline may inhibit apoptosis, or programmed cell death. Also, calcium channel blockers may be used for their better-understood prevention of apoptosis. In some degenerative neurological disorders, vitamin E has proven slightly helpful in reducing the rate of progression, and may likewise assist in managing PSP. Fetal brain cell implantation and pallidomy, however effective in Parkinson's, has not produced positive results in PSP (8).
Non-drug therapies are equally important in dealing with PSP. Speech therapy reduces some speech and swallowing difficulties. These processes are more affected as the disease progresses, resulting in choking and implantation of small food particles in the lungs, referred to as aspiration pneumonia. Difficulties with eating also could lead to problematic weight loss (3). A gastrotomy is a minimally invasive procedure entailing the placement of a feeding tube through the abdominal wall and into the stomach. This option is usually necessary later in the progression of the disease when swallowing abilities are most encumbered. Weighted walkers are used to prevent PSP individuals from falling backward. Bifocals or prisms occasionally improve the effects of the supranuclear vertical-gaze palsy. Ointments and eye drops are given to soothe dry eyes from infrequent blinking (1).
No one dies from PSP itself. However, repeated contraction of pneumonia from choking on secretions and food products is presently the number one cause of death. Starvation related to difficulty in swallowing is also prevalent. After the first seven years of progression, balance and rigidity problems generally make it impossible for the PSP individual to walk. Although death usually occurs about ten years after the initial symptoms present, if good general health and nutrition are maintained one may survive several years longer (3).
Research efforts by several medical institutions, including the National Institute for Neurological Disorders and Stroke (NINDS) and Johns Hopkins University, are being undertaken to more clearly understand the diagnosis and treatment of PSP (1). Some corollaries may be made with Parkinson's disease and other degenerative neurological disorders, but the significant implications of PSP remain unknown. What I find most curious about PSP is the rapid and extensive nature of the paralysis, coupled with a marginally affected intellect. I can only imagine how torturous it must be to experience such limited ability for movement and expression, yet maintain a high thinking capacity. Hope remains in present medical research and the capabilities of modern technology to generate a treatment for those suffering from PSP.
1)Healthtouch Health Information, Excellent summary of PSP
3)The Gale Encyclopedia of Medicine, A very good summary of the symptoms, treatments, and prognosis for PSP
4)Case Refernces of the Massachusetts General Hospital , Case study of a gentleman suffering from PSP.
5)The Progressive Supranuclear Palsy [PSP Europe] Associatiob
6)Society for Progressive Supranuclear Palsy, Comparison of Parkinson's disease and PSP.
7)Progressive Supranuclear Palsy, A good source for neuropathological and immunohistochemical studies on PSP.
8)Progressive Supranuclear Palsy (NWU), From the Northwestern University Medical School.
9)Progressive Supranuclear Palsy (Steele-Richardson-Olszewski Syndrome), From the Medical College of Wisconsin.
| Physical Brain Abnormality a Possible Cause of Sch Name: Balpreet B Date: 2002-02-25 16:18:45 Link to this Comment: 1156 |
Neuropathologists have been researching schizophrenia for approximately a hundred years. But, even with a hundred years of research, the neuropathology of schizophrenia is still obscure. Although scientists have come a long way since the beginning of research, when they first believed that it was a " 'functional' psychosis, a disorder with no structural basis," the cause of the chronic disease remains a mystery (1). However, with technological advances in science, researchers have found a common trend in diagnosed patients- physical abnormalities of their brains. These revelations cause scientists to wonder if brain abnormalities are a cause for schizophrenia and, if so, how these abnormalities arise.
Schizophrenia has long been considered the "graveyard of neuropathologists" (1). This chronic and disabling brain disease is characterized by a relapsing psychotic disorder that primarily affects the thought and behavior of the affected person. Although symptoms may vary from patient to patient, common ones include disturbances of thought, auditory hallucinations and multiple delusions (2). If all this is known, why is schizophrenia the graveyard of neuropathologists? Although the symptoms are now relatively simple to diagnose, neuropathologists still do not know what causes this disease. Many diseases are caused by genetic, behavioral and other factors, making scientists theorise that this is the cause of schizophrenia as well. However, neuropathologists still do not understand all the factors necessary for schizophrenia to exist (6).
With relatively recent technology of MRI scans, CAT scans, and PET scans, scientists have discovered that many patients with schizophrenia have physical abnormalities in portions of the brain. CT and MRI studies have improved resolution and sophistication of analyzing brain abnormalities in people diagnosed with schizophrenia, allowing many abnormalities to be identified, including ventricular enlargement and decreased cerebral volume. Brain ratio, or VBR, indicates an increase of 20-75% of the lateral ventricle while MRI studies show a median 40% increase in ventricular size. The enlargement of the lateral ventricle is accompanied by an average 3% loss of brain tissue, in which reduction is relatively greater in the axial than the sagittal plane, suggesting a relative decrease in mediolateral breadth and a greater involvement of regions which are typically included in axial slices, such as temporal lobes (1). There are also a few MRI studies which suggest that the thalamus is smaller in patients with schizophrenia; although this evidence is weak, it is complemented by strong neuropathological data.
However, many scientists emphasize that some of the abnormalities researched are quite subtle, in that these abnormalities have been found not to be 1) characteristic of all schizophrenia patients or 2) to occur only in individuals with schizophrenia (5). Also, although the structural pathology has been observed in schizophrenia patients, the brain abnormalities developed do not correlate with the disease duration. Abnormalities found in patients with schizophrenia remain relatively the same throughout the progression of the disease. Researchers have found that VBR and ventricular increase and brain tissue loss do not change drastically in patients with schizophrenia. This suggests that the alterations are largely static, and there is relatively no progression in the reduction of brain tissue, or increase in VBR (1).
Even though these technological advances have allowed neuropathologists to discover that brain abnormalities are characteristic in schizophrenia patients, how do these physical abnormalities develop? Developmental neurobiologists have found that schizophrenia may be a developmental disorder resulting when neurons form inappropriate connections during fetal development (6). However, symptoms of schizophrenia generally appear during adolescence or young childhood, when the body is undergoing the hormonal and physical changes of puberty. It has been suggested that the disease remains "dormant" during childhood, proposing that patients are born with schizophrenia and do not display the symptoms until adolescence, when the disease emerges (3). If this is the case, then perhaps it is the brain and body changes that occur during puberty that arouse the inappropriate connections during fetal development and result in the emergence of schizophrenia. Scientists have in fact discovered patterns of brain development that extend into the teenage years. Prior to this research, neuropathologists had observed brain development in the womb and in the first 18 months of life; but recently researchers have discovered structural changes that occur much later in adolescence (4). With this study, it becomes more likely that schizophrenia remains silent until adolescence, when brain abnormalities are formed during structural changes.
With new scientific technology, research in schizophrenia has been favored in that the discovery of brain abnormalities in schizophrenia patients help the search for the cause of this disease. It has become more likely that schizophrenia remains dormant until adolescence, when structural changes to the brain are being made resulting in the physical brain abnormalities found in patients diagnosed with schizophrenia. However, these recent studies arise some questions on the cause of this disease. What causes these brain abnormalities? Are these abnormalities spontaneous, are they genetic? Schizophrenia has shown hereditary trends; perhaps there is some genetic mutation which causes the abnormal brain development during adolescence. Although the cause is still unknown, the technological advances of MRI scans and CAT scans have moved the research foreword, hopefully finding a cause for this chronic disease in the near future.
1)The Neuropathology of Schizophrenia, a critical review of recent brain abnormality data and its interpretation
2)The Aetiology of Schizophrenia, a description of the possible causes for schizophrenia
3)Schizophrenia, background information concerning this disease
4)Teenage Brain: A work in progress, recent research concerning structural changes of the brain during adolescence
5)Schizophrenia: Questions and Answers, a source answering the most common questions about this disease
6)Schizophrenia, basic information on schizophrenia
| Adderall, Ritalin, AD/HD, and Abuse Name: Michele Dr Date: 2002-02-25 18:03:47 Link to this Comment: 1162 |
Attention Deficit Disorder and Attention Deficit Hyperactivity Disorder are behavioral disorders affecting attention span, impulse control, and self-discipline. They are usually associated with children, although adults can suffer from the same disorders. It is estimated that 4% - 6% of the U.S. population suffers from AD/HD, and children with the disorders carry them into adulthood more than half the time. Typically medicated with psychostimulants such as Ritalin or Adderall, (methylphenidate and dextroamphetamine, respectively), concern over these disorders surrounds problems such as over-diagnosis or misuse of the prescription medications.
ADD is characterized by an inability to concentrate, poor self-control, and short attention span. ADHD is essentially characterized by the same deficiencies except it includes hyperactivity and impulsiveness. The two are generally grouped together in the acronym AD/HD and are treated the same way, although each diagnosis can be labeled with a subtype of predominantly inattentive type, predominantly hyperactive-impulsive type, or a combination type. Treatment involves psychological, educational, and social remedial measures along with medication, but frequently the more time-consuming efforts for treatment are disregarded in today's impatient world, with parents and patients hastily looking to medication for a quick solution.
Ritalin is the brand name for methylphenidate hydrochloride, a stimulant which was introduced in 1956 and affects the way the brain filters and responds to stimuli. This can be helpful to a person with AD/HD who feels bombarded by stimuli and is easily distracted. Although its workings are still largely not understood, methylphenidate helps the brain to focus more selectively, and is therefore often prescribed for AD/HD.
In addition to increasing attentiveness, methylphenidate increases energy and a feeling of well being, and comfort, and often causes the user to become more loquacious. Other short term effects include faster heart rate and breathing, increased blood pressure, dilated pupils, dry mouth, perspiration, and a feeling of superiority. More severe side effects include aggression and hostility, or even strange, incessant behavior. Flushing, tremors, and hallucinations are common of overdose. The effects of methylphenidate are often likened to those of cocaine and studies have shown similarities in the two. Both drugs have the ability to block dopamine transporters. The reuptake of catecholamines noradrenaline and dopamine are blocked, leaving them in the synapse in increased concentrations, promoting the elevation of mood and the feelings of alertness, well-being, verboseness, or superiority (1). In addition, a study using baboons showed that the regions of distribution of methylphenidate and cocaine in the brain are similar, and there is competition for binding sites between the two on the post-synaptic terminal (1).
In 1996, the FDA approved Adderall, a combination of mixed amphetamine salts amphetamine and dextroamphetamine, for the treatment of AD/HD. Adderall is an alternative medication to Ritalin (methylphenidate), and is often prescribed as the Plan B when Ritalin is not effective. With duration in the brain lasting twice as long as methylphenidate, Adderall can be administered half as frequently and is advantageous to parents who would prefer to avoid in-school doses.
Like methylphenidate, this amphetamine combination may improve attention span, self-control, and the ability to concentrate. The cocaine-like feelings of courage and superiority are not as common in higher doses of Adderall as they are with methylphenidate, but the amphetamines of Adderall often improve the mood and productivity similarly to methylphenidate. Instead of blocking the dopamine reuptake, amphetamines trigger the release of more dopamine and noradrenaline.
However, the question lingers: Does giving amphetamines to kids make sense? Interestingly enough, CNS stimulants such as Adderall are known to decrease hyperactivity and aggression in children, while in adults they more frequently lead to increased motor activity, the common result for which they are usually known. The marketing strategies of this drug must be clever enough to differentiate Adderall from the alarming word 'amphetamine,' to relieve the concerns of parents associating the amphetamines in Adderall with the threatening cousin methamphetamine, whose name is associated with crank addicts and dangerous street speed. The difference is subtle, the addition of a methyl group on the amphetamine molecule gives the molecule better fat solubility and therefore somewhat quicker entry in the brain (4).
All this is fine for the 3rd grader who can't concentrate on his math homework, but what about adults suffering from AD/HD in an age of more responsibility? And with all these advantageous side effects, who couldn't use a little improvement in their concentration, productivity, and mood? Diagnoses of AD/HD and subsequent prescriptions of psychostimulants for adults are subject to rigorous clinical exams, involving psychiatric histories and histories of school, employment, health, and behavior patterns throughout their life, as well as psychological tests evaluating memory, attention, and intellectual function (5). The stringency of the basis for adult prescription causes many adults desiring the benefits of these psychostimulants to turn to the black market, where the illegal resale of Ritalin and Adderall provides a less guilty form of street cocaine or speed.
A major demographic of people who abuse or illegally obtain these drugs are college and graduate school students, with their attention spans and motivation waning in the long, late hours of all-nighters and cram sessions. Often pills are crushed and snorted, providing a quicker and stronger effect, which has been a major push for the latest releases of these psychostimulants to be manufactured in time release capsules, making it difficult to crush them into powder for snorting. Adderall and Ritalin are also becoming popular as party drugs on college campuses, high school scenes, and at raves, where they are combined with other drugs such as ecstasy to enhance the effects (6). Excessive recreational abuse can cause users to become irritable and withdrawn from normal social interactions, experience insomnia and depression, and seem vacant to their friends and family--much like the long term effects of cocaine or amphetamine abuse.
With psychostimulant prescriptions and their popularity rising in recent years, parental reports of abnormal behavior and concerns of overdiagnosis have been growing. However, according to the Journal of the American Medical Association, the percentage of patients being treated for AD/HD does not exceed the estimated percentage of the population thought to have the disorder (7). Still, although not necessarily receiving treatment, many people may be led to believe they have AD/HD by over-concern of related symptoms of which most people suffer to some degree. For example, the author of this paper was determined to be a potential candidate for AD/HD by the short self-exam link cited in reference (8).
Although the severity of symptoms leading to the diagnosis of AD/HD may be ambiguous to some, treatment via prescription is highly regulated by the DEA. The dopamine reuptake block or trigger of release is neurochemically similar to SSRIs like Prozac and the once prescription, now illegal mood-enhancing drug MDMA (ecstasy), with the exception of seratonin for dopamine. Everything in moderation--methylphenidate and amphetamines can be beneficial for academic focus, but dangerous if their guidelines are not respected.
1)Biopsychiatry, Methylphenidate/Cocaine Comparisons
2)CHADD Children and Adults with Attention Deficit/Hyperactivity Disorder,
3)National Attention Deficit Disorder Association,
| Bipolar Disorder Name: Kathryn Fo Date: 2002-02-25 19:44:31 Link to this Comment: 1169 |
It is generally understood that everyone has good and bad days. A phrase people are familiar with is "everyone has their ups and downs". Most people, to a certain extent, are able to control their moods, whether it is good or bad. However, people who suffer from bipolar disorder sometimes are unable to control their moods. People with bipolar disorder experience sudden and, at times, severe mood swings, shifting from manic to depressive moods. Bipolar disorder is not gender bias; both men and women are equally susceptible to it (3). About 1% of adults and children suffer from bipolar disorder, but this figure is probably not accurate because bipolar disorder is difficult to detect and is often misdiagnosed. The misdiagnosis often leads to the mistreatment of the disease (1).
People affected with bipolar disorder suffer from both mania and depression, experiencing manic symptoms, or extreme highs, and then suddenly experience depressive symptoms, or extreme lows. In between these mood swing episodes are periods of normal mood. The depressed mood often lasts longer than the manic mood, however, the duration of episodes vary from person to person. If left untreated, episodes can last from several days to several months. Some symptoms of mania are: increased energy, restlessness, rapid speech, racing thoughts, excessive euphoria, uncharacteristically bad judgment, denial, overspending money, and risky behavior. Some symptoms of depressions are: persistent sadness and anxiety, feelings of guilt, hopelessness, and pessimism, increased fatigue, loss of interest and pleasure, difficulty in concentrating and decision making, change in appetite, and thoughts of death and suicide. Sometimes, sufferers experience mixed episodes, when they feel both manic and depressive symptoms simultaneously (1).
Bipolar disorder can be classified into two categories, depending on the severity. Bipolar I disorder is used to classify sufferers who experience at least one mania or mixed episode each episode, and may or may not suffer from depression. Bipolar II disorder is used to classify sufferers who experience at least one depressive episode and at least on hypo mania (less severe than mania) episode. Those classified with bipolar II disorder do not experience a full manic episode or mixed episode. There are also different subtypes of bipolar disorder, depending on the frequency of the episodes. A person suffers from rapid cycling when he/she experiences four or more episodes per year. Ultra rapid cycling is similar to rapid cycling except the episodes occur more often, experiencing four or more episodes per week. Sometimes the occurrence of episodes may be predictable, or exhibit some sort of pattern. One of the patterns observed is the seasonal pattern. Observations show that the season, often spring or summer, affect the onset of episodes (1).
The cause of bipolar disorder is not completely known. Researches agree that there is a genetic component linked to the disorder. Studies show that first-degree relatives of people affected with bipolar disorder are about seven times more likely to develop bipolar disorder (4). Twin studies show if one identical twin has bipolar disorder, the second one has a 70% chance of developing the disorder within his/her lifetime. Despite the observations made, no specific gene has been located for the cause of bipolar disorder (5).
Molecular genetic researches hypothesize the cause may be abnormally programmed death among cells within the brain. Researchers are studying the affects of two chemicals used to treat bipolar disorder, lithium and valproate. Both these chemicals regulate the expression of a certain protein, the cytoprotective protein bcl-2, in the frontal cortex and hippocampus region of the brains in rats. Coincidentally, neuroimaging has shown that in that same region of the brain, affected individuals have a prominent number of cell loss. Based on these observations, researchers concluded that this abnormally programmed cell deaths might affect the expression of certain proteins, which in turn affect the critical brain circuitry that regulates emotions. Based on this hypothesis, antidepressants and mood stabilizers function by enhancing the cell survival pathways and improving cell resiliency (4).
The function of certain neurotransmitters has also been studied in relation to bipolar disorder. An electrical signal is needed for an action potential to travel across an axon of a neuron. The electrical signal is caused by a positive ion influx. Treatments for mania block the calcium channels of cell membranes. This shows that the different mood swings may be due to a disruption in calcium concentration in the neurons. A disruption in the neuron may also cause a disruption in the neurotransmitters. Those who suffer from bipolar disorder are shown to have an alteration in certain neurotransmitters. Some of these neurotransmitters include noradrenaline, dopamine, serotonin, and acetylcholine. Other factors such as drug abuse, head injury, and the surrounding environment are also speculated to influence the development of bipolar disorder (3).
Typically, drugs are used in combination of psychotherapy to treat bipolar disorder. Mood stabilizers are the standard form of drug treatment, and are used to treat manic, mixed, and hypo manic episodes. Lithium is the oldest and most prescribed mood stabilizer. It is usually the first drug prescribed after initial diagnosis of the disorder. In addition to mood stabilizers, anxiolytic may be prescribed to treat anxiety and insomnia, which is experienced during manic episodes (2). Anti-depressants are prescribed to treat depression. Some examples of anti-depressants are Tricycle's, SSRI's (Selective Serotonin Re-Uptake Inhibitors), and MAOI's (Monoamine Oxidase Inhibitor). For severe depression, ECT (Electro Convulsive Therapy) is used. Anti-depressants are usually taken in company with mood stabilizers, since taking anti-depressants alone can cause the patient to shift into a manic episode. Hospitalization may be necessary for additional supervision because affected people often feel suicidal or delusional (5).
Humans are complex organisms, unique from the other organisms of the animal kingdom. Humans are able to control their moods and thoughts. However, diseases like bipolar disorder takes this control away. It is diseases like this one which makes us reexamine the whole concept of brain=behavior. During manic-depressive episodes, the person control, and seems that a force more powerful than the person takes over his/her body and mind. It is uncertain to me if this "force" is the brain, or a force that overrides the brain. Since the cause of bipolar is still not completely known, my uncertainties and questions cannot be thoroughly answered.
WWW Sources
1) What is bipolar disorder?, on the Bipolar Home website
2)Mania, on the Bipolar website
3)Bipolar Education website
4)eMedicine Journal
5)Bipolar Home website
| Schizophrenia Name: Caitlin O' Date: 2002-02-25 20:35:15 Link to this Comment: 1171 |
It is a frightening disorder that strikes about one percent of the world population. It surfaces most frequently during puberty and has the potential to forever destroy the lives of the people who are unfortunate enough to be its victim. The disorder is schizophrenia and it manifests itself by disturbing normal psychiatric behavior. The symptoms of schizophrenia are characterized by both positive and negative symptoms. Positive symptoms include hallucinations, delusions, and other unusual or disorganized behavior. Unresponsiveness, lack of activity, and loss of interest characterize negative symptoms. Though it is possible for doctors to diagnose and treat patients with schizophrenia, the causes of schizophrenia are still unknown. Much research has been done to further the understanding of the disorder, yet it seems that the causes of schizophrenia are still under debate. (1)
According to recent research there are several things that can cause schizophrenia. Genetic makeup among individuals affected by the disorder seems to be a significant factor. The probability of an offspring with two unaffected parents developing schizophrenia is only one percent, yet this probability increases to thirteen percent among people with one affected parent. Offspring that have two schizophrenic parents have a 35 percent chance of developing the disorder. (1)
The environment surrounding an individual also can trigger the onset of schizophrenia. It has been observed that family stress, trauma, and poor social interactions all have the tendency to promote schizophrenic behavior, though it does not necessarily cause it. Going along with this, it is also possible that prenatal conditions affect the development of schizophrenia in offspring. Viral infections, malnutrition, and birth complications have been cited as other possible causes of schizophrenia. (4)
Perhaps what is most convincing, though, are the recent links made between schizophrenia and chemical imbalances in the brain. There are four main hypotheses that support the theory that biological chemistry is responsible for causing schizophrenia. The first is named the Membrane Hypothesis. Observations of persons suffering from schizophrenia suggest that a defect or impairment in nerve cell membranes could affect how neurotransmitter receptors send messages across the nerve synapses. Also, there is evidence of decreased enzymes and fatty acids among schizophrenics. (2)
A second hypothesis is the Single-Carbon Hypothesis. This theory explains that the single-carbon folate serves as a metabolic pathway for several reactions in the brain. One of these reactions is the synthesis of methionine. It has been found that methionine metabolism is defective in many sufferers of schizophrenia. This suggests that folate is somehow related to the disorder, though exact relationship remains unknown. (2)
The NDMA Receptor Hypothesis is another suspect in the search for the cause of schizophrenia. According to research, it is possible that NDMA receptor dysfunction may induce schizophrenic symptoms due to the fact that NDMA receptors operate with glutamate, an excitatory neurotransmitter. Drugs that affect NDMA receptors, such as ketamine and phencyclidine, have been found to produce hallucinations. Also, neuroleptic drugs like clozapoine have the ability to prevent hallucinations, therefore providing further evidence to support this theory. (2)
A final hypothesis is the Dopamine Hypothesis. By far it is the most supported of all the hypotheses in the modern scientific field of neurobiology. Dopamine is a neurotransmitter in the brain that allows nerve cells to send messages to one another in order to control certain behaviors. It has been hypothesized that there is an increased level of dopamine in the brains of schizophrenics, therefore causing mainly positive symptoms such as delusions and hallucinations. Though the exact relationship between dopamine receptors and the drugs that curb schizophrenic symptoms remain unknown, studies have shown that the best drugs to treat schizophrenia are ones that block excess amounts of dopamine from being produced in the brain. Therefore, neurobiologists suspect that dopamine plays an essential role in the causes of schizophrenia. (3)
After researching schizophrenia, it is apparent that there is no clear answer to the question of what causes the psychiatric disorder. Rather, there is much debate about the four hypotheses that seem to dominate the scientific community as of late. Many researchers believe that schizophrenia may be a combination of all or some of the hypotheses. Whether these hypotheses are true or not, it is important that more research be done to become less wrong in the understanding of schizophrenia.
1)“An Introduction to Schizophrenia”,
3)“The Role of Dopamine Receptors in Schizophrenia”,
| Reliving the Nightmare: Post-Traumatic Stress Diso Name: Amy Cunnin Date: 2002-02-25 20:48:37 Link to this Comment: 1173 |
After the terrorist attacks on September 11th, horrific images of the towers collapsing, survivors fleeing, and the rescue and recovery efforts inundated television viewers. In the weeks following the attacks, numerous news accounts reported increasing general anxiety among Americans, with many individuals reporting sleep difficulties and trouble concentrating. Additionally, much attention focused on the effects on those who directly witnessed and/or were injured the attacks, and whether they would suffer from post traumatic stress disorder, also known as PTSD (4). I will give a brief overview of the definition of PTSD, the neurobiology behind it, and what environmental factors may put certain people at heightened risk for developing the disorder.
Post traumatic stress-disorder is an anxiety disorder which results from exposure to an event which threatens the physical safety of an individual (1). PTSD originated as a mental illness category after the Vietnam War, when veterans exhibited sets of symptoms that did not fit into any current illness categories. However, in previous wars soldiers had complained of "shell shock" or "combat fatigue," which researchers now believe were essentially the same conditions as PTSD (2). As many as thirty percent of Vietnam veterans and eight percent of Persian Gulf War veterans exhibited symptoms of post-traumatic stress disorder (1).
Today the definition of PTSD has broadened to include not just those in combat, but people who have experienced any man-made or natural disasters, accidents, violent crime such as rape, and abuse. Symptoms may include flashbacks, nightmares, depression, anxiety, sleep problems, emotional detachment, anger, or guilt. In addition to emotional symptoms, physical symptoms such as chest pain, headaches, gastrointestinal problems, and generalized pain may occur. These symptoms must last for more than a month to be diagnosed as PTSD. Certain environmental cues that are reminiscent of the traumatic event may trigger symptoms, and anniversaries of the trauma are often difficult (1).
The biological roots of post-traumatic stress disorder also partly lie in serotonin. Serotonin is a neurotransmitter involved in such functions as hunger, aggression, sleep, and fear response. The neurons that produce serotonin have raphe nuclei in the brain stem and extend to other parts of the central nervous system, including the amygdala, a small, almond-shaped portion of the brain that controls fear response. Anxiety results in lower levels of serotonin (5), and these lower serotonin levels may act on the amygdala in some way to help produce the symptoms of post-traumatic stress disorder. The National Institute of Mental Health and the Anxiety Disorders Association of America co-sponsored a recent conference at which researchers declared that "circuits involving the central nucleus of the amygdala appear to process conditioned fear responses to specific stimuli, while circuits involving a closely related area, the bed nucleus of the stria terminalis, handle non-cue-specific, non-conditioned anxiety. Both circuits, in turn, connect to the hypothalamus , brainstem, and other brain areas mediating specific signs of fear and anxiety." However, further research on the amygdala's specific role in fear response is needed in order to understand its role in PTSD (6).
Also, traumatic events cause changes in norepinephrine and cortisol levels, which contributes to PTSD symptoms. Norepinephrine is a neurotransmitter that acts on the hippocampus, which is responsible for long-term memory storage. Norepinephrine is released in stressful situations and is present at elevated levels in individuals with PTSD. Additionally during stressful situations the hormone cortisol, which controls norepinephrine's action, is present in lower levels. As a result, in traumatic situations an elevated, less regulated level of norepinephrine acts on the hippocampus, resulting in especially vivid, long-term memories that affect PTSD sufferers (1).
Environmental factors also play an important role in the development of post-traumatic stress disorder. In the United States about 3.6 percent of 18 to 54 year-olds have PTSD (1). In the case of September 11th, approximately 70-100,000 New Yorkers were thought to be at risk of developing the disorder. Scientists believed that the number after a disaster such as the World Trade Center would be higher than for a natural disaster such as an earthquake because experiencing "deliberate violence" is generally more traumatic (4). Additionally, individuals who have previously experienced abuse or other types of trauma would be more at risk of developing PTSD after a second exposure to trauma, and women are twice as likely to develop PTSD as men (1).
Also, overall non-whites are more at risk of developing the disorder than whites. For instance, African- Americans are more likely to witness or be victims of violent crime than whites. One study found that 25 percent of African- American children who had been exposed to violence met the criteria for PTSD. Native Americans are also more likely to be exposed to violence than whites, and as a result have a PTSD rate of 22 percent. Among Asian-Americans, those who came to the United States as refugees have a particularly high chance of having post-traumatic stress disorder because of violence witnessed in their home countries and the trauma of being uprooted. For example, one-half of Cambodian adolescents who had been held in Pol Pot's concentration camps had PTSD. Similarly, Hispanic refugees from Central America have PTSD rates ranging from 33 to 60 percent (3).
The high rates among non-whites may also be worsened by a lack of access to treatment resources or a discomfort with seeking treatment from primarily white caregivers (3). However, early intervention is essential in successfully treating PTSD, since talking about the event soon after is thought to reduce the severity of symptoms. Therapists also use group therapy and exposure therapy, in which the individual gradually works through the traumatic experience again in order to confront their anxiety (1). Additionally, antidepressants such as selective serotonin reuptake inhibitors have been effective in treating PTSD, in part because individuals with PTSD often have other anxiety disorders, depression, and drug and alcohol problems that may be partly alleviated through antidepressants (1). However, further studies are needed to develop more effective medications, such as drugs that specifically target the amygdala (6).
In recent years awareness of PTSD has greatly increased as it has moved from general definitions such as "shell shock" to an official clinical condition with known symptoms and treatment. Researchers have uncovered biological bases for the disorder in the action of norepinephrine on the hippocampus and of serotonin on the amygdala. However, in treating the disorder therapists must be sensitive to the greater effect of trauma on women, and environmental factors such as the type of trauma experienced and previous exposures to traumatic events, as well as the co-occurrence of PTSD with other mental illnesses.
WWW Sources
1);National Institute of Mental Health information sheet on PTSD.
2)About.com website , On PTSD, with definitions and links to other web resources.
3) Surgeon General's Report: "Mental Health- Culture, Race, Ethnicity" . A supplement to "Mental Health: A Report of the Surgeon General 1999."
4) Scientific
American . Article on September 11th and PTSD.
5)
6)Anxiety
Cal State-Chico website on serotonin.
Disorders Treatment Target: Amygdala Circuitry" from the ADAA 18th annual
meeting.
| What is Addiction, and What Causes it? Name: Tara Monik Date: 2002-02-25 22:52:45 Link to this Comment: 1178 |
When a mother brings her young son along with her to a methadone clinic for her daily dose, each nurse and staff members looks upon the little boy with worry. Is this child in risk of falling into the same patterns simply because his mother will find it difficult to teach him differently? Or, is he predisposed to drug dependence due to his own DNA? While drug dependency has not yet been reduced to a few "undesirable" genes in the human genome, most, if not all, scientists will agree that the risk of drug dependence is largely heritable. Why does drug dependency depend on genetics, and are there environmental factors as well?
The first step towards understanding drug addiction is finding an acceptable definition of the affliction. Drug addition can be defined as a "compulsion to use alcohol and other drugs and the occurrence of withdrawal symptoms related to nervous system hyper excitability" (1). The nervous system grows dependent on the drugs in order to function, which creates a psychological need for the drugs. How does this develop?
Heroin, which is just one example of a drug to which the body can develop an addiction, originates from the juice of the opium poppy. It's effects the body's opiate receptors in the central nervous system act to reduce painful sensations. The opium receptors are proteins, which are located on the face of neurons along the nervous system (2). Researchers found through experiments with radioactive naloxone that the heroin binds to these receptors and in turn inactivates them. Heroin does this by mimicking natural molecules in the brain, such as endorphin and enkephalin, which also inhibit the receptors (2). Therefore the body grows accustomed to not making any of the natural products itself and becomes dependent on the drug in order to feel comfortable and relaxed. Withdrawal can set in as soon as 8 hours after previous heroin use, and can include any of the following symptoms: drug craving, restlessness, muscle and bone pain, insomnia, diarrhea and vomiting, kicking movements, goose bumps, and depression (3).
One question that arises from this discussion is, if heroin produces these effects on the central nervous system, then why are some people more likely to become addicted than others? Wouldn't everyone eventually become addicted to the drug? One possible answer to this question is that while everyone has the potential to develop a heroin dependency, some people may be more likely to do so, or may have a more severe problem with the addiction. For example, some people may have greater difficulty synthesizing endorphins and therefore would have more trouble forcing their bodies to make it on its own. In addition, some people are more likely to fall into depression which influences drug use. If a person has high cortisol levels to begin with (which influence depression), he or she may become more severely depressed and therefore have a more difficult withdrawal period (4).
It is also possible that heroin addiction is similar to alcohol dependence, which has been found to be genetic. For example, children of alcoholics are said to be 4 times as likely to become alcoholics as opposed to people without family history of alcoholism. However, part of this amount of risk can be accounted for by environmental influence.
In a study in Sweden, the alcohol habits of identical twins that were adopted and reared apart were examined. The incidence of alcoholism was slightly higher among people who were exposed to alcoholism only through their adoptive families. However, it was dramatically higher among the twins whose biological fathers were alcoholics, regardless of the presence of alcoholism in their adoptive families (4). This study suggests that alcoholism is influenced by biology and slightly by environment.
In another study being performed by Dr. Henry Kranzler of UConn Health Center, subjects are tested on their delay discounting rates (5). Delay discounting indicates whether people are likely to be able to wait for a period of time for a larger monetary reward, or whether they will take a smaller amount of money without being able to wait. For example, subjects are offered either 10 dollars today or 50 dollars in 2 days. The choices that they make demonstrate the type of personality they have, and whether they are more likely to fall into dependent habits such as drug addictions. These personalities have been found to be genetic, which could also link addiction to genetics (5).
The link between drug abuse and genetics seems to be one that is difficult to ever fully examine. However, drug abuse is probably influenced by a balance of genetic predisposal as well and environmental persuasion. While it may be possible for anyone to become dependent on alcohol or heroin, some people are more likely to develop an addiction than others. As Terence T. Gorski writes, "genes and environments are locked together in complex loops that affect each other. Certain environmental conditions stimulate the activity of certain genetic traits. Other environmental conditions inhibit the activity of certain genetic traits" (6). This means that genetics provides tendencies to act a certain way, yet these tendencies need to be activated in order to function properly. If the young boy had never been exposed to heroin, he would most likely never have a problem with a heroin addiction. However, the influence of his mother's addiction may activate his own disposal to a heroin dependency.
| Drug Addiction: A Brain Disease? Name: Nicole Pie Date: 2002-02-25 23:10:53 Link to this Comment: 1182 |
When people hear the words drug addict, these words have negative connotations and stigmas attached to them. People visualize a person who does not care about anything, including family, work, or commitments, except for obtaining money to buy drugs to get high. However, there are many people who are drug addicts that maintain a normal, functioning life. Before we can examine why these people are addicted to drugs, one must first define the word addict.
George F. Koob defines addiction as a compulsion to take a drug without control over the intake and a chronic relapse disorder (1). The Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association defined "substance dependence" as a syndrome basically equivalent to addiction, and the diagnostic criteria used to describe the symptoms of substance dependence to a large extent define compulsion and loss of control of drug intake (1). Considering drug addiction as a disorder implies that there are some biological factors as well as social factors.
There are many biological factors that are involved with the addicted brain. "The addicted brain is distinctly different from the nonaddicted brain, as manifested by changes in brain metabolic activity, receptor availability, gene expression, and responsiveness to environmental cues." (2) In the brain, there are many changes that take place when drugs enter a person's blood stream. The pathway in the brain that the drugs take is first to the ventral tegmentum to the nucleus accumbens, and the drugs also go to the limbic system and the orbitofrontal cortex, which is called the mesolimbic reward system. The activation of this reward system seems to be the common element in what hooks drug users on drugs (2).
Drugs seem to cause surges in dopamine neurotransmitters and other pleasure brain messengers. However, the brain quickly adapts and these circuits desensitize, which allows for withdrawal symptoms to occur (3). Drug addiction works on some of the same neurobiological mechanisms that aid in learning and memories (3). "This new view of dopamine as an aid to learning rather than a pleasure mediator may help explain why many addictive drugs, which unleash massive surges of the neurotransmitter in the brain, can drive continued use without producing pleasure-as when cocaine addicts continue to take hits long after the euphoric effects of the drug have worn off or when smokers smoke after cigarettes become distasteful." (4)
Since memory and pleasure zones are intertwined in the brain, many researchers have been using psychological approaches to stop drug use. Many rehabilitation centers have used classical conditioning to rehabilitate drug addicts. They combine exposure to drugs combined with cognitive scripts, like statements how drugs have destroyed a person's life or what can be accomplished without using drugs, according to DeLetis (5). By using classical conditioning, the drugs addicts pair the drugs with negative connotations and properties. "Adverse withdrawal symptoms can function as an instrumental negative reinforcer and can be linked to the opponent process theory of motivation." (6) However, drug addicts may relapse and start using again because of many environmental "cues", which are external forces that are associated with drug use in their lives. When the drugs addicts see these cues, their brain circuitry, especially the orbitofrontal cortex become hyperactive and causes these people to start craving drugs again (2). No matter how successful the rehabilitation treatment is, once those "cues" are around, the drug addicts remember how pleasurable the drugs felt and relapse into drug abuse again.
Through all of the research done about drug addiction and its affects on the brain, one can see how drug addiction is considered a brain disease. Drug addiction is a disabling disease and can ruin a person's life. By taking drugs, a person's brain becomes "rewired" to tolerate high amounts of dopamine neurotransmitters, but once those high amounts of dopamine cease to exist, the person experiences withdrawal symptoms. However, there are ways drug addicts can control their drug intake by using classical conditioning techniques, which allows them to associate drugs with negative attributes.
1) Neurobiology of Addiction: Toward the Development of New Therapies
2) Addiction Is a Brain Disease, and It Matters
3) Beyond the Pleasure Principle
4) Getting the Brain's Attention
5) Provider Uses Exposure Response Therapy for Addiction
6) Neurobiological Mechanisms of Nicotine Craving
| Webpaper #1: The bipolar brain and the creative mi Name: Sarah Eber Date: 2002-02-25 23:32:26 Link to this Comment: 1183 |
“Our hospital was famous and had housed many great poets and singers. Did the hospital specialize in poets and singers, or was it that poets and singers specialized in madness? …What is it about meter and cadence and rhythm that makes their makers mad?” (1)
The link between madness and creativity is one that has been hotly debated in both medical and literary circles for a long time. The two most common types of mental illness theorized to be an influence on creative people such as writers, artists, and poets were schizophrenia and bipolar disorder (2). However, various studies comparing the characteristics of schizophrenics, bipolars, and writers have concluded that schizophrenics do not share a common thought process with writers (2). In comparison, a study conducted at the University of Iowa declared that while both bipolar patients and writers tended to “sort in large groups… arbitrarily change starting points, or use vague distantly related concepts as categorizing principles” (p 107), the two differed in their abilities to control their thoughts (2). Where the exactly this line of control is located – or indeed if there is a line at all – is the debate in question.
Bipolar disorder, also called manic depression, is a complex and often cruel illness that takes sufferers on a rollercoaster ride of emotional highs and deep depressions. During the mania period, either euphoria or irritability manifest themselves, and sometimes a combination of the two, called “mixed mania”(3). A person in a manic phase can also exhibit symptoms known to physicians as the DIGFAST symptoms: distractibility is heightened; insomnia is present due to increased energy; grandiosity occurs in delusions of godliness or omnipotence; flight of ideas speeds up thought processes; activity is greatly increased; and thoughtlessness results in sexual promiscuity and/or shopping sprees (3).
The other half of bipolar disorder is that which accounts for the great number of suicides among the ranks of bipolar patients: depression (3). Roughly 20% of bipolars committed suicide before effective treatments for the ailment became available (2). Depression is characterized by such symptoms as feelings of exhaustion, sleeping either much more or much less than usual, lowered self-worth, lowered enthusiasm for life, and contemplation of suicide (3). These depressions can last as long as six months to a year. They are frustrating and frightening to deal with, for unlike other forms of depression there is often no cause for the reversal in mood (3). Patients can cycle rapidly through depressive and manic phases, from four times a year to as often as three or four times a day (3).
Manic depression can also be associated with such behavioral problems such as attention deficit disorder (3). Other problems that can appear as a result of the disease are addiction to drugs and alcohol as an attempt to “self-medicate,” using depressants like alcohol to slow down the manic thought process or using stimulants such as cocaine to attempt to prolong the sense of euphoria also associated with a manic phase (2). Most frightening of all, the disease has been found to be genetic; if one identical twin is bipolar, the other is 80% likely to suffer from it, whether the two are raised together or apart (4). While some people become violent while they are manic, these are usually patients with a very severe form of bipolar disorder (4). Most artists and writers diagnosed with bipolar disorder have a milder form of the disease, sometimes called hypomania (4). Patients with hypomania are subject to the same symptoms as mania except at a much lower intensity; combined with mild depression, these two result in a condition called cyclothymia, itself a milder form of the fully formed manic-depression that often follows it later in the patient’s life (2).
Artists and writers are often subject to these fluctuations in mood, accompanied by sudden periods of productivity. Nancy C. Andreason, a psychiatrist at the University of Iowa, conducted a study that began in the 1970’s to discover the link between bipolar disorder and writers (4). For the next 15 years she collected data on a group of 30 writers; as of the time of publication of the article, 43% of the writers had been diagnosed with manic depression, as opposed to 10% of the control group (4). More unsettling still, two of the 30 writers in the sample group had committed suicide during the time of the study (4). A similar study found that 33% of artists and writers said that they experienced acute mood swings; this subgroup was made up mainly of poets and novelists (4).
Writers have reported these rapid changes in mood in their own works. As Robert Burns wrote, “Day follows night, and night comes after day, only to curse him with life which gives him no pleasure” (2). William Cowper, a poet who in the 1700’s was thrown into an asylum due to the severity of his illness, describes his depression as if “a thick fog envelops every thing, and at the same time it freezes intensely” (2). Equally compelling are the descriptions of the mania that is twin to this deep depression, the irrational urges and speeding thoughts that wreak havoc on both mind and body of sufferers such as Theodore Roethke: “Suddenly I knew how to enter into the life of everything around me… All of a sudden I knew what it felt like to be a lion. I went into the diner and said to the counter-man, “Bring me a steak. Don’t cook it. Just bring it.” So he brought me this raw steak and I started eating it” (2). Yet those who suffered this swiftly flowing madness could describe their experiences so beautifully, as John Ruskin did: “I saw the stars rushing at each other…Nothing was more notable to me through the illness than the nerves… and their power of making colour and sound harmonious as well as intense” (2).
There are lists upon lists of those artists and writers who experienced the glorious highs and lethargic lows of bipolar illness. Virginia Woolf, John Berryman, and Robert Lowell are just a few on a long list of well-known writers (5); Tchaikovsky, van Gogh, and Pollock add composers and painters to the list of bipolar sufferers (6). This extensive documentation of writers’ own experiences with mood fluctuation is highly convincing of the link between bipolar illness and a creative temperament. Combine those writings with the overwhelming results of studies that find a far greater incidence of manic depression among artists and writers than among the general population, and the link is as well-established as a scientific truth can ever be.
This conclusion, however, leaves us with a few very pressing questions. These days, the automatic response to a diagnosis of manic-depression is to medicate the patient (3). While doubtless this creates a calmer life for both the patient and those around him or her, it is often doubtful whether the patient leads a happier life while on medication. As is described by a bipolar teenage girl on lithium: “How can I tell them I LIKE being high? …I feel dull. I feel robbed of my creativity. I feel robbed of who I am, or rather who I was” (7). From a slightly different perspective, is society better off with these artists and writers medicated? Psychiatist Joseph J. Schildkraut of Harvard Medical School studied the lives of 15 artists in the mid-1900’s; at least four had committed suicide (8). Even with these casualties, Schildkraut maintains, “Yet depression in the artist may be of adaptive value to society at large” (8). How would the literary world have changed without the mad genius of Virginia Woolf, Sylvia Plath, F. Scott Fitzgerald? Is it fair to allow a writer or artist to sacrifice their emotional stability or even their lives for the creation of new art? Where do we draw these lines between the public and the private good?
2) Jamison, Kay Redfield. Touched with Fire: Manic-Depressive Illness and the Artistic Temperament. The Free Press: New York, 1993.
3)Medscape article, facts on bipolar disorder
4)An article on the Pendulum website, about the possible links between bipolar disorder and creative personalities
5)A website to support those with bipolar illness, with a list of famous manic-depressives
7)A website to support those with bipolar disorder, with an essay by a teenage girl about her bipolar illness
8)An article posted from the Science News, about the relationship between creativity and bipolar illness
1) Kaysen, Susanna. Girl, Interrupted. Vintage Books: New York, 1993.
6)The Serendip webpage, an article entitled “Creativity and Psychopathology”
| Dissociative Identity Disorder: How Many Personali Name: Sook Chan Date: 2002-02-25 23:38:15 Link to this Comment: 1184 |
Dissociative Identity Disorder, commonly known as Multiple Personality Disorder, is estimated to afflict at least a tenth of the American population. Patients with this disorder suffer from constant memory loss due to the presence of two or more other personalities that "take over" the patient's consciousness at random times of the day. This switching of personalities may last for a couple minutes, a couple hours, to up to several weeks at a time (1). In the past 30 years, the prevalence of Dissociative Identity Disorder has sky rocketed.
The term dissociation refers to the disruption of one or more agents that constitutes "consciousness", such the formation of memories, making sense of them and maintaining a sense of identity (1). Dissociation results from forces beyond the patient's control. Proponents of Dissociative Identity Disorder believe memory loss occurs because the patient's consciousness is taken over by alter personalities believed to be formed during childhood (2). Personalities are usually found to be extremely different from the personality of the patient. The patient is usually shy, introverted and insecure, whereas some of her personalities may be flirtatious, outgoing, confident; and yet others may have issues surrounding anger management. Personalities may be older than the age of the patient, younger, or may have lived over a hundred years ago (1).
Patients who suffer from DID are usually women who have had a history of sexual or extreme physical abuse, or who have experienced repeated trauma beyond her control (3). Because the child cannot physically escape the pain, her only option is to escape mentally: by dissociating. Dissociation is said to defend against pain by allowing the maltreatment to be experienced as if it were happening to someone else. The distress of this childhood maltreatment is also endured by employing repression: a mental mechanism that allows the child to forget the abuse happened at all (3).
Does Dissociative Identity Disorder exist? The American Psychiatric Association states that an individual displaying at least two personality states in which these personality states take control of the patient's behavior can be diagnosed with Dissociative Identity Disorder (2). The individual diagnosed with this disorder tends to be depressed, passive, and often displays feelings of guilt (2). The patient is often unable to recall important personal information and has frequent gaps in their memory due to the "take over" of alter personalities (1). This suggests the employment of repression. Instead of allowing the self to helplessly accept the abuse, the child convinces herself that she is somewhere else and not directly receiving the pain (2). By convincing herself that the trauma did not happen, the child is able to feel safe. "I was never abused, Susie was". They allow these personalities to experience their pain, and as they grow older, more personalities arise to cope with everyday stressors. The personalities become overused, and eventually, the patient allows them to take over her life.
It is basic human nature to act differently and "beside" oneself when exposed to different environments and people with variable personalities. For example, one person may act differently towards a co-worker at the office as compared to a friend on the weekends. However, that does not mean that he has more than one personality. He is conscious of his behavior in the office and at the bar. Someone who suffers from multiple personality disorder is not conscious of these different behaviors because he is not consciously carrying out these actions. When other personalities take over, that frame of experience comes through as gaps of lost memories to the main personality.
There are many variations in the accepted definition of this disorder. One startling, yet well identified fact illustrates the range of the patient’s manifestation of the disorder. The disorder's most dramatic signs appear after, not before, patients begin therapy with proponents of the disorder (4). Patients who seek psychiatric help with symptoms of this disorder, skyrocket in the number and extravagance of their alter personalities as therapy progresses (4). It has been concluded from this pattern that patients who suffer from this disorder may be extremely insecure and attention seeking because they received little, if any attention when they were children. Proponents of this disorder, when approached with a case of probable DID, become extremely interested and excited by the mystery of the disorder. They validate the existence of these possible alter personalities, and the more they validate, the more arise. Is it possible that the patients, as insecure and undeserving as they feel, believe that if they do not come up with more personalities, the therapist might lose interest? Patients who suffer from DID are like emotional sponges, absorbing as much attention as they can to compensate for their childhood distress. The proponent-therapists of this disorder tend to encourage the displays of these alter personalities by engaging real-life conversations with them and accepting their stories as truth.
Another question that comes to mind is the issue of responsibility. As children, the patients managed to defend themselves from ever dealing with reality. As they reach adulthood and life becomes more complicated, these alter personalities seem like a good outlet for them to once again escape responsibility. Having a therapist who indirectly supports this principle allows the patients to escape responsibility of their actions. These personalities tend to be in the extremes of the behavioral spectra. They may be extremely promiscuous, or perform illegal activities (4). Some have anger management issues exhibited when the patient becomes scared or angry. These personalities take over to deal with the patient's emotions. When this happens, any outcome or blame is placed on the alter personality, and this is further validated by the therapist (1).
In 1988, a study found that 135 years prior to 1979, a mere twelve cases of dissociative identity disorder was found. Of these twelve, four were examples not of DID, rather "incipient" multiple personality disorder (4). In the recent years, however, thousands of adult cases have been discovered. This stark contrast cannot help but bring attention to the critics of this disorder.
Is it possible that this disease boomed in the past few years due to the bias therapy? Clinicians often become so fascinated with the psychodynamic defense constructs of the mind that they fail to adequately address the co-morbid personality, or the neurological phenomena underlying hypnotizibility and dissociative states (4). Some critics speculate the dissociation is a form of hypnosis used by vulnerable individuals to cope with trauma. It is probable that patients who come into therapy may have problems dealing with their emotions and self validation, and at the end of therapy, with the help and validation of therapists, discover multiple alter personalities.
Does Dissociative Identity Disorder exist? Maybe. Yet, one who is unable to integrate various emotions and memories should have less than one personality, not multiple.
1)Dissociative Identity Disorder: The Relevance of Behavior Analysis by Brady J. Phelps
2)Multiplying the Multiplicity in the British Journal of Psychology
3)The Treatment of Dissociative Identity Disorder With Neurotherapy and Group Self Exploration
4)An Analytical Review of Dissociative Identity Disorder
| Did it Already Happen, or is it Happening Now? Name: Tiffany Va Date: 2002-02-26 00:51:17 Link to this Comment: 1189 |
"Darling, what did you say was Sue's number?"
"I don't remember stripping at Dan's birthday party last year!"
"No officer, I don't know what happened after the accident. I can't even remember my name."
Amnesia is the partial or complete loss of memory, most commonly is temporary and for only a short period of time. (1). There are various degrees of amnesia with the most commonly occurrence being either retrograde or anterograde amnesia. Prior to my research into this subject I did not know much about amnesia besides what is portrayed in the Disney movie Anesthesia in which Anesthesia cannot remember her traumatic childhood. While I recognize that there is a huge difference between forgetting what to pick up at the grocery store and not remembering the past ten years of ones life, what exactly is the difference between the later and the former?
While there are several classified types of amnesia I choose to focus on retrograde and anterograde amnesia, because these are most common. Retrograde amnesia refers to the inability to remember events before the brain damage occurs, and anterograde is the inability to remember events after the brain damage. (2). Okay, so now I know the difference. One you cannot remember your past. The other you cannot remember your present. Now, the question to be posed is how exactly do these two degrees differ in relation to the way the brain operates when confronted with the trauma?
Making and storing memories is a complex process involving many regions of the brain. (3). Most experts agree that we have two stages of memories - short-term memory and long-term memory. Short-term memory is the immediate memory we have when we first hear or perceive something, however, it holds a definite limited amount of information. (2).
"What did you say the number was again? 555-2695. Okay, 555-2695. 555-2596, 555-2965. Wait, what did you say the number was again?
This is an example of short-term memory.
Long-term memory is the information we retain after a day, two weeks, or ten years. (4).
"In 1492 Columbus sailed the ocean blue."
This is an example of long-term memory as almost every child is asked to commit this fact to memory.
So, what does all this have to do with amnesia? Well, I'm glad you asked. Information flows in through the middle of our brain and branches out like a tree. Before that information goes to different areas, it goes through a channeling/filter system. In this regard, the brain is like a mailroom - this information goes into this box, and that letter goes into that box. (4). In order for short-term memory to become long-term memory, it must go through a process know as consolidation. During consolidation, short-term memory is repeatedly activated - so much that certain chemical and physical changes occur in the brain, permanently "embedding" the memory for long- term access. It is believed that consolidation takes place in the hippocampi, located in the temporal-lobe regions of the brain. Medical research indicates that it is the frontal and temporal lobes that most often damaged during head injury. (3).
As the amnesiac recovers, he or she usually recalls older memories first, and then more recent memories. (3). However, memories tend to return like pieces of a jigsaw puzzle; these bits and pieces return in random order. In general, the smaller the degree of retrograde amnesia, the less significant the head injury. Anterograde amnesia is caused as a result of the complex systems in the brain being damaged. The chemical balance in the brain is upset. As brain systems begin working, memory also starts to work. (4).
I am intrigued by the fact that short-term memory can work independently of long-term memory. While long-term memory can be achieved through the repetition of a fact that is in the short-term memory, it appears that in amnesiac patients their long-term memory tends to return faster than their short-term memory. They can remember their favorite childhood food, but cannot remember why they are in the hospital. In essence, the people who suffer from aterograde amnesia have the memory capacity similar to that of a goldfish.
So while I may not comprehend the complexity to which the brain controls our thought process, I can grasp the concept of retrograde and anterograde amnesia. What I do not understand is where is the memory contained prior to the amnesiac patient being able to retrieve the information? Does it just sit their collecting dust until the mailman comes back from his lunch break?
WWW Sources
1) 1)Mental Health, definition of amnesia.
2) 2)Amnesia, description of retrograde and anterograde amnesia.
3) 3)Question of The Day, lists types of amnesia and explains retrograde and anterograde amnesia.
4) 4)Memory,explanation of memory.
| Lets all go for a run! ----Does exercise really he Name: Rebecca Ro Date: 2002-02-26 01:12:49 Link to this Comment: 1190 |
Some people have thought that exercise positively affects the brain as well as the body. Preliminary evidence suggests that physically active people have lower rates of anxiety and depression than sedentary people do (2). It seems logical that an active lifestyle would help the brain. However, the scientific observations were lacking. Now several biological studies indicate that working out does benefit the brain. This new insight may point more towards the notion that exercise has overall health benefits and also may lead to specialized physical activity programs for patients (1). Exercise may improve mental health by helping the brain cope better with stress, according to research into the effect of exercise on neurochemicals involved in the body's stress response (2). These findings come from animal as well as human studies and are leading to a better understanding of the overall health rewards of exercise and heightened support for exercise regimens that could aid recovery from a wide range of illnesses. Furthermore, the ongoing research indicates that specialized exercise regimens may help repair damaged or aged brains (1).
Some research suggests that exercise positively affects the hippocampus. The hippocampus is vital for memory and learning. Studies with animals found that exercise increases brain concentrations of norepinephrine in brain regions involved in the body's stress response (2). In a recent study, researchers found that adult mice doubled their number of new brain cells in the hippocampus when they had access to running wheels (1). The fact that the adult brain can increase its number of brain cells is amazing. It was once thought that the brain stopped producing new brain cells early in its development and that brainpower dimmed as cells died over the years. But in the past decade, researchers have found evidence that the brain continues to generate new brain cells throughout life, even in humans. Studies indicated that challenging environments, which included a number of components, such as pumped-up learning opportunities, social interactions and physical activities, were key to boosting the growth (1).
In another study, scientists found that voluntary physical activity alone was enough to trigger a boost in brain cell proliferation in rats. However, this proliferation was seen in relation to the running wheel. Swimming produced no change in mice and rats. This could be because they had access to a pool for only a brief amount of time per day. The runners had round-the-clock wheel access. It's also possible that the rodents don't enjoy swimming and it causes a stress to their systems that counters any benefit. Researchers believe that rodents enjoyed the running wheel because they will voluntarily go on it. Mice will log some 20,000 to 40,000 revolutions or four to six miles per day (1).
Scientists are trying to map the biological steps that induce the brain cell proliferation in the running rodents. One factor in the growth phenomenon may be brain-derived neurotrophic factor, which supports the function and survival of brain cells. The factor increased in the hippocampi of rats that voluntarily exercised on running wheels, according to an earlier report. In addition, scientists are studying whether exercise alters the molecular mechanisms that are important for learning and memory (1). It seems possibly plausible, since the cell research shows that changes occur in the brain's learning and memory center. In addition, past behavioral research on mice indicated that treadmill running improved certain learning and memory tasks. Even members of a family of mice that were poor learners improved their performances on the tasks. The exercise also prevented an age-related decline in mouse performance (1).
Researchers also are finding biological evidence that exercise can help the brain on other fronts. For example, animal studies are determining that exercise prevents the negative effects of chronic stress on the brain at the molecular level and boosts the brain's biological battle against infection (1).
There was another study on rats, this time comparing exercise, to the antidepressant drug imipramine. It was found that unforced exercise provided more benefits than either imipramine or forced exercise. Researchers induced a depression like condition in rats using the drug clomipramine. The rats showed several behavioral signs of depression, including an impaired sex drive. Researchers then gave one group of rats 24-hour access to a running-wheel for 12 weeks. Another group ran on a treadmill for an hour a day, six days a week for 12 weeks. A third group received imipramine for the last six days of the 12 week experimental period. And a fourth group remained sedentary and received no treatment for the 12 weeks. The rats given imipramine showed an increase in brain concentrations of norepinephrine, an increase in serotonin metabolism, another neurotransmitter associated with depression, and a decrease in the density of beta receptors, the brain cell receptors that norepinephrine attaches to. Both exercise groups also showed these changes. But only the wheel running rats saw increased sexual activity, the behavioral measure that was used to rate depression (2). This study showed that all exercise is not equal. It might not be exactly fitness that provokes neurochemical benefits. According to this study, the treadmill trained rats exercised more and became more physically fit than wheel running rats. However, the wheel runners received the biggest behavioral boost as measured by increased sexual activity. Some say research in humans finds a similar trend. Does this mean that the real benefit of exercising comes from a combination of biological as well as social factors?
Biologically, exercise seems to give the body a chance to practice dealing with stress. It forces the body's physiological systems, which are involved in the stress response to communicate much more closely than usual. The cardiovascular system communicates with the renal system, which communicates with the muscular system. And all of these are controlled by the central and sympathetic nervous systems, which also must communicate with each other. This workout of the body's communication system may be the true value of exercise (2).
Running can promote brain cell survival in animals with neurodegenerative disease. Previous work had indicated that running can boost brain cell growth in normal mice. In the new study, however, scientists studied mice with a condition similar to the disorder ataxia-telangiectasia (A-T), which in humans leads to a loss of motor control that typically leaves patients wheelchair bound. The A-T mice that ran were found to exhibit higher levels of cell survival than did their non-running counterparts. In sedentary A-T mice it appears that most newly born brain cells die. Running appears to ‘rescue’ many of these cells that would otherwise die (8). This study suggests that staying active may help delay progression of neurodegenerative conditions. Hopefully, further investigation will reveal exactly how exercise helps brain cells to survive.
Previous research suggests that maintaining a healthy flow of blood and oxygen protects the brain. Running may in fact give the brain a workout. A new study found that individuals consistently scored higher on intellectual tests after embarking on a running program. Seniors at Duke University started a 4-month exercise program. These seniors showed significant improvement in memory and other mental skills, also known as cognitive function. After 12 weeks of jogging, scores on complex computer based tests ''significantly increased''. These tests showed that joggers had a clear improvement in prefrontal function and that scores began to fall again if participants stopped their running routine (3). If exercise can help young people improve their cognitive ability, why not try it for the elderly?
Researchers at Southwestern Medical School gave a group of people two computer-based tests. Then the participants ran for half an hour on a treadmill. Once their heart rates were back to normal, the subjects were hooked up to an electroencephalogram (EEG) machine that reads brain activity and were given the two tests again. After exercise, the participants were able to make quicker decisions when taking the tests, particularly with the more difficult tests. The EEG machine reported that brain activity increased more rapidly (6).
It is important that we expand on these studies so that we can learn exactly how exercise affects the brain. Overall these group of studies are suggesting that an active lifestyle plays an important role in maintaining the function of the brain. If exercise improves mood, it follows naturally that it would improve the thinking process. Most people cannot think their best when they are depressed (4). Chronic physical inactivity can break down the body and its systems (5). I think the study that shows that mice didn't experience an age related decline in performance must be investigated thoroughly (1). If this observation turns out to be true for humans it can be of great benefit in preventing or at least slowing down the effects of dementia and Alzheimer’s disease. With the aging of our population, more people are developing these mentally debilitating diseases. Although exercise cannot prevent dementia, if we can just find a specific exercise regimen that would halt or reduce the decline of mental impairment it would be a terrific breakthrough.
Further studies are needed to explain specific mental processes that are improved by exercise and to better understand the underlying mechanisms of these improvements. Afterall, science just works as a summary of observations and is always subject to challenges based on new observations. That is what is so fascinating about scientific research.
2)Exercise Fuels the Brain's Stress Buffers,American Psychological Association
3)Jogging May Make You Smarter, Study Says , Reuters Health
4)Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus , National Neuroscience 1999 Mar; 2(3):266-70
5)Mental exercise keeps the brain in motion, Canadian Press News Article, Health News, Tuesday, May 18, 1999
6)Exercise and Your Brain , Southwestern Medical Center
7)Exercise 'could halt mental decline' , BBC News, Tuesday, 16 January, 2001
8)Exercise For Your Brain's Sake , Scientific American News
| Anorexia and Bulimia Nervosa Name: Asra Husai Date: 2002-02-26 02:19:48 Link to this Comment: 1191 |
Today, both anorexia and bulimia are the most common eating disorders and affect almost 15 percent of American teenagers. Eating disorders are fifteen times more likely to occur in adolescent girls than adolescent boys. They can be fatal and thousands die from every year but this is one mental illness that can be beaten. Anorexia is increasing more rapidly in developed countries than in underdeveloped countries. Bulimia is becoming the more common type of eating disorder among teens. It is difficult to diagnose because many bulimics are deeply ashamed of their rituals and few share their problems with close friends (4). If these two eating disorders are becoming more and more widespread around the world and occurring in a certain age group, then is there a common chemical imbalance or erroneous thought process that leads to such behavior? If so, then how can these eating disorders be handled?
The distinct factor that separates anorexia nervosa from bulimia nervosa is the binging-vomiting/purging cycle and the role it serves in the maintenance of body weight for the sufferer (4). Bulimics are usually within normal weight range while anorexics are extremely underweight. The difference between anorexic and bulimic people are that bulimics can spend all day planning their next binge, while anorexics can spend all day thinking about what they can’t eat at their next meal. When recovering from the eating disorder those with anorexia work at valuing the accomplishments they’ve made, while those with bulimia work at gaining control of their lives (2).
Surveys show that people with anorexia tend to have high intelligence, and superior scholastic performance, but the two almost overwhelmingly consistent personality traits are those of perfectionism and obsessionality (4). Physical symptoms of anorexia result from the behavior of trying to achieve weight loss. Losing the insulated layer has consequences such as sensitivity to temperature, dry skin, brittle hair, vitamin deficiency, heart rate slows, and blood pressure falling due to the fact that the body maybe adjusting to the loss of energy intake (1).
This behavior has biochemical disturbances as well, which have more serious implications. The main disturbances are dehydration and changes in the levels of some electrolytes in the blood. Potassium and chloride fall causing the blood to become alkaline producing a metabolic alkalosis. Low levels of potassium and dehydration cause weakness and fatigue. Low body potassium and alkalosis can cause irregular heartbeat and alterations in the electro-cardiogram. (1)
An anorexics biggest fear is becoming overweight and continue to think they are overweight even after they become extremely thin, are very ill or near death. Often they will develop strange eating habits such as refusing to eat in front of other people. Sometimes the individuals will prepare big meals for others while refusing to eat any of it (5). The goal for an anorexic is to find ways to avoid eating food and exercising for long hours in order to keep the pounds off.
Bulimia is known as the “binge-purge syndrome” and was once considered to be in the same category of anorexia until recently. This syndrome mostly occurs in females starting in their late teens and who say that episodes of binge eating occur two or three times a week. The prevalence of bulimia may be as great as one-in-six tertiary students (3). Bulimics often feel as thought they have no control over their lives. So, it is a struggle between uncontrollable eating and desperate attempts to purge excessive food (2).
Some specific physical symptoms associated with bulimia is the potential for gastric rupture during periods of binging, inflammation and possible rupture of the esophagus during vomiting, and for those who habitually induce vomit may have a swelling look to their face due to the enlargement of the salivary glands as well as damaged teeth due to the acidity of the vomit (4). Bulimia has similar biochemical disturbances to anorexia.
Binging and purging are the behavioral aspect is a way of dealing with unpleasant emotions. A bulimic that is about to binge has a sense of anxiety and tension and once they start to binge they are overcome with a feeling of freedom and their negative thoughts disappear. During the binge period the bulimic may induce vomit, which can reduce tension. At the end of the binge, most binge-eaters feel less tense and anxious, but may not like themselves because of what they have done to their bodies (1). Feeling guilty about inducing vomit may cause more anxiety and tension and thus creating a vicious binge-purge cycle (1).
Anorexia and bulimia are mental illnesses that can be cured. One approach is cognitive therapy, which deals with the thoughts, beliefs, and the assumptions of individuals that affect their feelings and behaviors (6). Recently, scientists have found a decreased level of neurotransmitters such as serotonin and norepinephirne in bulimic and anorexic patients. Depression and irregular menstrual cycle are other factors that are usually associated with an eating disorder. So, the other approach is medical treatment that addresses these issues.
Cognitive therapy teaches you how certain thinking patterns are causing your symptoms (7). Anorexic and Bulimic people are constantly thinking about their body weight and shape. This is mainly due to the image of a woman in our culture today. The cultural pressure of the ideal woman seems to play a large role in affecting the female adolescent age group. A woman goes through a lot of physical and mental changes during the time period and so it is obvious that eating disorders would mainly affect this age group. Thinking patterns can be distorted as soon as a person begins to give into the ideal image of a man or woman that is portrayed in the media as well as other factors combining to worsen the thought process.
The medical approach involves recognizing other behaviors that are related to eating disorders such as depression and treating her in terms of depression. Also, it has been discovered that there are certain neurotransmitters that may cause such a behavior. Serotonin is a neurotransmitter that helps regulate mood (8). When levels of serotonin are low, the bulimic will binge on carbohydrate-rich foods, which increases tryptophan in the blood. The high levels of tryptophan stimulates the brain the synthesis and release of serotonin. Serotonin allows her to feel relaxed and drowsy, however this only lasts for a short time, which leaves her in the same place as before with low levels of serotonin (1). Dexfenfluramine and fluoxetine are two drugs that cause the release of serotonin and have shown some improvement in behavior.
Nonetheless, it is very unlikely to use one or the other method for the treatment of eating disorders. These two methods are combined to get the best possible result. The brain and the behavior of a person are related and therefore these two aspects cannot be separated from one another when treating a mental illness. It is quite clear that people who suffer from anorexia nervosa and bulimia nervosa have similar distorted thought processes and similar behavior. Since each individual is unique in his/her own way, their behavior will differ and may be triggered by different reasons. Two people can both be bulimic and have different factors that have led them to behave in similar fashions. This is where cognitive therapy is useful. Once the root of the problem is recognized, medical treatment can be administered if needed.
Anorexia and bulimia are eating disorders that are rapidly growing and affecting a large number of adolescents mainly women. The causes are for the most part due to the cultural standards of a woman and can also be due to chemical imbalances. Treatment for this mental illness usually entails cognitive therapy and medical attention. The main problems lies within the brain and thought process of body image, which seems to develop in the early teens. An excerpt from Scott’s Anorexia and Bulimia Nervosa says it best:
“Adolescence is one of the most crucial periods in a person’s life for the development or personality, and if this time of growth, challenge and integration is not made proper use of, the individual will be unable to cope efficiently with normal adult life. In particular, the development of a healthy mind and body identity, the establishment of adequate psychological and sexual intimacy and the development of normal stress-management skills suffer.” (4)
| The K+ Channel, A New Hope For a Better Understand Name: Gabrielle Date: 2002-02-26 06:05:29 Link to this Comment: 1192 |
The axons of our neurons are the pathway for the communication that exists in our nervous system. This communication takes the form of an electric signal, also called an action potential. The action potential occurs due to a change in voltage across the membrane of the axon. The change in voltage is achieved by a change in the concentrations of the ions, Na+, Ca+, and K+(1) . The cell starts with a large concentration of potassium ions, K+, inside the cell, and a large concentration of sodium ions, Na+, outside the cell. The action potential propagates down the axon due to openings and closing of different channels allowing changing of the concentrations of the ions(10).
Channels are proteins that span the membrane of the axon. These proteins have a structure so that they can be allow ions to flow through pores that are only open at the appropriate times. Some of the channels are opened and closed by other chemicals, while some are initiated by a change in the membrane potential.
This particular K+ channel, which is greatly studied, is a voltage-gated channel. This means that the channel opens in response to a certain voltage difference that occurs across the membrane. The channel is closed when the cell is at rest. Following inactivation the channel opens via a complicated mechanism, which scientists are still trying to decipher(7)(8). The specific voltage is that which occurs after the Na+ channel has opened and allowed a significant amount of Na+ to be released from the cell. So, the K+ channel is induced to an open state by a depolarization of the membrane potential. The K+ channel opens at the beginning of the repolarization, or after the depolarization has almost reached its peak. The opening of this channel allows K+ ions to flow outside of the membrane of the cell, bringing the voltage of the cell back down to its normal level. The K+ returns to the inside of the cell through a pump that exchanges it for Na+ so that there is little voltage change.
Scientists have struggled for a long time to understand how voltage-gated channels work. "How and where changes in the structure of the voltage-sensing domains [work] to gate ion conduction is not understood," said Li-Smerin et al. in a paper published in February 2000(2). Since then research in the field of voltage-gated channels has reached great heights. Now, scientists view K+ channels as those that are best understood(3). There have been multiple experiments done to determine the structure of the channel through x-ray crystallography, flourometry, and mutagenesis(2)(4). That picture has been almost perfected. Mutations have been done to determine structures that have a big influence on the voltage sensing and gating properties of the channel. For example, Li-Smerin et al. did a series of 37 mutations that led to two groups that they call the major impact and the minor impact residues(2). They were defined as being major or minor depending on how great of an affect the mutation had on the functionality of the resulting channel. When the major residues were mapped on the structure the scientists could make references as to what kind of contribution the original residue had.
The structure of the channel consists of four subunits, each with six helical segments, referred to as S1-S6. The six helices are separated based on whether they belong to the "domain that senses the voltage or the domain that surrounds the pore"(5). S1 through S4 are the helices that are thought to be the ones that respond to the voltage change. The two remaining sections of the protein are those that make up the pore, which opens and closes to allow ions in or out. The structure of these last two are almost exactly the same as a K+ channel that is non-voltage-dependant. This is further evidence that the first four are those that interpret the voltage change, since they are the difference between the two types of channels.
Knowing the structure was the one of the first steps scientists took towards understanding the channel. The basic idea is that the S1-S4 lie on the outer side of the pore, and influence the pore defining helices, S5 and S6. Near the center of the membrane is a water-filled cavity where some drugs, such as TEA, bind to block activation(3). When the pore closes it does it via changing into a teepee like structure. See (10) for a picture of the protein structure.
A portion of S4 is positively charged, and therefore the membrane potential change moves this portion, possibly even to the other side of the membrane. The closed state of the channel is more stable than the open state due to a series of hydrogen bonds in the protein structure(8). This is why such a strong energy changes, such as the depolarization are necessary to change the structure of the channel. The exact movement of the region is unknown. Originally the debate centered on the region moving laterally, but now there is a lot of evidence showing that the helix actually rotates around its inner axis, and slightly out of the membrane at an angle. This motion is comparable to that of a corkscrew. The S4 is also in very close proximity to the pore-forming segments, S5 and S6. S4 connects directly to the S5. This is still being evaluated, but the current proposal is that the torque in the S4 is translated directly to S5 and indirectly to S6. This seems very probable because the gating of channels that aren't voltage-gated rely on a twisting in S6 to open the channel. The other possibilities are that the S4 rotates the others the way gears work, or that it moves outward from the protein complex, opening the channel(5).
There are many differences that are recognizable between voltage-gated and non-voltage-gated channels. These differences help understand how the voltage-gated channel works. We have already discussed the fact that there are additional helices on the voltage-gated channels, and that there are minute differences in the structure of the pore-defining helices. Another important structure in a channel is the "residues" that line the helices. Residues are the amino acids that reside on the transmembrane surface(2). In non-voltage gated channels that residues only interact with the lipids of the membrane that surrounds them. In voltage-gated channel these residues also interact with the additional helices(2). This is beneficial because these residues can possibly show where the interactions are between the different helices. Mutants of the residues have been studied to see which ones change the voltage-sensing domain(2). Multiple scientists are currently working on studying these mutants. Some have no or little affect, while some eliminate gating altogether. Eventually these mutants should be able to tell us exactly how the channel is working.
Even without the difficulty of voltage-dependency scientists still don't know what the basic structure of the opening/closing structure of any of the channels are. It was originally thought that the channel was just a trap-door apparatus. Spin-labeling has shown that at least non-voltage-dependant channels work by rotating the inner helix(5). This may also be the formation in the voltage-dependant channel. There are two other types of gating observed in voltage-gated channels; N-type, and C-type. N-type is also referred to as the activation gate. It is near the interior of the cell, and it is open during activation. The C-type is also referred to as the slow inactivation gate, and it is located at the external part of the channel(7). Scientists are still working on identifying exactly where these sites occur. A major way of studying them is by blocking them with molecules of similar size to K+.
Eventually there will be a lot of helpful medical advances coming out of the knowledge of this channel works. Many diseases, from depression to Alzheimer's could possibly be affected by further knowledge of the ion channels. Drugs can be made that interact in more precise ways with the channels, maybe with less negative side affects. The possibilities are endless, and the knowledge is fast approaching.
1)Serendip Notes, Some notes are available from the class on the Neurobiology of Behavior which discuss Action Potentials.
2)A Localized Interaction Surface for Voltage-Sensing Domains on the Pore Domain of a K+ Channel
4)Reconstructing Voltage Sensor-Pore Interaction from a Fluorescence Scan of a Voltage-Gated K+ Channel
5)Taking Apart the Gating of Voltage-Gated K+ Channels
6)Reconstructing Voltage Sensor-Pore Interaction from a Fluorescence Scan of a Voltage-Gated K+ Channel
7)Tight Steric Closure at the Intracellular Activation Gate of a Voltage-Gated K+ Channel.
8)The Polar T1 Interface Is Linked to Conformational. Changes that Open the Voltage-Gated Potassium Channel
10)Lights, Camera, Action Potential, A site made for children that has great descriptions and visuals of an action potential.
| Transient Global Amnesia Name: Miranda Wh Date: 2002-02-26 08:09:59 Link to this Comment: 1193 |
A little while ago, my father and grandfather were driving in our car together. All of a sudden, my grandfather said that he was feeling dizzy and thought the beginnings of a migraine were coming on. My grandfather is extremely healthy and has an amazing memory, so my father was shocked when not long after, when grandfather asked where Ruthy, his recently deceased wife, was. When my father reminded him that she had died of cancer last year, my grandfather broke into tears, as if he was being told for the first time. In addition, he couldn't even remember what he had just eaten for dinner or any other events of the day. My father drove him straight to the emergency room, worried that he had perhaps just suffered a minor stoke. By the time that he got to the hospital, he was already beginning to regain some of the memories that had been lost. The doctors reassured him that it was not a stroke, but rather a memory disorder called transient global amnesia.
Transient global amnesia (TGA) is a type of amnesia involving the sudden, temporary disturbance in an otherwise healthy person's memory. The other main kinds of amnesia are called anterograde and retrograde amnesia. Anterograde amnesia is a type of memory loss associated with a trauma, disease, or emotional events. It is characterized by the inability to remember new information. (1) Retrograde amnesia is associated with the loss of distant memories usually preceding a given trauma. (2) In transient global amnesia, generally both distant memories and immediate recall are retained, as are language function, attention, visual-spatial and social skills. However, during the period of amnesia, people suffering from the disorder cannot remember recent occurrences nor can they retain any new visual or verbal information for more than a couple minutes. (3) Though patients generally remember their own identities, they are often very confused by their surroundings and the people around them. They continuously ask questions about events that are transpiring, for example where they are, who is with them, what is happening. However, once they are told, they immediate forget the answer, and repeat the question again. (4)
The period of amnesia can last anywhere from one to twenty-four hours. Some people suffer from a headache, dizziness, and nausea while others have only memory loss. TGA generally affects fifty to eighty-year-old men, about 3.4 to 5.2 people per 100,000 per year. (5) People afflicted with transient global amnesia always recover and can remember the memories that were lost during the episode. (6) Once they regain their memory, some people, such as my grandfather, can recall both the episode and the feeling of not being able to remember. However, others never recover the memories of the attack nor the events immediately before.
The cause of TGA remains in dispute. There is convincing evidence that external emotional stresses, such as sexual intercourse, immersion in cold water, or strenuous physical exertion, can trigger the associated loss of memory. (7) For example, my grandfather suffered from TGA directly after taking his sister to the hospital. TGA may be the result of a transient ischemic attack, a "mini-stroke." Transient ischemic attacks are caused by a temporary interruption of the blood flow to the brain. (8) Another possible cause of transient global amnesia is a basilar artery migraine, a type of migraine caused by the abnormal constriction and dilatation of vessel walls. (9)
Patients suffering from transient global amnesia have undergone medical imaging techniques, for example magnetic resonance imaging (MRI) and positron emission topography (PT), in order to find out what biological changes cause a temporary lapse in memory. The symptoms of transient global amnesia seem to be the result of dysfunction in such regions of the brain as the diencephalon and medial temporal lobes. (4) The diencephalon is composed of the thalamus, epithalamus, subthalamus, and hypothalamus. The thalamus is associated with memory, and changes in its structure have been proven to result in amnesia. (10) Some MRIs have shown evidence of changes in the medial temporal lobes, indicating that patients had suffered from a transient ischemic attack. Nonetheless, many people that have undergone such tests have not shown any changes in the functioning of their brains. (4)
These findings are in line with our neurobiological understanding of memory. Under normal functioning, there are three kinds of memory: working memory, declarative memory, and procedural memory. Working memory allows for short-term recollection, for example, it is responsible for your being able to remember the gist of the sentence you just read. It is associated with the temporary storage of verbal and visual information. The verbal working memory is localized to the frontal regions of the left hemisphere, while spatial working memory involves mainly the right hemispheres. Procedural memory is responsible for cognitive and motor skills, all learned, habitual actions, for example, my ability to type this paper without looking at the keyboard or my ability to ride a bicycle. (12) The anatomical basis for procedural memory appears to be the basil ganglia, thalamus, and the frontal lobes. Declarative memory, associated with the hippocampus, is all experiences and conscious memory, including people, events, objects, facts, figures, and names. The region of the brain termed the medial frontal lobe is particularly responsible for declarative memory function.
There is much evidence proving that damage to the medial frontal lobe, severely affects a person's ability to recall and form long-term memories. The most well-known clinical example involves a patient called H.M. H.M. was afflicted with epilepsy. Surgeons removed both of his medial temporal lobes in an attempt to cure him from his disease. However, in so doing, they profoundly damaged his memory. He could no longer form new memories, though all his memories from before the surgery were retained - in other words he had anterograde amnesia. (11) Therefore, it appears that the lack of functioning and blood supply of the medial temporal lobe produces the symptoms of transient global amnesia, and results in the inability to make and recall autobiographical memories.
Transient global amnesia fortunately has a very positive prognosis - its effects are never permanent and the episodes last for a relatively short period of time. However, the inability to remember can be extraordinarily frightening. It is a natural experiment because it shows fairly clearly that certain parts of the brain are involved with certain kinds of memory. We often see ourselves as unitary beings, but in fact we are made up of many different processes that make up who we are. Although much of the neurobiology associated with memory remains quite mysterious, transient global amnesia helps highlight the particular machinery of our personal narratives.
3)E Medicine, Transient Global Amnesia
4)Transient Global Amnesia Case Studies
7)HealingWell, What Happened to Afterglow
9)Basilar Artery Migraine Page
12)The Cognitive and Habit Subsystems , A great image of the anatomy of the brain.
| The Neurobiological Factors Associated with Depres Name: Mary Schli Date: 2002-02-26 08:39:40 Link to this Comment: 1194 |
Depression is a mood disorder that affects approximately ten percent of men and nearly twenty-five percent of women at least once in their lifetime (1). There are several types of clinical depression, such as unipolar depression and bipolar depression. Unipolar depression consists of primarily depressive states while bipolar depression involves a fluctuation between states of depression and mania (2). Some of the most common symptoms of depression include excessive feelings of sadness, guilt, or worthlessness, a significant change in appetite, insomnia or hypersomnia, energy loss, thoughts or attempts of suicide, and anhedonia (3), (4). While the symptoms of depression are understood fairly well, how the exact causes of the disorder interact in the development of depression remain somewhat of a mystery.
There are several biological factors that may contribute to the increased susceptibility to depression. Genetic links have been made as the result of twin studies suggesting that family members of depressed patients are more likely to be depressed or to develop depression than the general population. However, it is important to note that these results may be due to the similar environments of twins rather than genetic influence (5). Consequently, studies comparing twins who were reared apart have been conducted and the data suggest that the concordance rates for twins reared together or apart is nearly identical, although the rate is slightly lower for twins reared apart. This suggests that while the environment does play an important role in the development of depressive symptoms, genetic influences are also important (6). In addition, other genetic studies have suggested that Chromosomes 18 and 21 may play a role in depression, but these studies have yet to be replicated (5). While some of the findings from these genetic studies are still preliminary, several investigations have indicated that the role of certain neurotransmitters, called monoamines, in depression is immense (7).
Neurotransmitters are chemicals in the brain that bind to receptors in order to excite or inhibit the firing of neurons (6). The Catecholamine Theory of Mood was proposed as a major explanation for the cause of depression in the 1960s by Joseph Schildkraut (7). Schildkraut suggested that a deficiency of the neurotransmitter norepinephrine at receptor sites caused depression while increased levels of norepinephrine caused mania. Some evidence for Schildkraut’s account was established by the success rate of monoamine oxidase (MAO) inhibitor drugs, which block the reuptake of monoamines and facilitate the release of neurotransmitters such as norepinephrine and serotonin (8). Further evidence has been established by studies that found decreased norepinephrine levels in the cerebrospinal fluid of deceased depressed patients (5). More recently, drugs have been developed that selectively block the reuptake of norepinephrine by the presynaptic cell. It has been found in preliminary studies that the level of depression decreases in these patients, which provides further evidence for the role of norepinephrine in depression. While empirical support for the Catecholamine Theory of Mood has grown substantially, evidence from more recent studies highlights the important roles of other monoamines in depression (5).
Norepinephrine is not the only neurotransmitter that may contribute to depression; rather, evidence suggests that serotonin plays an important role in the disorder as well. Decreased serotonin levels at the synapses may actually moderate the decreased norepinephrine levels of a depressed patient. Several sources of support for this hypothesis have been found. For example, studies of depressed patients suggest that decreased levels of serotonin in the brain are associated with decreased mood, while increased levels of serotonin are associated with increased levels of mood (9). In addition, the cerebrospinal fluid of depressed patients contained lower levels of a substance that serotonin produces than the fluid of nondepressed patients, which suggests that the levels of serotonin in the brains of the depressed patients were lower than the levels of the nondepressed patients (5). Further evidence indicates that serotonin is present in regions of the brain that regulate behaviors associated with depression, such as the amygdala, which mediates emotions, and the hypothalamus, which is involved in sleep and hunger (9), (5). Autopsies revealed that a particular subtype of serotonin receptors were more dense in patients with depression than in nondepressed patients, suggesting that these receptors became more dense in order to counterbalance the effect of low serotonin levels (5). Finally, the treatments available for depression suggest that serotonin levels are an important factor in depression. For example, the selective serotonin reuptake inhibitors (SSRIs), which prevent the immediate reuptake of serotonin, are effective in alleviating the symptoms of depression. However, there are caveats in interpreting this data. Despite the fact that the SSRIs begin to affect the reuptake of serotonin almost immediately, the symptoms of depression are not noticeably relieved until approximately one to four weeks after beginning treatment. This discrepancy provides further support for the notion that there is not one particular factor that causes depression; rather, there are multiple factors that interact in the etiology of the disorder (10).
Dopamine, a neurotransmitter that moderates reward, is a third monoamine that may be involved in depression (11). It is believed that the role of dopamine may not be as profound as the role of other factors involved; nevertheless, evidence suggests that drugs that increase dopamine levels reduce the severity of depression that a patient may feel. However, because drugs of this type can become addictive, other drug treatment options are often favored or required (11). Finally, although unusually low levels of dopamine may be present in patients with depression, monoamines are not the only substances that may mediate the disorder.
Cortisol is a hormone that is released increasingly with increased stress (12). This elevated level of cortisol affects serotonin levels and is caused by the hypothalamus producing more corticotropin-releasing factor (CRF). This in turn triggers the production of adrenocorticotropic hormone (ACTH), which stimulates the production of cortisol (5). Research has shown that depressed patients have higher levels of cortisol in the hypothalamic-pituitary-adrenal system, which controls some brain regions that are aversely affected in depression such as those areas responsible for sleep, appetite, arousal, and pleasure (13). Furthermore, when these patients are given dexamethasone, which normally decreases cortisol levels, the amount of cortisol present only briefly decreases. The hypothalamic-pituitary-adrenal system then resumes its production of cortisol and ignores the inhibiting effects of the dexamethasone. This indicates that the person is highly stressed and at a high risk for becoming or remaining depressed (12).
Depression is a mental disorder that causes patients to display serious behavioral symptoms. There are several factors that may affect depression such as a genetic predisposition, abnormal neurotransmitter levels in the brain, and an increased production of cortisol. While many studies suggest that these factors have important roles in depression, further research is necessary in order to understand more completely how they interact in patients suffering from this disorder.
1) Stress. Grief. Postpartum Depression. Depression has many sources.
2) Mental Help Net – Depression (Unipolar)
3)Basic Information about Depression, Basic Information about Depression
4)Depression – Holistic Online.com
5)Scientific American Feature Article: The Neurobiology of Depression , Good resource of information about the neurobiological factors involved in depression
6) Papolos, Demitri & Papolos, Janice. Overcoming Depression: The Definitive Resource for Patients and Families Who Live with Depression and Manic Depression. New York: HarperCollins Publishers, 1997.
7)Depression: Beyond the Catecholamine Theory of Mood, A good overview of depression
8) Carlson, Neil. Physiology of Behavior. Massachusetts: Allyn and Bacon, 2001.
9)Carol Hart, Secrets of Serotonin, Chapter 2, Information about Serotonin
10) Depression: Beyond the Catecholamine Theory of Mood, A good overview of depression
11)The Chemistry of Depression
12) Gilbert, Paul. Overcoming Depression: A Step-by-Step Approach to Gaining Control Over Depression. Oxford: Oxford University Press, 2001.
13)Behavior: The Neurobiology of Depression, An interesting article by a psychiatrist at the University of Michigan
| Beauty and the Brain Name: Peffin Lee Date: 2002-02-26 09:20:28 Link to this Comment: 1195 |
Each year, billions of dollars are spent on cosmetics, facial firming, bacterial injections, double eyelid surgery, and the list goes on. All in the name of beauty. But, what is beauty? What defines it? Is there a universal beauty? Can it be obtained?
According to BBC, our perception of beauty begins in the womb. Studies show that babies have a tendency to look the longest at faces with smooth skin, round eyes, plump lips, and symmetry. In fact, BBC reports that our DNA is written to produce symmetry, yet factors such as environment produces asymmetry. Universally, these characteristics represent youth and fertility. Our faces are “an advertising hoarding which provide a potential mate with information about health, fertility and appropriateness as a partner” 1. Men look for young and healthy faces, translating to mates that are youthful with big eyes and plump lips 1. Whereas, females look for mates with the most testosterone, indicating fertility and strength. Bony protrusions such as the nose, cheek bones, brows and jaw indicate a potential for healthier children 1.
With the birth of the Golden Ratio, by Dr. Stephen Marquardt, dreams of achieving beauty have been made possible 1. This mathematically generated ratio claims to be the “essence of facial beauty” 1. It explains that the majority of people are attracted to faces that conform to the 1:1.618 Golden Ratio 1. As the founder of Marquardt Beauty Analysis in California, Dr. Stephen Marquardt and his researchers have taken it upon themselves “to develop and provide information and technology into which to analyze and positively modify (ie. improve) human visual attractiveness” 2.
So, we know that we are programmed to be attracted to beautiful faces and many of us spend our entire lives trying to understand it, but what exactly fuels our obsession?
According to a recent study done by Itzhak Aharon and his colleagues, it appears that the viewing of beautiful faces activates a reward circuitry in the brains of humans, similar to that activated when eating, having sex, using cocaine, or making money 3. The reward circuitry is activated by the neurotransmitter Dopamine, which is produced in the nucleus accumbens and released in the ventral tegmentum of the midbrain 4. Dopamine serves many purposes, for example it is needed for learning and memory processes 5, but for the purposes of this study, Dopamine is used as a method of motivating behavior 3. When a desired behavior is performed, a release of dopamine gives the person a sense of pleasure, causing a willingness to continue, repeat, and reinforce a specific behavior.
The study 3 consists of three components using four categories of faces: average female, beautiful female, average male, and beautiful male. Their main goal was to differentiate between aesthetic and rewarding qualitites.
The first component 3 required eight young heterosexual males to rate the attractiveness of faces using a rating from 1 (“very unattractive”) to 7 (“very attractive”). There was a significant difference in rating between average and beautiful for both male and female faces rated. As the number of exposures to the faces increased, the beautiful female faces increased slightly in ranking, while the average female faces decreased more in rating. Yet for the male faces, continued exposure resulted in increasing ratings for both average and beautiful faces, with the difference in rating between beautiful and average remaining the same. Regarding the viewing of female faces in the first component 3 , the increase in rating of beautiful faces and decrease in rating of average faces may be a result of a early release in dopamine. When looking at a beautiful face a little bit of dopamine is released. So, with continued exposure, when the subject views the picture, he is reminded of the first release of dopamine, then he is rewarded with another release of dopamine 6. Whereas, when looking at an average face, no dopamine is released, therefore there is no reason to continue the behavior.
The second component 3 involves fifteen young heterosexual males that were given the keypress task. In this test, the subjects were allowed forty minutes to view eighty images that were always in a new random order, meaning that the categories of faces were intermixed. The results were that the subjects only expended effort to increase the viewing time of beautiful female faces. Whereas for all the other categories, they keypressed to make the faces disappear. The additional effort to increase the viewing time of only beautiful female faces rather than both beautiful male and female in the second component 3 indicates that although the viewing of male faces may be aesthetically pleasing, it is not rewarding.
In the third component 3, the fMRI was used to monitor six specific regions of the brain that been previously associated with the reward circuitry: the nucleus accumbens, sublenticular extended amygdala fo the basal forebrain, amygdala, hypothalamus, orbitofrontal cortex, and ventral tegmentum of the midbrain. In these targeted regions, six regions of interest were selected to base the comparison between the four face categories. So, six young heterosexual males were shown a set of average faces with neutral expressions. This set would be the foundation for image focusing and centering. A couple minutes later a rapid presentation of faces intermixed with fixation points was shown, and the subjects were to focus on the fixation points. For the comparison, different signal changes were noted in the different regions or interest.
The use of the fMRI showed two important things. First, the neuroimaging patterns obtained matched those using drugs, eating, and money stimulus, indicating a generalized circuitry processing rewarding stimuli. And secondly, the similarity in signal profiles between viewing beautiful faces and using money as a stimulus, suggests that reward regions respond to reinforcing characteristics rather than aesthetics.
It is interesting to note that in the third component 3, for males viewed, either average or beautiful, no signal changes were noted. This coincides with the results of the first two components 3 demonstrating a separation between attractiveness and reward value regarding beautiful male faces. In another study 7, Berridge distinguishes the difference between “liking” and “wanting.” “Liking” shows pleasure while “wanting” shows incentive motivation. Therefore, when viewing beautiful females, the subjects expressed “wanting,” and while viewing beautiful males, the subjects expressed “liking.”
So, then where does that leave us? Well, I am not really too sure, but those of you who are in search of this universal beauty, I would like to end with a reminder from Dr. Marquardt who still believes that beauty is in the eye of the beholder and that the ones we love and admire become more beautiful with time 1.
2) Marquardt Beauty Analysis,Official Website
3) ”Beautiful Faces have Reward Value: fMRI and Behavioral Evidence”
4) Diagrams and Brief Descriptions of the Central Nervous System
5) “Increased Dopamine Release in the Human Amygdala During Performance of Cognitive Tasks"
7) "Food Reward: Brain Substrates of Wanting and Liking"
| Ecstasy, the Brain and Serotonin (MIA) Name: Amy O'Conn Date: 2002-02-26 09:21:00 Link to this Comment: 1196 |
3,4-methylenedioxymethamphetamine (MDMA), or ecstasy, is a synthetic, psychoactive drug with stimulant and hallucinogenic properties. Ecstasy is an often talked about drug due to its recent popularity and rapid spread amongst teenagers especially. Many newspapers and magazines have featured articles in the past 5 years highlighting the danger of this easily made drug, and its rampant use in the club/rave scene of almost all Western countries. The complete effects of ecstasy are still unknown, although much research has been produced that shows the deleterious effects of the drug on the brain. Ecstasy is also controversial because the content of pills varies widely; buyers and sometimes sellers don’t really know what each pill consists of (1).
The results of a survey published in 2002 set out with the purpose of examining the prevalence and patterns of ecstasy use among college students, and to determine characteristics, associated behaviors, and interests of ecstasy users. These results showed that from 1997-1999, ecstasy use increased significantly in every college subgroup except for noncompetitive schools. The variable most strongly associated with ecstasy use was found to be marijuana. In terms of social context, MDMA users were more likely to spend large amounts of time socializing, attend residential colleges, and belong to a fraternity or sorority.
The first study that provided direct evidence that chronic use of ecstasy causes brain damage was published in 1999. The study used advanced brain imaging techniques (PET scan) to show that MDMA harms neurons that release serotonin, a chemical that is thought to play an important role in memory, among other functions. The PET scans showed significant reductions in the number of serotonin transporters, the sites on neuron surfaces that reabsorb serotonin from the space between cells after it has completed its work. The lasting reduction of serotonin transporters occurred throughout the brain. This study and others suggest that brain damage and the amount of MDMA ingested are directly correlated (2).
But what are the functional consequences?
The functional consequences of ecstasy use have just begun to be explored in the past few years. Another study, published in 2000, found that heavy ecstasy users (30-1000 occasions) as opposed to non-ecstasy users, reported significantly higher scores on tests for somatisation, obsessionality, anxiety, hostility, phobic-anxiety, paranoid ideation, psychoticism, poor appetite, an restless or disturbed sleep. Another interesting effect of MDMA found was a significantly higher degree of impulsivity. This particular characteristic of ecstasy users has been found in other studies as well (3).
What is the connection between the neurobiology of MDMA use and the behavior of the user? How do reduced serotonin levels result in behavior changes such as impulsivity?
Various animal studies have demonstrated that MDMA selectively affects serotonin and related chemicals in the brain. Brain concentrations of TPH, 5-HIAA and serotonin were decreased in rats treated with MDMA, while dopamine and similar chemicals weren't affected at all. In another study, rats treated with MDMA were found to have a dose-dependent decrease of serotonin in the hippocampus, hypothalamus, striatum and neocortex. Another study revealed a lasting loss of serotonergic axons in the forebrain after MDMA use. Even 52 weeks after the last MDMA treatment, serotonin concentrations were significantly reduced in the cortex and hippocampus; serotonin transporter binding was also reduced (6).
While there are numerous studies with results like the aforementioned, no convincing direct causal relations between neurochemical alterations and neuropsychological parameters have been thus far established (6).
An equally important question is how can scientists present these relationships to the average ecstasy user in an understandable format? Sites such as dancesafe.org (4). and ecstasy.org aim to educate and provide users with literature and the most up-to-date research on ecstasy while not condemning using it (5). Approaches like this make imperative information much more accessible to users because it is both risk-free and personal.
The direct link between the neurotoxicity of MDMA and the psychosocial behavioral effects has not yet been figured out, but it is clear that a link does exist. Perhaps one day researchers will be able to find the missing link. Until then, ecstasy users can access web sites and science journals to attempt to use the drug in the safest possible way.
Works Cited
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a name="3">3) Parrot, A.C. et al. “Psychobiological Problems in Heavy ‘Ecstasy’ Users (MDMA) Polydrug Users. Drug and Alcohol Dependence. 60 (1999): 105-110.
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a name="6">6) McGuire, P. "Long Term Psychiatric and Cognitive Effects of MDMA Use." Toxicology Letters. 112-113 (2000): 153-156.
| Procrastination: Habit or Disorder? Name: Jenny Mary Date: 2002-02-26 09:25:43 Link to this Comment: 1197 |
Universally common to college students, procrastination is often addressed as a bad habit. Yet, in most cases, this isn't a nuance, but a perpetual occurrence - no longer qualifying for the term "habit." Typically thought of as a behavioral trait, procrastination thrives on a cycle of blame shifting and avoidance. Falling victim to this "habit" myself, I embarked on a mission to seek out the causes of procrastination.
The results of my findings, were debates over whether procrastination is in fact biological or psychological. Convincing evidence exists for both perspectives, which attempt to resolve the mysterious question - why do college students and people of all ages, alike, procrastinate? Today's technologically dependent society can opt for hyperefficiency, yet mindless procrastination continues, often manifested through electronics(3). Furthermore, an online survey by The Procrastination Research Group posed the question, "To what extent is procrastination having a negative impact on your happiness?" of the 2,700 responses: 46% said "quite a bit" or "very much" and 18% claimed "extreme negative effect"(3). The dismal results speak to a common problem of procrastination.
The traits of procrastination are obvious, more interesting are the traits of the procrastinator. Chronic procrastinators avoid revealing information about their abilities, prefer menial tasks, make poor time estimates, tend to focus on the past and do not act on their intentions. These characteristics have been related to low self-esteem, perfectionism, non-competitiveness, self-deception, self-control, self-confidence, depression and anxiety(4). From a neurobiology standpoint, the listed traits refer directly to the I-function in actions that consciously abuse the self. The importance of the I-function's interpretation of information and modification of behavior can be illustrated in the self-handicapping and decision-making components of procrastination. The complexity of procrastination has forced researchers to divide it into different types, the most pertinent in my opinion - behavioral and decisional.
Behavioral procrastination is equated with self-handicap. Essentially, this self-handicap provides a means for further blame shifting, as could be seen in an example of a student doing poorly on an exam and using procrastination as an excuse(3). Studies on self-handicapping have shown that people use a wide variety of strategies in order to construct barriers for their success(4). The placing of these mental barriers is the work of the I-function manipulating the internal experience. Two studies conducted by Ferrari and Tice in a laboratory setting had participants (men and women) perform an identical task twice. In the first study, participants were notified that they would be evaluated on their performance of the task. Time was allotted for practice or engaging in fun activities. Results found that participants procrastinated for 60% of the time. The second study described the identical task as a fun game. Results of activity during the time allotted showed that procrastinators, in comparison with non-procrastinators, spent the same of amount of time practices. Thus, the results suggest that procrastination was a behavioral self-handicap only when the task was deemed evaluative(4). The pervasive tendency of the self-handicap creates a cycle of self-defeating behavior, which in turn send negative feedback to the I-function. Correspondingly, this self-inflicted degradation and shame is translated into health problems.
The second type of procrastination - decisional, is the pattern of postponing a decision when dealing with conflicts and choices(5). People with high decisional procrastination display tendencies of perfectionism in taking longer to make decisions. Thus, the study by Ferrari and Dovido hypothesized that people with higher decisional procrastination, in comparison with people lower in decisional procrastination, seek out more information about a chosen alternative before making a decision(5). This hypothesis underscores the fear of error and necessity for perfection in people with high decisional procrastination. In addition, varying levels of decisional procrastination correlates to fundamental differences decisive strategies(5). The argument Ferrari and Dovido put forth associate decisional procrastination with caution and assurance of correctness, by collecting data, before making a decision. Clearly the implications of this form of procrastination differ from those of behavioral procrastination, characterized by distraction and avoidance. Decision-making or critical thinking, is an activity of the brain. Yet, it seems to me that people with high decisional procrastination take greater care in taking a step forward, thus the I-function would have to be considered in light of the fact that while a decision is being made, the thoroughness is connected to notions of concern, desire and fear; reflecting individual traits.
Up until this point, procrastination has been discussed from a psychological standpoint. The perspective countering previously stated information is biological. Research done by R.L. Strub links procrastination to physical disorders and lesions in the brain, particularly in the frontal lobe - specifically the bilateral hemisphere in globus pallidus(1). The prefrontal cortex (PFC) of the frontal lobe controls cognitive processes. Many of its functions are routinely used in daily life (i.e. judgment, planning, critical thinking, empathy, attention span, organization, etc.). As the most evolved part of the brain, the PFC is responsible for necessary behavior in a social sphere, consequently affecting our personalities. "The capacity of the individual to generate goals and to achieve them is considered to be an essential aspect of a mature and effective personality. It is not a social convention or an artifact of culture. It is hard wired in the construction of the prefrontal cortex and its connections"(2). Given the importance of the PFC, a dysfunction can cause problems with organization, procrastination, judgment, attention span and distractibility. The PFC sends signals to the limbic and sensory parts of the brain. When a person needs to focus, the PFC decreases the distracting input from the other brain areas(2). Therefore, if there is a problem with the PFC, there is no filter mechanism at work. Underactivity of the PFC is common with Attention Deficit Disorder. While this argument is compelling, it personally made me feel as though I experience underactivity of PFC all too frequently. The behavioral aspects of the frontal lobe are critical in functioning from day to day and it is the abundance of these characteristics that make it seem unlikely that they would all be working perfectly at any point in time. On a lighter note, the PFC offers the procrastinator a scientifically legitimized excuse for procrastination.
There is yet to be any treatment offered for biological procrastination. However, for those people who subscribe to psychological explanation, there is help after all. Researchers offer an oversimplified solution that recommends procrastinators change the way they think(3). On a more individual basis, to tackle the universal problem of procrastination, people can try becoming aware of internal excuses, breaking up difficult tasks, focus on the negative consequences, make lists and most importantly question the rationale behind procrastinating(6). While experts attempt to rehabilitate procrastinators in a psychologically, I question the success of such actions due to the presence of the I-function. If the I-function is the intrinsic self, can it be changed? Perhaps along the lines of changing a frame of mind, altering one's desired behavior is a difficult task.
To balance the negative connotation of procrastination, there is evidence in the decisional procrastination theory (overly cautious decision-making) that it may have positive long-term functions(5). In all fairness, the opposing view is that procrastination is essentially an obstacle to achievement in both the long-term and the present(7). The attitude one takes towards procrastination is connected to which argument is more convincing. I began my research to find out why my friends and I put off work until the last minute. In return I uncovered debates of psychological v. biological, underscored with mind v. brain. Procrastination is a strong act of agency supported by the I-function. The neurobiological perspective of PFC stripped procrastination of any elements of agency. While eradicating procrastination will never occur on a universal level, I have hopefully removed the myth surrounding the ever-common act and in effect may even encourage a student or two to start studying earlier.
2)Frontal Lobes, Information on the prefrontal cortex
3)The Danger in Delay, Procrastination as self-defeating behavior.
4)Procrastination as a Self-Handicap for Men and Women: A Task-Avoidance Strategy in a Laboratory Setting, Two studies on behavioral procrastination
5)Examining Behavioral Processes in Indecision: Decisional Procrastination and Decision-Making Style
6)A Cure for Procrastination, General information on what procrastination is, why/when it occurs and how it is treated
7)The Procrastination Syndrome: Signs, symptoms, and Treatment, Diagnosis and treatment information
| Causes of Sexual Dysfunctions Name: Lauren Wel Date: 2002-02-26 09:36:48 Link to this Comment: 1198 |
"Sexual dysfunctions are an important public health concern, to which general health and emotional problems contribute" (10). What is a sexual dysfunction? A sexual dysfunction is any condition that inhibits someone's ability to enjoy sex. Some common sexual dysfunctions are: hypoactive desire disorder (low sex drive), hyperactive sexual disorder (high sex drive), sexual aversion disorder, lack of lubrication (females), impotence (male erectile disorder), premature ejaculation, vaginismus (prolonged contractions of the vaginal wall that cause painful intercourse), or failure to orgasm during sex (8). In a study of happily married couples, 14% of men and 15% of women reported that they were either not very satisfied or not at all satisfied with their sex lives. In another study by Laumann in 1992, it was found that the prevalence of sexual dysfunction is 43% in women and 31% in men (10). Are these numbers surprising? What is causing this lack of sexual fulfillment?
Did you ever wonder why sexual desire varies from person to person? Or why and how your sexual drive can change over time? Did you ever wonder what causes things to go wrong sexually - sexual dysfunctions? What is controlling YOUR sexual desire?
Innervations of the organs of sexuality are mediated primarily through the autonomic nervous system (12). The autonomic nervous system is the part of the vertebrate nervous system that regulates involuntary action, as of the intestines, heart, and glands, and that is divided into the sympathetic nervous system and the parasympathetic nervous system (1). It is generally assumed that the parasympathetic system activates the process of erection via impulses that pass through the pelvic splanchnic nerves (S2, S3, S4), which cause the smooth muscles of the penile arteries to dilate. The sympathetic (adrenergic/adrenalin) system is responsible for ejaculation. Similarly for women, the sympathic system facilitates smooth muscle contraction of the vagina, urethra, and uterus that occurs during orgasm.
"The autonomic nervous system functions outside of voluntary control and is influenced by external events (for example, stress, drugs) and internal events (hypothalamic, limbic, and cortical stimuli)" (12). So, it is not surprising, therefore, that erection and orgasm are so vulnerable to dysfunction.
There are many possible psychological disorders that could cause a person to be sexually unsatisfied. If a person has a psychological disorder such as bi-polar disorder, schizophrenia, epilepsy, or depression - they tend to enter states of extreme fear, paranoia, or anxiety more often than a person without their disorder. These states are not normal states of consciousness for a healthy person, and many of these abnormal states of consciousness inhibit sexual interest (9). For example, a bi-polar person experiences non-normal states of extreme bliss or extreme depression. During each non-normal state of consciousness, the bi-polar person will be too consumed by either their elation or their depression to feel any sexual desire. Therefore, a person's sexual desire is related to the amount of time spent in non-normal states of consciousness.
Not only the psychological disorder itself can cause abnormalities in sexual desire, but so can the treatment of the disease. Drugs used to treat some psychological disorders - such as depression - can alter sexual desires by disturbing the normal processes in the brain that deal with desire and sexual arousal. Certain chemical agents such as antihypertensive, anticonvulsant, serotoninergic antidepressant and neuroleptic drugs may cause a loss of libido - sex drive (12). These drugs alter the production and uptake of certain chemicals called neurotransmitters in the brain that have been found to alter sexual desire/performance. Some of these neurotransmitters are: dopamine, epinephrine, norepinephrine, and serotonin. All have effects on sexual function. For example, an increase in dopamine is presumed to increase libido. Serotonin produced in the upper pons and mid-brain is presumed to have an inhibitory effect on sexual function (12).
There are other medical conditions in addition to psychological disorders that can be the cause sexual problems. In the U.S. there are two million men who are "impotent because they suffer from diabetes mellitus; an additional 300,000 are impotent because of other endocrine diseases; 1.5 million are impotent as a result of vascular disease; 180,000 because of multiple sclerosis; 400,000 because of traumas and fractures leading to pelvic fractures or spinal cord injuries; and another 650,000 as a result of radical surgery, including prostatectomies, colostomies, and cystectomies" (12). Some of the injuries are of the abdomen, lower spinal cord, or pelvic vascular areas, which can compromise circulation to the genitalia or sensory nerves to/from the genitalia - producing impotence or other changes in normal sexual responses.
In addition to psychological disorders, drugs, and varying medical conditions being the cause of sexual dysfunction, injury and/or brain surgery can also cause a range of affects on a person's libido (4). Examining the outcome of damage to certain, specific areas of the brain can help us understand the roles that those parts of the brain play in sexual drive/performance.
There are 4000 serious head injuries that occur each year in the U.S., of which about 100 are survivors. The disturbance of sexual functioning in these head injury survivors is the rule rather than the exception (4). Sexual drive, having to do with structures deep in the brain, are rarely disturbed by non-penetrating head injury. It is sexual motivation and initiation that are damaged by blunt frontal lobe trauma.
Experimentation with animals has demonstrated that the limbic system is directly involved with elements of sexual functioning. In all mammals the limbic system is involved in behavior required for self-preservation and the preservation of the species (12). The limbic system is the "link between higher cortical activity and the lower systems that control behavior" (3). It controls the neuroendocrine system, autonomic system, olfactory sensory processing, emotions and motivation, and memory. The limbic system is interconnected nuclei of the olfactory bulb and orbitofrontal cortex, amygdala, hippocampal formation, hypothalamus, anterior and mediodorsal nuclei of thalamus, septal nuclei, and the Limbic ring of neocortex (7).
Kluver and Bucy proved that the limbic system is involved with sexual functioning in their experiment with monkeys. The monkeys in their experiment were aggressive and raging prior to the operation. The operation consisted of the removal of the monkey's temporal lobe. After the operation the monkeys were docile, orally fixated, and had increased compulsive and sexual behaviors (2). Their findings led to the so-called Kluver-Bucy Syndrome. Humans can get Kuver-Bucy Syndrome when their temporal lobes get damaged from such things as tumors or surgery. Humans with this disorder also experience a disturbance in sexual function just as the monkeys did (3).
Temporal lobe epilepsy is another way in which the temporal lobe might function inadequately and cause sexual dysfunction. There is a high frequency of sexual disturbance in patients with temporal lobe epilepsy. Gastaut and Collomb (1954) were the first to draw attention to hyposexuality after specific inquiry in 36 patients with temporal lobe epilepsy. More than two-thirds showed marked diminution or absence of interest, appetite or sexual activity. Other forms of focal and generalized epilepsy appeared to be unassociated with such problems. Frequently, there was "a remarkable lack of sexual curiosity, fantasies or erotic dreams, yet little to suggest inhibition since the patients talked easily and without reserve about such matters" (12).
The amygdala has a large number of sexual phenomena associated with it. One of the more interesting is the observation that gay men have more connections between the amygdala on each side of the brain than straight men (9). The amygdala manages our emotions and helps to manage our states of consciousness (9). These normal and non-normal states of consciousness have a lot to do with sexual dysfunction (e.g. hyposexuality) as was discussed previously with psychological disorders.
Physiological disorders, medications, certain medical conditions, injury and/or brain surgery are only some of the causes of sexual dysfunction. Examining the neurological causes of sexual dysfunction will allow us to better understand the workings in our brain that have to do with sexual desire - and with this knowledge and better understanding we can hopefully help the many people in our society that suffer from sexual dysfunctions.
2)Brain and physiology of emotion
3)Neuroscience of emotions and sexuality
5)EMOTIONAL MEMORY AND THE AMYGDALA
9)Sex and states of consciousness
10)Sexual Dysfunction Secondary to Depressive Disorders
12)Sexual Dysfunction Following Injury:Time for Enlightenment and Understanding
| Walking a Difficult Line: Taking a Look at Borderl Name: Adria Robb Date: 2002-02-26 09:48:40 Link to this Comment: 1199 |
Individuals with Borderline Personality Disorder (BPD) live a difficult existence. These are people for whom maintaining normal interpersonal relationships, controlling anger, suffer from extreme self-doubt and drastic mood swings, among other symptoms. They comprise only 2% of the population, but have a disorder which the psychiatric and scientific communities have trouble acknowledging, and great difficulty treating. (4)
Individuals suffering from BPD suffer a range of symptoms which include the following: dramatic mood changes, depression, irritability, uncontrollable anger, negative impulsiveness (which includes reckless sex, substance abuse, binging), suicidal feelings, self-mutilation, extreme self-doubt about one’s capabilities. (6, 3) They also experience a kind of heightened awareness of their environment and thus are overly stimulated by it. (1) In addition to these and other symptoms, individuals with BPD often suffer from other mental disorders – such as depression, bipolar disorder, anxiety disorders – as well, making their BPD difficult to diagnose. (4) There is a great mystery surrounding the causes of all mental disorders, and this is also the case with BPD. Psychologists and scientists believe that it is both a biological and psychological disease, and that BPD as an illness is closely related to depression more than schizophrenia, which had been the previous though. Experts have also believe that attention-deficit disorders could be a cause factor, as well as childhood abuse or neglect. (6) Many people suffering from BPD experience very strong feelings of abandonment by parents, family and friends, that can be triggered by an incident that would be perceived as relatively insignificant by the outsider. (4)
Borderline Personality Disorder by definition is very difficult to treat. This is due to the fact that the nature of this psychological disorder affects the patient’s interpersonal skills, which is the basis of therapeutic treatment. Psychiatrists and psychologists find it near impossible to work with patients suffering from BPD because they have little ability to maintain a stable working relationship with anyone (and certainly not a therapist) and their intense mood swings and anger control issues, among other characteristics, are “…likely to lead to clinician burnout…”. (3) This is an obvious frustration for any family member or friend of a BPD individual, who wants nothing more than to have their loved seek out and be successful at getting help to treat their disorder. The is also evidence that medication diagnosed for specific symptoms of the individual with BPD can help, however, the administering and monitoring of psychotropic drugs is usually done in conjunction with some form of psychotherapy, which remains the problem site of treatment. (6,3)
Because of the difficulties in treating BPD patients, there are very few psychotherapists and psychologists who will work with them. Also, there is still relatively little known about this disorder and little research has been conducted in comparison with other severe mental disorders. (3)
There has been one breakthrough in treatment, however, by Dr. Marsha Linehan, a Professor of Psychology at the University of Washington. Her method of treatment – called Dialectical Behavior Therapy or DBT – is on its way to becoming the standard treatment for BPD patients. DBT’s is comprised of one-on-one psychotherapy and a skills training group. “The goals of skills training are to change behavioral, emotional and thinking patterns that cause personal misery and [interpersonal] distress.” (7) The results of Dr. Linehan’s treatment have been positive. During the period of treatment (typically one year), patients undergoing DBT develop fewer thoughts of hopelessness and suicide, were more likely to stick with the treatment and not drop out, and reported that they felt less anxiety and more success in changing behavioral patterns then with traditional forms of psychotherapeutic treatments and medication. (7)
More recently there has been an initiative by the National Institute of Mental Health and the Borderline Personality Disorder Research Foundation to bring neuro- and behavioral scientific researchers together to compare findings on mechanisms of BPD. (5) Some of this research shows that
“…people predisposed to impulsive aggression have impaired regulation of the neural circuits that modulate emotion. The amygdala, a small almond-shaped structure deep inside the brain, is an important component of the circuit that regulates negative emotion. In response to signals from other brain centers indicating a perceived threat, it marshals fear and arousal. …Areas in the front of the brain (pre-frontal area) act to dampen the activity of this circuit. Recent brain imaging studies show that individual differences in the ability to activate regions of the prefrontal cerebral cortex thought to be involved in inhibitory activity predict the ability to suppress negative emotion.” (4)
Despite the fact the discouraging facts that BPD is difficult to diagnose and treat and relatively little research has been done on this disorder, there are a growing number of support networks currently in existence, as well as support groups for families of BPD individuals, and books being published on the disorder. (1, 2) Through this steadily growing awareness there is some hope that eventually more will be discovered about Borderline Personality Disorder and as a result new treatment options will be developed to help patients.
Web Resources:
1) BPD Sanctuary , One of the leading resources and support sites on BPD
2) BPD Central , Another leading site with resources and basic information on BPD
3) The Borderline Personality Disorder Research Foundation
4) National Institute of Mental Health, BPD article “Raising Questions, Finding Answers”
5) National Institute of Mental Health , BPD article “Concept for Borderline Personality Disorder Initiative in FY 2003” research initiative
6) National Alliance for the Mentally Ill site on BPD
7) Dr. Linehan’s DBT course of treatment (“A Promising Treatment…”)
More Information:
8) More basic information on BPD
9) More information on DBT (treatment)
| What is Sleep and the Effects of Sleep Deprivation Name: Tina Chen Date: 2002-02-26 10:01:36 Link to this Comment: 1200 |
Sleep is one of the things that most students can say they do not get enough of. It is a time for us to rest and for a few blissful hours hopefully forget about the stress and worries of school and life. Unfortunately, due to too much work or too much studying to do, often enough, we do not get the amount we need each night to be fully rested the next day. But we have learned to cope with the sleep deprivation by drinking coffee in the morning to wake us up. Even though we are awake, how well can we function throughout the day when we have only had less than five hours of sleep? How much does our behavior change without enough sleep?
Before we get to what the effects of sleep deprivation are, let us first look at what sleep is. Sleep is controlled by neurotransmitters, which act on different neurons in the brain. Some of these neurotransmitters produced, such as serotonin and norephinephrine keep the brain active while we are awake. Researchers think that adenosine builds up in our blood while we are awake and the gradual breakdown of it causes drowsiness. There are five stages of sleep: stage 1, 2, 3, 4, and REM or rapid eye movement sleep. During stage 1-4 of sleep, our brain waves become slower and slower until we switch to REM sleep. At that point, our breathing is more rapid and irregular and our eyes move rapidly under our eyelids. (1).
Circadian sleep rhythm is the internal body clock that is controlled by the hypothalamus. Every twenty-four to twenty-five hours, the cycle repeats itself, which can be effected by light exposure. It is thought that light will reset the clock of your body. The low-point of the rhythm is in the morning, which is thought to help you stay asleep so that you are fully rested and aids in preventing you from waking up too early. Then there is the higher point of the circadian rhythm that allows you to wake up and stay active throughout the day. Then finally, there is again a downswing to make you sleep and the cycle begins all over again. (2).
Why is sleep so important to us? There have been studies done that suggest that sleep deprivation can be detrimental to or decrease the function of our immune systems. Just think, how often was it that after many days of continual sleep deprivation did you start to think that you had a cold? Sleep deprivation can also result in a decrease in core body temperature, decrease in the release of growth hormone, and possible cause an increase in heart rate variability. Sleep also seems to be important in order for our nervous system to work properly. Without sufficient amount of sleep, our behavior and our ability to do things are impaired. We feel drowsy and are unable to concentrate after not getting enough sleep. With enough sleep deprivation, it has been found that some begin to hallucinate and develop mood swings. Higher-ordered cognitive task become more difficult to do where it has been shown that tests that require speed and accuracy have lower results compared to those that are not sleep deprived. Judgment is also impaired; it has been tested that riskier behavior is more likely to occur when sleep deprived. (2).This is part of the reason why you should not drive when you are sleep deprived. Aside from the risk of falling asleep at the wheel, since judgment is impaired, you may make the wrong decision when driving that could cause an accident.
As stated before, when deprived of sleep high-ordered cognitive tasks are more difficult to accomplish. This is why sleep deprivation is so detrimental to students. It has been shown that verbal learning is highly affected by lack of sleep. Recalling things is also more difficult which is why it is important to have sufficient amounts of sleep before taking an exam. (3). It has also been found that thinking and speech can also be impaired. When you do not get enough sleep, it becomes more difficult to communicate to others. The problem is that it is hard to find the right words to say what you are thinking. This suggests that access to long term memory is impaired. Also, when speaking, a person who is sleep deprived will usually speak in a monotone. (4). Just remember to the last time you did not get enough sleep and recall how there were times when you found it difficult to communicate to your friends. Finding the right words, speaking them, and being able to concentrate must have been hard to do.
Sleep is important part of our daily lives. Without it, we would not be able to function well. However, many people, especially students, do not get enough of it. The results are not positive. With lack of sleep, many things are impaired such as memory, judgment, verbal learning and more. All of those things are vital to be a good student because without it, how can you study, do well on an exam or participate in discussions? The only effect of sleep deprivation that you can slightly counteract is drowsiness, which can be reduced by drinking coffee or anything that may have caffeine. Napping in the afternoon can help reduce some of the effects, but it is better to keep those naps short or else, you may end up more tired and groggy than before. So, without enough sleep our behavior will change making us worse students. Therefore, we can conclude that we all need more sleep!
2)http://www.emedicine.com/neuro/topic444.htm,
3)http://www.nature.com/cgi taf/DynaPage.taf?file=/nature/journal/v403/n6770/full/403655a0_fs.html,
4)http://www.lboro.ac.uk/departments/hu/groups/sleep/wellcome.htm,
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| Grow Little Cell Grow! Investigating Neurogenesis Name: Claire Alb Date: 2002-02-26 12:02:24 Link to this Comment: 1205 |
Neurons are the building blocks of the nervous system as they are responsible for the input, processing and transmission of information. Neurons are derived from stem cells as the latter differentitate into specialized cells and make progenitor cells which are responsible for the formation of neuron and glia cells. Although the majority of neurons are formed during the pre-natal and perinatal stage of development, neuron formation continues in the dentate gyrus of the hippocampus (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells. The hippocampus, which lies beneath the cortex is a major factor of learning and memory formation and can indirectly influence emotion
(3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth. Progenitor cells which are present in the subventricular zone of the hippocampus are responsible for such growth as they produce daughter neuron cells through division (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells .
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In the 1960s, Joseph Altman from MIT reported that new neurons were being produced in the dentate gyrus of the hippocampus of adult rat brains. Although such findings were groundbreaking, they failed to create the stir that Elizabeth Gould’s 1998 study caused . The Princeton University neurobiologist demonstrated that the marmoset brain generated neurons (1)The Scientist Magazine , Human neurogenesis. Group demonstrates that adult human brains grow new cells after all. BrdU or bromodeoxyuridine served as a marker when incorporated into the DNA of the progenitor cells and through autoradiographic techniques, the labelled progenitor cells were identified to produce daughter neuron cells. The neurons have “processes which go inward and follow paths to other structures within the hippocampus and get incorporated into basic circuitry of the brain”
(4)New Neurons in Neocortex? New Study Says NO! .
In 2000, Fred Gage of the Salk Institute reported that neurogenesis can take place in the hippocampus of adult animal brains. Progenitor cells were isolated from the adult brains of five subjects with tumors and analyzed in culture dishes. Brdu, was once again used as a marker while the ultimate division of the extracted progenitor cells to neurons observed
(4) New Neurons in Neocortex? New Study Says NO! .
Although these findings are not only revolutionary and exciting, there are many questions which have yet to be answered by neurogenesis. What is the functionality of these replicating neurons? When questioned, Gage stated that “we have theories as to the significance of their function but no proof yet” 1)The Scientist Magazine . Furthermore, as laboratories around the country are finding evidence of these new nerve cells in the hippocampus, the “so what?” question must be asked. How can such findings be applied to everyday life?
Studies on clinical depression demonstrate that patients with bouts of clinical depression have smaller volume sized hippocampus than their normal sized counterparts who do not suffer from it. There is also constant decrease in hippocampal volume due to a lifetime duration of depression (2)American Scientist Magazine. In 2001, Ron Dunman’s research brought not only association of the neurogenesis/depression phenomenon but possible application when demonstrating that treating rats with Prozac and ECT resulted in newly formed neurons in the hippocampus (3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth.
Progenitor cells which are inhibited from dividing throughout most of the brain, do so in the dentate gyrus of the hippocampus and the olfactory bulb as they develop into daughter neurons. Constant renewal of such neurons is thought to be necessary for learning processing and storage of new information (2)American Scientist Magazine. If the mechanisms which inhibit most progenitor brain cells from developing into neurons are found, there is the possibility of repair for damaged brain tissue due to illness, trauma or age. There are also exciting possibilities of stem cell development to diseases such as Parkinson’s and Alzheimer’s, all which are neurodegenerative (5)
Other studies have found that neuronal growth not fixed to the hippocampus. Elizabeth Gould has also published findings which support the neuron formation in the neocortex., as the latter is the most evolved and complex part of the brain which controls cognitive function and language. Pasko Rakic, who’s chairman of Yale’s neurobiology department has consistently contradicted her findings. In December 2001 publication, he concurred with current research that adult primate produce neurons in the hippocampus but could not support the same in the neocortex (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells. The politics revolving around such scientific rivalry and differences must be ignored as future research is done on the neocortex
(6) The Scientist Magazine.
| better to have a bottle in front of me than a fron Name: Lilian B Date: 2002-02-26 12:54:34 Link to this Comment: 1206 |
In the movie, “One Flew Over the Cuckoo’s Nest,” Mcmurphy, the main character, undergoes a frontal lobotomy (“cutting of the lobes”) to treat his ‘mental illness,’ after several rounds of ECT were unsuccessful in crushing his spirit. In the final scenes of the movie we see from his disposition that he has been reduced from an animated, hyperactive state to a vegetative state. McMurphy’s friend, Chief, tries to talk him, but he stares straight ahead and does not respond. The movie takes place in an insane asylum in the 1950’s, the height of the lobotomy craze in the United States. Between 1939 and 1950, nearly 20,000 documented lobotomies were performed, and thousands more in other countries (1). At first the procedure was used in lieu of Electronic Shock Therapy, for rowdy patients who did not respond well to ECT. The lobotomy was applied as a ‘”fix-all” solution for people with all kinds of major or minor mental disorders. Of course, such an invasive procedure is meant to be used only as a last resort in severe cases of debilitating illness. Many doctors, looking for a quick fix for their patients, used the procedure in cases of “undesirable behavior.” Unfortunately, such a broad criterion meant that anything from Schizophrenia to Obsessive Compulsive Disorder (OCD), to unruly behavior in general could be treated by lobotomy. In Japan many of the people lobotomized were just children who did not behave well or who performed poorly in school.
What started the lobotomy craze? As with any result, it is difficult to say what exactly prompted the explosion in popularity of such a gruesome surgery. We can begin by exploring the origins of lobotomy in general: In the late 19th century, the scientific community was beginning to understand that behavior was largely controlled by could be mapped out in the brain. The German scientist, Friederich Golz began by cutting the frontal lobes on dogs. He noted that even ferocious dogs became more tame and subdued after the surgery (1). In 1892, in an insane asylum in Switzerland, Gottleib Burkhardt was inspired by Golz to try the procedure on human subjects. He treated patients who were having hallucinations to lobotomies. Some of his patients did become more calm after the surgery, and others died from complications. Burkhardt’s strategy was widely criticized, and there was not much heard about lobotomies for nearly half a decade (1).
Why the frontal lobe?? It became more clear in observations of lobotomized patients that scientists’ theories about the frontal lobes of the brain were correct. The frontal lobe is thought to be a sort of control center, and the location of the self in the brain (5). It is involved in some motor function, problem solving (divergent thinking), spontaneity, memory, language, judgment, impulse control, social and sexual behavior. “Patients with frontal lobe damage exhibit little spontaneous facial expression, which points to the role of the frontal lobes in facial expression (Kolb & Milner, 1981). Broca's Aphasia, or difficulty in speaking, has been associated with frontal damage by Brown (1972),” (5). Also, lobotomy patients might seem more calm because frontal lobe damage results in a difficulty in interpreting one’s environment. The patient has trouble responding to questions, and his associative learning skills are impaired. Oddly enough, it’s also been documented that people with frontal lobe damage cannot get a “good-belly laugh,” that it, they have trouble comprehending the punch lines of jokes. In a study lead by Dr. Shammi of the University of Toronto, patients with all kinds of brain damage were subjected to the Three Stooges and other humorous material: “The study found that people with right anterior frontal damage had the most disrupted ability to appreciate written and verbal jokes -- and funny cartoons -- compared to the normal control group and people with focal lesions elsewhere in the brain. Individuals with right frontal damage chose wrong punch lines to written jokes and did not smile or laugh as much at funny cartoons or verbal jokes. They showed a preference for silly slapstick humor -- surprising but illogical endings which are the hallmarks of such acts as The Three Stooges.,” (5). So, it follows that the frontal lobotomy should result in drastic changes in social behavior.
Why was the change in behavior of subjects viewed as a change for the better? In the mid 1930’s, a scientist at Yale University (Carlyle Jacobson) began experimenting with ‘lobe cutting’ in chimpanzees. In Jacobson’s experiment, aggressive animals became much more calm. In chimpanzees, this change in behavior seemed to occur without any damage to memory or intelligence. A Dr. Fulton performed the same experiment on chimps, yielding similar results. The calm, docile chimps looked to be much better off then they were before the experiment.
At a neurological conference in England, Fulton shared his results with the Portuguese doctor Antonia Egas Moniz. “Moniz knew that certain psychoses, such as paranoia and obsessive-compulsive disorders, involve recurrent thought patterns that dominate all normal psychological processes. Based on Fulton's ideas, he proposed to cut surgically the nerve fibers which connect the frontal and prefrontal cortex to the thalamus, a structure located deep in the brain, which is responsible for relaying sensory information to the cortex. In this way, Moniz reasoned, there might happen an interruption of the repetitive thoughts, allowing a more normal life for the psychotic,” (1). Moniz worked to develop a procedure that he called ‘white matter cutting.’ Through two incisions on either side of the brain, 2 ‘ice picks’ were inserted. A few sweeps of the pick sliced through brain tissue in the frontal lobes. Some of his patients with anxiety or depression saw improvements in their disposition, while others saw no improvement at all or even the contrary. Moniz specified that his process, the leucotomy, should ONLY be used in cases where there was no other avenue. He believed that in that a morbidly fixed idea could be removed from the brain by destroying the tissue on which the idea was saved. He thought that patients with severe anxieties and depression, or compulsive or hallucinatory disorders could benefit from the removal of the ideas that plagued them(2). In 1949, Moniz was awarded the Nobel prize for medicine and physiology. Some years later, Moniz was shot in the back by an old patient of his. He became paraplegic.
So, the father of leucotomy was a paraplegic, and the procedure he created was at most a minor success. Why was this not the end of lobotomy? Perhaps unfortunately, a scientist named Walter Freeman was also at the London Conference with Moniz and Fulton. Freeman was hopeful about the potential of leucotomies in psychiatric medicine. The awarding of the Nobel Prize to Moniz was to Freeman an indication that the procedure was respectable and effective. In Sept. of 1936 Walter Freeman and his co-worker, James Watt, set out to reinstate the lobotomy as a medical procedure for those with mental ailments. They heralded the operation, believing themselves that it worked. They developed the “Freeman-Watts Standard Procedure,” in an attempt to refine the lobotomy methods being used at the time. The pair toured the country, promoting their procedure and performing it on many patients. Freeman was the driving force in the pair, and he strove to perfect the operation by making it less messy and less time consuming. Their efforts perpetuated the ‘lobotomy craze,’ and by the late 40’s it was an exceedingly popular operation.
People did not begin to realize the ramifications of such a gruesome operation until it became clear, through observation, that lobotomized individuals were far from normal or happy, and that in actuality, the appearance of a less crazed nature had simply been mistaken for (what was in some cases) a total loss of the individual’s personality. In addition, scientists were not getting the results they expected from empirical evidence. It seemed that only 1/3 of the cases yielded any improvement in the patient, while 2/3 of patients remained just as ill as they were initially or, in many cases, their illnesses became worse. Scientist in the 50’s began experimenting with the use of new kinds of psychiatric drugs (such as thorazine) in treating patients, as medication is reversible and brain surgery is not. By the late 50’s, lobotomies had become nearly obsolete, and the status of the procedure was downgraded from effective to experimental. All in all, the lobotomy era seemed to have been a sort of ‘oops’ in psychosurgical science.
Researchers from Mount Sinai Medical School have come to Pilgrim, one of the largest state hospitals in the country to hopefully gain something from the lobotomy tragedy. Dr. Peter Powchik says about the hospital, “If you want to learn why people don’t get better, you do it here.” “Powchik and his colleagues administer teststhat assess patients' thought processes and motor coordination. Their preliminary findings show that lobotomies did not help these patients and in some cases may have even triggered more mental illness. The project has turned up evidence that some people who had lobotomies for depression, anxiety or disruptive behavior developed symptoms of schizophrenia following the surgery,” (4). Philip Harvey, the coordinator of the research project at Mount Sinai hopes that his teams research may give scientists some clues as to how schizophrenia originates in the brain. He is driven finitude of available time for his research to be done. Lobotomies are so rarely performed now, that compiling data on such a massive scale in the future would be impossible. Their job is an emotionally taxing one, as many of the patients are frighteningly sick, and what is more sad, they will not recover:
“All are elderly and have spent most of their adult lives behind locked doors and barred windows. Some spend their days staring vacantly; others are forever agitated. They range from Frances Kichinski, who no matter what she is doing is always weeping, to Pauline White, who smiles constantly and wonders why the family that exists only in her mind never comes to visit,” (4). Harvey laments, "It may have caused some people to be hospitalized for the rest of their lives. It made so many people worse." As for McMurphy, it is clear in the end of the film that he has no way out of the mental hospital, for he is nearly a vegetable, and no one in such a state could be self-sufficient. And so, by killing him, Chief is giving his friend freedom and thus is actually demonstrating an incredible amount of love and reverence for his friend who fell victim to ‘the system,’ as so many others did who are STILL in asylums today.
1)History of Lobotomy,
2)PBS Website,
3)Nobel Prize Website,
4)Research Articles,
5)The Frontal Lobe,
| "Meat all the Way Down": Colin McGinn's The Myste Name: Hilary Hoc Date: 2002-02-26 13:13:53 Link to this Comment: 1207 |
"Meat all the Way Down":
Colin McGinn's The Mysterious Flame
Early in The Mysterious Flame, (1)., philosopher Colin McGinn's breezy but provocative discussion of the relationship between consciousness and the brain, McGinn presents a telling vignette from a science fiction story in which aliens are discussing their observations of humans:
"These creatures are the only sentient race in the sector and they're made out of meat. . . .They're meat all the way through."
"No brain?"
"Oh, there is a brain all right. It's just that the brain is made out of meat."
"So . . .what does the thinking?"
"You're not understanding, are you? The brain does the thinking. The meat."
"Thinking meat! You're asking me to believe in thinking meat!"
"Yes, thinking meat! Conscious meat! Loving meat. Dreaming meat. The meat is the whole deal. Are you getting the picture?" (1).
It is this apparent contradiction, that initially insensate organic material can create consciousness, a phenomenon without apparent material content or spatial location, which McGinn sets out to explain. Many philosophers and scientists have undertaken this journey before him, but McGinn contends that this long road of philosophical inquiry is actually a blind alley. While McGinn believes that the mind is indeed a product of the material qualities of the brain, he argues that the mind (or brain) does not itself possess the ability solve what philosophers denominate "the mind-body problem," (although "mind-brain problem" might be more accurate).
McGinn begins by rejecting both traditional materialism and dualism. Materialists propose that the brain and consciousness are one and the same: thus, brain waves not only correlate with consciousness, they are consciousness. McGinn faults this position for ignoring the very nature of conscious experience. The experience of consciousness, he argues, does not directly correlate with brain waves or the activity on a PET scan. Studying these physical phenomena alone will tell the observer nothing about the experience of consciousness, while endless introspective inspection of one's conscious state would not lead to any description of the brain's anatomy or physiology, let alone that neurons within it were firing as one thought.
Likewise, McGinn rejects dualism, the proposition that consciousness exists completely independent of the brain, because its proponents also ignore empirical observations. Were consciousness completely disconnected from the brain, a fully functioning brain could exist without consciousness, and consciousness could exist independent of the brain, thereby producing what McGinn terms ghosts (disembodied minds) and zombies (organisms with mindless brains, beings who can act but who do not perceive). Dualism thus does not account for empirical observations of conscious organisms, in which the consciousness's existence appears to depend on the brain's activity, and vice-versus. Yet neither science nor philosophy has yet offered a satisfactory explanation of this interdependence.
McGinn offers a third way out of the mind-brain problem: pessimism and acceptance of failure. McGinn agrees with materialists that it is properties of the brain, and the brain alone, which produce consciousness. These properties, however, are unknowable, emerging in their turn from properties of space and matter that the human brain cannot perceive. He postulates a theory he dubs "mysterianism," a respectable way of saying the world will never know. McGinn argues that, in contemplating the origin and nature of consciousness, the human mind has come to the edge of its conceptual capacity: the mind peers over the cliff, but can see nothing but an endless abyss below. While human intelligence can perceive the problem, it cannot understand the answer.
McGinn relies primarily on the concept of cognitive closure to support this argument. Human intelligence, he argues, evolved in response to the environment in which humans had to survive. Thus, certain human capacities are well developed, including the ability to navigate in three-dimensional space and to predict the effect of actions in a three-dimensional world. The imperatives of survival, however, have left other capacities undeveloped or nonexistent: for example, the human brain cannot perceive radar or infrared, or understand whale song. The ability to understand consciousness is simply not, McGinn argues, one of the human brain's talents. Specifically, because consciousness is a nonspatial phenomenon, which affects and is affected by objects that occupy space, McGinn argues that consciousness must have spatial characteristics not perceptible to the human brain. Similarly, while consciousness appears to be immaterial, it is created by and in turn affects matter. Therefore, McGinn reasons, consciousness must depend upon properties of matter imperceptible to the human brain and inaccessible to the mind. McGinn acknowledges that the key to consciousness is located in every sentient organism's genes, because genes code for the construction of all biological phenomena, including consciousness. Yet McGinn maintains that human intelligence as it is currently constructed will never unlock this code.
McGinn's exposition of the mind-brain problem is an intelligent and readable summary of centuries of philosophic debate. Explicitly addressing the layperson, he does not fall into the trap of spewing jargon, although he often belabors his points with one too many repetitious analogies. His straightforward and informal style effectively establishes a dialogue with the reader, although his bursts of self-revelation can become distracting. (Perhaps no one really needs to know about his infatuation with Seven of Nine on television's Starship Voyager.)
As interesting as his argument is, however, McGinn never quite proves his point. The concept of cognitive closure is intuitively appealing and supported by empirical observation: there are in fact various physical phenomena the brain cannot perceive or interpret. It is likely, then, that the brain's limitations similarly constrain the conscious mind. However, McGinn cannot provide a satisfactory account of why humans would experience cognitive closure with regard to consciousness, rather than any other mystery of the natural universe. His supposition that there are properties of space and matter that the human brain cannot perceive and that human intelligence has not yet deduced appears eminently reasonable. However, McGinn does not explain why the properties of space and matter that underpin the structure and formation of consciousness from its origin in the brain will always remain beyond human understanding.
McGinn's examples of human misconceptions about space, for example, undermine the very point he is trying to make. As he points out, contrary to what the brain perceives, humans have deduced that the Earth is not flat, nor does the sun revolve around it, and that matter is not solid. His examples support the idea that humans have been wrong about the natural and biological world, often because their own brains deceive them. Yet human intelligence can deduce, from empirical observations and analysis, physical properties not readily apparent to the brain; McGinn likens humans studying consciousness to pre-Einsteinian physicists, but never makes clear why this analogy presupposes failure rather than success.
Accepting McGinn's proposition of cognitive closure, then, does not necessarily lead to McGinn's ultimate conclusion. Indeed, if cognitive closure can be found anywhere, perhaps it is not in knowing what it is we do not know, but rather in recognizing what we cannot know. How can we know that we cannot know something? If human intelligence is cognitively closed to understanding consciousness, how can human intelligence ever deduce this?
McGinn rests his conviction that the problem of consciousness cannot be solved in part on his misunderstanding of the nature of scientific inquiry. He views science as a collection of disciplines which "ask answerable questions and moves steadily forward," while philosophers wrestle with the insoluble questions at the frontiers of cognitive closure. (1). Were McGinn convinced that scientific inquiry produces as much uncertainty as it dispels, he would find the distinction between science and philosophy less clear cut . Perhaps counterintuitively, his view of science as simple and unambiguous causes McGinn to demand more of science than it can deliver. Like philosophers, scientists often theorize well beyond their empirical observations, altering or abandoning theories as new observations undermine them, but never arriving at one single, immutable truth. As a philosopher, McGinn has assumed a level of certainty in science that is available nowhere in human inquiry and scholarship, be it scientific or philosophic (and his assumption that there is a clear line between these two fields bespeaks unfamiliarity with one or both of them). Seeing uncertainty before him, McGinn announces that the path is cognitively closed and turns back before the journey has truly begun.
References
(1) McGinn, Colin. The Mysterious Flame: Conscious Minds in a Material World. New York: Basic Books, 1999.
Related Web and JStor Resources:
By Colin McGinn:
The following papers and reviews by Colin McGinn are more detailed and technical discussions of aspects of the argument set forth in The Mysterious Flame:
"Can We Solve the Mind--Body Problem?" Colin McGinn. Mind, New Series, Vol. 98, No. 391. (Jul., 1989), pp. 349-366. Stable URL:
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Reviews of The Mysterious Flame
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| Differentiating Tic Disorders Name: Beverly We Date: 2002-02-26 13:33:45 Link to this Comment: 1208 |
Is it possible to differentiate Tourette tics from non-Tourette tics? Are all tics the same? What is a tic? What does a tic feel like? How does "ticcing" affect a person's sense of self or "I-Function"? Are Tic Disorders Inherited?
A tic is a repetitive, uncontrollable, purposeless contraction of an individual muscle or group of muscles, usually in the face, arms, or shoulders. These movements may be signs of a minor psychological disturbance. Such tics often occur in childhood and will probably be outgrown. There are also tics that are caused by neurological disorders that could have resulted from brain damage at birth, head trauma, or use of some specific medication (1). Tic disorders may be inherited. Genetic analysis of numerous pairs of siblings has shown several areas that may contain genes that, when mutated, may give rise, or increase susceptibility to, Tourette Syndrome. There is growing evidence that Tourette Syndrome is inherited from both parents (bilineal transmission), with the father typically affected by childhood tics and the mother typically having some symptoms of obsessive-compulsive disorder (8). Tics can present as motor or vocal and are categorized as Simple or Complex (3) according to age of onset, duration and severity of symptoms (2). There are several different categories of tic disorders.
Transient tic disorders can begin during the early childhood years and can occur in up to 18% of all children. Simple transient motor tics can present in the form of eye blinking, nose scrunching, grimacing and squinting, and other forms (2). Simple transient vocal tics are less common and include sounds repeatedly made such as clearing the throat, coughing, grunting, hiccuping, belching, and other sounds. Transient tics last for a short while, only several weeks or months, and are usually not associated with specific behavioral problems. These tics are more noticeable during stressful, fatiguing or emotional times (2). Boys are three to four times more likely to be affected than girls. Transient tics usually do not last for more than one year, although it is not uncommon to have these episodes over the course of several years. For many children, the symptoms never go beyond blinking and sniffing (or similar choices) and are often described as "nervous habits" or allergy symptoms.
Chronic tic disorders are differentiated from transient tic disorders in that their duration is over many years and the behavior is unchanging. With transient tic disorder, the tic may change from one type to another, (sniffing may be replaced by forehead furrowing and then the furrowing is replaced by finger snapping), while in chronic tic disorder the tic remains the same for a very long time.
Chronic multiple tics present often, and in series. Sometimes it is difficult to draw distinctions between transient, chronic and chronic multiple tics (2).
Tourette Syndrome (TS), first described by Gilles de la Tourette, can be the most debilitating of the tic disorders and is characterized by multiform, frequently changing motor and vocal or phonic tics. There are multiple diagnostic criteria, as defined in the Diagnostic and Statistical Manual of Mental Disorders IV.
A. In Tourette Syndrome, both multiple motor and vocal tics have been present at some time during the illness, although not necessarily concurrently.
B. The tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a period of more than 1 year, and during this period there was never a tic-free period of more than 3 consecutive months.
C. The disturbance causes marked distress or significant impairment in social, occupational, or other important areas of functioning.
D. The onset is before age 18.
E. The disturbance is not due to the direct physiological effects of a substance (e.g. stimulants) or a general medical condition (e.g. Huntington's disease or post-viral encephalitis) (2).
In Simple Motor tics, the movement is fast, darting and meaningless. In Complex Motor tics, the movement is slower and may appear purposeful (2). This form may include copropraxia (making obscene gestures), and echopraxia (mimicking movements that others make) (3). In Simple Vocal tics, the sound production contains meaningless noises. In Complex Vocal tics, there are linguistically meaningful words and phrases, including coprolalia (vocalizing obscene or other socially unacceptable words or phrases), echolalia (repeating what someone else has just said), and palilalia (repeating your own words over and over again) (3).
Tourette Syndrome is a spectrum disorder-it varies with each individual and may appear anywhere on the spectrum between very mild and severe (4). It does not affect intelligence, although in Tourette Syndrome the child may develop such additional behavioral and developmental disorders as Attention Deficit Hyperactivity Disorder, impulsivity, aggressivity, self-injurious behaviors, and varied learning disabilities (2).
When a person is engaged in tic behavior, what does he/she feel? A tic comes on the way a sneeze or a blink comes on; there is a need to complete the act. Tics are involuntary and compelling, and the person has little control over the onset of the tic. Some individuals have reported that they are conscious of the urge to tic before the action occurs (3). The person is fleetingly aware that there is a flashing thought (I-Function or consciousness) which manifests in the tic behavior. I-Function can also be part of unconscious behavior. The motor and/or vocal response that began as an unconscious thought brought awareness during the tic event. If I-Function serves as a filter of both consciousness and unconsciousness, then the tic behavior has been filtered before and during the behavior. Almost simultaneously, the thought and action occur. A tic can be "put off" temporarily, but later, when the person permits him/herself to complete the urge to tic, the ticcing may increase in intensity.
Tics increase in frequency and severity with stress, during relaxation after physical exercise, idleness, fatigue, exposure to heat, and use of dopaminergic drugs, such as steroids, caffeine, and CNS stimulants. Tics usually diminish with performance of engaging mental or physical activities (e.g., playing computer games, playing sports) or with consumption of marijuana, alcohol or nicotine (5). Some people can control the tic urges so that they only tic in the privacy of a safe place, such as their home (4).
Tic disorders challenge individuals because they must develop a sense of self, ("I-Function"), something besides being a person who has a tic disorder. Children must cope with the embarrassment of tic disorders (whether the cause is Tourette Syndrome or a milder tic disorder). They are challenged every day in school settings; their friendships are tested because their behavior is different. Even under the best of circumstances, children have social problems, but with tic disorders, children have a particularly difficult time, often being shunned by playmates and peers. Children will develop this sense of self, this "I-Function," but while the personality is developing they must make choices about how they view themselves. Without a good support system, the child could become depressed and self-loathing, thinking of him/herself only as a person who tics. Without an "I-Function," the body is simply discharging neurological output.
Adults with tic disorders have similar issues, but have the advantage of life experience. They are lawyers and teachers, doctors and artists, plumbers and nurses, mothers and fathers. A person with a tic disorder needs to have a "split personality," in essence two "I-Functions" that can differentiate between the tic disorder and the "other" self. One needs to be able to harmonize the tic behavior into the "I-Function," allowing the behavior to become a part of the individual, rather than having tic behavior that is merely neurological output. The "I-Function" will be the determining factor that distinguishes one person with this disorder from another. An individual's perception of him/herself will greatly predict how successful he/she feels in the company of other people. "I-Function" is that which gives a person a sense of self, whether the I-Function is conscious or unconscious.
No matter what label is given to the tic disorder, the tic probably signifies a subtle brain developmental disorder. Researchers have linked Tourette Syndrome to an area of the brain known as the basil ganglia, which is involved in controlling movement and which plays an important role in attention, concentration, and decision making (6). Tic disorders involve abnormalities in the Central Nervous System levels of neurotransmitters or neuro-peptides, particularly dopamine, norepinephrine, opioid peptides, and serotonin (5). It has been observed that dopamine-blocking agents suppress tics in some individuals (8).
All tics are movements or sounds that occur intermittently and unpredictably out of a background of normal motor activity. Some tics are the result of brain injury, head trauma, or encephalitis, although most tics are commonly called idiopathic, and are part of the spectrum, which includes Gilles de la Tourette Syndrome, or one of the other idiopathic tic disorders (7). Many people now believe that all tic disorders are closely related and are perhaps all part of the same spectrum (4).
The differentiation of Tourette Syndrome tics from other tics may be no more than semantic, a somewhat arbitrary assignment to a category. Furthermore, recent genetic evidence links Tourette Syndrome with multiple and transient tics of childhood; Tourette Syndrome, therefore, can only be differentiated in retrospect (2).
I heard Dr. Oliver Sacks speak on this subject a few years ago and I remember something quite poignant. He said that he had no knowledge of Tourette Syndrome until he was presented with a patient who had this disorder. After that, he saw people with tic disorders everywhere he went. I know several people with tic behavior; I never had a name for the disorder.
2) Tourette Syndrome and Other Tic Disorders ,
4) Tourette Syndrome and Other Tic Disorders ,
5) Is it a tic or Tourette's?,
6) Tourette's, Other Tic Disorders Far More Common Than Once Thought ,
7) Definition and Classification of Tic Disorders ,
8) We Move: Tourette Syndrome ,
| Social Order and Animal Consciousness Name: Porsha Gau Date: 2002-02-26 14:07:09 Link to this Comment: 1212 |
There is nothing new about the uncanny abilities of animals. People have noticed them for centuries. Millions of pet owners and pet trainers today have experienced them personally. But at the same time, many people feel they have to deny these abilities or trivialize them. They are ignored by institutional science. Pets are the animals we know best, but their most surprising and intriguing behavior is treated as of no real interest. Why should this be so, and what about the implications of animal consciousness and intelligence through the behavior observed by those with close relations to animals.
One reason for institutional science’s lack of interest is a taboo against taking ‘pets’ seriously. This taboo is not confined to scientist but is a result of the split attitudes to animals expressed in our society as a whole. During working hours we commit ourselves to economic progress fueled by science and technology and based on the mechanistic view of life. This view, dating back to the scientific revolution of the seventeenth century, derives form René Descarte’s theory of the universe as a machine. Though the metaphors have changed (from the brain as a hydraulic machine in Descarte’s time), life is still thought of in terms of machinery. Animals and plants are seen as genetically programmed automata.
Meanwhile, back at home, we have our pets. Pets are in a different category from other animals. Pet-keeping is confined to the private, or subjective, realm. Experiences with pets are kept out of the real, or objective, world. There is a huge gulf between companion animals, treated as members of the family, and animals in factory farms and research laboratories. Our relationships with our pets are based on different sets of attitudes, on I-thou relationships rather than I-it approach encouraged by science.
Whether in the laboratory or in the field, scientific investigators typically try to avoid emotional connections with the animals they are investigating. They aspire to a detached objectivity. They would therefore be unlikely to encounter the kinds of behavior and apparent consciousness that depend on the close attachment between animals and people. In this realm, animal trainers and pet owners are generally far more knowledgeable and experienced than professional researchers on animal behavior- unless they happen to be pet owners themselves.
Consciousness has been found to be one of the hardest things to define and study. The textbook definition of “Consciousness” is the full knowledge of what is in one’s own mind; awareness. "Consciousness" has many uses that may not be simplified into a single concept. Several useful distinctions among different senses of consciousness have been made though, and aided by these distinctions, it is possible to gain some clarity on the important questions that remain about animal consciousness. There are two notable senses of consciousness which are involved when a creature is awake rather than asleep, and the sense of consciousness shown in the primal ability of organisms to perceive and consequently respond to features of their environments, thus showing them as conscious or aware of of those features. Consciousness in both these senses has been identified in organisms belong to a wide variety of taxonomic groups.
One researcher, Pete Chernika, who has intimately studied consciousness, specifically in dolphins, observes "In experiments, for instance, dolphins appear to pass one consciousness test by recognizing themselves in mirrors. And dolphins also exhibit a keen awareness of the status and identity of other dolphins in their highly social groups. They know who mom is, who the leaders of the pod are, and how they should behave around different individuals," he says. "They appear to be able to envision themselves in relation to all these other animals and then act accordingly."
Many researchers agree that consciousness is more likely in highly social animals such as chimps and dolphins, who must be able to see themselves in relation to others in their groups in order to get along. "Complex social interaction puts a high priority on awareness of self and others," says Chernika.
It is impossible to observe these intangible bonds that form between social animals, that link together the members of their groups or families. The same is true of human social bonds. Our domesticated animals are by nature social, as are we. The bonds between animals and humans are a kind of hybrid between the bonds that animals form with each other and those that people form with each other.
Within these social bonds and interactions there exists an order which may suggest the consciousness of each individual of their function or position within their given social structure. For an animal to recognize its position within the hierarchy of a group, it seems that they would have to be vaguely cognizant of themselves as an individual. Factors such as size, ferociousness, being of the male gender, ect.,which are normally thought to dictate order in most social animal communities, are only fragments of establishing hierarchies and social structures. As an example, elephants usually associate in herds of about 20 individuals led by an old female, or matriarch. It has been observed that the eldest and most experience elephant is chosen as the matriarch and this position is not challenged. The other elephants are respectful and conscious of their place in the herd, and it is not until the matriarch dies is she replaced by the next oldest in the herd. Elephants happen to be very social and keenly sensitive to the motions and noises of the other elephants in their herd, fierce ‘animal’ competition does not dictate their order. Rather a sense of respect and an acute awareness of others behavior causes each individual to behave in a way that creates a cohesive social structure. In many animal social structures this deliberate self-modifcation of behavior and sense of place indicates an awareness of self.
Questions about animal consciousness are a fraction of the large set of questions about animal cognition and mind. The answers to these question of whether animals are conscious beings or "mere automata" could have serious moral consequences, considering the dependence of our societies the uses of animals for biomedical research and farming. The so-called "cognitive revolution" that occurred during the late 20th century has finally led to many experiments by psychologists and ethologists exploring the cognitive capacities of animals. Despite all this work, the topic of consciousness in animals has remained controversial, even taboo, among scientists, even while it remains a matter of common sense to most people that many other animals do have conscious experiences.
Resources:
1) Riba, Rebecca. ‘How Small is the Circle: The question of animal consciousness’ http://www.rso.cornell.edu/MBB/journal/riba.html
2) Animal Consciousness
3) ‘Nature: Inside the Animal Mind’
http://www.pbs.org/wnet/nature/animal mind/consciousness.html
4) Consciousness and Self-Conciousness
5) Griffin, Donald. ‘Animal minds’
6) Animal Cognition and Animal Minds
| Intrapsychic Omnipresence in Bodily Symptoms Name: Ms. Cass B Date: 2002-02-26 14:24:51 Link to this Comment: 1213 |
Sometimes disease and illness just show up. For these medical conditions, a doctor usually tells us what is "wrong" physically. These scientific observations determining diseases or symptoms leave people wondering if there is something behind the cell that created the malfunction. Perhaps one's psyche; which is the mind functioning as the center of thought, conscious or unconscious, and interconnected with the physical environment, can effect the body positively and negatively. An indirect way of dealing with psychological conflict is to intuitively or unconsciously convert it into symptomatic illness. However, this does not get rid of the emotions or the symptoms, for this is not the root of the problem. It is only through recognition of the their intuition or repressed emotions that people may come to heal themselves. It is difficult although possible for some to assign every illness or symptom to some underlying psychic cause; but that is usually whimsically referred to as "new age" and "mystical". It is a person's own personal belief whether she created her diabetes, or whether he created his cancer as a result of psychological and emotional conflict and trauma. Therefore, we can only look at the facts to postulate the argument that a lack of psychological well being manifests itself somatically. The best way to examine the notion that psychological factors affect medical conditions is with the neurosis Hysteria.
Hysteria is also known now as Conversion Disorder or Dissociation, in which unconscious or emotional psychological conflict converts into a bodily disturbance (2). An example of this is anxiety. Hysteria is diagnosed as psychological stress accompanied with physical symptoms. Interestingly, despite the multiple physical symptoms there is no anatomical or organic basis for any of them. Although conversion disorder is a physical manifestation, there is no physical cause. In the case of hysteria, the mind or the psyche is neglected by the person who represses emotional trauma, and these then divert themselves into the body as a means of expression or escape. These patients often times do not know what is wrong with themselves because the repression was unconscious and out of their control. Accordingly, the physical symptoms in hysteria are a result of the person's lack of psychological control, which is unconscious not voluntary.
During the 19th century, French Neurologist J.M. Charcot and Psychologist P. Janet emphasized that “morbid ideas could produce physical manifestations” and that hysteria was caused by the psyche not the body (1). This reference highlights the notion that physical symptoms reflect psychic states. Freud also believed that hysterical symptoms were symbolic of a repressed unconscious “event” or psychic trauma not properly expressed at the time (2). One must appreciate Freud’s assertion of unconsciousness in the pressed event. Some of the physical manifestations of hysteria or conversion are expressed as blindness, paralysis, ataxia, epilepsy, amnesia, anaesthesia, aphonia (loss of voice), and melancholia (3). The same symptoms were also seen in Breuer’s patients like Anna O. One of the most classic of all psychosomatic disorders was the hysteric Dora, Freud's patient. At the age of eighteen she had developed a range of symptoms such as hemicranial headaches, attacks of nervous coughing, tussis nervosa (inflammation of nose and throat), appendicitis, aphonia, fatigue, together with amnesia, dyspnoea (aggravation), hysterical unsociability, and depression. As Freud describes it, Dora "was clearly satisfied neither with herself nor with her family: her attitude towards her father was unfriendly, and she was on very bad terms with her mother....and she tried to avoid social intercourse" (6). Dora also had traumatic sexual encounters with a man which she repressed as well. Clearly Dora had psychological stress, and psychological trauma due to the resulting sexual fears. Dora diverted her repressed sexual encounters and familial conflict into her psyche, which created a plethora of symptoms.
Similar symptoms are also seen in dissociative states where the individual may suffer from "dissociative control" and "dissociative awareness" in that he or she can not consciously control actions and is not aware of what experiences took place (5). For example, amnesia and fugue states represent the person's inability to recollect what actions took place. In fugue states, they are consciously aware of the actions, but they do not remember. Amnesia in hysterics does not come as a result of brain lesion, but as a self-induced protective erasing of an emotional traumatic experience. These states, like hysteria, address the person's involuntary control of their internal experience and worldly actions. Since there was no organic basis for the physical symptoms, physicians like Breuer and Neurologist Charcot in this era used suggestion, free association and hypnosis to free the patients from their symptoms (1). They found that letting the hysteric talk through her conflicts "lead to the disappearance of her symptoms whenever she was able to recollect their root events" (1). This sort of treatment worked because the mental conflict was unknown as far as the patient was concerned. The symptoms served as a psychological defense to banish painful anxiety from consciousness. Therefore, the use of hypnosis, and what later became psychoanalysis, helped in ridding symptoms because the Psychoanalyst was able to draw out unconscious traumatic memories and bring them to conscious awareness to begin a process of mental and emotional healing.
When was the last time you heard about Hysteria? Probably the last time you talked about the Salem Witch Trials. Hsyteria is not a prominent illness as many others today. Where did it go? Have there been more mental illnesses that have taken over or are we just rolling up more names to the old one? Hysteria is the only disease or disorder that has an actual psychological basis. Even some of the psychological disorders like depression and schizophrenia are known to have some physical basis. However, maybe every disease has an underlying emotional memory that is only accessible when brought to consciousness. It could be that every symptom has a negative mental association, and when that is recognized, and released, then the person is able to heal. Perhaps physical and mental illnesses are different across people because they psychologically choose to deal differently with the external environment and certain experiences, and therefore the manifestation of their illnesses. When we hear about miracle cures it makes us wonder what it is that served to heal them spontaneously. It could be that psychologically the person decided what they needed to change in their life in order to be at ease and healthy with themselves. The psychological aspect may be more important in curing diseases than we may think. What is unknown to the normal observer or the people who are actually diseased, is whether or not they have the personal choice to control emotional fluctuations and mental patterns. Is conversion of psychological conflict automatic and involuntary, or can that be governed by our Self?
The tasteful opinion that the individual is in control of his or her health, mental or physical, comes down to personal beliefs. Perhaps all illnesses, diseases, and symptoms stem from psychological disturbance. Clearly, hysteria is conversion of psychological conflict into the body. History tells us that physical symptoms associated with hysteria and dissociative states are a result of negative mental and emotional states. These negative states rather than being released were pushed back further in the mind to the unconscious. It was only through the catharsis of psychotherapeutics that patients could understand the unconscious, which irrevocably led to their symptomatic illnesses. Hysteria is one of the few diseases that is psychological in origin, and may be the only one. Yet, it is possible that all other diseases follow the psychological path as well. Ph.D Louise Hay writes “I have learned that for every condition in our lives, there is a NEED FOR IT. Otherwise, we would not have it. The symptom is only an outer effect. We must go within to dissolve the mental cause. It’s like cutting down the weed and getting the root out” (8). Rather than viewing the sentiment as mystical there is a real basis for further research and understanding in its application in the field of mental health.
3) Notes on Neurotic Disorders
5) Hypnotizability and traumatic experience
6) Freud, Sigmund. Dora: An Analysis of a Case of Hysteria. New York: Simon & Schuster, 1997.
8) Hay, Louise L. Heal Your Body: The Mental Causes for Physical Illnesses and the Metaphysical Way to Overcome Them. Carlsbad: Hay House Inc., 1988
| Pick's Disease Name: Alisa Alex Date: 2002-02-26 14:31:07 Link to this Comment: 1214 |
Pick's disease is a form of dementia characterized by a progressive and irreversible deterioration of social skills and changes in personality, along with impairment of intellect, memory, and language. In 1892 Arnold Pick, a German neurologist studied a patient who in his life had dementia and lost of speech. When the patient died, his brain shrunk, with the brain cells having died (atrophied) in the specific areas of the brain. In Pick’s disease, the frontal and temporal lobes of the brain are most affected. Changes occur in the cerebral cortex (which is how the frontal lobe is affected.) Pick's disease affects the temporal lobes of the brain in 25%, frontal lobes in 25% and both frontal and temporal lobes in 50% of cases (1). Damage to the frontal lobes leads to alterations in personality and behavior, changes in the way a person feels and expresses emotion, and loss of judgment. On a microscopic level, there is severe neuron damage in the cerebral cortex. The brain cells in these areas are found to be abnormal and swollen. These abnormal cells define Pick’s disease and are called Pick’s cells. Pick’s disease is often confused with Alzheimer’s disease where the degeneration generally affects mostly the temporal and the parietal lobes of the brain (2). When such typical cells are not seen on post-mortem examination but the same areas of the brain are affected by cell death the case may be described as Pick's syndrome (3).
In the early stages of Pick’s disease, unlike Alzheimer’s in its early stages, the patient can recognize people and places. Usually, an infected person is diagnosed with “probable Alzheimer’s”, it is later discovered that the patient has Pick’s disease (2). There are three stages of the development of Pick’s disease. The first is usually psychological, behavior, and judgment problems. There may be a change in their social behavior. The second is the development of other symptoms i.e. lost of speech and obsessed behavior. The last is generalized dementia.
There are personality changes where the person may talk to strangers, become withdrawn, impatient or rude. The person may develop insensitivity to others. The person’s actions may seem childish to others (3). Another sign of Pick's disease is that the person often becomes quite obsessed during the early stages, insisting that things are very neat and in order, or constantly washing his/her hand, or observing the methods in which things are carried out. Mathematical skills are usually relatively well preserved in Pick’s disease patients.
The person may develop changes in their diet and crave certain types of foods. These symptoms are often accompanied by weight gain. The person may even become an alcoholic. The may have an overall compulsion to put things in their mouth. They usually develop short attention spans and can barely hold lengthy conversations. The person may have speech problems. Repetition is a common symptom especially in brief words and phrases. Towards the end of the disease, the patient usually becomes completely mute. Unfortunately, people with Pick's disease often suffer from significant lack of knowledge into the effects of their behavior.
There is very little known about the causes of Pick’s disease. Through research, it is known that Pick’s disease is not found in any particular age or race. Researchers have come out with different outcomes. Some researchers say that it affects women more than men while others suggest men are at a greater risk. Anyone can develop Pick's disease. It affects men and women alike. Although it typically affects people in their 50s and 60s it has been diagnosed in people from the ages of 20 to 80. The most severe cases of Pick's disease occur before the age of 60 years . Pick's disease is the cause of less than 10% of all dementias. A brain scan is necessary to help define Pick's disease by showing the degree and location of the degeneration in the brain. There is no cure or effective treatment available. Information and risk factors for Pick's disease are less understood than for Alzheimer's disease. Some people with Pick's disease can live for a very long period of time, and others have a more rapid illness. Doctors can give diagnosis to the living patient through EEG’s to determine whether they have Pick’s disease or something like Alzheimer’s.
Research has not been conclusive as to whether or not the disease is genetic, but it does exist as an inherited disease in some families. The majority of case studies show that the patients affected have no family history of the disease.
The rate of progression varies enormously between people ranging from a duration from 2-15 years . The death is usually caused by infection. Medication can be used to treat some of the behavioral problems. Pick’s disease alone is a very mentally and physically draining disease but along with medication, it maybe almost impossible for patients to continue a normal life once they are diagnosed with the disease and begin treatment.
1)Frontal Lobe Dementia and Pick’s Disease
2)Pick’s Disease from Alzheimer’s Outreach
References
| The Correlation Between Music and Math: A Neurobio Name: Cindy Zhan Date: 2002-02-26 14:34:22 Link to this Comment: 1215 |
I remember the first time I heard the statement ¡° Did you know that listening to classical music enhances your mathematical abilities?¡± I was both intrigued and excited, intrigued because I did not understand how music and math, two seemingly unrelated subject could possibly affect each other. I was also excited because I began to view classical music as some kind of magical potion that would transform my math skills from decent to extraordinary. When I had the opportunity to write this web paper, I immediately jumped into the topic of music and math. The questions that I wish to answer throughout this paper are; does listening to music really help you do better in math? If so, which part of the brain is controlling the correlation between math and music? In addition, how does music stimulate the brain in a way that enhances mathematical abilities?
It turns out that there is much evidence that supports the positive effects of music on one¡¯s ability to do math. Most research shows that when children are trained in music at a young age, they tend to improve in their math skills. The surprising thing in this research is not that music as a whole is enhancing math skills. It is certain aspects of music that are affecting mathematics ability in a big way. Studies done mostly in children of young age show that their academic performance increases after a certain period of music education and training. One particular study published in the journal ¡°Nature¡± showed that when groups of first graders were given music instruction that emphasized sequential skill development and musical games involving rhythmn and pitch, after six months, the students scored significantly better in math than students in groups that received traditional music instruction. (1)
The result of this study posed another important question. How does this type of music that emphasized sequential skills, rhythmn and pitch manage to improve children's ability to do math? It turned out that there are two distinguished types of reasoning, spatial temporal (ST) reasoning and Language analytical (LA) reasoning. LA reasoning would be involved in solving equations and obtaining a quantitative result. ST reasoning would be is utilized in activities like chess when one needs to think ahead several moves. The effect of music on math sometimes termed the Mozart effect. The Mozart effect gain its name after the discovery that listening to Mozart's compositions, which is very sequential, produces a short-termed enhancement of spatial-temporal reasoning. Some key reasoning features used in spatial temporal reasoning are
1. The transformation and relating of mental images in space and time
2. Symmetries of the inherent cortical firing patterns used to compare physical and mental images and
3. Natural temporal sequences of those inherent cortical patterns (3).
The same people who conducted the Mozart effect experiment also suggested that spatial-temporal reasoning is crucial in math. The areas of math that require ST reasoning are geometry and certain aspects of calculus, which require transformations of images in space and time. In higher mathematics, the ability to write mathematical proofs is also associated with ST reasoning because proof writing is a task that requires intuitive sense of natural sequences and the ability to think ahead several steps.
As to the question, what part of the brain controls the correlation between math and music, there are also many resources that provide answers. Dr. Gottfried Schlaug, found that certain regions of the brain such as the corpus callosum and the right motor cortex, were larger in musician who started their musical training before the age of 7 (2). As to what happens in that area of the brain when one listens to music, we turn to the experiment performed by Xiaodeng Leng and Gordon Shaw. Gordon and Leng developed a model of higher brain function, which is based on the trion model. The trion model is a highly structured mathematical realization of the Mountcastle organization principle, with the column as the basic neuronal network in mammalian cortex. The column comprises minicolumns called trions. One particular columnar network of trions has a large repertoire of spatial-temporal firing patterns, which can be excited and used in memory and higher brain functions (3). Shaw and Leng performed an experiment in which they mapped the trion model of firing patterns in that particular column onto various pitches and instruments producing recognizable styles of music. This mapping of the trions gaves insight to relate the neuronal processes involved in music and abstract spatial-temporal reasoning (3). It shows that the part of the cortex, which contains the repertoire of spatial-temporal firing patterns, can be excited by music and is utilized in higher brain functions such as spatial-temporal thinking in mathematics.
In conclusion, my research into math and music does seem to suggest that music enhances mathematics skills. Music targets one specific area of the brain to stimulate the use of spatial-temporal reasoning, which is useful in mathematical thinking. However, as to the question of whether or not music is the magical portion that will elevate anyone¡¯s ability to do math, the answer unfortunately . . .would be no. Just because most mathematicians are fond of music, dosen't mean that all musicians are fond of mathematics. I found a letter posted on the web written by a fourteen-year-old overachiever to a mathematics professor. The student expresses his fraustration that even though he is an excellent musician, math is one of his weakest subjects. In math, he is not making the grades that he needs to stay in a certain prestigious academic program (4).
This letter seems to suggest that listening to music, or being able to master a musical instrument does not automatically guarantee that one can perform well in math. In other words, there are many musicians who are good in music but not in math. Music is a lot more than notes conforming to mathematical patterns and formulas. Music is exhilarating because of the intricacies of the patterns that occurs. Whether or not these patterns resemble math has no relevance to many musicians. More often than not, musicians are inclined to practice music because of the wonders and awe that they feel for music even if they are not aware of the math that is in music.
WWW Resources
(1)Making the case of music education
(2)Music on the mind
(3)Spatial-temporal versus language-analytical reasoning: the role of music training
(4)Letter written by a young musician
| Pick's Disease Name: Alisa Alex Date: 2002-02-26 14:42:45 Link to this Comment: 1216 |
Pick's disease is a form of dementia characterized by a progressive and irreversible deterioration of social skills and changes in personality, along with impairment of intellect, memory, and language. In 1892 Arnold Pick, a German neurologist studied a patient who in his life had dementia and lost of speech. When the patient died, his brain shrunk, with the brain cells having died (atrophied) in the specific areas of the brain. In Pick’s disease, the frontal and temporal lobes of the brain are most affected. Changes occur in the cerebral cortex (which is how the frontal lobe is affected.) Pick's disease affects the temporal lobes of the brain in 25%, frontal lobes in 25% and both frontal and temporal lobes in 50% of cases (1). Damage to the frontal lobes leads to alterations in personality and behavior, changes in the way a person feels and expresses emotion, and loss of judgment. On a microscopic level, there is severe neuron damage in the cerebral cortex. The brain cells in these areas are found to be abnormal and swollen. These abnormal cells define Pick’s disease and are called Pick’s cells. Pick’s disease is often confused with Alzheimer’s disease where the degeneration generally affects mostly the temporal and the parietal lobes of the brain (2). When such typical cells are not seen on post-mortem examination but the same areas of the brain are affected by cell death the case may be described as Pick's syndrome (3).
In the early stages of Pick’s disease, unlike Alzheimer’s in its early stages, the patient can recognize people and places. Usually, an infected person is diagnosed with “probable Alzheimer’s”, it is later discovered that the patient has Pick’s disease (2). There are three stages of the development of Pick’s disease. The first is usually psychological, behavior, and judgment problems. There may be a change in their social behavior. The second is the development of other symptoms i.e. lost of speech and obsessed behavior. The last is generalized dementia.
There are personality changes where the person may talk to strangers, become withdrawn, impatient or rude. The person may develop insensitivity to others. The person’s actions may seem childish to others (3). Another sign of Pick's disease is that the person often becomes quite obsessed during the early stages, insisting that things are very neat and in order, or constantly washing his/her hand, or observing the methods in which things are carried out. Mathematical skills are usually relatively well preserved in Pick’s disease patients.
The person may develop changes in their diet and crave certain types of foods. These symptoms are often accompanied by weight gain. The person may even become an alcoholic. The may have an overall compulsion to put things in their mouth. They usually develop short attention spans and can barely hold lengthy conversations. The person may have speech problems. Repetition is a common symptom especially in brief words and phrases. Towards the end of the disease, the patient usually becomes completely mute. Unfortunately, people with Pick's disease often suffer from significant lack of knowledge into the effects of their behavior.
There is very little known about the causes of Pick’s disease. Through research, it is known that Pick’s disease is not found in any particular age or race. Researchers have come out with different outcomes. Some researchers say that it affects women more than men while others suggest men are at a greater risk. Anyone can develop Pick's disease. It affects men and women alike. Although it typically affects people in their 50s and 60s it has been diagnosed in people from the ages of 20 to 80. The most severe cases of Pick's disease occur before the age of 60 years (3). Pick's disease is the cause of less than 10% of all dementias. A brain scan is necessary to help define Pick's disease by showing the degree and location of the degeneration in the brain. There is no cure and no effective treatment yet available. Information and risk factors for Pick's disease are less understood than for Alzheimer's disease. Some people with Pick's disease and frontal lobe dementia can live for a very long period of time, while others have a more rapid illness. Doctors can give probable diagnosis to the living patient through EEG’s to determine whether they have Pick’s disease or something like Alzheimer’s.
Research has not been conclusive as to whether or not the disease is genetic, but it does exist as an inherited disease in some families. The majority of case studies show that the patients affected have no family history of the disease.
The rate of progression varies enormously between people ranging from a duration from 2-15 years (2). The death is usually caused by infection. Medication can be used to treat some of the behavioral problems. Pick’s disease alone is a very mentally and physically draining disease but along with medication, it maybe almost impossible for patients to continue a normal life once they are diagnosed with the disease and begin treatment.
1)Frontal Lobe Dementia and Pick’s Disease
2)Pick’s Disease from Alzheimer’s Outreach
| Does a split reality exist? D Name: Kornelia K Date: 2002-02-26 16:18:47 Link to this Comment: 1217 |
Where or When (Words by Lorenz Hart, Music by Richard Rogers)
When you are awake; The things you think come from the dreams you dream; Thought has wings-; And lots of things- are seldom what they seem; Sometimes you think you have lived before; All that you live today.; Things you do – come back to you,; As though they knew the way.; Oh, the tricks your mind can play!; It seems we stood and talked like this before.; We looked at each other in the same way then; But I can’t remember where or when.; The clothes you’re wearing are the clothes you wore.; The smile you are smiling you were smiling then,,; But I can’t remember where or when.; Some things happen for the first time,; Seem to be happening again - ; And so it seems that we have met before, and laughed before and loved before,; But who knows where or when! (1)
It happens to many people – you are there and it’s as if you have already been there, you know what is going to happen next and it seems a part of another life you have lived. Some claim that déjà vu is signifying problems in your mental state, that you are probably losing your mind and start living in the hallucinating world of a person with mental problems. Others accept it as a fact of life. But in a survey, over 80% of the participants who reported having experienced déjà vu, denied a possibly clinical condition before their déjà vu incidents, such as mental and physical fatigue, depression, stress, anger, fear. And surveys among random groups of population show that nearly all people experience déjà vu. The statistics varies from 30% to 96%. (3)
The concept of déjà vu is not very well studied. Even though a common phenomenon, most of the studies have concentrated on clinical populations such as psychopathological patients. (6) Neppe’s definition describes déjà vu as any subjectively inappropriate impression of familiarity of the present experience with an undefined past. (2)The term “already seen” was first used in 1876 by E.Letter Boirac who called it “la sensation du déjà vu.” In 1896 F.L. Arnaud introduced it to science. (7)Many researchers are cautious when dealing with instances of déjà vu because of the chance the person who experienced the sensation may have read or seen something that is in his unconsciousness triggering the impression. There exist seven major phenomenological classifications of the déjà vu experience: a disorder of memory, a disorder of ego state, an ego defense, a temporal perceptual disturbance, a recognition disorder, a manifestation of epileptic firing, or a subjective paranormal experience. (2)While reading the different models of explanation that are used (psychodynamic model, physiological model, holographic model, dream and reincarnation, distortion of the sense of time) in discussing déjà vu, I decided to focus on the physiological explanation and the temporal perceptual disturbance. (3)
Of all the five senses it seems that déjà vu occurs only to the sense of sight. A possible explanation of the phenomenon could be the fact that everything seen by a person is in reality perceived independently by the two eyes. So if the signal path to the brain has a slightly different length for the two eyes, then the brain can get signals from one of the eyes faster, process them and turn them into a memory. By the time the signal from the second eye has arrived, there would already exist a memory of the experience, and thus the feeling of a déjà vu happens. The interesting thing is whether individual memories are in some way time marked or whether the brain’s memory keeps “time stamps” on them. (8) Often times we have a time concept of an experience because the memory involves a certain moment of the day, a certain stage in our life. But if the memories are recorded with almost now time difference between each other, and in the case when you do not get déjà vu, do they just mold together and form some kind of a puzzle composed of very fast recorded memories. Experiments have shown that the human brain can only distinguish two individual visual events with respect to time if they occur more than 25 milliseconds apart. (8) So if a person has an optical signal path impairment which results in the image from one eye coming after the other with more than 25 milliseconds, then the brain can think that they are two different incidents instead of parts of one and the same. Once the optic nerves deliver signals to the thalamus, it is responsible for transferring the information to the primary visual cortex in the occipital lobe. But there can be a delay in any part of this journey which would result in two separate images arriving in the memory at different times. If the time difference is great enough a déjà vu can happen. (8) Sno describes this as the event “being experience and recalled simultaneously.” (5)
There is a research done by Vilayanar Ramachandran on the rare condition of blind sight. A person is unable to see but experiences some things that can only occur due to sight. Dr.Ramachandran has discovered that humans actually have two totally separate brain processing methods regarding visual information – the standard thalamus-centered pathway and a more primitive method which is not used in most cases because of evolution and the better efficiency of the thalamus one. However, the argument goes, if the extinction of the primitive method has not completely taken place in some individuals, then maybe they would experience much more occurrences of déjà vu. (8)
In any case, the thing that is most interesting to me is what does déjà vu signify for our memories formation. The wholeness of a memory depends on how fast the perception of the different eyes reached the thalamus. And what becomes an objective reality then? Because something that has objectively happened as a single incident, depending on the functionality of our visual pathway, could become two separate incidents, a split reality. St.Augustine mentiones the phenomenon of “falsae memoriea” in relation to déjà vu, but is a split memory a false memory?
WWW Resources
1)Dreams and Deja Vu
2)The Psychology of Deja vu
3) Deja vu
4)On Deja vu
5)Been There, Done ThatTime magazine
6)The Déjà vu Phenomenon and Personality
7)The Déjà vu
8)A Theory on the Déjà vu Phenomenon
| Attachment and Monogamy as Studied in People and R Name: Ashley Far Date: 2002-02-26 16:32:54 Link to this Comment: 1219 |
“It had to be you, it had to be you
I wandered around, and finally found - the somebody who
Could make me be true, and could make me be blue
And even be glad, just to be sad - thinking of you.”
-Written by Gus Kahn and Isham Jones (10)
The mystery of monogamy has puzzled the human race for a long time. Monogamy is usually reasoned to be the result of an attachment that is strong enough to make someone be true to their loved one. Writers, artists, great lovers, the broken-hearted, and many other people, have entertained the question: if there is such a thing as monogamy, what is responsible for it? Recently scientists have started to seriously ponder the same question. Within the past few years exciting studies and experiments have been done with the intent to delve into this complicated question, which ultimately pertains to love. In 1999, scientists at Emory University led experiments with voles and mice to study monogamy. (1) In 2000, scientists from the University College of London studied the brain activity in a group of people who were “truly, deeply and madly in love” entitled The Neural Basis of Romantic Love. (2) Although no conclusions can be reached, many interesting observations are being made about monogamy and romantic attachment.
Prairie voles are monogamous creatures, so much that eighty percent of the time males refuse to mate with any vole other than their first mate, and both parents tend to their offspring. (3) Montane voles, who are a very closely related species to prairie voles, are polygamous. (4) Both female and male montane voles leave each other and their offspring after mating. "Prairie voles spend more than 50% of the time in close physical contact with each other, whereas montane voles spend less than 5% of the time in close proximity to other individuals.” (5) After studying the social patters of other species of voles, like pine and meadow voles, it is apparent that two neuropeptides are responsible for the difference in social interaction. (4) Oxytocin, in females, and vasopressin, in males are the two chemicals which help prairie voles to be monogamous. (4) These same chemicals are present in montane voles, but do not have the same effect. (5) Oxytocin and vasopressin are released after the prairie voles mate, so that they form an “attachment.” (1)
When the scientists injected male prairie and montane voles with vasopressin, the prairie voles reacted to a female much more than usual. (4) The montane voles, however, did not react significantly to the female vole. (4) The difference in behavior is explained by different vasopressin receptor patterns between the prairie and montane voles. To further test this, the scientists made a mouse with an extremely similar vasopressin receptor pattern to that of the prairie vole. (4) The mouse became more sociable with the female mice. (4) He did not become monogamous, but his social patterns were greatly affected. (4) From this mouse experiment, they were able to conclude that it is not the amount of chemical in brain that had an effect, but the pattern. (6)
When non-monogamous behavior is shown in humans, one often wonders if it is due to a lack of love and a low level of attachment. The study on romantic love does not explain what love is, but shows where love is in the brain. Seventeen people, who were determined by a lie-detector test and a questionnaire to be really in love, had brain scans taken when showed a picture of their loved one, and some close friends. (7) The friends had known the subject at least as long as the loved one, but totally different parts of the brain lit up on the brain scan when showed a picture of a friend than their lover. (2) The parts of the brain that were activated when the picture of the significant other was shown were the “regions implicated in happy states, attention to one's own emotional state and especially social interactions which involve assessing one's own and other people's emotions and states of mind." (2) The parts of the brain that were deactivated were the parts of the brain that are activated when experiencing depression and when these parts are artificially inactivated, they treat depression. (2) It is clear that love creates an intensely happy state in the brain, but this study actually has an even greater implication: the areas activated by drugs, such as cocaine, overlap with the areas activated by romantic love. (2) So, can love really become an addiction? This is a popular question which might hold more weight than we’d like to give it. If love is an addiction, than is attachment a genuine feeling, or just an effect from the ‘drug?’
Another study shows that changing a single gene in a normally solitary roundworm affects it’s eating behavior. (8) When a specific gene is changed, the asocial species eats with the group of normally social roundworms, whereas it would normally eat by itself. (8) This indicates that there is, at a simple level at least, a biological reason for social interactions. Monogamy has not yet been directly linked to a certain chemical, and neither has attachment or love. This is because love and personal relationships are very complex. Love can produce many different bodily symptoms ( i.e. sweating, dizziness) and far more emotional feelings. (9) Love is an abstract concept and thus is hard to be objectified by scientists. Countless studies will need to be done, because all studies and experiments having to do with love will almost certainly be fallible. To attempt to solve the puzzle, one must look at all the different components of love, such as monogamy and attachment, in order to get to the bigger picture. When we do have it all figured out (yeah, right) the song “It had to be you” will hold a whole new meaning. We’ll no longer wonder why it had to be that one person, but will appreciate them even more because of those (presently mysterious) reasons.
(1)Monogamy May Be in the Genes, Discovery Channel Canada
(2)The Neural Basis of Romantic Love, Published Papers from the Laboratory of Neurobiology
(3)Love is All in Your Head -- Or is it in Your Genes?, Web MD Health site
(4)Increased affiliative response to vasopressin in mice, nature.com site
(5)Neuroendocrine bases of Monogamy, sciencedirect.com site
(6)Insel, Young discover ‘sociability gene’ in prairie voles, emory university site
(7)The Science of Love, ABC News site
(8)Dinner together and mating forever -- Is it in the Genes?, Web MD Health site
(9)What is love, medically speaking? Sonoma county medical association site
(10)It had to be you, The Sinatra Songbook
| Mental Imagery: Can a Figment of Imagination Help Name: Erica Carl Date: 2002-02-26 17:01:26 Link to this Comment: 1220 |
“It all comes from the mind. I've seen the most incredible success stories...because a person had a dream and it was so powerful no one could touch it. He'd feel it, believe it, think about it all day and night. That would inspire him to do things necessary to get the results he wanted (2).” -Arnold Schwarzenegger
For the past few weeks, the world has been glued to their television screens, mesmerized by the breathtaking accomplishments of the 2002 Olympic athletes. As an avid watcher of ice skating events, I couldn’t help but wonder what athletes like the bronze medallist Micelle Kwan and the gold medallist Sarah Hughes were thinking prior to their final skating performances. Before the final skating event, both skaters physically practiced their performances. I noticed that in addition to physically preparing themselves by repeatedly running through their performances, Sarah and Michelle closed their eyes and listened to music before they skated. Did mental imagery help either of the athletes prepare and successfully execute their presentations? In other words, what are the effects of mental imagery on the performance of athletes such as Michelle Kwan and Sarah Hughes? Does it make a difference on performance if mental imagery of the desired outcome is absent or present?
What is mental imagery? In The Effects of Mental Imagery on Athletic Performance, Anne Plessinger describes mental imagery as the imagining of the execution of an action without actually performing the action. Plessinger also explains that mental imagery not only includes visual senses, but also auditory, olfactory and kinesthetic senses (4). Studies have demonstrated that mental imagery prior to athletic performance leads to better results than the execution of the action alone. Plessinger describes an experiment that consisted of a control group and an imagery group who were told to complete specific golf skills. It was concluded that the imagery group performed better because they had higher goals and expectations of themselves (4). Perhaps the mental preparation helped the imagery group’s brains acquire the right skills needed. Also, other studies have shown specific physiological differences (breathing, heart rate…etc.) with the addition of mental imagery before performance (1).
Does this mean that mental imagery is linked to motor performance? Would athletes achieve the same or different results if they mentally prepare themselves or not? To answer these questions, I looked at the neurological aspect of mental imagery and motor preparation. In general, motor performance originates from the specific region of the cortex (that controls the visual, auditory…etc. senses) that is stimulated by signals or neurotransmitters traveling by neuromuscular pathways (3). These signals move towards the brain, which turns on motor activities and also effects physiological functioning (1). Thus, if mental imagery and motor performance correlate, shouldn’t the two have the same neural mechanisms (6)? In 1977, Ingvar and Philipson performed experiments demonstrating that mental imagery and motor performance have different neural mechanisms (6). They studied the effects of mental imagery versus motor performance of unilateral hand movements by measuring brain activity. Results showed that two regions of the brain, the supplementary motor area (SMA) and the rolandic region were activated by executed movements whereas only the rolandic regions were stimulated by only imagined movements (6). In 1973, Fujita carried out an experiment that tested the physical versus the mental execution of an activity (3). EMG results demonstrated that a distinction did exist between physical and mental execution because the intensity of the two, represented by their amplitudes, differed. These studies prove that mental imagery and motor performance are separate entities, but are they linked? There is no doubt that mental imagery before execution of an action leads to better results, according to the mentioned studies. Personal experience has shown me that envisioning a perfect piano performance aids in the actual achievement of that goal. In addition, various accounts show that imagery encourages better behavior and heightened confidence (1).
So what about beyond the athletic world? How does mental imagery relate to how we view the world and the universe in general? I came across a few articles that explored the concepts of mental imagery, mental representation, and consciousness. How are these three concepts related to the execution of our actions and how we perceive things (5)? In 1664, Descartes described mental imagery as representational pictures fabricated in the pineal gland of our brains and that these pictures are accessible as information (4). If Descartes idea of mental imagery equating mental representation is valid, then is what we see actually what we see? A very interesting article entitled, The Science of Consciousness by Norman Stubbs, explores this question. Stubbs talks about the idea that our brains are like internal maps that contain patterns of accessible information from the external world (7).
“The world is our brains’ fabrications that we experience rather than something at which we look. It is an internal map; a navigation room in our brains, where information provided by our sensory apparatuses is transformed into a model of our environment. Using this model, as a strategic and tactical planning tool, we are able to formulate action patterns that are sent out on motor neurons for execution and thus we are able to navigate in the environment (7).”
How does Stubbs above quote relate to the Olympics? Doe this mean imagery feeds a better internal map that in turn helps us navigate better in the external environment? Could Michelle Kwan have won the gold if her internal map was better constructed compared to Sarah Hughes’s internal map, and if so, did mental imagery play any part? My findings do lean towards the belief that there is a distinction between mental imagery and motor preparation. However, although they are both separate from each other, mental imagery can affect performance. Should all athletes follow Arnold Schwarzenegger’s advice of success by taking dreams from the mind and turning them into realities? Further research could explore how different types of mental imagery can influence different types of performances. Perhaps experimenting on a greater amount of variables, for example age groups, or looking deeper into the neurological aspect of mental imagery could better our understanding.
WWW Resources
1)Guided Imagery, a good definition of imagery
2)Illegal link - Click on the LeatherPage.com logo for the ... , a good quote about the mind
3)INTRODUCTION TO IMAGERY IN PHYSICAL PERFORMANCE , a source for the neurological aspect of imagery
4)Mental Imagery , a good overall source
5)Mental Imagery, Philosophical Issues About. , another good overall source
6)THE REPRESENTING BRAIN: NEURAL CORRELATES OF MOTOR , a source for neurological aspects
7)Science of Consciousness, an interesting source for the external world and mental imagery
| Locked-In Syndrome and PVS: Implications for Brain Name: Gavin Impe Date: 2002-02-26 20:02:05 Link to this Comment: 1229 |
During our first few class sessions, I became very intrigued by the brain = behavior idea and the I-function. I kept searching for what I thought to be an easy way to approach these complicated issues. We discussed extensively the example of Christopher Reeve, as someone with an intact I-function, but who has lost a certain element of connectedness between total I-function control and his actual body. I became very interested in how the I-function and brain = behavior interrelate. I thought that looking into some information about the persistent vegetative state and the locked-in syndrome would yield a satisfying and definitive answer once and for all. Is a brain still a brain without the I-function? I found no definitive answer, but I was able to convince myself of the "less-wrongness" of the brain = behavior idea.
I first looked into the persistent vegetative state. Below I have reproduced a somewhat technical explanation of how PVS patients are believed not to have an I-function:
Three lines of evidence suggest that PVS patients are "noncognitive, nonsentient, and incapable of conscious experience [12]." First, motor and eye movement, and facial expressions in response to stimuli occur in stereotyped patterns rather than learned reactions. Second, positron emission tomography reveals cerebral glucose metabolism at a level far below those who are aware or in locked in states. PVS levels are comparable to those in deep general anesthesia and as such are totally unaware and insensate. Third, neuropathological examinations of PVS patients show "lesions so severe and diffuse [12]" that it would be almost impossible, giving our current understanding of neural anatomy and function, to have any sort of awareness. (1) [see site for references within]
As the above passage clearly indicates, patients in PVS lack an I-function. They are totally removed from the world of perceptive experience – they are simply not there. A PVS patient goes through normal periods of sleep and wakefulness, can "grind their teeth, swallow, smile, shed tears, grunt, moan, or scream" (2). When I discovered this, I was quite puzzled. I didn’t understand how someone who is ostensibly not in control of such actions, could exhibit behavior that in my everyday life I observe to be a clear indication of emotion and feeling. These are things that seemed to me should to be absent from the lives of people with this syndrome.
What troubled me I later found out, was simply the fact that these things are remarkably similar to things we might normally think are clear evidence of the I-function. So, my problem with the I-function then became the following: if a human being has no I-function then does brain still equal behavior? It seemed very interesting to me that that the things a PVS patient can do don’t require a functioning mind to do them. That is, the brain, even when seriously injured, can control a range of functions within the body, even when the patient has no awareness, no sense of self, and is for all intents and purposes, "not there." I put the last phrase in quotes to highlight it as the first thing that came to my mind when thinking about the relationship between brain, mind, and body in a PVS patient. The body of a PVS patient seemed to me almost like an unmanned vehicle, like a plane on autopilot. Things are happening, but no one is at the controls. The body has lost its I-function, and yet continues to function.
The dynamic relationship between brain, behavior, and the I-function also surfaced in our discussion of paralysis and Christopher Reeve. Intrigued by the fact that despite an almost total disconnection with his body, Christopher Reeve exhibits all the complex manifestations of an intact I-function. How can the I-function still be there, but the ability to control all of one’s body be gone? This seemed to contradict what I learned about PVS patients, who have no I-function, but nonetheless behave with the gesturing of normal healthy humans. Christopher Reeve exhibits the reverse of this scenario. I had discovered at this point that there is evidence beyond the shadow of a doubt that there can be no I-function in patients with PVS. However, I was not as convinced about patients with locked-in syndrome. I wondered if finding more out about patients with this condition could help me to understand more about the brain = behavior idea and the I-function.
The locked-in syndrome describes a condition in which a person is "unable to communicate orally or gesturally due to paralysis of motor pathways" (3). There are numerous grades of this syndrome, with Christopher Reeve as an example of someone who has much of his ability to communicate orally still intact. In Christopher Reeve’s case, it seemed obvious to me that an I-function was intact. However, when did the I-function cease to exist? Some patients with more serious cases of the locked-in syndrome can be fully awake, and aware of what is happening around them, but are unable to effect even the most minor response (4). I was initially unsure of what to make of these patients. How could one objectively determine if these patients had an I-function? What if an I-function were present, and we just could not prove it? In looking at more sites on the web, I found that there are numerous new technologies being tested which can help in both the diagnosis and therapy of patients are with varying degrees of this syndrome. One such technology is called the Eyegaze Communication System and is used as both a therapeutic and diagnostic device (5). The technology employed here relies on tracking movement in the patients eyes, and this can be a tremendously valuable asset when this is one of the only types of motion that can be generated by the patient. Even if the movement is small, it can be used to determine if the patient can in fact respond to commands using his or her limited motor output abilities. The goal of this technology is essentially to harness as much power as one can from the limited amount of output the patient can generate, and to in turn translate this power into meaning and purpose. Even with small eye movements, we can determine if the I-function is present. A patient can be instructed of a set of motions that will convey meanings.
Another such device I read about is a thought translation device that was developed by researchers who noted that it is often very difficult to evaluate a patient’s level of consciousness and awareness when he or she is locked-in and unable to participate in human communication (6). The researchers of this particular study were surprised to find that their belief in a hierarchy of complexity information processing in humans was not validated. Patients in the study often demonstrated complex abilities in the absence of rudimentary ones. Formerly I would have espoused this as clear evidence that brain does not equal behavior. However, when came upon this information, I realized that there is in fact a gray area here that scientists don’t completely understand. We don’t know everything that goes on the brain, but this certainly does not damage the credibility of the brain = behavior model; it simply makes it a little more of a challenge to think of it as still "less wrong."
This led me to the observation that we as humans are naturally attuned to macroscopic and simplistic demonstrations of behavior to prove that our I-functions are intact. In reality, testing for the existence of the I-function in these types of patients is an enormous challenge. So, in my quest to simplify the questions we had been asking in class, I made things more complicated. Overall, the activity of the brain is something that is taken for granted in conscious individuals. It seems odd that people can be vegetative and do so little, yet still be alive. It also seems strange that patients can exhibit a range of behaviors (even laughing) which would normally suggest some sort of cognition when in fact they have no sense of self. The discoveries began to make me feel more comfortable with the brain = behavior notion.
My initial thinking on these subjects was affected by my finding something inherently unsettling when any idea surfaced that would challenge the fact that the I-function is in control at all times. I did not think that the brain = behavior idea could hold when there was no I-function present. It seems a fairly natural human feeling to want to know that one is able to have control over one’s own behaviors and actions all the time. The idea that our brain is in control when "we" are not is unnerving. I found the fact that biological processes can occur without any problem in PVS patients and patients with the locked-in syndrome to be a very difficult concept to grasp. What originally seemed to be a manageable foray into the big question of does brain = behavior turned into something more complicated than I would have thought. In the end, I am much more comfortable with the idea of brain = behavior, having read extensively that documentable neurophyisiological happenings can give satisfactory explanations of the behavior of persons with PVS or in a locked-in state. I know believe that even in patients who are vegetative or locked-in, brain does equal behavior regardless of I-function status.
References:
1)UPENN bioethics site
2) independent patient resource site
3) The Locked-In-Syndrome by Philippe Van Eeckhout.
4) medical summary of conditions and examinations, E. Valenstein & S. E. Nadeau.
5) Use of an Eye-Operated Eyegaze Communication System in Locked-In Syndrome, by: James E. Chapman, M.D.
6) Results and Reflections on the Boundaries of Consciousness, Niels Birbaumer.
| Searching for the Location of Creativity Name: melissa ho Date: 2002-02-26 20:33:47 Link to this Comment: 1231 |
What causes an artist to feel so passionate about his work? What leads the artist in his choice of an outlet for his creativity? What is it that inspires the artist? Is it possible that all of this is formed completely in the artists mind? Is it the case that the “gift” of creativity and genius is given to some individuals and not others, or is the gift of creativity merely the plague of a mental disorder? Do these artists even have anything in common?
Whitman tends to believe that someone does have something in common with him. This is best demonstrated through his poem “Among the Multitude.”
Among the men and women the multitude,
I perceive one picking me out by secret and divine
signs,
Acknowledging none else, not parent, wife, husband, brother, child,
Any nearer than I am,
Some are baffled, but that one is not – that one knows me.
Ah lover and perfect equal ,
I meant that you should discover me so by faint indirections,
And I when I meet you mean to discover you by the like in you.
Here Whitman demonstrates a similarity between people because of some common ground. Although this poem is meant to express a hidden love between a man and a woman, the idea of a common ground work between people can be positioned between artists. In this work Whitman is saying that people with this tie between them know that it is there and can recognize it in an instant. Great artists with a creative nature share a passion for their art as well as a unique way of expressing it. Where does this passion and ability for unique expression come from?
There seems to be a myth encompassing the artists with “madness.” Could it be that this genius is only the result of a mental disorder? Diana Applegate seems to have explored this in her paper “Toward a Neurobiology of Creativity? Making Connections Between Art, Manic-Depressive Illness, and the Frontotemporal Dementia.” She uses Dr. Kay Redfield Jamison’s book, Touched With Fire: Manic-Depressive Illness and the Artistic Temperament, as a main resource. Her final conclusion from this is that, “Jamison's book does not provide us with any answers, but it raises several new and interesting questions. If the behavioral characteristics of the creative process are similar to those of a genetic, neurobiologically-related disorder, then it is conceivable that creativity arises from the interaction of certain neurons in the brain.” Earlier in her paper she also explicitly goes through the process that Jamison uses to illustrate that creativity is very possibly a result of manic depression. Jamison’s support being that many artists have a history of having manic depression. Also that manic depression causes an increased sensitivity to emotion and allows for easier expression of these emotions through art during succeeding highs and lows.
Another approach to the neurobiological idea of creativity is introduced by Semir Zeki in his article “Artistic Creativity and the Brain.” In this artile Zeki says that he hopes that neuroscience will “study the neural basis of artistic creativity and achievement, starting with the elementary perceptual process.” By the perceptual process he is restating the idea that artists precieve life and it’s material things differently than most individuals. He feels that as John Constable says “"The whole beauty and grandeur of Art consists ... in being able to get above all singular forms, local customs, particularities of every kind.... [The painter] makes out an abstract idea ... more perfect than any one original." Zeki says that this is because an artist has a special gift for the attention to detail where generally in our brains this is disregarded because it is not needed. Zeki, also makes no final conclusions only that he has an opinion on the matter.
Scientists have not yet found where creativity is located in the brain. So therefore there is no definite answer as to what causes the differences in artistic variation. However there are many different ideas on this subject. Some scientists believe that it has to do with the “right and left brains”, whereas others feel that it is caused from a mental disorder. These ideas all have flaws and none give an accurate scientifically supported theory. Therefore I am still left with my initial question. Where does creativity come from and what causes variations in this creativity, which causes artists to express their work so uniquely.
I am still left to believe that the only way in which to find an answer to these questions is through Neurobiology. My belief stems from at this point in our exploration of brain and behavior it is fair to say that our brain has an effect on our bodily movement and stimulation through receptors. This idea can best be described through the I-function box, which demonstrates the input and output through the brain. Through this we are shown that through different inputs into the brain we are able to form different outputs. Therefore through a different experience as someone else we are able to form individual personalities. These different personalities cause us to express ourselves differently from any other individual because we have not had the same life experiences as they have had.
So, an artist is as I see it a unique variation of the common man. A common man, is this an artist? I have no direct conclusions only ideas from myself and others because of the nature of this topic. When no scientists have come up with sound theories and scientific evidence to support them, we are left with only one choice. The choice is to come up with our own ideas and thoughts on the topic.
2) "Creativity and Psychopathology", by Rachel Friedman, on the Harvard Brain's Website
http://hcs.harvard.edu/~husn/BRAIN/vol7-spring2000/creativity.htm
4) SCIENCE magazine archives "Artistic Creativity and the Brain" Semir Zeki.
http://www.sciencemag.org/cgi/content/full/293/5527/51
5) THE GIFT OF SATURN: CREATIVITY AND PSYCHOPATHOLOGY
ANTONIO PRETI, MD
http://serendipstudio.org/serendipia/Serendipia-Preti.html
6) Metacognitive Musings, by: John Dalton http://serendipstudio.org/local/suminst/bbi01/projects/dalton/
7) Untitled, by: Elaine de Castro
http://serendipstudio.org/bb/neuro/neuro98/202s98-paper1/deCastro.html
8) Synesthesia: Phenomenology And Neuropsychology - A Review of Current Knowledge by Richard E. Cytowic
http://psyche.cs.monash.edu.au/v2/psyche-2-10-cytowic.html
9) Precis of "THE CREATIVE MIND: MYTHS AND MECHANISMS", What is creativity? - by Margaret A. Boden, School of Cognitive and Computing Sciences, University of Sussex, England
http://www.cogsci.soton.ac.uk/bbs/Archive/bbs.boden.html
| The Link Between Down Syndrome and Alzheimer's Dis Name: Aly Dymkow Date: 2002-02-26 21:40:54 Link to this Comment: 1234 |
The individuals with Disabilities Education Act states that "all children with disabilities, including mental retardation, be educated to the maximum extent appropriate with students who are not disabled" (2). In an ideal world, society would have no problem following this decree, but the world is less than perfect and, therefore, stigmas are unfortunately attached to those suffering from mental disabilities, especially the mentally retarded. One has to question whether this group of people deserves these stigmas. Having grown up with two severely retarded cousins and, for that matter, a great uncle suffering from Alzheimer's Disease, I often wondered as to what was happening within their brains. It was evident that they were unable to respond to me in a normal fashion, but I challenged whether this was just a veneer. Being a spiritual person and believing the mind to be akin to 'the soul', I always felt it must be separate from the brain. A part of me hoped that their minds were still cognizant even though their brain appeared to have a different physiology and they seemed to be unable to respond to me in a normal fashion. However, upon researching the link present between Down Syndrome and Alzheimer's Disease, I began to question whether my previous beliefs were indeed true. I think the questioning of this raises ethical issues about how we treat the mentally disabled and gives quite an argument for the brain = behavior debate.
As more and more adults live longer, age-associated mental disease is becoming more and more of a concern. Present estimations state that soon nearly 10 million Americans will suffer from the disabling disease called Alzheimer's. Alzheimer's sufferers endure the progressive deterioration of cognitive, physical, and adaptive skills, and have a distinctive model of neuropathology (11). The fact that individuals displaying the same symptoms have similar abnormalities in their brains gives supporting evidence to the brain = behavior argument. In further support, studies have suggested that mentally retarded adults have the same risk as other adults of developing Alzheimer's disease, which affects roughly 6% of adults over 65 in the general population. However, adults with Down Syndrome have a much higher rate of developing the disease. 25% of adults with Down Syndrome develop the disease by age 40, and the rate sky-rockets to 65% after age 60. Upon autopsy at death, nearly all adults that suffered from Down Syndrome show brain patterns analogous with those of Alzheimer's (9) . If the brain is responsible for the behaviors demonstrated by the sufferers of both Down Syndrome and Alzheimer's, then one has to question what the link is. What makes the transition from one to the other more frequent than in the general population and why are the mentally retarded not afflicted by Alzheimer's as often as those with Down Syndrome?
Down Syndrome is the most common genetic form of mental retardation and occurs in about 1 out of every 800 births. It has distinctive characteristics that allow it to be easily distinguished from other forms of mental retardation (3). Factors such as maternal age, hormonal abnormalities, x-rays, viral infection, immunologic problems, and genetic predisposition can cause the improper cell-division during meiosis responsible for the syndrome. As a result of this, individuals with Down Syndrome have an extra trisomic chromosome 21 (8). Like Alzheimer's patients, the Down Syndrome brain is different than that of the general population. Down Syndrome's patients have a hindered ability to perform tasks involving cognitation and suffer from other physiological and mental differences (3). The behaviors displayed by individuals with Down Syndrome are similar to those displayed by individuals with Alzheimer's. However, they are not the same and the two diseases can be distinguished from one another. One of the main differences between the two mental diseases is that people are born with Down Syndrome, unlike Alzheimer's, which sets in late in life. One has to remember that even though a person with Down Syndrome has limitations in intellectual functioning, he or she can often function quite normally in the community and can utilize daily living skills, which often disappear with the onset of Alzheimer's (1).
If Down Syndrome patients already display problems with cognitation, then one must wonder as to how the transition from Down Syndrome to Alzheimer's can be witnessed. The problem of Alzheimer's for those with Down Syndrome is especially disconcerting because the progression from the onset of the disease to death takes less time than in the general population. The disease can run its course in 2-8 years depending on the individual and is not always apparent in the beginning. Because the brain is already impaired, memory loss is not always noted at first. With the onset of Alzheimer's, the retarded individual's behaviors often change. These changes may include: the development of seizures, the changing of personality, the occurrence of long periods of inactivity or apathy, the development of hyperactive reflexes, the loss of activity and utilization of daily living skills, the visual retention deficits, the loss of speech, the onset of disorientation, the increasing of stereotyped behavior, and the appearance of abnormal neurological signs (9).
Alzheimer's Disease is identified by senile plaques, made of amyloid peptides, which are derivatives of a large precursor protein, encoded by genes on chromosome 21, and neurofibrillary tangles in the brain. Due to the presence of three copies of chromosome 21 in Down Syndrome patients, scientists are investigating whether the overexpression of the precursor protein may explain the increased occurrence of Alzheimer's Disease in those afflicted with Trisomy 21 (8). It has been demonstrated by a rare genetic defect that mutations of the amyloid percurson protein gene lead to the early development of Alzheimer's Disease. A number of genes found on chromosome 21 may also be responsible for this as well. A gene located on Chromosome 14, coding for the S182 protein, was discovered in 1995 and may be a cause of early onset Alzheimer's Disease. Other genes were discovered recently, including a gene on chromosome 1 that shares similarities with the S182 gene. A protein called APOE4 has been found to be present in almost half of all Alzheimer's cases. It is coded by a gene on chromosome 19 and binds to the amyloid, (the substance present in the Alzheimer brain) (12). A mouse model for partial trisomy 16 is now being used to study the onset of Alzheimer's Disease in those with Down Syndrome because this segment is homologous with chromosome 21 in humans (8). If the Alzheimer's is caused by the presence of this third copy, then there is no explanation as to why Alzheimer's occurs in the general population as well. One of the greatest arguments found for the link between the two diseases comes from Huntington Potter, associate professor of neurobiology at Harvard Medical School. Potter suggests via his findings that all Alzheimer's is due to an extra copy of chromosome 21. This explains the early onset of the disease in those with Down Syndrome. In the general population, some cells undergo improper segregation and thus a small percentage of cells have three copies of the chromosome. The presence of these trisomy cells, would therefore cause the disease later than if all the cells of the body had the trisomy (13).
Because those with Down Syndrome already are afflicted with mental retardation, there has not been as much concern over this growing problem. Some, although seemingly indifferent to the problem, believe that, because the inflicted are already impaired, it is not a major concern. When society takes the attitude of such comedians as Bill Maher of ABC, and equates the mentally retarded with "dumb" animals, respect for human life becomes downgraded. Does a human's value come only from the ability of his or her brain to function correctly or should value be placed on all human life simply by virtue of one's belong to the species? How does one argue that it is more acceptable to help one group of people over another, both of whom suffer from the same disease, just because their brains have functioned at different levels? How do we know that the level of understanding in these individuals has not changed, but rather their ability to make us aware of that understanding has? What if the physiology of their brains allows for understanding, but not responding? What do our judgments then become formulated on? Based on the findings it seems apparent that the brain determines the behavior of the body. However, I can not help but hope that there is something innate within all of us that make us more than just behavioral depictions of the models of our brains.
1)Introduction to Mental Retardation, Site for National Organization of and for People with Mental Retardation and Related Deveopmental Diabilities and Their Families
2)Education Position Statement, Site for National Organization of and for People with Mental Retardation and Related Deveopmental Diabilities and Their Families
3) Task-Related Social Behavior in Children with Down Syndrome, Site for American Association on Mental Retardation
4)Emotion Recognition by Children With Down Syndrome, Site for American Association on Mental Retardation
5)Mental Retardation and Developmental Disabilities Branch (MRDD), Site for National Institute of Child Heath and Human Development
6)Questions, About Down Syndrome, by Dr. Ira Lott, University of California , Good Site for Alzheimer’s questions
7) Alzheimer's disease, Good Online Encyclopedia
8)New Research Into Down Syndrome Homepage, The link between Alzheimers disease and Down Syndrome, Risk of Down Syndome with Increasing Maternal and Paternal Age, Good Detailed Site
9)Alzheimer's Disease and People with Mental Retardation, Good Detailed Site
10)Developmental Disabilities and Alzheimer's Disease, Good Detailed Site by The Arc
11)Epidemiology of Alzheimer Disease in Mental Retardation, Periodicals Index
12)Fact Sheet: Alzheimer's Disease, Family Caregiver Alliance
13)Harvard Researchers Link Alzheimer's to Problem With Chromosome Segregation Presenilin Proteins are Found in Cell Structures Involved in Mitosis, Recent Press Release
| Struggling to Remember Name: Nawal Al-K Date: 2002-02-27 14:45:42 Link to this Comment: 1259 |
The brain gathers, processes, and stores information in a number of ways. When we perceive something, a set of cells in our brain is activated in a specific sequence. If not fully pursued, the perception fades and the cells return to their original state (1). However if the thought or perception is ‘entertained,’ the cells interact, forming a network of communication and signal transmission. The set of cells becomes a memory engram; a neuronal network representing encoded fragments of past experiences. “The set of cells with facilitated synapses is now the anatomical correlate to the memory (1).” Recollection of an event or rather activation of an engram can occur via a stimulus to any of the parts of the brain where a neural connection for the memory exists. Once the engram is activated the hippocampus facilitates activity at the synapse, strengthening the relationship between neurons in the network, thus solidifying the memory (1). The chances of remembering improve by this process of consolidation. Thus, memories play an integral role in our lives; they are the bits and pieces of our experience.
Just as remembering plays a critical role in shaping or lives, so does the process of forgetting. What happens when we forget or lose our memories? Perhaps forgetting is due to poor encoding, an error in the process transforming something a person sees, hears, thinks, or feels into a memory (2). Maybe the absence of proper stimulus prohibits retrieval of information or maybe forgetting serves as a drive to keep us sane, purging the brain of irrelevant data. “If we remembered everything, we should on most occasions be as ill of ass if we remembered nothing (William James, The Principles of Psychology).”
Memory plays a central role in mental health and thus its impairment is one of the most distressing psychological dysfunctions. Amnesia or memory loss is an extreme case of forgetting that occurs often as a result of severe brain injury or traumatic experience. The term amnesia is associated with a broad category of memory deficits ranging from Alzheimer’s disease and anterograde and retrograde amnesia to infantile and childhood amnesia and progressive memory loss due to aging (3). However, clinical cases of amnesia tend to fall into two main categories-psychogenic amnesia and organic amnesia. Psychogenic amnesia refers to instances in which memory loss is presumed to have a purely psychological basis. Traumatic events may have altered the patient’s brain but no physical damage is observed. Organic amnesia on the other hand, is a direct result of brain injury that can be caused by any number of factors: impaired blood supply, tumors, infections, etc (4). Amnesia can affect recollection of experiences occurring either subsequent to the appearance of the disorder (anterograde amnesia) or those that took place prior to its onset (retrograde amnesia) (3).
What stages or aspects of the memory processes are impaired? Neuropsychologists have devoted considerable attention to the nature of memory deficits, specifically with regard to anterograde amnesia (4). The hippocampus and other structures in the medial temporal lobe mediate the consolidation and storage of new memories and thus it seems likely that if some error in memory processing did occur, it would be in these areas of the brain (3). Some theories propose a disruption in the memory process at the initial registration of information. Amnesic patients have the ability to encode sensory properties of information but fail to process it into something meaningful. Another theory suggests the problem lies at the stage of memory consolidation, where information is established into permanent form. Other theories suggest accelerated forgetting or the failure to store or retrieve encoded sensory input is responsible (4).
“Memories are us. They are a function of our past experiences and a framework for our future selves. Moreover, what we individually chose to remember or forget is intrinsic to who we are (1).” Do memories create our identity? What if we lose the ability to choose what we remember or forget, as is the case for those suffering from amnesia? Does this mean they have somehow lost their identity? ‘Mr. Nobody,’ as referred to by the British media, once had a name, a birth certificate, and a career. He used to be a 'somebody' until he was robbed of his wallet, his memory, and essentially his identity on the streets of Toronto. In November of 1999, he awoke in a hospital bed without a clue of who he was and now, three years later is still suffering from a detrimental memory disorder. “Mr. Nobody lives in a vacuum, haunted by a past he cannot remember and a future he cannot plan (5).” In this case, Mr. Nobody’s inability to recall the events of his past has striped away his identity-his mere existence is unbearable without a past to define it. Mr. Nobody however, has not lost the ability to create new memories, but perhaps part of who we are includes memories both from the past and from the present.
“Memory is history recorded in our brain, memory is a painter, it paints pictures of the past and of the day (Grandma Moses).” Are we then, by definition, a product of our memories and experiences past and future?
1) Now where did I put my keys. World and I. volume 13, 1998 (160-168).
2)Memory
3)Amnesia
4)Amnesia
5)The Case of 'Mr. Nobody'
| At a Loss for Words Name: Miriam Shi Date: 2002-02-27 16:46:42 Link to this Comment: 1262 |
“I did not feel like A.H. Raskin. I now had a new self, a person who no longer could use words with mastery.” ~A.H. Raskin, editor for the NY Times
Language is the principal means whereby we formulate our thoughts and convey them to others. It allows us to disclose our fondest memories of the past and communicate our emotions. Language has been instilled in us ever since we were babies inside our mother’s womb. We often take language for granted since most of us have never had to live a life of silence. It is perhaps because of this that people who have suffered brain damage caused by strokes, gunshot wounds, brain tumors, or other traumatic brain injuries feel a loss of self when they lose their ability to speak (1) . If we can’t talk then we can’t communicate right? Wrong.
We often speak of our brains being lateralized. What is brain lateralization exactly? Brain lateralization pertains to the fact that the two halves of our so-called “symmetrical” brain are not exactly alike. There are functional specializations that are specific to each hemisphere (2). For the most part language areas are concentrated in the left hemisphere. Surprisingly, only about three percent of right-handers and nineteen percent of left-handers have language controlled by the right hemisphere (3). Two major areas of the brain, Broca’s area and Wernicke’s area are responsible for language production and language comprehension, respectively. It is fairly difficult to assess exactly what parts of the brain control language, anything really, by any means other than clinical reports of people with brain injuries or diseases. Approximately one million people in the United States currently have aphasia, the language disorder that results from damage to portions of the brain responsible for language (1). Some people with aphasia have problems primarily with expressive language often termed Broca’s aphasia, whereas others have problems with receptive language often dubbed Wernicke’s aphasia (3). The two get their names from Paul Broca, a French neurosurgeon, and Carl Wernicke, a German neurologist who identified their respective parts in the mid-1800s (2). Broca’s area describes the lower rear portion of the frontal lobe on the left side that is in front of the motor strip (4). Patients with Broca’s aphasia often omit small words such as “is”, “and”, and “the (5).” A person with this type of aphasia may say, “Walk dog” meaning, “I will take the dog for a walk.” What is said usually makes sense and is understood, but it is very compressed. Broca’s aphasics are often aware that they are having language difficulties. This level of self-awareness means that they often respond well to treatment. On the other hand, Wernicke’s area is located in the temporal lobe behind the primary auditory cortex (4). Patients with Wernicke’s aphasia tend to speak in long sentences that have no meaning, often creating new words (5). Someone with Wernicke’s aphasia may say, “You know that smoodle pinkered and that I want to get him round and take care of him like you want before,” meaning “The dog needs to go out so I will take him for a walk (5).” Opposite of Broca’s aphasia, people with Wernicke’s aphasia have difficulty with comprehension, yet they often remain unaware of their language difficulties and become annoyed or frustrated when others can’t understand them. Due to this lack of self-awareness, Wernicke’s aphasics rarely respond to treatment.
The idea of self-awareness is an interesting one in the case of aphasics. Psychology textbooks often teach us that self-awareness stems from being aware of others of your species, and then becoming aware, possibly from how others treat you, that you are one of them (6). Furthermore, self-awareness, especially in humans, includes not only awareness of one’s physical self, but also of one’s own personality and character, reflected psychologically in the reactions of other people (6). So then could we presume that Wernicke’s aphasics would respond better to treatment if we didn’t look at them funny every time they spoke? Surely anyone’s recovery or responsiveness to treatment depends on your surroundings and the encouragement from other people.
Although we may think of aphasics as having a huge disadvantage in today’s society where language seems to be the root of any sort of success, after all being able to express one’s desires or goals is appealing. Aphasics have actually been shown to have an interesting advantage over those of us dominated by our left-hemispheres. They are skilled at spotting liars by reading facial expressions (7). Who would have thought? Aphasics in a study done by Nancy Etcoff were shown to have an unusual ability to tell when someone is lying seventy-three percent of the time (7). Non-aphasics had only about a fifty-fifty chance of spotting a liar (7). This would suggest that the brain’s right hemisphere, the undamaged half in aphasia patients, is better than the left half at detecting emotions. Human language includes a strong nonverbal component often hidden under the verbal components. Research in the 1960s has shown that each half of the brain is specialized in a complementary manner for different ways of thinking (8). It has been observed that the mode of the left hemisphere is verbal and analytic, whereas that of the right is nonverbal and global (8). Loss of language due to damage to the left hemisphere may free aphasics to pick up on unspoken cues to deception. When we normally speak to someone else, we get facial expressions, gestures, and words. What we really focus in on is language, and that may be blinding us to some other cues. Our society, mainly our education system largely neglects the nonverbal form of understanding. Although the right and left hemispheres work together, each side processes information differently. Most information in classrooms is geared to the left hemisphere. Therefore, we often forget to use the right side of our brains, which interprets information visually, creatively, and emotionally. What about those students whose right side is dominant? Maybe people who do poorly in school just aren’t “left-brained.”
Damage to the right hemisphere can lead to a loss of the ability to express emotions, leading speech to become lifeless and flat. On the contrary, a person with damage to the left hemisphere, although unable to truly talk, can still sing songs and in fact learn new ones (9). Often scientists and psychologists argue that who we are is our brain. Essentially that our brain is what makes us walk, talk, think, and feel the way we do. Perhaps based on the above findings, who we really are isn’t the brain per se, but the right hemisphere. Oftentimes many have difficulty in accepting that our brain equals who we are because we can’t easily attribute our emotions to the brain. Maybe who we are is based on our personality, in that if we are logical then we are our left hemisphere, and if we are more creative and intuitive we are our right. If our right hemisphere is responsible for such things as intuition and imagination, then wouldn’t we all benefit from a world where children were taught at an early age to use the right side of their brains more often? Would people become more open-minded and insightful? Would we all be able to sit on a jury and correctly incarcerate those who have broken the law? Wouldn’t it be nice if those who were innocent on death row could walk free because an aphasic was able to tell they were telling the truth? Clearly the left and right side of our brains influence us in different ways. No one is completely right-brained or totally left-brained. If we learn to understand how each side functions, then maybe we can better understand how we process information best and learn to adapt specific strategies in ways that work best for us.
WWW Resources
1)American Speech-Language-Hearing Association, Aphasia Facts
2)Handedness and Brain Lateralization, Brain Lateralization
3)Language and the Brain, summary of different types of Aphasia
4)Conversations with Neil’s Brain, story about a man in the operating room Aphasia
5)NIDCD Health Information, Aphasia Facts
6) Gray, Peter. Psychology: Third Edition. New York, NY: Worth Publishers, 1999.
7)C-Health, article on aphasics and lie detecting
8)
9)Aphasia, asymmetry of the brain and aphasia
| What does the placebo effect say about the mind-bo Name: Priya Puja Date: 2002-02-28 12:58:09 Link to this Comment: 1269 |
When I was seven years old my family and I took my grandmother on a trip around northern India. It was her desire to make pilgrimages to the temples that were considered to be the holiest by the Swaminaryans, an orthodox sect of Hindus. At that time in my life, I couldn't even pretend to be interested in the activities occurring within the temples. Instead, I was mesmerized by my proximity to the wildlife that was lounging just outside of the actual walls of temples. In a two-week span of time I must have seen more than twenty temples, and by the end they all blurred together except for one.
Although the temple itself was not magnificent, what was occurring inside has remained with me to this day. A male priest, who was sitting at the main alter, was pulling on elderly woman's hair causing her to scream hysterically. I discovered that the woman was suffering from a headache and was having it cured by the priest. More accurately, she was having the "ghosts" removed from her brain. For the individuals who were directly involved in the ceremony and for many of the people with whom I was traveling, exorcism was a perfectly legitimate way of curing an illness of the body. The cure had no pharmaceutical basis, but it was based in the people's belief system. The belief system for the circumstance that I witnessed was a ritualistic aspect of Hinduism. In the case of the exorcism, the individuals involved expected that the treatment would work, and as a result the treatment did work. The idea that people benefit from expectation alone is called the placebo effect, and it is not unique to India or to the east.
Placebos are medications or treatments that are benign and have no pharmacological properties 1)The Placebo Effect Real of Imagined. The category of placebo includes everything from the hair pulling I witnessed in India to the starch pills that millions of American women take along with their birth control. Until recently, placebos were considered important to Western medicine, in so far as they were part of a rigorous scientific method of testing and approving new medicine. In particular, a standard part of clinical trials is the division of patients into two categories. One category is given the medication being tested and the other is given placebo pills. The trials are such that neither the patients nor the researchers know who is in what category (double blind trials). The purpose of these types of trials is to control for the influence of attitude both on the part of researchers and patients 1)The Placebo Effect Real of Imagined. However, the accumulation of clinical studies that seem to suggest that placebos themselves promote positive health outcomes has caused an explosion in the research of the placebo effect. The placebo effect is "the measurable, observable, or felt improvement in health not attributable" to conventional medical treatment. More importantly, the improvement is believed to be due to the placebo itself 6)The Placebo Effect, good source of general information about the placebo effect.
In the past decade, the most premiere scientific journals have published articles that look at the placebos themselves, outside of their primary role in new drug approval. Last year, a Canadian study suggesting the effectiveness of placebo treatment was published in Science. The study concerned Parkinson's disease, a neurodegenerative disorder that causes impaired coordination and tremors. Parkinson's causes the destruction of brain cells that produce the chemical messenger dopamine. The study demonstrated that similar levels of dopamine are released after injection of a drug or a placebo 3)Great Expectations, summary of a study done on placebo effect in Parkinson's patients. Although dopamine is primarily found in the movement control circuits that degenerate in Parkinson's, the researchers surmised that dopamine is also released by expectation of a therapeutic reward 3)Great Expectations, summary of a study done on placebo effect in Parkinson's patients. According to the researchers, one possible explanation for the phenomena of dopamine release with placebo in take, lies in the connections between the regions of the cerebral cortex and those involved in memory with the substania nigra (the region of the brain affected in Parkinson's) 2)Scientists Show How the Placebo Effect Works. More specifically, memory of earlier benefits from Parkinson's drug could cause dopamine release 2)Scientists Show How the Placebo Effect Works.
There are several recent other studies suggesting that placebos themselves are beneficial. According to a paper presented to the American Psychological Association's (APA) 104th annual convention, the placebo effect accounts for fifty percent of improvements in depressed patients taking antidepressants 4)Listening to Prozac but Hearing Placebo: A Meta-Analysis of Antidepressant Medication, a controversial study done on the effectiveness of using pharmaceuticals in treatment of depression. According to another study, when placebos are given for pain management, the course of pain relief follows that of an active drug 9)The Placebo Prescription, comprehensive non-scientific article on the placebo effect. For both the placebo and the active medicine, peak relief comes about an hour after administration. The placebo effect seems to be acknowledged, perhaps unwittingly, by most medical doctors when one considers that until recently prescribing antibiotics for viral colds and flus was a common practice 5)Understanding It Can Help Avoid Flawed Study Designs.
In western society, the schools of thought regarding the explanation for the placebo effect divide along lines similar to those that divide the schools of thought regarding the mind-body relationship. One explanation for the placebo effect is that it is psychological, "due to a belief in the treatment or to a subjective feeling of improvement" 6)The Placebo Effect, good source of general information about the placebo effect. In other words, "a person's beliefs and hopes about a treatment, combined with their suggestibility, may have a significant biochemical effect" 6)The Placebo Effect, good source of general information about the placebo effect. This type of belief that faith heals can most closely be aligned with dualists who believe that the mind is an "immaterial substance, capable of existence as a conscious, perceiving entity independent of the physical body" 8)Mind, good source of general information on mind body dilemma. As such, the mind can both influence and overcome the body.
Throughout India, people rely on ayurvedic and homeopathic medicine. Although many of these treatments may promote health in some way or another, the belief, and therefore the reality, that these methods actually cure specific physiological illnesses are rooted in the idea that the mind and body are the same thing. Within both eastern and western medicine there are treatments that may be labeled as placebos according to current definitions of the word. Traditional medicine, in all of its varied forms, is no less valuable as a form of treatment when compared to pharmaceutical and non-pharmaceutical placebos that are routinely administered by medical doctors in the west.
The difference between eastern and western medicine is that western philosophy makes distinctions between the mind and body. This results in the unwillingness of western medical practitioners to accept and utilize what they know to be fundamentally true. For example, the very inclusion of a placebo group in clinical studies seems to be an admission that the mind influences the body, yet the placebo effect has until recently been ignored by most scientists. This stands in stark contrast to traditional medicine, which maintains a legitimate place for placebo treatment. The very fact that placebos are not considered to be merely placebos, but actual treatments for specific ailments makes these treatments effective in the circumstance in which they are used. Their effectiveness is not based on the actual pharmaceutical value of specific molecules being inserted into the body, but rather on the belief in getting better.
The placebo effect seems to be proof of the fact that the mind and body are fundamentally connected. The conclusion is not that illnesses and injuries can be healed simply by a belief in the cure being applied. However, the placebo effect suggests that physiological health outcomes are without a doubt influenced by the mind. All of this brings to the forefront the question of what the mind actually is. Although this is a topic for another paper, what can be said is that the placebo effect is essentially a result of beliefs, and beliefs seem to fall partly in the category of non-physiological.
(1) The Placebo Effect Real or Imagined
(2) Scientists Show How the Placebo Effect Works
(3) Great Expectations
(4) Listening to Prozac but Hearing Placebo: A Meta-Analysis of Antidepressant Medication
(5) Understanding It Can Help Avoid Flawed Study Designs
(6) The Placebo Effect
(7) Placebo Effect: The Power of the Sugar Pill
(8) Mind
(9) The Placebo Prescription
, BUT NOT BOTH). REFERENCES (IF ANY) GO IN A NUMBERED LIST AT THE END (SEE BELOW). TO CITE A REFERENCE IN THE TEXT, USE THE FOLLOWING AT EACH NEEDED LOCATION: (YOUR REFERENCE NUMBER).
SUCCESSIVE REFERENCES, LIKE PARAGRAPHS, SHOULD BE SEPARATED BY BLANK LINES (OR WTIH , BUT NOT BOTH)
FOR WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY
REFERENCE NUMBER)NAME OF YOUR FIRST WEB REFERENCE SITE, COMMENTS ABOUT IT
FOR NON-WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY
REFERENCE NUMBER) STANDARD PRINT REFERENCE FORMAT
Other theories regarding the placebo effect are more biological in nature. For example, according to one theory, the placebo effect is merely an illness or injury taking its natural course. In other words, humans can spontaneously heal with time. In addition, illnesses themselves wax and wane 6)The Placebo Effect, good source of general information about the placebo effect. This argument, with its more biological basis, seems to indicate that the body is a distinct entity with the biological potential to heal itself. Another argument that also focuses on the body itself, suggests that the placebo effect "is an organic effect that occurs in patients due to Pavlovian conditioning on the level of abstract and symbolic stimuli" 7)Placebo Effect: The Power of the Sugar Pill, provides a more scientific perspective on the placebo effect. In other words, the placebo effect is a product of an involuntary conditioned reflex of the patient's body 7)Placebo Effect: The Power of the Sugar Pill, provides a more scientific perspective on the placebo effect. Another scientific theory, suggests that the actual process of treatment-touching, showing attention, interpersonal communication-may trigger physical reactions in the body while promoting healing 7)Placebo Effect: The Power of the Sugar Pill, provides a more scientific perspective on the placebo effect. In terms of the mind body debate, the individuals who believe in these more biological explanations of the placebo effect can most likely be grouped together in the camp with metaphysical materialists. According to this school of thought, the mind is the brain itself or an emergent reality of the brain
8)
References
www.studysonline.com
www.healthy.net
www.nature.com
http://journals.apa.org
www.pubs.acs.org
http://skepdic.com
www.epub.org.br
http://skepdic.com/mind.html
www.nytimes.com
YOUR TEXT. REMEMBER TO SEPARATE PARAGRAPHS WITH A BLANK LINE (OR WITH References
| Ecstasy, the Brain, and Serotonin (MIA) Name: Amy O'Conn Date: 2002-02-28 14:32:12 Link to this Comment: 1270 |
stimulant and hallucinogenic properties. Ecstasy is an often talked about drug due to its
recent popularity and rapid spread amongst teenagers especially. Many newspapers and
magazines have featured articles in the past 5 years highlighting the danger of this easily
made drug, and its rampant use in the club/rave scene of almost all Western countries. The
complete effects of ecstasy are still unknown, although much research has been produced that
shows the deleterious effects of the drug on the brain. Ecstasy is also controversial
because the content of pills varies widely; buyers and sometimes sellers don't really know
what each pill consists of (1).
The results of a survey published in 2002 set out with the purpose of examining the
prevalence and patterns of ecstasy use among college students, and to determine
characteristics, associated behaviors, and interests of ecstasy users. These results showed
that from 1997-1999, ecstasy use increased significantly in every college subgroup except
for noncompetitive schools. The variable most strongly associated with ecstasy use was
found to be marijuana. In terms of social context, MDMA users were more likely to spend
large amounts of time socializing, attend residential colleges, and belong to a fraternity
or sorority.
The first study that provided direct evidence that chronic use of ecstasy causes brain
damage was published in 1999. The study used advanced brain imaging techniques (PET scan)
to show that MDMA harms neurons that release serotonin, a chemical that is thought to play
an important role in memory, among other functions. The PET scans showed significant
reductions in the number of serotonin transporters, the sites on neuron surfaces that
reabsorb serotonin from the space between cells after it has completed its work. The
lasting reduction of serotonin transporters occurred throughout the brain. This study and
others suggest that brain damage and the amount of MDMA ingested are directly correlated href="#2">(2).
But what are the functional consequences?
The functional consequences of ecstasy use have just begun to be explored in the past few
years. Another study, published in 2000, found that heavy ecstasy users (30-1000 occasions)
as opposed to non-ecstasy users, reported significantly higher scores on tests for
somatisation, obsessionality, anxiety, hostility, phobic-anxiety, paranoid ideation,
psychoticism, poor appetite, an restless or disturbed sleep. Another interesting effect of
MDMA found was a significantly higher degree of impulsivity. This particular characteristic
of ecstasy users has been found in other studies as well (3).
What is the connection between the neurobiology of MDMA use and the behavior of the user?
How do reduced serotonin levels result in behavior changes such as impulsivity?
Various animal studies have demonstrated that MDMA selectively affects serotonin and
related chemicals in the brain. Brain concentrations of TPH, 5-HIAA and serotonin were
decreased in rats treated with MDMA, while dopamine and similar chemicals weren't affected
at all. In another study, rats treated with MDMA were found to have a dose-dependent
decrease of serotonin in the hippocampus, hypothalamus, striatum and neocortex. Another
study revealed a lasting loss of serotonergic axons in the forebrain after MDMA use. Even
52 weeks after the last MDMA treatment, serotonin concentrations were significantly reduced
in the cortex and hippocampus; serotonin transporter binding was also reduced href="#6">(6).
While there are numerous studies with results like the aforementioned, no convincing direct
causal relations between neurochemical alterations and neuropsychological parameters have
been thus far established (6).
An equally important question is how can scientists present these relationships to the
average ecstasy user in an understandable format? Sites such as dancesafe.org href="#4">(4). and ecstasy.org aim to educate and provide users with literature and
the most up-to-date research on ecstasy while not condemning using it (5).
Approaches like this make imperative information much more accessible to users because it is
both risk-free and personal.
The direct link between the neurotoxicity of MDMA and the psychosocial behavioral effects
has not yet been figured out, but it is clear that a link does exist. Perhaps one day
researchers will be able to find the missing link. Until then, ecstasy users can access web
sites and science journals to attempt to use the drug in the safest possible way.
Works Cited
1)Drug Abuse Home Page, a government
supported cite, strongly anti-drug, and useful reference
sub-group of the NIH
3) Parrot, A.C. et al. "Psychobiological Problems in Heavy 'Ecstasy' Users
(MDMA) Polydrug Users. Drug and Alcohol Dependence. 60 (1999): 105-110.
4)dancesafe homepage, a great resource for
youth especially, not anti-drug
5)ecstasy homepage, independent site for basic
information on using ecstasy safely
6) McGuire, P. "Long Term Psychiatric and Cognitive Effects of MDMA Use."
Toxicology Letters. 112-113 (2000): 153-156.
| Ketamine: An Escape From Reality Name: Kathryn Ro Date: 2002-02-28 16:32:24 Link to this Comment: 1271 |
Ever since I was little, people have warned me about the horrible effects that illegal drugs have on your life. My generation has been taught to think of mind altering drugs in a very negative light yet many people still take these drugs. The general reason that people give to explain this is that the drugs feel good. This seems like a very vague response especially since we have been taught that the negative effects outweigh the bad. Why does it feel good and how good do they feel? It appears that there must be a deeper reason why people take drugs since it is such a risky thing to do. Many drug users, especially those who use psychedelic drugs, say that these drugs give them valuable insights that change their lives for the better. Is it possible that a drug can do this? If so, how do they work?
The reason why many drugs feel so good is due to the dopamine reward system. Whenever one experiences an intense feeling of elation due to something good such as a good grade on a test, a delicious dessert, or hearing your favorite song, she is experiencing the brain’s chemicals acting as a reward (1). In 1954, James Olds and Peter Milner discovered that rats would learn to press a lever if rewarded with a brief burst of electric stimulation. This discovery was significant because it suggested the existence of a pleasure center in the brain. The electrical self-stimulation was most effective when applied to the medial forebrain bundle, which goes from the midbrain to the hypothalamus and then triggers the activity of other cells that extend from the ventral tegmental area in the midbrain to the nucleus accumbens in the forebrain. This pathway relies on the neurotransmitter dopamine and possibly norepinephrine which are enhanced by drugs such as cocaine and amphetamine (2). Drugs can trick the brain into thinking that the body deserves a reward and a flood of dopamine is released, which creates an intense feeling of pleasure.
Pleasure is a feeling that all people seek, and experiencing intense pleasure or euphoria is one very important reason why people use drugs. Drugs can also offer the user an escape from the self and reality. Some people want to escape from an undesirable situation, but many probably want to escape from more than this, they want to escape themselves too. Self awareness is highly evaluative and it can be very stressful to maintain a certain image of the self (7). Using drugs allows some to forget the parts of themselves that they find unacceptable and sometimes it allows them to look into different parts of the self that they are not familiar with. Drugs can also provide temporary relief from the stressful burden maintaining one’s identity. Finally, drugs can allow the user to seek transcendence. Loss of the self entails bliss and is another reason why drugs feel so good (7).
Some of those who use drugs to escape the self hope that this separation will offer insights about the self. These people generally use psychedelic drugs such as ketamine, ecstacy, and LSD. The word psychedelic means ‘mind revealing’ (3). Some believe that these drugs may tell us more about how the mind constructs reality, personality, and a sense of meaning or sacredness (3). For these reasons, some psychologists think that these drugs can be effective ways to enhance therapy.
Ketamine is an especially interesting drug because it can induce near death experiences, which many people believe offer great insight into the self. The way ketamine works is it blocks the N-methyl-D-aspartate receptors in the brain for the neurotransmitter glutamate. These receptors in the temporal and frontal lobes of the cerebral cortex play a key role in cognitive processing, memory, and perception. In a near death experience, a flood of glutamate is released, overactivating NMDA receptors which results in neurotoxicity. When this happens, it is very likely that a flood of neuroprotective agents called endopsycosins bind to NMDA sites to protect them from neurotoxicity are released. Ketamine acts the same way as the neuroprotective agents do, leaving an altered state of consciousness (6).
A near death experience is when a person reports leaving the physical body and possibly going through a tunnel towards a light. One way to classify them is on a five stage continuum (6). First the person experiences feelings of peace and contentment. Second there is a sense of detachment from the body. Next they feel as if they are entering a transitional world of darkness, usually through a tunnel. At the end of this tunnel, they emerge into a bright light and finally enter into this light (6). Ketamine can reproduce all of these features. One ketamine user describes the experience as, “I was convinced I was dead. I was floating above my body. I reviewed all the events of my life and saw a lot of areas where I could have down better (6).” Experiences like these can be therapeutic. Some positive changes resulting from an experience like this include an enhanced joy of living, reduced fear of death, increased concern for others, reduced levels of anxiety and neurosis, and reduced addiction (3).
One of the biggest studies involving ketamine and psychotherapy took place in St. Petersburg, Russia. Over 1,000 patients have been given ketamine to aid alcoholism treatment. These trials were well planned with proper control groups, which is not true of many studies with psychedelic drugs. The results of this study seem to show that ketamine can be an effective supplement to treatment. The subjects who took ketamine had very good rates of sobriety at one and two year follow ups compared to the control group. They also seemed to improve in personality changes as well, with decreased depression, anxiety, and increased ego strength. People seemed to think life was more meaningful. Some believe that ketamine psychedelic therapy can reconnect the ego with denied parts of the self (3).
Ketamine seems to be fairly safe in a hospital setting. It can block nerve paths without depressing respiratory and circulatory functions, which is why it can be used as an anaesthetic (5). In low doses, it actually acts like a stimulant rather than a sedative. However, the hospital is not the only place where ketamine is used. It is becoming an increasingly popular club drug. It also has a bad reputation for being known as date rape drug, since it is colorless, odorless, and can cause amnesia. Common street names for ketamine are “K”, Special K, Vitamin K, and Ket. It can be taken orally, injected, or most commonly snorted. Its original form is a liquid, but is usually microwaved or boiled into a powder form (4). The dosage used in these setting usually does not induce a near death experience, but if it does occur it is commonly called a “k” hole. Some common negative side effects include muscle spasms, blurred vision, slurred speech, dizziness, and impaired coordination (4). It is not physically addictive like cocaine or heroin, but some can because psychologically addicted. The Drug Enforcement Administration just declared it to be a controlled substance in 1999, and is illegal to possess without a prescription or license.
The reasons why people take drugs certainly seem to be more complex in most cases than the simple answer that people take drugs because they feel good. People often use drugs as a way to escape their situation or themselves, and sometimes even to gather insights about themselves. Ketamine seems to be an interesting drug for escape since it provides an experience that seems like the ultimate escape, death. Many swear that drugs like ketamine can change lives for the better and that these drugs have therapeutic effects. However, there is not any conclusive evidence that supports this. While the user probably does gain some insights from ketamine, how valuable or accurate they actually are is questionable. Another question that is raised is what exactly is reality and why do drugs like ketamine change that reality? It is very interesting that those who use ketamine to escape from reality and themselves can end up becoming more in touch with themselves. Of course not all people that use ketamine do so for a life changing experience. The people who use it in clubs or at raves are probably the ones who are using to feel good and have fun, but at the same time this could be an attempt to escape the self and forget about the aspects of the self that are stressful.
3)Ketamine and Quantum Psychiatry
| Attention Deficit Hyperactivity Disorder / Persona Name: Shannon Le Date: 2002-02-28 17:54:23 Link to this Comment: 1272 |
For a typical person with Attention Deficit Hyperactivity Disorder (ADHD) sitting down to do a task such as homework can be agonizing, the physical act of staying in place, being as difficult as concentrating on the work. The person with ADHD may go on in life to have social problems because symptoms such as hyperactivity, inattention, and impulsivity, are mistaken as laziness or self-centeredness (14). The problems of ADHD often develop further manifesting as compulsive disorder, depression, school and job failure, relationship trouble, and substance addiction (5). ADHD is a psychiatric disorder, first documented by the medical society in 1902, that is diagnosed in 3%-5% of school age children (14). Although, there have been many changes in the understanding of the still puzzling disorder, the diagnostic criteria now given for ADHD are given by the DSM-IV, which provides lists of symptoms for three types. The person can have the hyperactivity type, the inattentive type, or a combination of the two, which is a third type. In order to be diagnosed with either type the person must express six of the symptoms from one category or the other, and the symptoms must have been present for at least six months. The person has the combination type if they have six symptoms from both categories (8) .
Many of the symptoms listed in the DSM-IV make ADHD sound more like a personality type rather than a disorder. A person has a 30% chance of having ADHD if a sibling or parent has the disorder, which is not surprising considering personality types also tend to run in families (1). Approximately 2/3 of the children diagnosed with ADHD are comorbid, but then the other 1/3 are otherwise deemed normal (6). Many people with only ADHD may have attention and memory problems, but then also have characteristics that can be looked at in a positive light. For instance these same people are often spontaneous, creative, and outgoing (4). In a world where most of the successful are those who can sit behind a desk for lengthy hours at a time, there are naturally going to be people who have great difficulties doing well in this life style. To what point should people be able to conform to the sit, stay, and focus lifestyle before they are labeled with a disorder?
There has been a great deal of studies done in attempts to find the neurobiological brain differences between normal people and those diagnosed with ADHD. According to MRI and other studies it is believed that a primary problem area for those with ADHD is the frontal lobe, specifically the cortex, an area with functions such as attention, concentration, memory, and learning (12). The frontal lobe is also an area where the neurotransmitter dopamine is synthesized and used. There seems to be lower levels of dopamine in the frontal lobes of those having ADHD. Another study shows 48% higher DOPA decarboxylase activity, which breaks down dopamine, in the right midbrain of those with ADHD (10). Stimulants such as Adderall are thought to increase dopamine levels in this area of the brain by decreasing re-uptake (11). Studies show that 70%-80% of children with ADHD respond positively to the stimulant medications. Other drugs that have been used to treat ADHD include antidepressants that have effects on the neurotransmitters, norepinephrine and dopamine. The diagnosis of ADHD and the prescription of medication to treat ADHD are on the rise (8). Is this because more people are educated about the disorder and are seeking treatment, or is this because many parents are abusing the disorder as an excuse for poor parenting or a child that is not motivated to sit and study? Although, it seems the latter could sometimes be the case, many of the new cases are adults who were never diagnosed because the disorder and the treatments were not as publicly known as they are today. New research shows that 2%-4% of adults have ADHD(). Also more girls that were overlooked, because on average they are naturally less hyperactive then boys, are now being diagnosed (14).
Some of the newer studies supporting differences in the ADHD brain are as follows. Quantitative EEG (QEEG), a highly sensitive and common test for abnormality, shows that children with ADHD have abnormal QEEG scans of up to 80% higher than in normal children. The most abnormal areas are in the thalamocortical and septal-hippocampal pathways located in the frontal part of the brain (3). Another study that suggests differences in the brain of people with ADHD involves DRD4, the dopamine D4 receptor gene. The study suggests an association between the gene and ADHD but the connection is still unclear (13). Perhaps this study will one day reveal the reasons behind lower levels of dopamine in those with ADHD. There was also a study implemented to observe differences in the working memory of those with ADHD and those without. A functional neuroimaging device, positron emission tomography (PET) study, was used to compare regional cerebral blood flow changes in the areas related to working memory. Although, the normal people had more cerebral blood flow change in the frontal and temporal regions, the people with ADHD had changes in blood flow over a larger area, with most of the change focused in the occipital lobe (2). This is important because it suggests that the ADHD brain uses other methods to try to overcome the impaired ability to focus on specific tasks or stimuli. PET studies have also given evidence to support decreased glucose levels, and therefore activity levels, in the frontal regions of the brain during learning for many with ADHD (7). The National Institute of Mental Health (NIMH) is in the process of recruiting volunteers for many new studies to be done concerning ADHD. These studies will be used to gain more knowledge about the biological basis of ADHD. Studies include, more "Brain Imaging of White Matter in Children", "Study of ADHD Using Transcranial Magnetic Stimulation", and "Biological Markers in Childhood Psychiatric Disorders (15,16,17)."
There are a lot of neurobiological differences between the ADHD brain and a normal brain supporting that those diagnosed with ADHD do have a disorder rather than a hyperactive or inattentive personality type. Regardless, personality difference or disorder, those with the symptoms will certainly have a difficult time successfully conforming in today's society. People diagnosed with ADHD have been shown to have deficits in executive functions of the brain, which are responsible for "activating, organizing, integrating, and managing other functions", such as learning memory (9). Executive function is highly important for success in life, and therefore, if the symptoms were before a personality, the personality is now dysfunctional in this society and constitutes being called a disorder. The demands and structure of social, educational, and occupational life will present more of a challenge for those with ADHD than those without, and these people should be given the same chance to succeed if possible. Medications such as stimulants and antidepressants, as well as lessons on how to deal with the symptoms are being used to help people with ADHD conform to the societal norm. Hopefully the many planned and already implemented ADHD studies will bring further insight into the differences of the ADHD brain. This further understanding will foster new ideas of ways to help the people who many times cannot seem to sit still and be calm, and the people who just cannot seem to stay focused, better be able to sit, listen, and concentrate.
1) “Frequently Asked Questions About ADD”, Article from the National ADDA World Wide Website
2) “Alterations in the Functional Anatomy of Working Memory in Adults with ADHD”, An article from The American Journal of Psychiatry
3) “The Clinical Role of Computerized EEG in the Evaluation and Treatment of Learning and ADHD in children and Adults” , An article from The American Journal of Psychiatry
4) “Close Relationships, Intimacy, and ADHD” , Article From CHADD website
5) “Adult ADHD and Social Skills: What Does Everybody Else Know that I Don’t?” , Article from CHADD website
6) “Fact Sheet: ADHD” , Article from the American Psychiatric Association
7) “What Causes ADD?” , Article from ADDA
8) “DSM IV for AD/HD” , Article from the Mental Health website
9) “ADD/ADHA: Reticular Activating System, Neurological Issues with ADD/ADHD Discussed” , Article from About.com
10) “High midbrain F DOPA Accumulation in Children with ADHD” , Article from The American Journal of Psychiatry
11) “ADHD Gets Some Attention” , Article from Neuroscience for Kids, off the Serendip website
12) “Hypofrontalityin ADHD During Higher-Order Motor Control: A Study With Functional MRI” , Article from The American Journal of Psychiatry
13) “Meta-Analysis of the Association Between the 7-Repeat Allele of the Dopamine D4 Receptor Gene and ADHD” , Article from The American Journal of Psychiatry
14) “CHADD Fact Sheet On ADHD Adult Symptoms” , Article from the CHADD website
15) “MRI Brain Imaging of White Matter in Children” , A current Study being carried out by NIMH
16) “Study of ADHD Using Transcranial Magnetic Stimulation” , A current Study being carried out by NIMH
17) “Biological Markers in Childhood Psychiatric Disorders” , A current Study being carried out by NIMH
| Adolescents, Mental Health, and Cigarette Smoking Name: biz martin Date: 2002-03-01 00:03:42 Link to this Comment: 1273 |
I began this research interested in looking at mental health and its relationship to cigarette smoking. By searching the Internet, I found myself being drawn into the discourse surrounding cigarette smoking, mental health and adolescents/adolescence. By seeing nicotine as addictive, and therefore an abuseable substance, and understanding the neurological effects nicotine has on the brain, we can see how cigarette smoking is connected to mental health. In adolescents the effect is even more pronounced because their relationships to peers and parents create situations where their mental health is compromised.
Nicotine is one of the many chemicals found in cigarettes, and is the “primary component in tobacco that acts on the brain.” (1). You would think that after two hundred years of studying nicotine we would have a relatively sound understanding of it, and yet it still produces unexpected side effects on the brain and body.(1). Nicotine addiction in America is most commonly expressed and seen through cigarette smoking. “Most cigarettes in the U.S. market today contain 10 milligrams (mg) or more of nicotine. Through inhaling smoke, the average smoker takes in 1 to 2 mg nicotine per cigarette.” (1).
How does nicotine enter a person’s body and where does it go once it’s inside? “Nicotine is absorbed through the skin and mucosal lining of the mouth and nose or by inhalation in the lungs. Depending on how tobacco is taken, nicotine can reach peak levels in the bloodstream and brain rapidly. Cigarette smoking, for example, results in rapid distribution of nicotine throughout the body, reaching the brain within 10 seconds of inhalation”. (1).
How nicotine interacts with the brain significantly affects behavior. “Of primary importance to its addictive nature is the finding that nicotine activates the brain circuitry that regulates feelings of pleasure, the so-called reward pathways...nicotine increases the levels of dopamine in the reward circuits.” (1). Smoking increases dopamine, which in turn increases pleasurable feelings. The enjoyable effects of nicotine are even more enhanced by the subsequent feelings of craving and withdrawal. This positive reinforcement from needing to sustain increased dopamine levels by smoking, while coping with the addictive qualities of smoking, make this a hard habit to quit. Generally speaking, a smoker will take about 10 puffs on a cigarette in a five-minute period. If one smoked 30 cigarettes a day (1.5 packs), that person would get 300 hits of nicotine a day. “These factors contribute considerably to nicotine's highly addictive nature.” (1).
Even though most smokers would “identify tobacco as harmful and express a desire to reduce or stop using it,” most smokers, who try, fail to quit. “Addiction is characterized by compulsive drug-seeking and use, even in the face of negative health consequences, and tobacco use certainly fits the description.” (1). This makes it all the more significant when you learn that “three-quarters of the adults who currently smoke started their habit before the age of 21.” (2). If adults are already addicted by age 21, when did they start? It turns out that “teenage years are critical ones in the habituation of cigarette smokers.” (2). Cigarette companies know that if they can hook a young consumer in their early years, they will have a customer for life, as long as they can keep them addicted. Since the adolescent years are among the most tumultuous ones, it is important to look at the effects cigarette smoking might have on this population.
It is easy to think of cigarette smoking and nicotine addiction as occurring in a vacuum. Seeing it as just a habit, though, will rule out any connection to mental health. The NIMH and NIDA have both found that “chronic cigarette smoking during adolescence may increase the likelihood that these teens will develop a variety of anxiety disorders in early adulthood.” (3). Since there are strong connections between panic disorders and breathing problems, researchers hypothesized that “smoking might also relate to risk for panic disorder in children and adolescents through an effect on respiration.” (3). This type of correlation is useful aside from empirical research if one wanted a more applied approach when studying this population. Because it “highlights how cigarette smoking may rapidly and negatively affect a teen's emotional health-perhaps even before any of the widely known physical effects such as cancer may occur,” (3). it is able to appeal to something within their realm of imagining. The risk of cancer is in the distant future, but teen’s think with their emotions. Emotional health is something they can understand, relate to and actually want to protect, perhaps by altering their smoking habits.
The National Comorbidity Survey found that “thirty-one percent of those adolescents who smoked 20 or more cigarettes per day had anxiety disorders during early adulthood. Among those who smoked every day and had an anxiety disorder during adolescence, 42 percent began smoking prior to being diagnosed with an anxiety disorder and only 19 percent were diagnosed with anxiety disorders before they reported daily smoking.” (3). The NCS found that mood, anxiety, antisocial personality disorder, and substance use disorders were highly comorbid in a general population sample aged 15 to 54. (4). At the same time, the life span of mental disorders co-existing with addictive disorders was estimated at 50 percent, and in 83.5 percent of these cases, the mental disorder developed during adolescence and before the addiction. (4). The theories concerned with the relationship between substance use and mental disorders have emphasized the interaction between the symptoms of the mental disorder and the mood-altering characteristics of specific substances. (4). In the case of cigarettes and nicotine, the mood altering characteristics would be first and foremost, pleasurable feelings. Don’t underestimate the feelings of irritability and crankiness that occur as dopamine levels fall during withdrawal. This results in a positive feeling when a cigarette is smoked, and a negative feeling when cigarettes are not around: a very obvious reinforcement of cigarette smoking behavior, which is only compounded with the addictive quality of nicotine.
“It has been proposed that substance use is an attempt to self-medicate for difficult feeling states such as depression and anxiety...Adolescence is a difficult developmental period that may precipitate the onset of emotional problems or substance use. Self-medication and using substances to forget unpleasant experiences, or to fulfill a need state that cannot be otherwise gratified have been identified as motivations for adolescent substance use.” (4). It has also been shown that at any one time “between 10% and 15% of the child and adolescent population has some symptoms of depression. The prevalence of the full-fledged diagnosis of major depression among all children ages 9 to 17 has been estimated at 5%.” (5). These aren’t flat out correlations between depression and cigarette smoking, but they do offer reasonable implications on the relationship between the two. Adolescence is a time when depressing thoughts crowd the mind; it’s reasonable to believe that much of smoking begins due to depression and the need to self medicate the dopamine levels in the brain.
Adolescent onset smoking is only now being recognized as a problem. “Although an estimated 1 million adolescents begin smoking annually, and although cigarette smoking continues to be the largest cause of preventable illness and death in the United States, the number of studies dedicated to smoking cessation interventions was woefully small.” (6). Complying with the realization that the risk of emotional instability over the risk of cancer would cause greater reactions in adolescents, is Hurt’s conclusion that, “the nicotine patch therapy plus minimal behavioral intervention does not appear to be effective for treatment of adolescent smokers.” (6). More effort needs to be placed into creating a more effective smoking cessation program aimed at adolescents, as well as making the treatment available to them.
One source of prevention is, of course, the parents. “Children living with nonsmoking parents-and particularly those youngsters who also have mothers with a strong antismoking attitude--are 50% less likely to take up the tobacco habit compared with their peers,” researchers report. (7). One study, supported by the NIH, was concerned primarily with the role of the mother’s attitude about smoking. They found that “children in households where neither parent smoked and the mother had strong antismoking beliefs were 50% less likely to take up the habit than other children.” (7). When compared to houses where either parent smoked, there was “no reduction in adolescent smoking associated with mothers' antismoking attitude. This joint effect of parental attitudes and behaviors suggests that mothers' attitudes have a substantial influence on children and adolescents, but that this influence occurs only when the attitudes are strongly held and both parents behave in a manner consistent with those attitudes and do not smoke." (7).“Do as I say, not as I do,” has rarely carried much weight though. Kids will often mimic their parents behavior even when they are told not to.
The concern lies in keeping teenagers from starting smoking, so they will have less chances of
starting this habit as they grow up. Because mental health is tied into cigarette smoking, there are even
more levels on which to appeal to someone’s sensibilities. It’s hard to explain to someone who is so young, that their health in old age depends on choices they make when they are young. It might be more relevant to talk with an adolescent about their emotional state and to correlate that with any cigarette smoking behavior. Cigarette smoking creates changes in brain neurology by heightening activity in the pleasure zone. It is important to realize what the interactions are that occur between cigarettes and the brain, because they have implications for mental health and behavior.
1) National Institute of Drug Abuse page on nicotine, describes nictotine’s addictive qualities
2)Division of Alcohol and Drug Abuse smoking fact sheet, good source for smoking fact sheet
3)National Institute of Health paper, good paper linking adolescent cigarette smoking to anxiety disorders
4)Substance Abuse and Mental Heatlh Services Administration, paper explaining comorbidity of smoking and mental health
5)American Medical Association, mental health and adolescents
6)Archives of Pediatric and Adolescent Medicine, paper about promoting adolescent smoking cessation
7)Medline Plus Health Information, relating a parents expectation to whether or not a kid will smoke
| Attention-Deficit Hyperactivity Disorder, Ritalin, Name: Sujatha Se Date: 2002-03-01 00:06:19 Link to this Comment: 1274 |
Attention-Deficit Hyperactivity Disorder, more commonly referred to as simply ADHD, is the most commonly diagnosed disorder among American children today. According to the National Institute on Mental Health an estimated 3 to 5 percent of school age children are affected by this disorder. (1) There are more diagnosed cases of ADHD of in the United States than there are anywhere in the world. The main symptoms of ADHD include "developmentally inappropriate levels of attention, concentration, activity, distractibility, and impulsivity." (1) While the number of people diagnosed with ADHD increases dramatically every year, there is still much about the disorder that is not understood. While scientists have deduced that ADHD originates in the brain, they still have many questions about the nature of it. The classification of Attention-Deficit Hyperactivity Disorder has become quite a controversial topic in American society today. There are some who believe that by recognizing the symptoms associated with the disorder as ADHD; science is simply putting a band-aid on a problem that could be otherwise corrected with behavior modification.
The lack of a complete understanding of ADHD has led scientists to question how to go about treating ADHD. While at the moment the disorder cannot be cured, they are methods that scientists have come up with to address the symptoms displayed by ADHD. These approaches range all the way from psychotherapy, and cognitive-behavioral therapy, to the prescription of pyschostimulant medications. (3) The most popular of these medications include amphetamines, such as Aderall, and methylphenidates such as Ritalin. (1) The use of such drugs has caused controversy among scientists and general American society alike. If we do not understand the exact nature of Attention-Deficit Hyperactivity Disorder is it appropriate to use drugs as methylphenidates to deal with it? While studies conducted on the short-term use of these drugs have indicated strongly favorable results in reducing the symptoms of ADHD, at the present there have not been any conclusive studies to show the long-term effects of methylphenidate.
To look at the other side of the debate on ADHD one must also consider the argument that while scientists at the moment do not completely understand the nature of ADHD, they are obligated to learn more. If the use of Ritalin has shown obviously beneficial effects is it not logical to use it? The debate surrounding the use of psychostimulants drugs, and more specifically Ritalin, has mainly to do with the lack of understanding concerning ADHD than it does with the drugs themselves. Scientists believe that one first one has to recognize ADHD as a disorder before one can proceed to evaluate its treatments. Ultimately the battle over Ritalin and ADHD demonstrates the lack of understanding we as humans have of the brain and how it functions.
Attention-Deficit Hyperactivity Disorder most popularly associated with an inability to concentrate has been identified by the American Psychiatric Association as displaying nine possible symptoms. To be diagnosed with ADHD a person must display at least six of the nine symptoms. These symptoms include:
-Making careless mistakes in schoolwork
-Difficulty sustaining attention to tasks
-Not listening to what is being said
-Losing and misplacing belongings
-Fidgeting and squirming when seated
-Talking excessively
-Interrupting or intruding on others
-Difficulty in playing quietly (2)
There is still much that is unknown as to what causes ADHD. While it has been determined that the disorder is a result of a behavior in the brain, there are still specific questions that are unanswered. Research has led scientists to believe that the prefrontal cortex, a part of the cerebellum, and a group of nerve cells, referred to as the basil ganglia are involved in ADHD. (3) Studies of children with ADHD have showed that their prefrontal cortex and their basil ganglia were smaller when compared to children who did not have the disorder. The prefrontal cortex in the brain is one of the areas responsible for editing a person's behavior. The basil ganglia coordinate neurological input activity in the brain. (3) While the prefrontal cortex and the basil ganglia have been identified as playing a role in ADHD scientists do not yet understand what causes these areas to shrink. Among children studied the shrinkage in their brain has been associated with a mutation of genes. This has provided scientists with the clue that ADHD is possibly caused by malfunction of more than one gene, making it a polygenic disorder. (3)
The question scientists are now asking is which genes specifically are defective? A great amount of research has been focused on the role that dopamine, a neurotransmitter in the brain, plays. (2) Dopamine is released by neurons in specific parts of the brain to control the activity of other neurons. There are dopamine receptors that sit on the outside of specific neurons. The dopamine then enters these neurons through the specific receptor. There are also dopamine transporters that sit on the outside of other neurons. These transporters gather dopamine that has been released in the brain, but not used, together again. In persons with ADHD it is these transporters that are either unreceptive, or overly receptive. The result is an imbalance in the level of dopamine present in the brain. (3)
The incorrect transportation of dopamine causes a person with ADHD to have limited control over their executive functions. These executive functions include four operations: the operation of working memory, the internalization of self-directed speech, the controlling of emotions, and the reconstitution of behavior. (3) Scientists' understanding of the role that dopamine plays in ADHD has led them to try and control the levels of dopamine released in the brain. This has been done by the use of psychostimulants. The most popular of these psychostimulants is methylphenidate, better known as Ritalin. Ritalin affects ADHD by preventing dopamine transmitters from collecting released dopamine. In one study the use of psychostimulants seemed to help improve the behavior of 70 to 90 percent of children who took it. (3)
The sharp increase in the number of diagnosed cases of ADHD has led to a dramatic increase in the number of people using pyscholstimulants. The prescription of methylphenidate has increased so much so that it has sparked a debate among scientists and mainstream American society alike. Many ask what the effects of the dependency on pyschostimulants are. What does it mean to have such a large number of people on such powerful drugs? While the use of any powerful drug can cause debate, the one surrounding the use of Ritalin is so intense in part because of the nature of the nature of the drug. Methylphenidate belongs to the same family of drugs that cocaine does. (6) While several studies have shown that Ritalin when administered in small dosages can have an overtly positive effect on ADHD, many are worried that a dependency on Ritalin will lead to greater problems. (4)
Ritalin functions by creating a balance in the level of dopamine transmitted in the brain. It is in fact a pyschostimulant, but it works by preventing the stimulation of dopamine transporters. Ritalin is prescribed in the form of a tablet. It is given in 5, 10, or 20 mg dosages. (5) Once taken Ritalin produces a calming effect. It aids the brain in performing its executive functions. The side effects associated with Ritalin can include lack of hunger, loss of ability to sleep, and headaches. (5)
One of the biggest things that scientists have been trying to learn about is the long-term effect of Ritalin on the brain. At the moment they are unsure. A research project conducted at the University of Buffalo showed that methylphenidate has the potential to cause long lasting changes in brain cell structure. In the study 20 mg per kg were prescribed to mice. (The prescribed dosage for a human would be .3 to .7 mg per kg). The changes produced in the brains of the mice resembled changes in the brain caused by cocaine usage. (8) The study concluded that Ritalin as it is prescribed among humans not only appears to be safe, but beneficial.
There is great uncertainty in the medical world surrounding Attention-Deficit Hyperactivity Disorder. While scientists now understand part of the process of how ADHD develops its, they are still unsure about a lot. The biggest debate concerning ADHD is how to treat it. Science and society alike have contrasting views on how ADHD can be best dealt with. One's opinion on how to treat ADHD goes in accordance with one's interpretation of the disorder. Scientists who see ADHD as the result of a chemical imbalance look to drugs for a solution. Others who see ADHD as simply a behavioral problem look to behavior modification techniques for help. Ultimately the debate surrounding ADHD demonstrates how the little we as humans understand about the brain and its functions. While this is only natural, for science is simply a system of trial and error, . . . the question then becomes how do we proceed to become "less wrong" about Attention-Deficit Hyperactivity Disorder?
1)Attention Deficit Hyperactivity Disorder (ADHD)-Questions and Answers, National Institutes of Health
2) Attention Deficit Disorder (ADD), Attention Deficit Hyperactivity Disorder (ADHD, AD/HD) A Developmental Approach, National Information Center for Children and Youth with Disabilities (NICHCY)
3)Attention-Deficit Hyperactivity Disorder, Scientific American Online
4) Methylphenidate (Ritalin), National Institute on Drug Abuse
5) Ritalin: Prescribing Information, Novartis Pharmaceuticals Corporation
6) The Hazards of Treating "Attention-Deficit/Hyperactivity Disorder" with Methylphenidate (Ritalin), The Journal of College Student Psychotherapy
7) Information About ADD, Scientific American Online
8) University At Buffalo Research on Long-Lasting Effects of Ritalin in Brain-Cell Function, Science Daily
| Panic Disorder Symptoms and Causes Name: Natasha Gj Date: 2002-03-01 00:13:43 Link to this Comment: 1275 |
Panic Disorder Symptoms and Causes
By: Natasha Gjivoje
Everyone, at one point or another, has felt anxious. It could have been due to stress. It could have been as a result of having to perform in front of an audience. It could have been for fear of not being accepted by the graduate school of your choice. But have you ever had episodes of intense anxiety and fear, unexpectedly and in the absence of any real external threat? If you have, then you were very likely experiencing a “panic attack,” the hallmark of panic disorder, which occurs when the brain’s normal mechanism for reacting to a threat become used inappropriately (9). This disorder is associated not only with a number of somatic and cognitive symptoms, but has a large number of possible causes as well. Generally, it is possible to have healthy people experience an isolated panic attack and not actually have the panic disorder. Up to ten percent of people with panic attacks fit in this category (6). In order to be diagnosed with the panic disorder, a person must experience at least two unexpected panic attacks and develop constant concern about having another attack (4). In the United States, about three million people will experience panic disorder at some point in their life(3).
So what are the symptoms of a panic disorder? As mentioned above, a person can have a panic attack and not have a panic disorder, but all panic disorders begin with panic attacks. During the attack, the person might experience just several or more than several of the following symptoms (to be deemed a panic disorder, the person must experience at least four of the following symptoms): racing or rapid heart beat, chest pain, breathing difficulties, choking sensation, nausea and/or vomiting, a feeling of detachment from the body, dizziness, shaking/trembling, excessive perspiration, sleeping difficulties, and among others, a lack of concentration, and a fear of dying/having a heart attack (1). Most panic attacks last for only several seconds, but the symptoms may persist for several hours (2).
A person with a panic disorder, in which the panic attacks recur often, eventually develops a fear of having another attack. This often actually induces a panic attack and the cycle just keeps on going (6). Many times the patient will convince himself/herself so fervently that they are dying that many sufferers often feel the need to go to the emergency room and get tested. Even though this disorder is easily as well as successfully treatable, if it is not diagnosed it can become very debilitating to the individual (9).
But what causes a panic disorder? There is no definitive answer when it comes to this question. It is believed that there are a number of causes for this type of disorder, ranging form causes of genetic nature, to causes tied to the brain and biochemical abnormalities (6). Sometimes panic disorders run in families. It is not unusual for a mother and a daughter to have a panic disorder, just like it has been proved through research that if one of genetically identical twins has the disorder, it is likely that the other will also (9). Thus the conclusion is that in some cases a genetic factor, in combination with the environment, may play a role in the individual’s predisposition to the mental illness.
On the other hand, some individuals are believed to have panic disorder due to biochemical abnormalities in the brain. Research suggests that this type of mental illness many be a result of increased activity in the hippocampus and locus coeruleus, portions of the brain that monitor internal and external stimuli and control the brain’s responses to them (6). There is also indication that the amygdala plays a role in this disorder. The amygdala, along with the hippocampus are major centers of the limbic system—a system that “controls” our emotions (5).
Also, in this type of disorder, many neurotransmitter alterations exist. Those neurotransmitters include serotonin, norepinephrine, gamma-aminobutyric acid, corticotropin-releasing hormone, and cholecystokinin. Since all these neurotransmitters are closely related and work together in the body, it only takes a change in one to cause a change in all of them, resulting in a number of extensive feedback mechanisms (6). For that reason, panic disorders are treated with, for example, Selective Serotonin Reuptake Inhibitors, which work block the reuptake of serotonin in the body so that its presence is increased in the brain. This is very important because serotonin is a neurotransmitter that plays a major role in “quieting” the stress response (7).
But a panic disorder can also be triggered by an “overdose” of a stimulant such as caffeine or cocaine. Caffeine is a stimulant that interferes with a chemical in the brain called “adenosine.” This chemical acts as a natural tranquilizer or a sedative in our body, and when it is meddled with, it can not work properly to calm the body down and therefore the individual is more likely to experience a panic attack (8).
In addition to the above causes, medical professionals believe that panic disorders focus on bringing underlying conflicts in an individual to expression—such as anger and unexpressed conflicts in intimate relationships. Also, those who believe in the above notion place emphasis on the importance of a person’s way of thinking, a person’s response to stress, and their overall perception. Individuals with panic disorder often feel that they are unable to control their lives and are unable to attain certain goals and achievements. Statistically speaking, women are twice as likely to develop a panic disorder then are men, probably due to their more “vulnerable” nature and increased likeliness of taking things more seriously and letting events effect them more permanently then men (6).
There are many theories concerning the causes of panic disorder. And they are probably all applicable and necessary for everyone is an individual, and everyone has different predispositions, whether those happen to be genetic, or biochemical, or both. That is why it is much easier to point out a symptom of a panic disorder than it is to point out its cause. Panic disorders are currently widely studied and researched. This type of disorder, although treatable, can be very devastating and debilitating to the person if it goes on untreated—it can cause specific phobias such as fear of driving a car, or fear of leaving the house. It can cause the loss of a job, and it can cause relationship problems (4). Luckily, even with this disorder’s rather undefined nature of causality, there is much treatment available that has helped at least eighty percent of panic disorder sufferers cope with this problem (6).
WWW Sources
1)Anxiety and Panic Hub, resource about anxiety and panic attacks
2)APA Online, Answers to Q’s about panic disorder
3)Panic Disorder, good overview of disorder and its treatments
4)Anxiety Disorders- including Panic Disorder and Phobias, additional info on panic attacks
5)Anxiety Disorders Treatment Target: Amygdala Circuity, explains how amygdala may have a role in anxiety and panic disorder
6)Mental Health: A Report of the Surgeon General, great site for panic disorder info
7)SSRI’s and Panic Disorder, All about Paxil, Prozac, Zoloft, and Luvox
8)Caffeine…Panic Attacks and caffeine don’t mix, effects of caffeine on panic attacks
9)Understanding Panic Disorder, additional info about panic disorder
| Differentiating Tic Disorders Name: Beverly We Date: 2002-03-01 10:09:06 Link to this Comment: 1279 |
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Is it possible to differentiate Tourette tics from non-Tourette tics? Are all tics the same? What is a tic? What does a tic feel like? How does "ticcing" affect a person's sense of self or "I-Function"? Are Tic Disorders Inherited?
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A tic is a repetitive, uncontrollable, purposeless contraction of an individual muscle or group of muscles, usually in the face, arms, or shoulders. These movements may be signs of a minor psychological disturbance. Such tics often occur in childhood and will probably be outgrown. There are also tics that are caused by neurological disorders that could have resulted from brain damage at birth, head trauma, or use of some specific medication (1). Tic disorders may be inherited. Genetic analysis of numerous pairs of siblings has shown several areas that may contain genes that, when mutated, may give rise, or increase susceptibility to, Tourette Syndrome. There is growing evidence that Tourette Syndrome is inherited from both parents (bilineal transmission), with the father typically affected by childhood tics and the mother typically having some symptoms of obsessive-compulsive disorder (8). Tics can present as motor or vocal and are categorized as Simple or Complex (3) according to age of onset, duration and severity of symptoms (2). There are several different categories of tic disorders.
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Transient tic disorders can begin during the early childhood years and can occur in up to 18% of all children. Simple transient motor tics can present in the form of eye blinking, nose scrunching, grimacing and squinting, and other forms (2). Simple transient vocal tics are less common and include sounds repeatedly made such as clearing the throat, coughing, grunting, hiccuping, belching, and other sounds. Transient tics last for a short while, only several weeks or months, and are usually not associated with specific behavioral problems. These tics are more noticeable during stressful, fatiguing or emotional times (2). Boys are three to four times more likely to be affected than girls. Transient tics usually do not last for more than one year, although it is not uncommon to have these episodes over the course of several years. For many children, the symptoms never go beyond blinking and sniffing (or similar choices) and are often described as "nervous habits" or allergy symptoms.
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Chronic tic disorders are differentiated from transient tic disorders in that their duration is over many years and the behavior is unchanging. With transient tic disorder, the tic may change from one type to another, (sniffing may be replaced by forehead furrowing and then the furrowing is replaced by finger snapping), while in chronic tic disorder the tic remains the same for a very long time.
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Chronic multiple tics present often, and in series. Sometimes it is difficult to draw distinctions between transient, chronic and chronic multiple tics (2).
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Tourette Syndrome (TS), first described by Gilles de la Tourette, can be the most debilitating of the tic disorders and is characterized by multiform, frequently changing motor and vocal or phonic tics. There are multiple diagnostic criteria, as defined in the Diagnostic and Statistical Manual of Mental Disorders IV.
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A. In Tourette Syndrome, both multiple motor and vocal tics have been present at some time during the illness, although not necessarily concurrently.
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B. The tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a period of more than 1 year, and during this period there was never a tic-free period of more than 3 consecutive months.
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C. The disturbance causes marked distress or significant impairment in social, occupational, or other important areas of functioning.
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D. The onset is before age 18.
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E. The disturbance is not due to the direct physiological effects of a substance (e.g. stimulants) or a general medical condition (e.g. Huntington's disease or post-viral encephalitis) (2).
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In Simple Motor tics, the movement is fast, darting and meaningless. In Complex Motor tics, the movement is slower and may appear purposeful (2). This form may include copropraxia (making obscene gestures), and echopraxia (mimicking movements that others make) (3). In Simple Vocal tics, the sound production contains meaningless noises. In Complex Vocal tics, there are linguistically meaningful words and phrases, including coprolalia (vocalizing obscene or other socially unacceptable words or phrases), echolalia (repeating what someone else has just said), and palilalia (repeating your own words over and over again) (3).
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Tourette Syndrome is a spectrum disorder-it varies with each individual and may appear anywhere on the spectrum between very mild and severe (4). It does not affect intelligence, although in Tourette Syndrome the child may develop such additional behavioral and developmental disorders as Attention Deficit Hyperactivity Disorder, impulsivity, aggressivity, self-injurious behaviors, and varied learning disabilities (2).
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When a person is engaged in tic behavior, what does he/she feel? A tic comes on the way a sneeze or a blink comes on; there is a need to complete the act. Tics are involuntary and compelling, and the person has little control over the onset of the tic. Some individuals have reported that they are conscious of the urge to tic before the action occurs (3). The person is fleetingly aware that there is a flashing thought (I-Function or consciousness) which manifests in the tic behavior. I-Function can also be part of unconscious behavior. The motor and/or vocal response that began as an unconscious thought brought awareness during the tic event. If I-Function serves as a filter of both consciousness and unconsciousness, then the tic behavior has been filtered before and during the behavior. Almost simultaneously, the thought and action occur. A tic can be "put off" temporarily, but later, when the person permits him/herself to complete the urge to tic, the ticcing may increase in intensity.
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Tics increase in frequency and severity with stress, during relaxation after physical exercise, idleness, fatigue, exposure to heat, and use of dopaminergic drugs, such as steroids, caffeine, and CNS stimulants. Tics usually diminish with performance of engaging mental or physical activities (e.g., playing computer games, playing sports) or with consumption of marijuana, alcohol or nicotine (5). Some people can control the tic urges so that they only tic in the privacy of a safe place, such as their home (4).
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Tic disorders challenge individuals because they must develop a sense of self, ("I-Function"), something besides being a person who has a tic disorder. Children must cope with the embarrassment of tic disorders (whether the cause is Tourette Syndrome or a milder tic disorder). They are challenged every day in school settings; their friendships are tested because their behavior is different. Even under the best of circumstances, children have social problems, but with tic disorders, children have a particularly difficult time, often being shunned by playmates and peers. Children will develop this sense of self, this "I-Function," but while the personality is developing they must make choices about how they view themselves. Without a good support system, the child could become depressed and self-loathing, thinking of him/herself only as a person who tics. Without an "I-Function," the body is simply discharging neurological output.
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Adults with tic disorders have similar issues, but have the advantage of life experience. They are lawyers and teachers, doctors and artists, plumbers and nurses, mothers and fathers. A person with a tic disorder needs to have a "split personality," in essence two "I-Functions" that can differentiate between the tic disorder and the "other" self. One needs to be able to harmonize the tic behavior into the "I-Function," allowing the behavior to become a part of the individual, rather than having tic behavior that is merely neurological output. The "I-Function" will be the determining factor that distinguishes one person with this disorder from another. An individual's perception of him/herself will greatly predict how successful he/she feels in the company of other people. "I-Function" is that which gives a person a sense of self, whether the I-Function is conscious or unconscious.
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No matter what label is given to the tic disorder, the tic probably signifies a subtle brain developmental disorder. Researchers have linked Tourette Syndrome to an area of the brain known as the basil ganglia, which is involved in controlling movement and which plays an important role in attention, concentration, and decision making (6). Tic disorders involve abnormalities in the Central Nervous System levels of neurotransmitters or neuro-peptides, particularly dopamine, norepinephrine, opioid peptides, and serotonin (5). It has been observed that dopamine-blocking agents suppress tics in some individuals (8).
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All tics are movements or sounds that occur intermittently and unpredictably out of a background of normal motor activity. Some tics are the result of brain injury, head trauma, or encephalitis, although most tics are commonly called idiopathic, and are part of the spectrum, which includes Gilles de la Tourette Syndrome, or one of the other idiopathic tic disorders (7). Many people now believe that all tic disorders are closely related and are perhaps all part of the same spectrum (4).
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The differentiation of Tourette Syndrome tics from other tics may be no more than semantic, a somewhat arbitrary assignment to a category. Furthermore, recent genetic evidence links Tourette Syndrome with multiple and transient tics of childhood; Tourette Syndrome, therefore, can only be differentiated in retrospect (2).
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I heard Dr. Oliver Sacks speak on this subject a few years ago and I remember something quite poignant. He said that he had no knowledge of Tourette Syndrome until he was presented with a patient who had this disorder. After that, he saw people with tic disorders everywhere he went. I know several people with tic behavior; I never had a name for the disorder.
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\n2) Tourette Syndrome and Other Tic Disorders ,
\n4) Tourette Syndrome and Other Tic Disorders ,
\n5) Is it a tic or Tourette's?,
\n6) Tourette's, Other Tic Disorders Far More Common Than Once Thought ,
\n7) Definition and Classification of Tic Disorders ,
\n8) We Move: Tourette Syndrome ,
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| Grow Little Cell Grow! Investigating Neurogenesis Name: Claire Alb Date: 2002-03-01 10:59:32 Link to this Comment: 1280 |
Neurogenesis, the production of new nerve cells, has been a revolutionary finding as nerve formation has always been thought to end with adulthood. It has not been until recently that such dogma has been contradicted as research findings report that neurogenesis continues in the hippocampus throughout most of the adult life of mammals and primates (1)The Scientist Magazine , Human neurogenesis. Group demonstrates that adult human brains grow new cells after all. Recent correlations have been further made between neurogenesis and depression as the latter depletes neuron cells in the brain while antidepressive drugs have demonstrated to increase neuronal growth (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells .
\nNeurons are the building blocks of the nervous system as they are responsible for the input, processing and transmission of information. Neurons are derived from stem cells as the latter differentitate into specialized cells and make progenitor cells which are responsible for the formation of neuron and glia cells. Although the majority of neurons are formed during the pre-natal and perinatal stage of development, neuron formation continues in the dentate gyrus of the hippocampus (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells. The hippocampus, which lies beneath the cortex is a major factor of learning and memory formation and can indirectly influence emotion
\n (3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth. Progenitor cells which are present in the subventricular zone of the hippocampus are responsible for such growth as they produce daughter neuron cells through division (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells .
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\nIn the 1960s, Joseph Altman from MIT reported that new neurons were being produced in the dentate gyrus of the hippocampus of adult rat brains. Although such findings were groundbreaking, they failed to create the stir that Elizabeth Gould’s 1998 study caused . The Princeton University neurobiologist demonstrated that the marmoset brain generated neurons (1)The Scientist Magazine , Human neurogenesis. Group demonstrates that adult human brains grow new cells after all. BrdU or bromodeoxyuridine served as a marker when incorporated into the DNA of the progenitor cells and through autoradiographic techniques, the labelled progenitor cells were identified to produce daughter neuron cells. The neurons have “processes which go inward and follow paths to other structures within the hippocampus and get incorporated into basic circuitry of the brain”
\n (4)New Neurons in Neocortex? New Study Says NO! .
\nIn 2000, Fred Gage of the Salk Institute reported that neurogenesis can take place in the hippocampus of adult animal brains. Progenitor cells were isolated from the adult brains of five subjects with tumors and analyzed in culture dishes. Brdu, was once again used as a marker while the ultimate division of the extracted progenitor cells to neurons observed
\n(4) New Neurons in Neocortex? New Study Says NO! .
\nAlthough these findings are not only revolutionary and exciting, there are many questions which have yet to be answered by neurogenesis. What is the functionality of these replicating neurons? When questioned, Gage stated that “we have theories as to the significance of their function but no proof yet” 1)The Scientist Magazine . Furthermore, as laboratories around the country are finding evidence of these new nerve cells in the hippocampus, the “so what?” question must be asked. How can such findings be applied to everyday life?
\nStudies on clinical depression demonstrate that patients with bouts of clinical depression have smaller volume sized hippocampus than their normal sized counterparts who do not suffer from it. There is also constant decrease in hippocampal volume due to a lifetime duration of depression (2)American Scientist Magazine. In 2001, Ron Dunman’s research brought not only association of the neurogenesis/depression phenomenon but possible application when demonstrating that treating rats with Prozac and ECT resulted in newly formed neurons in the hippocampus (3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth.
\nProgenitor cells which are inhibited from dividing throughout most of the brain, do so in the dentate gyrus of the hippocampus and the olfactory bulb as they develop into daughter neurons. Constant renewal of such neurons is thought to be necessary for learning processing and storage of new information (2)American Scientist Magazine. If the mechanisms which inhibit most progenitor brain cells from developing into neurons are found, there is the possibility of repair for damaged brain tissue due to illness, trauma or age. There are also exciting possibilities of stem cell development to diseases such as Parkinson’s and Alzheimer’s, all which are neurodegenerative (5)\nhref="http://www.nimh.nih.gov">National Institute of Mental Health.
\nOther studies have found that neuronal growth not fixed to the hippocampus. Elizabeth Gould has also published findings which support the neuron formation in the neocortex., as the latter is the most evolved and complex part of the brain which controls cognitive function and language. Pasko Rakic, who’s chairman of Yale’s neurobiology department has consistently contradicted her findings. In December 2001 publication, he concurred with current research that adult primate produce neurons in the hippocampus but could not support the same in the neocortex (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells. The politics revolving around such scientific rivalry and differences must be ignored as future research is done on the neocortex
\n(6) The Scientist Magazine.
| better to have a bottle in front of me than a fron Name: Lilian B Date: 2002-03-01 11:03:22 Link to this Comment: 1281 |
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\nBiology 202
2002 First Paper
On Serendip
\nIn the movie, “One Flew Over the Cuckoo’s Nest,” Mcmurphy, the main character, undergoes a frontal lobotomy (“cutting of the lobes”) to treat his ‘mental illness,’ after several rounds of ECT were unsuccessful in crushing his spirit. In the final scenes of the movie we see from his disposition that he has been reduced from an animated, hyperactive state to a vegetative state. McMurphy’s friend, Chief, tries to talk him, but he stares straight ahead and does not respond. The movie takes place in an insane asylum in the 1950’s, the height of the lobotomy craze in the United States. Between 1939 and 1950, nearly 20,000 documented lobotomies were performed, and thousands more in other countries (1). At first the procedure was used in lieu of Electronic Shock Therapy, for rowdy patients who did not respond well to ECT. The lobotomy was applied as a ‘”fix-all” solution for people with all kinds of major or minor mental disorders. Of course, such an invasive procedure is meant to be used only as a last resort in severe cases of debilitating illness. Many doctors, looking for a quick fix for their patients, used the procedure in cases of “undesirable behavior.” Unfortunately, such a broad criterion meant that anything from Schizophrenia to Obsessive Compulsive Disorder (OCD), to unruly behavior in general could be treated by lobotomy. In Japan many of the people lobotomized were just children who did not behave well or who performed poorly in school.
\nWhat started the lobotomy craze? As with any result, it is difficult to say what exactly prompted the explosion in popularity of such a gruesome surgery. We can begin by exploring the origins of lobotomy in general: In the late 19th century, the scientific community was beginning to understand that behavior was largely controlled by could be mapped out in the brain. The German scientist, Friederich Golz began by cutting the frontal lobes on dogs. He noted that even ferocious dogs became more tame and subdued after the surgery (1). In 1892, in an insane asylum in Switzerland, Gottleib Burkhardt was inspired by Golz to try the procedure on human subjects. He treated patients who were having hallucinations to lobotomies. Some of his patients did become more calm after the surgery, and others died from complications. Burkhardt’s strategy was widely criticized, and there was not much heard about lobotomies for nearly half a decade (1).
\nWhy the frontal lobe?? It became more clear in observations of lobotomized patients that scientists’ theories about the frontal lobes of the brain were correct. The frontal lobe is thought to be a sort of control center, and the location of the self in the brain (5). It is involved in some motor function, problem solving (divergent thinking), spontaneity, memory, language, judgment, impulse control, social and sexual behavior. “Patients with frontal lobe damage exhibit little spontaneous facial expression, which points to the role of the frontal lobes in facial expression (Kolb & Milner, 1981). Broca's Aphasia, or difficulty in speaking, has been associated with frontal damage by Brown (1972),” (5). Also, lobotomy patients might seem more calm because frontal lobe damage results in a difficulty in interpreting one’s environment. The patient has trouble responding to questions, and his associative learning skills are impaired. Oddly enough, it’s also been documented that people with frontal lobe damage cannot get a “good-belly laugh,” that it, they have trouble comprehending the punch lines of jokes. In a study lead by Dr. Shammi of the University of Toronto, patients with all kinds of brain damage were subjected to the Three Stooges and other humorous material: “The study found that people with right anterior frontal damage had the most disrupted ability to appreciate written and verbal jokes -- and funny cartoons -- compared to the normal control group and people with focal lesions elsewhere in the brain. Individuals with right frontal damage chose wrong punch lines to written jokes and did not smile or laugh as much at funny cartoons or verbal jokes. They showed a preference for silly slapstick humor -- surprising but illogical endings which are the hallmarks of such acts as The Three Stooges.,” (5). So, it follows that the frontal lobotomy should result in drastic changes in social behavior.
\nWhy was the change in behavior of subjects viewed as a change for the better? In the mid 1930’s, a scientist at Yale University (Carlyle Jacobson) began experimenting with ‘lobe cutting’ in chimpanzees. In Jacobson’s experiment, aggressive animals became much more calm. In chimpanzees, this change in behavior seemed to occur without any damage to memory or intelligence. A Dr. Fulton performed the same experiment on chimps, yielding similar results. The calm, docile chimps looked to be much better off then they were before the experiment.
\nAt a neurological conference in England, Fulton shared his results with the Portuguese doctor Antonia Egas Moniz. “Moniz knew that certain psychoses, such as paranoia and obsessive-compulsive disorders, involve recurrent thought patterns that dominate all normal psychological processes. Based on Fulton's ideas, he proposed to cut surgically the nerve fibers which connect the frontal and prefrontal cortex to the thalamus, a structure located deep in the brain, which is responsible for relaying sensory information to the cortex. In this way, Moniz reasoned, there might happen an interruption of the repetitive thoughts, allowing a more normal life for the psychotic,” (1). Moniz worked to develop a procedure that he called ‘white matter cutting.’ Through two incisions on either side of the brain, 2 ‘ice picks’ were inserted. A few sweeps of the pick sliced through brain tissue in the frontal lobes. Some of his patients with anxiety or depression saw improvements in their disposition, while others saw no improvement at all or even the contrary. Moniz specified that his process, the leucotomy, should ONLY be used in cases where there was no other avenue. He believed that in that a morbidly fixed idea could be removed from the brain by destroying the tissue on which the idea was saved. He thought that patients with severe anxieties and depression, or compulsive or hallucinatory disorders could benefit from the removal of the ideas that plagued them(2). In 1949, Moniz was awarded the Nobel prize for medicine and physiology. Some years later, Moniz was shot in the back by an old patient of his. He became paraplegic.
\nSo, the father of leucotomy was a paraplegic, and the procedure he created was at most a minor success. Why was this not the end of lobotomy? Perhaps unfortunately, a scientist named Walter Freeman was also at the London Conference with Moniz and Fulton. Freeman was hopeful about the potential of leucotomies in psychiatric medicine. The awarding of the Nobel Prize to Moniz was to Freeman an indication that the procedure was respectable and effective. In Sept. of 1936 Walter Freeman and his co-worker, James Watt, set out to reinstate the lobotomy as a medical procedure for those with mental ailments. They heralded the operation, believing themselves that it worked. They developed the “Freeman-Watts Standard Procedure,” in an attempt to refine the lobotomy methods being used at the time. The pair toured the country, promoting their procedure and performing it on many patients. Freeman was the driving force in the pair, and he strove to perfect the operation by making it less messy and less time consuming. Their efforts perpetuated the ‘lobotomy craze,’ and by the late 40’s it was an exceedingly popular operation.
\nPeople did not begin to realize the ramifications of such a gruesome operation until it became clear, through observation, that lobotomized individuals were far from normal or happy, and that in actuality, the appearance of a less crazed nature had simply been mistaken for (what was in some cases) a total loss of the individual’s personality. In addition, scientists were not getting the results they expected from empirical evidence. It seemed that only 1/3 of the cases yielded any improvement in the patient, while 2/3 of patients remained just as ill as they were initially or, in many cases, their illnesses became worse. Scientist in the 50’s began experimenting with the use of new kinds of psychiatric drugs (such as thorazine) in treating patients, as medication is reversible and brain surgery is not. By the late 50’s, lobotomies had become nearly obsolete, and the status of the procedure was downgraded from effective to experimental. All in all, the lobotomy era seemed to have been a sort of ‘oops’ in psychosurgical science.
\nResearchers from Mount Sinai Medical School have come to Pilgrim, one of the largest state hospitals in the country to hopefully gain something from the lobotomy tragedy. Dr. Peter Powchik says about the hospital, “If you want to learn why people don’t get better, you do it here.” “Powchik and his colleagues administer teststhat assess patients' thought processes and motor coordination. Their preliminary findings show that lobotomies did not help these patients and in some cases may have even triggered more mental illness. The project has turned up evidence that some people who had lobotomies for depression, anxiety or disruptive behavior developed symptoms of schizophrenia following the surgery,” (4). Philip Harvey, the coordinator of the research project at Mount Sinai hopes that his teams research may give scientists some clues as to how schizophrenia originates in the brain. He is driven finitude of available time for his research to be done. Lobotomies are so rarely performed now, that compiling data on such a massive scale in the future would be impossible. Their job is an emotionally taxing one, as many of the patients are frighteningly sick, and what is more sad, they will not recover:
\n“All are elderly and have spent most of their adult lives behind locked doors and barred windows. Some spend their days staring vacantly; others are forever agitated. They range from Frances Kichinski, who no matter what she is doing is always weeping, to Pauline White, who smiles constantly and wonders why the family that exists only in her mind never comes to visit,” (4). Harvey laments, "It may have caused some people to be hospitalized for the rest of their lives. It made so many people worse." As for McMurphy, it is clear in the end of the film that he has no way out of the mental hospital, for he is nearly a vegetable, and no one in such a state could be self-sufficient. And so, by killing him, Chief is giving his friend freedom and thus is actually demonstrating an incredible amount of love and reverence for his friend who fell victim to ‘the system,’ as so many others did who are STILL in asylums today.
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References
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\n1)History of Lobotomy,
\n2)PBS Website,
\n3)Nobel Prize Website,
\n4)Research Articles,
\n5)The Frontal Lobe,
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| "Meat all the Way Down": Colin McGinn's The Myster Name: Hilary Hoc Date: 2002-03-01 11:08:07 Link to this Comment: 1282 |
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\nBiology 202
2002 First Paper
On Serendip
\n"Meat all the Way Down":
\nColin McGinn's The Mysterious Flame
\nEarly in The Mysterious Flame, (1)., philosopher Colin McGinn's breezy but provocative discussion of the relationship between consciousness and the brain, McGinn presents a telling vignette from a science fiction story in which aliens are discussing their observations of humans:
\n"These creatures are the only sentient race in the sector and they're made out of meat. . . .They're meat all the way through."
\n"No brain?"
\n"Oh, there is a brain all right. It's just that the brain is made out of meat."
\n"So . . .what does the thinking?"
\n"You're not understanding, are you? The brain does the thinking. The meat."
\n"Thinking meat! You're asking me to believe in thinking meat!"
\n"Yes, thinking meat! Conscious meat! Loving meat. Dreaming meat. The meat is the whole deal. Are you getting the picture?" (1).
\nIt is this apparent contradiction, that initially insensate organic material can create consciousness, a phenomenon without apparent material content or spatial location, which McGinn sets out to explain. Many philosophers and scientists have undertaken this journey before him, but McGinn contends that this long road of philosophical inquiry is actually a blind alley. While McGinn believes that the mind is indeed a product of the material qualities of the brain, he argues that the mind (or brain) does not itself possess the ability solve what philosophers denominate "the mind-body problem," (although "mind-brain problem" might be more accurate).
\nMcGinn begins by rejecting both traditional materialism and dualism. Materialists propose that the brain and consciousness are one and the same: thus, brain waves not only correlate with consciousness, they are consciousness. McGinn faults this position for ignoring the very nature of conscious experience. The experience of consciousness, he argues, does not directly correlate with brain waves or the activity on a PET scan. Studying these physical phenomena alone will tell the observer nothing about the experience of consciousness, while endless introspective inspection of one's conscious state would not lead to any description of the brain's anatomy or physiology, let alone that neurons within it were firing as one thought.
\nLikewise, McGinn rejects dualism, the proposition that consciousness exists completely independent of the brain, because its proponents also ignore empirical observations. Were consciousness completely disconnected from the brain, a fully functioning brain could exist without consciousness, and consciousness could exist independent of the brain, thereby producing what McGinn terms ghosts (disembodied minds) and zombies (organisms with mindless brains, beings who can act but who do not perceive). Dualism thus does not account for empirical observations of conscious organisms, in which the consciousness's existence appears to depend on the brain's activity, and vice-versus. Yet neither science nor philosophy has yet offered a satisfactory explanation of this interdependence.
\nMcGinn offers a third way out of the mind-brain problem: pessimism and acceptance of failure. McGinn agrees with materialists that it is properties of the brain, and the brain alone, which produce consciousness. These properties, however, are unknowable, emerging in their turn from properties of space and matter that the human brain cannot perceive. He postulates a theory he dubs "mysterianism," a respectable way of saying the world will never know. McGinn argues that, in contemplating the origin and nature of consciousness, the human mind has come to the edge of its conceptual capacity: the mind peers over the cliff, but can see nothing but an endless abyss below. While human intelligence can perceive the problem, it cannot understand the answer.
\nMcGinn relies primarily on the concept of cognitive closure to support this argument. Human intelligence, he argues, evolved in response to the environment in which humans had to survive. Thus, certain human capacities are well developed, including the ability to navigate in three-dimensional space and to predict the effect of actions in a three-dimensional world. The imperatives of survival, however, have left other capacities undeveloped or nonexistent: for example, the human brain cannot perceive radar or infrared, or understand whale song. The ability to understand consciousness is simply not, McGinn argues, one of the human brain's talents. Specifically, because consciousness is a nonspatial phenomenon, which affects and is affected by objects that occupy space, McGinn argues that consciousness must have spatial characteristics not perceptible to the human brain. Similarly, while consciousness appears to be immaterial, it is created by and in turn affects matter. Therefore, McGinn reasons, consciousness must depend upon properties of matter imperceptible to the human brain and inaccessible to the mind. McGinn acknowledges that the key to consciousness is located in every sentient organism's genes, because genes code for the construction of all biological phenomena, including consciousness. Yet McGinn maintains that human intelligence as it is currently constructed will never unlock this code.
\nMcGinn's exposition of the mind-brain problem is an intelligent and readable summary of centuries of philosophic debate. Explicitly addressing the layperson, he does not fall into the trap of spewing jargon, although he often belabors his points with one too many repetitious analogies. His straightforward and informal style effectively establishes a dialogue with the reader, although his bursts of self-revelation can become distracting. (Perhaps no one really needs to know about his infatuation with Seven of Nine on television's Starship Voyager.)
\nAs interesting as his argument is, however, McGinn never quite proves his point. The concept of cognitive closure is intuitively appealing and supported by empirical observation: there are in fact various physical phenomena the brain cannot perceive or interpret. It is likely, then, that the brain's limitations similarly constrain the conscious mind. However, McGinn cannot provide a satisfactory account of why humans would experience cognitive closure with regard to consciousness, rather than any other mystery of the natural universe. His supposition that there are properties of space and matter that the human brain cannot perceive and that human intelligence has not yet deduced appears eminently reasonable. However, McGinn does not explain why the properties of space and matter that underpin the structure and formation of consciousness from its origin in the brain will always remain beyond human understanding.
\nMcGinn's examples of human misconceptions about space, for example, undermine the very point he is trying to make. As he points out, contrary to what the brain perceives, humans have deduced that the Earth is not flat, nor does the sun revolve around it, and that matter is not solid. His examples support the idea that humans have been wrong about the natural and biological world, often because their own brains deceive them. Yet human intelligence can deduce, from empirical observations and analysis, physical properties not readily apparent to the brain; McGinn likens humans studying consciousness to pre-Einsteinian physicists, but never makes clear why this analogy presupposes failure rather than success.
\nAccepting McGinn's proposition of cognitive closure, then, does not necessarily lead to McGinn's ultimate conclusion. Indeed, if cognitive closure can be found anywhere, perhaps it is not in knowing what it is we do not know, but rather in recognizing what we cannot know. How can we know that we cannot know something? If human intelligence is cognitively closed to understanding consciousness, how can human intelligence ever deduce this?
\nMcGinn rests his conviction that the problem of consciousness cannot be solved in part on his misunderstanding of the nature of scientific inquiry. He views science as a collection of disciplines which "ask answerable questions and moves steadily forward," while philosophers wrestle with the insoluble questions at the frontiers of cognitive closure. (1). Were McGinn convinced that scientific inquiry produces as much uncertainty as it dispels, he would find the distinction between science and philosophy less clear cut . Perhaps counterintuitively, his view of science as simple and unambiguous causes McGinn to demand more of science than it can deliver. Like philosophers, scientists often theorize well beyond their empirical observations, altering or abandoning theories as new observations undermine them, but never arriving at one single, immutable truth. As a philosopher, McGinn has assumed a level of certainty in science that is available nowhere in human inquiry and scholarship, be it scientific or philosophic (and his assumption that there is a clear line between these two fields bespeaks unfamiliarity with one or both of them). Seeing uncertainty before him, McGinn announces that the path is cognitively closed and turns back before the journey has truly begun.
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References
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\nReferences
\n (1) McGinn, Colin. The Mysterious Flame: Conscious Minds in a Material World. New York: Basic Books, 1999.
\nRelated Web and JStor Resources:
\nBy Colin McGinn:
\nThe following papers and reviews by Colin McGinn are more detailed and technical discussions of aspects of the argument set forth in The Mysterious Flame:
\n"Can We Solve the Mind--Body Problem?" Colin McGinn. Mind, New Series, Vol. 98, No. 391. (Jul., 1989), pp. 349-366. Stable URL: The answer is no.
\n This paper discusses the limits of human knowledge, with an emphasis on Chomsky's theories.
\n) This paper discusses the need to discover new properties of space to better understand consciousness, and impossibility of doing so
\n) A review of Steven Pinker's How the Mind Works, in which McGinn elaborates on his theory of the mind.
\nReviews of The Mysterious Flame
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| Intrapsychic Omnipresence in Bodily Symptoms Name: Cass Barne Date: 2002-03-01 11:10:48 Link to this Comment: 1283 |
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\nBiology 202
2002 First Paper
On Serendip
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\nSometimes disease and illness just show up. For these medical conditions, a doctor usually tells us what is "wrong" physically. These scientific observations determining diseases or symptoms leave people wondering if there is something behind the cell that created the malfunction. Perhaps one's psyche; which is the mind functioning as the center of thought, conscious or unconscious, and interconnected with the physical environment, can effect the body positively and negatively. An indirect way of dealing with psychological conflict is to intuitively or unconsciously convert it into symptomatic illness. However, this does not get rid of the emotions or the symptoms, for this is not the root of the problem. It is only through recognition of the their intuition or repressed emotions that people may come to heal themselves. It is difficult although possible for some to assign every illness or symptom to some underlying psychic cause; but that is usually whimsically referred to as "new age" and "mystical". It is a person's own personal belief whether she created her diabetes, or whether he created his cancer as a result of psychological and emotional conflict and trauma. Therefore, we can only look at the facts to postulate the argument that a lack of psychological well being manifests itself somatically. The best way to examine the notion that psychological factors affect medical conditions is with the neurosis Hysteria.
\nHysteria is also known now as Conversion Disorder or Dissociation, in which unconscious or emotional psychological conflict converts into a bodily disturbance (2). An example of this is anxiety. Hysteria is diagnosed as psychological stress accompanied with physical symptoms. Interestingly, despite the multiple physical symptoms there is no anatomical or organic basis for any of them. Although conversion disorder is a physical manifestation, there is no physical cause. In the case of hysteria, the mind or the psyche is neglected by the person who represses emotional trauma, and these then divert themselves into the body as a means of expression or escape. These patients often times do not know what is wrong with themselves because the repression was unconscious and out of their control. Accordingly, the physical symptoms in hysteria are a result of the person's lack of psychological control, which is unconscious not voluntary.
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\nDuring the 19th century, French Neurologist J.M. Charcot and Psychologist P. Janet emphasized that “morbid ideas could produce physical manifestations” and that hysteria was caused by the psyche not the body (1). This reference highlights the notion that physical symptoms reflect psychic states. Freud also believed that hysterical symptoms were symbolic of a repressed unconscious “event” or psychic trauma not properly expressed at the time (2). One must appreciate Freud’s assertion of unconsciousness in the pressed event. Some of the physical manifestations of hysteria or conversion are expressed as blindness, paralysis, ataxia, epilepsy, amnesia, anaesthesia, aphonia (loss of voice), and melancholia (3). The same symptoms were also seen in Breuer’s patients like Anna O. One of the most classic of all psychosomatic disorders was the hysteric Dora, Freud's patient. At the age of eighteen she had developed a range of symptoms such as hemicranial headaches, attacks of nervous coughing, tussis nervosa (inflammation of nose and throat), appendicitis, aphonia, fatigue, together with amnesia, dyspnoea (aggravation), hysterical unsociability, and depression. As Freud describes it, Dora "was clearly satisfied neither with herself nor with her family: her attitude towards her father was unfriendly, and she was on very bad terms with her mother....and she tried to avoid social intercourse" (6). Dora also had traumatic sexual encounters with a man which she repressed as well. Clearly Dora had psychological stress, and psychological trauma due to the resulting sexual fears. Dora diverted her repressed sexual encounters and familial conflict into her psyche, which created a plethora of symptoms.
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\nSimilar symptoms are also seen in dissociative states where the individual may suffer from "dissociative control" and "dissociative awareness" in that he or she can not consciously control actions and is not aware of what experiences took place (5). For example, amnesia and fugue states represent the person's inability to recollect what actions took place. In fugue states, they are consciously aware of the actions, but they do not remember. Amnesia in hysterics does not come as a result of brain lesion, but as a self-induced protective erasing of an emotional traumatic experience. These states, like hysteria, address the person's involuntary control of their internal experience and worldly actions. Since there was no organic basis for the physical symptoms, physicians like Breuer and Neurologist Charcot in this era used suggestion, free association and hypnosis to free the patients from their symptoms (1). They found that letting the hysteric talk through her conflicts "lead to the disappearance of her symptoms whenever she was able to recollect their root events" (1). This sort of treatment worked because the mental conflict was unknown as far as the patient was concerned. The symptoms served as a psychological defense to banish painful anxiety from consciousness. Therefore, the use of hypnosis, and what later became psychoanalysis, helped in ridding symptoms because the Psychoanalyst was able to draw out unconscious traumatic memories and bring them to conscious awareness to begin a process of mental and emotional healing.
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\nWhen was the last time you heard about Hysteria? Probably the last time you talked about the Salem Witch Trials. Hsyteria is not a prominent illness as many others today. Where did it go? Have there been more mental illnesses that have taken over or are we just rolling up more names to the old one? Hysteria is the only disease or disorder that has an actual psychological basis. Even some of the psychological disorders like depression and schizophrenia are known to have some physical basis. However, maybe every disease has an underlying emotional memory that is only accessible when brought to consciousness. It could be that every symptom has a negative mental association, and when that is recognized, and released, then the person is able to heal. Perhaps physical and mental illnesses are different across people because they psychologically choose to deal differently with the external environment and certain experiences, and therefore the manifestation of their illnesses. When we hear about miracle cures it makes us wonder what it is that served to heal them spontaneously. It could be that psychologically the person decided what they needed to change in their life in order to be at ease and healthy with themselves. The psychological aspect may be more important in curing diseases than we may think. What is unknown to the normal observer or the people who are actually diseased, is whether or not they have the personal choice to control emotional fluctuations and mental patterns. Is conversion of psychological conflict automatic and involuntary, or can that be governed by our Self?
\nThe tasteful opinion that the individual is in control of his or her health, mental or physical, comes down to personal beliefs. Perhaps all illnesses, diseases, and symptoms stem from psychological disturbance. Clearly, hysteria is conversion of psychological conflict into the body. History tells us that physical symptoms associated with hysteria and dissociative states are a result of negative mental and emotional states. These negative states rather than being released were pushed back further in the mind to the unconscious. It was only through the catharsis of psychotherapeutics that patients could understand the unconscious, which irrevocably led to their symptomatic illnesses. Hysteria is one of the few diseases that is psychological in origin, and may be the only one. Yet, it is possible that all other diseases follow the psychological path as well. Ph.D Louise Hay writes “I have learned that for every condition in our lives, there is a NEED FOR IT. Otherwise, we would not have it. The symptom is only an outer effect. We must go within to dissolve the mental cause. It’s like cutting down the weed and getting the root out” (8). Rather than viewing the sentiment as mystical there is a real basis for further research and understanding in its application in the field of mental health.
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References
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\n 1) The Freud Page
\n 2) Encyclopedia.Com
\n 3) Notes on Neurotic Disorders
\n 4) Pediatric On Call
\n 5) Hypnotizability and traumatic experience
\n 6) Freud, Sigmund. Dora: An Analysis of a Case of Hysteria. New York: Simon & Schuster, 1997.
\n 7) Psychiatric Terminology
\n 8) Hay, Louise L. Heal Your Body: The Mental Causes for Physical Illnesses and the Metaphysical Way to Overcome Them. Carlsbad: Hay House Inc., 1988
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| The Placebo Effect: How Strong Is The Power of Sug Name: Cassidy Ga Date: 2002-03-01 12:22:01 Link to this Comment: 1284 |
For years, scientists have sought to find an explanation for the placebo effect. Although many hypotheses exist, there is no one reason defining why or how the placebos work. Some researchers argue that the phenomenon doesn't even occur; that the placebo effect is merely random error and that any improvement said to be caused by a placebo is simply a spontaneous recovery in the patient's condition (2)(3). Other scientists argue that Pavlovian conditioning supports an explanation for the effect: If patients have previously shown improvement from being in a medical setting or from taking medicine, they are conditioned to experience positive effects every time they are in the same situation (1). A second explanation for the placebo effect is that any drug (or placebo) given to a patient will reduce their stress levels. Because many illnesses begin under high-stress circumstances, or exhibit more extreme symptoms under stressful situations, many of the patient's symptoms are likely to improve (2)(4).
The first question that must be answered before delving into the hypotheses behind the placebo effect is whether or not the phenomenon even exists. Certain physicians and scientists claim that "positive effects" of a placebo are, in actuality, just the body's natural ways of healing itself and the immune system's defenses kicking in soon after the placebo is taken (2). Basically, these researchers argue that improvement in a patient's condition after being administered a placebo is merely a coincidence. Negative effects that are often blamed on placebos are viewed by these researches in the same way: nausea or headaches that are claimed to be a placebo's side effects may be spontaneously occurring symptoms (3).
It has been established that colds, nausea, headaches and flus will indeed go away eventually, regardless of whether we take drugs or not. But how can studies that show that placebos have an effect on more serious and chronic illnesses, or potentially fatal conditions, such as hypertension, asthma, Parkinson's disease and schizophrenia be explained?
One theory comes from Pavlov's experiment on conditioned reflexes. In this experiment, Pavlov rang a bell before giving food to a dog. After a numerous trials, no food was given after the bell rang, but the dog still salivated and expected the food. This reflex was an involuntary bodily response to an outside stimulus. Similarly, many people have experienced relief after visiting a physician or taking a medication. Therefore, the patient would be conditioned to respond positively to any visit to a physician's office or any medication administered to them, even if that medication is a placebo (1). This is where the strength of suggestion comes into play-- if the physician tells the patient that the medication is a drug that will help the patient's condition, and if the patient has been previously conditioned as mentioned above, then the patient's body will respond accordingly in about 50-60% of all the cases (3)(4). The number of cases in which the placebo causes positive, healing effects sometimes even exceeds the number of cases in which the actual drug does the same (4).
Another theory behind the placebo effect has to do with the placebo and positive suggestions from the physician reducing stress levels in the patient. Many ailments are at least partially stress-related, including hypertension, asthma and panic and anxiety disorders. According to the scientists who subscribe to this theory, stress can impair the immune and endocrine systems (5). Being removed from an environment which a patient associates with illness and being placed in a different environment which is commonly associated with healing, such as a physician's office or a hospital, can immediately reduce the patient's stress level. This means that placebos are not always in the form of medicines, and that merely changing environments can trigger the placebo effect (5). Also, the reassurance from a physician that the patient will feel better immediately reduces stress. The theory that stress reduction is responsible for the placebo effect can be likened to the Pavlovian conditioning theory, in that the change of environment or positive reassurance from the doctor acts as a stimulus. The conditioned response to the stimulus would be a lowered stress level.
Contrary to what some scientists argue, the placebo effect does seem to exist, according to numerous studies conducted throughout the past century. I am curious about why doctors don't prescribe placebos more often since there is so much data supporting their positive effects. Are doctors just too anxious to prescribe drugs, or is there an ethical reason behind it? Although scientists can't agree on the explanations behind the placebo effect, I think it is obvious that the body is very susceptible to the power of suggestion. Does it matter why the placebo effect occurs, as long as its consequences are positive?
1) Placebo Effect: The Power of the Sugar Pill
2) Scientific American; All In The Mind by W. Wayt Gibbs
4) The New York Times Magazine; The Placebo Prescription by Margaret Talbot
5) Hospital Practice; Harnessing The Placebo Effect by Miroslav Backonja and Walter A. Brown
| Grow Little Cell Grow! Investigating Neurogenesis Name: Claire Alb Date: 2002-03-01 13:21:11 Link to this Comment: 1285 |
Neurogenesis, the production of new nerve cells, has been a revolutionary finding as nerve formation has always been thought to end with adulthood. It has not been until recently that such dogma has been contradicted as research findings report that neurogenesis continues in the hippocampus throughout most of the adult life of mammals and primates (1)The Scientist Magazine , Human neurogenesis. Group demonstrates that adult human brains grow new cells after all. Recent correlations have been further made between neurogenesis and depression as the latter depletes neuron cells in the brain while antidepressive drugs have demonstrated to increase neuronal growth (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells .
\nNeurons are the building blocks of the nervous system as they are responsible for the input, processing and transmission of information. Neurons are derived from stem cells as the latter differentitate into specialized cells and make progenitor cells which are responsible for the formation of neuron and glia cells. Although the majority of neurons are formed during the pre-natal and perinatal stage of development, neuron formation continues in the dentate gyrus of the hippocampus (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells. The hippocampus, which lies beneath the cortex is a major factor of learning and memory formation and can indirectly influence emotion
\n (3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth. Progenitor cells which are present in the subventricular zone of the hippocampus are responsible for such growth as they produce daughter neuron cells through division (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells .
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\nIn the 1960s, Joseph Altman from MIT reported that new neurons were being produced in the dentate gyrus of the hippocampus of adult rat brains. Although such findings were groundbreaking, they failed to create the stir that Elizabeth Gould’s 1998 study caused . The Princeton University neurobiologist demonstrated that the marmoset brain generated neurons (1)The Scientist Magazine , Human neurogenesis. Group demonstrates that adult human brains grow new cells after all. BrdU or bromodeoxyuridine served as a marker when incorporated into the DNA of the progenitor cells and through autoradiographic techniques, the labelled progenitor cells were identified to produce daughter neuron cells. The neurons have “processes which go inward and follow paths to other structures within the hippocampus and get incorporated into basic circuitry of the brain”
\n (4)New Neurons in Neocortex? New Study Says NO! .
\nIn 2000, Fred Gage of the Salk Institute reported that neurogenesis can take place in the hippocampus of adult animal brains. Progenitor cells were isolated from the adult brains of five subjects with tumors and analyzed in culture dishes. Brdu, was once again used as a marker while the ultimate division of the extracted progenitor cells to neurons observed
\n(4) New Neurons in Neocortex? New Study Says NO! .
\nAlthough these findings are not only revolutionary and exciting, there are many questions which have yet to be answered by neurogenesis. What is the functionality of these replicating neurons? When questioned, Gage stated that “we have theories as to the significance of their function but no proof yet” 1)The Scientist Magazine . Furthermore, as laboratories around the country are finding evidence of these new nerve cells in the hippocampus, the “so what?” question must be asked. How can such findings be applied to everyday life?
\nStudies on clinical depression demonstrate that patients with bouts of clinical depression have smaller volume sized hippocampus than their normal sized counterparts who do not suffer from it. There is also constant decrease in hippocampal volume due to a lifetime duration of depression (2)American Scientist Magazine. In 2001, Ron Dunman’s research brought not only association of the neurogenesis/depression phenomenon but possible application when demonstrating that treating rats with Prozac and ECT resulted in newly formed neurons in the hippocampus (3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth.
\nProgenitor cells which are inhibited from dividing throughout most of the brain, do so in the dentate gyrus of the hippocampus and the olfactory bulb as they develop into daughter neurons. Constant renewal of such neurons is thought to be necessary for learning processing and storage of new information (2)American Scientist Magazine. If the mechanisms which inhibit most progenitor brain cells from developing into neurons are found, there is the possibility of repair for damaged brain tissue due to illness, trauma or age. There are also exciting possibilities of stem cell development to diseases such as Parkinson’s and Alzheimer’s, all which are neurodegenerative (5) \nOther studies have found that neuronal growth not fixed to the hippocampus. Elizabeth Gould has also published findings which support the neuron formation in the neocortex., as the latter is the most evolved and complex part of the brain which controls cognitive function and language. Pasko Rakic, who’s chairman of Yale’s neurobiology department has consistently contradicted her findings. In December 2001 publication, he concurred with current research that adult primate produce neurons in the hippocampus but could not support the same in the neocortex (2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells. The politics revolving around such scientific rivalry and differences must be ignored as future research is done on the neocortex
\n(6) The Scientist Magazine.
| better to have a bottle in front of me than a fron Name: Lilian B Date: 2002-03-01 13:28:49 Link to this Comment: 1286 |
\nIn the movie, “One Flew Over the Cuckoo’s Nest,” Mcmurphy, the main character, undergoes a frontal lobotomy (“cutting of the lobes”) to treat his ‘mental illness,’ after several rounds of ECT were unsuccessful in crushing his spirit. In the final scenes of the movie we see from his disposition that he has been reduced from an animated, hyperactive state to a vegetative state. McMurphy’s friend, Chief, tries to talk him, but he stares straight ahead and does not respond. The movie takes place in an insane asylum in the 1950’s, the height of the lobotomy craze in the United States. Between 1939 and 1950, nearly 20,000 documented lobotomies were performed, and thousands more in other countries (1). At first the procedure was used in lieu of Electronic Shock Therapy, for rowdy patients who did not respond well to ECT. The lobotomy was applied as a ‘”fix-all” solution for people with all kinds of major or minor mental disorders. Of course, such an invasive procedure is meant to be used only as a last resort in severe cases of debilitating illness. Many doctors, looking for a quick fix for their patients, used the procedure in cases of “undesirable behavior.” Unfortunately, such a broad criterion meant that anything from Schizophrenia to Obsessive Compulsive Disorder (OCD), to unruly behavior in general could be treated by lobotomy. In Japan many of the people lobotomized were just children who did not behave well or who performed poorly in school.
\nWhat started the lobotomy craze? As with any result, it is difficult to say what exactly prompted the explosion in popularity of such a gruesome surgery. We can begin by exploring the origins of lobotomy in general: In the late 19th century, the scientific community was beginning to understand that behavior was largely controlled by could be mapped out in the brain. The German scientist, Friederich Golz began by cutting the frontal lobes on dogs. He noted that even ferocious dogs became more tame and subdued after the surgery (1). In 1892, in an insane asylum in Switzerland, Gottleib Burkhardt was inspired by Golz to try the procedure on human subjects. He treated patients who were having hallucinations to lobotomies. Some of his patients did become more calm after the surgery, and others died from complications. Burkhardt’s strategy was widely criticized, and there was not much heard about lobotomies for nearly half a decade (1).
\nWhy the frontal lobe?? It became more clear in observations of lobotomized patients that scientists’ theories about the frontal lobes of the brain were correct. The frontal lobe is thought to be a sort of control center, and the location of the self in the brain (5). It is involved in some motor function, problem solving (divergent thinking), spontaneity, memory, language, judgment, impulse control, social and sexual behavior. “Patients with frontal lobe damage exhibit little spontaneous facial expression, which points to the role of the frontal lobes in facial expression (Kolb & Milner, 1981). Broca's Aphasia, or difficulty in speaking, has been associated with frontal damage by Brown (1972),” (5). Also, lobotomy patients might seem more calm because frontal lobe damage results in a difficulty in interpreting one’s environment. The patient has trouble responding to questions, and his associative learning skills are impaired. Oddly enough, it’s also been documented that people with frontal lobe damage cannot get a “good-belly laugh,” that it, they have trouble comprehending the punch lines of jokes. In a study lead by Dr. Shammi of the University of Toronto, patients with all kinds of brain damage were subjected to the Three Stooges and other humorous material: “The study found that people with right anterior frontal damage had the most disrupted ability to appreciate written and verbal jokes -- and funny cartoons -- compared to the normal control group and people with focal lesions elsewhere in the brain. Individuals with right frontal damage chose wrong punch lines to written jokes and did not smile or laugh as much at funny cartoons or verbal jokes. They showed a preference for silly slapstick humor -- surprising but illogical endings which are the hallmarks of such acts as The Three Stooges.,” (5). So, it follows that the frontal lobotomy should result in drastic changes in social behavior.
\nWhy was the change in behavior of subjects viewed as a change for the better? In the mid 1930’s, a scientist at Yale University (Carlyle Jacobson) began experimenting with ‘lobe cutting’ in chimpanzees. In Jacobson’s experiment, aggressive animals became much more calm. In chimpanzees, this change in behavior seemed to occur without any damage to memory or intelligence. A Dr. Fulton performed the same experiment on chimps, yielding similar results. The calm, docile chimps looked to be much better off then they were before the experiment.
\nAt a neurological conference in England, Fulton shared his results with the Portuguese doctor Antonia Egas Moniz. “Moniz knew that certain psychoses, such as paranoia and obsessive-compulsive disorders, involve recurrent thought patterns that dominate all normal psychological processes. Based on Fulton's ideas, he proposed to cut surgically the nerve fibers which connect the frontal and prefrontal cortex to the thalamus, a structure located deep in the brain, which is responsible for relaying sensory information to the cortex. In this way, Moniz reasoned, there might happen an interruption of the repetitive thoughts, allowing a more normal life for the psychotic,” (1). Moniz worked to develop a procedure that he called ‘white matter cutting.’ Through two incisions on either side of the brain, 2 ‘ice picks’ were inserted. A few sweeps of the pick sliced through brain tissue in the frontal lobes. Some of his patients with anxiety or depression saw improvements in their disposition, while others saw no improvement at all or even the contrary. Moniz specified that his process, the leucotomy, should ONLY be used in cases where there was no other avenue. He believed that in that a morbidly fixed idea could be removed from the brain by destroying the tissue on which the idea was saved. He thought that patients with severe anxieties and depression, or compulsive or hallucinatory disorders could benefit from the removal of the ideas that plagued them(2). In 1949, Moniz was awarded the Nobel prize for medicine and physiology. Some years later, Moniz was shot in the back by an old patient of his. He became paraplegic.
\nSo, the father of leucotomy was a paraplegic, and the procedure he created was at most a minor success. Why was this not the end of lobotomy? Perhaps unfortunately, a scientist named Walter Freeman was also at the London Conference with Moniz and Fulton. Freeman was hopeful about the potential of leucotomies in psychiatric medicine. The awarding of the Nobel Prize to Moniz was to Freeman an indication that the procedure was respectable and effective. In Sept. of 1936 Walter Freeman and his co-worker, James Watt, set out to reinstate the lobotomy as a medical procedure for those with mental ailments. They heralded the operation, believing themselves that it worked. They developed the “Freeman-Watts Standard Procedure,” in an attempt to refine the lobotomy methods being used at the time. The pair toured the country, promoting their procedure and performing it on many patients. Freeman was the driving force in the pair, and he strove to perfect the operation by making it less messy and less time consuming. Their efforts perpetuated the ‘lobotomy craze,’ and by the late 40’s it was an exceedingly popular operation.
\nPeople did not begin to realize the ramifications of such a gruesome operation until it became clear, through observation, that lobotomized individuals were far from normal or happy, and that in actuality, the appearance of a less crazed nature had simply been mistaken for (what was in some cases) a total loss of the individual’s personality. In addition, scientists were not getting the results they expected from empirical evidence. It seemed that only 1/3 of the cases yielded any improvement in the patient, while 2/3 of patients remained just as ill as they were initially or, in many cases, their illnesses became worse. Scientist in the 50’s began experimenting with the use of new kinds of psychiatric drugs (such as thorazine) in treating patients, as medication is reversible and brain surgery is not. By the late 50’s, lobotomies had become nearly obsolete, and the status of the procedure was downgraded from effective to experimental. All in all, the lobotomy era seemed to have been a sort of ‘oops’ in psychosurgical science.
\nResearchers from Mount Sinai Medical School have come to Pilgrim, one of the largest state hospitals in the country to hopefully gain something from the lobotomy tragedy. Dr. Peter Powchik says about the hospital, “If you want to learn why people don’t get better, you do it here.” “Powchik and his colleagues administer teststhat assess patients' thought processes and motor coordination. Their preliminary findings show that lobotomies did not help these patients and in some cases may have even triggered more mental illness. The project has turned up evidence that some people who had lobotomies for depression, anxiety or disruptive behavior developed symptoms of schizophrenia following the surgery,” (4). Philip Harvey, the coordinator of the research project at Mount Sinai hopes that his teams research may give scientists some clues as to how schizophrenia originates in the brain. He is driven finitude of available time for his research to be done. Lobotomies are so rarely performed now, that compiling data on such a massive scale in the future would be impossible. Their job is an emotionally taxing one, as many of the patients are frighteningly sick, and what is more sad, they will not recover:
\n“All are elderly and have spent most of their adult lives behind locked doors and barred windows. Some spend their days staring vacantly; others are forever agitated. They range from Frances Kichinski, who no matter what she is doing is always weeping, to Pauline White, who smiles constantly and wonders why the family that exists only in her mind never comes to visit,” (4). Harvey laments, "It may have caused some people to be hospitalized for the rest of their lives. It made so many people worse." As for McMurphy, it is clear in the end of the film that he has no way out of the mental hospital, for he is nearly a vegetable, and no one in such a state could be self-sufficient. And so, by killing him, Chief is giving his friend freedom and thus is actually demonstrating an incredible amount of love and reverence for his friend who fell victim to ‘the system,’ as so many others did who are STILL in asylums today.
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\n1)History of Lobotomy,
\n2)PBS Website,
\n3)Nobel Prize Website,
\n4)Research Articles,
\n5)The Frontal Lobe,
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| "Meat all the Way Down": Colin McGinn's The Myster Name: Hilary Hoc Date: 2002-03-01 13:32:55 Link to this Comment: 1287 |
\n"Meat all the Way Down":
\nColin McGinn's The Mysterious Flame
\nEarly in The Mysterious Flame, (1)., philosopher Colin McGinn's breezy but provocative discussion of the relationship between consciousness and the brain, McGinn presents a telling vignette from a science fiction story in which aliens are discussing their observations of humans:
\n"These creatures are the only sentient race in the sector and they're made out of meat. . . .They're meat all the way through."
\n"No brain?"
\n"Oh, there is a brain all right. It's just that the brain is made out of meat."
\n"So . . .what does the thinking?"
\n"You're not understanding, are you? The brain does the thinking. The meat."
\n"Thinking meat! You're asking me to believe in thinking meat!"
\n"Yes, thinking meat! Conscious meat! Loving meat. Dreaming meat. The meat is the whole deal. Are you getting the picture?" (1).
\nIt is this apparent contradiction, that initially insensate organic material can create consciousness, a phenomenon without apparent material content or spatial location, which McGinn sets out to explain. Many philosophers and scientists have undertaken this journey before him, but McGinn contends that this long road of philosophical inquiry is actually a blind alley. While McGinn believes that the mind is indeed a product of the material qualities of the brain, he argues that the mind (or brain) does not itself possess the ability solve what philosophers denominate "the mind-body problem," (although "mind-brain problem" might be more accurate).
\nMcGinn begins by rejecting both traditional materialism and dualism. Materialists propose that the brain and consciousness are one and the same: thus, brain waves not only correlate with consciousness, they are consciousness. McGinn faults this position for ignoring the very nature of conscious experience. The experience of consciousness, he argues, does not directly correlate with brain waves or the activity on a PET scan. Studying these physical phenomena alone will tell the observer nothing about the experience of consciousness, while endless introspective inspection of one's conscious state would not lead to any description of the brain's anatomy or physiology, let alone that neurons within it were firing as one thought.
\nLikewise, McGinn rejects dualism, the proposition that consciousness exists completely independent of the brain, because its proponents also ignore empirical observations. Were consciousness completely disconnected from the brain, a fully functioning brain could exist without consciousness, and consciousness could exist independent of the brain, thereby producing what McGinn terms ghosts (disembodied minds) and zombies (organisms with mindless brains, beings who can act but who do not perceive). Dualism thus does not account for empirical observations of conscious organisms, in which the consciousness's existence appears to depend on the brain's activity, and vice-versus. Yet neither science nor philosophy has yet offered a satisfactory explanation of this interdependence.
\nMcGinn offers a third way out of the mind-brain problem: pessimism and acceptance of failure. McGinn agrees with materialists that it is properties of the brain, and the brain alone, which produce consciousness. These properties, however, are unknowable, emerging in their turn from properties of space and matter that the human brain cannot perceive. He postulates a theory he dubs "mysterianism," a respectable way of saying the world will never know. McGinn argues that, in contemplating the origin and nature of consciousness, the human mind has come to the edge of its conceptual capacity: the mind peers over the cliff, but can see nothing but an endless abyss below. While human intelligence can perceive the problem, it cannot understand the answer.
\nMcGinn relies primarily on the concept of cognitive closure to support this argument. Human intelligence, he argues, evolved in response to the environment in which humans had to survive. Thus, certain human capacities are well developed, including the ability to navigate in three-dimensional space and to predict the effect of actions in a three-dimensional world. The imperatives of survival, however, have left other capacities undeveloped or nonexistent: for example, the human brain cannot perceive radar or infrared, or understand whale song. The ability to understand consciousness is simply not, McGinn argues, one of the human brain's talents. Specifically, because consciousness is a nonspatial phenomenon, which affects and is affected by objects that occupy space, McGinn argues that consciousness must have spatial characteristics not perceptible to the human brain. Similarly, while consciousness appears to be immaterial, it is created by and in turn affects matter. Therefore, McGinn reasons, consciousness must depend upon properties of matter imperceptible to the human brain and inaccessible to the mind. McGinn acknowledges that the key to consciousness is located in every sentient organism's genes, because genes code for the construction of all biological phenomena, including consciousness. Yet McGinn maintains that human intelligence as it is currently constructed will never unlock this code.
\nMcGinn's exposition of the mind-brain problem is an intelligent and readable summary of centuries of philosophic debate. Explicitly addressing the layperson, he does not fall into the trap of spewing jargon, although he often belabors his points with one too many repetitious analogies. His straightforward and informal style effectively establishes a dialogue with the reader, although his bursts of self-revelation can become distracting. (Perhaps no one really needs to know about his infatuation with Seven of Nine on television's Starship Voyager.)
\nAs interesting as his argument is, however, McGinn never quite proves his point. The concept of cognitive closure is intuitively appealing and supported by empirical observation: there are in fact various physical phenomena the brain cannot perceive or interpret. It is likely, then, that the brain's limitations similarly constrain the conscious mind. However, McGinn cannot provide a satisfactory account of why humans would experience cognitive closure with regard to consciousness, rather than any other mystery of the natural universe. His supposition that there are properties of space and matter that the human brain cannot perceive and that human intelligence has not yet deduced appears eminently reasonable. However, McGinn does not explain why the properties of space and matter that underpin the structure and formation of consciousness from its origin in the brain will always remain beyond human understanding.
\nMcGinn's examples of human misconceptions about space, for example, undermine the very point he is trying to make. As he points out, contrary to what the brain perceives, humans have deduced that the Earth is not flat, nor does the sun revolve around it, and that matter is not solid. His examples support the idea that humans have been wrong about the natural and biological world, often because their own brains deceive them. Yet human intelligence can deduce, from empirical observations and analysis, physical properties not readily apparent to the brain; McGinn likens humans studying consciousness to pre-Einsteinian physicists, but never makes clear why this analogy presupposes failure rather than success.
\nAccepting McGinn's proposition of cognitive closure, then, does not necessarily lead to McGinn's ultimate conclusion. Indeed, if cognitive closure can be found anywhere, perhaps it is not in knowing what it is we do not know, but rather in recognizing what we cannot know. How can we know that we cannot know something? If human intelligence is cognitively closed to understanding consciousness, how can human intelligence ever deduce this?
\nMcGinn rests his conviction that the problem of consciousness cannot be solved in part on his misunderstanding of the nature of scientific inquiry. He views science as a collection of disciplines which "ask answerable questions and moves steadily forward," while philosophers wrestle with the insoluble questions at the frontiers of cognitive closure. (1). Were McGinn convinced that scientific inquiry produces as much uncertainty as it dispels, he would find the distinction between science and philosophy less clear cut . Perhaps counterintuitively, his view of science as simple and unambiguous causes McGinn to demand more of science than it can deliver. Like philosophers, scientists often theorize well beyond their empirical observations, altering or abandoning theories as new observations undermine them, but never arriving at one single, immutable truth. As a philosopher, McGinn has assumed a level of certainty in science that is available nowhere in human inquiry and scholarship, be it scientific or philosophic (and his assumption that there is a clear line between these two fields bespeaks unfamiliarity with one or both of them). Seeing uncertainty before him, McGinn announces that the path is cognitively closed and turns back before the journey has truly begun.
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\nReferences
\n (1) McGinn, Colin. The Mysterious Flame: Conscious Minds in a Material World. New York: Basic Books, 1999. \nRelated Web and JStor Resources: \nBy Colin McGinn: \nThe following papers and reviews by Colin McGinn are more detailed and technical discussions of aspects of the argument set forth in The Mysterious Flame: \n"Can We Solve the Mind--Body Problem?" Colin McGinn. Mind, New Series, Vol. 98, No. 391. (Jul., 1989), pp. 349-366. Stable URL: \n \n) \n) \nReviews of The Mysterious Flame \n) \n) \n) \n) \n
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| Intrapsychic Omnipresence in Bodily Symptoms Name: Cass Barne Date: 2002-03-01 13:39:12 Link to this Comment: 1288 |
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\nSometimes disease and illness just show up. For these medical conditions, a doctor usually tells us what is "wrong" physically. These scientific observations determining diseases or symptoms leave people wondering if there is something behind the cell that created the malfunction. Perhaps one's psyche; which is the mind functioning as the center of thought, conscious or unconscious, and interconnected with the physical environment, can effect the body positively and negatively. An indirect way of dealing with psychological conflict is to intuitively or unconsciously convert it into symptomatic illness. However, this does not get rid of the emotions or the symptoms, for this is not the root of the problem. It is only through recognition of the their intuition or repressed emotions that people may come to heal themselves. It is difficult although possible for some to assign every illness or symptom to some underlying psychic cause; but that is usually whimsically referred to as "new age" and "mystical". It is a person's own personal belief whether she created her diabetes, or whether he created his cancer as a result of psychological and emotional conflict and trauma. Therefore, we can only look at the facts to postulate the argument that a lack of psychological well being manifests itself somatically. The best way to examine the notion that psychological factors affect medical conditions is with the neurosis Hysteria.
\nHysteria is also known now as Conversion Disorder or Dissociation, in which unconscious or emotional psychological conflict converts into a bodily disturbance (2). An example of this is anxiety. Hysteria is diagnosed as psychological stress accompanied with physical symptoms. Interestingly, despite the multiple physical symptoms there is no anatomical or organic basis for any of them. Although conversion disorder is a physical manifestation, there is no physical cause. In the case of hysteria, the mind or the psyche is neglected by the person who represses emotional trauma, and these then divert themselves into the body as a means of expression or escape. These patients often times do not know what is wrong with themselves because the repression was unconscious and out of their control. Accordingly, the physical symptoms in hysteria are a result of the person's lack of psychological control, which is unconscious not voluntary.
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\nDuring the 19th century, French Neurologist J.M. Charcot and Psychologist P. Janet emphasized that “morbid ideas could produce physical manifestations” and that hysteria was caused by the psyche not the body (1). This reference highlights the notion that physical symptoms reflect psychic states. Freud also believed that hysterical symptoms were symbolic of a repressed unconscious “event” or psychic trauma not properly expressed at the time (2). One must appreciate Freud’s assertion of unconsciousness in the pressed event. Some of the physical manifestations of hysteria or conversion are expressed as blindness, paralysis, ataxia, epilepsy, amnesia, anaesthesia, aphonia (loss of voice), and melancholia (3). The same symptoms were also seen in Breuer’s patients like Anna O. One of the most classic of all psychosomatic disorders was the hysteric Dora, Freud's patient. At the age of eighteen she had developed a range of symptoms such as hemicranial headaches, attacks of nervous coughing, tussis nervosa (inflammation of nose and throat), appendicitis, aphonia, fatigue, together with amnesia, dyspnoea (aggravation), hysterical unsociability, and depression. As Freud describes it, Dora "was clearly satisfied neither with herself nor with her family: her attitude towards her father was unfriendly, and she was on very bad terms with her mother....and she tried to avoid social intercourse" (6). Dora also had traumatic sexual encounters with a man which she repressed as well. Clearly Dora had psychological stress, and psychological trauma due to the resulting sexual fears. Dora diverted her repressed sexual encounters and familial conflict into her psyche, which created a plethora of symptoms.
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\nSimilar symptoms are also seen in dissociative states where the individual may suffer from "dissociative control" and "dissociative awareness" in that he or she can not consciously control actions and is not aware of what experiences took place (5). For example, amnesia and fugue states represent the person's inability to recollect what actions took place. In fugue states, they are consciously aware of the actions, but they do not remember. Amnesia in hysterics does not come as a result of brain lesion, but as a self-induced protective erasing of an emotional traumatic experience. These states, like hysteria, address the person's involuntary control of their internal experience and worldly actions. Since there was no organic basis for the physical symptoms, physicians like Breuer and Neurologist Charcot in this era used suggestion, free association and hypnosis to free the patients from their symptoms (1). They found that letting the hysteric talk through her conflicts "lead to the disappearance of her symptoms whenever she was able to recollect their root events" (1). This sort of treatment worked because the mental conflict was unknown as far as the patient was concerned. The symptoms served as a psychological defense to banish painful anxiety from consciousness. Therefore, the use of hypnosis, and what later became psychoanalysis, helped in ridding symptoms because the Psychoanalyst was able to draw out unconscious traumatic memories and bring them to conscious awareness to begin a process of mental and emotional healing.
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\nWhen was the last time you heard about Hysteria? Probably the last time you talked about the Salem Witch Trials. Hsyteria is not a prominent illness as many others today. Where did it go? Have there been more mental illnesses that have taken over or are we just rolling up more names to the old one? Hysteria is the only disease or disorder that has an actual psychological basis. Even some of the psychological disorders like depression and schizophrenia are known to have some physical basis. However, maybe every disease has an underlying emotional memory that is only accessible when brought to consciousness. It could be that every symptom has a negative mental association, and when that is recognized, and released, then the person is able to heal. Perhaps physical and mental illnesses are different across people because they psychologically choose to deal differently with the external environment and certain experiences, and therefore the manifestation of their illnesses. When we hear about miracle cures it makes us wonder what it is that served to heal them spontaneously. It could be that psychologically the person decided what they needed to change in their life in order to be at ease and healthy with themselves. The psychological aspect may be more important in curing diseases than we may think. What is unknown to the normal observer or the people who are actually diseased, is whether or not they have the personal choice to control emotional fluctuations and mental patterns. Is conversion of psychological conflict automatic and involuntary, or can that be governed by our Self?
\nThe tasteful opinion that the individual is in control of his or her health, mental or physical, comes down to personal beliefs. Perhaps all illnesses, diseases, and symptoms stem from psychological disturbance. Clearly, hysteria is conversion of psychological conflict into the body. History tells us that physical symptoms associated with hysteria and dissociative states are a result of negative mental and emotional states. These negative states rather than being released were pushed back further in the mind to the unconscious. It was only through the catharsis of psychotherapeutics that patients could understand the unconscious, which irrevocably led to their symptomatic illnesses. Hysteria is one of the few diseases that is psychological in origin, and may be the only one. Yet, it is possible that all other diseases follow the psychological path as well. Ph.D Louise Hay writes “I have learned that for every condition in our lives, there is a NEED FOR IT. Otherwise, we would not have it. The symptom is only an outer effect. We must go within to dissolve the mental cause. It’s like cutting down the weed and getting the root out” (8). Rather than viewing the sentiment as mystical there is a real basis for further research and understanding in its application in the field of mental health.
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\n 1) The Freud Page
\n 3) Notes on Neurotic Disorders
\n 5) Hypnotizability and traumatic experience
\n 6) Freud, Sigmund. Dora: An Analysis of a Case of Hysteria. New York: Simon & Schuster, 1997.
\n 8) Hay, Louise L. Heal Your Body: The Mental Causes for Physical Illnesses and the Metaphysical Way to Overcome Them. Carlsbad: Hay House Inc., 1988
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| Learning to Read and Write: Language on the Brain Name: Tua Chaudh Date: 2002-03-05 12:19:10 Link to this Comment: 1366 |
When I was little, my favorite book was Happy Birthday Moon. For a while, it was my nightly bedtime story. Anyone who offered to read aloud to me was immediately proffered this book. After some time, I knew the story by heart, word for word. I could not quite read the book but I had memorized the framework of it and so could tell the story myself. The day that I learned to finally recognize the words themselves was so exciting. When the blur of squiggly lines on the page became letters with sound and meaning, a whole new dimension opened up. Every form of human expression is codified within some framework of language. As an English major, I study how people manipulate and interpret language in order to communicate. As a tutor with a reading enrichment program, I sometimes encounter kids who do not share this love of reading and writing. As it is my job to help them master and gather more enjoyment from their dealings with language, and since brain equals behavior, I thought this web paper the perfect opportunity to ask few questions. How does the brain process language? Why do some people enjoy reading and writing better than others do? Why is it easier for some people to learn to manipulate language? And which came first the brain, or the linguistic framework that defines and identifies it? I have learned that language, like the nervous system, is a complicated blueprint which humans use to communicate with, navigate, and interpret, the world.
1)
2)
5)
For most people, the parts of the brain that process language are located in the left hemisphere
Words are the signifiers in our system of linguistics. When a person sees a word, the brain associates that word with a representation or picture of whatever it is that word signifies. In order to be able to process the connection, the brain has to recognize the thing itself, and the group of letters that form the word that represents it. Reading is almost like speaking, the difference lies in the extra activity of the occipital lobe
American linguist Benjamin Lee Whorf believes that language and thought influence each other. Language expresses thought, but language also shapes thought References
| Grow Little Cell Grow! Investigating Neurogenesis Name: Claire Alb Date: 2002-03-22 15:10:29 Link to this Comment: 1566 |
Neurons are the building blocks of the nervous system as they are responsible for the input, processing and transmission of information. Neurons are derived from stem cells as the latter differentiate into specialized cells and make progenitor cells which are responsible for the formation of neuron and glial cells. Although the majority of neurons are formed during the pre-natal and perinatal stage of development, neuron formation continues in the dentate gyrus of the hippocampus (2). The hippocampus, which lies beneath the cortex is a major factor of learning and memory formation and can indirectly influence emotion. Progenitor cells which are present in the sub ventricular zone of the hippocampus are responsible for such growth as they produce daughter neuron cells through division (2).
In the 1960s, Joseph Altman from MIT reported that new neurons were being produced in the dentate gyrus of the hippocampus of adult rat brains. Although such findings were groundbreaking, they failed to create the stir that Elizabeth Gould's 1998 study caused . The Princeton University neurobiologist demonstrated that the marmoset brain generated neurons (1). BrdU or bromodeoxyuridine served as a marker when incorporated into the DNA of the progenitor cells and through autoradiographic techniques, the labeled progenitor cells were identified to produce daughter neuron cells (4). The neurons have "processes which go inward and follow paths to other structures within the hippocampus and get incorporated into basic circuitry of the brain" (2).
In 2000, Fred Gage of the Salk Institute reported that neurogenesis can take place in the hippocampus of adult animal brains. Progenitor cells were isolated from the adult brains of five subjects with tumors and analyzed in culture dishes. Brdu, was once again used as a marker while the ultimate division of the extracted progenitor cells to neurons observed (4).
Although these findings are not only revolutionary and exciting, there are many questions which have yet to be answered by neurogenesis. What is the functionality of these replicating neurons? When questioned, Gage stated that "we have theories as to the significance of their function but no proof yet" (1). Furthermore, as laboratories around the country are finding evidence of these new nerve cells in the hippocampus, the "so what?" question must be asked. How can such findings be applied to everyday life?
Studies on clinical depression demonstrate that patients with bouts of clinical depression have smaller volume sized hippocampus than their normal sized counterparts who do not suffer from it. There is also constant decrease in hippocampal volume due to a lifetime duration of depression (2). In 2001, Ron Dunman's research brought not only association of the neurogenesis/depression phenomenon but possible application when demonstrating that treating rats with Prozac and ECT resulted in newly formed neurons in the hippocampus (3).
Progenitor cells which are inhibited from dividing throughout most of the brain, do so in the dentate gyrus of the hippocampus and the olfactory bulb as they develop into daughter neurons. Constant renewal of such neurons is thought to be necessary for learning processing and storage of new information (2). If the mechanisms which inhibit most progenitor brain cells from developing into neurons are found, there is the possibility of repair for damaged brain tissue due to illness, trauma or age. There are also exciting possibilities of stem cell development to diseases such as Parkinson's and Alzheimer's, all which are neurodegenerative(5).
Other studies have found that neuronal growth not fixed to the hippocampus. Elizabeth Gould has also published findings which support the neuron formation in the neocortex., as the latter is the most evolved and complex part of the brain which controls cognitive function and language. Pasko Rakic, who is chairman of Yale's neurobiology department has consistently contradicted her findings, however. In December 2001 publication, he concurred with current research that adult primate produce neurons in the hippocampus but could not support the same in the neocortex. The politics revolving around such scientific rivalry and differences must be ignored as future research is done on the neocortex (6).
Constant neuronal generation in the hippocampus can have many purposes. Throughout its lifespan, an adult has new experiences which require the storage and processing of new information. Since such demand is constant, new neurons may be required to store such information. However, when taking such perspective, there are many new questions which arise. If new neurons may needed for new information, then what happens to the old neurons in the hippocampus? Does lack of usage lead to their degeneration or do they continue to be functional? Stored memories are often recalled in adults thus leading to the possibility that older neurons may needed for the processing and transmission of such needed information.
Neurogenesis is a complex issue with an array of possibilities for the future. Further investigations will have to answer some of the questions and issued raised.
WWW Resources
(1)The Scientist Magazine , Human neurogenesis. Group demonstrates that adult human brains grow new cells after all.
(2)American Scientist Magazine, Depression and the Birth and Death of Brain Cells.
(3)National Depressive and Manic Depressive Association, Antidepressants and Brain Cell Growth.
(4) Neuroscience for Kids, New Neurons in Neocortex? New Study Says NO!
(5)
(6) The Scientist Magazine.
| The Brain and Violence: An Unhealthy Combination Name: Balpreet B Date: 2002-04-07 14:33:28 Link to this Comment: 1735 |
"Jack was walking down the street enjoying a snack he had just bought at a convenience store. Feeling good, he smiled at the stranger coming toward him while continuing to eat. The stranger suddenly pulled out a knife and began stabbing Jack. Bystanders pulled the knife away, but too late."
"After the killing, the attacker said that he was deeply sorry. He had sensed a strange aura, then experienced a flashback of having been bitten and of having a hernia operation under local anesthesia. That was followed by hallucinations about Jack cutting off his flesh, testicles, and heart to eat them" (6).
Everyday on the news one hears stories of crimes and murders such as the one above. Murders are committed every day; stores are robbed every hour; crimes are committed constantly. The truth is that violence has sadly become a common and prevalent occurrence in society today. In essence, one must ask himself whether or not these violent tendencies have any biological relation whatsoever. Is violence caused by disruptions or damage to the brain? Is there a genetic correlation? Or is violence brought about by something else, such as economic difficulties or social or cultural differences? And one must ask himself an even broader question-whether a cause for violence even exists.
In 1848, a railroad worker, Phineas Gage, was working when an explosion caused an iron rod to impale his skull, damaging the front part of his brain. Although Gage miraculously survived, his behavior severely changed in that the intelligent and respectful man everyone knew suddenly because fitful, impulsive, and rude (2).
This case is one of the first indications that violence may be related to some kind of damage or abnormality in the brain. Researchers have found correlations between violent and aggressive tendencies to damage or abnormalities to a specific part of the brain. Gage's accident probably resulted in damage to the prefrontal cortex. The prefrontal cortex is the brain's foremost outer position, located behind the eyes. This area of the brain is especially important because of it's importance in the orchestration of emotion, arousal, and attention. The prefrontal cortex seems to be the part of the brain that enables people to restrain themselves from acting on all of their impulses and is extremely vital for a child's ability to learn to feel remorse, conscience, and social sensitivity (5).
However, although the function of the prefrontal cortex is known, why, or how, would prefrontal deficits cause violent tendencies or a more aggressive character? Adrian Raine, a psychopathologist from USC suggests that damage or abnormalities of the prefrontal cortex may result in a condition known as Antisocial Personality Disorder, or APD. This disorder is characterized by irresponsibility, deceitfulness, impulsiveness, lack of emotional depth and antisocial behavior. Raine, in his study, suggested three reasons why prefrontal deficits may cause such a personality (5). Firstly, the prefrontal cortex is responsible for self-restraint and deliberate foresight. If this part of the brain was damaged, then one effect that would arise would be the tendency for one to act on all his impulses without thinking ahead or thinking of the consequences. Second, the prefrontal cortex is important for learning conditioned responses. This area of the brain has been thought to be central to a child's ability to learn to feel remorse, conscience, and social sensitivity (7). If the prefrontal cortex was to function abnormally, how is the child supposed to learn how to have a conscience? For example, one study reported that children who received damage to their prefrontal cortex before the age of seven developed abnormal social behavior, which was characterized by their inability to control their aggression and anger (2). Lastly, Raine suggests that if prefrontal deficits underlie the APD group's low levels of autonomic arousal, these people may unconsciously be trying to compensate through stimulation-seeking (5).
There have been many studies done concerning violence and its relationship to the prefrontal cortex. In July, 2000, UW-Madison psychologist Richard Davidson analyzed brain imaging data from a large, diverse group of studies on violent subjects and those predisposed to violence to find any connections between the brain and violent tendencies. His studies focused on individuals diagnosed with APD, convicted murderers, and those with childhood brain injuries (4). He hypothesized that impulsive aggression and violence arise as a consequence of faulty emotion regulation (3).
Davidson and his colleagues found common neurological trends among many of their subjects in the brain's inability to properly regulate emotion. One core finding that Davidson's study found dealt with the interplay among several distinct regions of the brain, primarily the orbital frontal cortex, the anterior cingulate cortex, and the amygdala. They found that normal brain activity in the orbital and anterior regions were either entirely absent or slowed in many of their studies, while the amygdala showed normal or heightened activity. The inability of these two regions of the brain to counteract the response of the amygdala may explain how threatening situations can become explosive in some people with damage to the prefrontal cortex (4).
There also exist many recent studies that attempt to relate genetics to the increased tendencies for violence in some people. Although no single gene for human violence has been discovered yet, data from molecular geneticists suggest that multiple genes may interact to prime individuals to this behavior (1). Davidson's study also described a large group of subjects who had a genetic deficit that caused a disruption in the brain's seretonin levels. Seretonin has been hypothesized to hold inhibitory control over impulsive aggression. Disruption of the seretonin level may contribute to increased aggression within the individual (3).
However, although these recent studies such as Davidson's correlate genetics and prefrontal damage to increased violent tendencies, can one actually say that this is the only cause of violence? When analyzing and/or observing behavior, one automatically relates his observations to the brain; however, in stressing the function of the brain, one cannot ignore the importance of social influences on behavior (8). Adrian Raine stresses this case: "We are talking about a predisposition to antisocial behavior. Some people who have prefrontal deficits do not become antisocial, and some antisocial individuals do not have prefrontal deficits. It's important to make clear that biology is not destiny" (5). Non-biological factors such as socioeconomic and cultural influences may play a major role in violent tendencies. Issues such as unemployment, lower educational level, alcohol use, and access to firearm all contribute to violent crimes (1). Not only do biological factors need to be stressed, but so do cultural factors. Violence is found all over in movies, video games, the nightly news, professional sports and many more socially accepted types of media and entertainment. Couldn't exposure to violent events profound behavioral consequences?
Although all the above trends and relationships implied by these studies exist, do they prove that violence is ultimately caused by some type of biological disorder or social influence? By implying this, one is assuming that every man or woman who commits a crime or acts with violent tendencies does so by some type of brain damage, genetic disorder, or social problem. If anything, by believing this, society is giving people an excuse to commit crimes and act on their violent behavior; if biological or social influences ultimately cause violence, does that redeem one's actions? Does this give criminals an excuse to murder, cheat, and steal? Can their violent tendencies and criminal actions be reasoned in the court of law as being out of their hands because of damage to their prefrontal cortex when they were a child? Although these studies express a trend between brain damage to the prefrontal cortex and violence, one cannot use this to makes excuses for those who act on this aggressive behavior. A correlation between brain damage and violence might have been found, but how to act on this newfound discovery still needs to be discussed before anything else can be done.
1) Violence and Brain: An Urgent Need for Research
2) Brain Briefings: Violent Brains
3) Dysfunction in the Neural Circuitry of emotion Regulation-A Possible Prelude to Violence
4) Violent Behavior Linked To Specific Brain Dysfunction
5) Size of Brain Linked to Violence
6) Sudden Brain Seizures Said to Trigger Violence
7) Brain Size Linked to Violence
8) Mark, Vernon H. Violence and the Brain. New York: Harper & Row Publishers, 1970.
| Battle of the Sexed Brain Name: Tiffany Su Date: 2002-04-11 00:15:19 Link to this Comment: 1790 |
All kinds of research have shown that the bigger the brain, generally, the smarter the animal. (1) However, as Emily Dickinson might agree, it is not the size of the brain that counts, but rather what is contained within the brain. Human male brains are, on average, approximately 10% larger than that of the female, but this is because of men's larger body size: more muscle cells imply more neurons to control them. (3) If the size of the brain is not the determinate factor of the differences between the male and female brain what is?
Of special interest to researchers of this subject was the amount of gray matter, the part of the brain that allows us to think. The researchers wanted to know if women have as much gray matter as men. (1) It would be logical to conclude that if there is less gray matter, the component of the brain associated with the thinking process, than obviously, biologically men and superior in intellect to women. However, as is the case with many biological researches, more questions arose than were answered. According to one psychology professor at the University of Pennsylvania, there is no difference in the amount of gray matter in men and women. To make up for the smaller brain size, women have 55.4% gray matter vs. 50.8% in men. (1) Thus disputing the hypothesis that the difference in amount of gray matter is the reason for the difference in the way men and woman perform various tasks. If this is an accurate conclusion, the question still remains, why are men more inclined to perform better on spatial, intuitive, nonverbal tasks, such as mathematics, while woman tend to excel at verbal, sorting, detail-oriented tasks such as English? (4) Some scientists believe that the answer to this question lies in the evolutionary development of the brain.
Over the last couple of decades, proponents of evolutionary psychology have been piecing together a case that the mind is naturally sexed. Our male and female forebears faced different evolutionary pressures in their struggle to survive and reproduce in the Pleistocene grasslands, and as a result they have different mental aptitudes and even differently organized brains. (5) This would suggest that since men were the ones that hunted they are better equipped to analyze spatial-oriented tasks. At first this appears a logical conclusion. In order to hunt for food the male would have to be aware of how far the prey is. However, I have to question, if humans are simply animals, then why can this logical not be applied to all animals? In the jungle the lioness is the one that hunts, not the lion. Yet, although the lioness is the provider, and is capable of defending herself, since they travel in packs, the lion is considered the King of the jungle. I believe that it would be viewed as preposterous to suggest that we would have a Queen of the jungle instead of a King. The reason for this is not biological, but rather a social aspect.
Recent decades have witnessed two contradictory processes: the development of scientific research into the differences between the sexes, and the political denial that such differences exist. A hundred years ago, the observation that men were different from women, in a whole range of aptitudes, skills, and abilities, would have been leaden truism, a statement of the yawning obvious. Such a remark, uttered today, would evoke very different reactions. Said by a man, it would suggest a certain social ineptitude, a naïveté in matters of sexual politics. A woman venturing such an opinion would be scorned as a traitor to her sex, betraying the hard-fought "victories" of recent decades as women have sought equality of status, opportunity and respect. (2) Imagine a Bryn Mawr woman saying that biologically women are inferior to men. This would be an affront to the feminist movement that our "politically correct" society has been forced to include.
Yes, women tend to be more verbal; this has been supported by tests, which revealed that females speak twice as many words as the man, and has done so even before the age of two. (4) Yes, men tend to receive higher scores on logic-oriented tests; comparing the scores of SATs can support this. Women score significantly lower than men on the SAT. In 1994, the most recent information available, they had an average score of 881 (out of a possible 1600 points, 400 is the minimum), while men scored an average of 926 points, nearly 50 points higher. (6) Despite the information presented to show that there is a difference in the way the male and female brain operates, I still fail to see how any of the information presented proves that one sex is superior to that of another. There are several well-known female mathematicians and scientists. This fact disproves the idea that men are superior to women in logical tasks. Langston Hughes is a famous male poet, which would disprove the idea that females are superior to men linguistically. However, the addition of the word "generally" does make a difference. I would have to agree that generally there are intellectual tasks that men are better at than females. However, I am not convinced that this is a biological superiority, rather than social.
Are women naturally more inclined to play with Barbie Dolls, or is the societal expectation to do this the cause. Is it the societal expectation for a man to use his wit to be the "bread winner" in the family, the real reason why male dancers are not as respected as a male scientist? What is biological predisposition, and societal demand? So far, research has only been able to point out the aesthetic differences of the male and female brain, and to speculate what these differences mean in terms of the way in which the two sexes perform various tasks. Therefore I must still maintain the phrase that was instilled in me by my father; I am capable of doing anything I put my mind to.
WWW Sources
1}Gender gaps on the Brain,Size of brain not determinate factor of intelligence.
2. 2}Excerpts From Brain Sex,The biological vs. The political brain.
3. 3}Are There Differences between the Brains of Males and Females?,Intellectual differences among the sexes.
4. 4}Left/Right Brain?,Left or right brained.
5. 5}La Difference,Who is the better sex?
6. 6}Traumatic Tests: Gender Bias and the SATs,SAT statistics.conclude that men are superior to women in intellect, right? Now I would not be a proud Bryn Mawr woman if I were to agree with this logic. However, I would not be
| Gambling and the Brain Name: Rebecca Ro Date: 2002-04-11 00:47:48 Link to this Comment: 1791 |
Compulsive gambling is a behavior which may rely on brain circuits that evolved to help animals assess rewards important to their survival. Researchers have found that those same circuits are used by the human brain to assess social rewards. They found that the brain systems that detect and evaluate such rewards generally operate outside of conscious awareness. The study said that much of what happens in the brain goes outside of conscious awareness. There are automatic brain circuits which affect activities such as gambling (2). However, this challenges prior notions which say that people make conscious choices about their everyday decision making. If people can get themselves to work unconsciously, how does the brain really know what it must pay conscious attention to? Also, how did evolution create a brain which makes such distinctions?
Experiments performed on animals and humans are showing that the brain has evolved to shape itself according to what it encounters in the external environment. Dr. Montague, of Baylor College of Medicine said that ninety percent of what people do everyday is carried out by an autonomic unconscious system that is evolved to help creatures survive (2). According to research, we use these circuits to know what to attend to and what to ignore. Brain imaging machines directly measure the activity of human brain circuits. The two circuits that have been studied most extensively are involved in how we assess rewards. The chemical dopamine is used in these two circuits. The first circuit is in the middle of the brain and helps us assess rewards. Learning takes place only when something unexpected happens and dopamine firing rates increase or decrease. When nothing unexpected happens, the dopamine system is quiet. In humans, the dopamine signal is sent to a higher region of the brain, the frontal cortex. The anterior cingulate is located in part of the frontal cortex and part of its function is detecting errors and conflict in the flow of information being processed automatically. Brain imaging shows that when a person gets an unexpected reward, more dopamine reaches the anterior cingulate. However, when a person expects a reward and does not get it, less dopamine reaches that region. Also, when a person expects a reward and gets it, the anterior cingulate is quiet (2). From these observations it looks like winning in gambling can affect the dopamine system, similar to the neural circuitry involved in the highs and lows of abusing drugs. Therefore, people can become addicted to gambling too. Do compulsive gamblers have vulnerable dopamine systems? The first win would be a dopamine rush, but does that then get embedded in their memory? According to the study, gamblers keep gambling and the occasional dopamine rush of winning overrides their conscious knowledge that they will lose in the long run (2).
A research team headed by Dr. Hans C. Breiter used magnetic resonance imaging to map the brain responses of twelve men while they participated in a game of chance involving winning or losing money. The tests were divided into two stages -- expectancy and outcome. During the expectancy phase, the subjects were shown how much money they could potentially win, depending on where the arrow stopped on a spinning disk. During the outcome phase, the arrow stopped on a designated monetary value on the disk, and the subjects found out whether they had won or lost money on that spin. This experiment showed that blood flow to the brain changed in ways similar to that seen in other experiments where an infusion of cocaine is given to cocaine addicts. Similar changes in blood flow to the brain occur when low doses of morphine are given to drug-free individuals. The changes varied in accordance with the amount of money involved, and a broadly distributed set of brain regions were involved in anticipating a win. The more money involved, the more excited the person became. The primary response to winning, or the prospect of winning, was seen in the right hemisphere of the brain, while the left hemisphere was more active in response to losing (3). This similarity suggests that common brain circuitry is used for various types of rewards (4). This study is also important because identifying regions of the brain and then mapping the neural pathways that process the anticipation and rewards could possibly lead to the development of medications or interventions that could block these circuits and provide other treatment approaches.
William Gehring, of the University of Michigan, and his colleagues, used an EEG to monitor the brain waves of experimental subjects as they played a gambling-type game. There were twelve subjects who played a video game in which they had to choose two numbers: 5 and 25. If they picked 5 and it won; they would get five cents. If 5 lost, they would lose that amount and so forth. Choosing the 25, would result in a gain or loss of 25 cents. He found that when people lost either amount, the anterior cingulate would become active within a quarter of a second. In the next round after a loss, subjects almost always chose the 25 (1). Choices made after losses were riskier and were associated with greater loss-related activity than choices made after gains (7). Subjects could have been gambling more because the brain was expecting them to win. However, we should keep in mind that his subjects were paid enough so that they could not leave with less money then they came with (1). Another problem with this study is that people tend to gamble more freely with money that is not their own. I can go to Atlantic City, walk around, watch others gamble, and not even spend a nickel. However, when I go with my grandparents who give me money, I am ready, willing, and able to gamble. I always try to win the money back that I lost. I also know that if I play a gambling game on my computer, I bet large sums of money since I know it is not real. Another problem with Gehring's experiment was the small amount of money that was involved. If we were talking about gambling in Las Vegas or in Atlantic City, the stakes would be much higher. Then again there is the other side, in which people become more averse to loss after they lose a lot of money. It happens to my friends when they bet on a sporting event. If their team loses, they are more cautious the next time.
A challenge for the future is to determine how different parts of these brain circuits affect the thinking, emotion and motivation involved in anticipation, evaluation, and decision-making. The findings in these studies show how the brain evaluates the choices made. Neuroscience may provide new constructs for understanding economic decision-making. An interesting topic for future research would be to look at how people play the stock market.
If we continue to look at unconscious reward circuits in human behaviors we may be able to understand why people act the way they do. Are we processing information at the unconscious level? That may scare many people since we look at most of our decisions and behavior as conscious decisions. We want to believe that we are fully aware of the choices that we make. Ongoing research will help us look more closely at systems that process reward and organize behavior in humans. Further research might help us try to determine the roles played by the different components of brain circuitry. This in turn may help scientists understand the development of drug abuse and compulsive gambling. If we know the cognitive processes related to gambling, we can understand compulsive gambling better and give those people the treatment that they need.
2)Hijacking the brain circuits with a nickel slot machine, NY Times, NY Times Newspaper article
3)Gambling has drug-like effect on brain,USA Today Newspaper article
4)Gambling—Like Food and Drugs—Produces Feelings of Reward in the Brain , Scientific American
5)You Bet Gambling Is Addictive , Business Week Online
6)The Good, the Bad, and the Anterior Cingulate, Science Journal, Science Magazine
7)The Medial Frontal Cortex and the Rapid Processing of Monetary Gains and Losses, Science Journal, Science Magazine
| Do Men and Women Experience Pain Differently? Name: Amy Cunnin Date: 2002-04-13 15:15:40 Link to this Comment: 1803 |
Pain has been an under-researched area of medicine, but today physicians are increasingly interested in the workings and treatment of various types of pain. In particular, a growing body of research exists on the different ways in which men and women may experience pain and the implications of these differences for medical treatment. Does the sex of an individual make a difference in their pain experience? Numerous researchers believe that women are more sensitive to pain than men, while others believe that the differences between the pain experiences of men and women are not significant. Over the course of my research I found that part of the problem in trying to answer the question lies in how scientists measure the pain experience of men and women.
The difference in the pain experience of men and women is an understudied area because most previous studies of pain and its potential treatments have only used men or male animals. For scientists, using only males was simpler since women have reproductive hormone cycles that could complicate the studies. The implication of this, of course, is that sex differences in the experience of pain (and in many other aspects of health) has remained an understudied area. However, in 1993 President Clinton signed the NIH Revitalization Act, which requires the inclusion of women in NIH research. In 1996 the NIH formed a Pain Research Consortium, and in 1998 the NIH held a conference entitled "Gender and Pain" (1).
At the NIH conference, some researchers argued that sex differences in pain are substantial and argued specifically that women are more sensitive to pain. For example, women report pain more often and also report it at higher levels than men. Additionally, when men and women are exposed to the same pain stimulus, women will say that they are in pain more quickly than men (1).
However, others believe that sex differences in the experience of pain may not be so significant. The higher reported pain levels of women may be due more to gender socialization than to biological differences between men and women. For example, in most laboratory pain studies women report about twenty percent more pain than men (2). However, researchers at the University of Florida examined pain reporting of chronic pain patients in a clinical setting and found that women reported only three to ten percent more pain than men, a significantly smaller difference. The researchers believed that women may not always experience more pain, but rather are socialized to acknowledge pain and thus are more likely to report it in both laboratory and clinical settings. Men are taught to not acknowledge pain, so in a short-term lab experiment they are less likely than women to admit that they are in pain. However, men experiencing chronic pain want relief for their long-term suffering, so gender socialization in less of a barrier to acknowledging pain in a clinical setting (2).
A recent University of Washington study, presented at the NIH "Gender and Pain" conference, also suggests that men and women with chronic pain experience similar levels of pain. The study had two rounds, the first examining 202 men and 226 women with chronic non-cancer related pain. The researchers examined "prior treatment for pain, pain severity, emotional distress, interference of pain with life, and impact of pain on functional activities." Researchers did not find women reporting more severe pain, or "interference of pain with life" or "functional activities." The only area of significant difference between men and women was emotional distress, since women reported higher levels of depression. Since depression is generally thought to be higher among women, the researchers did not believe that the depression was necessarily pain related (3).
The second round of the study examined 91 men and 52 women with cancer-related chronic pain. In this sample, the researchers found no differences between the sexes in the various measures of pain. Unlike the first study, there was no difference in depression levels between men and women, perhaps because in the second sample all of the patients were suffering from a potentially deadly illness (cancer) and therefore more generally prone to depression. The University of Washington researchers concluded that in treating chronic pain, the sex of the patient is less important than their psychosocial characteristics such as coping ability, marital satisfaction, and the impact of outside life activities (3).
Additionally, research on a genetic basis for pain differences between men and women is inconclusive. Researchers on pain differences in animals such as mice have found that generally the female animals appear more sensitive to pain and do not respond as much to pain relievers as males. However, the differences between males and females do not tend to be large (4). Furthermore, researchers believe that "even within gender, there are individual differences in feeling pain that are linked to still undiscovered genes" large (4). Researchers at Johns Hopkins University and the National Institute on Drug Abuse have located a gene that may be responsible for individual variations in pain sensitivity. The gene codes for the mu opiate receptor, which binds with endogenous painkillers such as endorphins as well as exogenous painkillers such as morphine and heroin. These receptors are found primarily in the thalamus, the cerebral cortex, the visual cortex, and the basal ganglia, but with a great deal of individual variation in their number large (5). Researchers examined eight mouse strains with variations in the mu opiate gene, and found that the mice with more active form of the gene had a greater number of mu opiate receptors in the brain and a higher pain tolerance. While still a new area of research in humans, studies on human mu opiate genes have found individual variations in the regulatory portion of the gene that may account for individual variations in pain experience large (5).
How, then, do we know whether men and women experience pain differently? The genetic evidence for a gender basis of pain is not conclusive and points to individual variations as more significant than sex variations. Another challenge is that we cannot "see" pain, only a subject's reaction to a painful stimulus. In the case of humans, we also can use their description of their physical discomfort. However, women are socialized to more freely acknowledge their pain and men to minimize theirs, how can we know if the actual pain experience of men and women is different? I found it difficult to reach a conclusion, in part since this is a relatively new area of research. Additionally, while I used research focusing on chronic pain, there is a huge range of types of pain that humans can experience. Therefore, examining pain solely through the person's sex gives an incomplete picture. The differences may lie more at the level of the individual and the intersection of their current pain experience with their psychological and social background.
WWW Sources
1) NIH website, Overview page for the April 1998 NIH Gender and Pain Conference.
2) American Psychological Association Monitor Online, article on sex differences in pain.
3)NIH website, abstract of a chronic pain study presented at the NIH Gender and Pain conference.
4) Intel Health article,"Gender, Genes Are Linked to Pain Response."
5) Scientific American article entitled "Personal Pain", on the role of the mu opiate gene in pain sensitivity.
| Overestimation of the Placebo Effect Name: Beverly We Date: 2002-04-14 19:34:09 Link to this Comment: 1809 |
The purpose of this paper is to investigate whether the Placebo Effect is overestimated through misinterpretation of the data. Specifically, the objective is to explore whether the passage of time during clinical trials accounts for many results widely attributed to the placebo effect. That is, the passage of time in itself-through a combination of spontaneous changes in symptoms, regression effects, and homeostatic changes-produces most of the favorable results credited to the placebo.
Despite its widespread acceptance for approximately fifty years, the Placebo Effect has recently become controversial, with several researchers claiming that the presumed benefits of placebos are overestimated. Dr. Asbjorn Hrobjartsson and Dr. Peter C. Gotzsche of the University of Denmark and the Nordic Cochran Center reviewed journal articles looking for the original research stating that 35% of patients improve if given a placebo. Interestingly, none of the papers they examined included original research on the placebo effect, but all cited the same reference. The original source was a 1955 article, "The Powerful Placebo," published in the Journal of the American Medical Association and written by Henry Beecher, chief of anesthesiology at Massachusetts General Hospital in Boston. Dr. Beecher had analyzed about a dozen studies and had come up with the 35% figure (1).
Challenging the validity of this finding, Drs. Hrobjartsson and Gotzsche hypothesized that two important factors were ignored. First, that the natural course of many diseases is to wax and wane. Second, that a patient who feels terrible one day will almost certainly feel better the next day.
Hrobjartsson and Gotzsche analyzed 114 studies conducted between 1946 and 1998 that used not the usual two, but three groups of patients. One group received appropriate medical treatment, one group received placebo treatment, and the third group received nothing. (The studies involved 7,500 patients with 40 different medical conditions, including high blood pressure, high cholesterol levels, asthma, behavior disorders, such addictions as alcohol abuse and smoking, and such neurological diseases as Alzheimer's Disease, Parkinson's Disease, epilepsy, as well as bacterial infections and the common cold (5). As Hrobjartsson and Gotzsche predicted, the patients in this third group improved as often as the patients in the placebo group (1).
Carol Hart (2) cites Shapiro and Shapiro, who offer possible confounds that lead to overestimation of the placebo effect. Observations of the third control group-the group with neither treatment, nor placebo-may have improved because of three mechanisms. The first possibility was Spontaneous Improvement. Chronic pain conditions or mood disorders wax and wane, and often show improvement with no provocation (3). Patients may choose to enter treatment or a medical trial when the symptoms of the complaint have reached a high degree of variability. Pain, depression, cholesterol levels may have peaked, and, thereafter, improvement may follow without any intervention.
The second possibility was Fluctuation of Symptoms, particularly Regression to the Mean, the tendency for random increases or decreases to be followed by observations closer to the average (3). When a patient is in great pain on day #1, it is possible that the pain may diminish somewhat on day #2. Very bad experiences are followed by improved experience. Rheumatoid Arthritis and Multiple Sclerosis are examples of diseases whose symptoms may change from day to day (4). Regression accounts for natural and inevitable fluctuations. Periods of pain are followed by periods of remission of pain. The intensity and duration of pain from arthritis, chronic backache, gout, and other illnesses, fluctuate, and eventually move toward the average-away from the extremes. [Sir Francis Galton, in a study in 1885, coined the term regression in a study called Regression Toward Mediocrity in Heredity Stature, which was a study of average heights of sons of very tall and very short parents (5).]
A third possibility to account for the improvement of symptoms with no intervention is the body's natural process to achieve a state of homeostasis. This natural occurrence precipitates Time Based Healing. The body will attempt to repair itself. Illnesses and injury often heal spontaneously as the body's immune and hormonal systems act to regulate and return the body to a healthy state (4). Except for extreme illnesses and severe conditions, most ailments are self-limiting and improve with time, regardless of treatment. There is a common saying: If you treat a cold, the symptoms will last for a week, but if you leave it alone, the cold will be gone in seven days. Even serious diseases have periods of exacerbation and remission. Some cancers inexplicably disappear. The main logical error (fallacy) in plotting disease progress is known by the Latin expression post hoc, ergo propter hoc-after it; therefore because of it (6). Spontaneous healing occurs because something inside the body causes a major response in the immune system. The dozens of types of white blood cells produced by our lymphatic system, spleen, and thymus literally flood the body and attack everything that is foreign and might cause illness (7).
If new studies show that the Placebo Effect is overestimated, then its apparent benefits may be attributable to the passage of time. Placebos are best known for their use as inactive substitute treatments in randomized clinical trials of drugs. Placebos are meant to provide a benchmark for measuring the efficacy of those compounds, but instead often confound results by seeming to be effective themselves. Placebos do not help disease, only the way patients perceive disease (8).
A variety of researchers have argued that a combination of expectancy (suggestion) and endorphin release accounts for the benefits of placebos. Still others believe that the researchers in a double blind study may be exhibiting a Hawthorne Effect, an increase in productivity, merely because they are involved in an investigation, which affects patient outcomes (9).
Indeed, many holistic and alternative therapies are generally held to be based upon the phenomenon of the placebo effect. If the hypothesis in this report is true, then one must be skeptical toward the variety of holistic and alternative therapies available that claim to exploit the Placebo Effect for the benefit of patients. According to Lawrence Sullivan, a historian of religion at the Harvard Divinity School, the placebo is a "toxic waste site, nobody wants to own it. Even shaman and witch doctors would be offended by the idea that their healing powers depended on the Placebo Effect" (8).
Some interesting background information: The word, placebo entered the English language through a particular mistranslation of the 116th Psalm that read "I will please the Lord" rather than "I will walk before the Lord." In the medieval Catholic liturgy, this verse opened the Vespers for the Dead; because professional mourners were sometimes hired to sing vespers, "to sing placebos" came to be a derogatory phrase describing a servile flatterer. By the early 19th century, "placebo" had come to mean a medicine given "more to please than to benefit the patient" (2).Outside the context of modern clinical trials, "placebo" has been a term reserved for characterizing the substandard practices of other less ethical or knowledgeable healers. Using treatment drugs that have no efficacy against an ailment is considered by some another form of placebo. For example, some physicians today will prescribe antibiotics for viral colds and flu, because the patient requests them, even though the physician knows that the antibiotics are useless in treating viral infection (2). The dangers that exist within the belief that placebos have curative powers have allowed charlatans and alternative curative practices to perpetrate a fraud on the gullible.
2) MDD July 1999: The Mysterious Placebo ,
3) Spontaneous Remission and the Placebo Effect ,
5) Regression and the Regression Fallacy ,
6) Skeptical Inquirer/January/1997/ The Mysterious Placebo ,
7) Health News Network-The Placebo Effect ,
8) Mind, Brain, Behavior: The Pleasing Placebo ,
9) Clinical Research-Journal of Prosthetics and Orthotics ,
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| Voices Name: Michelle T Date: 2002-04-15 14:01:36 Link to this Comment: 1812 |
Albeit that their have been many case studies performed by psychologists, the words of a schizophrenic give new meaning to the disease. For paranoid schizophrenia, an increase in recent literature reveals the point of view of the ill person. No two cases are exactly the same, so what follows is a conglomeration of experiences of paranoid schizophrenia survivors. As one schizophrenic has stated: "The schizophrenic experience can be a terrifying journey through a world of madness no one can understand, particularly the person traveling through it. It is a journey through a world that is deranged, empty and devoid of anchors to reality. You feel very much alone. You find it easier to withdraw than cope with a reality that is incongruent with your fantasy world. You feel tormented by distorted perceptions. You cannot distinguish what is real from what is unreal. Schizophrenia affects all aspects of your life. Your thoughts race and you feel fragmented and so very alone with your 'craziness,'" (6). Paranoid schizophrenia is a very debilitating disease -- it takes over one's life and creates a downward spiral into one's own surreal world. No longer can one communicate or relate to other people. Reality is distorted to fit the pattern of paranoia inside one's mind. M.E. McGrath delineates her experience as a survivor of paranoid schizophrenia:
"I know all the negatives: schizophrenia is painful, and its craziness when I hear voices, when I believe that people are following me, wanting to snatch my very soul. I am frightened too when they whisper, every laugh is about me; when newspapers suddenly contain cures, four-letter words shouting at me; when sparkles of light are demon eyes. Schizophrenia is frustrating when I can't hold onto thoughts; when conversation is projected on my mind, but won't come out of my mouth; when I can't write sentences but only senseless rhymes; when my eyes and ears drown in a flood of sights and sounds ... and on and on ... always more ..." (1). Schizophrenia heightens one's sensitivity to emotions, stress, sound, and other stimuli while inflating the ego of the schizophrenic to believe that the world in fact revolves around him. As a schizophrenic, suddenly it seems that the spotlight is on you alone. One is at once extremely important, yet persecuted. People are talking about you. People are conspiring against you. You are the chosen one. The schizophrenic's world is full of turmoil and distress, which is also, at the same time, very isolating.
Auditory hallucinations are often experienced by schizophrenics, whereby, usually, voices are criticizing the patient or are telling that individual to hurt themself. It seems that the feelings and thoughts of the schizophrenic take on an identity or some times several identities, each of which attempts to interpret the environment. "Emotions that would normally be comfortably catalogued as unacceptable take on a life of their own as voices that seem more real than the real world outside" (2). New characters are created by the imagination that distracts the schizophrenic from reality. The voices seem like they are coming from somewhere outside of the self; they are very real for the person experiencing them. "I heard them coming at me from the outside, as real as the sound of the telephone ringing... Occasionally they were friendly, but mostly they reviled me, shouting in their hoarse, harsh tones: 'You must die, you bitch,' they shrieked. 'Die! Die! Die!'" (2). Everyone feels at one point in his life that he is not performing as well as he would like. In the prior passage, Lori's perfectionism and eagerness to please her family turned into self-hatred. The slight awkwardness or embarrassment of a situation turned into a barrage of criticism from within. Not only did the voices chastise her for her mistakes, they eventually demanded that Lori hurt herself. They became so strong that Lori's own identity was becoming intertwined with the voices. "The Voices were twisting themselves around me. It was hard to tell where they left off and I began. They threatened me, and I believed them. If I squealed on the Voices, they might kill me. If I ratted on them, the person I told would have to die," (2). The voices inside the schizophrenic's head become so dominating and frightening that, in the mind of the schizophrenic, the voices are in control. Once that has happened, the situation becomes more tragic, for the free will of the patient has been lost. The schizophrenic often times withdraws from the community because the voices are so strong. He starts behaving as if he was afraid of people in general, when really what scares him is the voices. He does not trust himself to engage with others, because the voices are usually telling him that other people are dangerous or that they are making fun of him. There is also fear that other people might define themm as crazy and not understand. "It got to the point where I couldn't decipher reality from what the Controller was screaming. So I withdrew from society and reality. I couldn't tell anyone what was happening because I was afraid of being labeled as 'crazy.' I didn't understand what was going on in my head. I really thought that other 'normal' people had Controllers too," (1). This schizophrenic was so fearful of what was going on inside his head that he could not express it to anyone. He assumed that other people had "controllers" also. Assumptions like this can get schizophrenics into a pit of fear, because they are essentially lost in their own worlds without any basis of reality.
In addition to the hallucinations, one other symptom - delusions - also plays a major role in dissociating the schizophrenic from the world. There are many different types of delusions. The thought pattern of a delusional person is itself very unique. One wonders how such grandiose conspiracies develop in the schizophrenic mind. Dr. Frese, who is also schizophrenic, has a theory as to how delusions are capable of occurring: "When our rational processes break, our cognitions become dominated by the activities of the paleocortex... We begin to lose our confidence in rational processing and begin to see truth in nonlinear relationships," (4). Dr. Frese suggests that the neocortex stops functioning correctly so that the delusional person relies on more primitive manners of thinking. These more primal manners of thinking do not incorporate information into a rational pattern, but instead take bits and pieces of inconsequential material and string them together to fit the already paranoid thought pattern. When one is paranoid, he begins to look for signs that fit into his perception of reality. The delusions get more surreal as new information is incorporated. Some times, the delusions involve that person having a special mission in life, for example, Maurizio wrote: "I began to have delusions about the state of the world around me. Suddenly the noises made by cars and planes going by outside my house took on secret and deliberate meanings. I became convinced that I was involved in the start of a nuclear war and the only way for me to survive was to find the answer to a difficult riddle," (5). Maurizio's delusions were kept aflame by the hallucinations that he heard in the noise that the traffic made outside his house. He does not explain why he thought that a nuclear war was about to occur, but he does state that he was the one destined to be in control of the war. Another common delusion that schizophrenics have is thought broadcasting -- where everything that goes through a schizophrenic's mind is thought to be heard by the people around him. "I thought perhaps I had a special calling in life, something beyond normal... It progressed to where I thought the world could read my mind and that everything I imagined was being broadcast to the entire world," (6). Thought broadcasting is especially interesting for it is so common among paranoid schizophrenics, yet there really is no reasonable foundation for the delusion. What could make one believe that other people could hear their thoughts? Maybe there were coincidences that caused the schizophrenic to feel that another person knew how he felt about something. The delusions that are created make the illness especially difficult to treat, for the ill person must come to trust another and believe him over one's own irrational thinking.
Hope for the schizophrenic comes in the form of antipsychotic medication, which can alleviate some of the symptoms. However, these same medications can wreack havoc on the body and cause disorientation. One is never the same on antipsychotics as he was before the illness struck. Emotions often become flattened. As an anonymous schizophrenic has said: "Medication upon medication made my thoughts return to reality, but my body seemed suspended in time and space. There was no laughter; there were no tears; there was only existence," (1). What kind of life can one lead without emotion? It is as if a zombie has taken over the life of a once active person. The meaning has been stripped from these medicated patients. Antipsychotics do not work for everyone. As Lori, who was resistant to most medications, put it: "I felt like I was getting worse and worse with each trial of new medication. I felt like a tree being cut down. The more the doctors and medications hacked away at me, the closer I was to falling," (2). Finding a medication that works is extremely frustrating. The patient clings to the hope that this new drug will "cure" him, all the while suffering from the horrible side-effects of each drug. There is no method to figure out which medication will work for that individual. Psychiatric medications mostly work by trial and error with some consideration for the seriousness of the side-effects. This shopping period for antipsychotics can be tortuous in itself. Often, one has to take other medications to offset the side-effects of another. Some people, like Lori, have to take several different kinds of medication four times a day. Lori was at one time on so much medication that she did not know what to do with herself. "Because the medications made me at once lethargic and restless, I often just stood in one spot, moving my weight back and forth from one foot to another. I was taking so much medicine that I found it difficult to even smile. I walked around the house sluggishly, doing what I had to like a robot," (2). Lori, at that instance, was clinging to life out of the love for her family. For her, life was unbearable without motivation or feeling. Eventually, Lori found that she could offset the side-effects of the antipsychotics by taking illegal drugs. This is a trap that many schizophrenics fall into, for it gives their life a superficial meaning. One lives just to get high so that they can feel "normal" again. Illegal drugs make the case more difficult, because the drugs, along with the delusions, create an ever more surreal world for the schizophrenic.
Although paranoid schizophrenia is a deadly spiral that can be very difficult to escape from, there are many who have survived to retell their incredulous stories. Those who have spoken throughout this paper are survivors that have managed to get the help they need through psychiatric medicine and counseling. As Maurizio had put it, "my experiences with schizophrenia were initially very devastating, derailing my career and almost destroying my future" (5). The illness for him was a great obstacle to hurdle, but his life progressed once he learned how to cope with schizophrenia. For M.E. McGrath, schizophrenia has altered her life so much that she still feels the repercussions. "The illness has certainly stripped me of any pretense now, leaving me, instead, feeling hollow, yet hurting. I twist and turn, hoping to find a comfortable position in which just to be me," (1). Each schizophrenic's illness is different. Some are not cured by antipsychotics. Others are still in denial believing that there is nothing wrong with them. Unfortunately, with psychiatric care focusing on medication instead of housing the schizophrenics, many ill people are forced to live on the street. Pamela's picture of how schizophrenics are treated is glim. "Schizophrenia is, for most people, an uncharted and terrifying shadowland that they seek to avoid along with the sufferer whose torments, pain and oddness scare them. In the past, such people were put behind locked doors of asylums. Today they are simply consigned to the anonymity and powerlessness of poverty, and are forgotten," (3). It is true that there are many schizophrenic individuals that are homeless because the disease itself is so hindering to one's existence. If one is so poor that one cannot afford antipsychotic medication, then there is a very slim chance that he will be able to get a job. Schizophrenics need to be taken care of while they are in the depths of their illness. Unfortunately, people do not want to spend the money on those individuals in society that cannot fend for themselves. One wonders whether the reformation in psychiatric care really helped the nation or hindered it. Certainly, in the case of paranoid schizophrenia, a change needs to be made to help those that suffer. Empathy is a great place to start helping those with schizophrenia. Hopefully, this paper has helped to bring the schizophrenic's perspective into focus.
1) Gottesman, Irving I. Schizophrenia Genesis: the Origins of Madness. W.H.Freeman and Company, New York, 1991.
2) Schiller and Bennett. The Quiet Room. Warner Books Inc., New York, NY. 1996.
3)Schizophrenia Home Page,Wagner, Pamela. "A Voice from Another Closet."
5)Mental Health,Frese, Frederick. "Coping with Schizophrenia"
5)Mental health, Baldini, Maurizio. "Maurizion Baldini's Story" 5)Mental Health Home Page, Jordan, J. "Schizophrenia - Adrift in an Anchorless Reality"
| Munchies and More: The Effects of Marijuana on the Name: Kathryn Fo Date: 2002-04-15 18:57:59 Link to this Comment: 1816 |
To many, marijuana is seen as a horrible narcotic that causes many physical and social problems. To others, it's a harmless drug that gives the body a relaxing sensation. Marijuana can be found on many college campuses and high schools. It is estimated that at least 70 million Americans have tried it, and of those people, 10-14% become dependent of the drug (1). Marijuana is often referred to as the "gateway" drug, leading the user to more serious narcotics. Marijuana users experience different sensations, from excessive mellowness, fuzzy memory, to the munchies. Some of the typical effects are impairment of memory, alteration of memory, motor coordination, posture, cognitive ability, and sensory perception. So what is it in marijuana that keeps users wanting more?
The active ingredient in marijuana is delta-9-trans-tetrahydrocannabinol, or THC. The structure of THC is very similar to the endogenous cannabinoids, or endocannabinoids for short, which are naturally occurring chemicals in the body (1).The THC binds to the receptors of the endocannabinoids, and activates the neurons, causing the different sensations experienced during a high. These receptors are spread throughout the brain. THC affects the central nervous system, as well as the peripheral tissue systems. THC can reduce pain, lower body temperature, and enhance appetite. It can also be used for anti-inflammatory, bronchodilatory, and anti-convulsant, which is why THC is used for medicinal purposes. THC is used as a popular treatment for glaucoma by reducing ocular pressure, and for neurological disorders such as multiple sclerosis, Huntington's Disease, and spinal cord injury (4).
The THC acts on the receptors of the endocannabinoids. Two known endocannabinoid receptors are CB1 and CB2, which are found in the nervous system and the periphery nervous system, respectively. The receptors are coupled with G-proteins and mediate the inhibition of adenylyl cyclase activity, which in turn reduce the production of cyclic AMP, cAMP. The reduction of cAMP formation blocks calcium ion flow into the cells, which would disrupt the formation of action potentials. This may attribute to some of the side effects to marijuana use (4). Cyclic AMP and calcium ions regulate several neurotransmitters, including acetylcholine and dopamine (1). This may account for the nice and mellow feeling people experience when smoking pot.
The precise physiopathological responses between the stimulation and inactivation of endocannabinoid receptors are still unclear, however, it is known that the performance of the nervous system and the peripheral processes, such as modulation of neurotransmitters, control of immune, gastrointestinal, reproductive, and cardiovascular systems are impacted. By observing the actions of the CB1 receptor, researchers are able to determine different response pathways. The actions of the CB1 receptors interact with thermoregulatory systems in the body. CB1 receptors also interact with sensory perception such as hearing, color vision, and touch. Motor responses are also affected by CB1 receptors, some motor responses being movement, coordination, posture, and muscle function. THC has a high affinity to CB1 receptors, which may account for the different sensations when one gets "high. Often times, a person under the influence of marijuana feels an increase of body temperature, hallucinates, seeing colors and objects that are not really there, has trouble walking, or staggers around. It is the binding of the THC to the receptors that cause this. The CB1 receptors and their corresponding enzymes and proteins can be found in the thalamus, hippocampus, cortex, striatum, substantia nigra, and cerebellum. This shows that endocannabinoids and their substrates have a role in motor and cognitive response (2).
THC may also affect the endocrine system. The CB1 receptors are found in the hypothalamus of the brain, which regulates the secretion of pituitary hormones. The release of the pituitary hormones can also lead to the secretion of adrenocorticotropic hormones (2).
It is still unknown if marijuana is addictive, or contains any addictive agents. An experiment was done with monkeys, in which every time they hit a lever, they would get injected with THC. After the monkeys figured out how to operate the levers, they hit the lever about 30 times per minute. This however, does not prove whether the monkeys were addicted or whether they just enjoyed the sensation, and felt it was a reward. In humans, about 10-14% of users become dependent. There are many treatment programs that help those addicted to marijuana (3). It may more difficult to diagnose a marijuana addict because the symptoms of marijuana addiction are not as noticeable as symptoms of different dependence, such as alcoholism (1).
One thing that I wanted to find information on, but was not able to was about the "munchies". My friend and I came up with the same question: Do people actually experience the "munchies", or are it because they heard that everyone experiences "munchies" after they smoke marijuana, so they get the "munchies" too. Are the "munchies" a physiological effect of marijuana use, or just a psychological effect? Though I did not get an answer, I think it may be related to THC. This question may require more research for the future.
1) Carrol, Linda, Marijuana Effects: More Than Just Munchies, New York Times, January 29, 2002
2)endogenous signaling system: chemistry, biochemistry, and physiology, from the Internet Journal of Science - Biological Chemistry
3)Hooked on Hash, from New Scientist, 2000
4. 4)The Pharmacology and Biochemistry of Cannabinoid Receptors, May 1997
| Migraines: That Ache In Your Head Name: Nicole Pie Date: 2002-04-15 21:49:34 Link to this Comment: 1819 |
Have you ever had a headache? That pounding pain that would not go away, it was probably a headache, however there is another type of headache that happens to one side of the head and could also cause nausea, sensitivity to light, sound or odors. Also accompanying the migraine is a aura, which could be flashes of light, or temporally lose your vision, in any case it is a visual impairment. (1) Migraines differ from headaches because a migraine is a neurological disease. (2) Many Americans are affected by migraines, it is estimated that eleven to eighteen million people are affected, which most of them are women. Migraines are very disabling as well as having life-threatening outcomes. (2) Now you might be saying to yourself, "Well we know the symptoms of a migraine but what causes migraines?" Well the causes are unknown, since triggers, external forces that cause the migraine to occur, vary from person to person. Triggers range from stress, smells, sights, noises and even things a person eats. (3) However there are many theories on what occurs within the brain to cause the pain and throbbing.
One of the theories on what occurs within the brain during migraines is blood vessels increase blood flow, which makes the blood vessels expand. The expansion of the blood vessels triggers nerves within the brain and this nerve activity cause a person to feel pain as well as causes the tissue around the brain to become inflamed. (2)
Another theory suggests that the brain stem becomes overly activated which causes the release of chemical messengers. The chemical messengers causes inflammation and pain in the fibers surrounding blood vessels. (4)
A similar theory to the one described above suggests that, the nervous system is more sensitive to the environment. (1) Because the nervous system has a heightened sensitivity, the nervous system responds to triggers by causing spasms in nerve-rich arteries at the base of the brain. These spasms constrict the arteries and blood flow is reduced. As a result of this decrease in blood flow, platelet cells clump together, which causes the release of serotonin. Since serotonin causes the constriction of arteries, blood flow is reduced further, making the brain's oxygen supply decrease as well. Since the brain needs oxygen, some arteries will dilate to meet the brain's oxygen needs. This dilation will eventually spread outward through the brain and down the neck and scalp. Some scientists believe that this dilation causes the sensation of pain. (1) (3) (5) (6)
Another theory deals with the presence of the aura and how that causes the onset of a migraine. The presence of the visual aura is caused by visual neurons firing out of sync without any visual stimulus, as well as firing without passing information on to the next neuron. These neurons that abnormally fired, released high amounts of potassium ions, which spread from the visual neurons into the meningies of the brain. The nerves located in the meningies begin to fire, which releases neuropeptides that cause the blood vessels to dilate and register pain. Once this loop is set in effect, it continues to cycle over and over again which causes the pain of the migraine. (6)
In my lifetime I have experienced migraines as well as read the literature cited below and therefore I have my own theory, which is a combination of all the theories. My theory is the brain is working on a corollary discharge system. By having a hypersensitive nervous system, leads to having triggers which causes spasms within the arteries of the brain. These spasms cause the arteries to constrict and nerves to release seriotonin, which constricts the arteries even further. (1) (3) (5) (6) This constriction of the arteries cause the pulsating sensation a person feels when they have a migraine. Since the brain has a certain oxygen level, the brain must trigger the arteries to dilate. Because the brain has an expectation of a certain level of oxygen, the neurons within the brain send a corollary discharge signal to other neurons. This corollary discharge is perceived as pain within the head.
Since doctors and scientists know the blood vessels in the brain constrict in the beginning of a migraine, they have ways of preventing and managing migraines. One of the ways is to identify triggers that cause the onset of a migraine, as well as changing the person's lifestyle into a healthy lifestyle. (1) Doctors also prescribe medicine that is anti-inflammatory, which causes the blood vessels to remain at a normal diameter. There are many medicines that can prevent migraines as well. These medications are the serotonin agonists, which mimic the effects of serotonin in the brain. Other medications are vasoconstrictor, which counteract the effects of the dilation phase. (1) (5)
Migraines are a debilitating disease for many people in America. Since doctors and scientists know what happens within the brain, they can prescribe and create drugs that will reverse the affects of migraines. There are many theories about what happens within the brain when a migraine occurs, however the common thread in each theory is the constriction and dilation of arteries in the brain. There is no cure for migraines but there are preventive and management measures a person can use to help their condition.
1)What is a Migraine Headache?
| Schizophrenia: A Matter of Perception? Name: Sook Chan Date: 2002-04-16 01:31:18 Link to this Comment: 1822 |
Schizophrenia is one of the most severe psychopathologies present today. Its causes are still vague, and the symptoms vary across a large spectrum. However, two generalized grouped of symptoms have been identified for schizophrenics: positive symptoms, and negative symptoms. Negative symptoms include lack of activity, anhedonia, and loss of interest. Positive symptoms include disorganized speech, hallucinations, and delusions experiences (1).
Individuals with schizophrenia commonly experience a disorder in their perception. Their surroundings are unreal and their external sensory environment seems different from what they previously knew. In fact, their perceptions become derailed; misinterpreting situations and the chronology of events. They are unable to distinguish between reality and imaginary. They have a false sense of reality and are unable to interpret the real context of situations. This could be due to the testimony that their experiences are fragmented. Does the brain put these pieces of fragments together, molding them to what is expected and most logical based on the limited contextual information?
"Everything is in bits. You put the picture up bit by bit into your head. It's like a photograph that is torn to bits in your head" (2).
Every experience from the sensory environment undergoes a processing mechanism where it is placed into two categories: something that has already previously been experienced, or an experience that is completely new. Our brain makes associations with the past, forming reactions and thoughts based on the past consequences and outcomes. It activates the schemata experiences (2). Ever smelled cotton candy and your brain immediately brings you memories of fairs and innocent bliss? However, schizophrenic individuals have difficulties in accessing their schemata. There is a lack of common sense in schizophrenic individuals which results from three interrelated problems experiences (2). They do not hold the same constant sets of beliefs about the world which we normally take for granted. They are unable to understand how other people feel or think about a particular matter. And their judgement about the likelihood of events is impaired. Their schemata, stored traces of earlier experiences, are impaired experiences (2). It has been suggested that during a psychotic episode, they are unable to control the contents of their consciousness because their input and output processes are not automatically supported by their cognitive schemata experiences (3). Yet, a study using PET scans found that during hallucinations, areas within the brain core were activated. The core regions served as meeting ground for thoughts, emotions, and perceptions, a place where present and past experiences may be compared experiences (3). One idea is that the brain creates and believes its own reality when the network core areas are activated. However, the same areas are also activated when a normal person sees and hears a real voice or incident. Is there a possibility that it isn't the inaccessibility of their past experiences that is of error, it is the error in circuitry that accounts for the impaired sense of reality experienced by a schizophrenic patient?
Fragmented sensory inputs may cause a flawed perception of situations. The different sensory inputs that make up an experience for normal individuals, are no longer interconnected for schizophrenic individuals. Also, schizophrenics have difficulties with memory due to poor organization in the encoding phase (2).
A common proof of skewed perception v. reality experienced by many schizophrenics involves extreme paranoia and the feeling of conspiracy against them. For example, a patient may see two people talking in hushed tones as he passes them on the street, and assume that they are conspiring against him. Experience is arbitrary. Two individuals may be presented the same painting, yet, they notice different things, Variation occurs in both what one chooses to see and what is interpreted from the things seen. Take the example above of a situation. He sees two people talking. Any normal person might ignore this incident, but the schizophrenic thinks that the individuals are talking about him. Yet, is the schizophrenic's perception flawed or just different from the average generalized reaction? Nonetheless, there is a definite problem with the way schizophrenics approach and interpret situations. Hallucinations and delusions are secondary conditions to the distortion of reality (4). One might say that hallucinations and delusions exists from the inability to correctly rationalize confusing situations by certain bits of information.
Patients with schizophrenia process irrelevant information that intrudes into their consciousness and causes distractibility. During a psychotic episode, the cognitive defect plays a major part. They are unable to organize inputs into a larger picture to provide context. Hence, schizophrenics fail to control the contents of their consciousness (2). The main question is what is the cause of this distractibility and flawed perception?
The prefrontal cortex and the hippocampus are the brain structures that are believed to be impaired in schizophrenic individuals (5). The prefrontal cortex elicits responses guided by internalized knowledge that include one's schemata and memory. The hippocampus stores memory and allows for its retrieval. It is the structural framework that provides the brain with a sense of context by binding together sites in the neocortex that represents the correct contextual framework (5). A strong correlation has been found between the prefrontal cortex physiological activation and the reduced hippocampus volume in schizophrenic subjects.
Much of the neurobiology of schizophrenia remains unknown. However, effective anti-hallucinating, anti-psychotic drugs such as clozapine target the dopamine receptors of the brain, indicating a possibility that dopamine D4 receptors may be a critical site of action (1). Auditory hallucinations are more common to schizophrenics than visual hallucinations. It has also been hypothesized that auditory verbal hallucinations arise from misinterpreted inner speech and aberrant activation of the primary auditory cortex (5). It has been summarized that the brain fills in the missing pieces of our sensory environment, making us see things that may not be there. A schizophrenic individual's brain is unable to correctly retrieve stored past experiences to format a current experience into context. Hence, the brain starts afresh, with no prior training of how to fill in the different fragments of sensory input. Schizophrenics experience an impaired sense of reality because as the brain is sticking the fragments of experiences together, it fills in pieces that are not there, making the individual believe in things that are out of context and out of reality.
"My perception of the world seemed to sharpen the sense of strangeness in things. In the silence and immensity, each object was cut off by a knife ... spaced off from other things. If you move it's frightening. The picture you had in your head is still there but it's broken up. If I move there's a new picture that I have to put together again." (2).
1) What Happens to the Body and Brain of Individuals With Schizophrenia.
2) Context and Cognition in Schizophrenia: Main source of my paper, very interesting as it covers many of the themes discussed in class.
3) Cause Identified.
4) Cerebral Activity Associated With Auditory Verbal Hallucinations: A Functional Magnetic Imaging Case Study
5) Impaired Recruitment of the Hippocampus During Conscious Recollection in Schizophrenia: Interesting article on the role of the hippocampus in memory and perception.
| I Love You From the Bottom of My Brain: The Neurob Name: Miranda Wh Date: 2002-04-16 01:51:13 Link to this Comment: 1823 |
You're at a typical weekend party. You spot someone across the room. They look over in your direction. "Wow, they're so beautiful," you think. You want desperately to go over and talk to them, but at the very thought of it, your heart starts racing and your palms begin to sweat. Looking over at them again, you see that amazingly enough they are coming over to you. Even before speaking to them, you feel like you have just fallen in love. Is this feeling really love at first sight? Or is it merely the release of hormones in the brain? What causes the feeling of being in love? How can we know for sure if we really are in love?
Love is one of the strongest and most elusive emotions. Nearly every person seeks to experience the feeling of being in love. And once it is achieved, one's life is forever changed. Yet, most people would have extreme difficulty describing what exactly love is, how they know for sure that they are in love, or why love is so universally important. Understanding the neurobiology behind love might help to give us a more clear perspective on social bonding and raises the question of whether love is nothing more than the release of certain chemicals.
The hormone oxytocin plays a significant role in many animals' instinct to love and form social bonds. In fact, it has been called jokingly, "the cuddle hormone." (1) Oxytocin is a small protein composed of nine amino acids. It is produced in the hypothalamus and is released by the pituitary gland. (2) Oxytocin is also produced in the ovaries of women and the testes of men. However, the hormone's most well known function is specific to females. (3) First, it plays an integral role in the delivery of a baby. When a woman goes into labor, oxytocin levels increase. This stimulates contraction in the smooth muscle of the uterine walls, thereby facilitating delivery. Secondly, oxytocin plays a role in milk letdown in nursing mothers. Milk is initially released into small sacs, called alveoli, which are surrounded by smooth muscle cells. Oxytocin stimulates contractions of this smooth muscle, causing the milk to be released to the mouth of a nursing baby. (3) Lastly, and most importantly, oxytocin causes the formation of maternal behavior. Successful reproduction and survival for many species relies upon a mother's attachment to and caring for her offspring. There is a drastic increase in the levels of oxytocin in the body and brain of a woman who is in labor. This upsurge is the main cause of the establishment of the strong bond of love a mother initially feels for her child. (4)
It is very strange to think that mothers nurture and care for their children mainly due to the release of a hormone at the moment of birth. We tend to believe that the relationship between a mother and a child goes beyond biology - that there is something much deeper than merely instinct or the release of chemicals that causes a mother to love. However, there is very convincing evidence that proves that hormones like oxytocin are largely the cause of maternal behavior. A number of experiments have been done, showing the importance of oxytocin in the formation of the mother-child relationship. In many species (for example sheep and rats), blocking the release of oxytocin caused mothers to abandon their young. Similarly, when virgin female rats were injected with oxytocin, they exhibited mother-like behavior. They cared for and cuddled with the offspring of other females as if they were their own. (1)
Oxytocin does not only play a role in the bond between mother and child but also between two mates. The attachment formed between sexual partners is predominantly caused by the release of oxytocin during sexual intercourse. Oxytocin is intricately tied with the biology of sex - it causes penile erections and shortens both the time for ejaculation and the refractory period after ejaculation. (4) The release of oxytocin can be learned. In other words, after repeatedly having sex with the same partner, simply seeing him or her could set off the release of oxytocin. As a result, one becomes attached to that particular partner and learns to prefer them to other possible mates. Thus the monogamy practiced by humans and other species is also the result of the release of oxytocin.
To prove that oxytocin creates monogamy and social bonding, an experiment was conducted using a mouse-like rodent called a prairie vole. Prairie voles, much like humans, form life-long monogamous relationships. Both parents live together and meticulously care for their offspring. Both males and females show a strong preference to their mate over other voles, and the male aggressively guards the female from possible harm. On the other hand, montane voles do not form lasting bonds nor do they protect and care for their young. They are promiscuous maters, showing no loyalty to one partner over another. Researchers blocked the release of oxytocin in prairie voles to test if it was the key ingredient in their monogamous preferences. Not so surprisingly, mating pairs formed no lasting bonds. In a similar experiment, scientists did not allow the prairie voles to mate, but they administered oxytocin to the females and vasopressin (a hormone much like oxytocin found mainly in males) to the males. Even without sex, the voles still created monogamous social bonds and strong preference to their mate over other voles. (5)
Unfortunately, there has been no real data regarding oxytocin levels in humans in relation to the formation of relationships. And there are, of course, some very significant differences between voles and humans. Obviously the vole brain and the human brain are not identical, nor are their mating habits or reasons for forming social attachments. (5) However, studying the biology behind love and social bonding in other animals could help us in understanding our own species. The vole experiments show how extraordinarily important oxytocin is in the formation of social relationships. (6)
Knowing that love is so chemically influenced and based brings up many interesting issues. It is strange to think that motherly love and romantic or sexual love are so intricately related, both caused by the release of the same hormone. We tend to see our mother's love for us as completely different from her love for her husband. In much the same way, there is something uneasy about that thought that merely one hormone could be the reason behind our most intimate social relationships and one of our most intense emotions. Is love nothing more than instinct? Does the way we feel about the people we love really have anything to do with that person or is it simply connected to hormones? Are there really no emotions that are beyond the brain? Understanding the role that hormones like oxytocin play will be very instrumental in our figuring out just how much neurobiology dictates the perception of our emotions.
1)Oxytocin Web Site, a rich resource with a lot of information about oxytocin
2)Oxytocin Web Site, the structure of oxytocin
3)Oxytocin, The Hormone of Love, an in depth look at oxytocin
4)The Chemistry of Love, a look at the chemicals that cause all the manifestations of being in love
| Pain: Understanding the Subjective, Objectively Name: Gavin Impe Date: 2002-04-16 03:39:44 Link to this Comment: 1824 |
Pain is a universal element of the human experience. Everyone, at some point in their lives, experiences pain in one form or another. Pain has numerous causes, effects, and is itself a highly complex biological phenomenon. It also carries with it important emotional and social concerns. Pain cannot be entirely understood within the context of any one field of scientific inquiry. Indeed, it must be examined across a range of disciplines, and furthermore considered in relation to important non-scientific influences, such as emotional responses and social determinants. I conducted my explorations regarding pain with the following question in mind: to what degree is pain subjective? I found several avenues of inquiry to be useful in my explorations: they are (1) the expanding specialty in the medical profession of pain management; (2) pain in individuals with spinal cord injuries (SCIs) and (3) pain experiences of children. Examining these issues led to the conclusion that pain is in fact a highly subjective phenomenon.
"The philosophy that you have to learn to live with pain is one that I will never understand or advocate," says Dr. W. David Leak, Chairman & CEO of Pain Net, Inc. (1). Indeed, the notion that pain is an essential element of life, and that one must endure pain to achieve something positive (as conveyed in the omnipresent athletic mantra "no pain, no gain") has informed our sense as a society of how pain is to be dealt with. Only recently, with increasing awareness in the health care community that managing a patient's pain is a complex, yet crucial aspect of their care, has society's view of pain and its management begun to change. "Pain Management" is itself a neologism, and the establishment of pain management as a legitimate sub-specialty in the medical profession has no doubt encouraged people previously untreated for serious pain to obtain medical treatment. The existence of pain management clinics and services has altered the greater social understanding of pain from one that posited it as an imperative, to one that posits it as an unnecessary and entirely treatable condition. It is conceivable that formerly, when individuals did not have access to such services, that they conditioned themselves to make their pain less of an issue. Most people have had the experience of being required to actively control their pain, and therefore we can conclude that pain is heavily influenced by such social factors. These factors are almost impossible to understand in any objective sense, but to objectively understand pain, we must realize that they contribute to the notion of pain as a subjective phenomenon:
Pain is not just a physical issue, but effects all aspect of you physical and mental health. Despite centuries of trying to separate mind and body, treatment of chronic pain forces us to admit this can't be done. We will never say your pain is in your head but thoughts and emotion are related to pain. We call this the pain/stress/depression cycle. Biofeedback can give us the opportunity to interfere throughout this cycle. The more places and ways we can interfere with the pain- stress cycle, the more likely we are able to be of lasting help (2).
The recent recognition that pain is a complex entity that is affected by issues such as stress and depression is a recent one. Along with this recognition has come the implication that a satisfactory definition of pain must include what are inherently definition-resistant quantities. How can one scientifically define emotions and stress? That pain encompasses a variety of such issues requires that it be established as a subjective phenomenon.
An examination how pain affects children is also useful in establishing its subjectivity. Evidence suggests that experiences with pain, especially during childhood, are crucial in affecting an individual's subsequent experiences with pain. Indeed, it is recognized that differing levels in individual pain tolerance can be affected by differences in what people have learned about how to respond to pain:
A child's age, past experience with pain, and family and cultural styles, McGrath said, influences his or her response to new, painful situations. Parents serve as models. Young children often fall down, she observed, and then look at a parent for cues on how to react. In general, the younger the child, the greater his or her overt distress, and the more the child has to be physically restrained, she said, the more painful the experience will be (3).
As this excerpt illustrates, pain also has a significant component of learned experience. Individuals exhibit different levels of tolerance to a controlled application of physical pain. If two people touch a hot bowl, they will not necessarily react in the same manner to the apparent discomfort. These reactions may be attributable to how children develop differing thresholds, boundaries, and levels of tolerance of pain via interaction with other people during formative experiences with pain. If pain were an entirely objective phenomenon, the dynamics of these interactions would have no effect on the child's subsequent understandings of exactly what pain is: "Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life" (4). Interaction with the environment can indeed alter an individual's conception of what they find to be "painful." Therefore, there is no way to objectively determine parameters for what is painful and what is not. The effect of experiences with pain during formative years is thus another way of establishing the subjectivity of pain.
A third manifestation of the subjectivity of pain lies in the experiences of individuals with spinal cord injuries (SCIs). Such injuries have an objective and clinically demonstrable effect on a patient's ability to feel and to sense stimuli. However, this does not mean that individuals with spinal cord injury that renders a part of their body "senseless" do not feel pain in these regions: "In fact, a number of people with SCI experience chronic pain in areas that otherwise have no sensation" (5). By objective medical criteria, patients in such a condition should in fact not be experiencing pain. The reality is that the biological process of pain is something that cannot be entirely understood by the shortsighted idea that pain cannot exist when there it has no apparent physical cause. Pain is more than the sum of the biological interactions that would purport to explain it. Here again the importance of the emotional and psychological aspects of pain can be seen, necessitating the establishment of pain as subjective.
What then, makes us resistant to the idea that pain is subjective? Part of the answer to this question lies in the fact that a good deal of pain has a concrete neurophysiological basis. Indeed, there are a number of scientific measures that can serve as clear indicators of the presence of conditions that are known to induce pain. Imaging studies that reveal tissue or nerve damage are an example of such indicators. Indeed, even less technological methods of assessment can still conclude what exactly is at the root of someone's pain. If a person has injured their knee, it is common for them to be asked to describe the pain they are feeling. Dull pain, sharp shooting pain, pain that waxes and wanes - these different types of pain are each indicators that can be helpful in determining the exact nature of the person's injury. However, one must resist this tendency to view pain as a simple phenomenon with a clear-cut cause/effect duality as there are other factors that must be taken into consideration. An examination of the emergence of the field of pain management, pain in individuals with spinal cord injuries (SCIs), and the dynamic of the childhood experience with pain provides evidence that the emotional, psychological, and social aspects of pain require that it be considered a subjective phenomenon.
1)Pain Net, Inc., an organization that provides educational and support services to physicians, and other health care professionals throughout the nation.
2)American Academy of Pain Management.
3)"Children and Pain," from the National Institutes of Health.
4)International Association for the Study of Pain.
5)University of Washington Medical School Department of Rehabilitation Medicine.
| Munchausen Syndrome by Proxy: Sick kid or sick par Name: Jenny Mary Date: 2002-04-16 03:52:41 Link to this Comment: 1825 |
In relating the details of Munchausen Syndrome by Proxy (MSBP), the initial reaction is usually shock, followed quickly by fascination. The reason for the latter is that the medical community has yet to make up their minds about what exactly MSBP is. The debate: psychiatric disorder v. child abuse. Essentially the arguments for both create a divide between the brain and behavior, though not relating the two.
Munchausen Syndrome "is a condition manifest by persons feigning or inducing illness in themselves for no other apparent gain than adopting the sick role and thus exposing themselves to painful and sometimes damaging and disfiguring medical procedures (7)." The name of the syndrome originates from an eighteenth-century Baron, Hiernymous Karl Friedrich von Munchausen, who was a military mercenary widely known for regaling fantastical stories of exploits (6). While the Baron had no psychiatric condition or any further ties with the medical nature of the syndrome, as it is known today, his connection to the syndrome derives from the proven fabrication of all his tales. In 1977, the British journalist Roy Meadow first used the term "Munchausen By Proxy" in an article that named children as the primary victims of the syndrome.
At the time, the literature revealed the natural mother of the child to be the perpetrator of induced and at times actual, illness (3). It is important to note that Meadow's intended to apply MSBP to the problem of child abuse and while it is still extensively classified as such in child abuse and medical journals, the boundaries of the syndrome have been stretched with increased prevalence. The popular view of MSBP remains that it is a form of child abuse in which a parent of caretaker continually fabricates information about the child's health in order to assume the sick person's role by proxy (1).
The perpetrator is often a parent and typically the mother. However, there have been cases where the father acts as perpetrator. The first reported case of MSBP with a male caretaker occurred in 1990 when a father complained to physicians that his newborn baby would often stop breathing, turn blue and have seizures. Following extensive evaluation of apnea, it was discovered that the father, himself was suffocating and shaking the baby (5). Perpetrators show an avid interest for hospital care and usually have experience in the medical field. Munchausen syndrome is present in 10% of such perpetrators (3).
Munchausen syndrome and MSBP are included in the DSM-III R category of factitious disorders and therefore are elusive syndromes that are difficult to diagnose and recognize (2). "Because symptoms in factitious disorders are not connected with obvious gain, the absence of external gain suggests that factitious disorders like Munchausen syndrome serve some psychological need, but do so by maladaptive methods (2)." The syndrome is not recognized by the American Medical Association or the American Psychiatric Association (10). Lack of official recognition from the medical community has created an air of confusion around MSBP. Munchausen syndrome is decidedly a psychiatric disorder involving the patient assuming a role, but the reason for skepticism concerning MSBP is that is clearly a form of child abuse, as well as a vehicle for further role assumption by the perpetrator. Therefore, diagnosis is often relegated to close surveillance of the perpetrator's behavior toward the child.
While the medical community questions the validity of MSBP, I am more likely to adopt the opinion that the two can be reconciled - the syndrome being a form of child abuse that demonstrated behavior typical to that of a psychological disorder. The debate over the status centers on the perpetrator. Studies have shown that the perpetrator "rarely suffers from overt mental illness..." though, they have been known to have "one of various personality disorders associated with attempts to deceive - most commonly, the historic and borderline disorder types (1)." Some past medical history could show Munchausen syndrome, depression, family dysfunction, and somatization disorders (1). Thus, it is clear that MSBP serves a psychological need for the perpetrator because there is no external evidence of physical gain.
MSBP is a sort of enigma - which brings me to my original purpose; a quest for the truth about MSBP. The most important question for me being: what causes Munchausen Syndrome By Proxy? It is a disturbing disorder, which is closely tied to behavior and, on the surface, loosely connected to the brain. No concrete psychological or neurological data exists on the causes of child abuse. Most theories on the causes of child abuse point to past abuse, family dysfunction and depression - the same symptoms existing in MSBP perpetrators. However, it seems far too simple to write off MSBP as child abuse and ignore the psychological components of the syndrome, such as the perpetrator assuming the role of a sick individual by proxy. Above all, this speaks to the prevalence of the I-function in the individual.
The I-function provides an idea of self, from an objective perspective. Therefore, the perpetrator's I-function is closely linked to their behavior as individuals and caretakers. The behavior of the perpetrator involves imagining themselves in a role outside of their bodies and I would argue this aspect can be attributed the I-function. The notion of fictitious experience takes the perpetrator away from the physical reality and to a completely psychological, imaginary space. The correlation between I-function and the perpetrator's actions can informally explain their motives for MSBP. To clarify, I am not suggesting that the I-function is a cause of, or an indicator of intent to engage in MSBP for two reasons: 1. There is no physical evidence of the I-function to point to, 2. The I-function could only account for the perpetrator's personal experience (imagination, dreaming, planning, etc.) in order to isolate the person from other caretakers that do not partake in MSBP. Arguably, the role of the I-function is to individualize each human, but working in conjunction with a history of psychological disorders and abuse, it helps in producing the mind frame of a perpetrator of MSBP.
Information on Munchausen Syndrome By Proxy is unanimous on several basic points: the identification, symptoms of the perpetrator and consensus (more or less) that is at least, a form of child abuse. The vast black hole of diagnosis, treatment for the perpetrator and victim and concrete warning signs poses a great risk to the victims. The perpetrators are not overtly inadequate caretakers, but in fact the very opposite. Furthermore, coupled with their ability to deceive and lie to obtain their desired ends creates difficulty in diagnosing MSBP for doctors. The perpetrator is most likely deeply caught in their psychological, internal experience, while the child suffers through physical, external experience. Lack of medical data and psychological mapping of the perpetrator causes MSBP to continue and increase in frequency over time. The issue of the proxy further complicates the reality in questioning what is true and what ailments are genuine. Surveillance is the only answer offered right now, but I hope that there will soon be medical aid available for the perpetrators.
WWW Sources
1) General information on MSBP, Clinician Reviews (August, 2001) article.
2) Information on Munchausen syndrome and Munchausen syndrome by proxy, The Journal of Psychology (May, 1997) article.
3) Case reports of MSBP, Journal of Toxicology: Clinical Toxicology (April, 2001) article.
4) Case of MSBP, Newsweek (April, 1996) article.
5) MSBP: father as perpetrator, Pediatrics magazine (March, 1990) article.
6) MSBP - The deadly game; Saturday Evening Post (July, 1996) article.
7) MSBP: child abuse in the medical system, Archives of Pediatrics & Adolescent Medicine(July, 1996) article.
8) Fabricated or induced illness in children, British Medical Journal (August, 2001) article.
9) Information on MSBP.
10) Mothers Against Munchausen Syndrome by Proxy Allegations (M.A.M.A) home page.
| What is Intelligence? Name: Asra Husai Date: 2002-04-16 04:54:49 Link to this Comment: 1826 |
Intelligence can be defined in many different ways since there are a variety of individual differences. Intelligence to me is the ability to reason and respond quickly yet accurately in all aspects of life, such as physically, emotionally, and mentally. Anyone can define intelligence because it is an open-ended word that has much room for interpretation. Thus my paper is an attempt to find the meaning of human intelligence. There are a couple of scientists who have tried to come up with theories of what makes a human being intelligent.
Jean Piaget, a Swiss child psychologist, is well known for his four stages of mental growth theory (1). In the sensorimotor stage, from birth to age 2, the child is concerned with gaining motor control and getting familiar with physical objects. Then from age 2 to 7, the child develops verbal skills, which is called the preoperational stage. In the concrete operational stage the child deals with abstract thinking from age 7 to 12. The final stage called the formal operational stage ends at age 15 and this is when the child learns to reason logically and systematically. (1)
Piaget's theory provides a basis for human intelligence by categorizing the major stages in child development and how they contribute to intelligence. Each of these invariant stages has major cognitive skills that must be learned. Knowledge is not merely transmitted verbally but must be constructed and reconstructed by the learner (3).
Thus this development involves a few basic steps. The first fundamental process of intellectual growth is the ability to assimilate the new events learned into the preexisting cognitive structures. The second fundamental process is the capability to change those structures to accommodate the new information and the last process is to find equilibrium between the first two processes. (3)
Even though Jean Piaget's theory was interesting, I found Howard Gardener's, a psychologist at Harvard University, theory even more intriguing. He arranged human intelligence into seven sections and they are body-kinesthetic, interpersonal, intrapersonal, linguistic, logical-mathematical, musical, and spatial intelligence. Gardner believes that everyone has a mixture of all the categories varying at different levels. We can see a couple of intelligences that stand out in people we know and including ourselves. (2)
For example, as a math major, I would consider the logical-mathematical intelligence to be more predominant than my linguistic intelligence based on the name of the categories. In fact, Gardner characterizes the logistical-mathematical intelligence as people who think logically and are able to transfer abstract concepts to reality. These people enjoy solving puzzles and can be good inventors because they can visualize an invention even before making a prototype (2). They normally do better in school, which is for the most part due to the fact that schools are designed for logical-mathematical type of thinkers.
The linguistic type, as you may have guessed, are the natural born writers and poets. They usually have excellent storytelling skills, spelling skills, and love to play with words. They tend to be bookworms and can easily learn more than one language. Best form of learning is through hearing, speaking, or seeing words. This type of intelligence seems to be located in the Broca's Area, since damage to one portion of the brain will cause a person to lose the ability to express themselves in clear grammatical sentences, though that person's understanding of vocabulary and syntax remains intact (4).
Even musical intelligence has been scientifically traced in certain areas of the brain. Impaired or autistic children who are unable to talk or interact with others have exemplified exceptional musical talent (4). People of this type of intelligence show great aptitude for music, have excellent pitch, and good sense of rhythm. They concentrate better with music playing in the background and a particular concerto by Mozart has scientifically shown changes in the brains of listeners (2). Thus, musical intelligence can be a form or a means of learning.
Another form of intelligence is the interpersonal intelligence. This category is for people who are very well aware of their environment. They tend to be sensitive to people around them, have an excellent idea of how people behave, and are especially sociable. Politicians, leaders, counselors, mediators, and clergy are excellent examples of people with this type of intelligence. Damage to the frontal lobe has shown damage to person's personality and the ability to interact with others.
Intrapersonal intelligence is almost the opposite of interpersonal intelligence. This kind of intelligence deals with how well you know yourself. People who possess a higher degree of this type of intelligence have a high self-esteem, self-enhancement, and a strong sense of character. They are usually deep thinkers, quite, self-teachers, skilled in music or art, and have an inner discipline (2). This sort of intelligence is hard to measure since it is often difficult to recognize externally.
Spatial intelligence is the ability to perceive and interpret images or pictures in three-dimensional space. The right hemisphere of the brain has been proven to control this form of intelligence and scientists are certain that spatial intelligence is clearly an independent portion of this intellect (4). A person of this intellect enjoys making maps and charts.
Lastly, Gardner classifies people who are athletically inclined into the body-kinesthetic intelligence. They perform the best in atmospheres of action, touching, physical contact, working with their hands. Dancers and athletics are good examples of this form of intellect. I am a little skeptical that Gardner considers this a form of intellect since it is only a physical component of intelligence, but nonetheless, the brain does use both hemispheres to control movement.
All of the seven components of intelligence are independent from one another and I believe that it serves as an excellent understanding of the various forms of human intelligence. Whereas, Piaget's theory shares his idea of when intelligence is formed and how childhood development affects our adulthood intelligence. Thus, what is intelligence?
Well, I agree with both of the scientists approach in defining human intelligence. I believe that intelligence is the ability to utilize our entire brain, which will most definitely include Gardner's theory but more. Since we only use a small percentage of our brain, I imagine our brains have a lot more forms of intelligence than the ones Gardner proposes as well as more stages of child development than the ones Piaget proposes. As I mentioned before, intelligence is an open-ended word that may never have an agreed upon definition, but we all have our own definition.
References:
1)Jean Piaget, Swiss Child Psychologist
2)The Seven Human Intelligences
| The Human Perception of Pain Name: Cass Barne Date: 2002-04-16 08:24:16 Link to this Comment: 1827 |
There is more research surfacing supporting the notion that people can control their pain. What is left under-examined is the notion of whether the pain is mediated by the brain, mind, or both. We all know that pain is an instinctive "sense" if you will, necessary to the survival of all living beings. Without pain, it would go unrecognized and exacerbate to the point of death. Pain is a protective mechanism essential to survival. There are three important claims here: One is that pain is actually a perception. The second, is the brain mediates the suppression of pain through a "gate" in the spinal cord. Lastly, since pain is a perception, the mind may decide the degree to which the "gate" is open, which therefore influences to amount of pain reaching the brain. Recent research provides evidence that certain brain structures mediate the spinal cord gate. Still controversial is whether receptivity to pain is biological in origin and completely dependent on the brain, or whether the mind, the entity in an individual responsible for thought, and feelings, conscious or unconscious, controls the nervous system and in the end manipulates one's perception of pain.
Pain is defined by the International Association for the Study of Pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage" (1). When pain is described in these terms we can see that pain is a perception, sort of like seeing and hearing. When pain is processed there are a number of brain structures activated, commonly referred to as the "central pain matrix" (2). It may seem irrelevant to delve into pain signal activation in the brain since what we are talking about is the brain controlling pain, not receiving it. However, it is important to recognize that when there is an incoming stimulus, it goes to the brain and creates one's perception of pain. In a sense, this means that the brain creates the mental state or the percept of pain. It is also important to discuss the brain structures associated with the pain activation because these structures are essentially the means to the end state of what we call "pain".
The pain process starts out with a stimulus which activates somatosensory axons from the skin, muscles, or internal organs to enter the nervous system via spinal nerves. Axons that convey sharp localized information, like fine touch, ascend through the dorsal columns of the spinal cord, referred to as the fast pathway, to the nuclei in the lower medulla (3). From the medulla, the axons cross the brain and ascend through the medial lemniscus to the ventral posterior nuclei of the thalamus, the somatosensation receiver (bodily sensation). Axons from the thalamus project to the primary somatosensory cortex which are then relayed to the secondary somatosensory cortex. Conversely, axons that convey less localized information, like pain or temperature, ascend through the spinothalamic tract, the slow pathway, and terminate in the ventral posterior nuclei of the thalamus (3),(9). The end site for both of these pathways is in the somatosensory cortex.
These pathways also activate the anterior cingulate cortex, a region of limbic cortex on the medial side of cerebral hemispheres, which processes and understands pain. Studies show that this region is not involved with pure perception of pain, but with the emotional reaction that a painful stimulus can cause. That is, when activated, the aversiveness of pain increases (9). Still under investigation is whether the primary and secondary somatosensory cortex are involved in the perception of pain. A 1997 study produced pain sensations by having subjects put their hands in ice water. Under one condition, the subjects were hypnotized so as to reduce the pain. What they found was that the hypnosis worked in that the pain was not too unpleasant, although intense. The PET scan, a device for detecting brain activity, showed that the stimulus activated both the primary somatosensory cortex and the anterior cingulate cortex. Although the perception of pain remained high with activation of the somatosensory cortex, the anterior cingulate cortex in the hypnotized subject was less active than the others. Those hypnotized also reported less pain even though they could feel ice water. This offers that those who were hypnotized had less of an aversion to the pain although a high perception of pain. Therefore, this system "is activated when a harmful stimulus is potentially threatening to a person, which in turn activates a number of reactions and changes in affect and mood" (2). This change of mood suggests that the stimuli, be it internal or external, lead to the perception of pain. Yet, when a person is not fully conscious, the claim that less pain is produced or perceived, seems valid. In effect, this leads to the idea that the percept of pain may be psychologically induced or reduced. Although pain perception may always be activated with the appropriate stimuli, a person's level of consciousness or degree of interest in the pain may attribute to the intensity of the pain itself. All the while though, the biology of the nervous system seems to be activated first with a noxious stimulus, and with that, this model upholds that the brain creates the mind because the physical structures make the person conscious of perceiving the pain.
Ronald Melzack and Patrick Wall's research of the 1960's proposed the gate-control theory of pain explaining that "pain transmission is blocked from reaching higher centers necessary for perception of pain" (3). This theory holds that ascending and descending pain signals may be blocked in the dorsal horn at the base of the spinal cord therefore inhibiting these areas of the brain from perceiving the pain (3),(4). Essentially, the gate cuts off the ascending axons and disables them from getting to the brain, with the end result being the non-percept of pain. Perhaps the "gate" on those who were hypnotized was closed, therefore allowing less transmission through, and in the end inhibiting pain. However, the study showed that there was still perception of pain, with less aversion to the pain. This would mean that the signals were actually getting through. Therefore, in this case, being less conscious seemed effective in psychologically reducing the perception of pain. On the other hand, when we think about daily "painful" stimuli and how the same stimuli can affect two people differently, it makes one wonder whether the lack of pain perception in one person is a result of the gate closure. Speculatively, the ability to ignore the pain, or not perceive the pain, may be due to the conscious self being in control. This theory suggests that incoming pain is suppressed by certain areas of the midbrain, in particular the anterior cingulate cortex (9).
Perhaps the reason this is mind boggling is because the spinal gate is a hypothetical gate. The spinal gate theory pain is just that, a theory. But, there is still the question of why some people are tougher than others. Are some more susceptible to pain because of childhood rearing in that they never learned mind over matter and how to "close the gate"? What about an Army Ranger? Through disciplinary training he learns to be "tougher" and how to survive with essentially no food or rest, in addition to days of walking and trenching through difficult terrain. Is the ability to suppress the pain from walking for three weeks straight without falling to exhaustion, due to learned behavior, which changes the brain and thus the ability to close the gate to incoming pain? Does one learn to take conscious control of his body and therefore pain? This is where the mind-body connection comes into play.
The mind-body problem argues that there is a relationship of the mind to the body (or brain) and that mental processes affect the physical (5),(6). What the mind is, depends on one's philosophy, but the most common definition is as follows: the entity in an individual responsible for consciousness or unconsciousness, thought and feelings, having its origin in the brain (7),(8). Or, the mind may just be what we are conscious of and therefore in control of. Left unbeknownst, is if the mind makes a decision that leads to suppression of pain since the brain does. That is, a thought in the mind could transform into an action potential in the brain, which could then be sent down the spine to close the gate and inhibit the pain signals from coming through. There is no evidence for this kind of connection of the mind to the brain. However, this does not mean that the mind is not interconnected with the body and can affect certain feelings and sensations.
Previous studies on the other hand, provide us with clues to psychologically induced pain. For instance, Seligman and Buchanan at the University of Pennsylvania, found that those who were psychologically distressed had higher levels of chronic pain than those who were less distressed (5). Such findings would suggest that one's mind can influence the receptivity to pain. Perhaps the mind-body/brain problem, how mental processes affect the physical, is a similar way of saying that the mind controls the spinal gate. Perhaps the more one is in control of his pain, the less pain he has because his conscious mind communicates with the nervous system to close the gate. The hypnosis study, however, refutes the notion that the mind has power over pain since the subjects were unconscious while perceiving pain. Science has observed and supported the theory that the brain is involved in receptivity and activation of pain or the perception of pain, and that in fact may suppress pain. Indeed however, the power of positive thinking is more accepted, and supports the mind-body connection and is seemingly demonstrative of being in control of his ability to perceive or not perceive pain. Alas, there is no evidence that the mind controls the opening and closing of this spinal cord gate.
The truth of the matter, is that we will never really know what makes one "tougher" than another. All people are different and therefore their perceptions are different. This difference may be due to the fact that we each have different brains and perceive pain with more or less aversiveness than others do. There is strong scientific evidence in the study of pain supporting that certain brain parts are activated during painful stimuli and more interestingly, active during the aversiveness to pain. There are also meaningful observations suggesting the brain mediates the suppression of pain. This view of pain, we must remember is dependent on the notion that pain is a perception. Pain as a perception leaves the window open for discussion on the mind-body problem. If pain is one's own perception of a stimulus, then it follows that the mind may have conscious control of these perceptions. The scientific world is for the most part confident that the brain is involved in pain, in both suppressing it and receiving it. Still controversial, is which regions of the brain are in control of certain metacognitions of pain, such as perception and understanding. Especially one sided, is if the conscious self, the mind, can alter the nervous system and thus the perception of pain. Let it be known that there is still plenty of room for more observations and conclusions. In addition, we must note that this is also a very limited view of pain. For example, the body's endogenous opioid system was left out despite the increasing well supported belief that endorphins suppress pain as well. It is important to bear in mind that the brain has a role in allowing pain in and out through the theorized spinal gate. However, it is also worthwhile to consider the possibility that one's entire perception of pain may be conscious in origin and simply correlate to the mechanisms of the brain, rather than stem from just the brain entirely.
2) 2)The Human Perception of Pain
4) 4)Modification of pain within the spinal cord
6) 6)Mind and Body Interactions
9) 9) Carlson, Neil R., Physiology of Behavior. Needham Heights: A Pearson Education Company, 2001.
| The Human Perception of Pain in Conjunction with t Name: Cass Barne Date: 2002-04-16 08:48:53 Link to this Comment: 1829 |
There is more research surfacing supporting the notion that people can control their pain. What is left under-examined is the notion of whether the pain is mediated by the brain, mind, or both. We all know that pain is an instinctive "sense" if you will, necessary to the survival of all living beings. Without pain, it would go unrecognized and exacerbate to the point of death. Pain is a protective mechanism essential to survival. There are three important claims here: One is that pain is actually a perception. The second, is the brain mediates the suppression of pain through a "gate" in the spinal cord. Lastly, since pain is a perception, the mind may decide the degree to which the "gate" is open, which therefore influences to amount of pain reaching the brain. Recent research provides evidence that certain brain structures mediate the spinal cord gate. Still controversial is whether receptivity to pain is biological in origin and completely dependent on the brain, or whether the mind, the entity in an individual responsible for thought, and feelings, conscious or unconscious, controls the nervous system and in the end manipulates one's perception of pain.
Pain is defined by the International Association for the Study of Pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage" (1). When pain is described in these terms we can see that pain is a perception, sort of like seeing and hearing. When pain is processed there are a number of brain structures activated, commonly referred to as the "central pain matrix" (2). It may seem irrelevant to delve into pain signal activation in the brain since it is seemingly unrelated to the ability of the brain to suppress pain. However, it is important to recognize that an incoming stimulus goes to the brain and creates one's perception of pain. In a sense, this means that the brain creates the mental state or the percept of pain. It is also important to discuss the brain structures associated with the pain activation because these structures are essentially the means to the end state of what we call "pain".
The pain process starts out with a stimulus which activates somatosensory axons from the skin, muscles, or internal organs to enter the nervous system via spinal nerves. Axons that convey sharp localized information, like fine touch, ascend through the dorsal columns of the spinal cord, referred to as the fast pathway, to the nuclei in the lower medulla (3). From the medulla, the axons cross the brain and ascend through the medial lemniscus to the ventral posterior nuclei of the thalamus, the somatosensation receiver (bodily sensation). Axons from the thalamus project to the primary somatosensory cortex which are then relayed to the secondary somatosensory cortex. Conversely, axons that convey less localized information, like pain or temperature, ascend through the spinothalamic tract, the slow pathway, and terminate in the ventral posterior nuclei of the thalamus (3),(9). The end site for both of these pathways is in the somatosensory cortex.
These pathways also activate the anterior cingulate cortex, a region of limbic cortex on the medial side of cerebral hemispheres, which processes and understands pain. Studies show that this region is not involved with pure perception of pain, but with the emotional reaction that a painful stimulus can cause. That is, when activated, the aversiveness of pain increases (9). Still under investigation is whether the primary and secondary somatosensory cortex are involved in the perception of pain. A 1997 study produced pain sensations by having subjects put their hands in ice water. Under one condition, the subjects were hypnotized so as to reduce the pain. What they found was that the hypnosis worked in that the pain was not too unpleasant, although intense. The PET scan, a device for detecting brain activity, showed that the stimulus activated both the primary somatosensory cortex and the anterior cingulate cortex. Although the perception of pain remained high with activation of the somatosensory cortex, the anterior cingulate cortex in the hypnotized subject was less active than the others. Those hypnotized also reported less pain even though they could feel ice water. This offers that those who were hypnotized had less of an aversion to the pain although a high perception of pain. Therefore, this system "is activated when a harmful stimulus is potentially threatening to a person, which in turn activates a number of reactions and changes in affect and mood" (2). This change of mood suggests that the stimuli, be it internal or external, lead to the perception of pain and an emotional response to the pain. Yet, when a person is not fully conscious, the claim that less pain is produced or perceived, seems valid. In effect, this leads to the idea that the percept of pain may be psychologically induced or reduced. Although pain perception may always be activated with the appropriate stimuli, a person's level of consciousness or degree of interest in the pain may attribute to the intensity of the pain itself. All the while though, the biology of the nervous system seems to be activated first with a noxious stimulus, and with that, this model upholds that the brain creates the mind because the physical structures make the person conscious of perceiving the pain.
Ronald Melzack and Patrick Wall's research of the 1960's proposed the gate-control theory of pain explaining that "pain transmission is blocked from reaching higher centers necessary for perception of pain" (3). This theory holds that ascending and descending pain signals may be blocked in the dorsal horn at the base of the spinal cord therefore inhibiting these areas of the brain from perceiving the pain (3),(4). Essentially, the gate cuts off the ascending axons and disables them from getting to the brain, with the end result being the non-percept of pain. Perhaps the "gate" on those who were hypnotized was closed, therefore allowing less transmission through, and in the end inhibiting pain. However, the study showed that there was still perception of pain, with less aversion to the pain. This would mean that the signals were actually getting through. Therefore, in this case, being less conscious seemed effective in psychologically reducing the perception of pain. On the other hand, when we think about daily "painful" stimuli and how the same stimuli can affect two people differently, it makes one wonder whether the lack of pain perception in one person is a result of the gate closure. Speculatively, the ability to ignore the pain, or not perceive the pain, may be due to the conscious self being in control. This theory suggests that incoming pain is suppressed by certain areas of the midbrain, in particular the anterior cingulate cortex (9).
Perhaps the reason this is mind boggling is because the spinal gate is not a physical gate. The spinal gate theory pain is just that, a theory. But, there is still the question of why some people are tougher than others. Are some more susceptible to pain because of childhood rearing in that they never learned mind over matter and how to "close the gate"? What about an Army Ranger? Through disciplinary training he learns to be "tougher" and how to survive with essentially no food or rest, in addition to days of walking and trenching through difficult terrain. Is the ability to suppress the pain from walking for three weeks straight without falling to exhaustion, due to learned behavior, which changes the brain and thus the ability to close the gate to incoming pain? Does one learn to take conscious control of his body and therefore pain? This is where the mind-body connection comes into play.
The mind-body problem argues that there is a relationship of the mind to the body (or brain) and that mental processes affect the physical (5),(6). What the mind is, depends on one's philosophy, but the most common definition is as follows: the entity in an individual responsible for consciousness or unconsciousness, thought and feelings, having its origin in the brain (7),(8). Or, the mind may just be what we are conscious of and therefore in control of. Left unbeknownst, is if the mind makes a decision that leads to suppression of pain since the brain does. That is, a thought in the mind could transform into an action potential in the brain, which could then be sent down the spine to close the gate and inhibit the pain signals from coming through. There is no evidence for this kind of connection of the mind to the brain. However, this does not mean that the mind is not interconnected with the body and can affect certain feelings and sensations.
Previous studies on the other hand, provide us with clues to psychologically induced pain. For instance, Seligman and Buchanan at the University of Pennsylvania, found that those who were psychologically distressed had higher levels of chronic pain than those who were less distressed (5). Such findings would suggest that one's mind can influence the receptivity to pain. Perhaps the mind-body/brain problem, how mental processes affect the physical, is a similar way of saying that the mind controls the spinal gate. Perhaps the more one is in control of his pain, the less pain he has because his conscious mind communicates with the nervous system to close the gate. The hypnosis study, however, refutes the notion that the mind has power over pain since the subjects were unconscious while perceiving pain. Science has observed and supported the theory that the brain is involved in receptivity and activation of pain or the perception of pain, and that in fact may suppress pain. Indeed however, the power of positive thinking is more accepted, and supports the mind-body connection and is seemingly demonstrative of being in control of one's ability to perceive or not perceive pain. Alas, there is no evidence that the mind controls the opening and closing of this spinal cord gate.
The truth of the matter, is that we will never really know what makes one "tougher" than another. All people are different and therefore their perceptions are different. This difference may be due to the fact that we each have different brains and perceive pain with more or less aversiveness than others do. There is strong scientific evidence in the study of pain supporting that certain brain parts are activated during painful stimuli and more interestingly, active during the aversiveness to pain. There are also meaningful observations suggesting the brain mediates the suppression of pain. This view of pain, we must remember is dependent on the notion that pain is a perception. Pain as a perception leaves the window open for discussion on the mind-body problem. If pain is one's own perception of a stimulus, then it follows that the mind may have conscious control of these perceptions. The scientific world is for the most part confident that the brain is involved in pain, in both suppressing it and receiving it. Still controversial, is which regions of the brain are in control of certain metacognitions of pain, such as perception and understanding. Especially one sided, is if the conscious self, the mind, can alter the nervous system and thus the perception of pain. Let it be known that there is still plenty of room for more observations and conclusions. In addition, we must note that this is also a very limited view of pain. For example, the body's endogenous opioid system was left out despite the increasing well supported belief that endorphins suppress pain as well. It is important to bear in mind that the brain has a role in allowing pain in and out through the theorized spinal gate. However, it is also worthwhile to consider the possibility that one's entire perception of pain may be conscious in origin and simply correlate to the mechanisms of the brain, rather than stem from just the brain entirely.
2)The Human Perception of Pain
4)Modification of pain within the spinal cord
7)Mind-Body-Medicine
8)Mind and Body Wellness
9) Carlson, Neil R., Physiology of Behavior. Needham Heights: A Pearson Education Company, 2001.
| What doesn't kill you makes you stronger: true or Name: Sarah Eber Date: 2002-04-16 09:03:10 Link to this Comment: 1830 |
What doesn't kill you makes you stronger. How true is this axiom? In many cases, dealing with life's problems will indeed help create a stronger person. There are times, however, when this may not be true.
Child abuse is a widespread problem in America and beyond. In Pennsylvania alone, there were 5109 physical injuries in kids ages 5-14 in 1989, and a further 55 fatalities in children age 4 and under, all due to child abuse (1). For many years, experts believed that the negative effects of child abuse, such as emotional problems, flashbacks to traumatic events, and even learning problems, were psychological phenomena only, able to be cured with therapy. Now, however, beliefs are being changed with the help of tools such as MRI imaging, able to detect actual changes in brain anatomy, and it appears that what doesn't kill you may still permanently weaken you, at least when it comes to child abuse.
The chief danger to the brain in child abuse, besides direct injury by the abuser, is the stress placed on fragile, developing tissue. Traumatic stress placed on the brain, such as that caused by abuse, will activate the locus ceruleus, which through a release of the neurotransmitter norepinephrine will cause the release of neurotransmitters such as epinephrine, dopamine, and more norepinephrine (2). These neurotransmitters are called catecholamines and are complemented by glucocorticoid stress hormones such as cortisol (2). Stress hormones and neurotransmitters are necessary to the normal function of the brain, and are to some point beneficial, but unusually high levels of these chemicals caused by abuse, especially over an extended period of time, can be very harmful (3). When levels of glucocorticoid hormones are elevated for an extent of several days due to stress, the neurons receiving these hormones begin to be damaged (4). Neurons begin to atrophy and the growth of new neurons is halted (4). If the stress continues for too long, neurons will die (4). This problem is exacerbated by the hormones themselves, which due to their water-insoluble properties will stay in the bloodstream for hours or days (3). The water-soluble neurotransmitters, on the other hand, only last for seconds (3). This persistance of the stress hormones makes it hard for the brain to return to its natural, unstressed state.
The brain develops in such a way that it leaves itself vulnerable to these negative influences. The prenatal brain develops an overabundance of neurons, some of which are then carefully eliminated before age 4 (5). In a process similar to this, the amount of synapses between neurons is built up during early childhood and then pruned back for the next 30 years of life (5). These two processes are both disturbed by elevated levels of stress hormones (5). The two centers of the brain with the most postnatal changes, including the growth of new neurons after birth, are the hippocampus, which is part of the limbic system, and the cerebellar vermis (6). The hippocampus is in charge of creating and retrieving memories, working together with the other parts of the limbic system, such as the amygdala, which records the emotions for each memory. The vermis controls the production and release of two of the catecholamine neurotransmitters, dopamine and norepinephrine (6). Both the vermis and the limbic system have higher concentrations of receptors for the stress hormone cortisol than anywhere else in the brain (6). Due to this fact, these still-developing areas are the most vulnerable to the damage done by elevated levels of stress hormones.
The limbic system shows the most dramatic effects of abuse. As stated before, an overexposure to stress hormones will cause the atrophy and eventual destruction of neurons, while halting the growth process of new neurons. This effect is clearly seen in MRI brain scans of adults who were abused as children: the left side of the hippocampus is markedly smaller than the right (1). Interestingly, when similar MRI testing was performed on a group of young people, ages 18-22, who had also suffered abuse in childhood, the left hippocampus was found to be equal to the size of the right (1). There are several hypotheses to explain this phenomenon. One is that the steady growth of the hippocampus through three decades prevents a change from being seen until later on in life (5). Another possible explanation is that abuse of alcohol or use of cocaine, used as an escape from painful memories of abuse, could cause the decrease in the hippocampus seen in older subjects (5).
Another alarming indicator of damage to the limbic system can be seen in brain-wave abnormalities detected by an electroencephalogram (EEG) (6). Temporal lobe epilepsy is a condition in which the limbic system is subjected to an "electrical storm" of wayward brainwaves, causing various symptoms of nausea, tingling, or vertigo (6). Tests performed by Martin Teicher in 1994 on 115 children and adolescents, abused and non-abused, showed that 54% of those who had undergone abuse early in life showed abnormalities on the EEG, while only 27% of those who were not abused showed abnormalities (6).
The effects of the overload of stress hormones on the vermis are is difficult to tell. However, it is clear that the vermis plays an essential role in the brain (6). Problems in the vermis are linked to bipolar disorder, autism, schizophrenia, and attention-deficit/hyperactivity disorder (ADHD) (6). The vermis is also partially in charge of the electrical activity in the limbic system, and an electrical stimulus applied to the vermis causes seizure activity in the limbic system to halt (6). If this suppression of improper electrical signals in the limbic system is part of the vermis' regular duties, damage to the vermis may be partially responsible for the brain-wave abnormalities of the limbic system described in the paragraph above.
Child abuse has a distressing effect upon learning ability as well. The hippocampus performs the essential task of storing and retrieving verbal memories, for which it retains a plasticity in order to learn and remember (6). However, the hippocampus is not the only part of the brain affected by abuse. In a study of children and adolescents diagnosed with posttraumatic stress disorder (PTSD) due to physical or sexual abuse, an unsettling relationship was seen between brain development and degree of abuse (5). The intracranial volume of PTSD subjects was smaller than the control group, and the longer the subject had been abused, the smaller the intracranial volume was (5). This decrease of intracranial volume was also shown to have a direct correlation to the decrease of IQ in the PTSD subjects, and the longer the child had been abused, the lower the IQ would be (5). Brain size in general also decreased as intensity and length of abuse increased (5).
The possibility of mental disorders is also raised. In the same study, the PTSD subjects were found to have larger lateral ventricles the greater the extent of abuse was, which is probably caused by the destruction of neurons due to the overabundance of stress hormones (5). While no direct link has been made, enlargement of lateral ventricles is a symptom of many mental health problems, such as schizophrenia, Alzheimer's disease, alcoholism, bipolar disorder, and depression (5).
The proof of brain damage due to child abuse is plain. Rather than simply causing emotional or psychological distress, child abuse causes the brain to physically "rewire" itself. There is a theory that this rewiring is a throwback to the earlier history of humans, in which increased aggression and fear served to increase the lifespan of the beleaguered human (6). Some even believe that the promiscuity sometimes seen in teens and adults who were abused as children is a continuation of that pressure to survive: if survival is dubious, reproduction is best done as soon as possible (6).
The conclusion of "rewiring" the abused brain presents a far more depressing view of the many behavior problems apparent in abused children, for then a great deal of the aggression, depression, and learning problems of an abused child are physical rather than emotional, and thus will require more than a visit to a therapist to fix, if indeed they can be fixed at all. This conclusion raises more questions. How to fix the "scarring" of the brain caused by trauma in childhood? How much of the emotional and learning problems of an abused child can be fixed, and how many are physical phenomena? Most important of all, perhaps: How to prevent the cycle of abuse from continuing on into another generation?
1) Kolko, David J. "Characteristics of Child Victims of Physical Violence: Research Findings and Clinical Implications." Journal of Interpersonal Violence 7.2 (1992): 244-276
2)< href="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T4S-3WK3RV4-3&_user=400777&_coverDate=05%2F15%2F1999&_alid=40836662&_rdoc=1&_fmt=full&_orig=search&_cdi=4982&_sort=d&_st=13&_acct=C000018819&_version=1&_urlVersion=0&_userid=400777&md5=b56f7b8e13ccaf122404bcc148bf3926">Developmental traumatology part I: biological stress systems
3)Development of the Cerebral Cortex: XII. Stress and Brain Development: 1, an article from the Journal of the American Academy of Child and Adolescent Psychiatry, dealing with the effects of stress hormones and neurotransmitters upon the brain in situations of extreme stress
4)Development of the Cerebral Cortex: XIII. Stress and Brain Development: II, an article from the Journal of the American Academy of Child and Adolescent Psychiatry, about the damaging effects of stress hormones on the developing brain
5)Developmental traumatology part II: brain development, an article detailing a study of the effect of post-traumatic stress disorder upon the brains of abused children
| The Never-ending Story: Sexual Orientation and Gen Name: Amy O'Conn Date: 2002-04-16 09:16:48 Link to this Comment: 1831 |
It is my observation that the average person gains insight into the nature vs. nurture debate when some particular human trait that is politically or socially volatile at the time is announced as having a specific genetic origin. This observation was confirmed when, in surfing the web, I came across an article entitled, "Female Inner Ear Comes Out of the Closet (1)." While reporting on a study published by a UT psychology professor who found that homosexual women exhibit tones in the inner ear similar to those of male test subjects, the Daily Texan journalist, with no explanation or sources, effortlessly mixes and confuses the social construction with the "science" of sexual orientation—even in her or his title. Attempting to get to the root of how an individual's sexual preference is determined, and the subsequent attempt to designate these individual tendencies into definitive statements regarding large groups in society has become a seductive topic for numerous media sources within the past decade or so. A closer look at this debate reveals the relative error of exploring one side without an equal exploration of the other.
Dean Hamer et al at the National Cancer Institute published the initial paper that is accountable for the explosion of interest and argument regarding genetic determination of sexual preference in 1993 (2). Hamer's study found that, of thirty-two pairs of brothers who were "exclusively or mostly" homosexual, twenty-two pairs of brothers shared the same type of genetic material. This introduced the idea that there is a gene for homosexuality. Hamer went on to identify a specific genetic sequence that exists on the maternally passed-on X chromosome. The extent of this sequence's influence on sexual preference was not and is not known. Another study published in 1993 by Macke et al studied the same locus, but found that it had no bearing on sexual preference (2).
In fact, all that any study can definitively say is that scientific "suggestions," that homosexuality and heterosexuality (bisexuality is far-less explored, or often placed within the former categories) can be partially determined by genetics exist; the essential contradiction of these suggestions and the definitive ideal that the public identifies with science is inherent within these studies. It was this perplexing contradiction that caused me to ask, what is the point of these studies, and do they really benefit us as a society?
The means by which studies themselves are carried out could play a part in the opposing conclusions of nearly identical studies that, by definition, should produce concurrent conclusions. It seems that the most common method for obtaining a sample population for relevant studies is to advertise in gay-identified magazines and newspapers, seeking volunteers to self-identify their sexual orientation, and if necessary, that of their siblings, etc.; information verification, if it is possible, is not always attempted (3). It is very probable that difficulty in obtaining an unbiased and random study sample has a large influence on a study's outcome. Also, when dealing with a politically charged issue, one must be aware of bias on the part of the researcher (3). The fact that certain groups can and will use studies to discriminate, to end discrimination, to essentially further any number of politically or socially motivated agendas certainly should be acknowledged by both professional and lay people when confronted with these studies.
Ruth Hubbard identifies questionable motives or biases of researchers, among others, in a conversation that she had in 1993 with Frank Aqueno, a writer/performance artist (4). Earlier that year, Hubbard and her son wrote, Exploding the Gene Myth: How Genetic Information is Produced and Manipulated by Scientists, Physicians, Employers, Insurance Companies, Educators, and Law Enforcers. She defines the gene myth as the idea that everything we are or do comes out of our genes, and that through finding out about our genes, we are going to learn what it means to be human. She and many others cite the conservative interpretation of the gene myth as its' intrinsic danger: that society can now write off certain people as defective, and possibly use this to write off societal wrongs.
Wanting to simplify the fluid relationship between genetics and environment is tempting; wanting to reduce homosexuality and bisexuality to static states of being puts this particular debate in the spotlight at the present. The danger lies in precisely not recognizing the political and social implications of these studies—without which makes them useless to society at this point in time (4). There are members of the gay community and others who react positively to the recognition that their lifestyle is not necessarily a personal choice, as many homophobes argue (2). And as I already mentioned, there are also those who use genetics to justify societal inadequacy and discrimination.
There are many "whys?" to the ongoing debate between proponents of the nature vs. nurture argument when it comes to sexual preference. What really are the benefits of ascribing particular behaviors that the status quo deems abnormal as attributable to genetics? I'm not so sure that scientists, sociologists, social activists, or anyone else should ever be allowed to work independently of one another; it seems that on all sides misconceptions abound regarding the outcome, the method, and even the motives of studies produced by those who fall on opposite or just different sides of the debate.
Researching this debate leads me to believe that all involved must work hard to not use ambiguous or socially constructed ideals and rhetoric. Until there is some agreement between the aforementioned, Daily Texan and other medias will continue to misconstrue the how and why of the nature vs. nurture debate. Until then, perhaps the obsession with "decoding" the human genome or utilizing social theory in this particular debate reveals something more important about our society than whether or not sexual preference is a choice: that humans today are too focused on the why and the how of society and not the what and for what good.
1)University of Texas Psychology Page, a short article from a local newspaper citing new and strange study
2)Bryn Mawr College Student Biology Page, good overview of major genetics of sexual orientation studies in last decade
3)Hampshire University Website, thoughtful and comprehensive discussion of genetics of sexual orientation
4)Frank Aqueno Website, an interesting but biased conversation between a famous professor/author and an gay rights activist
| Parkinson's Disease - the chances of a trembling b Name: Kornelia K Date: 2002-04-16 09:20:07 Link to this Comment: 1832 |
I have been closely following the news in the past months and I have noted a continuum in the coverage of the medical condition of one person who for many symbolizes the virtues of man, has been associated with the liberation of the minds of people under the communist era, has firmly supported the foundations of the Catholic faith and has been inspiration for many - the current Pope John Paul II. The newspaper photos of his almost expressionless face and the constant trembling hand which have started hindering his public activities and my deep respect to the his achievements made me look into the roots of the Parkinson's disease and its effects on behavior.
Parkinson's disease, or the "shaking palsy" as first defined by Dr.Parkinson in the early 19th century, is defined as a disorder of the central nervous system, affecting about 2% of the world's population. It is more common among older people and there is a higher percentage of men affected by it. (1)Cells in the part of the brain that control movement are lost, causing sometimes severe difficulty in performing movements with a variable intensity depending on the individual cases(2) The widely recognized symptoms include muscular rigidity, resting tremors, bradykinesia, inconsistency of posture, dementia. All of these symptoms directly or indirectly affect the patient's behavior. The symptoms only appear after the death of 80% of the cells which produce dopamine. (4) The loss of dopamine causes the nerve cells of the basal ganglia to fire out of control, leaving patients unable to direct or control their movements in a normal manner. Thus, the early diagnosis is very hard, especially in the sporadic cases. Early symptoms of the disease include a drop in energy or a loss of coordination, impaired handwriting, reduced arm swing, a tremor on one side of the body, soft voice, depression. (7)
The explanation of the processes in the nervous system, which lead to the distressing results of a completely changed lifestyle as well as behavior, is important for understanding the origins of the disease. For all movements/actions the body performs, the brain gathers information about the body position which comes together in the striatum. The striatum, in cooperation with the substantia nigra and other parts of the brain, sends out commands for balance and coordination. The substantia nigra produces dopamine, the neurotransmitter which is crucial to human movement and controlling of balance. In Parkinson's disease, there is a dying off of the nerve cells producing dopamine in the substantia nigra, resulting in a large loss of dopamine in the brain, which causes a disbalance in the dopamine/acetylcholine cooperation. (6)The effects are a lack of coordination of movements, manifesting through tremor, stiff muscles, difficult moving.
There appear to be two categories of the disease - the sporadic form which does not seem to be inherited and the non-sporadic or the familial form. For a long time the wide spread hypothesis had been that the causes were almost exclusively due to environmental factors, even though in many cases the exact environmental factor has not been pinpointed. However, in 1996 there was a breakthrough discovery which suggested that a genetic alteration is capable of causing the disease. (5)A gene mutation on a gene, called alpha-sunuclein, found on the so-called long arm of chromosome 4, was identified by studying a large Italian family which had a relatively high number of Parkinson's disease cases. (6)However, the symptoms of familial Parkinson's are identical to those in families with no history of the disease, except that sometimes the disease may develop earlier in life. (5) Additionally, the sporadic-form patients did not have the gene mutation. This demonstrated the fact that at least two types of Parkinson's disease, with and without mutation, exist at the molecular level. (6)
In terms of treatment, the most widespread way has been through medications, mainly concentrated on increasing the level of dopamine or mimicking the role of dopamine in the brain. As of this moment, there has been not found a way to stop the loss of dopamine. All cures have extended their function to slowing down the decline of the loss or of the function of the neurotransmitter. There is also the Pacemaker which is a wire surgically implanted within the brain, similar to the cardiac pacemaker. Patients can activate manually the device in the occurrences of tremors. The more drastic treatment involves surgical intervention whose long-term effects are, however, still questionable. The newest research advancements have shown that implanting pig embryonic cells, which are similar to human dopamine cells, into the brains of people with Parkinson's may help improve symptoms. (8)
While doing my research on the topic, I encountered numerous websites for consultation, discussion groups, chapters and support networks for people suffering from Parkinson's. While reading some of the testimonies of those people, I was shocked by the extent to which the disease has influenced their lifestyle, their relationships, and more generally their behavior. (9) Patients talk about the inability to relate to people, the incredible difficulty in keeping their old life, the motivation, the pursuing of personal interests. There is, apparently, a very drastic change in behavior, both in terms of the visible syndromes as well as the attitudes of the patients. This could very well serve as a clue towards our discussion of the relationship between brain and behavior. How can we account for such drastic alternations in people's behavior and disregard the direct dependency on processes in the brain?
1) Parkinson's disease: An Overview
2) Parkinson's Disease Society.
3) Parkinson's Information.
4) BBC Health News. , BBC News Agency with certain articles on current research
5) Research News.
6) Molecules of the Mind: Dreaming of Parkinson's. , interesting article
7) The Parkinson's Institute
8) An Active Web Resource for Parkinson's Disease Information
9) An Online Support Group for Patients
| Lasting Effects of Pain Name: Peffin Lee Date: 2002-04-16 09:29:35 Link to this Comment: 1833 |
Once upon a typical sunny day, Mary, Susie, and Jackie are jumping rope. Unbeknownst to them, as they chant their rhymes, Mikey and Kenny hide in the bushes planning a surprise attack. Just as Mary's little feet barely lift off the ground, the two boys leap towards the girls and push them into the dirt.
"Ouch!!!" they all scream as everyone hits the dirt.
Mary is up on her feet with her knees skinned and bleeding. A smile slowly crept on her face as she tried to hold back a chuckle.
"What's so funny?" asked Mikey, as everyone turned to look at her. "Aren't you supposed to get mad and chase us around?"
Mary shrugs and looks down at her knees.
"Doesn't that hurt?" asks Jackie.
So what exactly does Mary feel when she hurts her knees?
Pain, of course. But, how exactly does she experience it?
Well, inside Mary's tissues lie nociceptors. Nociceptors are specialized sensory nerves that are activated when there is a potential for danger, such as Mary falling to the ground. The stimulation of nociceptors, first, allows large-diameter, myelinated axons to carry rapidly conducted action potentials. This causes the sensation of a sharp, well-localized, pricking or cutting pain. It is then followed by a diffuse burning or aching pain caused by more slowly propagated action potentials that are carried by smaller, less heavily myelinated axons (1).
The action potentials are generated and conveyed to the central nervous system by way of a difference in electrical potential (2). When the threshold potential difference for each nocicpetor is reached, a signal is sent to the central nervous system. As the signal continues to travel to the spinal cord, the medulla, the thalamus, and then the cerebral cortex, it must pass through a series of gates (3). According to the gate theory of pain, the awareness of pain can only get to the brain by passing through a series of gates (Melzack and Hall, 1965). To open a gate, a group of small neurons that form a "pain pool" must reach their threshold. When it is reached, the signal is allowed to be sent higher.
So as Mary and everyone else who falls to the ground, their body is undergoing this awareness of pain.
Kenny is next to stand up.
"Owww, there's sand in my leg," he whimpered unhappily.
"Hey, you pushed us, and now you're crying?," said Mary defiantly, "You are the biggest crybaby ever!"
"I am not!" shouted Kenny.
"Yea you are, I heard your mom tell my mom yesterday! She said you always cry and scream when you fall down!" said Mary.
"That's not true!" said Kenny, "my mom always said I was a premium baby!"
"Premium baby? What's that?" asks Susie.
Jackie and Mary giggle.
"What's so funny?" asks Kenny.
Mikey takes Kenny's arm. "Let's just go home Kenny."
REWIRING OF THE NERVOUS SYSTEM
Up until the mid-1980s, popular belief was that babies did not experience pain. Even the International Association for the Study of Pain (IASP) defined pain in two criteria: "(a) it insists on verbal expression as the only authentic source of evidence for establishing any painful experience, and (b) it suggests that the experience of pain is learned from injuries in early life" (Narsinghani). This definition excluded non linguistic beings, thus allowing physicians to perform surgery on infants without anesthesia for many years. Since then, new studies have found that pain experienced by newborns may have lasting effects.
One such groundbreaking study led by neuroscientist M.A. Ruda of the National Institute of Dental and Craniofacial Research (NIDCR) at the National Institutes of Health (NIH) reported that painful stimuli delivered to rat pups shortly after birth permanently rewired the spinal cord circuits that respond to pain (4). Ruda and her colleagues began with two groups of rat pups. The first group was injected with an irritant (Freud's adjuvant) into the left hind paw when they were one day old, equivalent to that of a 24 week neonate in humans. The second group was injected at fourteen days old, equivalent to that of adolescence in humans. Both groups immediately reacted with shaking, licking of the paw, and occasional vocalization, shortly resulting in skin lesions persisting for 5 to 7 days.
About eight to twelve weeks later, the rat pups', now adults, spinal cords were stained with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to determine the pattern of nerve fibers. The dye stained the pain-sensitive axons and indicated any appearance of new axons formed. Ruda and her colleagues discovered that the rat pups, who received the injection at one day old, had an increase of about 25% more stained axons (5) in the left side of the dorsal horn, corresponding to the side injected. The dorsal horn is the layered structure in the spinal cord that propels pain signals up to the brain. In addition, several spinal segments exhibited an increase in density of axons, specifically the caudal segments.
The increase in pain-sensitive axons can be seen in the adult rats' behavioral response to pain. Once again, the adult rats were injected with an irritant in the left hind paw, then the paw was subjected to heat. The adult rats who had been injected at one day old were much quicker to withdraw their paw than normal rats. These results coincide with the mechanisms of pain. The increased number of activated axons, result in a more intense pain. This accounts for the lower pain threshold experienced by adult rats who had been injected.
The increased sensitivity of pain was only witnessed during a distinct developmental window (5), if the injection was given at one day old to three days old, more neurons are formed. But, as the rat pup increases in age to day fourteen, the physiological and behavioral changes match that of untreated rat pups.
Therefore according to this study, abnormal stimulation during a distinct developmental window can cause changes in the pain circuits. This leads researchers to study the effects of pain on premature infants because they are still considered to be undergoing basic brain development. In my continuing revision of this paper, I will investigate how intensity of pain affects development.
2) Information on Pain
3) Web paper Reference
4) Altered Nociceptive Neuronal Circuits After Neonatal Peripheral Inflammation
5) Neuroscience: Early Insult Rewires Pain Circuits
| OCD: What's in Control? Name: Lauren Wel Date: 2002-04-16 09:40:44 Link to this Comment: 1835 |
Obsessive Compulsive Disorder (OCD) is an anxiety disorder that is the fourth most common mental illness in the U.S. (8). OCD affects five million Americans, or one in five people (3). This is a serious mental disorder that causes people to think and act certain things repetitively in order to calm the anxiety produced by a certain fear. Unlike compulsive drinking or gambling, OCD compulsions do not give the person pleasure; rather, the rituals are performed to obtain relief from the discomfort caused by obsessions (2). OCD is more common than schizophrenia, bipolar disorder, or panic disorder, according to the National Institute of Mental Health (6). This disorder can be therapeutically treated, but not cured. The causes of OCD are not completely understood, and warrant further exploration of self-control and autonomy.
There are many branches or types of OCD. Within all branches, ninety percent of people suffer from both obsessions and compulsions, rather than solely one or the other (1). One category of OCD sufferers tend to check and recheck items from 10-100 times - such as a locked door. The overwhelming impulse to recheck remains until the person experiences a reduction in tension despite the realization that the item is secure (1). OCD sufferers also tend to habitually wash due to fear of contamination. Another form of OCD is hoarding, which is excessive saving of typically worthless items such as shoes or computer disks due to an overwhelming fear that one day these items might be of use. People who suffer from the ordering branch of OCD, feels compelled to place items in a designated spot or order to alleviate worries of disorder and mayhem. Pure-O sufferers are those people who grapple with unwanted and unethical thoughts. They tend to be superstitious and compulsively do problem solving in order to control their thoughts. OCD sufferers can also be subject to hyperscrupulosity, which involves extreme worry and anxiety for the safety of others. Another form of OCD is body dysmorphia. This is a condition where people become excessively focused on some body part which they perceive to be grossly malformed (1). Hypochondriacs -people who have an extreme fear of sickness - fall into this category of OCD. General behaviors that may indicate OCD are: excessive washing, repeating, checking, touching, counting, ordering/arranging, hoarding, or praying (2). OCD patients live in a vicious cycle. They have obsessions about certain things and cause anxiety. To relieve this anxiety, compulsions are performed, and then attention can be paid again to the obsessions that have not truly been alleviated. The difference between OCD sufferers and other people, is the OCD sufferers use up at least an hour of their day thinking or doing these incessant tasks and they interfere with the person's work, social life, and relationships (2).
If OCD is found in conjunction with another disorder, it is usually found with a ticking disorder or depression. Ticking is involuntary motor behavior that results from a feeling of discomfort (much like the compulsions of OCD), and depression usually is exemplified from the person's disappointment or shame for having the OCD. Sixty to ninety percent of people with OCD have suffered from at least on major episode of depression at some point in their lives (3). However, OCD is usually easy to distinguish from schizophrenia, delusional disorders, and other psychotic conditions because unlike psychotic individuals, people with OCD continue to have a clear idea of what is real and what is not (4). Eighty percent of people with OCD are painfully aware that their behaviors are unreasonable and irrational (1). A person with OCD, in eighty percent of cases, is conscious that their actions are not normal, and cannot stop them. The person seems to be suffering from a separation between self and behavioral instincts. Their self is no longer in control of their actions or thoughts, is this separation possible? What is the purpose of the 'self,' the person, in patients with OCD if they have lost control over their mind and body?
In order to better understand the changes that have overcome a person with OCD, it is helpful to analyze what is going on in their brains, even though there is no single cause for OCD. OCD involves problems in communication between the orbital cortex, the front part of the brain, and the basal ganglia, deeper structures. These parts of the brain are used in motor control, and have been found in OCD patients to have impaired inhibitory mechanisms. The inhibition is shown by lower levels of synchronization of the prefrontal area and basal ganglia after simple self-paced movement, and may extend the concept of reduced inhibition in OCD patients to refrain from performing impelling actions (9). These parts of the brain use the messenger seratonin, and when there are low levels of seratonin, the symptoms of OCD increase. When there are high concentrations of seratonin, the communication between these two areas of the brain involved in processes that in some way mediate OCD behaviors is increased, and the symptoms of OCD decrease (2). Drug therapy is one answer to OCD. Medicines that function as seratonin reuptake inhibitors are most affective at relieving the compulsions of OCD patients. The purpose is to increase the availability of seratonin in the synapses of the brain so that the orbital cortex and basal ganglia can communicate more efficiently. If OCD is treated by a drug that acts as a selective seratonin reuptake inhibitor (SSRI) the symptoms of OCD typically decrease from forty to ninety-five percent (3).
An overly sensitive amygdala, the small portion of the brain stem that responds to emergency circumstances, is also thought to play a large role in OCD patients. Brain mapping studies tests were used on OCD patients. The brain activity of the amygdala increased dramatically when an OCD patient was presented with a 'stressor' or a fear that would provoke a habitual compulsive response to mediate and relieve that fear (8). Because OCD patients have a heightened response to emergency situations, the innate response to seek a soothing and relieving action or thought is made. The OCD patients find relief from their overly active emergency response by habitual and calming compulsions. Because the amygdala is not involved in cognitive and rational abilities, not responding to obsessive thoughts can only be learned by contradictory, repetitive acts (8). This is one form of cognitive behavioral therapy (CBT); it is called exposure and response prevention (E/RP) (7). The person suffering from OCD is presented with his/her fear and is forced to inhibit their usual, calming response. The OCD patient could be made to rub their hands on the floor before eating a sandwich to prove to them that their fear of germs is irrational and does not really cause sickness or death. The person clearly can understand that his/her fears are superfluous and uncalled for, but they cannot control their response or fears. The I-function, therefore, cannot be involved in the human's response to fear, fright, or anxiety, except through learned responses. Can the I-function and the self 'teach' more primal parts of the brain to act differently?
Another form of treatment given to OCD patients is cognitive therapy (CT), which is usually paired with E/RP. CT helps to reduce the catastrophic thinking and exaggerated sense of responsibility often seen in OCD sufferers by challenging the inaccuracy of faulty assumptions in the person's obsessions (5). The first thing that OCD patients are taught in CT, is to understand that they are not crazy even though they are troubled by so many thoughts and actions that they know are inappropriate (8). The patients with OCD are taught to say, "It's not me, it's my OCD," or "It's not me, it's how the natural brain works." Usually when a person does not, and thus cannot, control a behavior then they are unaware of the processes underlying that behavior. We are not conscious of the blind spot when our brain 'fills in' the empty area created by the blind spot, and thus have no control over our blind spot. However, OCD patients are aware of their brain's autonomous control over their behavior that causes obscure actions and thoughts that are typical of OCD patients. The I-function is not involved in the blind spot, but is it or is it not involved in OCD behaviors? How can the OCD patient be aware of what is going on, but not be able to control himself? Surveys show that eighty percent of the American population experiences violent and upsetting thoughts, which are speculated to occur due to automatic associations produced by the brain (8). Can we control any of our thoughts? Are we all as helpless as OCD patients, but we just are upset by this fact to a lesser degree than OCD patients seem to be? The OCD sufferers are shown that everyone has abnormal, strange thoughts, but that OCD sufferers accompany these thoughts with incredible anxiety. CT attempts to make the person understand that giving into an obsessive response increases the brain's sensitivity to the threat that caused the obsessive response, thus creating a negative affect on the persons ability to create a determination in avoidance of relief seeking, obsessive behaviors (8).
OCD is present in many people, 5 million in the US, all to differing degrees - to what degree is relevant? When does OCD behavior become a factor in one's life and personality? Although OCD is not completely understood, and the treatments are not one hundred percent accurate, there has been a majority of decreased suffering after treatment. In one form of treatment, OCD patients are taught to "discover the ability to make their own choices" by understanding that they can successfully ignore obsessions (8). Doesn't the I-function involve "choices," which would implicate that OCD patients are not able to have full use of their I-function? If the I-function seems to be aware of OCD behavior, but has no control, what implications does this have on our understanding of the I-function and autonomy? How much control DO we really have?
1)What is O.C.D.?
2) Obsessive Compulsive Foundation-What is OCD?
3) Most Frequently asked questions about OCD
4) Obsessive Compulsive Foundation, related Disorders
5) Obsessive Compulsive Foundation-How is OCD treated?
6) OCD and Tic Disorders
7) A Cognitive Therapeutic Differentiation Between Conceptualizing and Managing OCD
8) Obsessive Compulsive Disorder: OCD
9)Letizia et al. 2001. Abnormal Pattern of Cortical Activation Associated with Voluntary Movement in Obsessive Compulsive Disorder: an EEG Study. American journal of Psychiatry. 158: 140-142.
| Video Game Addiction: Do we need a Video Gamers An Name: Mary Schli Date: 2002-04-16 09:55:17 Link to this Comment: 1836 |
Super Mario Brothers, Sonic the Hedgehog, and Street Fighter are familiar names to nearly all of us. They are all best selling games of major video game consoles. Over 9.8 billion dollars were spent on video games in the United States during 2001 alone, and video game consoles are present in 36 million homes in the United States (1). With the increasing amount of time that people are spending on video games, one is left to wonder if it is possible to become addicted to video games. Do we need a Video Gamers Anonymous?
Addiction has been defined as "A primary, chronic disease, characterized by impaired control over the use of a psychoactive substance and/or behavior. Clinically, the manifestations occur along biological, psychological, sociological and spiritual dimensions (2)." While there is currently no category for video game addiction in the Diagnostic and Statistical Manual of Mental Disorders (3), which is the manual utilized to diagnose psychological disorders, video game addicts are often described by clinicians in the field as displaying many symptoms characteristic of other addictions. These behaviors include failure to stop playing games, difficulties in work or school, telling lies to loved ones, decreased attention to personal hygiene, decreased attention to family and friends, and disturbances in the sleep cycle (4). Withdrawal symptoms can even include behaviors as severe as shaking (5).
All addictions can be dangerous and harmful to the addicted person and others around him; however, video game addiction can be particularly detrimental to children. Video games are becoming increasingly popular with children of young ages, which in turn may raise the likelihood that these children will develop addictions to video games. Furthermore, playing violent games may be associated with a tendency to behave more aggressively, although the data are inconclusive about the cause and effect nature of this relationship (6). In a study by Irwin and Gross, children who played a violent video game displayed a higher level of aggression than children who played a nonviolent game (6). Similarly, in a study by Calvert and Tan, college students who played a violent video game reported more aggressive thoughts after playing the game than college students who played a nonviolent game (6). Although several researchers advocate the position that video games cause violent behavior in children and adults, there are also many researchers who support the opposite belief, which is that video games purge one's desire to act violently and thus reduce the amount of violence in which a person will engage (5). Other detrimental effects of video games include taking time away from a child's studies or homework and decreased social skills (5). Finally, despite possible detrimental effects of excessive video game playing, there are benefits to playing video games in moderation. For instance, video games may improve spatial abilities, the ability to create and apply multiple strategies, and may help develop critical analyzing techniques (7). Due to the nature of video games, psychological, social, and neurological factors have all been associated with excessive video game playing.
The psychological cycle of substance addiction and other maladaptive behaviors can be applied to video games as well. A person playing a video game feels an emotional high, commonly known as an adrenaline rush, as a result of his gaming tactics (8). He then plays the game more and pushes his physical and psychological limits in order to experience the emotional high. Eventually, he will again reach a level that stimulates the production of adrenaline. The cycle may continue until it leads to an unhealthy level of interaction with video games, which some professionals may label video game addiction. Even famous psychological effects such as the sunk cost fallacy can influence the addictive cycle. This fallacy occurs when a person feels compelled to continue performing a certain behavior because he has previously invested time in the behavior and does not want to feel as though his investment was wasted (9). Similarly, Dr. Timothy Miller, a clinical psychologist, states that many video game players may feel that they have wasted their efforts if they do not reach the next goal in a game, which may lead to additional time spent playing the game that the person otherwise would have spent in a more constructive task (4).
According to Dr. Orzack, the Director of Computer Addiction Services at McLean Hospital, social pressure or lack of social skills can also lead to video game addiction (4). Dr. Orzack suggests that many video game addicts have struggled with finding their place in society and as a result play video games in order to become part of a crowd. The players then may feel compelled to reach the next level of achievement in the game in order to flaunt their abilities in front of their peer group (4). While these social effects are important to consider when investigating the development of excessive video game playing, it is equally important to discuss the neurological effects as well.
Not only can excessive video game playing cause behavioral and social changes in a person, but it can also result in neurological changes as well. A recent study utilized positron emission tomography in order to show that levels of the neurotransmitter dopamine increased while playing video games (10). Dopamine is believed to mediate several behaviors, one of which is the experience of pleasure. For example, dopamine levels increase in emaciated rats when the rats are presented with food, and similar effects are found when water deprived rats are presented with water. Despite the positive effects of dopamine, high levels of the neurotransmitter have also been associated with addictions to drugs and substances (11). Because increased levels of dopamine have been found in people who are playing video games and because these effects are similar to the increased levels of dopamine in drug addicts, some researchers have hypothesized that higher levels of dopamine can produce a dangerous cycle leading to addiction of video games (11). However, because this research is fairly novel, studies replicating the data are necessary. Furthermore, the possibility of involvement of other neurotransmitters during video game play should be explored since it is possible that multiple neurotransmitters may interact in addictive behaviors. Finally, because this area of research is fairly new, many interesting questions can be raised. For instance, does excessive playing of video games cause a fundamental and permanent change in the dopamine system? If so, what are the subsequent effects on the pleasure systems of these individuals? Do these people require more dopamine to be released as a result of a decreased sensitivity to dopamine that was caused by the excessive play, in a way similar to other addictions (10)? If future studies demonstrate these patterns, and if they are considered in unison with the psychological and social ramifications of excessive video game playing, it can be concluded that the video game addiction can and does exist. In that case, the answer to the initial question of "Do we need a Video Gamers Anonymous?" is most certainly yes.
1)Assorted Gaming Statistics, A good reference for game statistics
2)Definitions in Addiction Medicine,
3)Computer and Cyberspace Addiction,
5)Video games: Cause for concern?,
6)Video games: Research, ratings, and recommendations, Contains many references for empirical studies
8)Are video games really so bad?,
10)Positron Emission Tomography ,
11)The Biochemistry of Human Addiction, Discusses the role of dopamine in addiction
| The Medicinal Marijuana Debate Name: Cassidy Ga Date: 2002-04-16 13:17:40 Link to this Comment: 1839 |
For years research groups, certain state governments, pharmaceutical companies and even some physicians have battled with the federal government over the legalization of the marijuana plant for medicinal purposes. Large amounts of research have been devoted to both sides of the argument; however, many of the studies contradict each other when naming the benefits and risks of marijuana. How can we decide whether the therapeutic values of marijuana outweigh the hazards of the drug when there have been no definitive findings? First we must review what is known about marijuana, such as how the chemicals in it affect the body, and then pick which study results seem more scientifically sound.
For over 4000 years and in many different cultures, marijuana has been used medicinally for pain relief and treatment of many ailments. These ailments include digestive disorders, hemorrhaging, congestion, asthma and insomnia. The drug has been administered orally, topically and through inhalation. It was not until 1937 that using marijuana became a federal offense with the introduction of the Marijuana Tax Act ((6)). Today, marijuana is classified as a Schedule 1 drug, which defines it as "highly addictive with no medical usefulness"-the same definition given to heroin ((4)).
The opioids in heroin and the cannabinoids in marijuana are used similarly by the brain. They either bridge synapses in the brain so that messages can be transmitted, in which case they are acting as agonists, or they block the agonist's binding site so that messages cannot be transmitted across synapses. In the latter case, the cannabinoids or opioids are acting as antagonists ((3)).
Cannabinoids and opioids do not cause identical effects, however. There is a naturally occurring chemical in the brain called anandamide, which is very chemically similar to the cannabinoids in marijuana. Anandamide triggers certain nerve receptors that are involved with pain control, memory and cognition, motor functioning, nausea and vomiting, and internal eye pressure ((7)). Therefore, it is not surprising that in many studies marijuana has been found to:
1) Ease nausea and vomiting while stimulating the appetite;
2) Reduce pain;
3) Relieve intra-ocular pressure in glaucoma patients;
4) Control muscle spasms, which has proven helpful to sufferers of spinal cord injuries, Parkinson's disease, multiple sclerosis and Tourette's syndrome ((2), (6)).
Do the risks of using marijuana prevail over all of these supposed benefits? The federal branch of the Drug Enforcement Administration issued a statement containing the arguments behind why the government opposes medicinal marijuana. According to the DEA, marijuana is highly addictive, usually serves as a "gateway drug", weakens the immune system and causes cancer ((4)). But how can we believe all these statements when the government lists very few sources for their data? One study conducted by the United States concluded that marijuana smoke may lead to cancer by causing abnormalities in the cells that line the lungs. Although this verifies one of the DEA's claims, the study also claimed that dependence on the drug is rare. The same study found no evidence for the argument that marijuana is a gateway drug; actually, the research states that the true gateway drugs are common legal substances, namely, tobacco and alcohol ((1)).
Other arguments against using marijuana medically often concern the fact that if it were legalized, it would be the only prescribed drug that would have to be smoked. Scientists are attempting to discover the chemicals and cannabinoids in marijuana that lead to positive medical results. They hope that these chemicals can be isolated and administered in other ways ((3)). So far, the only legal alternative to marijuana is the synthetic version of THC, Marinol, which is taken in pill form. Marinol, however, has its own disadvantages: First, absorption of a pill takes much longer than absorption of inhaled smoke, too long to be of much use to nausea sufferers. Also, Marinol causes more severe psychoactive effects than marijuana. And who wants to pay 500 to 900 dollars a month for Marinol when marijuana can be grown free of cost ((5))?
It seems as if the only source that provided entirely negative information on marijuana was the federal government. Is there any way our leaders can compromise with advocates of medicinal marijuana? What should be done about the situation? I think that more studies should be done on which chemicals in marijuana cause which reactions in the body. Also, I think that it should be determined whether the rare instances in which people become addicted to marijuana are physical addictions or psychological addictions. If it is discovered that the addictions are merely psychological, what is the difference between marijuana and most other drugs? Almost anything can be psychologically addictive. Finally, from what I have read, most results seem to show that marijuana could easily be reclassified as a Schedule II drug, which would allow it to be used as medicine but with severe restrictions. Why deny ill people almost definite relief?
.
1) Marijuana and Medicine: Assessing the Science Base
2) Medical Marijuana: full analysis of the Institute of Medicine's commissioned report
3) Scientific American: Healing Haze?
4) Drug Enforcement Administration: The Medical Myths of Marijuana
5) ARDPArk, Inc.: Synthetic THC/ Marinol
6) Why all the controversy? What does the research actually show?
| The Percept of Pain: Where does it come from? Name: Raquel P. Date: 2002-04-16 14:17:31 Link to this Comment: 1840 |
In class we have discussed the concept of pain, concluding that a conflict between what the brain anticipates occurring and what actually occurs has the potential to cause the perception of pain. Furthermore, it was suggested that genetics might have a role in the experience of pain, particularly when applied to the discussion of phantom limb pain. However, I found these inferences a bit unsatisfying and walked away with more questions than answers. Where does chronic pain come into the picture? Why is a stimulus that is painful for one person not for another? And the question that puzzled me the most: how, from a neurobiological perspective, can an individual experience pain in her arm if she was born without one?
Pain, a component of the somatosensory system, is defined by the International Association for the Study of Pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" (1). The perception of pain serves as a defense system to maintain homeostasis, warning of injury that should be avoided and/or treated. Injured limbs actually inhibit voluntary movement to promote necessary healing processed (2). So essential is the painful response that those individuals born with congenital pain insensitivity do not react to pain, often resulting in severe, permanent tissue damage, and even premature death.
A crucial concept in the definition of pain is that it is indeed a perception, therefore involving the brain's rumination and elaboration on corresponding input. This may be paralleled to another sensory perception, vision. Although the optic nerve head should cause a "hole" in an individual's sight, no discontinuity is appreciated; the brain evaluates the environment surrounding the hole and produces the most appropriate continuous image. Likewise, there is the possibility that the nervous system's influence can change aspects of pain.
What is happening during a painful experience? Two classes of pain have been delineated: nociceptive pain and neuropathic pain. The latter division involves only direct injury to nerves in both the central and peripheral nervous systems. Tissues containing specialized sensory receptors, called nociceptors, are activated by noxious stimuli and have been discovered to exist in almost all multicellular animals on Earth, as well as in some bacteria (2). Nociceptors are most abundant in superficial areas of the skin, joint capsules, inside the periostea of bones, and around vessel walls (3).
Although nociceptors are involved with pain perception, stimulation of a nociceptor does not invariably result in a painful response. Unlike other sensory receptors, nociceptors become increasingly sensitive with continued stimulation. Damaged tissue releases prostaglandins and leukotrienes, chemicals that sensitize nociceptors (4). These nociceptors respond to stimuli that would not normally be interpreted as painful (this is sometimes called allodonia). For example, sunburn pain is exacerbated by a gentle touch or breeze due to the hyperactivity of the nociceptors. Aspirin and similar drugs reduce sensitization by inhibiting the production of prostaglandins (5).
Three types of nociceptors have been classified: A delta (I and II), medium-diameter cell bodies with lightly myelinated axons, and C fibers that have small-diameter cell bodies and non-myelinated axons (4). The myelinated A delta fibers conduct impulses faster and thus communicate with the brain sooner than the C fibers. Further categorization of identifies nociceptors as mechanical, thermal, and polymodal. Mechanical nociceptors involve the activation of A delta conducting at 5-30m/s fibers during the experience of intensive pressure. Likewise, thermal nociceptors are activated by extreme hot or cold temperatures (>45°C or <5°C), and also involve thinly myelinated A delta fibers. Polymodal nociceptors are activated by high intensity mechanical, chemical, and thermal stimuli, involving non-myelinated C fibers. All classes of nociceptors are present on skin and tissues and work together in forming the pain response. For example, one may initially experience a feeling of "sharp" pain when hitting their thumb with a hammer, proceeded by a prolonged "aching." The first pain occurs when A delta fibers transmit information from mechanical and thermal nociceptors to the brain. C fibers transmitting polymodal nociceptors are responsible for the later, prolonged aching experience (6).
A delta and C fibers travel through the pain gate and synapse with other nerve fibers in the marginal layer (lamina I) and the substantia gelatinosa (lamina II) of the superficial dorsal horn (6). The fibers then release a neurotransmitter, substance P, into the synaptic cleft, sending an impulse up to the thalamus. The thalamus then sends two signals; one to the cerebral cortex and one back to the original location of pain to inhibit nociceptors from transmitting further unnecessary pain impulses. The signaled cerebral cortex considers the tissue damage and transmits messages to both the limbic system and the autonomic nervous system (ANS). The limbic system functions to increase or subdue pain by controlling the individual's emotional responses. Blood flow, pulse rate, and breathing are moderated by the ANS, therefore ANS assistance helps to provide an ideal environment for damaged tissue restoration (4).
Chemical messages transmitted by hormones also influence conduction of pain signals to the brain. The previously mentioned prostaglandins increase the frequency of impulses in addition to sensitizing nociceptor nerve endings. Substance P stimulates nociceptors at the site of injury to intensify the incidence of pain sensation. For pain reduction, the hormones Serotonin and Norepinephrine are released to promote the liberation of endorphins by nociceptors (4). Thus, by the release of hormones both an individual's pain experience and perception are altered. This leaves additional room for variation in such experience among people.
As mentioned above, A delta and C fibers travel through the pain gate before any further signal transmission occurs. The gate control theory of pain was presented in 1965 by Melzak and Wall, and has crucial implications for the painful experience. The "pain gate" is positioned in the dorsal horn at the base of the spinal cord. It serves to screen nerve impulses; the majority of impulses from a certain class of fiber are permitted to travel through the spinal cord and to the brain. For example, if touch/pressure impulses (A delta I fibers) outnumber painful impulses (A delta II fibers), then only the touch/pressure impulses are received by the brain (7). This is why intensely massaging a pain site tends to reduce the perception of pain. Acupuncture works similarly. By applying strong pressure to a very localized site, pain signals will not successfully pass through the pain gate and hence little or no pain is perceived by the individual (4).
Having explored the conventional explanation for pain, I was more comfortable with how variations among persons can exist in their perception of pain. However, the idea of phantom limb pain still eluded me. Under the conventional pain theories, phantom pain is explained by central sensitization of dorsal horn neurons. Some noxious conditions are severe and persistent enough to cause prolonged stimulation of C fibers, also eliciting a progressively more intense response from the dorsal horn neurons. Long-term changes in dorsal horn neurons result, altering the biochemical properties and excitability of the neurons (3). Changes at the molecular level are thought to involve modification of the genetic transcription of neurotransmitters and receptors (8). These alterations are responsible for spontaneous pain events evidenced by amputees. It is proposed that the insult of the surgical procedure triggered a central sensitization state in an individual's dorsal horn nerves. Also, chronic pain may be attributed to a similar process of neuronal hypersensitivity (3). One study on phantom limb pain examined the MEG map differences from a cohort of amputees. It was concluded that an appreciable degree of somatosensory cortical reorganization was evident and should be considered (9).
Although this explanation sounds feasible, it does not explain why individuals having been born missing a limb experience phantom pain. The nervous system is not responding to, or has been altered by, a devastating surgical procedure. Yet the individual relates not only pain and movement experiences, but also acknowledges a persistent sense of spatial position of the missing limb (7).
I discovered a paper written by Ronald Melzak, one of the "pain gate theory" formulators. He was similarly frustrated by the existing explanations for phantom pain and explored the possibility of an entirely revised system for regulation by the nervous system. Other neurological research has not able to assign the perception of pain to a specific part of the brain. In fact, so many sensory and cognitive processes are involved in perception that it is almost irrefutable that the majority of the nervous system must be related to the full perceptual experience. Using data from the evaluations of paraplegics with spinal cord sections and individuals suffering from phantom pain, Melzak concluded that the body we feel (the "body-self" identity) and the phantom limb are regulated by the same neural pathways. Furthermore, the qualities we associate with the body, including pain, are also experienced in the absence of sensory inputs from the body (7). Melzak is proposing that the origins for patterns of basic experiences are generated in neural networks in the brain; these patterns are intrinsic to the brain. Therefore, stimuli do not cause these pre-existing pattern generators, but rather initiate the activation of them. It would not be necessary to possess a body to experience one.
Melzak coins the term "neuromatrix" to explain a possible mechanism for pattern generation and the nervous system's interaction with the environment. The neuromatrix refers to a function that is continuously aware of the entire body, producing a feeling of unity. Although millions of nerve impulses are hitting the nervous system each moment, it is essential for the sense of body to be maintained. Details from inputs are integrated into the neuromatrix as they arrive, allowing for continual revision, and inputs are analyzed and synthesized to produce appropriate responses. Using this logic, it can be inferred that commands originate in the brain and actually produce experiences. This may explain why amputees suffer genuine fatigue from the experience of persistent bicycling movements, or amputees relate the feeling of pain from clenching an imaginary fist (7). Unfortunately, there exists no delineated cure from chronic pain and phantom pain; the neuromatrix involves many parts of the brain and it is possible that these pattern generators cannot be mechanically altered without causing disturbance of deeper levels of perception.
The implication that a brain can generate perceptual experience without first acquiring input is provocative to say the least. However, the same phenomenon has been accepted when discussing the absence of a blind spot in vision. Can we attribute enough authority to the brain to suggest that it controls our experiences? Should pain now only be defined in terms of perception and not physical injury? It think this theory should be explored and may be useful in understanding the human perception of reality in general. Although typically cynical about notions that are not physiologically observable, I am surprisingly excited by the idea of a neuromatrix and look forward to rethinking my pervious understandings of the nervous system's workings. It may be interesting to see how the I-function is involved with this process and why pain treatments such as biofeedback have been known to produce positive results.
1) Journal of Physiology , An article on the Journal of Physiology website.
2)Chronic Pain Solutions, A paper on the etiology and treatment of pain.
3) Kandel, Schwartz, and Jessel. Principles of Neural Science, 4th Edition. New York: McGraw-Hill, 2000.
4)Pain Receptor Anatomy, The introductory page of a website discussing neurobiological basis for pain.
5)Brain Briefings, An excerpt from the Society of Neuroscience web page discussing nociceptors and pain.
6)Nociceptors, A paper describing the molecular identity and function of nociceptors.
7) Pain: Past, Present, and Future. , An article published by Ronald Melzack.
8)Pain, A general website discussing the causes and treatments of pain.
9)MEG Research on Pain, A research piece discussing MEG and pain.
| Speaking From Within: A Discussion on Our Innate A Name: Cindy Zhan Date: 2002-04-16 14:23:39 Link to this Comment: 1841 |
For years since I moved to the United States after the age of nine, I've always been frustrated at the lack of improvement in my ability to speak English without a trace of foreign accent and my ability to write without any grammatical errors. It always seemed to me that learning languages is unlike learning anything else, I can logically understand the pronunciation of the a word or the rules of grammar, but for reasons unknown, I always found it hard to incorporate logical knowledge of language into the actual speaking and writing of English. I started to surf the web in attempt to find the reasons to why, even after spending more than half of my life in the U.S, I still cannot speak and write as well as people who were born or came here at a much younger age.
At first I though the answer would be something to the extend of finding a region of the brain that is specialized for the learning of languages and that region is more developed in people other than I, who are good at linguistics. However, it turned out that the answer entails more than specialized regions in the brain, while there are regions in the brain that are specific for processing languages, what I found more interesting is that there is much evidence that supports the selectivist theory, found by Noam Chomsky that the ability to learn language is innate. Here innate means that ¡°the language template is pre-organized in the neuronal structure of the brain, so that the fact of being an integral part of a given environment selects the borders of each individual neuronal structure without affecting its fine organization, which pre-exists.¡± (1) In this paper, I wish to point out evidence that supports this theory of the innateness of language, and to exam how the language template develops. In conclusion, I wish to gain a better understand of my own language learning process in light of these new findings.
One evidence that points to the innateness of language is the accuracy and speed at which humans process language and the accelerating rate at which children acquire language. ¡°¡ the average speaker produces approximately 150 words per minute, each word chosen from somewhere between 20000 and 40000 alternatives, at error rates below .1%. The average child is already well on her way toward that remarkable level of performance by 5 years of age, with a vocabulary of more than 6000 words and productive control over almost every aspect of sound and grammar in her language.¡±(2)Therefore, unlike learning of other things, which depends on the firing of neuron to make connections, the connections for the learning of language already exist before humans are expose to language through their environments, which accounts for the accuracy of processing language and the speed of acquisition of language.
One particular supporter of the selectivist theory, Bob Hadley, who is a professor of computer science at SFU, incorporated the Chomskian view that an innate structure of language exist in our brains and constructed a model of language learning systems which contains explicit, conceptual structures in the brain that are specifically there to enable language learning.(3) His system is a clear improvement upon the model made by connectionist- researchers who use computerized neural networks (computer programs that try to replicate the connections between neurons in a human brain.) The neuron networks learn languages without pre existent structures, it is based on the believe that ¡°language is built up constantly from a continuous interaction with a well-structured environment.¡±(1)
The model designed by Hadley works more like the natural language learning system in humans in that, unlike the connectionist models, which uses the same word in the one grammatical context, Hadley¡¯s model demonstrates strong semantic systematicity-the ability to generalize use of the same word in many different grammatical roles which is unique to humans. Take the noun ¡°cat¡± for example, the connectionist model can only recognize cat as a subject as in ¡°the cat chases the mice.¡± However, if ¡°cat¡± is used as an object as in ¡° I am looking for the cat.¡± The connectionist model would fail to recognize the word where as Hadley¡¯s model would not. This computer model experiment demonstrates more concretely the validity of the selectivist theory.
So how does the innateness of language account for my lack of improved proficiency in English? It turned out that language learning has a critical period. During the acquisition of language, the brain goes through ¡°pruning¡± of unnecessary connections as language development takes place. In other words, the neuronal synaptic connections are not created, or built as we learn language: they pre-exist: unnecessary ones merely decay as language learning takes place.(1) As a result of this pruning period, the ability to learn language fluently decreases with age. Young children deprived of languages acquire language fully if learning takes place before puberty. If after puberty, they are very inept at language.(4) ¡°Among Chinese and Korean children who have immigrated to the United States there is a linear relationship until puberty between the age of arrival and proficiency in English.¡±(1)
Alas, this is the answer to my question. Because the ability to learn language is innate and it has a critical development period before the puberty age, when I arrived at the United States, perhaps the innate structure in my brain had already begun its regression in acquiring languages. The language template within my brain had been filled with the Chinese language, it had already gone through most of the ¡°pruning¡±, meaning it had strengthened the neuronal connection needed for the Chinese language and gotten rid of the ones that is not needed for learning other languages. The quote in the previous chapter about the age of arrival and proficiency in language, support my speculation about the difficulties in attaining language proficiency after a certain age. Because I arrived just a little bit before pre teenage years, while there is still room to learn another language, the ability to learn language had already begins its stage of decline and therefore, acquisition and proficiency of the English Language does not come easily for me compared to immigrant children who came to this country earlier than I.
Of course knowing that the structures for learning languages pre-exist within our brain is only the first step to understanding how our brain processes languages. While I gained a basic understanding of the innateness of the ability to learn language and how it accounts for, to some degree, my struggles in achieving proficiency of English, there is still a lot to learn about the structures of the language-learning template. From researching the broad topic of brain and language, I also learned about the lateralization and localization of language on the brain. Even though it would take another web paper to elaborate on these two topics, writing the this web paper is a good start because while there is a lot to learn about how the brain functions specifically in response to language, knowing that the innate structure exist for the acquisition of language is a start for understanding how language is processed in our brains.
References
(1)The Biological Foundations of Languages, An extensive site about neurobiology of Language
(2)On the Nature and Nurture of Language,A detailed research paper
(3)Is Language Innate or Learned ,An artical about language learning computer models
(4)Higher Cortical Function-Language,An introduction to Language and the brain
| Neurobiology of Human Sexuality Name: Tania Rome Date: 2002-04-16 15:39:40 Link to this Comment: 1842 |
Tania Romero
Neurobiology of Human Sexuality
Human sexuality is a topic that has been taboo for many centuries. The orgasm, for example, is one aspect of sexuality that has been overlooked. In particular, the female orgasm is an important function to address because it's a subject that has been socially steeped in silence and shame, and is directly connected to female health in general. Not many people are willing to admit, that orgasms actually benefit a woman physically and psychologically in many ways (i.e. easing menstrual cramps to alleviate stress). One mystery about the female orgasm is why some women "fake" orgasms during sexual activity. One thing that is for sure, is that even though the male orgasm is reached quicker, the female orgasm is capable of repeated pleasure. Why do so many women have difficulty experiencing an orgasm and why do men climax so fast? Interestingly enough, most women will confess that their partners do not give them orgasm. Instead, they allow themselves to have orgasms. Not only that, but they can have a variety of different types of orgasms at the same time. (i.e. clitoral orgasms, G-spot orgasms, vaginal orgasms, ejaculatory orgasms, blended orgasms, etc). Men will comment for example, that the scent of a woman is what drives them crazy during sexual activity and makes them unable to hold the sensation for long. So do women have more control over physical pleasure in the brain than men? How do sexual problems happen in the brain?
There is a combination of things that come in effect when it comes to an orgasm in the brain. Neurotransmitters, and neuro-peptides for example, are heavily involved in the sexual response. To reach an orgasm, the central nervous system sends orders to the heart, so that it pumps faster, sending blood to oxygenate the increase of blood flow in muscles involved in sexual activity. Nitric oxide, serotonin, dopamine, epinephrine, and norepinephrine, are just a few of the neurotransmitters and neuro-peptides involved in sexual activity. Nitric oxide (NO) plays a critical role in both male and female sexuality. In penile erections, NO stimulates the release of guanylate cyclase, which, in turn, converts GTP to cGMP and produces relaxation of smooth muscles and increased blood flow into the penis. This information is used in the popular drug sildenafil (ViagraTM) that inhibits the metabolism of cGMP to prolong the effects of the erection. (1) Serotonin's role in sexual function is that of constriction of smooth muscles in the genitals, and peripheral nerve function. Epinephrine appears to be involved in maintaining the penis in a flaccid state. This increases the rate and force of the muscle's contractions during sexual activity. Conversely, in women, epinephrine has been shown to increase vaginal pulse amplitude. Norepinephrine is another neurotransmitter that mediates chemical communication in the sympathetic nervous system, a branch of the autonomic nervous system. Like other neurotransmitters, it is released at synaptic nerve endings to transmit the signal from a nerve cell to other cells. Levels in the brain of neropinephrine vary according to sexual arousal. They increase significantly with arousal and sexual activity in men as well as in women.
Hormone levels are also involved in sexual activity. In males, testosterone levels remain generally above the threshold required for sexual interest and activity. Thus increases testosterone above this threshold are believed to have additional influences on sexual interest or behavior. Interestingly, estrogen(the "female hormone") seems to have little impact on sexual desire on either males or females. Estrogen deficient women, however, can cause a decrease genital lubrication caused by the thinning of the vaginal epithelium. All factors can impair both the physiological and psychological aspects of sexual arousal. (2)
Other hormonal influences in sexual function include oxytocin, cortisol, pheromones, and prolactin. There is some evidence showing that oxytocin (produced by dopamine) levels increase during sexual arousal and orgasm in both men and women. (3) Also the combination of oxytocin and female hormones like estrogen in women, encourage an emotional attachment with a partner. In men, the bonding effect is muted, due to the male's higher testosterone levels. As a result, men form emotional ties slower, and are more likely to regard initial sexual contact as just sex. Studies of men and women with elevated levels of prolactin report decreased sexual interest, arousal, orgasm as well as mood disturbances such as anxiety and depression. Dysfunction in remaining erect has been described in men with both abnormally low and abnormally high prolactin levels. In women, high prolactin has been associated with infertility and decreased sexual activity. Animal studies also suggest that prolactin has an inhibitory influence on both male and female sexual behavior, although short-term prolactin elevations may play a role in some elements of sexual behavior in male rats.
Clearly, this molecule plays many roles in humans but the exact role is uncertain. It is known that prolactin shares a close connection with dopamine in the brain, particularly in the tubero-infundibular tract, which runs along the base of the hypothalamus and releases dopamine into the portal veins of the pituitary gland. Dopamine acts to inhibit the release of prolactin. This, in turn, affects dopamine release. Blockade of dopamine receptors in the tuberoinfundibular tract releases prolactin from the tonic inhibitor control of dopamine, allowing prolactin levels to rise. This self-regulation is critical to prolactin homeostasis, since any disturbance in the connection between the hypothalamus and the pituitary may lead to hyperprolactinemia (high prolactin levels). (4)
Knowing what happens in the brain during sexual arousal and orgasm can help to speculate why so many men and women have problems during sexual activity. There are various factors for both men and women that can cause sexual dysfunction such as depression(caused by low level of serotonin), everyday stress, etc. Understanding the sexual differences in both men and women, can also help differentiate male and female behaviors. But there is still on-going research being done on these issues because not much in known about how these chemicals work together in the brain to affect sexual behavior. There are speculations for example, that the olfactory sensors in men are highly sensitive to the "smell" of estrogen and in fact, cause quick arousal. But this kind of triggering in the "female" brain is less receptive. Perhaps this is why women have to "think" about having an orgasm in order to feel one. Whether women control their orgasm or not, is still questionable. But it is obvious that the levels and ways that these chemicals work together in the brain are different for men and women.
),
1) Scientific American: News In Brief: Study Lays Bare the Physiology of Erection: March 19, 2002
2) Chan, John, Dellovade, Tammy L., Forrest, Douglas, Pfaff, Donald, W, The Two Thyroid Hormone receptor genes have opposite effects on estrogen-stimulated sex behaviors, Nature Neuroscience Vol 3 number 5 pp 472-475 2000.
3) Bartlik, Barbara, Gelenberg, Alan J., Legere, Regina, Villaluz, Jose, Sexual Dysfunction Secondary to Depressive Disorders The Journal of Gender-Specific Medicine, 2[2]:52-60 1999
4) Michele A. Kelly, Marcelo Rubinstein, Sylvia L. Asa, Ge Zhang , Carmen Saez , James R. Bunzow , Richard G. Allen, Robert Hnasko , Nira Ben-Jonathan , David K. Grandy , and Malcolm J. Low Pituitary Lactotroph Hyperplasia and Chronic Hyperprolactinemia in Dopamine D2 Receptor-Deficient Mice Neuron, Vol. 19, 103–113, July, 1997
| Effects Valium has on Seizures Name: Deb Charam Date: 2002-04-16 18:33:10 Link to this Comment: 1846 |
I decided to write about this topic because it is something that effects my family directly. My sister is a victim of a disease called Rett Syndrome which causes her to have intense seizures. She is seventeen now and has had seizures her whole life. Having faced these for many years now, my parents have been through lots of different types of medications to help treat and control her seizures. The newest type of medication is Valium and so I though that I would take this opportunity to learn more about it and its effect on seizures.
First off, it is important to understand what a seizure is. A seizure is caused by abnormal discharge of electric stimulation in the brain. They may also be caused by salt imbalances in the blood, gastrointestinal disease, poisoning, head injury, brain disease such as a tumor, a malformed blood vessel, or anything that causes sudden lack of oxygen to the brain.((1).) Seizures are also grouped into different categories depending on how severe they are and also depending on which part of the brain is effected. For example, if the entire brain is involved it is a generalized seizure as opposed to if only a portion of the brain is effected and in that case the seizure is a partial seizure. ((2).) There are two types of partial seizures, simple partial and complex partial. There are also two types of generalized seizures, generalized absence (petit mal) and tonic-clonic (grand mal). The seizures that my sister has are tonic-clonic or grand mal, which are considered the most severe type of seizure to have. With a tonic-clonic seizure, there are two phases. In the tonic phase, the person loses consciousness and falls, as the body grows rigid. In the clonic phase, body extremities jerk and twitch. After the seizure, consciousness returns slowly. ((2).)
Over the years, my sister has been through various different medications whose intent was to control her seizure activity. A new type of treatment that her neurologist suggested trying is Valium (Diazepam). Valium is a drug that effects the limbic, thalamic and hypothalamic regions of the central nervous system. ((3).) Valium slows the central nervous system and is used to treat anxiety related disorders and conditions that cause severe muscle spasms and convulsions. ((4).) Valium is administered rectally. Liquid Valium is absorbed fast from the rectum. The effect should take place 5-15 minutes after the injection.((3).) Valium should not be used on a daily basis because it can cause withdraw and it also has many other side effects.
My sister has her seizures in clusters. When she has them she will usually have about five or six seizures over the course of two or three days. Because her seizures come in clusters, her neurologist thought that Valium may help stop or at least decrease the intensity or frequency of her seizures. The last time two times that she had seizures, my mom rectally gave her the Valium and my mom thought that the Valium did have an effect. She said that once she gave her the Valium that the seizures went away, but that my sister was very tired and it took her two or three days to regain her strength, but those two or three days were seizure free. My parents have had many discussions about whether
They should continue to use the Valium and for right now they are going to continue to use it when her seizures come because the Valium did make them stop. We think that because we are not going to use it on a regular basis that her body will not become dependent on it. But as of right now, the Valium is supported by us as a way to treat a tonic-clonic cluster of seizures.
SUCCESSIVE REFERENCES, LIKE PARAGRAPHS, SHOULD BE SEPARATED BY BLANK LINES (OR WTIH
, BUT NOT BOTH)
FOR WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY
2)Types of Seizures, COMMENTS ABOUT IT
3)Treating Cluster Seizures With The Rectal and Oral Valium Protocol, COMMENTS ABOUT IT
FOR NON-WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY
REFERENCE NUMBER) STANDARD PRINT REFERENCE FORMAT
| St. John's Wort As A Treatment For Depression: Her Name: Adria Robb Date: 2002-04-16 23:41:31 Link to this Comment: 1852 |
This country has its share of major health issues, and Depression has remained a prominent one. With a prevalence rate of one in twenty suffering from this psychological disease in the US, (8) it is no wonder that many varying treatment options now exist for sufferers. The most common approach to treating Depression is with some form of psychotherapy coupled with prescription drugs. However, this traditional course of treatment now has the so called 'alternative' approaches to contend with. One such alternative therapy is Hypericum, an herb that is more commonly known as St. John's Wort. There is a bubbling debate between believers in the herbal treatment and non-believers (comprised mostly of doctors and researchers) who think St. John's Wort does nothing for Depression. From both sides of the debate, however, there have been some interesting findings.
There is a common understanding that St. John's Wort was named after John the Baptist. Hypericum perforatum is its Latin name. St. John's Wort is a naturally occurring plant characterized by its black-spotted yellow flowers. Historically it has been hailed as an effective treatment for an array of ailments, including digestive disorders, lung ailments, skin abrasions, and as a general inducer of state of 'well being'.
From its supporting side, the argument is that St. John's Wort should be treated as comparable to prescription antidepressants and as just another available option for the millions who are depressed in this country. Supporters often site the fact that German doctors endorse millions of doses of the herb daily, and elsewhere in Europe, the medical community readily acknowledges its positive effects. They also argue that the process of prescribing the right antidepressant to a patient is an extremely time consuming and pain staking process, as one medication might be changed to another and dosages fluctuate in an attempt to stabilize the patients mood. The process can take close to a year. With St. John's Wort, however, the herb is easily obtainable, does not need a prescription, and is available at a much lower cost than prescription drugs. It also boasts few side effects and mild ones at that, versus the multiple side effects that go along with such popular prescription antidepressants such as Prozac. (2)
Now we will turn to the other side of the coin, as it were. The US Food and Drug Administration has not yet approved St. John's Wort as an effective treatment for depression. This lack of approval is mostly due to the fact that little research has been conducted on the effects of St. John's Wort. That is, until recently.
In April 2001 and again this month (April 2002) The Journal of the American Medical Association (JAMA) published the results of clinical trials conducted to test whether St. John's Wort works to treat Depression. (4,10,11) Both times the results did not favor the use of the herb. The most recent JAMA report concluded, "...hypericum should not be substituted for standard clinical care of proven efficacy, including antidepressant medications and specific psychotherapies, for the treatment of major depression of moderate severity." (4)
When interviewed about the results of the JAMA reports, Psychiatrist Mark I. Levy, MD (University of California, San Francisco) expressed concern with the popular belief that St. John's Wort treats Depression. "The danger is the illusion of effect, given that untreated depression has a 15% death rate. If people think they are going to treat it [Depression] by taking a relatively ineffective medication, that scares me." (11) In other words, there are likely thousands of people using St. John's Wort who are remaining under-treated for an extremely serious and potentially deadly psychiatric disease. Considering the research results and the prevailing popularity of Hypericum, this is indeed a valid concern.
Countering this, however, from the pro- Hypericum side, is the fact that no one ever claimed St. John's Wort could treat severe forms of depression, and that for mild forms of the disease, St. John's Wort can be effective in allaying symptoms. (10)
Turning again to the con side, Hypericum has serious interactions with prescription drugs. And not just a few, but many, including, HIV/AIDS medications, cancer, and heart treatment drugs. In most cases, these drugs are non-negotiable: i.e. a patient has no choice as to whether they take them or not, as their life depends on the drug(s). With millions of Americans taking drugs for these and other common conditions, and millions suffering from Depression, there is bound to be overlap. So, for millions of people already on prescription drugs for things like heart disease, if they are also depressed, St. John's Wort should truly not be considered as a treatment option. (9,11)
So what is a consumer to do? When battling Depression, or even a periodic sad mood, a cheap, accessible, over-the-counter mood-booster seems like a miracle. And many consumers think of St. John's Wort in that way. For mild forms of depression, the herb appears to be quite an effective treatment. For more severe forms, this appears not to be the case, say researchers, but there are still some patients who swear by it.
However, because of the high probability of severe interaction with other drugs, it is best to consult your doctor or psychiatrist before self-prescribing St. John's Wort. And that goes for all other over-the-counter treatments as well.
While finding as many ways as possible to treat Depression is a priority for medical researchers, and the wish of all sufferers and others effected by it, it is also imperative that one not get carried away with new discoveries. Consult medical doctors, go through the research, weigh both sides of the coin, and then make a personal decision as to which treatment will best help your condition.
Resources Cited:
1) CNN.com Health , article on St. John's Wort
2) Hypericum.com , basic information about the herb Hypericum perforatum
3) JAMA April 2002 Report on the Hypericum efficacy research study
4) WebMD (Online consumer medical information) , article "Are Herbs Good Medicine?"
5) WebMD , article "St. John's Wort Not Effective – Again", after release of JAMA report
6) WebMD , article "A Dangerous Prescription", mixing herbs with prescription drugs
For More Information:
7) Newsweek article "A Natural Mood Booster", treating Depression with St. John's Wort
8) National Institute of Mental Health (NIMH), "Information About St. John's Wort" page
9) National Center for Complementary and Alternative Medicine , St. John's Wort Fact Sheet
10) National Center for Complementary and Alternative Medicine , St. John's Wort Q & A
11) Health World Online , index of articles on Depression and herbal remedies
| Beauty, Biology, and Society Name: Sujatha Se Date: 2002-04-17 01:52:21 Link to this Comment: 1856 |
What is beauty? How do human beings decide who is attractive and who is not? Society is full of messages telling us what is beautiful, but what are those definitions based on? Do we consciously decide whom we are attracted to, or is biology somehow involved? The issue of beauty and how we define it has been studied for centuries. Scholars from all fields of study have searched for the "formula" for beauty. Darwin in his book The Descent of Man wrote, "It is certainly not true that there is in the mind of man any universal standard of beauty with respect to the human body. It is however, possible that certain tastes in the course of time become inherited, though I have no evidence in favor of this belief." (1) Science has tried to look at beauty beyond the conscious level. It has tried to determine what roles biology plays in human attraction. Scientists have discovered that symmetry and scent play a role in defining human attraction. (3) But while this can begin to explain beauty on the most basic of levels, what accounts for variations in the standard of beauty? The idea of beauty varies within different societies and communities. Do these cultural preferences have a biological basis? What is the relationship between biology and society in relation to the idea of beauty? How do they relate to each other, and how do they differ? In particular what role does science play in the preference that many societies, (in particular South Asian, East Asian, and North American Cultures), have for fairer skin?
Beauty is experienced through visual stimuli. The human being's intake of beauty is through both conscious and unconscious decisions. (4) (4) The question is what motivates our unconscious decisions? Mathematicians have for hundreds of years studied facial structure as a possible explanation for the formula for beauty. ((1)Through an analysis of the human face they have determined that symmetry is involved. The human face is designed symmetrically. While there are variations, in general the human face is symmetric in design. (2) Because the tendency towards symmetry is a dominant trend in physical structure, humans tend to look for symmetry in each other. This desire is often times unconscious. The Golden Ratio, also known as the Phi Ratio, defines human facial structure as following a symmetrical ratio of 1:1.618. (1) Another factor involved in attractiveness is scent and more specifically pheromones. (4) While the intake of human scent may be unconscious is seems to have a positive impact on beauty as well. Pheromones are unconscious indicators that the human body releases. In a study conducted by Anja Rikowski and Karl Grammer the relationship between physical symmetry and scent was conducted. Through the experiment it was determined that individuals with a high level of facial symmetry, also give off high levels of pheromones. (2)
Why are symmetry and scent so important? What does the Golden Ratio and pheromones tell us about the science of beauty? In a biological sense beauty and physical attractiveness, serve the purpose of reproduction. Humans have the innate desire to want to reproduce, and more specifically pass on their genes. (3) Attractiveness aids the reproduction process by helping humans find partners. The physical features of a person are indicators of how they rate as a potential mate. (5) A high correlation between symmetry and health has been found. Because humans tend to follow a symmetrical pattern, the more a person's features are symmetrical, the more desirable they are. In addition pheromones are unconscious indicators of the body's readiness and ability to reproduce. (3)
Do men and women read each other's bodies in the same way? Male and female play different roles in the reproduction process. (2) Because of this there is some variation in what they look for in a partner. The female's level of involvement in the reproduction process is higher than the males. After nine months of pregnancy she is responsible for ensuring that her children reach adulthood. This assures the successful passing on of her genes. Males in comparison have the biological ability to pass their genes on quicker and more frequently. Potentially a male could reproduce through many females, increasing the chance of their genetic success. (4)Science has looked to see how the biological formula reflects this difference. Through studies females have indicated a preference for male faces that have sharp lines. In addition well-defined muscular bodies are considered attractive. These features have been associated with health, success, and power on the male's part. Females search for potentially successful and powerful mates because they want a partner who can help to raise their children. (4) The female body reaches maturity before the males. Because of this she can look to older males as possible partners. The male image of female beauty tends to be based more on physical attraction. Because he has the potential of having more than one partner, he looks for females who look like they can successfully pass on his genes. Males are attracted to women's faces that are smaller and rounder. Symmetry in a woman's facial features and overall physical features are important. In addition a female's scent, the level of pheromones she gives off, indicates her potential success rate. (4)
The definition of beauty and what is considered attractive has changed with time. (6) In addition definitions of beauty vary within cultures. How does biology explain this? What is the link between societal definitions of beauty and the biology of attractiveness? The underlying factor behind it all is the need to pass on one's genes. But with time as indicators of success have changed, so has the definition of beauty. Look at the preference that many societies have for fair skin. In particular South Asian, East Asian, and North American cultures have a strong preference for lighter complexions. (7) (9) (10) This can be seen through the images of beauty that these societies promote, as well as the considerable market for skin lighteners within them. In Asian cultures one of the most important indicators of a good potential match is a fair complexion. (9) This holds true in particular for women whose complexion can be considered more important than her level of education and her financial status. The ethnic make up of the United States is very diverse, yet the model of beauty does not reflect this diversity. The prototype of beauty is blond hair, blue eyes, and fair skin. What is the logic behind the preference for fair skin? Is there a biological explanation for the preference in for lighter complexions?
Historically fair skin has been associated with power. ((8) In societies that have experienced colonization, or have been ruled by other groups, the definition of beauty is based on the prototype of those who are in power. The ideal for beauty has changed with history. For example a hundred years ago the model of a beautiful woman in Indian society was one who had a darker complexion and a round physical appearance. The present day model of a beautiful Indian woman is one who is fair skin, slim, and has western facial features. In the history of the United States, in particular during slavery, light skin was desirable. A white complexion was strictly enforced as being correct, and anything less than white was defined as inferior. African-American slaves with lighter complexions were given preference over those with darker ones. (7) (7) Biologically humans are driven to want to find partners who are successful. If a society's image of successful person is one who has fair skin, and we innately look for successful mates, what role does biology play in color preference? Can a person's desire for a successful mate lead them to follow society's definitions of what is beauty?
Beauty can be defined by both biology and society. The standards for beauty evolve with time as well. While society's definition of beauty can change, there is a biological basis behind determining attractiveness. The innate need to reproduce, and pass on our genes, drives human beings to be attracted to each other. The example of lighter skin was meant to look at the relationship between biology and society. There is much more involved in what determines societal definitions of beauty than just biology. But it is important to question the role biology plays in relation to those standards. How can we distinguish between what is society's influence and what is biology's influence in relation to definitions of beauty? Another question is how much of an effect biology has on determining our lives. There is not a clear answer. As with all aspects of life biology determines the basis in how we live. But with time and discovery we will gain more of an understanding of that basis..
3) Symmetry, and Attractiveness
4) Female Phermones and Male Physiology
5) Evolutionary Psychology of Sexual Attraction
6) The Biological Purpose of Beauty
7) The Role of Afrocentric Features in Person Perception: Judging by Features and Categories , Journal of Personality and Social Psychology
8) When Black Isn't Beautiful, , The Guardian.
| Life After Brain Injuries: Are We Still the Same P Name: Alyson Dym Date: 2002-04-17 03:04:02 Link to this Comment: 1857 |
During the summer of my junior year, a friend of mine, we will call her "Jen", got into a horrible car accident. Apparently sitting in the middle of the backseat, only strapped in with a lap belt, my friend hit her head on the side window, smashing the window upon impact. After 3 weeks of being in a coma, my friend eventually recovered. Even though she was deemed "physically" healed, my friend was truly never the same. Not only had her demeanor and interests changed, but also it seemed as if she had become a completely different person after her accident. I thought it very sad at the time, because the friends who had been close to her before were no longer close. I did not understand what they meant when they said that she had become a different person. Certainly, I realized that she had changed, but I could not fathom that she was now so different that they could no longer treat her like the old "Jen". I believed that this new "Jen" was still the same person as before-that the inner soul with which they had become friends had never and, indeed, could never change. However, after reading Descartes' Error: Emotion, Reason, and the Human Brain, by Antonio R. Damasio, I regret the harsh judgments I made about "Jen's" friends. Dealing with someone who has suffered from a tremendous change in personality is not as easy as one would expect.
Descartes, a famous philosopher, once made the statement, "Cogito ergo sum" (6). Like, Descartes, I previously believed that a separation between the mind and one's body existed. I believed that the mind of an individual was his or her soul and that the brain and body were just the machinery used to share that soul with the outside world. I never thought that an injury to the brain could cause a change in the entire essence of a person. However, Damasio espouses beliefs which are the exact opposite of Descartes. Damasio argues that the brain and mind are two inseparable entities and that thinking is the function of the brain. Aristotle once stated, "If the eye had a soul, it would be seeing". Using this format, a soul is defined as the function of something. If the function of the brain is to think, then it would follow that the soul of a person exists in one's mind, where the capability to think is lodged. If this mind is the consequence of a functioning brain, then it can be said that when a brain suffers an injury, an individual's entire essence is injured as well. This idea of a person's essence, or soul, changing is controversial. I believe this controversy arises because it is too frightening for a person to fathom that his intrinsic being could be permanently changed as a result of an unpreventable action. However, the evidence in favor of the premise that the mind is a function of the brain, or the brain is equal to one's behavior, is astonishing (5).
Brain injury is any injury that results in damage to the brain. For many people who suffer from brain injury, the problems associated with it become a permanent part of their lives. The problems that develop depend upon which part of the brain is injured. People can lose cognitive and motor functions as well as their ability to express thoughts and perceive their surroundings. The most unnerving consequence of a brain injury can be a change in personality. Often after being injured victims, like my friend "Jen", develop an apathy and decreased motivation for life. Emotion can run to both extremes: a forever high, or as in the case of my friend, an absence there of (1). In society there is a difference in the response shown to someone who has suffered a brain injury that changes his or her personality, and someone whose injury has affected any other part of the body, or even other types of injuries to the brain. What accounts for this difference? If an individual loses a limb, he loses the function of that limb as well. It makes sense then that when an individual loses part of his brain, the function of that part goes too. This is in correlation with the statement, brain = behavior. Each part of the brain seems responsible for different behaviors, a fact that is reinforced when examining injuries to different areas of the brain and the varying results that occur. For example, if an individual suffers injury to their amygdala, he becomes calm and almost devoid of emotional ups and downs. People have therefore reasoned that this area of the brain is responsible for exhibiting anger and possessing violent emotions (9). If the function of a specific area of the brain is a defining characteristic of an individual's personality, then it is almost as if a new person develops, in place of the old, when an injury to that area occurs.
In the summer of 1848, a man named Phineas Gage incurred a traumatic injury to the frontal lobe region of his brain after a sudden explosion sent a rod straight through his head. Against many odds, Phineas survived, but afterwards his demeanor changed dramatically. Once a calm, balanced, and levelheaded man, Gage became an overly emotional, unbalanced and quite vulgar man upon recovery. Friends he had had previously, now compared him to an animal and made the perplexing statement, "Gage was no longer Gage" (3). The most frightening thing about this story is that, although Gage was very different, he was not aware of the changes within himself. In class we have explored the nervous system and noted that there is a separate I-function involved, making one aware of the "self". With each class, it becomes more evident that this I-function has less and less control on the rest of the nervous system. Many times the I-function is not aware of things that the nervous system is doing until the person is told what his or her nervous system is doing, (i.e., when the brain makes up an image for the place of vision, the optic nerve, where no sensory receptors are located). So the question I have for people like Gage, who seem to be totally dissimilar people after suffering a brain trauma, is whether or not their I-functions are aware of the change in personality? People suffering from a personality change are unable to will themselves back to their old personality, even after their I-function is made aware. This furthermore, supports that brain equals behavior, because if behavior was independent of the brain, one would be able to change their personality back despite the brain changes. However, can we ever be sure that, because we are not mind readers, that even though their personality changes, they are not thinking in the same manner, as Descartes would argue? And if the individual thinks in an entirely new manner, would that really be enough to consider him or her a totally different person?
The likely reality is that when someone's brain is injured, the function is forever injured as well. There is no separation between mind and brain. Popular opinion of the mind's function is that it is a result of a brain process. Although when the brain loses a function, it is not unlike the reaction incurred in any other part of the body, but the more important query remains. Which characteristics do we use when defining a person's being? If Gage had suffered from a trauma to any other part of his body and survived, his friends would never have said that Gage was no longer the same person. Often when people undergo a personality change, their IQ remains unaffected by the injury. This is because of the various tasks delegated to the brain. The frontal lobe has evolved to be the main organizer. If people, like Gage, damage this region of their brain, their persona changes because this region is imperative for defining one's personality. However, if Gage had suffered from an injury to his temporal region, his personality would seem the same, only his memory would be adversely affected (9). An example of a personality change as a result of frontal lobe damage is a 12 year old boy who was in a car accident. Since the accident, the child has been aggressive and suffers from unpredictable destructive fits. Although his I.Q remains at 128 since the accident he has been expelled 3 times from different schools for his hostile persona, brought about after the damage to his brain (4). What, then, is the most important factor accounting for the way a person becomes defined; what has happened to make the various regions of the brain become so specialized? Has there been a gradual process through evolution that makes the loss of the frontal lobe harder to deal with than the loss of other regions of the brain, or other body parts? Or has the brain always functioned in this manner? When examining the responses to what appears to be injuries that are all serious in nature, it becomes apparent that some injuries are, indeed, more acute than others. Although an injury which is noticeable may on the surface seem more life changing, it cannot be argued that it is the injuries which are held within one's mind that are the most devastating to a person's being. Yes, they are all injuries to the body, but only those touching the brain have the capacity to change the "soul" of a person.
1)Brain Injury Society, A good site defining what brain injury is, its causes, and its treatments
2)Traumatic Brain Injury Resource Guide, a good diagram of the frontal lobe of the brain and a good description of its functions
3)Cyber Museum of Neurosugery, a good site about Phineas Gage
4)Alasbimn Journal, a legal page discussing the issues of aggressive personality change and the law
5) Antonio R. Damasio, Descartes' Error, New York: Avon Books, Inc., 1994, a great book with much about Phineas Gage and other Brain injury victims
6) Rene Descartes, Discourse on Method and Meditations on First Philosophy, Indianapolis, Indiana: Hackett Publishing Co., Inc., 1998, can't read one without the other!
7)Athiest Site, a site dedicated to atheism that explores some of the questions this paper raises
8)American University, a site outlining the neurospychology of emotion
9)University of Northern Iowa, a site dedicated to the effects of different injuries to the brain
| Dyslexia, and what it can teach us. Name: Gabrielle Date: 2002-04-17 10:09:18 Link to this Comment: 1860 |
What is a learning disorder and what can knowing more about learning disorders tell us about our own learning? Scientific research has acknowledged that many learning disorders are really just the edge of what is the normal spectrum in human capabilities.(1) Children with reading disabilities differ from one another and from other readers along a continuous distribution.(2) The aptitude to read depends upon fast and precise understanding and decoding of single words.(2) A disabled readers IQ tells very little about their skills. Disabled readers with varying IQ can display exactly the same progress, and neurobiological symptoms. This tells us that the IQ is not a suitable indicator of disability in basic reading skills. That is just one example of the many things that we can learn from people with learning disabilities that we can apply to all people. We will also see that by studying students with dyslexia we can see some of the important brain functions in reading.
For a long time, research in the scientific community in respect to learning disabilities was slim. One problem in recent decades is that scientists have spent a lot of time searching for the basis of the disorder as opposed to the solution. This has created a chasm between the scientific and the educational worlds. Teachers were experiencing frustration with the influence that PhD's and MD's have on their curriculum.(2) Some teachers feel that when help is provided it can be in a non-helpful manner. Researchers don't always take into consideration what it was really like to be teaching.
When we think about learning in a broad scale we think about it as repetition of memorization. On a cellular level learning is the result of change in the strength of a connection due to synaptic activity.(3) At larger levels Hebbian ideals can't really be taken much farther than simple behaviors. We can use Hebbian learning to explain repetitive actions that allow us to learn, say a piece of music. A musician plays a piece of music over and over again, until he/she knows it really well. At this point the synapses that were being used in the musicians brain have physically and chemically changed so that there is now a stronger connection.
Can we explain learning disorders with Hebbian theory? Surprisingly we can. It turns out that dyslexics fail to increase activation in order to make the connections between phonologic structures and sounds.(4) This was discovered in an experiment in which a group of defined dyslexics and a group of non-dyslexics were shown different stimuli while an MRI was imaging their brain. They were given different tasks which were varied to require diverse amounts of visual-spatial, orthographic, and phonological processing. Orthographic processing demands the subject to understand patterns amongst figures. Asking subjects to decide whether or not the letters "t" and "v" rhyme is a phonological task. An example of a task requiring only visual-spatial decisions, is one in which the subject would be shown two series of letters, dDdd and dDdd, and then be asked to acknowledge that they were equivalent.
There are multiple factors to lead to the result of a diagnosis with dyslexia. At this point we are able to clearly pick out students who may have future problems by the first grade.(5) Dyslexia is commonly known as a reading disorder. Dyslexics commonly have trouble reading because they cannot keep track of all the rules of phonological connections to visual and orthographical cues from writing. Another component of dyslexia, which isn't as evident, is a lack of understanding of sound presentations. It seems that many dyslexics have trouble interpreting nuances in rapid sound alterations, limiting their ability to distinguish between sounds.(6) They therefore have a more difficult time differentiating syllables, and fluctuations in voice that indicate context(such as the difference between a question and a statement).
New computer games were developed to train children to read words more accurately. These games require the students to use audio-visual skills to match abstract objects. For example one specific program used in a recent study used different thickness and heightened rectangles in patterns. Two would be shown to the student, and a sound would be played. The student then had to identify which of these patterns was related to the sound.(7) Without knowing it, the student was improving their reading skills. They were training their brain to make connections between symbols and sounds. Reading tests were given to students before and after these computer games. The tests afterwards showed marked improvements in the speed of reading, and accuracy of word identification.(8)
These new forms of computer-based teaching seem to be surpassing the innate learning form. They are teaching the child in a way so that the way the child thinks so that it will be able to continue doing so outside of the classroom. This allows the child to learn in an unconventional way that the regular learning process was blocking. We could possibly examine this blocking as having been caused by the I-function. The I-function requires that the student memorize the coding of language. Dyslexics however, seem to not be able to memorize in this fashion. They can however still recognize patterns, and the computer program teaches them to recognize patterns more accurately.
We can make some generalizations about learning disorders in general after looking at dyslexia. This is possible because dyslexia is "a problem with managing verbal codes in memory,"(5) and the majority of learning disorders are the result of a deficit in phonological understanding, or understanding the codes of language.(2)
There are many other factors that come into play when thinking about learning disorders. There is always the fact that students' minds are occupied with other things. There has to be a limit to how much a person can be learning at one time. The environment may be affecting how that person is learning. If the person needs to keep their mind sharp for another skill, their mind may put that in front of reading in the ranking of importance for survival. Many researchers' have found evidence that dyslexia seems to have economic and familial reasons also.(3)
From our studies of learning disabilities we should take a few things. We should use our new and varied teaching tactics for everyone, to possibly help people that we don't recognize as needing aid. Since learning disorders are just part of the spectrum, what aids a learning disorder may also aid an average learner. We can also take advantage of these deficits to help us better understand the processes in the brain, such as conversion of short-term memory to long-term, complex analyses, and many other questions we have about the brain.
1)"The science of literacy; From the laboratory to the classroom."
4)"Functional disruption in the organization of the brain for reading in dyslexia"
6)"Auditory stream segregation in dyslexic adults "
7)"Neuroimaging Studies of Word Reading"
8)"Plastic neural changes and reading improvement in reading-impaired children"
| Proprioception: how and why? Name: Shannon Le Date: 2002-04-17 21:59:53 Link to this Comment: 1872 |
There are five common senses that are discussed and learned from an early age: sight, hearing, taste, touch, and smell. The I-function, the conscious part of the brain, is very aware of these senses. It voluntarily checks information obtained by these senses in order to experience the environment, and also when a strong enough stimuli has signaled attention to these specific receptors. There are other equally important sensory systems set up that are essential for normal body functioning, but these are not so easily recognized by the I-function because the nervous system keeps the input unconscious.
One overlooked sense, known as proprioception, is as important, if not more important as the other senses, for normal functioning. Proprioception is "the process by which the body can vary muscle contraction in immediate response to incoming information regarding external forces," by utilizing stretch receptors in the muscles to keep track of the joint position in the body (1).
Proprioception and kinesthesia, the sensation of joint motion and acceleration, are the sensory feedback mechanisms for motor control and posture. Theses mechanisms along with the vestibular system, a fluid filled network within the inner ear that can feel the pull of gravity and helps the body keep oriented and balanced, are unconsciously utilized by the brain to provide a constant influx of sensory information (2). The brain can then send out immediate and unconscious adjustments to the muscles and joints in order to achieve movement and balance. Why has the nervous system developed the sense of proprioception, and why is it an unconscious aspect of the sensory system?
Proprioception, also often referred to as the sixth sense, was developed by the nervous system as a means to keep track of and control the different parts of the body. An example that enables one to best understand this sensory system is one showing what happens if this sensory system is no longer there. Ian Waterman lost his sixth sense along with the ability to feel light touch when a virus killed the necessary nerves. The man still had all the nerves to control muscle movement but had no feedback from the outside world about where his limbs were except that obtained by sight. A normal person is able to move a finger, knowing where and what the finger is doing, with little effort. The normal person could just volunteer the finger to move back and forth and proprioception would make this an easy task. Without proprioception, the brain cannot feel what the finger is doing, and the process must be carried out in more conscious and calculated steps. The person must use vision to compensate for the lost feedback on the progress of the finger. Then the I-function must voluntarily and consciously tell the finger what to do while watching the feedback (3).
The eyes have to also be trained to judge weights and lengths of objects. As Waterman attempts to lift objects there is no feedback on how hard to flex the muscles except from what clues vision gives. Studies of Waterman support that through feedback from proprioception the brain is able to calculate angles of movement and command the limb to move exact distances. If vision is taken away, the lights are cut out, then Waterman will fall in a heap on the floor, with no ability to make successful voluntary movements. The examples of Waterman illustrate the type of information obtained because of proprioception and the great importance of this information. Without this sense humans would be forced to spend a great amount of their conscious energy moving around or would not be mobile at all (3).
The proprioception sensory system is carried out utilizing proprioceptors in the muscles that monitor length, tension, pressure, and noxious stimuli. The muscle spindles, the most complex and studied of the proprioceptors, informs other neurons of the length of the muscle and the velocity of the stretch. The density of muscle spindles within a muscle increases for muscles involved in fine movements, as opposed to those involved in larger course movements. The brain needs input from many of these spindles in order to register changes in angle and position that the muscle has accomplished. There is also more spindles found in the arms and legs, muscles that must maintain posture against gravity (1).
Another proprioceptor, the golgi tendon organ, is found where the tendons meet the muscle. They send detailed information about the tension occurring in specific parts of the muscle. There are also proprioceptors sending information to the nervous system from joints and ligaments. Depending on the amount, where in the body, and from what proprioceptors the different input is coming from, determines if the information will be made conscious or processed unconsciously. All the input coming into the nervous system is processed, and then depending on the state of the muscle, there are commands sent back to the muscle (1).
After thinking of Waterman's plight to accomplish many basic movements without the help of proprioception, the realization of the importance of this sense becomes apparent. I can possibly imagine the species successfully evolving without eyesight, especially if the sense of hearing evolved more keenly. However, it is much harder to imagine the human species evolving without the ability to easily move. Waterman's situation also makes the reasoning become clearer as to why the nervous system evolved keeping the I-function separate from most proprioceptor feedback. Proprioception is extremely important and encompasses so many areas of the body. The sensory information being processed is a constant and a monumental amount. If the I-function, which can only focus on a few aspects at once, had to be responsible for all of the input coming in from all the different muscles there would be difficulties. The confusion would be overwhelming and the I-function would be useless in making decisions at the speed necessary, because it would need to think first. Thinking takes time, where the unconscious nervous system responds immediately through processes wired to specifically deal with the type and amount of input coming in. Systems like proprioception and other unconscious, yet crucially essential, systems allow the I-function to develop without having to be bothered with all functioning of the body. These unconscious systems allow a lot to get done at once. The I-function may spend time learning new skills and developing ideas without being inhibited by the large amount of stimulus needed for a successfully functioning of the body.
The I-function is most likely very aware of senses such as sight, hearing, and smell, because it can focus on the details that it wishes to consciously concentrate on. A lot of stimulus can be discounted by the I-function very quickly, if not ignored before it reaches that far, so that the I-function can concentrate. This is a necessary property of the I-function because we are multi-task beings that are constantly surrounded by stimuli. The I-function must have the ability to make decisions and be able to identify the stimuli in the environment relevant to our well being. The information coming in from the proprioceptors cannot be ignored, just as the neurons that are signaled to pump the heart cannot ignore the stimulus, because the majority of the information coming in is necessary for normal movement.
While proprioception is necessary for learning a type of movement or skill involving muscle, concentration from the I-function is essential as well. Once the skill, such as the appropriate movements of driving or the movements a baby must accomplish to walk, have been conquered and learned the I-function is not as functional during these tasks. The proprioception and motor systems can take over, utilizing a feedback system to accomplish a job that the unconscious brain already has learned. The I-function can go on to do other things, because it would mainly just hinder smooth muscle processes with to much thought and analysis. That is why humans do so many learned things best if not thought about. For example, the harder a driver focuses on what her muscles are doing as she drives, the choppier her movements will be, and the worse the driving will be.
The phantom limb also indirectly supports reasoning for the evolution of proprioception. A person with a phantom limb still feels pain or some sort of sensation even though they were born without the limb or it was amputated. The evidence that people having no limb at birth still can experience a phantom limb supports Ronald Melzack's idea of there existing a "neuromatrix" (4). The brain has a particular matrix, or map of the body, genetically installed in the brain that both responds to stimuli from proprioception and continuously sends impulses to different parts of the body to check on the condition and location of the body parts. The matrix can be altered due to experience such as storing memory or changing synaptic connections, but the overall organization is set from birth. Studies show that the matrix can record the experience of pain and generate experiences of sensation on its own (4).
When the matrix sends out signals to the missing limb and receives no response from proprioception the matrix registers a problem in the limb instead of no limb. When the brain recognizes something wrong it reports a painful sensation to clarify that there is a problem in the area of the limb to the rest of the brain, and the person experiences a painful limb even though they know it is not there (4).
There is a matrix in the brain monitoring all of the sensory information and constantly checking to see where the limbs are. This matrix is able to adjust; recording data and generating certain sensation long after the stimulus has stopped. Therefore, it may also have the ability to record patterns of action by the muscles, while the I-function consciously works the muscles through new unfamiliar patterns of movement. The patterns recorded or learned, like those of pain, could be triggered by the I-function to signal for a pattern of movement. Then a learned pattern of movement could be set forth, initiating smooth muscle movements, such as a free throw during a basket ball game, without the I-function monitoring or interfering.
If this is a way that the brain records and utilizes sensory input to conquer and utilize movement pattern, then proprioception is a primary building block in the human's ability to learn, repeat, and become comfortable with so many movements throughout life. Therefore, it is essential that the I-function not be bothered by the sense of proprioception, unless learning a new movement, because these movement patterns would be useless if the I-function had to deal with the incoming proprioception anyway. With proprioception as an unconscious sense and the matrix giving unconscious feedback to muscles, utilizing my already learned movement patterns, I can concentrate on what I am saying in my paper without having to also consciously tell my fingers to hit certain keys at certain times.
With the sense of proprioception our lives are made less complicated, and we are given the ability to learn and utilize many movement patterns freeing the I-function to focus awareness on new tasks and thoughts. The I-function seems to be one of the most complicated aspects of the brain. Was the I-function one of the last aspects to evolve in the human brain thus far? If so was it because the necessities for survival were accomplished by the species, proprioception allows movement and eating is instinctual to the brain? Why did evolution cause the human to develop the I-function?
1)Proprioception, A simplified overview of anatomical structures and neurophysiological actions involved in joint stability.
2)Mixed up in Space, An article concerning how the vestibular and proprioceptor systems react in space.
3)Why can't this man feel whether or not he is standing up?, The story of one man's loss of proprioception
4)Phantom Limbs, Discussions about what and why there are phantom limbs
| Bipolar Disorder and Drug Treatment Name: Joan Stein Date: 2002-04-18 10:27:14 Link to this Comment: 1879 |
1)NIMH-Bipolar Disorder
2)Dr. Ivan's Depression Central
3)Antisuicidal Effects of Lithium
4)British Journay of Psychiatry
5)Doctor's Guide - Lithium and it's Anti-Depressive Effect
| Meditation: Does it Alter the Mind and the Body? Name: Erica Carl Date: 2002-04-18 10:40:52 Link to this Comment: 1880 |
BEEP BEEP BEEP!!!! 9:00 am starts flashing on your alarm clock and you immediately run through your "to do list" for the day. It's a long list, filled with classes, meetings, homework, meals, exams...etc. Being the master of multitasking, I have a tendency to perform various tasks at once. As a result, my concentration level decreases while my stress level increases. How can this lack of concentration and stress level be fixed? Many people turn to meditation, but does this practice actually work? And if so, how does meditation work to change the mind and the body?
Meditation is defined as "...engagement in contemplation, especially of a spiritual or devotional nature...an attempt to concentrate mind on a single form or an idea or an aspect of divinity at the exclusion of all other forms and the ideas. The mind is focused inwards, and this effort of concentration acts as stimulus to gain access to the knowledge of the object of meditation" (1). The practice of meditation involves both psychological and physiological changes. For example, the altering of breathing patterns and thought processes. But does meditation guarantee mental and physical change?
Meditation forces an individual to gain complete control of their inner self. But, what exactly is the inner self? The subconscious is an integral constituent of the internal mind. It is located deep in the core of the mind, acting as the center of emotions, behavior, creativity, and imagination. In addition, subconscious maintains good health (2). Does meditation allow an individual to open the hidden doors of the subconscious mind? What is the difference between the subconscious and conscious mind? You can think of the conscious mind as known knowledge while the subconscious mind is unknown knowledge. Meditation taps into the subconscious mind and uncovers veiled realities about the inner self. To investigate whether meditation affects the mind, studies were performed on subjects practicing meditation techniques. In conclusion, the experimenters discovered an increase in productivity, improved relations at work, increased inner potential, increased strength of self-concept, and reduced anxiety (3). All these factors can be thought of as being an element of an individual's subconscious mind because it involves behavior and thought procedures. Moreover, the focus of one image steers an individual away from multitasking and toward greater concentration. In a sense, an individual becomes more aware of their inner self as a result of focused attentiveness.
How does meditation physiologically change the body? There has to be a reason why so many therapists suggest meditation as a solution to some physical dilemmas. Experiments were performed demonstrating that meditation does better the health and well being of an individual by altering the autonomic system of the brain. Instead of the fight or flight mechanism, which causes blood pressure to rise, the rate of the heart beat to speed up...etc., meditation aims to replace the sympathetic panicked feelings. Rather, meditation calms the nervous system. Among the various physiological changes experienced by subjects practicing meditation are lower blood pressure, slower heartbeat, rate of respiration, and rate of metabolism, and skin (stimuli) resistance (1). This particular web site stresses the presence of changes in neurophysiology with meditation, concluding that neurotransmitters and neuro-modulators, chemical substances released at the synapse, are modified when meditation is a constant stimulus. The website further explains how neurotransmitters and neuro-modulators create new brain connections and activate undeveloped neurons. This hypothesis along with the experiments investigating the effects of meditation on the body may elucidate the question of how meditation alters the physiological state.
Meditation effects both physiological and psychological changes of the mind and the body. It forces an individual to put the conscious mind aside and unleash the hidden truths about one's inner self. The conscious mind equates exposed knowledge while the subconscious mind is the unexposed deeper knowledge. Meditation can serve as a tool to cleanse the mind and reveal unknown components of an individual's inner self. Becoming aware of one's inner self may shed light on factors like behavior patterns, which can ultimately be changed to better the well being of the individual. Even practicing Buddhists use meditation as a cleansing tool to rid them of evil and negative thoughts and exchange them with good and positive ones (4). Physically, meditation can improve an individual's health by altering the body's condition. Therefore, meditation changes mental and physical well being through a heightened sense of control, concentration, and relaxation. This exploration of mediation on the mind and the body opens up a can of new questions. For example, does mediation result in an out-of-body experience or is it a learned concept of thinking? Does meditation remove a person from their mind and body? Or, does meditation require a new philosophy of learned behavior? Further investigations may be able to answer these questions. For now, sign up for that yoga class or take time out of your busy day to breath slowly, close your eyes, and focus on one image. Meditation can alter your lifestyle and ultimately your mind and body.
1)qnest home page, a good source about meditation. The practice of meditation
2)Inner Sphere Home page, another good meditation source.
3) TM Home Page, defines meditation
4)Self Hypothesis Home Page, Great source describing a hypothesis about meditation
| Phantom Limbs: Sensations When There Should be Non Name: Tina Chen Date: 2002-04-19 09:48:30 Link to this Comment: 1889 |
It has been found that it is not necessary to have had an amputation to experience the phantom limb phenomenon. It has been reported that after avulsion of the brachial plexus of the arm, even though no injury to the arm itself occurred, that there is extreme pain felt in the arm. For surgery, patients that receive an anesthetic block of the brachial plexus experience phantom arm. It also occurs in the legs when there is an anesthetic block of the lower body, and when there is a block of the spinal cord at the thoracic level, patients have experience phantom body. (2).
Not only can one experience phantom limb due to an anesthetic block, but it has been reported that people born without limbs also experience it as well. Ronald Melzack, psychologist from McGill University in Montreal found that children born without arms or legs experience phantom limbs. He studied 125 people, mainly teenagers, who had been born with a limb below the elbow. Melzack found that the phantom limb occurred by rain or by dreams where it was thought that there were two normal hands. An 11 year old girl reported that she felt pain in her fingers (she had no arm below the elbow) if she bumped her funny bone. Others have said that they felt tingling, itching or even numbness in arms or legs that they did not have. (3).This study concur the findings of a Swiss group who had a woman with no limbs that still felt movement when they stimulated parts of her brain that usually sense limb movement magnetically. (4).
Learning that people who were born without limbs can experience phantom limbs have made scientists reevaluate the theories they have about how the nervous system develops. The Swiss group showed through experience performed on this woman that her brain still has a sensory map for the limbs that she does not have. If was believed before that if a person did not have an arm that they did not develop the neurons to feel an arm. It is believed that for amputees that the neurons that used to receive feelings from the limbs are still firing which is the cause of phantom limbs. But with this woman, magnetic resonance imaging showed neuronal activity in parts of the brain, when she said she was moving her phantom limb. (4).
Phantom limb occurs not only in those who lose a limb or were never born with one, it can occur in people who are paraplegic that have a complete break in the spinal cord. Even though no signals can get through the break in the spinal cord, patients still report feeling in their legs and lower body. (2).
For years, scientists have been trying to figure out why phantom limbs occur. In the 1930s, it was discovered that the surface of the cerebral cortex had a map of the human body called the homunculus. The sensory stimuli are close to the cortex of the brain so that the primary sensory regions are excited by stimuli. This occurrence is that scientists refer to as a map. In the recent years, it has been found that this cortical map is very plastic (the ability for neurons to adapt to change) in humans and in animals. There is one theory that believes that if part of the somatosensory cortex has no input then the map will reorganize itself so that the unaffected part of the cortex represents a different part of the body surface. This idea is known as cortical reorganization. There is a big debate within the scientific world on whether or not the cause of the phantom limbs is due to cortical or non-cortical contributions. (1).
For the cortical model side of the debate, it is thought that the cortex has the ability to reorganize itself so that the signals received from residual limbs are perceived to be coming from the lost limb. To support this theory, Ramachandran studied the localization of touch sensations on the body post amputation. He found that when he lightly touched certain parts of the body, a sensation was felt in the phantom limb. He found that there were two specific regions (the face and a line above the amputation) that evoked sensations in the phantom limb. Ramachandran theorized that in the homunculus, the area for the hand is surround on both sides by areas for the face and the line of amputation. (1).
Although some believe that cortical model is correct, many believe in the non-cortical model. It is thought that perhaps it is peripheral signals or signals at the level of the spinal cord are the cause of phantom limbs. Katz believed that spontaneous input from the cortex increased the speed of firing of the post-ganglionic sympathetic fibers of the spinal cord. The increased firing causes these fibers to be excited which activates the primary afferent fibers which then discharges. These discharges ultimately cause the phantom sensations. Non-cortical theory believes that spontaneous activity at the edge of the amputation causes phantom limbs. (1).
There is still a debate going on as to why phantom limbs occur. Only through further study of the nervous system can we hope to fully understand and hopefully one day stop its occurrence. Until then, we can only try to find ways to ease the pain of amputees, paraplegics and people who were born without limbs.
2) http://cognet.mit.edu/MITECS/Entry/melzack
3) http://www.findarticles.com/cf_0/m1511/n2_v19/20159526/p1/article.jhtml
4) http://www.sciencenet.org.uk/slup/CuttingEdge/Jun00/phantom.html
| Why do I have the Baby Blues? An Investigation of Name: Claire A. Date: 2002-04-20 17:56:22 Link to this Comment: 1895 |
Mental illness has been a reality not only for Yates but for millions of women throughout the country. Depression tends to be one of the most prevalent consequences of childbearing as 50% of new mothers report slight bouts of depression, 10% have manic depression and .2% suffer from psychosis(2). Yonkers et. al, further investigated postpartum depression rates for minority women in comparison to their Caucasian counterparts. After conducting a postpartum three trial screening which included the Structured Clinical Interview, it was found that depression rates for Latino, Blacks and White racial groups was between 6.5% to 8.5% (3). Regardless of race, all groups of women were susceptible to similar rates of PPD at 3-5 weeks postpartum. Other studies have found that depressive disorders begin even before giving birth. Evans et. al, conducted a study which monitored 12,509 women throughout their pregnancy up to 8 months postpartum. Depression scores were actually higher at 8 months of pregnancy with 13.5% of the participants assessed as depressed. Such percentage lowered to 9.1% at 8 weeks and 8.1% at 8 months postpartum
(4).
Postpartum depression is categorized into three forms according to symptoms experienced:
1. Postpartum blues is a common and usually short-lived condition which is characterized by weeping, emotional instability, low-self esteem, anxiety and vulnerability immediately after giving birth (5).
2. Postpartum depression (PPD) is more intense and incapacitating as it can often interrupt with the woman's everyday activities. It can be accompanied by feelings of despair, anxiety, fatigue and irritability which linger and reoccur for months if no medical attention is given (5).
3.Women with postpartum psychosis suffer from insomnia, hyperactivity and hallucinations and delusions about death and possibly hurting the child. Psychosis is further accompanied with schizophrenia and has an onset of three months but can appear 18-24 months postpartum(6).
Although the three categorizations may be useful for the identification and possible treatment of the illness, there are hormonal, psychological, social and environmental aspects which can also contribute to psychiatric illness. Fluctuations in estrogen and progesterone hormone levels during pregnancy are considered a possible source of depression. Upon 24-48 hours after giving birth and delivering, progesterone levels fall ten times the levels held throughout the pregnancy. Women who have the highest hormonal fluctuation postpartum, are reported to be the most at risk for depression (6). PPD has further been linked to estrogen's ability to activate the gene for corticotropin releasing hormone (CHR). Once CHR is secreted out of the hypothalamus, it regulates pituitary gland release of adrenocorticotropic hormone (ACTH), which regulate the secretion of cortisol in the adrenal glands. If high levels of estrogen are present, they affect the abundant buildup of cortisol in the blood as negative feedback inhibition is be unable to regulate it. Since cortisol is responsible for activating metabolic pathways, its prolonged presence leads to increased stress levels and depression. Thus, women with increased levels of cortisol have been found to have PPD (5).
Psychologists have further suggested that the patient's psychological construct could make them more susceptible for postpartum depression. Those who with a negative outlook of the world would most likely have low self-esteem, helplessness and disturbed emotional feelings leading to PPD. Such theory is contradictory as optimistic patients are often affected by PPD, while not all women with negative outlooks become medically depressed (5).
The role of social and environmental factors are also considered important links in maintaining and prolonging the illness. For example, new role expectations can bring uncertainty about the future as the woman has additional responsibilities and obligations. There may be added pressure to be a "good mother" while enduring exhaustion, fatigue and extended periods of isolation (5). Social networks composed of family and partner's support are also necessary as they create a support system which facilitate the transition after childbirth.
Is it possible that Andrea Yates lacked a cohesive social network, while suffering from the psychological and physical strain of taking care of her children? There's evidence that Yates suffered from depression throughout her five pregnancies as she attempted suicide twice and was hospitalized four times from 1999 to 2001(1). There is also evidence that gender role expectations left her with a large load of housework. "Man is the breadwinner and the woman is the homemaker" stated her husband in testimony(1). When at the Oprah Winfrey Show, Rusty explained how he and Andrea were planning to have as many children as possible because they loved and valued their family. Multiple pregnancies for a woman with a history of PPD can cause the illness to recur. Yates was undoubtedly at higher risk due to her subsequent pregnancies.
A study conducted in the UK demonstrated that midwifery visits prolonged mental stability and early detection of mental illness. Midwives visited for 28 days and closely monitored the new mothers with mental screenings. The visits further provided structural support as the mothers were able to reach out to the medical establishment and address their fears and concerns. Although the program may be helpful in preventing mental illness early on, it is problematic as it does not provide an outlet for women who may have a later onset of PPD. What can be drawn from such study is the need for changes in the current "drive thru" system of childbirth. Hospital stays have been reduced as new mothers are quickly sent home without medical resources at their disposal(8).
The Andrea Yates trial was significant in that it raised awareness of mental illness under a media firestorm. It made the American public aware of the potential actions such illness can cause a person to do. Dialogue, however, is not a sufficient means in which to properly target and treat PPD. The medical establishment must ensure prevention through mental health screenings and subsequent psychiatric check-ups for new mothers. Through educational campaigns, awareness must be brought to the masses so that the stigma attached to mental illness be eradicated. Hopefully, people will seek proper treatment as there are millions suffering with depression in isolation and silence.
WWW Sources
(1)Newsweek , Psychosis or Vengeance? Prosecutors suggest Andrea Yates may have not have been delusional when she killed her children.
(2) An Introduction to Postpartum Illness , Postpartum Support International.
3. Yonkers, Kimberly. Onset and Persistence of Postpartum Depression in an Inner-City Maternal Health Clinic System. Journal of the American Medical Association. 287: 168-169. Retrieved April 16, 2002 from Bryn Mawr College's connection to Expanded Academic.
(4) Cohort Study of Depressed mood during pregnancy and after childbirth BMJ.
(5) Women and Postpartum Depression ,Office of Women's Health.
(7) Scientific American, Why Are So Many Women Depressed?.
8. Albers, Leah and Williams, Deanne. Lessons for US postpartum care. The Lancet. 359: 370. Retrieved April 16, 2002 from Bryn Mawr College's connection to Expanded Academic
| Of A divided Mind: Human Responses to the Human Sp Name: Hilary Hoc Date: 2002-04-21 20:59:18 Link to this Comment: 1901 |
When neuroscientists first made direct contact with the right hemisphere of the brain, during neurological tests of "split brain" human subjects, it was as if they had found intelligent, albeit speechless, life on Mars. At a time when brain imaging techniques were crude or nonexistent, the only way to observe and communicate with the brain's right hemisphere unimpeded by the left hemisphere was by testing split brain subjects (1). The right hemisphere, previously supposed mute, illiterate, mentally retarded, and completely subordinate to the left hemisphere, had a mind of its own (1). While it could not speak, it could respond to commands and questions via its contralateral control of the left hand. It had different abilities and even opinions and emotional states than the neighboring left hemisphere (2). These discoveries led to a model of hemispheric specialization of normal human brain function, with an analytic, verbal, problem solving left hemisphere and a visuospatial, synthetic, creative right hemisphere (1, 2). The formation of this model in turn offers insight into the brains of the observers as well as the observed. The observers' behavior supported some of their own hypotheses about the human brain, split or unsplit.
The term "split-brain" is commonly used to describe a person whose corpus callosum has been surgically severed (3). The corpus callosum, comprised of approximately 200 million neuronal fibers connecting the left and right hemispheres of brain, exists only in mammals' brains, and is largest in human brains (1, 3). Until the 1960's neuroscientists were unsure what purpose the corpus callosum served (3). By observing deficits in split brains' functions, scientists could better assess the corpus callosum's function (1).
Roger Sperry and his colleagues pioneered the operation severing the corpus callosum, known as callosal commisurectomy, in the 1960s, as a last ditch effort to control the seizures of life threateningly severe epilepsy by creating a fire wall to prevent electrical impulses from traveling between hemispheres (1). This treatment was successful, and after recovering from the surgery, the split-brain patients appeared normal in every day interactions and even during a routine physical exam (1). However, Sperry and his colleagues, after extensive and specific neurological tests of split brain patients, posited that the corpus callosum communicated stimuli and responses between the two hemispheres, each specialized for different cognitive functions (1).
Using a tachistoscope, Sperry delivered visual stimuli to a single visual field of the subject (1). He discovered that, with the exception of olfactory stimuli, the hemispheres of the brain receive sensory stimuli and exercise motor control contralaterally (1, 3, 5). Thus, when a word or picture of an object was flashed to the right eye, the patient was able to name the object or read the word. However, when a picture of an object was flashed to the left eye, the patient could not name it and in fact would deny seeing the object. Simultaneously, the left hand could point to the object or pick it out of a group of concealed objects (1). Thus, if a strong smell such as garlic or ammonia were presented to the right nostril, whose olfactory receptors connect directly to the right hemisphere, the patient would grimace with disgust while verbally denying that she smelled anything. However, her left hand could point to the object the right nostril had smelled, as the patient continued to say she smelled nothing (1, 5). .
Thus, with the primary information pathway between the two hemispheres severed, subjects apparently could not transfer information received as sensory stimuli between hemispheres. The researchers believed, however, that the two hemispheres attempted to communicate through external cues (4, 6). For example, when a subject was told to retrieve with his left hand a pencil palpated with his right hand, the right hand jabbed the left hand with the pencil (6). Researchers commonly observed subjects in similar tests saying aloud the name of the object touched with the right hand; the right hemisphere can sometimes understand many individual words and will then know what object to retrieve (4, 6). Researchers often saw subjects using facial expressions, such as frowning and smiling, in apparent attempts to cue the hemisphere that was attempting to complete a task (6).
These and similar experiments led Sperry to conclude that the corpus callosum served as the information pathway between the human brain's two hemispheres (1, 2). The results also suggested that the left hemisphere had exclusive control of language, and consequentially a split brain person could only speak about sensory input of which the left hemisphere was aware (1, 2, 4). Likewise, the researchers concluded that the hemispheres attempted to exchange information through external cues when internal pathways were severed (6). However, contrary to initial expectations, the right hemisphere could understand and respond to simple language, possessed a fund of general information, and had the same memories as the left hemisphere (1, 2).
Based on tests of a small pool of split brain subjects, a somewhat rigid functional portrait of the right and left hemispheres was developed (7). The right and left hemispheres were assigned respective areas of competence in a detail that sometimes rose to the level of assigning each hemisphere a personality: the left brain was analytic, language competent, and sequential in its thought; able to solve complex problems. The right hemisphere, by contrast, was visuospatial, synthetic, more emotionally attuned and creative (2,7). In sum, the researchers succumbed to the temptation to extrapolate general principles from a small set of individual observations.
However, as experiments continued, as researchers developed equipment able to deliver more information for longer periods of time to a single hemisphere (4)., as the effects of time on the split brain subjects began to manifest, and as more split brain subjects became available for study, the mapping of the brain became at once more detailed and less definite (2,7). Researchers discovered that the location of brain functions sometimes varied from patient to patient. The most dramatic example was a split brain patient who had speech in the left hemisphere, but writing in right hemisphere (2,8). . Younger patients, who were twelve to fourteen years old at the time of the operation showed significantly less lateralization of function than did older patients whose hemispheres had decades in which to specialize before commisurectomy (10). Finally, some experimental data suggested that split brain subjects developed and/or made greater use of subcortical connections between the hemispheres to integrate sensory input and motor output (11,12).
All of these findings provided evidence that individual brains can vary widely and respond to changes in conditions by developing and/or using different neural networks as well as coping strategies external to the brain (2, 5, 7). However, there was little discussion of the possibility that the frequent testing of the right hemisphere in isolation may have helped stimulate it to develop language. Likewise, requesting that test subjects integrate stimuli separately but simultaneously delivered to each sphere may have helped stimulated the subjects' brains to develop or use existing subcortical connections to compensate for lack of callosal connections. Attention focused not on the potential contribution of the experiments to the results, but rather on the left hemisphere's responses to behavior in response to stimuli received exclusively by the right hemisphere.
The left hemisphere of a split brain has no experience of stimuli delivered exclusively to the right hemisphere, yet the left hemisphere attempts to craft explanations for behavior initiated by the isolated right hemisphere. For example, a split brain subject's left eye received a command to stand. The person stood, but when asked why she stood up, she responded, using the language center of the left hemisphere, that she wanted a soda (7). . Likewise, when the left and right hemispheres were each asked to pick an appropriate picture to accord with an image flashed only to that hemisphere, the left selected a chicken to match the chicken claw in the picture it saw, while the right hemisphere correctly chose a shovel to remove the snow it saw. When asked why the person chose those images, he replied that the claw was for the chicken, and the shovel was to clean out the shed. (5). Similarly, the left hemisphere will generate false memories to fill in blanks in a sequence it is attempting to recall, while the right brain will not. (5).
Michael Gazzaniga, one of the original members of Sperry's laboratory and now head of the cognitive neuroscience program at Dartmouth College, suggests that this ability of the left hemisphere to confabulate is the product of its unique efforts to interpret actions and experience (2, 5, 7). The interpreter attempts to organize experience into patterns and responds to these patterns (2, 5, 7). The interpreter is driven to create explanations for experience and individual phenomena; when it does not know the facts, it makes its best guess (2, 5, 7).
The behavior of neuroscience researchers as they examined split brain subjects can also be construed as supporting the existence of this interpreter, offering explanations and finding patterns in an effort to make sense of their observations. The study of split brains presents a version of the light in the refrigerator problem: as Kandel points out, split brain studies, while essential in identifying the role of the corpus callosum, show much more about how separate hemispheres operate in its absence than they do about how the hemispheres function when connected (3).. Once the hemispheres are split, they function in isolation, with lateralization of function emphasized unless and until the brain develops adaptive strategies. Indeed, the split brain experiments may have themselves contributed to the development of different functions and coping strategies in and between the split brain's hemispheres. Yet eagerness to find a pattern, to interpret experience, however limited, perhaps impelled by the left hemisphere's interpreter, moved researchers to reject one hypothesis only to enshrine another equally rigid and equally, albeit differently, distorted picture of reality. The researchers' initial inclination was to assume that the first split brain patients' brain functions were representative not only of all split brain patients but of the hemispheres' functions in a brain with an intact corpus callosum. The left brain interpreter may well have been at work in the experimenters as well as in their subjects.
1) Nobel e-Museum, the official web site of the Nobel Foundation, filled with articles and information about Nobel laureates.
2) Gazzaniga, Michael, "The Split Brain Revisited," pp. 50-55, Scientific American, 1998 from theWeb page of Dr. Gary Laver, an assistant professor of psychology at California Polytechnic State University. The Web page is not of great interest but the article is free.
3) Kandell, Eric, Schwartz, J., and Jessel, T., Principals of Neural Science, 4th Ed., McGraw-Hill: NY, 2000.
4) Nobel e-Museum Zaidel, Eric, Zaidel, D., and Bogen, J., "The Split Brain," at Dr. Joe Bogen's home page
5) Gazzaniga, Michael, "Organization of the Human Brain," pp. 947-956, Science, Sept., 1989. Available on the Bryn Mawr College library server through http://web7.infotrac.galegroup.com.
6) Puccetti, Ronald, "The mind with a double brain," The British Journal for the Philosophy of Science, p. 675-692, Dec. 1993. Available on the Bryn Mawr College library server through http://web7.infotrac.galegroup.com.
7) Connors, Diane, "Michael Gazzaniga (neuroscientist) (interview)," pp. 99-106, Omni, Oct., 1993.
8) Strauss, Evelyn, "Writing, speech separated in split brain," pp. 827-828, Science, May, 1998. Available on the Bryn Mawr College library server through http://web7.infotrac.galegroup.com.
9) Bogen, J.E., Dezure, R., Tenhouten, W.d., and Marsh, J.F., "The Other Side of the Brain IV. The A/P Ratio," on Dr. Joe Bogen's Web page.
10) Gazzaniga, M.S., Eliassen, J.C., Nisenson, L., Wessinger, C.M., Fendrich, R., Baynes, K., "Collaboration between the hemispheres of a callosotomy patient. Emerging right hemisphere speech and left hemisphere interpreter," pp. 1255-632, Brain; a Journal of Neurology, Aug., 1996.
11) Sergent, J., "A new look at the human split brain," pp. 1375-1392, Brain; a Journal of Neurology, Oct., 1987.
12) Corballis, Michael, "Visual Integration in the Split Brain," pp. 937-959, Neuropsychology, 1995.
Other Web sites of interest:
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| Aggression: Biological, Psychological and Cultural Name: Ashley Far Date: 2002-04-22 21:54:18 Link to this Comment: 1916 |
Most people will agree that aggression can become dangerous and that it is a serious problem. The source of different acts of aggression is trying to be understood from medical, psychological and cultural perspectives. Some scientists try to treat the abnormal aggressive behavior with medication, while others go deeper and try to find out why they have abnormal behavior. Some answers are biological, like genes and hormones, other answers are psychological, like rejection as a cause of aggression, and still others are cultural, blaming aggression on violence in the media.
Some men who are aggressive are being treated by scientists who are using SPECT, Single Photon Emission Computerized Tomography, to identify regions of the brain that are causing the problems with aggression. (1) SPECT creates a color picture of the blood flow and activity in the brain and variation in color reveals abnormalities and damaged regions. (1) Unusual increased or decreased activity that are key in causing aggression are often found in three areas of the brains. (1) Aggressive thoughts reside in the left temporal lobe; the anterior cingulate gyrus controls repeated thoughts and amount of attention given to something; and the prefrontal cortex controls impulse. (1) Usually aggressive men have too much or too little activity in the left temporal lobe, too much activity in the anterior cingulate gyrus and too little activity in the prefrontal cortex so that they cannot control themselves. (1) By identifying which region or regions are abnormal scientists can prescribe the best drug treatment for that specific person. Drugs help balance the activity in their brains, but why are they imbalanced in the first place?
In a few cases, faulty genes have been found to be the cause of over aggression. There is a Dutch family that has a long history of maternally linked men with aggression problems. (2) Because it is maternally passed down and only affects the men it is decidedly a problem with a recessive gene on the X chromosome. (2) After years of research there was a breakthrough that allowed them to pinpoint the defect to the MAO gene area, which consists of the genes MAOA and MAOB. (2) Both genes produce monoamine oxidase enzymes, so they measured the levels of the different enzymes to determine the specific gene. (2) Eventually a defect in the gene MAOA was found to be the cause of their abnormal aggression. (2) How does this discovery help the aggression problem so prevalent in today's society? Well, it is not clear yet whether this gene is a problem for people outside of the family who are aggressive, and generalizing could be dangerous. One scientist warns that "it would be a disaster if people suddenly decided to begin screening babies for monoamine oxidase deficiencies--as some did for the XYY defect." (2) Whatever scientists do with this new information it is another step towards answering questions about the origin of aggression.
Scientists have also been studying aggression in animals. Male mice that don't have the gene that allows nitric oxide, a neurotransmitter, to be produced in the brain are extremely physically and sexually aggressive. (3) On the other hand, when the brains of female mice were not producing nitric oxide they were remarkably not aggressive in situations where they would normally be aggressive. (4) The surprising difference has not yet been explained. Rats without gene mutations also show a difference in amount of aggression between males and females. (5) The fact that male rats are much more aggressive than females is related to the finding that male rats have depleted amounts of dopamine and serotonin in their brain compared to female rats. (5) Levels of serotonin also have a negative correlation to aggressive behavior in humans. (6) When there is more serotonin, there is less aggressive behavior. Many correlations have been found between aggression and certain chemicals in the body. One study has shown that low levels of cortisol in saliva of boys are correlated with the boys antisocial and aggressive behaviors. (7) Another study found that aggressive criminals have abnormal ratios of serum copper and plasma zinc in their blood, when compared to non-aggressive non-criminals. (8) One thing to keep in mind, however, is that correlation study findings only show associations and do not show cause and effect, so lack of serotonin could cause high aggressive behavior, or high aggressive behavior may cause low levels of serotonin.
Many times aggression in youth has been blamed on media, specifically TV and video games. One longitudinal study done by Leonard Eron and L. Rowell Heusmann found that eight year olds who watch a lot of violent TV are more likely to be arrested by the time they're thirty years old. (9) This study has been strongly disputed by Jonathan Freedman and Richard Rhodes on the basis that the numbers are not as significant as Eron and Heusmann claim. (9) Freedman and Rhodes go so far as to postulate that watching violence can be good for people. (9) Craig A. Anderson and Karen E. Dill found that the effects of video game violence exposure largely depend on whether or not an individual has an aggressive personality. (10) If one has a high aggressive personality and high exposure to video game violence, their aggressive behavior increases dramatically more than those with low aggressive personalities and high video game exposure. These results could be expected or surprising depending on the viewpoint taken, and as there is no such thing as a perfect study there are probably valid arguments against these studies. As a coping mechanism people create different scripts in their mind to deal with different problems. One concern about violent video games and TV is that the violence is presented as a solution to problems and that kids might develop scripts that use violence. (10) On the other hand playing violent video games do not cause direct harm to people, so it can be argued that playing these games are a way of releasing anger in a healthy way- much like hitting a pillow instead of one's sister.
It is thought by some people in this country that if there were less exposure and promotion of weapons, there would be less violence and aggression. One response to this is the saying 'guns don't kill people, people kill people.' But there have been many studies that show that the presence or pictures of guns make people more aggressive. (11) One recent study has explained this occurrence by showing that exposure to weapons increases aggressive thoughts. (11) When aggressive thoughts are more prominent in the brain, then people are less likely to act rationally and more likely to act on their aggressive impulse when provoked. (11) Another study focused on rejection in youths and the aggressive behavior elicited by being rejected by peers. (12) Rejection was found to be a direct cause of aggression. So, both the presence of weapons and the feeling of being rejected aid in increased, abnormal aggressive behavior.
We have begun to look at different explanations of the why's and how's of aggression. Different biological, social and psychological reasons are presented and are equally supported and rejected. One thing that can be determined by acknowledging the different possible causes of aggression is that there is not one thing that causes aggression, because everyone acts differently to different problems. Not everyone who is rejected acts out aggressively, so maybe some of the people who do act aggressively have other problems that are biological in nature. Aggression is a bio-psycho-social issue that is being addressed, and needs to be addressed in the future, from all different perspectives.
(2) Evidence found for a possible 'aggression' gene.
(3) Scientists Discover a Genetic Basis for Aggressive Behavior in Male Mice
(4) Brain Chemical Mellows Male Mice, Makes Mouse Mothers Tough
(5) Male aggression: inborn, not learned behavior
(6) Relationship between 5-HT function and impulsivity and aggression in male offenders with personality disorders
(7) Low Levels Of Salivary Cortisol Associated With Aggressive Behavior
(8) Copper, Zinc Levels Linked to Aggression
(9) Should You Let Them Watch?
(10) Video Games and Aggressive Thoughts, Feelings, and Behavior in the Laboratory and in Life
(11) Presence of Weapon Increases Aggressive Behavior
(12) If You Can't Join Them, Beat Them -- Psychologists Find Rejection Causes Aggression
| Phantom Limbs: A Neurobiological Explanation Name: Tara M Raj Date: 2002-04-23 01:09:28 Link to this Comment: 1921 |
Severely injuring a digit or limb can result in unrepentant damage and amputation. However, the painful sensations experienced in regard to that limb do not necessarily cease after amputation. The concept of feeling sensations in a limb that is no longer attached to the body is referred to as feeling a "phantom limb." This phenomenon is experienced by approximately 80%-100% of all patients who have lost a limb (1), and has therefore sparked wide interest in scientific community.
Phantom limb sensations are common for people with missing limbs or digits. In most cases, a phantom arm hangs straight down at the side when the person sits or stands (2). The subject feels as though the limb is there even though he or she is consciously aware that it is no longer attached to the rest of the body. For example, a story by S. Weir Mitchell was written in 1866 in which a civil war soldier undergoes amputation of both legs after a battle. Before the patient knows that his legs have been amputated, he asks the nurse to scratch them for him as he feels discomfort. The nurse and doctor are surprised and dumbfounded since they both are aware that the soldier no longer has these limbs and therefore should not being feeling any pain or discomfort stemming from them (2).
While the story of this soldier is fictitious, similar events occur constantly in patients who suffer the loss of a limb. There are phantom sensations that are not painful, including warmth, tingling, itching, movement, and uncomfortable positioning (1).. However, phantom pains are also common in which the subject feels stabbing, cramping, burning, and shooting pains in the phantom limb (1).
The biology behind phantom limbs is especially important in understanding and trying to treat the phenomenon. Since the senses are prompted by sensory neurons, phantom pains must also be the result of action in sensory neurons. However, if the leg is no longer attached to the body, then how can the neurons in the leg transport signals to the nervous system in order for the body to feel sensations?
One possible explanation is the existence of neurons from the phantom limb even after amputation. Even though the neuron's axons were cut, the neurons could still be present due to regeneration of broken axons. This would allow for an action potential to travel back to the spinal cord even though the leg itself is no longer attached. The sensory neurons are still in tact with the central nervous system and the body can therefore still feel sensations coming from the missing limb (4).
A study was performed by Merzenich in 1986 in which the index finger of a monkey was amputated, and signals were monitored in the corresponding part of the monkey's corticol map (3). Since the monkey's finger was no longer attached to the body, the logical hypothesis is that there would be no signals coming from the finger's area to the nervous system. However, every time the two fingers adjacent to that of the amputated one were touched, there were nerve impulses in the spinal cord. This led the scientists to believe that there are existing axon branches that become unbranched after normal input ends.
Similarly, Pons et al. demonstrated in 1991 that in adult monkeys in which one or more arms had been removed, the representation of the arm could be occupied in other representations of the body (1). In essence, if one part of the somatosensory cortex is deprived of input, the somatosensory cortex will reorganize the inputs so that the idle areas of the cortex become active.
Support of this theory includes a study done by Romachandran in 1992 that studied a subject soon after losing an upper limb and one digit. The subject was lightly touched in varying places to try to localize where phantom pains originated (1). It was found that certain regions, called reference fields, evoked phantoms pains for a specific limb or digit.
Since the senses are actually felt in the thalamus and cerebral cortex, it also makes sense that certain areas also experience more intense phantom sensations than others. For example, the most distal areas are the thumb and index fingers, which have the most extensive representations in the thalamus and cerebral cortex (1). This fact shows that phantoms pains correlate with the firing of sensory neurons to the brain, and those appendages with more complicated representations in the central nervous system mean more intense and more frequent phantom feelings.
Further support for the hypothesis axons exist in areas after normal input ceases is that amputation is not necessarily required for phantom pains. In an accident in which the shoulder is strongly thrown forward and all of the neurons are ripped from the spinal cord, phantom pains are also experienced (2). In this example, the axons of the neurons are torn, but the neurons are still present and can still pass action potentials to the nervous system which lead the brain to believe that it can feel the limb, even though it brain cannot physically move the limb.
Phantoms limb pains are experiences that biology and neurology are together beginning to uncover and understand. Perhaps after finding a definitive explanation for the sensations, subjects experiencing uncomfortable phantom pains will be able to seek some kind of therapy or treatment. The phenomenon is an excellent example of the interesting ways that neurons and the nervous system function, and it continues to question the concepts of knowing and consciousness.
1)Biological and Neural Network Models of Phantom Limbs
2)Scientific American: April 1992. Phantom Limbs
| Laughter Name: Michele Dr Date: 2002-04-23 04:28:33 Link to this Comment: 1923 |
"Analyzing humor is like dissecting a frog. Few people are interested and the frog dies of it." --E. B. White
Why do people laugh? Laughter is contagious and therapeutic. It helps us cope with stress, and relax with friends. It is an indication of happiness, the sole reason we go on living. But what causes people to laugh? People laugh at jokes, semantic humor, which relies on cognitive ability to process the "humor" therein, or sometimes at slapstick type behavior requiring no intellectual understanding. People laugh at different things and for different reasons, and for the few that are interested at the expense of the frog, it can be interesting to investigate.
Every individual varies in their neurological pathways through their "boxes" in their brain to reach the output of laughter from a number of different inputs. Laughter is caused by certain visual or audio stimuli, often by perception of the unexpected or the incongruous. A surprise in expected input can result in an emotional change, however major or minor. As H. Spencer says in his Physiology of Laughter, "the nervous system in general discharges itself on the muscular system in general: either with or without the guidance of the will" (1). Incongruous input causes an emotional change, and in the case of humorous response, resulting in the contraction of facial muscles and certain muscles in the abdomen. The epiglottis half closes the larynx, resulting in giggling, guffawing, or gasping, and tear ducts are activated. These outputs of the nervous system we refer to as laughter can be arrived at through a number of pathways through the boxes of the brain, fabricated in each individual throughout their life to that point.
Although different parts of the brain are involved in understanding different types of input necessary for the laughter output, the median ventral prefrontal cortex is a key player in the physical response. Using functional magnetic resource imaging, scientists at the Institute of Neurology in London scanned the brains of people listening to jokes, and found that for example, semantic jokes, playing on the meaning of words, activate the posterior temporal lobe, and puns, which work with the sound of words, activate the left inferior prefrontal cortex. At any rate, however the input is initially processed to be found incongruous with normal expectations, the median ventral prefrontal cortex is signaled to handle the response. This area is incidentally also involved in the reward system in humans and primates, explaining why humor and laughter are enjoyable and continue to be sought as a form of entertainment (2).
Primates laugh too? As Robert R. Provine puts it, "chimpanzee laughter has the sound and cadence of a handsaw cutting wood," explaining why one might not recognize the laughter responses of animals (3). Furthermore, the laughter response of rats is merely an ultrasonic chirp (4). Animals lack the cognitive complexity that humans possess, restricting the less advanced, such as rats, to laughter induced only by tickling. However, the rats that chirped most were also the most eager to be tickled (4). This corroborates allegations that the reward system of the prefrontal cortex is responsible for the enjoyment of laughter. This reward system is involved in the compulsion to continue all enjoyable activities, invoking through desire those activities necessary for life, such as eating and sex, and entreating others that are unnecessary, such as drug addiction. In any case, the reward system relies on the release of dopamine in the prefrontal cortex, a pleasure-inducing neurotransmitter (5). This pathway is activated by a reward stimulus, and in the case of personal amusement, the reward stimulus is something that causes the subject to laugh.
Reward stimuli vary in humans, due to our increasingly complex intrinsic variability compared to those of primates and rats. An interesting example is the concept of contagious laughter, where the response activity in the brain is not the prefrontal cortex, but the anterior motor cortex and the nucleus accumbens, an area also associated with the reward system (6). Although no typically unexpected stimuli are present, the laughter continues. The anterior motor cortex and nucleus accumbens are not responsible for processing "funny" information anyway, they are merely acting as pawns of the reward system in this case, and this may explain the addictive nature of the laughter reward.
Laughing has various causes, but in general, stimuli incongruous with the expected input cause the majority of responses. This type of input doesn't always cause laughter, however. Unexpected events or stimuli can cause either 1) acute stress, if the implications are negative, or 2) humorous response, if the significance is negligible. Stress is dealt with in a number of ways, but the primary physical responses to relieve stress are laughing and crying. Both are completely natural responses and relieve the muscle tension caused by stress. Although it is understandable that one would prefer to laugh than cry for obvious reasons, there are also biological benefits to laughing for stress relief. Laughter boosts endorphins, and causes the reduction of certain neuroendocrine hormones: epinephrine, cortisol, dopac, and growth hormone, all of which are part of the body's stress response. For example, during stress, the adrenal gland releases corticosteroids, converted to cortisol in the bloodstream, which has an immunosuppressive effect. The experience of laughing lowers cortisol levels in the bloodstream and consequently boosts T-cell activity (7).
We know what parts of the brain are involved in laughter and what it can do biologically and neurologically. We know laughter requires external input or internal realizations, since is impossible to laugh on cue--making laughter one of the few physical actions humans cannot will themselves to sincerely perform. The origins of laughter are primitive and still largely not understood, but its benefits are many, and unmistakably clear.
1)H. Spencer: Physiology of Laughter,
2)Where in the brain is the funny bone?,
4)The Biology of Humor: The Laughter Circuit,
| Generalized Anxiety Disorder Name: Joan Stein Date: 2002-04-23 11:17:44 Link to this Comment: 1927 |
Anxiety is a common occurrence and emotion in everyday life. Yet there are several individuals today who suffer from great pangs of anxiety and feelings of panic at such extremely high levels that it becomes quite debilitating. A normal, everyday environment can become so overwhelming that the day itself can stop dead in it's tracks while the sufferer rides through the wave of intense emotions and thoughts which seem to be going a million miles a minute and showing no signs of stopping or slowing down.
Generalized Anxiety Disorder (GAD) is one of a multitude of Anxiety Disorders that affect many people around the world. An individual suffering from GAD differs from anyone else dealing with natural anxiety due to the chronic and exaggerated worrying that can occur on a daily basis. The worries and anxieties usually are not provoked by anything, and finding the source of the worries is usually quite difficult. They are associated with daily things, such as but not limited to, health, money, family, or work. People with GAD cannot alleviate their concerns and usually become so overwhelmed by the anxiety that getting through the day and doing their usual activities proves too difficult.(1)
As a disorder, GAD is diagnosable. However, it is usually a difficult thing to do since GAD, unlike many of the other Anxiety Disorders out there, does not have any definite symptoms like a "panic attack". Individuals are diagnosed with GAD when they spend at least six months worrying excessively about a number of everyday problems and the worrying happens more often than not. Other symptoms of GAD may include: Trouble falling or staying asleep, muscle tension, sweating, nausea, gastrointestinal discomfort or diarrhea, cold and clammy hands, difficulty swallowing, or jumpiness.(2)
The cause of GAD is relatively unknown. Many believe and have evidence that GAD can be genetic and may run in families, while others see a correlation to GAD and situations of extremely high pressure and stress. Some research even suggests that there could be a specific gene related to disorders like GAD. GAD often coexists with other anxiety disorders, clinical depression and substance abuse.(3) Doctors who treat patients with diagnosed clinical depression find symptoms of anxiety to be a good sign, because it means that the individual hasn't simply accepted their depressed mood as they would a free meal. They are depressed and they are anxious because they are concerned about the ego dystonic nature of their depressed mood. A thorough initial evaluation is rudimentary to ruling out other possible and more appropriate diagnoses.(4) Some also find GAD caused by an overdose or overproduction of serotonin, a chemical in the brain that usually fights depression and anxiety, but too much can cause a reverse affect.(5)
About ten million adults or 3-4% of the population suffer from GAD, and women are more likely to have it than men. It can start at any time during childhood and adolescence, but can begin in adulthood too, usually around the early twenties.(3)
There are a few ways to go about treatment of GAD. The most common approaches are with psychological treatment, and if necessary medication. GAD patients have been shown to respond best to cognitive-behavioral therapy, an active form of therapy that involves more than just talking to a therapist. The individual gradually learns to see situations and problems in a different perspective and learns the methods and techniques to use to alleviate and reduce anxiety.(6) Drug treatment, although suggestively not the best way to go about treatment is another commonly used alternative. Certain medications are used to help relieve some of the symptoms of GAD, such as Valium and Ativan, the two most prescribed benzodiazepines. A non-benzdiazepine medication used for treatment is buspar (buspirone), a better alternative for long-term treatment. And, of course, self-help and support groups are another source of treatment that is encouraged.(4)
As amazing and complex as the brain is, the development and recognition of the numerous conditions and problems that can go on with the brain show how delicate a human's mentality and stability is, and how vulnerable it seems to be to the rapidly changing times and developments of society. It seems to be the nature of the brain and mentality to be slow in adjusting to the various new outputs that are created as society and the world progresses. Will science be able to find a way to make the brain adjust and accept change more quickly? This can be seen as a task similar to making evolution as fast as the first world's rate of development.
1)http://www.nimh.nih.gov/anxiety/anxiety/gad/gadinfo.htm
2)http://www.adaa.org/AnxietyDisorderInfor/GAD.cfm
3)http://www.nimh.nih.gov/anxiety/anxiety/gad/gadfax.htm
4)http://psychcentral.com/disorders/sx24t.htm
5)http://www.buspar.com/whatis.htm
6)http://www.anxietynetwork.com/gawhat.html
| ADHD and My Family: Searching for a More Scientifi Name: Priya Puja Date: 2002-04-23 13:03:47 Link to this Comment: 1929 |
My father, like many Asian immigrants, left India to pursue his educational goals in America in
order to provide a better life for his family. He arrived in the U.S. with fourteen dollars in his
coat pocket, a suitcase in his hands, and a will to succeed. For my father, in a place like America
where opportunities were plentiful and where hard work actually paid off there was no excuse
not to succeed. The practical translation of this belief meant that if his children worked hard in
school there was nothing they too could not achieve. As such, in my father's household, not
doing well in school was not an option.
Because of his cultural background my father found my brother's poor performance in school
incomprehensible. I too was puzzled by my brother's attitude towards school. He and I grew up
in the same house with the same parents and the same set of values. Yet, he seemed to not care
about school at all. For a long time, my family and I attributed my brother's C's in school and
obvious inability to concentrate to laziness and a lack of motivation.
My brother's diagnosis with Attention Deficit Hyperactivity Disorder (ADHD) was both a
welcomed explanation and a shock to my parents. On the one hand, my mother and father had
begun to question their parenting abilities, and this allowed them to shift the blame from
themselves. On the other hand, they had a very limited understanding of mental illness. In
particular, the concept of mental illness itself was not something they were terribly familiar with.
For my parents, problems of the mind were problems that existed within the scope of personal
will power.
In many ways, I partially subscribe to the world-view that my parents hold. As such, until
recently, I've been skeptical of my brother's diagnosis. In particular, at the time, it seemed to me
that distractibility was something that I too suffered from. I didn't enjoy forcing myself to
concentrate, but I did it because I knew that I had to. In addition, my brother seemed perfectly
capable of concentrating when he was playing soccer, watching the Discovery channel or playing
video games. In my mind, his problems appeared to be that he was spoiled and didn't like being
told what to do. In addition, I think that ADHD gave everyone in my family the excuse that they
needed. My parents could absolve themselves of any blame and my brother could walk way
continuing to be distracted. Beyond my family, I thought that ADHD as a distinctly Western
phenomenon. Most kids regardless of culture don't like sitting still in desk in school, but only in
America is such a commonplace occurrence given the legitimacy of medical label. In fact, it
seemed to me that labeling kids with ADHD was a clever way for society to avoid reforming its
educational system. Needless to say my recent studies of ADHD have shown me how ignorant I
was about the disorder.
ADHD, often referred to as ADD (Attention Deficit Disorder) affects between 3 to 5 percent of
school age children 1)National Institutes of Health,gives the most recent official opinion on ADD.
According to a recent consensus paper by the National Institutes of
Health, the core symptoms of ADHD are developmentally inappropriate levels of attention,
concentration, activity, distractibility, and impulsivity 1)National Institutes of Health,gives the most recent official opinion on ADD.
In addition, the "exact nature and severity of ADHD symptoms varies from person to person" 2)Attention Deficit Disorder Association,information geared to people who have ADD.
These symptoms have to be excessive, long term and pervasive and they must create a real handicap in at least 2 areas of the
person's life. It is these criteria that set ADHD apart from normal distractibility 3)Attention Deficit Disorder Association,information geared to people who have ADD.
ADHD is a complicated disorder the causes of which are not well understood. As a result, there
are several controversies surrounding ADHD. In particular, there are controversies about the
actual existence of the disorder, whether it can be reliably diagnosed, and how it should be
treated 1)National Institutes of Health,gives the most recent official opinion on ADD.
This is because at some level defining the boundaries of developmentally
"appropriate" behavior and "normal" distractibility is a matter of personal opinion. The
previously mentioned core symptoms are just one example of the subjective nature of the
disease. According to one doctor, "If the behaviors or symptoms are not severe enough then by
definition it's not ADHD" 4)Attention Deficit Disorder Association,interview with a physician, Dr. Peter Jaksa.
The problem with diagnosing ADHD is that there is very little
consensus as to what is "severe enough" to be considered ADHD. In particular, no independent
diagnostic tests to date exist and interview tests are the only means to diagnose the disease.
Fortunately, advances in neurological screening and genetics are beginning to shed light on the
biological aspects of ADHD. As a result of this progress, in the future, more objective
diagnostic criteria may be available. Imaging studies have implicated certain regions of the
nervous system. According to one study, the prefrontal cortex, the two basal ganglia (the
caudate nucleus and the globus pallidus), and the vermis region are significantly smaller in
children who have ADHD 5)Scientific America,great article about research surrounding ADD.
These findings are telling because each of these regions is closely
associated with the core symptoms of the disorder. In particular, the prefrontal cortex is the
considered the command center of the brain and is involved in regulating the ability to inhibit
responses 6)WebMD Lycos,general informationon ADD.
The basal ganglia, clusters of nerve cells located near the center or the brain,
manage the impulses coming to and from the prefrontal cortex. Taken together abnormalities in
these regions provide an insight into the impulsive nature of individuals who have ADHD 6)WebMD Lycos,general informationon ADD.
Although the exact role of the vermis region is not understood, previous studies suggest that it
may be involved in regulating motivation 5)Scientific America,great article about research surrounding ADD.
According to several studies, the shrinkage of these particular structures in individuals with ADHD may be due to mutations
in several genes that are normally active in these regions 5)Scientific America,great article about research surrounding ADD.
Not only are there anatomical differences in individuals who have ADHD, there are
pathophysiological differences in individuals who have ADHD. In particular, the
neurotransmitter dopamine has recently become the focus of much ADHD research. Dopamine
is "secreted by neurons in specific parts of the brain to inhibit or modulate the activity of other
neurons, particularly those involved in emotion and movement" 5)Scientific America,great article about research surrounding ADD.
The impetus for the interest in researching dopamine can be traced to the fact that the standard medications for ADHD, such
as methylphenidate, target dopamine transporters. According to one 1999 study, in comparison
to individuals without ADHD, the density of dopamine transporters was elevated by
approximately 70% in individuals with ADHD 7)Internet Association for Biomedical Sciences,research article.
Not surprisingly, genetics seems to be the missing link between the anatomical and the
pathophysiological aspects of the disorder. Several studies have shown that the genes that
encode for dopamine receptors and transporters are very active in the prefrontal cortex and basal
ganglia 5)Scientific America,great article about research surrounding ADD.
However, there is other proof beyond this that suggests that genetic factors are a
major factor in the disorder. In particular, studies have shown that ADHD has a heritability
approaching 80% 5)Scientific America,great article about research surrounding ADD.
Although most researchers agree that ADHD is a polygenic disorder, the
genes coding for the dopamine receptors (D4) and transporters (DAT 1) have been the focal
points of recent research. Dopamine binds to receptors on certain neurons and thereby transmits
its message to these neurons. Mutations in these receptors can result in them being less sensitive
to dopamine 5)Scientific America,great article about research surrounding ADD.
As such, this could lead to a marked increase in extracellular dopamine.
Dopamine transporters, on the other hand, exist on the surface of dopamine secreting cells. They
function by actively recycling unused dopamine so that it can be used again 8)Med InfoSource,information about dopamine.
Mutations that render transporters inefficient would also lead to an increase in extracellular dopamine. A 1992
study showed that the 3'-noncoding region of DAT contains a polymorphic variable nucleotide
tandem repeat (VNTR) 7)Internet Association for Biomedical Sciences,research article.
In particular, a 10-copy repeat of a 40-base unit was found to be
associated with ADHD 7)Internet Association for Biomedical Sciences,research article.
These studies seem to suggest that elevated dopamine transporter levels may be a trait of ADHD.
As such, if further studies confirm this hypothesis, physicians
may have a concrete method for diagnosing ADHD
ADHD is not unique in that it is difficult to diagnose. Like many other neurobiological disorders
it is complicated and multifaceted. The recently discovered genetic basis for ADHD reveals the
extent to which genetics influences the brain equals behavior. For me, personally, my
experiences with brother's ADHD have taught me to be wary of my own personal biases when it
comes to mental health.
1)National Institutes of Health,gives the most recent official opinion on ADD
2)Attention Deficit Disorder Association,information geared to people who have ADD
3)Attention Deficit Disorder Association,information geared to people who have ADD
4)Attention Deficit Disorder Association,interview with a physician, Dr. Peter Jaksa
5)Scientific America,great article about research surrounding ADD
6)WebMD Lycos,general informationon ADD
7)Internet Association for Biomedical Sciences,research article
8)Med InfoSource,information about dopamine
| Psychological Effects of Medicinal/Recreational Ma Name: Alisa Alex Date: 2002-04-24 02:19:47 Link to this Comment: 1942 |
Is there a difference in the psychological/healing effects between the use of "recreational" marijuana and medicinal marijuana?
Before researching this question, I could not understand what difference medicinal marijuana would have on cancer patients that was not already known through previous studies on the drug. I thought I fully understood marijuana's effects on the brain until the issues of medicinal marijuana arose. Prior to the research on the subject, I assumed that much of what is known now about the drug is due to the extensive research on its affects on Cancer and AIDS patients. If the use of marijuana is controlled for therapeutic purposes, are the effects different if used regular for non-medicinal purposes? This is the question I attempt to answer through extensive web research.
In the past 5 years, there has been an increased debate about the use of medicinal marijuana in treating cancer and AIDS patients. Marijuana has been used in alternative medical treatment by doctors around the country and by patients themselves who seek relief from the pain caused by cancer and AIDS. Controlled use of marijuana has been used to treat a number of diseases:
"AIDS. Marijuana can reduce the nausea, vomiting, and loss of appetite caused by the ailment itself and by various AIDS medications.
Glaucoma. Marijuana can reduce intraocular pressure, thereby alleviating the pain and slowing -- and sometimes stopping -- the progress of the condition.
Cancer. Marijuana can stimulate the appetite and alleviate nausea and vomiting, which are common side effects of chemotherapy treatment.
Multiple Sclerosis. Marijuana can limit the muscle pain and spasticity caused by the disease, as well as relieving tremor and unsteadiness of gait.
Epilepsy. Marijuana can prevent epileptic seizures in some patients.
Chronic Pain. Marijuana can alleviate the chronic, often debilitating pain caused by myriad disorders and injuries." (1)
Institutions nationally have conducted studies on the use of medicinal marijuana on disease stricken patients. The Institute of Medicine published a journal on the use of marijuana and the effects it as a recreational drug and medicinal drug. Because the substance, when used medicinally, is monitored/controlled, the psychological effects on the patient is slightly different, and its effects also vary depending on the type of the disease the patient is suffering from. A complete report done by the National Academy of Sciences details the psychological effects of recreational and medicinal marijuana. In the 20th century, marijuana has been used more for its euphoric effects than as a medicine. Its psychological and behavioral effects have concerned public officials since the drug first appeared in the southwestern and southern states during the first two decades of the century. (2) After extensive research of the drug in the past decade, its actual effects used medicinally and recreationally were found. Research on cannabinoid biology offers new insights into clinical use, especially given the scarcity of clinical studies that adequately evaluate the medical value of marijuana. For example, despite the scarcity of substantive clinical data, basic science has made it clear that cannabinoids can affect pain transmission and, specifically, that cannabinoids interact with the brain's endogenous opioid system, an important system for the medical treatment of pain. (3)
When marijuana is taken without regulation of the intake, the effects are quite similar. Those taking the drug, whether recreationally or medicinally experience similar effects. Marijuana has been linked to psychological dependence but not proven to be physically addictive.
"Many users describe two phases of marijuana intoxication: initial stimulation, giddiness and euphoria, followed by sedation and pleasant tranquility. Mood changes are often accompanied by altered perceptions of time and space and of one's bodily dimensions. The thinking process becomes disrupted by fragmented ideas and memories. Many users report increased appetite, heightened sensory awareness and pleasure. Negative effects can include confusion, acute panic reactions, anxiety attacks, fear, and a sense of helplessness and loss of self-control." (4)
Some researchers conclude that constant recreational use of marijuana in high doses can cause lung cancer, respiratory problems and brain impairment. Those advocating the use of medicinal marijuana argue that because it will be controlled by the doctor administering the drug, there isn't a chance of psychological addiction or any other problems believed to be connected with marijuana use.
Only long-term research can show concrete long-term effects of marijuana use. The short-term usage of the drug is helping many cope with their illness, it is because of these effects doctors, patients, and medicinal marijuana supporters rally for legal use of the drug in America. Many who rally for legal use of the drug do so because the statistics fail to prove any long-term psychological effects even when used recreationally.
WWW Sources
1)Medical Marijuana Briefing Paper
2)National Academy Press
3)National Academy Press
4)The Effects of Marijuana
| A Little Thinking Music Name: Tua Chaudh Date: 2002-04-24 16:29:18 Link to this Comment: 1948 |
When you hear a piece of music, the ear converts the sound waves into vibrations in specific parts of the inner and middle ear. These vibrations are then translated into action potentials that travel through the eighth cranial nerve to the brain stem, the thalamus, and the auditory cortex (1). It seems that the brain takes a song and translates it into it's own neurosymphony-sending electrical impulses to various parts of your brain. These varying patterns of impulses generate thoughts, feelings, and emotions (3) . It sounds almost as though we store various different patterns of these impulses in our brains and when the same pattern of sounds matches a pattern of impulses, it triggers a set of images. The interesting thing is that the same set of frequencies or pattern of impulses generates different images for different people. For instance, when I hear the Beatles' Yellow Submarine, I think of Mr. C, my fifth grade teacher, his old record player, and rock and roll Tuesdays. When my roommate's brain registers the same pattern of impulses, it brings up the memory of her family's tan colored Volkswagen Rabbit. When I hear Beethoven's Moonlight Sonata, I hear raindrops and soft footsteps, while another person might hear rays of light falling on water. We all have distinct visions of the same pattern of sounds. Neurobiologists, like Harvard's Mark Tramo, have yet to figure out exactly how this comes about (3) .
Music is one thing that stimulates and utilizes most parts of the brain (2). Both the right and left hemispheres are involved because while one codifies lyrics the other tackles melody. According to Michael Tramo in his recent Science article, "the brain does not have a specific musical center", it involves parts of the brain normally utilized in other types of thinking (4). It makes sense then that music has the ability to generate emotions and memories, it actually stirs these sections of the brain. Because music is not visual or tangible, our brains can not use those senses to interpret it. Perhaps that is the reason the music draws on so many aspects of the brain to be heard and understood. The mechanisms of the ear and the auditory cortex bring music into the brain but it is a combination of many brain functions that help us to fully understand it. Along with the pleasure of sound we get memories, images, and thoughts. We enjoy music so much because it stimulates and exercises the entire brain.
Although everyone has differing experiences of this form of expression, music is commonly identified as the 'universal language'. Perhaps, the common enjoyment and understanding of music lies in the fact that we are all born with an ability to "process music" (5). Why is this so? What purpose does it serve humans as biological systems to be able to listen to and enjoy music? I think that in the beginnings, in most early civilizations, music and musical instruments were a form of communication. We sing, because, like other animals, we need to relate our perceptions of the world to one another. But we also listen to music for the pure aesthetic of it. It has recently been discovered that even the Neanderthals had flutes that were used to play melodies for entertainment. There is something about the beauty of music that appeals to our brains. It probably has something to do with the fact that listening to music involves relatively effortless enjoyment. When reading a book, one has to concentrate on the subject, the formation of the words, the plot, etc. But one does not necessarily have to do anything while listening to music. The stimulation that these patterns of sound generate in our brains in turn produce images, memories, and thoughts without us having to make a conscious effort. It could be argued that the I-function box experiences music vicariously through the other parts of the brain.
For a long time now music has been thought to be good for people. The Mozart Effect Experiment, though not proof positive of anything, did suggest that children who study music or play musical instruments, enhance their math and language skills (4). Exercise makes things stronger, so it makes sense that studying music, which exercises the language and cognition centers of the brain, would enhance their performance abilities. An interesting aspect of music, however, which has only recently been explored scientifically, is its healing capabilities. Melodic Intonation Therapy is being used on stroke victims to help them recover from language aphasia. Therapists have their patients sing what they wish to say in very particular tones or pitches. The right brain stimulates impulses in the damaged left brain and in doing so helps it to regain its abilities (5). Patients' improvements are better and faster with this type of therapy than with ordinary language and speech therapy. Music is used to soothe babies in intensive care units, ease the pain of patients who have experienced to severe trauma, jostle the memories of Alzheimer's sufferers, and prepare athletes mentally and physically for games (3). Although more research needs to be done to discover the details of why musical therapy is so effective, it is clear that we respond psychosomatically to these strangely powerful noises.
It would seem that there is something inherent in our brains which makes music an essential for survival. It isn't so much that we would die if we never heard a single note, or hummed a tune, or played a melody, but that our experiences of everything else would be slower, less vivid, not remembered as well. Music thoroughly exercises and stimulates the brain, and in doing so, makes it stronger, more capable, and more in-tune with the world inside and outside it. So, in agreement with the ABBA song, that I danced to as a kid,
I say thank you for the music, the songs I'm singing.
Thanks for all the joy they're bringing.
Who could live without it? I ask in honesty, what would life be?
Without a song or a dance what are we?
So I say thank you for the music for giving it to me.
1) Neuroscience for Kids-The Musical Brain
2) Music Making and the Brain
3) Music on the Brain
4) Newshour: Brain Music
5) Music and the Brain
6) How Your Brain Listens to Music
7) Scientific American: Explore!: Exploring the Musical Brain
8) MEHB - Music's Effect on the Human Brain
9) Music and the Brain
10) Preliminary Report on the Effects of Musical Intonation Therapy
| Creativity, the Subconcious, and Daydreaming Name: melissa ho Date: 2002-05-01 21:18:00 Link to this Comment: 2023 |
When an artist of any sort is inspired they have what can very closely be compared with a spiritual feeling. Some have said that this state in which, the imagination flows so freely is that of a conscious dream. In this short essay I will explore the ideas behind creativity and this dreamlike state of inspiration. In order to do so we must first decide what creativity is and then how it is affected.
Creativity¡¦ is it merely the expression of ones ideas, or must it be something that none has ever thought of before? My answer to this question is that neither idea is a proper definition for creativity. To be creative is the ability of the individual to express themselves in a passionate manner that is unique. The expression must be unique in the fact that the way in which it is expressed demonstrates the emotions and feelings of the creator. Also there are other forms of creativity such as inventing in which although the idea itself may not be completely new, or unrelated to something else, but that this idea is a composite of the information, which one has obtained throughout their life. This idea in order to be creative cannot be just a regurgitation of the ideas, but rather it must be an individual perspective. Creativity can be found in every day life in the simplest things, as in the way in which a person observes a flower that they are passing. However, what causes a creative genius is the way in which they express their unique perspective.
Creative Geniuses when asked about their feelings of inspiration have often said that they feel that their spiritualized feeling is similar to that of a dream. Could the dream-like state which artists experience during inspiration be similar to that of daydreaming? Absolutely, Day dreaming is when one¡¯s mind drifts from the task that it has been set to do. In this state we are still conscious unlike in sleeping dreams, but our mind is able to, so to speak drift into the depths of itself. There have been studies done that say that daydreaming is connected with intelligence and creativity. This is partially because sometimes our brain needs time to process information and although this is generally done during our REM sleep cycle sometimes it can carry over to our wakeful states. The benefits of daydreaming to creativity stem from the idea that, when our mind is in a sleep cycle it wanders to the subconscious.
When our minds are able to wander the subconscious, while conscious of our thoughts, and are able to regurgitate the ideas that are within our subconscious we are at the beginning basis for creative genius. Some artists that have been very interested in the subconscious are Dahli and Michael Parks, just two very well known surrealist painters. These painters try to visually relate what they see within their subconscious, and to spark thoughts within your subconscious. Also, many poems, songs, and stories stem from the subconscious. Much poetry is based upon deep human emotion felt at a level that few people truly feel. For a blade of grass or a cloud to inspire one as they have inspired Wordswoth is unthinkable. I believe that these inanimate objects to Wordsworth, as they are demonstrated in his poetry, show that these objects were merely a springboard for other emotions. Songwriters, such as Bjork and Anastio (songs are written for Phish) generally try to find a universal subject such as love, or inner turmoil so that it will affect a number of people whenever they hear it. Fictional stories such as those done by Edgar Allen Poe or J.R. Tolkien explore the limits of the human mind. Stories such as these could only be thought of by ones inner thoughts because they are so far from reality.
Imagination and artistic passion must stem or at least be easier to retrieve from our subconscious mind. The subconscious mind contains the runoff of emotions that are so passionate that although our brain produces them, they are inappropriate to express within normal social limitations. Perhaps the brains of true creative geniuses produce more emotions than most individuals or they merely suppress more emotions. However these so called geniuses definitely do have the gift of expressing these emotions.
That is what makes them geniuses and causes millions to admire their work. So, in my next paper I will begin to explore further the manner in which these emotions are expressed. In this paper I have set a basis for the next with the ideas of where the emotions and creativity itself stems from in order to form a work of creative genius.
1) (1983). The Journal of Creative Behavior (Vol.17). Buffalo, NY: The Creative Education Foundation.
2) Summerfield (Ed.). (1960). The Creative Mind and Method. Austin, Texas: University of Texas.
3) Singer, Jerome L. (1975). The Inner World of Daydreaming. New York, NY: Harper and Row, Publishers.
4) Sartre, Jean-Paul. (1948). The Psychology of Imagination. New York, NY: Philosophical Library.
5) Solomon (Ed.). (1979). Myth, Creativity, Psychoanalysis. Detroit Michigan: Wayne State University Press.
6) Boden, Margaret A. (1992). The Creative Mind. New York. NY: Basic Books.
7) Stein, Morris I. (1974). Stimulating Creativity. New York, NY: Academic Press.
8) Damasio, Antonio R. (1994). Descartes Error. New York, NY: Quill.
| Social Phobia or Just Shyness? Name: Amy Cunnin Date: 2002-05-08 10:39:04 Link to this Comment: 2063 |
As pharmaceutical companies began advertising on television several years ago, many prescription drug advertisements flooded the airwaves. One such drug was for the treatment of "social anxiety disorder," also called "social phobia." In investigating the causes, symptoms, and treatment of social anxiety disorder, I found that while drug companies and some researchers have hailed the unveiling of a drug for social anxiety as an important step, others feel that the disorder is poorly defined and its prevalence is exaggerated. Therefore, the following questions emerged: how did the diagnostic category of "social anxiety disorder" come about? How much of the disorder is rooted in cultural views of shyness? While certain individuals may indeed suffer from social phobia, it may be over-diagnosed because shyness is viewed as a condition in need of a cure.
This disorder consists of an intense fear of being watched by others or of being embarrassed in social situations. Such situations can include eating or writing in public, using public bathrooms, giving presentations and participating in a class discussion (1). Social phobia can also include fear of talking with strangers or "important people" and difficulty "being assertive" (2). Individuals may also experience physical symptoms such as sweating, shaking, and nausea. Additionally, before stressful situations individuals with social anxiety anticipate having these physical symptoms, often making them more severe. As a result, socially phobic individuals may avoid certain social situations, some to the point of missing school or work (1). Additionally, social phobia often co-occurs with other conditions, most often depression and alcoholism. An estimated one-half of all socially phobic patients have drug, alcohol, or other mental health problems: socially phobic individuals have a depression rate four times higher than average, and sixteen percent have alcoholism (2).
The disorder typically begins in childhood, and the National Institute of Mental Health estimates that 3.7 percent of 18 to 54 year olds in the United States have social anxiety disorder, with women diagnosed twice as often as men (1). Although researchers are not completely sure of the biological basis of social anxiety, some believe that its basis may lie in the amygdala, a small portion of the brain that controls fear response. NIMH scientists have also found a possible genetic component: through research on mice, they have found a gene that relates to fearfulness (1). Additionally, hormones may play a role, specifically fluctuations in estrogen and progesterone levels in women (4). Environment may also be important, as people with social anxiety may learn the behavior from watching and patterning those around them (1). Treatment may include the use of medications such as selective seretonin reuptake inhibitors (SSRIs), monamine oxidase inhibitors (MAOIs) and beta blockers specifically for "performance phobias." Individuals may also benefit from behavioral therapy, which involves gradual exposure to feared situations (1).
However, some believe that the category of "social phobia" or "social anxiety" is not so clear-cut. For example, the diagnosis of social anxiety can be difficult because of its co-occurrence with depression and other mental health conditions and the sometimes overlapping symptoms of these conditions (2). Another question that arises from reading literature on social anxiety is the difference between social anxiety and shyness. Researchers emphasize that social anxiety is a more extreme condition; however, some argue that the distinction is not always clear. Doctors diagnose social anxiety by asking patients questions about their anxiety levels in various social situations (7), which is of course a subjective measure that depends on the patients' perception of their anxiety.
Furthermore, some believe that the category of social anxiety came about because of changes in social perceptions of shyness and its resulting "medicalization." In her recent article in the Journal of Social History, historian Patricia McDaniel chronicles changing perceptions of shyness in the United States from the 1950s to the 1990s. McDaniel examined self-help books through the years, which were particularly targeted at white, middle-class consumers. She found that in the 1950s, shyness was viewed as a positive trait in women. In particular, women were advised to be shy in their interactions with potential husbands (3).
However, by the 1970s the women's movement had made shyness a less desirable trait: and excerpt from The Intelligent Woman's Guide to Dating stated that "tied tongue and locked legs were no longer attractive in a world where women commonly open up their needs and hearts to new acquaintances" (3). This change in advice books reflected general changes in societal attitudes about shyness. By the 1970s, shyness was seen as a problem in need of a "cure." For example, psychologist Philip Zimbardo stated in the late seventies that "shyness ... touches all of our lives in some way. What we each thought was our own secret hang-up is actually shared by an incredibly large number of people. And we can take great comfort in knowing we are not alone in our suffering." Additionally, the idea of shyness as rooted in biology gathered steam through the 1980s and 1990s (3).
As a result, some critics believe that the creation of the category of social anxiety disorder reflects that shyness moved from being a simple personality trait to a "syndrome" or "disorder" that needs to be cured. For example, from the 1970s to the 1990s an increasing number of Americans described themselves as shy (5), and the number diagnosed with social anxiety disorder rose as well. Additionally, social anxiety disorder first appeared as a diagnostic category in the American Psychiatric Association's Diagnostic and Statistical Manual in 1980 (5). While the original definition of social anxiety disorder included "avoidance of situations," later versions omitted this symptom and replaced it with "significant distress," amore general term which allowed more individuals to be diagnosed with the disorder (6). As a result, while in 1980 the percentage of American thought to have social anxiety was two to three percent (6), the percentage is now estimated as five to ten percent (4). Social anxiety is the third most common mental health problem after depression and alcoholism (6). Interestingly, while women are described as more likely to suffer from social anxiety disorder, men are more likely to seek treatment for the problem. The discrepancy may be because shyness is still considered more of a "feminine" trait that is looked upon more negatively in men (4) and therefore what might be considered "social anxiety" in men is considered "normal" in women.
Critics also believe that the recent rise is in part due to the aggressive marketing efforts of drug companies such as SmithKline Beecham, which in 1999 began marketing its antidepressant Paxil as a treatment for social phobia. The television and print ads for Paxil gave gloomy portraits of those suffering from social anxiety and framed it as a "pathology." Additionally, the media has devoted increasing attention to the disorder, including testimonials from celebrities who claim to suffer from the disorder (5). Social phobia researchers and advocates may have also overestimated the prevalence of the disorder in order to garner more attention and funding. As a result, social phobia became a "hot disease" like attention deficit disorder, which has also had a huge increase in prevalence in recent years (6).
While such critics acknowledge that certain individuals may indeed suffer from crippling social anxiety, the increasing publicity on social anxiety disorder may lead certain individuals to seek treatment who may be shy but not necessarily have a disorder. For example, the Paxil website states that "some people find comfort just by learning social anxiety is a medical condition (emphasis added) and that medication can put you "in control of your anxiety"(7). The website implies that the construction of social anxiety disorder as a medical category with an accompanying drug treatment legitimates it as a "real" problem. While some individuals may take comfort in the idea of social anxiety as a medical condition, critics believe that the sharp rise in individuals seeking treatment for social anxiety reflects the medicalization of a personality trait (6). Also, researchers point out that a certain level of anxiety or nervousness is normal, and an edge of anxiety before a major event may actually be beneficial (6).
As stated earlier social anxiety disorder has a broad definition (6) and the diagnosis is subjective, consisting of a patient rating their anxiety in social situations (5). Additionally, its relationship to depression and alcoholism needs to be further explored, since its symptoms may overlap with symptoms of these conditions. It appears that certain biological factors such as the amygdala and hormone fluctuations may contribute to social anxiety (1), but further research in these areas is necessary
Also, how to "draw the line" between shyness and social anxiety is a question that needs to be addressed further (5). Whether shyness is considered a "trait" or a "disorder" depends on the intensity of symptoms (1). I do not want to minimize the suffering of individuals with social anxiety. Some people indeed suffer from social anxiety disorder and need medication and therapy. However, others may simply be seeking medical assistance for a personality trait that may not need correcting. The rise in the diagnosis of social anxiety disorder may in part be because of increasing awareness of the disorder, but also reflects a society that frowns on shyness. As a writer recently asked in The New York Times Magazine, "Is somebody out there inventing the drug to treat excessive perkiness?" (5).
WWW Sources
1) "Facts about Social Phobia", from the National Institute of Mental Health
2) "Social Anxiety Disorder: A Common, Unrecognized Mental Disorder", on the American Academy of Family Physicians site.
3)"McDaniel, Patricia "Shrinking Violets and Caspar Milquetoasts: Shyness and Heterosexuality from the Roles of the Fifties to the Rules of the Nineties", Journal of Social History, Spring 2001, v34:3 (Available online on Gale Group)
4) "Social Phobia- Not Just Another Name for Shyness", on the JAMA website.
5) "The Shyness Syndrome", a reprinted version of a recent New York Times Magazine article
6) "Is Shyness Catching? Docs are on a hot new disease: social phobia", from the "Utne Reader Online"
7) Social Anxiety Disorder site, by Paxil.
| Hey, I Smelled Him First! (Smelling and the Brain) Name: Tiffany Va Date: 2002-05-09 02:41:15 Link to this Comment: 2064 |
Most creatures that wiggle, slither, swim, walk or just plain sit, survives by their noses. (4). The story mentioned above is just an example of the power that the olfactory system posses, or rather another example of the extraordinary brain at work as it is the brain that interprets the information received by the olfactory system and attempts to make sense of it. Stephen was able to distinguish one individual from the other nineteen people present at the clinic by simply using his sense of smell. My curiosity of the olfactory system lies within this primary question; can the nose's ability to distinguish between such scents as food and wet grass also be intricate enough to "sniff out" a potential mate?
Our culture places such low value on olfaction that we have never developed a proper vocabulary for it. In A Natural History of the Senses, poet Diane Ackerman notes that it is almost impossible to explain how something smells to someone who has not smelled it. There are names for all the pastels in hue, she writes - but none for the tones and tints of a smell. (1). Why would we choose to ignore the importance of one of our primitive senses? Some anosmics suffer from depression and their quality of life is severely affected primarily because many expectancies of life, such as memories, taste, and the possibility of finding a mate, have all been hindered by their inability to smell. (11). Yet, sometimes we fail to see the value of this sense, and its potential genetic worth; i.e. finding a mate.
(13).
In order to understand how this sense might, (I use the word might because scientists have not agreed that it is a fact), aid in heightening sexual desire and consequently our choice of lovers, we must first examine the olfactory system itself. We think that we smell with our noses, but this is a little like saying that we hear with our ear lobes. (7). That simple, short rush of air up the nose that we inhale when we breathe plays an integral role in our sense of smell. Specialized receptor cells of the olfactory epithelium detect and recognize smells. The air passes through the nasal cavity through a thick layer of mucous to the olfactory bulb. The smells are recognized here because each smell molecule fits into a nerve cell like a puzzle piece. The cells then send signals to the brain via the olfactory nerve. The brain then interprets those molecules as the sweet flowers, or the curdling milk that you've held up in your nose, or as some scientist want us to believe as the sweet aroma of love. In this sense each receptor is like a key on a typewriter, and each molecule types on several letters to produce a word, the odor. The "words" are then sent to the olfactory bulb, a pine nut-sized part of the brain right above the nose, where the words are turned into olfactory sentences. (4).
(11).
Humans can detect over ten thousand different smells. The sense of smell is a primal one. It is one of the most important means by which our environment communicates with us. (3). Smells are really airborne molecules that find their way onto our noses from the outside world. Inside the nose are the sensitive receptors that can detect a huge range of smells. The brain then works out whether you have encountered this smell before and if so, what it is. Pleasant? Repulsive? (5). In this respect, you can think of sensory systems as little scientists that generate hypotheses about the world. (6).
(13).
Each sensory system has a code for the information it receives. The olfactory system encodes odors by chemical composition. There are over one thousand different olfactory receptor proteins found on neurons in the nose, each of which recognizes a particular chemical feature of some odor molecules. The neurons send their signals to the brain's olfactory bulb, where each of the thousands of little clusters of neurons called glomeruli receives input from olfactory neurons with just one receptor type. That means each smell should activate a unique pattern of glomeruli - the "code" for that smell. (2). If humans can distinguish between over ten thousand different smells, could at least one of those detectable smells be that of our potential mates?
(14).
Poets have swooned over it since the invention of the written word; singers started crooning about it even before that time. It is the central theme in our daily lives, from the books we read to the people who make our hearts beat a little faster. Attraction to another individual is what insures any specie's survival. Certainly, a person smitten for the first time at a bar does not ask for genetic sequence and specifics about that special someone's immune system before approaching him or her. Yet perhaps some of that information is received and interpreted at a subconscious level, yielding all of the necessary information to trigger attraction. (8). Almost forty years ago, scientists Karlson and Luscher coined the term pheromone as a way of explaining the attraction within a species. (9).
Pheromones are chemical signals secreted by one individual and received by another individual of the same species, in which they trigger a specific behavior or developmental process. One of the hottest debates in the study of chemical senses is whether humans can produce and detect pheromones, and if so, whether they can use pheromone signaling to drive behavioral responses. The strangest behavioral data supporting pheromone - based communication in humans have come from work on menstrual synchrony. It has been shown, for example, that female college roommates begin to menstruate at the same time. Interestingly, this synchronization effect may be achieved solely by wiping underarm sweat from "donor" women onto the upper lips of "recipient" women, strongly suggesting that human pheromones may be contained in sweat. (10). So if our sense of smell is strong enough to coordinate and entourage of women who have never interacted to have the same menstrual cycle then it is arguable to say that our sense of smell has the same capability of attracting us to another individual sexually.
Humans, like other animals, emit odors from many parts of their bodies. Personal body odor represents secretion from several types of skin gland, most of which are concentrated in the underarm (axillary) area. The biochemical composition of these secretions (and the resulting individual body odor) depends on genetic, hormonal, metabolic, dietary, psychological, social and environmental influences. It is not known whether the olfactory signals from one individual's secretions are perceived consciously, and processed through the main olfactory system, or whether a portion of the signals are pheromones, which are presumably processed unconsciously through the accessory olfactory system. Some scientists believe that mammals usually (although not exclusively) detect pheromones through receptors found in a specialized structure called the vomeronasal organ (VNO). This is a small tubular structure lined with receptor cells, and it is close to the nasal cavity. Pheromonal information sensed by the VNO is transferred to the accessory olfactory bulb and other regions of the brain, including the anterior part of the hypothalamus. This region controls the neuroendocrine systems responsible for aspects of reproductive physiology and behavior. The NVO -to-brain pathway constitutes the accessory olfactory system, and it is distinct from the main olfactory system, the receptors for which are in the olfactory epithelium in the nose. (9).
Based on the fact that personal body odor represents a biochemical composition of genetic, hormonal, metabolic, dietary, psychological, social and environmental influences, it would appear plausible that we can "sniff out" our mate. After all we are animals. However, I would argue that our evolutionary development has made it so that we have surpassed the primitive nose as being the sole explanation for why we chose whom we choose as a partner. If we can use our sense of smell to find a potential mate, which includes that person having a desired genetic make-up which would ensure our survival, would this not exclude homosexual relationships as, in this combination there is no natural fertilization of one partner by the other? Yet, they are humans too and are attracted to one another. Would the theory of using our sense of smell to be attracted to another individual within our own species also exclude beastiality, a practice that is still done today and is postulated that Catherine the great died from in 1796? (12).
Indeed, one must always take into consideration the role of free will in attraction. Humans are complicated creatures whose actions cannot be simplified to suit one theory of rationalization for said actions. Scientist do not know for sure if pheromones contribute to mate selection in humans. Even if pheromones get the proverbial foot in the door; from there, the course of the relationship is controlled by many other factors, both conscious and sub-conscious.
(4).
WWW Sources
1) The Mystery of Smell: The Vivid World of Odors., Expresses sentiments about olfactory system
2)Mapping Smells in the Brain., Discusses codes in Olfactory system
3)How do We Smell?, Explains air flow in nasal cavity
4)What's that Odor?, Discusses receptors function in the nose
5)Science Year Kit, Explains smells and pheromones
6)Illusions Reveal the Brain's Assumptions, Brain makes an educated guess about what the information it receives is
7)Finding the Odorant Receptors, Discusses the function of odorant receptor
8) The Science of Attraction, Discusses pheromones and human attraction for one another
9)Human Pheromones: Communication Through Body Odour, Discusses the VNO
10)Evidence Found of Human Brain Detection of Pheromones, Discusses the possibility that the brain can detect pheromones
11) Role of Smell, Discusses how smell effects the other senses
12)Catherine II Empress of Russia, A Biography of Catherine the great
13)Olfaction, Explains how the olfactory system operates
14)Smell and the Olfactory System, Used for picture. It discusses the correlations between smell and the olfactory system
| Animals as agents of socialization and their invol Name: elizabeth Date: 2002-05-09 16:07:48 Link to this Comment: 2066 |
It has been three hundred years since 1699, when John Locke first advocated giving children, "dogs, squirrels, birds or any such things to look after" in order to encourage them to develop "tender feelings and a sense of responsibility for others." (1) In the 1700's, the idea was just developing whereby "nurturing relationships with animals could serve a socializing function, especially for children." (1) Many 18th C. reformers believed that children could learn to "reflect on, and control, their own innately beast-like characteristics through the act of caring for and controlling real animals." (1) It was also at this time that theories, which had been focused on the "socializing influence" of animals, began to focus on animals as treatments for mental illness.
An early experiment at the York retreat, a mental institution in England, allowed patients to freely wander the grounds. The courtyards of the retreat "were supplied with a number of animals; such as rabbits, sea-gulls, hawks and poultry." (1) It was believed that these creatures would be comfortable for the residents to be around and interactions with the animals would "tend to awaken social and benevolent feelings." (1)
"During the 19th C., pet animals became increasingly common features of mental institutions in England and elsewhere." (1) In a report about the deplorable conditions of the Bethlehem Hospital in the 1830's, the British Charity Commission suggested, "that the grounds of the lunatic asylum 'be stocked with sheep, hares, a monkey, or some other domestic or social animals' to create a more pleasing and less-prison like atmosphere." (1) Thirty years later and both the men and women's wards at Bethlehem Hospital are stocked with animals. "Some patients pace the long gallery incessantly, pouring out their woes to those who listen to them, or, if there be none to listen, to the dogs and cats." (1)
The beneficial effects of animal companionship also appear to have been recognized as serving a therapeutic role in the treatment of physical ailments during this period. Florence Nightingale wrote, "a small pet is often than excellent companion for the sick, for the long chronic cases especially." (1) As usual, though, "progress" sloughed off the peripheral contributors to society as it plowed ahead into the advent of modern medicine. The increased obsession with cleanliness and germs "eliminated animals from hospital settings by the early decades of the 20th C." (1)
Sigmund Freud was concerned with the origin of neurosis and often expressed Hobbesian ideas about "mankind's inherent beast-like nature." (1) The term "animal-like qualities" refers to "being ruled by instinctive cravings or impulses organized around basic biological functions such as eating, excreting, sexuality, and self-preservation." (1) Freud said, "as children mature, their adult caretakers tame or socialize them by instilling fear or guilt whenever the child acts too impulsively in response to these inner drives. Children, in turn, respond to this external pressure to conform by repressing these urges from consciousness." Mental illness results, or so Freud maintained, "when these bottled up animal drives find no healthy or creative outlet in later life, and erupt uncontrollably in consciousness." (1) Were the mentally ill driven to be the way they were? And if they were, was it treatable?
Boris Levinson, the founder of pet facilitated therapy, wrote "one of the chief reasons for man's present difficulties is his inability to come to terms with his inner self and to harmonize his culture with his membership in the world of nature. Rational man has become alienated from himself by refusing to face his irrational self, his own past as personified by animals." (1) Levinson believed that man's inability to integrate his relationship to nature within the context of his culture has led to a difficult existence. The very aspect of human life that separates us from the animals, culture, is the very aspect that keeps us from realizing our own potential. Culture acts as a barrier to a natural existence, and functioning within these constrictions becomes difficult.
Levinson suggests that to combat the alienation, to harmonize, we must "restore a healing connection with our own, unconscious animal natures by establishing positive relationship with real animals, such as dogs, cats, and other pets." (1) He considers animals to be mediators and mile markers on the road to emotional well-being. It follows suit that if "our relations with animals played a prominent role in human evolution, so that they have now become integral to our psychological well-being," then it is logical to see "animals as allies, to reinforce our inner selves." (1) Animals are more connected to the human condition than previously believed, a phenomenon, which has begun to be documented in the field and literature of human-animal interactions. "During the last 20 years, the theoretical emphasis has shifted away from these relatively metaphysical ideas about animals as psycho-spiritual mediators, toward more prosaic, scientifically "respectable" explanations for the apparent therapeutic benefits of animal companionship." (1)
The research projects supporting this changing viewpoint showed there was a lot of significance to and variety in the types of roles animals played in human health. For example, in 1995, Dr. Karen Allen, a prominent contributor to the field of animal related health, found that disabled people who used service dogs "scored higher for psychological well-being, self-esteem, community integration and the amount of control they could exert over their environment" than those who do not use animals. (2) It seemed that the "concept of pets serving as sources of social support" offered an explanation for the more long term benefits of animal companionship;" (1) "social support" being defined as "information leading the subject to believe that he is cared for and loved, esteemed and a member of a network of mutual obligations." (1)
Dr. James L Lynch, another researcher in the field, was interested in "the medical consequences of loneliness," and how loneliness had emerged "as one of the single most important contributors to premature death in America." (3) Single people who live alone "had death rates from all causes that ranged anywhere from 2 to 10 times greater than the rates of those who were married." (3) There was also a very strong correlation of loneliness as a "major contributor to heart disease." (3) In research conducted with Dr. Aaron Katcher, the two men uncovered the "powerful influence that pet animals had on the long-term survival of heart patients." (3) They found that those heart patients who had pets "had a better change of living than those who did not have pets." (3)
They were stumped on how to understand this, when, in 1978, they obtained one of the first devices that could measure heart rate and blood pressure automatically, without the silence previously needed when measuring them. They found that whenever a person began to talk, "there was an immediate increase in blood pressure," and when they were quiet, it immediately reduced again. (3)This appeared to contradict the previous findings that loneliness contributed to premature death through increasing heart disease. A lonely person would theoretically talk less, thus not increasing their heart rate the way a person who talked to people would have. It was only through more research that they revised their theory, stating, "Those who found communicating the most difficult (as measured in pressure surges) were also most likely to withdraw from communication and social interactions and end up in a vicious, downwardly spiraling cycle of events," ending in premature death. (3)Animals, as a means to lower blood pressure and heart rate, not only act on physiologically to maintain health, but they also act as buffers against loneliness. They offer the often-mentioned unconditional love and devotion, which doesn't require quite the same maintenance and energy that a human relationship does. They also don't require the same amount of verbal communication that humans require, thus cutting back on talking-related blood pressure increases.
Since research had been dominated by studies on the elderly, everything revolved around sickness and aging, only giving a fragment of the effects of animals. Researchers decided to study children, so they focused on kids reading aloud in the presence of an animal. This provided similar aspects to the other studies, such as the talking, as well as the presence of the animal. "The presence of a pet dog resulted in lower blood pressure and heart rates, both when the children were quiet as well as when they read a book aloud." (3) These studies support the idea that pets are therapeutic. Their presence leads to lowered heart rates and blood pressures, even when people perform tasks that are shown to increase them both. Congruously, a study performed at the Johns Hopkins Medical School showed that dogs' blood pressure also decreased significantly when being pet by humans.
Animals and humans react to each other in these contexts in therapeutic and beneficial ways. We can profoundly impact our physiological health as well as our mental health by interacting with animals and nature. By separating ourselves from nature, we are punishing not just our physical health but our psyches as well. Humans are social creatures, and yet we still try to distinguish ourselves from the animals. Loneliness is not just the absence of "social support," (1)it is also the absence of physical contact. Since time immemorial, societies have used "solitary confinement, exile, and social ostracism as methods of punishment." (1)Animals can ameliorate our physical loneliness and physiological stress. They can provide us with a lens through which we can examine ourselves within the context of the big picture. They remind us that it's not less-than-human to be an animal.
1) Serpell, James. "Animal Companions and Human Well-Being: A Historical Exploration of the Value of Human-Animal Relationships." From Handbook on Animal Assisted Therapy: Theoretical Foundations and Guidelines for Practice. 2000. Academic Press.
2)"Health Benefits of Animals", good site, although it is biased towards several main authors' take on animal assisted therapy, which I've only realized through more extensive research and interviews on this topic.
3)"Developing a Physiology of Inclusion: Recognizing the Health Benefits of Animal Companions." , neat article about author's experience with animal influence to human health
4)life care web page, Offers more detailed references to health related studies involving animals.
| A Look at Humor, Laughter, Tickling and, of course Name: Rebecca Ro Date: 2002-05-10 00:00:32 Link to this Comment: 2067 |
Although there is considerable information on the neuronal representation of speech, little is known about brain mechanisms of laughter (2). While many researchers have tracked the brain mechanisms of depression, fear and anger, they have ignored positive emotions and have just begun to study humor. Their investigations are shedding some light on how the brain processes humor and prompts laughter.
Take this joke for instance: How many Bryn Mawr college students does it take to change a lightbulb? Answer: None, they were all so busy studying that they didn't even notice the light was out. If you found this old joke funny, you will get some activity going on in the brain. Investigations into how humor and laughter influence the brain are leading to a clearer understanding of how positive emotions affect brain mechanisms. This in turn may lead to creative ideas for new therapies for emotion disorders and pain (1).
The physiological study of laughter has its own name, "gelotology". Research has shown that laughing is more than just a person's voice and movement. Laughter requires the coordination of many muscles throughout the body. Laughter also increases blood pressure and heart rate, changes breathing, reduces levels of certain neurochemicals (catecholamines, hormones) and provides a boost to the immune system (3). Can laughter improve health? It may be a good way for people to relax because muscle tension is reduced after laughing. Human tests have found some evidence that humorous videos and tapes can reduce feelings of pain, prevent negative stress reactions and boost the brain's biological battle against infection (1). More studies are needed in this field to uncover whether humor or some other component such as distraction, is the predominant factor in these results.
Researchers believe we process humor and laughter through a complex pathway of brain activity that encompasses three main brain components. In one new study, researchers used imaging equipment to photograph the brain activity of healthy volunteers while they underwent a sidesplitting assignment of reading written jokes, viewing cartoons from The New Yorker magazine as well as "The Far Side" and listening to digital recordings of laughter. Preliminary results indicate that the humor-processing pathway includes parts of the frontal lobe brain area, important for cognitive processing; the supplementary motor area, important for movement; and the nucleus accumbens, associated with pleasure (1). Investigations support the notion that parts of the frontal lobe are involved in humor. Subjects' brains were imaged while they listened to jokes. An area of the frontal lobe was activated only when they thought a joke was funny. A study that compared healthy individuals with people who had damage to their frontal lobes, the subjects with the damaged frontal lobes were more likely to choose a wrong punch line to written jokes and didn't laugh or smile as much at funny cartoons or jokes (1).
A paper published in the journal Nature has provided information about how the brain is involved with laughter. Electrical stimulation was applied at 85 discrete sites on the cortical surface of the left frontal lobe of a 16-year-old girl (A.K.) undergoing monitoring by intracranial subdural electrodes to locate the focus of chronic intractable seizures. The patient's seizures were never accompanied by laughter. During stimulation A.K. performed a variety of tasks such as naming of objects, reading a paragraph of text, or counting. A small area measuring about 2 cm x 2 cm was identified on the left superior frontal gyrus where stimulation consistently produced laughter. The laughter was accompanied by a sensation of merriment or mirth. Although it was evoked by stimulation on several trials, a different explanation for it was offered by the patient each time, attributing the laughter to whatever external stimulus was present. The duration and intensity of laughter increased with the level of stimulation current. At low currents only a smile was present, while at higher currents a robust contagious laughter was induced (2).The results suggest that electrical stimulation in the anterior part of the supplementary motor area (SMA) can elicit laughter. The observation that A.K. was able each time to invoke a stimulus context that explained the laughter suggests a close link between the motor, affective and cognitive components of laughter. Analysis suggests that smiling and laughter might involve similar mechanisms which are closely related phenomena on a single continuum. This shows that the areas of the brain that caused laughter in A.K. are part of a larger circuit involving several different brain areas. The movement of face muscles for a smile would be the motor part of humor and the understanding of the joke would be the cognitive, thinking part of humor.
Even though we may know more about what parts of the brain are responsible for humor, it is still hard to explain why we don't laugh or giggle when we tickle ourselves. Some scientists believe that laughing caused by tickling is a built-in reflex because even babies do it (3). If we tickle ourselves in the same spot our friend tickled us, we do not laugh as we did previously. The information sent to your spinal cord and brain should be exactly the same. Apparently for tickling to work, the brain needs tension and surprise. When you tickle yourself, you know exactly what will happen...there is no tension or surprise. How the brain uses this information about tension and surprise is still a mystery, but there is some evidence that the cerebellum may be involved (3).Because one part of the brain tells another: "It's just you. Don't get excited". Investigations suggest that during self-tickling, the cerebellum tells an area called the somatosensory cortex what sensation to expect, and that this dampens the tickling sensation (7). It looks as if the killjoy is found in the cerebellum.
Damage to any one part of the brain may affect one's overall ability to process humor. Peter Derks, a professor of psychology, conducted his research with a group of scientists at NASA-Langley in Hampton. Using a sophisticated electroencephalogram (EEG), they measured the brain activity of 10 people following exposure to a humorous stimuli. How quickly our brain recognizes the incongruity that deals with most humor and attaches an abstract meaning to it determines whether we laugh (6). However, different people find different jokes funny. That can be due to a number of factors, including differences in personality, intelligence, mental state and probably mood. But, according to Derks, the majority of people recognize when a situation is meant to be humorous. In a series of experiments, he noticed that several patients recovering from brain injuries could not distinguish between something that was funny and something that was not. As follow-up to his latest research, Derks has been trying to identify the connection between mood and responsiveness to humor. Derks had originally thought that mood played a vital role in whether a person responded to humor. Someone feeling happy would be more inclined to laugh at a joke than someone feeling sad. However, early findings suggest that there is no apparent consistent pattern among people. Individuals seem to respond to humor in different ways that can't be predicted from their mood (6). Derks traced the pattern of brainwave activity in subjects responding to humorous material. Subjects were attached to an EEG and their brain activity was measured when they laughed. In each case, the brain produced a regular electrical pattern. Within four-tenths of a second of exposure to something potentially funny, an electrical wave moved through the cerebral cortex, the largest part of the brain. If the wave took a negative charge, laughter resulted. If it maintained a positive charge, no response was given. During the experiment, researchers observed the following specific activities. The left side of the cortex (the layer of cells that covers the entire surface of the forebrain) analyzed the words and structure of the joke. The brain's large frontal lobe, which is involved in social emotional responses, became very active. The right hemisphere of the cortex carried out the intellectual analysis required to get the joke. Brainwave activity then spread to the sensory processing area of the occipital lobe (the area on the back of the head that contains the cells that process visual signals). Stimulation of the motor sections evoked physical responses to the joke (4). Emotional responses appear to be confined to specific areas of the brain, while laughter seems to be produced via a circuit that runs through many regions of the brain. Damage to any of these regions can impair one's sense of humor. Derks's work only provides a basic picture of how the brain responds to humor. More comprehensive findings could be made if an EEG, Positron Emission Tomography (PET) scanner and Magnetic Resonance Imaging (MRI) were used on a subject simultaneously. However, only a few laboratories in the world are equipped for such testing.
Dr. Shibata of the University of Rochester School of Medicine said our neurons get tickled when we hear a joke. The brain's 'funny bone' is located at the right frontal lobe just above the right eye and appears critical to our ability to recognize a joke. Dr. Shibata gave his patients MRI scans to measure brain activity. Dr. Shibata tried to find out what part of the brain is particularly active while telling the punch line of a joke as opposed to the rest of the joke and funny cartoons in comparison to parts of the cartoon that's not funny. The jokes "tickled" the frontal lobes. The scans also showed activity in the nucleus accumbens. Activity in the nucleus accumbens is likely related to our feeling of mirth after hearing a good joke and our "addiction" to humor (9). While his research was about humor, the results could help lead to answers and solutions about depression. Parts of the brain that are active during humor are actually abnormal in patients with depression. Eventually brain scans might be used to assess patients with depression and other mood disorders. The research may also explain why some stroke victims lose their sense of humor or suffer other personality changes. The same part of the brain is also associated with social and emotional judgement and planning.
Laughter is a complex human behavior that occurs unconsciously. While we can consciously inhibit it, we don't consciously produce laughter. That is why it is very hard to laugh on command or to fake laughter. We know that many sensations and thoughts trigger laughter, and that it activates many parts of the body. While we know that certain parts of the brain are responsible for certain functions and tasks, it seems that laughter cannot be traced to one specific area of the brain. Furthermore the relation between laughter and humor is not understood, despite their evident connection.
Humor plays a powerful and unique role in human life with wide-ranging effects on many aspects of functioning. Humor can tie people together, help us cope with daily stress, and have a positive effect on the immune systems (5).Hopefully, uncovering the brain's specific response to positive stimuli like humor and laughter may lead to new therapies for depression.
Although Derks's early findings suggest that mood has no correlation to responsiveness to humor more studies are needed. I know when I am sad, I do not find many things funny. However, when I am in a good mood I laugh much more readily. Although the purpose of humor and laughter is still largely unknown, having a sense of humor is a key part of our personalities and it can play a powerful role in balancing negative emotions, such as fear and anxiety. If we can increase the humor processing abilities of depressed people then we may be able to combat some forms of depression. Even though there have been few studies of humor's place in the brain, understanding the basis of positive emotions will likely be as helpful as understanding the negative ones.
2)Electric current stimulates laughter, Nature Journal
3)What is so Funny and Why: Laughter and the Brain
7)Brain may hinder sense of self-tickling
| Recent Studies Concerning Violent Tendencies and t Name: Balpreet B Date: 2002-05-10 01:05:26 Link to this Comment: 2068 |
"It was an urge. . . . . A strong urge, and the longer I let it go the stronger it got, to where I was taking risks to go out and kill people-risks that normally, according to my little rules of operation, I wouldn't take because they could lead to arrest." -Edmund Kemper (6)
Ted Bundy. Charles Manson. Timothy McVeigh. Bundy murdered pretty women. Manson had followers who killed on his command. McVeigh is responsible for one of the most horrendous terrorist attacks on America, the Oklahoma State bombing. While these three serial killers had different methods for their acts, the one thing they have in common is that their killers. Murderers who took a number of innocent lives.
Perhaps to not the same extent, but sadly enough the world is full of Charles Manson's and Ted Bundy's. Violence has become a common and prevalent occurrence in society today. Everyday on the news one hears stories of crimes-murder, robbery, rape, assault, extortion, kidnapping, homicide, an endless list. Law enforcement works day and night protecting neighborhoods and cities from crimes and violence, but the truth of the matter is that crime still exists and all one can do is ask himself why. Why do such treacherous violent acts exist in society? In essence, one must ask himself whether or not these violent tendencies have any biological relation whatsoever. Do violent tendencies occur as an affect of disruptions or damage to the brain? Is there a genetic correlation? Is violence brought about by some other factor, such as economic difficulties or social or cultural differences? All these questions remain unanswered. But one even significant, broader question that one must consider is whether or not these factors, biologically related and non, effect the occurrence of violent tendencies in individuals.
In 1848, a railroad worker, Phineas Gage, was working when an explosion caused an iron rod to impale his skull, damaging the front part of his brain. Although Gage miraculously survived, his behavior severely changed in that the intelligent and respectful man everyone knew suddenly because fitful, impulsive, and rude (2).
This is one of the first dated cases insinuating that violence may be related to some kind of damage or abnormality in the brain. However, with increasing technology, researchers have found many correlations between violence and aggressive tendencies to damage or abnormalities to a specific part of the brain. Gage's accident probably resulted in damage to the prefrontal cortex. The prefrontal cortex is the brain's foremost outer position, located behind the eyes. This area of the brain is especially vital because of it's importance in the orchestration of emotion, arousal, and attention. The prefrontal cortex seems to be the part of the brain that enables people to restrain themselves from acting on all of their impulses and is extremely critical for a child's ability to learn to feel remorse, conscience, and social sensitivity (5).
However, although the function of the prefrontal cortex is known, why, or how, would prefrontal deficits cause violent tendencies or a more aggressive character?
Adrian Raine, a psychopathologist from USC suggests that damage or abnormalities of the prefrontal cortex may result in a condition known as Antisocial Personality Disorder, or APD, which is characterized by irresponsibility, deceitfulness, impulsiveness, lack of emotional depth and antisocial behavior. In his study, Raine suggests three reasons why prefrontal deficits may cause such a personality (5). Firstly, the prefrontal cortex is responsible for self-restraint and deliberate foresight. If this part of the brain was damaged, then one effect that would arise would be the tendency for one to act on all his impulses without thinking ahead or thinking of the consequences. Second, the prefrontal cortex is important for learning conditioned responses. This area of the brain has been thought to be central to a child's ability to learn and to feel remorse, conscience, and social sensitivity (7). If the prefrontal cortex was to function abnormally, how is the child supposed to learn how to have a conscience? For example, one study reported that children who received damage to their prefrontal cortex before the age of seven developed abnormal social behavior, which was characterized by their inability to control their aggression and anger (2). Lastly, Raine suggests that if prefrontal deficits underlie the APD group's low levels of autonomic arousal, these people may unconsciously be trying to compensate through stimulation-seeking (5).
There have been many studies done concerning violence and its relationship to the prefrontal cortex. In July, 2000, UW-Madison psychologist Richard Davidson analyzed brain imaging data from a large, diverse group of studies on violent subjects and those predisposed to violence to find any connections between the brain and violent tendencies. Davidson and his colleagues found common neurological trends among many of their subjects in the brain's inability to properly regulate emotion. One core finding that Davidson's study found dealt with the interplay among several distinct regions of the brain, primarily the orbital frontal cortex, the anterior cingulate cortex, and the amygdala. They found that normal brain activity in the orbital and anterior regions were either entirely absent or slowed in many of their studies, while the amygdala showed normal or heightened activity. The inability of these two regions of the brain to counteract the response of the amygdala may explain how threatening situations can become explosive in some people with damage to the prefrontal cortex (4).
Although the primary focus in research deals with the prefrontal cortex, there also exist many recent studies that attempt to relate DNA and genetics to the increased tendencies for violence. Scientists have not found any specific gene for human violence, yet data from molecular geneticists suggest that multiple genes may interact to prime individuals to this behavior (1). Davidson's study also described a large group of subjects who had a genetic deficit that caused a disruption in the brain's seretonin levels. Seretonin has been hypothesized to hold inhibitory control over impulsive aggression. Disruption of the seretonin level may contribute to increased aggression within the individual (3). These biological studies-abnormalities to the prefrontal cortex and genetics-may in fact greatly influence violent and aggressive acts amongst individuals. Even though these studies cannot say for certain whether or not this is substantial evidence, researchers are on the right path for determining any biological or physiological influences towards violence.
Although such biological studies are being performed, one must also consider social influences. Adrian Raine stresses this case: "We are talking about a predisposition to antisocial behavior. Some people who have prefrontal deficits do not become antisocial, and some antisocial individuals do not have prefrontal deficits. It's important to make clear that biology is not destiny" (5). For example, socioeconomic problems may play a major role in violent tendencies. Socioeconomic problems have no biological relation whatsoever; however, it can still cause an individual to act in violent ways. Issues such as unemployment, lower educational level, alcohol use, and access to firearms all contribute to violent crimes (1). However, some of these factors can be seen as acting by way of the brain. Alcoholism can definitely have correlations to the brain. While it might not be a direct effect of prefrontal cortex damage, alcoholism might be related to genetic mutations or the brain's behavior. But other factors of society, such as socioeconomic problems or unemployment, still influence violence and criminal actions performed by individuals. Thus, not only do biological factors need to be stressed, but so do cultural and social factors.
If one believes in morals and ethics, one can also include conscience in the factors that influence violent activity. When watching serial killers and rapists on the news, a question that frequently comes up is whether or not these individuals have a conscience, the idea of knowing what is right and what is wrong. It has already been said that the prefrontal cortex has a part in teaching children the difference between wrong and right and that it develops a conscience. But if one believes that the brain is not entirely responsible for behavior and that there is something else, such as a soul, or conscience, then a lack of conscience can be an influential factor that is not related to the brain or any biological or physiological factors.
Although all the above trends and relationships implied by these studies exist, do they prove that violence influenced by some type of biological disorder or social factor? By implying this, one is assuming that every man or woman who commits a crime or acts with violent tendencies does so by some type of brain damage, genetic disorder, or social problem. If anything, by believing this, society is giving people an excuse to commit crimes and act on their violent behavior; if biological or social influences ultimately cause violence, does that redeem one's actions? If one looks at what Timothy McVeigh, Charles Manson, and Ted Bundy have done, and said that their actions can be justified by a disorder in their prefrontal cortex or some other physiological factor, what does that leave us as a society with? Are the crimes committed by these serial killers justified? Should they be set free because they couldn't "control" their actions?
Perhaps, in some to many cases, an individual's tendency to act in violence is influenced by biological abnormalities of the brain or other physiological factors. But how can one know for certain whether or not this is the case? Currently, there is no way to determine how extensive the these factors influence violence and aggression. One could believe the criminal when he says he wouldn't have committed a crime if his prefrontal cortex was damaged. But then that brings up the question on whether or not his word is reliable. On the one hand, criminals could use these factors as an excuse to get out of jail and commit more crimes; or, on the other hand, the individual could be telling the truth, and, with treatment and medications, he could live the rest of his life without even littering a gum wrapper. But the truth of the matter is there is no way of knowing yet if these factors discussed are the reasons for violence. Unless technology advances in the future allowing scientists to know for sure if violence is influenced by factors, the crimes committed by the Ted Bundy's and Timothy McVeigh's in the world cannot be justified.
There are many issues when discussing violence. While it is a serious issue, it is also a rather sensitive one. One would think that after seeing acts of violence constantly everywhere-in movies, video games, the nightly news, professional sports and other forms of entertainment-society would be used to it by now. But how can one ever get used to violence? All these issues remain unanswered. While there is a substantial amount of recent research that involves different biological and physiological factors for violent tendencies, it is still too soon to make any determinations. Aside from scientific research, there arises the moral issues as well, whether or not these criminals should be free in society instead of locked away in prison. Criminals like Ted Bundy, or Timothy McVeigh. Can these influential factors justify the murders, rapes, robberies, and other crimes that occur every day in society? A correlation between brain damage and violence might have been found, but how to act on this newfound discovery still remains ambiguous. And until the next step is taken in research and discussing what should be done, society cannot move forward in eliminating the everyday violence.
1) Violence and Brain: An Urgent Need for Research
2) Brain Briefings: Violent Brains
3) Dysfunction in the Neural Circuitry of emotion Regulation-A Possible Prelude to Violence
4) Violent Behavior Linked To Specific Brain Dysfunction
5) Size of Brain Linked to Violence
7) Brain Size Linked to Violence
8) Mark, Vernon H. Violence and the Brain. New York: Harper & Row Publishers, 1970.
| Pediatric and Adult Migraines...are they different Name: Amy O'Conn Date: 2002-05-10 05:23:44 Link to this Comment: 2070 |
What is a migraine headache?
Many people are surprised to find that children get migraines. It is one of those illnesses that are associated with adults only. A migraine is an intense, pounding headache with nausea that occurs infrequently. The headache starts around the eyes, the forehead, or the sides of the head. Bright lights and loud noises also make the headache worse, and any movements make this headache worse. Migraines last from a few hours to a few days in serious cases (1).
Over 8 million children get migraines a year, which results in over 1 million lost schooldays cumulatively. 20% of adolescents in high school suffer from migraines as well. Pediatric migraines commonly stop when a child becomes an adult. Migraines occurring prior to puberty are about evenly split between boys and girls, and after puberty many more girls than boys experience them. Older children experience migraine pain typically on only one side of the head. Younger children, however, experience pain on both sides of the head. Some people also see a "warning aura," which is a pattern of lines or shadows in front of their eyes as the headache starts (2). Types of migraines are therefore classified as either common (no aura warning) or classic (with aura warning). Aura symptoms usually occur 30 to 60 minutes before the acute headache and generally are resolved by that time (3).
Why are pediatric and adult migraines different?
There are many different stimulants that trigger a migraine headache. Certain foods, like cheese, processed meats, chocolate, caffeine, MSG, nuts, or pickles are common triggers. Stress and too much exercise can also trigger an attack (1).
Most children with migraines have a family history of the illness. If both parents suffer from migraine, there IS A 70% risk that the child will also develop migraines. If only one parent suffers from migraine, the child has only a 45% risk of developing migraine (3).
Does pediatric migraine display both physiological and psychosocial symptoms?
Yes, children with migraines as well as their parents have noted the existence of both social and psychological symptoms of migraine, in addition to the physiological symptoms of migraine.
Physiological Symptoms:
Physicians look for slightly different symptoms when diagnosing a pediatric migraine. These symptoms include recurrent conditions such as vomiting, abdominal pain, or dizzy spells. Other symptoms include appetite loss, diarrhea, constipation, hot flashes and cold hands and feet. Unlike adults, children's migraines can wake them up from sleep, or are present upon waking (4). It is often not the child who is sick, but those around the child (typically parents), who notice that about 24-28 hours before the headache begins, the child is irritable, fatigued, pale, or depressed. Sometime children and adults both experience periods of elation, restlessness, and wakefulness. Many children, as opposed to adults, feel relief after sleeping for a few hours (3).
Psychosocial:
A controlled study by Aromaa et al from 2000 is the most recent study to report the pain experience of children with headaches and their families (5). Researchers followed 1143 families expecting their first child for over seven years. A questionnaire inquiring about the children's headaches was sent 6 years after their birth to 1132 of the original families followed. The results of the study indicate that children with headaches were more often very sensitive to pain, were more excited about physical examinations, cried more often during blood sampling or vaccination, avoided playing games for fear of getting hurt, and had recurring abdominal and growing pains. Researchers were able to conclude that migraine was recorded as being more intensive pain than tension-type headaches. They also concluded that although migraine has a large hereditary component, the child's pain-coping mechanisms could be influenced by parents' information.
Another study by Christiane Hermann and E.B. Blanchard tested the hypothesis that physiological responses of migraine patients are symptom–specific (6). Researchers applied both laboratory and parental conflict stressors to children and measured six of the autonomous, physiological responses of 26 children with migraine history and 10 control children. The two stressors were specifically chosen because the most frequently cited migraine triggers in children, this article claims, are achievement situations and emotional stress. The purpose of the study was to examine the psychophysiological response of children with migraine in comparison to control children (non-headache). The main theory behind the hypothesis was that children suffering from migraine usually show more cranial vasodilatation and peripheral vasoconstriction in response to stress. Like previous migraine studies with adults, results showed that children with migraine had similar heart rate (HR), finger temperature, and skin conductance level (SCL). The study also concluded that, despite opposite results from Aromaa et al's study, the children suffering from migraine did not subjectively experience more intense stressors than the control children. Blood Volume Pulse Amplitude (BVP) was expected to be greater for migraine children, but was insignificantly different than the rate for the control group. This suggests that the temporal artery may be the only extracranial blood vessel that contributes significantly to migraine pathogenesis. Hermann and Blanchard finished their study by saying that it is possible that factors other than psychophysiological reactivity may be most relevant for onset of migraine disorder.
After the above study was published, another study further attempted to determine the relationships between neurophysiological and psychosocial factors within the pathogenesis of migraine (9). Researchers investigated the contingent negative variation (CNV), parent-child interactions, and the relation between the two using an experimental group composed of 30 families with a migraine child and a control group of 20 families. The results showed that both groups showed the same results according to CNV measurements. The study also demonstrated that parents from migraine families exerted a lot more control over migraine children than over healthy siblings. Furthermore, the relation between CNV and parent-child interactions was shown to be strong only for very young children with migraine. Researchers were able to conclude that there's a strong influence of family interactions on the development and management of the neurophysiological aspects of the migraine disorder.
The most important tool for diagnosing migraines in children is the detailed history, which hopefully elicits a particular headache profile or pattern. Certain therapies are also specifically better for children. Biofeedback and relaxation techniques work better with children simply because they are more enthusiastic about these types of therapy. Some physicians recommend that parents maintain a regular sleep pattern and meal schedule, and that the child avoid doing an overload of activities. Like adults, many children can decrease the pain of a migraine by identifying certain migraine triggers. If drug treatment is needed for a child, the physician will prescribe simple analgesics (pain relievers). Depending on whether or not painkillers are enough, the physician might add preventive medicines to the child's regimen. Drugs that work for adults also work for children; the most commonly prescribed drug for children is an antihistamine, cyproheptadine. This drug is taken in both syrup and tablet form every 8-12 hours, and possible side effects include drowsiness and weight gain (2).
Sartory et al conducted a study that compared the efficacy of psychological vs. pharmacological treatments for children with migraine (7). The psychological treatment entailed either progressive relaxation or cephalic vasomotor feedback (CVF), both with stress management training via ten sessions for six weeks; pharmacological treatment entailed taking metoprolol (8), an oral beta-blocker for ten weeks. Results showed two main differences in correlation with treatment variation: the first is that relaxation and stress management training reduced the frequency and intensity of headaches more effectively than metoprolol with CVF and stress management in between. The other is that when compared to pre- and post-treatment data, children treated with relaxation training improved significantly in headache frequency and intensity; those treated with CVF improved significantly in headache frequency and duration, and mood. The medication had little effect on children's headache activity in this study. Researchers suggest that a calcium-channel blocker may have been more effective. Also, metoprolol is regarded as having a preventive effect and therefore acted as a psychological treatment instead of a pharmacological treatment.
Conclusions:
Pediatric and adult migraines do seem to be slightly different from one another, although not enough to categorize either as unique. The fact of the matter is, migraine research still has a long way to go because researchers have done few studies that are comprised of large sample sizes, or that can comprehensively separate psychosocial and physiological influences as well as therapies. It is, in fact, not yet clear whether genetic factors (the accepted physiological "cause" of migraine) or societal/psychological factors exert more influence over the other in determining the specific pathogenesis of migraine.
1) American Academy of Family Physicians. "Migraine Headaches in Children and Adolescents." American Family Physician 65:4 (2002): 635."
2)Migraine homepage for the Journal of the American Medical Association, a comprehensive review of diagnostic and therapeutic aspects of migraine
2)Diamond, Seymour. "Migraine in Children: how to recognize-how to treat." Consultant 39:7 (1999): 2045-2050.
4)Private Information Page, basic generalities about migraine
7)Sartory, G. et al. "A comparison of psychological and pharmacological treatment of pediatric migraine." Behaviour Research and Therapy 36 (1998): 1155-1170.
8) Pivate Pharmacological Information site, greeat online pharmacist answers to questions about metoprolol medication.
5) Aromaa, M. et al. "Pain Experience of Children With Headache and their Families: A Controlled Study." Pediatrics 106 (2000): 270-275
.
6) Hermann, C. and Blanchard, E.B. "Psychophysiological Reactivity in Pediatric Migraine Patients and Healthy Controls." Journal of Psychosomatic Research44:2 (1998): 229-240.
| POST-TRAUMATIC STRESS DISORDER: IMPLICATIONS FOR B Name: Gavin H. I Date: 2002-05-10 15:41:21 Link to this Comment: 2071 |
INTRODUCTION
Throughout the course of this semester we have examined numerous issues which have all had different implications for the brain = behavior argument. Some who have been skeptical of the validity of this idea have been swayed by observations that processes and behaviors they originally thought to have a cloudy neurobiological basis in fact have a sound biological and physiological underpinning. One such phenomenon which can help elucidate the ongoing brain = behavior debate is Post-Traumatic Stress disorder, or PTSD. Most people are familiar in some sense with the phenomenon of PTSD. This phenomenon has been renamed, reworked, and redefined numerous times over the past century. The approach to understanding PTSD and the more general notion of traumatic experience has been an interdisciplinary undertaking, involving the fields of medically oriented psychiatry, psychology, sociology, history, and even literature (1). The reason for this interdisciplinary approach is that the greater perception of the phenomenon is seen as having much more than a simple biological basis. It is seen as having multiple external influences. This view is a result of the often overwhelming sense that whatever biological mechanisms are present must be unintelligibly complex. However, there are certain aspects of PTSD which, upon examination, allow one an easy foray into the neurobiology of the disorder. Cathy Caruth, a leading trauma theorist, discusses the definition of PTSD: "While the precise definition of post-traumatic stress disorder is contested, most descriptions generally agree that there is a response, sometimes delayed, to an overwhelming event or events, which takes the form of repeated, intrusive hallucinations, dreams, thoughts, or behaviors stemming from the event, along with numbing that may have begun during or after the experience, and possibly also increased arousal to (and avoidance of) stimuli recalling the events" (1) . It is the goal of this paper to demonstrate that the phenomenon of PTSD, despite the fact that its multiple emotional and psychosocial effects are constantly being debated, is soundly rooted in neurobiology, and that this aspect of PTSD lends support to the notion that brain = behavior.
The general problem in the assessment of PTSD is that "Traditional psychotherapy addresses the cognitive and emotional elements of trauma, but lacks techniques that work directly with the physiological elements, despite the fact that trauma profoundly affects the body and many symptoms of traumatized individuals are somatically based" (2). Popular belief is that traumatic events affect an individual at the level of the I-function - that is, in the part of the brain responsible for cognition, emotion, and feeling. It is indeed true that the symptoms of PTSD can affect mood and the nature of interpersonal interaction. However, there is strong evidence that responses to trauma are rooted in neurobiological processes independent of the I-function, and have a somatic basis. As the above excerpt states, most treatment modalities focus on the non-somatic elements of PTSD, neglecting to recognize the important physiological effects that the disorder entails.
Dianthe Lusk, a character in Pauline Hopkins' novel Of One Blood, is diagnosed by a physician after she has been rescued from the scene of a train accident: "As I diagnose this case, it is one of suspended animation. This woman has been long and persistently subjected to mesmeric influences, and the nervous shock induced by the excitement of the accident has thrown her into a cataleptic sleep" (3). This passage underscores much of how PTSD is configured in the public mind. It is seen as a mysterious and indefinable affliction - something more akin to being possessed by a demon or a ghost than actually having an identifiable pathology in the nervous system. Despite the tendency to view PTSD as a phenomenon that exists outside the boundaries of our known knowledge of the nervous system, there are several important observations which lend support to the idea that PTSD is soundly rooted in such a basis. This connection may be used to help elucidate the overarching notion that brain = behavior.
THE PHYSICAL IN THE TRAUMATIC
The role of the physical in the phenomenon of traumatic events is often overlooked because it is not entirely evident how it plays into these scenarios. If anything, it is usually recognized that "a victim may instantaneously freeze rather than act, a driver may not have time to execute the impulse to turn the car to avoid impact, or a person may be overpowered when attempting to fight off an assailant." (2). However, it is this precise lack of a physical response that can lead to subsequent psychodynamic maladjustments: "Over time, such interrupted or ineffective physical defensive movement sequences contribute to trauma symptoms" (2). The very psychological problems that most associate with PTSD are in fact, brought into existence because of these physical movement defensive sequences. This recognition enables us to see the importance of non-psychological factors in traumatic experience.
MECHANISM OF SUPPRESSION
As Cathy Caruth states, "it is only in and through its inherent forgetting that [trauma] is first experienced at all" (1). Despite what may seem like a phenomenon whose biological basis is very cloudy, there is in fact a "general biological function of the process by which experience passes into the region of the unconscious" (4). The elucidation of this mechanism is made possible by "observations on the sensory changes which accompany the regeneration of a divided and reunited nerve" (4). Suppression, which is the mechanism by which memories enter into the unconscious, has been demonstrated experimentally to occur in the process of nerve regeneration. This very complex process involves demonstrating, using the modality of heating and cooling a human limb in which the nerve regeneration is taking place, that it is possible to suppress and recover different types of sensations that occur during the process of regeneration (4). The relevant message with regard to PTSD that can be drawn from this demonstration is "the special importance of suppression on the reflex and sensori-motor levels is that it reveals clearly the biological significance of the process" (4). The process of suppression is clearly rooted in physiology, and is experimentally reproducible. This all-important observation allows us to see that the brain = behavior argument plays significantly into the discussion of PTSD. The suppression of traumatic memory that occurs in the wake of such an event is "a process of reaction to the pleasures and pains" (4) of the event in question. The experiment described above helps us to see how many of the vague and imprecise terms such as "somatization", "conversion", "hysterical", "psychological", or "psychosomatic" distort the idea that what is actually happening in a patient with PTSD is a neurobiologically definable suppression which is independent of the conscious processing functions of the patient's brain (5).
PSYCHOBIOLOGICAL EFFECT OF CHILDHOOD TRAUMA
Van der Kolk et al. state: "Though the biological underpinnings of response to trauma are extremely complex, forty years of research on humans and other mammals have demonstrated that trauma (particularly trauma early in the life cycle) has long term effects on the neurochemical response to stress, including the magnitude of the catecholamine response, the duration and extent of the cortisol response, as well as a number of other biological systems, such as the serotonin and endogenous opioid system" (6). Another tremendously important observation that lends support to the idea that PTSD is characterized by an objective effect on the nervous system can be seen in the manner in which traumatic situations affect humans of different ages. It is well documented that the early childhood years witness a significant amount of development with regard to the nervous system. We deduce that an objective change in the nervous system takes place as a result of a traumatic stress, because a child will experience much more substantial and long-lasting effects than an adult in response to a similar traumatic event. A considerably large body of research has shown that the effect of such stresses on the nervous system can cause deficiency in or induce the following: "capacity to modulate emotions, difficulty in learning new coping skills, alterations in immune competency, and impairment in the capacity to engage in meaningful social affiliation" (6). Children affected by trauma thus exhibit behaviors throughout the course of their subsequent lives that are owed to neurochemical and neurobiological alterations and deficiencies that are brought about by the given traumatic event. This recognition helps us to see that subsequent psychological problems in the lives of traumatized children are the direct result of neurobiological disruptions that occur during a crucial developmental phase of the child's nervous system.
PHARMACOLOGIC TREATMENT OF PTSD
Another observation in support of the link between PTSD and an objective neurobiological basis is the efficacy of certain drugs on the numerous psychological manifestations of the disorder. Studies of the effects of drugs used to treat PTSD have largely centered on antidepressants and MAO inhibitors. The results of such studies have not been convincing (6). However, "during the past few years evidence has accumulated that serotonin reuptake blockers are likely to be the most effective drugs in the treatment of chronic PTSD" (6). Animal researchers have been able to demonstrate that "serotonin receptor blockers reverse the suppression of fear-induced behavior, probably because an increase in available serotonin in the limbic system amplifies the signals necessary to distinguish punishment from reward" (7). This linkage, while it has not been completely elucidated, does speak to a significant correlation between the neurobiology of PTSD and the ability to treat its numerous psychodynamic maladjustments. We are able to see PTSD then, not solely as a mysterious psychological phenomenon, but rather as a disorder whose pathology can be traced to a sound neurobiological basis and whose symptomatology can be treated by drugs whose mode of action is to affect said neurobiology.
CONCLUSION
Numerous observations regarding PTSD lead us to the conclusion that it is a disorder whose basis in neurobiology, while largely unrecognized in the lay public, is in fact very sound. These observations include: the manner in which physical responses play into traumatic scenarios; the presence of a biological mechanism of suppression, the documented effect of trauma in early life, and the ability to remedy the symptoms of PTSD through psychopharmacologic treatment. The tendency to see PTSD as a pure psychosocial disorder distorts the notion that traumatic events do in fact result in neurochemical and neurobiological changes in the nervous system. This association lends support to the notion of brain = behavior as it shows that psychological problems subsequent to traumatic events do not simply arise because the person was somehow "affected" by the event. Such a person's neurobiology was in fact altered from the normative state, and although a complex undertaking, his or her behaviors can be traced to this objective underpinning.
1) Trauma: Explorations in Memory , by Cathy Caruth, a leading trauma theorist.
2) Sensorimotor Psychotherapy: One Method for Processing Traumatic Memory," from Traumatology , by Pat Ogden and Kekuni Minton.
3) Of One Blood , a novel by Pauline Hopkins.
4)"The Repression of War Experience" , by W.H.R. Rivers.
5) "The Neurophysiology of Dissociation and Chronic Disease," from Applied Psychophysiology and Biofeedback , by Robert C. Scaer.
6) "Approaches to the Treatment of PTSD" , by Bessel A. van der Kolk and Onno van der Hart.
7) The Psychology of Fear and Stress , by J. Gray.
| Video Games: A Source of Benefits or Addiction? Name: Mary Schli Date: 2002-05-10 15:58:14 Link to this Comment: 2072 |
Super Mario Brothers, Sonic the Hedgehog, and Street Fighter are familiar names to nearly all of us. They are all best selling games of major video game consoles. Over 9.8 billion dollars were spent on video games in the United States during 2001 alone, and video game consoles are present in 36 million homes in the United States (1). With the increasing amount of time that people are spending on video games, one is left to wonder what effects video games have on the people who play them.
Video games, especially those that contain violence, are becoming increasingly popular with children of young ages. Playing violent games may be associated with a tendency to behave more aggressively, although the data are inconclusive about the cause and effect nature of this relationship (2). In a study by Irwin and Gross, children who played a violent video game displayed a higher level of aggression than children who played a nonviolent game (2). Similarly, another group of researchers found that college students who played a violent video game reported more aggressive thoughts after playing the game than students who observed the game (2). However, it should be noted that simply because these students reported more aggressive thoughts does not indicate that they were more likely to behave in a violent manner. Furthermore, it is likely that participants would have been focused on a particular behavior, regardless of the type of behavior, after they had previously spent a significant amount of time engaged in that activity; therefore, there do not appear to be firm conclusions that can be drawn from this study. Future studies could more effectively investigate this topic by exposing participants to different types of video games and then observing the types of behaviors in which the participants engage after playing the games. A study of this nature would allow a causal conclusion to be drawn about the relationship between video games and behavior since the actual behavior, rather than the thoughts, of the participants would be directly recorded. Although several researchers advocate the position that video games cause violent behavior in children and adults, there are also many researchers who support the opposite belief, which is that video games purge one's desire to act violently and thus reduce the amount of violence in which a person will engage (3). Other negative effects of video games may include taking time away from a child's studies or homework and decreased social skills (3) . Despite these possible detrimental effects of excessive video game playing, there are educational benefits to playing video games in moderation.
Video games can be utilized to benefit players in several ways, such as through education about important topics. A recent study conducted on the benefits of video games found games can provide a context in which participants can discuss scenarios and outcomes in order to facilitate their understanding of important concepts (4). Other researchers have found that children's reading and spelling abilities significantly improved with exposure to educational video games (5). Video games may also improve spatial abilities, the ability to create and apply multiple strategies, and may help develop critical analyzing techniques (6). They provide immediate feedback, so students can explore and learn how to alter their gaming techniques in order to be successful in a particular game. Teachers have also reported that video games led to collaboration among students (4). Many games require that participants work together in order to succeed in the game, which may improve players' social skills. Moreover, Fein, Campbell, and Schwartz found that in classrooms that contained a computer, children were more likely to engage in parallel play and peer interaction (5). Finally, many popular games teach children the value of economics through acquiring money and then trading it for objects that facilitate the playing of the game. Players are also required to meet and exceed challenges, which may increase their desire to meet challenges in other contexts as well (7).
Video games are often portrayed in a negative manner because they are seen as having an "addictive" quality. Addiction has been defined as "A primary, chronic disease, characterized by impaired control over the use of a psychoactive substance and/or behavior. Clinically, the manifestations occur along biological, psychological, sociological and spiritual dimensions (8)." While there is currently no category for video game addiction in the Diagnostic and Statistical Manual of Mental Disorders (9), which is the manual utilized to diagnose psychological disorders, video game addicts are often described by clinicians in the field as displaying many symptoms characteristic of other addictions. These behaviors include failure to stop playing games, difficulties in work or school, telling lies to loved ones, decreased attention to personal hygiene, decreased attention to family and friends, and disturbances in the sleep cycle (10). Withdrawal symptoms can even include behaviors as severe as shaking (3).
The psychological cycle of substance addiction and other maladaptive behaviors can be applied to video games as well. A person playing a video game feels an emotional high, commonly known as an adrenaline rush, as a result of his gaming tactics (11). He then plays the game more and pushes his physical and psychological limits in order to experience the emotional high. Eventually, he will again reach a level that stimulates the production of adrenaline. The cycle may continue until it leads to an unhealthy level of interaction with video games, which some professionals may label video game addiction. Even famous psychological effects such as the sunk cost fallacy can influence the addictive cycle. This fallacy occurs when a person feels compelled to continue performing a certain behavior because he has previously invested time in the behavior and does not want to feel as though his investment was wasted (12). Similarly, Dr. Timothy Miller, a clinical psychologist, states that many video game players may feel that they have wasted their efforts if they do not reach the next goal in a game, which may lead to additional time spent playing the game that the person otherwise would have spent in a more constructive task (10).
Despite the possible negative psychological effects of video game playing, there are many positive effects that may outweigh the negative consequences. For instance, the creativity of players may be enhanced by their involvement with video games. Players often create their own games with computer technology that allows them to use their own music and visual patterns (7). This may allow players to stimulate their brains and thought processes in order to create the often elaborate scenarios involved in complex video games. Furthermore, video games often allow players to use their imaginations in order to transport themselves into scenarios completely different from real world situations. While there are certainly creative benefits to playing video games, it is important to remember that players must be actively interested in these types of games and must be invested in them in order to gain these benefits.
According to Dr. Orzack, the Director of Computer Addiction Services at McLean Hospital, social pressure or lack of social skills can lead to video game addiction (10). Dr. Orzack suggests that many video game addicts have struggled with finding their place in society and as a result play video games in order to become part of a crowd. The players then may feel compelled to reach the next level of achievement in the game in order to flaunt their abilities in front of their peers (10). However, despite the fact that video games may have a detrimental effect on social skills, they may also positively affect development in this area.
Video games may facilitate players' social development in several ways. Because players may discuss the games with their peers and may share their tactics for success, players often benefit from these positive social interactions (7). Furthermore, simulation games may provide an environment in which players can improve their observation skills, which may lead to enhanced social interactions (13). For example, a player who is inexperienced in making correct judgments through observation of his peers may flourish in this area after playing games that rely upon careful observations for success. These games may incorporate a type of scaffolding nature that allows the player to slowly improve his skills in this area. Researchers have shown that programs that contain a substantial amount of scaffolding also may improve language skills (5). Scaffolding is a principle proposed by Vygotsky that entails presenting tasks to a person that he does not currently understand, but that are within his ability to understand. The assistance in the tasks then decreases, which allows the player's abilities to gradually grow in the area (14). Finally, some simulation video games may present players with unfamiliar words that they need to understand in order to succeed in the game; therefore, the vocabularies of players may increase as a result of playing these types of games (13). With an increase in vocabulary span and language development, players may be able to communicate with their peers in a more effective and enriched manner. One weakness in these arguments, however, is the fact that many players may not be invested in learning new vocabulary words and therefore may neglect to take the initiative in learning these new words when they are presented. Rather, these players may try to use the visual images and context in order to determine how to proceed in the game. However, despite the fact that these players may not be actively seeking a dictionary in order to expand their language skills, they may still benefit from the exposure to new words since it is probable that they can deduce the meaning of the words from the other aspects, such as visual images, of the games. Although these social effects are important to consider when investigating the effects of video game playing, it is equally important to discuss the neurological effects of playing video games.
Not only can video game playing cause psychological and social changes in a person, but it can also result in neurological changes as well. A recent study utilized positron emission tomography in order to show that levels of the neurotransmitter dopamine increased while playing video games (15). Dopamine is believed to mediate several behaviors, one of which is the experience of pleasure. For example, dopamine levels increase in emaciated rats when the rats are presented with food, and similar effects are found when water deprived rats are presented with water. Despite the positive effects of dopamine, high levels of the neurotransmitter have also been associated with addictions to drugs and substances (16). Because increased levels of dopamine have been found in people who are playing video games and because these effects are similar to the increased levels of dopamine in drug addicts, some researchers have hypothesized that higher levels of dopamine can produce a dangerous cycle leading to addiction of video games (16). However, because this research is fairly novel, studies replicating the data are necessary. Furthermore, the possibility of involvement of other neurotransmitters during video game play should be explored since it is possible that multiple neurotransmitters may interact in addictive behaviors. Finally, because this area of research is fairly new, many interesting questions can be raised. For instance, does excessive playing of video games cause a fundamental and permanent change in the dopamine system? If so, what are the subsequent effects on the pleasure systems of these individuals? Do these people require more dopamine to be released as a result of a decreased sensitivity to dopamine that was caused by the excessive play, in a way similar to other addictions (15)? On the other hand, is it the case that the dopamine levels were high simply because the players were happy and experiencing pleasure in playing the games, and so there was no relationship between dopamine levels and addiction?
The nature of video games has led researchers to discuss several psychological, social, and neurological effects that are associated with video game playing. It appears that playing appropriate video games in moderation can lead to beneficial effects, but more controlled studies investigating the role of video games in this type of development is necessary. Furthermore, many of the current studies available are inconclusive about the cause and effect relationship between video games and behavior, especially violent actions. Many authors of these studies have speculated that their results indicate that video games cause players to become more violent, when in fact this causal conclusion should not be made from the data collected. Until there are more studies of an appropriate nature, it can only be concluded that playing many types of video games, but perhaps not all, appears to provide benefits for players such as increased social skills, educational lessons, and language development; however, excessive playing of video games may lead to poor peer interactions and patterns of behavior similar to addiction.
1) Assorted Gaming Statistics , A good reference for game statistics
2) Video games: Research, ratings, and recommendations , Contains many references for empirical studies
3) Video games: Cause for concern?
4) The relevance of video games and gaming consoles to the Higher and Further Education learning experience. , Discusses benefits to playing video games in education
5) Din, F.S., & Calao, J. (2001). The effects of playing educational video games on kindergarten achievement. Child Study Journal, 31(2), 95 - 102. Available online at infotrak.
7) Computer games and Learning , Suggests positive ways to use video games in learning
8) Definitions in Addiction Medicine , A good resource for definitions
9) Computer and Cyberspace Addiction
11) Are video games really so bad?
13) Thinking and Learning Skills Potentially Developed by Playing Some Simulation/Adventure/Role-playing Video Games , Discusses some positive benefits to video game playing
14) Berk, L.E. (2000). Child Development (5th ed.). Boston, MA: Allyn and Bacon.
15) Positron Emission Tomography
16) The Biochemistry of Human Addiction , Discusses the role of dopamine in addiction
| beliefs and healing the body Name: elizabeth Date: 2002-05-11 15:43:31 Link to this Comment: 2075 |
I became interested in researching faith healing on the web, as a means of understanding belief and the idea of the brain healing the body. I knew a little about Christian based faith healing: the evangelical preachers on T.V. who smack the heads of the skeptical, and then they fall backwards, unconscious, and are healed, but I wanted to learn more specific information about the general practice of faith healing. What are the different forms faith healing takes? What are the underlying beliefs of the proponents of this form of belief and healing? How are these people portrayed and delivered over the Internet? Is there anything substantive to the notion of faith healing? What I found was a mix of strange ideas, which I simultaneously believed and scoffed at, depending upon their contexts and the information used to back their claims up.
To begin with, I learned about a type of faith healing performed in the Philippines called psychic surgery. It is an ancient practice that was used to relieve pain and promote healing. However, the context it finds itself in today is much more complex than that. To begin with, let me describe what might occur in a session, because it does not embody exactly what the name implies, although many believe it to. There is a lot of "laying of the hands, balancing of magnetic forces, and massaging with divinely sanctioned oils;" these are the pre-"surgery" activities that are performed while "awaiting spiritual guidance." (1) At the meeting of actor Andy Kaufman and a psychic surgeon, the actor was hoping to have his lung cancer removed. After the surgeon received "divine intervention," he appeared to have pulled out "the offending material" in the midst of a lot of blood. (1) However, two months later, Kaufman died, and X-rays showed that no surgery had ever been performed. (1) How was this possible, if the surgeon claimed to have pulled the cancer out? ...because psychic surgery, seen as a form of faith healing, is a hoax.
Dr. William Nolen, a Minnesotan surgeon who has operated in over 6000 surgeries, wanted to see for himself if psychic surgery was a hoax. He went into his personal investigation with no pre-conceived, set-in-stone beliefs. As he put it, "I was making a very sincere effort not to pre-judge the merits of the psychic surgeons whom I was about to investigate. If I had already been persuaded they were charlatans, I would never have undertaken the assignment." (1) He spent only two weeks shuttling around the Philippines, and in that short amount of time, was able to conclude that it was indeed a hoax. "His training as a surgeon enabled him to see the various tricks that were perpetrated by the healers." (1) The objects they claimed to remove were really "bullets" which they palmed, then proceeded to remove from the bodies of the afflicted. The "bullets" came in the form of wads of cotton drenched in fake human blood, animal intestines passed off as human organs, and other objects that the "surgeon" procured beforehand to use in the course of their meetings to create the illusion of surgery. (1) He knew of a woman who had screws in her hip and had them "removed," only to have them show up on an X-ray later. He even saw a lump of sugar passed off as a kidney stone. "These examples prove that psychic surgeons are nothing more than magicians and not even good ones at that." (1) And while some can be cured and helped by psychic surgeons, "the percentage of people cured, is much lower than articles written about the subject lead one to believe. And the healings do not result from the operations which are fake, but from the operations' psychological effect on people who believe they are real." (1)
Nolan realized that one of the reasons psychic surgeons are so popular is that they offer more compassion than their western medicine counterparts. "Compassionate healers can sometimes do more for patients than cold uncaring doctors-not because they have any supernatural powers, but because most ailments are psychological in nature and will often disappear given the warmth and reassurance the healers offer." (1) The placebo effect often works for those who think they are sick, but who sometimes, "need to be told they will get well soon before they actually do." (1) "Psychosomatic disorders can produce physical symptoms...as a result of stress." (1) These symptoms may be a way for the patient to get attention and sympathy. As their anxiety is relieved, like in a meeting with a psychic surgeon, the symptoms disappear.
Covering up the symptoms is, however, not the way to healthy living, according to those who practice Natural Hygiene. The act of practicing Natural Hygiene consists of "correct thinking and correct living." (2) This involves TONS of sleep, because they believe that when the eyes are closed, mental and physical health can be achieved. "Closing the eyes rests the brain and mind. An electric rhythm starts as soon as the eyes are closed and ceases immediately when they are opened. This rhythm serves to clear 'negative charges' from the brain. Activity of the eyes prevents recuperation from occurring." (2) Natural Hygiene is also about maintaining a strict vegetarian diet interlaced with fasting techniques to relieve illness. The personal attitude of Natural Hygienists is about "maintaining emotional poise, loving, forgiving and tolerating all other living beings, harming no other living beings, and being aware." (2) They are also against the use of drugs or medicine to alleviate symptoms, because they believe that "drugs only suppress the body's efforts at healing itself and maintaining its normal condition." (2)
Most importantly, to the Hygienists, is the belief that within everyone is the knowledge needed to heal your own self. Drugs get in the way of the body's natural defenses by "annulling bodily functions and impairing its structures, suppressing the power to feel." (2) The body's awareness of its diseased condition is altered by the presence of drugs by "diverting the organic attention away from the normal processes of life to the task of expelling the chemical." (2) These believers feel that the body can recover from illnesses as a result of the "operations of the processes of life and the conditions that maintain health." (2) Drugs do not effect change, but rather cover up the symptoms that point toward the real problem and which are the body's defenses against illness. "We should not alleviate or suppress the symptoms of disease. When a remedy is used, the body's energy is redirected toward dealing with the new problem, the remedy, and way from the original problem, the toxins that prompted the body to institute the disease process." (2)
They believe that "the disease is in reality not the entity at all...it is itself the process of purification-of 'getting well.'" (2) They also believe that "medication is far worse than the original malady." It is important to note that this is a very hard-core view of Natural Hygiene promoted by Dr. Bernarr, which is not echoed as rigidly in the "Standards of Practice" of the International Association of Professional Natural Hygienists, which states, "medication in some conditions, and other techniques of emergency medicine may be necessary." (2)
Not treating a disease, or treating it falsely, can lead to more pain and suffering, even death, by the believer. Simply to rest, to eat a vegetarian diet, or to keep a positive outlook, is not going to save a seriously sick person. However, covering up a symptom with drug use is also not going to cure them. Belief, it turns out, can affect your health, but belief alone is not going to save you. The case of Bob Shepherd's daughter, Debbie, belies this truth.
In the 1960's, Bob joined Christ's Church of Restitution, a very fundamental Christian group, who lived on a secluded farm in Northern California. He "was attracted by the certainty and security [he] saw in a tight-knit sect of Christian Bible-believers, who encouraged strict loyalty, an ardent faith in God and in divine healing, acceptance of the Lord's chastening as a Father's loving spanking." (3) His daughter developed a tumor in 1982, but due to his and his wife's beliefs about God, it was only treated by the head minister of their church, Brother Bee, through "the prayer of faith and Bible-ordained intercession." (3) As her growth worsened, Debbie's parents took her to the child welfare authorities. As members of a church devoted to "God and faith-healing," (3) rather than western medicine, they were scared of being outside the law if they left her to be taken care of their way. The doctors said Debbie had a cancerous Wilms` Tumor. Over the next year they did all they could to save Debbie, but on November 5, 1983, the Wilms` cancer claimed her. A couple doctors said she probably would have died no matter what. One of the nurses said, "Sometimes we will never understand why God saves one and not another." (3) But one of the people in thier own church implied that the fault was the Shepherds, for not trusting God. Bob and his wife went through turmoil, finally leaving the church, determined to lead a life with less stringent beliefs about God, faith and health.
Faith in God or in any higher power does help focus a person on acting a certain way, or leading their lives within certain guidelines. However, there are limits to what faith can achieve. Leading a good life will lead to better social relationships, as well as a more contented spirit, however it cannot cure a disease. Faith in western medicine is not altogether healthy, either, because of the quickness with which doctors prescribe medicine and fall back on surgery. Symptoms are not the cause of a problem, and medicine often covers up symptoms. There are times when medicine does get to the cause; for instance diabetics require insulin, which a lack thereof, is the cause of their problem.
The placebo effect of spychic surgery refers to easing someone's mind, which allows them to release the tension causing them illness. But again, the placebo effect will not cure cancer; it is an organic disease, not psychosomatic. I found it interesting to research for this paper, because I found SO much information. No matter what I looked at, the facet of life called "belief" was mentioned. This common thread ties the whole field of health and effectiveness together. Choices people make about their health and health-care seem to be wrapped around their belief systems, less on quantitative analysis of the effectiveness or positive results of a certain style of healing. And while belief is certainly strong in some individuals, enough to influence their lives effectively, often times, belief can overshadow the truth: which is that belief cannot cure organic diseases existing independently from mind-control, however closely tied the mind and body are to each other.
1)The Facts About Faith Healing, ever heard of psychic surgery? read this!!! some pretty weird stuff
2)Natural Hygiene: Nobody Knows, Understands, or Practices it. Why?, kind of fanatical support of Natural Hygiene
3)Deborah Elizabeth Shepherd, interesting piece on a fundamentalist Christian family who lost their daughter due to their faith in God and desire to forego medical intervention until it was too late
| Obsessive Compulsive Disorder: What it is, cause a Name: Tina Chen Date: 2002-05-11 17:13:52 Link to this Comment: 2076 |
OCD is an anxiety disorder that is described as someone with obsessive thoughts and/or compulsive behavior. People with OCD are caught up in repetitive behavior and thoughts that they cannot stop. Obsession is defined as unwanted, recurrent, and disturbing thoughts that a person cannot stop. These thoughts are unable to be suppressed and can result in severe anxiety. Compulsions are the result of the obsession. These are repetitive, ritualized behaviors that are done to alleviate the anxiety caused by the obsession. (2) The most common obsessions are fear of contamination, fear of causing harm to another, fear of making a mistake, fear of behaving in a socially unacceptable manner, need for symmetry or exactness, and excessive doubt. The most common compulsions are cleaning/washing, checking, arranging/organizing, collecting/hoarding, and counting/repeating. (3) Some people with OCD have rituals that help relieve the anxiety; however, that relief is only temporary. (4) Most patients (at least 80%) with OCD have both obsessions and compulsions. Less than 20% of the patients have one or the other. (2)
Most people with OCD sometimes know that their obsessions are senseless. This usually occurs when they are not obsessing. They know that their obsessions and compulsions are based on unwarranted fears. However, there are other times when they feel that their fears are completely valid. Even though people with OCD know that their fears are unwarranted, many try to rid themselves of these unwanted, obsessive thoughts and to stop performing their compulsive behaviors. Some can control themselves more while at work or at school. However, over the months or years, people's abilities to resist their feelings weaken and in the some cases, these rituals that the people with OCD perform can become so time-consuming which impedes their ability to have a full and normal life. Although OCD can consume one's life, people try to keep their disorder from their friends rather than to seek help. Most of the time people are successful in keeping it a secret from their friends and co-workers, but the downside is that they do not get the necessary help until years later after which they have learned to work their lives around their obsessions and compulsions. (4)
OCD can begin at any age from preschool age to adult, usually by age 40. Unfortunately, OCD is often unrecognized and a person with OCD can see three or four doctors can spend a decade seeking treatment before being properly diagnosed. It has been found that takes about 17 years from time that symptoms first appear to receiving proper treatment. The reason why so many are incorrectly diagnosed and treated incorrectly is that people with OCD are usually secretive about their symptoms or do not realize that they might not fully understand the potential reason behind their symptoms. Another reason is that many healthcare providers are not familiar with OCD and do not have the proper training to diagnose and treat OCD. The downside of the delayed diagnosis and treatment is that aside from finding the proper medication, people can avoid any suffering associated with OCD. (5)
The need to diagnose OCD early leads to the question of whether or not OCD is an inherited disorder. As of now, there has been no identification of a specific gene. However, research has found that it is possible that genes do, in fact, have a role in the development of OCD. When OCD develops at childhood, it has been found that OCD runs in the family. If a parent has OCD, then there is a slightly higher possibility that the child will also develop OCD. However, the risk is still low. Due to the nature of OCD, the child may inherit the disorder but not the symptoms. For example, if the parent with OCD washes compulsively, the child may check compulsively. (5)
Although it is not known whether OCD is inherited, there are several possibilities that researchers think are the cause. It is that that OCD could be due to abnormalities of the frontal lobe, basal ganglia, and cingulum. The function that the basal ganglia are involved with is routine behaviors, like grooming. The frontal lobe is involved with organizing behaviors and in planning. Finally, the cingulum is involved with communication in the brain's behavioral and emotional messages. Cingulum is comprised of fibrous bands. There has been evidence to support the hypothesis that cingulum is involved with OCD. This evidence is that when the cingulum is surgically severed, the result is that people with OCD are cured of the disorder. (6) What researchers believe is that OCD is caused by problems in communication between the frontal lobe and basal ganglia. (5) When PET scans of people with OCD were compared to PET scans of people without OCD, it was found that those with OCD burned energy more quickly in the frontal lobe and cingulate pathway. The cingulate pathway is made of cingulum, so the cingulate pathway is what connects the frontal lobe to the basal ganglia. The energy that is burned the more severe OCD is. So it is possible that this increased use of energy is the cause of OCD. (7)
The other possible cause of OCD is the abnormally low levels of serotonin found in people with OCD. Serotonin is a neurotransmitter that sends messages from one nerve to another throughout the brain. The way the neurotransmitter works is that it is released by a nerve ending, known as a synapse, it then crosses a gap and is then picked up by another nerve ending. The serotonin is usually cleaned out of the synapses by enzymes located in the brain. (6) It has been found that drugs that increase the levels of serotonin in the brain reduce the OCD symptoms. Therefore, it is reasonable to deduce that the reduced amount of serotonin inhibits a person's nerve cells to communicate effectively. (7)
There are two possible treatments for OCD: psychotherapy and medication. Cognitive behavioral psychotherapy (CBT) is one of the possible treatments of OCD. This type of treatment helps patients internalize a strategy to resist OCD for the rest of their life. The way behavioral therapy works is that it helps people learn to change their thinking and feelings by first changing their behavior. For OCD, behavior therapy involves exposure and response prevention (E/RP). The idea behind exposure is that anxiety will go down after being in long enough contact with what the person fears. A person's anxiety should decrease after repeated exposure until the fear is gone. The next part of the treatment is the response or ritual prevention (RP) used in combination with exposure. In RP, the person's rituals are blocked, so for example, someone who is always concerned about germs is not allowed to washing their hands all of the time. The purpose of this part of treatment is to help decrease compulsive behavior. Cognitive therapy (CT) is added to E/RP to help reduce the catastrophic thinking and exaggerated sense of responsibility. CT will helps end faulty assumptions made by obsessions. CBT is free of side effect, but all patients undergoing this type of treatment have some type of anxiety. (8)
Medication is the other type of treatment. It has been found that serotonin reuptake inhibitors (SRIs) are very effective in treating OCD. What this medication does is increase the concentration of serotonin in the brain. Five commonly prescribed SRIs in the United States are clomipramine, fluoxetine, fluvoxamine, paroxetine, and sertraline. Fluoxetine, fluvoxamine, paroxetine, and sertraline are different from clomipramine because they primarily affect only serotonin, so they are called selective serotonin reuptake inhibitors (SSRIs). Since clomipramine affects other nuerotransmittors, there are more side effects than SSRIs. Because of this, SSRIs are usually tried first. When on this type of treatment, improvement was seen after 8-10 weeks on SRIs. The downside is that less than 20% of those treated end with no OCD symptoms. For this reason, it is thought that SRI used in combination with CBT might be the best course of action. (9)
Obsessive compulsive disorder is a disorder that can be more debilitating than one would think. With this disorder, a person can become obsessed with something like germs which leads to compulsive hand washing, as a mild example. This can lead to a person washing his or her hands multiple times a day. This can disturb their work and relationships. It has been found that the cause of OCD is either due to brain abnormalities or a chemical imbalance. There are various types of treatments out there to treat OCD. The important thing is that OCD is diagnosed and treated early so that people can get the help that they need so that they do not have to suffer long.
1) http://health.yahoo.com/health/dc/000929/0.html
2) http://www.1-obsessive-compulsive-disorder.com/what-is-ocd.html
3) http://www.1-obsessive-compulsive-disorder.com/obsessions.html
4) http://www.nimh.nih.gov/publicat/ocd.cfm#ocd1
5) http://www.ocfoundation.org/ocf1010a.htm
6) http://www.mentalhealthchannel.net/ocd/
7) http://www2.health-center.com/mentalhealth/obsessivecompu/cause_of_ocd/default.htm
| Behavioral Genetic Determinism: Do Genes Equal Beh Name: Raquel P. Date: 2002-05-11 20:58:11 Link to this Comment: 2077 |
Human behavior is a loosely defined foundation for individuality, generally considered to be influenced and developed by the environment. However, recent molecular studies have exposed genetic factors that suggest a more biological origin for behavior. Gene segments in the genome of humans and other animals have been identified and associated with particular behavioral traits. Is it possible that the presence or absence of even a single gene may predispose one to alcoholism, increased irritability, or enhanced intelligence? Clearly exploration of the nature versus nurture argument with regard to genetic predisposition has social, political, and legal significance.
Employing "behavior" as the experimental variant requires identification of intrinsic behavioral characteristics that may be very difficult to define. Intelligence is considered an expression of behavior, yet the delineation of what makes an individual intelligent has been highly debated. Does IQ determine intelligence? Or is economic success indicative of intelligence? Once an experimenter is comfortable with his proposed definition for a behavior, the characteristic must be reliably and validly measured. However, if the relationship between, for example, intelligence and IQ is not clear, then assigning parameters for levels of intelligence will be even more challenging (1).
Genetically influenced traits tend to be polygenic in character, involving many genes acting in concert to produce a certain response. Therefore, association of one gene with one behavior is usually only partially conclusive. Behavior depends on the interaction of multiple gene sequences with environmental influences. These multiple gene systems are referred to as "quantitative trait loci" (QTL), reflecting their ability to quantitatively distribute phenotypic characteristics. The recently completed human genome sequence has greatly assisted the detection of QTLs and polymorphisms (2). It must also be emphasized that genes do not directly dictate action, but rather are mediated by the proteins that they code for. It is necessary to examine not only the genes but also the assortment of proteins responsible for expression of particular traits (3)It is anticipated that detailed analysis of the human genome will contribute to understandings about gene organization and transcription, and hence regulatory elements that control expression. By utilizing genomic and proteomic tools, the relationship between gene/protein and behavior may be more accurately described.
Effective behavioral genetic research requires investigation of families and populations, rather than individuals. Environmental factors influencing populations must also be considered. The heritability patterns of a behavior are compared with a control population experiencing similar environmental factors. A theoretical formula to account for variability is frequently employed: total phenotypic variability of a specific trait equals the genetic component plus the environmental component plus the interaction of the two (4). However, research has determined that environmental influences tend to disengage behavioral traits among family members rather than unify them. Furthermore, traditional belief asserted that genetic influences were critical only in infancy and early childhood, being superceded by environmental factors during later maturation. Recent genetic-behavioral findings support an opposite conclusion. It appears that the influence of certain genetic traits actually intensify through adolescence (5). Despite attempts to eliminate variability between studied populations, it is virtually impossible to account for the myriad of social experiences contributing to one's unique behavioral profile.
There are several existing indications that support biologically-based behavioral characteristics. Behavior tends to be species specific; varying species of birds utilize different methods for mating and feeding. Behaviors also reproduce themselves in successive generations, or "breed true." This is particularly evident in artificial selection for traits in domestic animals. However, behaviors do change when exposed to altered biological processes. For example, expression of undesirable social manifestations in mental illnesses is commonly controlled with drugs that alter brain chemistry (1).
Behaviors such as mental illness are also found to run in families. In fact, nearly all of the studied behaviors are found to be more heritable than common physical diseases (2). The incidence of schizophrenia in the general population is relatively low, but the siblings of schizophrenics are about 10 times more likely to suffer from the disorder, while the average incidence among children of schizophrenics is about 13 percent. Risks of subsequent generations are comparatively lower. A study investigated the incidence of schizophrenia among fraternal and identical twin populations. Identical twins, who essentially possess identical genomes, maintained a 46 percent rate of tandem schizophrenia. The rate for fraternal twins, however, was only slightly higher than that of non-twin siblings, at an incidence of 14 percent. The exact location of the schizophrenia gene (or genes) has not yet been verified (5).
Most importantly, behavior has an evolutionary history that links related species. The genomes of humans and chimpanzees are genetically very similar, varying principally in organization and assortment of genes. These two populations share traits of highly social primates, including behaviors such as nurturing, cooperation, and altruism. These behavioral characteristics enhance the survivorship of each species (1). Likewise, traits that prove detrimental to a species' survival are eliminated by natural selection. A study performed by Harvard and MIT scientists involved the silencing of the gene responsible for coding of an important enzyme, CAMKII, in lab mice. Mutated mice were found to be unusually aggressive and daring. When placed in an open field, a mutated mouse would dawdle. However, when under the same conditions, a normal mouse would immediately run to the perimeter for cover. The atypical brazen attitude of a mutant mouse would make it much more susceptible to attack by prey in nature. Therefore, this trait is not frequently observed among mouse populations because it has been naturally selected against (6).
Research regarding the genetic influence on obesity has received a lot of media attention. A study in 1994 found that mice possessing the "obese gene" were not only obese, but also suffered from type 2 diabetes and lacked the protein leptin, which acts on the hypothalamus to regulate appetite and energy use. This research was applied to obese children, and several families in the United Kingdom were found to be leptin deficient. Children were obese as long as food was available for their consumption (7). It has been suggested that the obesity and type 2 diabetes epidemics among American children has an bio-evolutionary component. Simply, humans have old genes in a new environment. Our species evolved to sustain a hunting-gathering lifestyle with frequent famine and mandatory physical activity for survival. Food is made readily available in our society, and many children are become increasingly less physically active. Unfortunately, the genes governing metabolism have not changed to accommodate this indulgent, inactive lifestyle. It has been estimated that genetics contributes to about 40 percent of obesity variance, while over 200 genes and gene markers for obesity have been identified (8). This is a classic example of how both environmental and biological factors are influencing behavior.
A rare genetically based neurodevelopmental disorder, Williams Syndrome (WS), may provide the most compelling evidence for parallel functional networks within the brain, as well as expose how these functions are influenced by genetic processes during neurodevelopment. WS is caused by a micro-deletion on the long arm of chromosome 7 (7q.11.23) with an incidence of 1 in 20,000 live births. This deletion encompasses a 1.5 mega base chromosomal segment, coding for an estimated 17 genes, and is thought to occur by unequal recombination during meiosis. The deleted segment includes elastin (ELN) and four genes that are understood to be highly expressed in the brain (FZD9, STXIA, LIMK1, CYLN2) (9).
WS is associated with multiple morphological and physiological manifestations. In addition to distinctive facial characteristics, WS is identified with cardiac problems, particularly supravalvular aortic stenosis, peripheral pulmonary stenosis, and hypertrophy. Other physical issues in WS include additional vessel narrowing, lax joints, joint contractures, hernias, short stature, and a hoarse voice. It is suspected that the ELN deletion is responsible for these connective tissue problems (9). Although the incidence of premature death due to cardiovascular and other organ complications in WS has been reported to be moderately high, contemporary methods of specialized and vigilant medical care have greatly improved and increased the lives of WS individuals (10).
The WS cognitive profile is particularly intriguing. Affected individuals possess a social-emotional phenotype that includes unusually elevated sociability and empathy coupled with a fervent attraction to music, probably due to emotional factors. WSI are associated with gregarious and loquacious personalities, involving excessive sociability with strangers. The disparity between cognitive strengths and weaknesses in the WS profile is considerable. The average IQ s of WS individuals (WSI) is fairly depressed, averaging at about 60. However, variation among WSI does exist and IQ s as high as 100 have been measured. WSI demonstrate great strengths with face perception and recognition memory, affective prosody, short-term auditory memory, and select aspects of languages, despite functioning in the range of mild mental retardation. However, individuals struggle with visuospatial, motor, vasomotor integration, and arithmetic skills. WSI can maintain differences between verbal and non-verbal skills that exceed two or three standard deviations on standardized measures. Overall language abilities are delayed, but phonological processing, verbal fluency, vocabulary, and morpho-syntax are impeccably developed (9).
Whole brain volumes in WS are about 15 percent smaller than normal. However, the superior temporal gyrus, which contains the primary auditory cortex and regions associated with auditory inputs necessary for language and music processing, are within normal volumes. Alteration of function in this area may explain the high rate of hyperacusis in WS, as well as involve the signature language and musical perceptions. An exaggerated leftward symmetry of the planum temporale is also observed. This pronunciation has been observed in musicians with perfect pitch and is linked to hemispheric dominance for language (9). A particular portion of the midline cerebella vermis is considerably larger than in the unaffected population. A growing body of evidence suggests that the neo-cerebellum participates in higher cognitive function, particularly with regard to fluent speech (11). The fore mentioned neurological peculiarities not only demonstrate how altered genetics in WS is closely related to language and musical abilities, but also suggest that a broad range of variation in diverse brain regions contribute to the unique characteristics of WS.
WS and autism are frequently compared to elucidate key neurological concepts. Autism is essentially the converse of WS, in that it involves low sociability, lessened empathy, and deficits in face recognition and non-verbal features of communication. Individuals suffering from autism fail to engage the fusiform gyrus (FG) during face perception exercises. However, preliminary evidence supports that WSI are normal in their engagement of the FG during corresponding exercises (9). Therefore, evaluation of WS not only reveals various neurological functions that are affected by the gene deletion, but also shed light into how the brain operates in other neurodevelopmental disorders. Neural systems employed by WSI for sensory, cognitive, and language processing is not identical to systems employed by the unaffected population for the same tasks (11). It is possible that the systems mediating behavior in WS may be mechanistically and anatomically distinct from the norm; high linguistic functions are maintained despite severe general cognitive deficits.
My interactions with Williams Syndrome children and adults have provided insight into their individual similarities and diversities. In July of 2000 the International Williams Syndrome Conference was held in Michigan, featuring both human genetics professionals and WSI accompanied by their families. The ages of WSI ranged from infancy to late adulthood. Although they all maintained characteristic morphological features, there was a substantial degree of unique physical difference in each person. Similarly, the presence of organ involvement varied among individuals.
Being surrounded by hundreds of WSI provided me with plenty of opportunity to socially interact with them, as well as allowing them to interact with each other. Conversation with a WSI is sometimes described as typical "cocktail conversation." Often times one unfamiliar with the disorder will not detect any social disparity. WSI have mastered their linguistic abilities and not only use an impressive vocabulary, but also exercise flawless syntax and grammatical complexity (12). However, their gregarious and trusting nature frequently leads them to become inappropriately friendly or even affectionate with strangers. In fact, the parents of young WSI are encouraged to reprimand their children when they exhibit this behavior. This emphasizes how innate this affability is in WS. A common conversation between two WSI during the conference involved countless superlatives and repeated affectionate gestures such as hugging or holding hands.
On the last evening of the conference, a banquet and dance was held for all participants. WSI of all ages engaged in singing and dancing, as long as the music was not played too loudly (hyperacusis). At one point, a young girl injured her foot while on the dance floor and began to cry. Immediately dozens of WSI surrounded her, providing kisses, hugs, and comforting words. A number of others were so affected by the misfortune of the young girl that they began to cry as well. This episode lasted for about fifteen minutes, and then the celebration resumed. These experiences demonstrated how unusually compassionate and concerned this cohort is toward people they barely know (or are not acquainted with at all).
The basic function and organization of the WS brain preserves linguistic abilities associated with higher cognitive function. It may be concluded that there exists a disproportionate conservation of the most autonomous aspects of human linguistic processing in this gene deletion. Particular social and musical affinities are also exhibited by those who possess the WS gene deletion. However, great variation between and among WS populations does exist. Not all WSI are musically inclined, nor are they all equally socially engaged. Likewise, the ELN gene deletion exists in all WSI, but not all suffer from the cardiovascular or other connective tissue manifestations.
To possess the genes for obesity does not automatically condemn one to a life-long battle with weight gain, but in many cases does predispose an individual to metabolic struggles. WS may be used as a convincing example of genes affecting behavioral traits. By utilizing the method of attacking "smaller rocks" to reach the mountain, the mysteries of genes and behavior may be revealed. Genes do not code for behavior, but rather proteins. In researching the translation and function of these proteins, and perhaps any neurological interactions, the scientific world may uncover the fundamentals of human behavior. The genes equal behavior presumption seems no less assuming than brain equaling behavior: genes, after all, are responsible for the function and organization of the brain.
1) What is behavioral genetics?
4) Evolution: Genetics and Behavior
5) Recent Developments in Human Behavioral Genetics: Past Accomplishments and Future Directions
6) The Maniacal Mouse: Linking Genetics and Behavior
7) Genes Do Play a Role in Obesity
8) Is Obesity Grounded in Genetics or Behavior-- or Both?
9) Genetics of Childhood Disorders: Williams Syndrome and Brain-Behavior Relationships
10) Deering, R., Kaplan, P., Nicholson, S. Williams Syndrome and Anesthesia: Evaluation of a Large Unselected Cohort. Presented at the Williams Syndrome Conference in MI (2000). In publication, Journal of Pediatrics.
11) Williams Syndrome: An Unusual Neuropsychological Profile
| Senior Moments: The Neurobiology of Memory and Ag Name: Tara Monik Date: 2002-05-12 11:14:04 Link to this Comment: 2078 |
"I lost my keys again," my mother exclaimed at dinner a few nights ago, "I really am getting old." This use of old age as a justification for memory deficits is extremely common. Many people relate old age with loss of memory and other neurobiological functions. Why is it that aging seems to go hand in hand with losing and forgetting things? Is there a neurobiological explanation for this phenomenon?
It is clear to neurobiologists that aging results in a decrease in brain size as well as a decrease in the efficiency of brain functions. It has been a widely held belief that aging causes neurons to die and for the overall number of neurons to decrease as one reaches old age. Studies conducted by Dr. David Merrill refute this idea, sighting a lack of neuronal loss in the entohinal cortex after running an MRI on a healthy subject. Instead, Merill indicates that loss of neurons may occur in degenerative disorders, such as Alzheimers, but not in healthy brains. However, it remains true that some aspects of cognition do decline as age increases, such as short term and long term memory. Since these effects are not caused by a decrease in the number of neurons present, there must be another neurobiological explanation.
In order to understand memory loss it is necessary to understand how memory works in a normal brain without any cognitive deficits. Memory can be separated into three distinct parts: working memory, declarative memory, and procedural memory (1). Working memory is the most short term, and it involves repeating something that someone has just said in conversation or remembering something you had just seen briefly. This part of memory does not ever become fully stored in the brain, does not become permanent memory, and can be erased once something new is put into the same part of the brain. (1). Therefore, once one sees something else or takes part in a new conversation is it difficult to remember all of the details from the one before. Declarative memory includes remembering facts one has used effort to learn in the past, and things one has tried to remember. The last part of memory, procedural memory, consists of everything one has learned by repetition, such as playing an instrument or sport, driving a car, or walking.
The brain is dividing into several sections, including the cerebellum, the frontal lobe, and the temporal lobe, among others. The temporal lobe exists in two parts, one on each side of the brain close to the ears. It is largely responsible for the memory system (2). On the medial surface of the temporal lobe there are three important structure that are essential for human functioning. These structures are named, in order from rostral to caudal, the olfactory cortex, the amygdala, and the hippocampus. Together these three structures are referred to as the "limbic system" (1). Their functions became understood after studying how the brain functions upon loss of each structure. For example, in 1953, a patient suffering from epilepsy underwent surgery which removed most of his medial temporal lobe (1). After the surgery, the patient was able to remember who he was and was able to carry out coherent, intelligent conversations. However, if the person with whom he was talking left the room, he would have no recollection of the conversation when it was over. This led scientists to believe that declarative memory is recorded in the mendial temporal lobe. Without this lobe, the patient could not remember any facts.
The mechanism of recording memories in the hippocampus is not yet fully understood. However, there are speculations on how the hippocampus functions in order for the brain to remember facts and figures. Information is initially stored in the neocortex, then travels to the hippocampal trace (3). The hippocampus allows for a one-way flow of information (1), in which synapses move through the gap between two areas of the hippocampus (called the subiculum to the dentate gyrus). After the information jumps between the gap, it continues in a loop formation and ends up in the subiculum again. Here in the subiculum it is involved in a short term memory consolidation, referred to as cohesion, followed by long term consolidation (3). Once the information has been fully consoliated and is ready to be stored in long term memory it is either sent to the hypothalamus or mammillary bodies, or to the entohinal cortex to be relayed back to the sensory cortex (1). The flow of information through this complicated hippocampal network is speculated to provide for memory storage.
Patients who suffer from degenerative Alzheimer's disease have a particularly difficulty with memory. In early stages of Alzheimer's disease, patients are unable to remember things on a short term basis. As the disease progresses, patients become fully dependent on others and can be unable to walk, move, or involve themselves in other basic activities (4). Since Alzheimer's disease is best known for degeneration of memory, the study of the disease is extremely helpful in understanding how memory collapses, and how memory changes as a function of age.
Researchers made two important observations in studying a brain with Alzheimer's and comparing it to a normal brain: the brain with Alzheimer's was smaller, and contained traces of a plaque build-up (5). The shrinkage of the brain seemed to be due to neuronal loss in the entohinal cortex, which is a section of the brain that controlled memory storage. The plaque build-up was found to be amyloid proteins which cannot be broken down in the brain due to the indigestible quality of their fibers (6). As the plaque grows, the sections of the brain it surround is pushed tightly compressed, limiting neural function. The amyloid plaque builds up in the gray matter of the brain, littering the space between synapses and making brain functions highly inefficient.
The cause of amyloid plaque build-up is still uncertain, but it is speculated that it is linked to an amino acid glycoprotein called Apolipoprotein E (5). This protein is synthesized mainly in the liver but is also found in small amounts in the central nervous system. It can be inherited in three different forms, as an E2, E3 or E4 allele. However, the E4 allele is the only one that seems to have an effect on amyloid plaque build-up. Scientists believe that Apolopoprotein E in the E4 form promotes the synthesis of amyloid plaque, therefore heightening the risk for Alzheimer's disease in any individual possessing this gene (7).
While memory loss in a hallmark trait of Alzheimer's disease, it also occurs in normal aging processes. Studies have shown that in normal aging, subjects have small amounts of difficulty processing and retrieving new information, specifically on recalling words and concentrating under divided attention (8). In Alzheimer's disease, subjects have greater difficulty learning new tasks and moving new information into long-term memory (8).
One study suggested that stress too could be a factor in memory loss in elderly individuals. Individuals with high levels of cortisol, a hormone associated with stress, had increased difficulty with memory (9). The same observation was true in individuals with Alzheimer's disease. In order to understand these findings, magnetic resonance imaging (MRI) tests were done on individuals with high cortisol levels as well as normal to low cortisol levels. The results were compared, and it was found that those with high cortisol levels had significantly smaller hippocampus sections in their brains (9). These findings show that high stress levels have an effect on hippocampus shrinkage and also promote memory loss. Therefore, hippocampus shrinkage is most likely a factor in memory loss for both normal aging subjects as well as for patients with Alzheimer's disease.
Other studies have also shown the importance of the hippocampas in memory. According to Dr. Stephen Salloway, in normal aging the structure of the hippocampus varies (10). As individuals grow older, the hippocampus still functions but its formation changes slightly, making it difficult for individuals to use their declarative memory as they used to. In addition, amnesia has been found to be the effect of hippocampus degradation or disruption. In certain cases of amnesia in which spatial memory and autobiographical memory is effected, MRIs have been done that demonstrate damage in the hippocampus.
In conclusion, age does indeed have a profound effect on brain function. A study conducted at the Univeristy of Kuopio in which a random sample of eldery individuals were tested for neuropsychological processes showed that the eldery had difficulty not only in memory tests, but also in tests of functions associated with the frontal lobe of the brain (11). Memory, along with executive functions of the frontal lobe, involve the hippocampus and other parts of the medial temporal lobe. This indicates that this part of the brain is responsible for certain aspects of memory, and a loss of memory most likely is the result of either degradation of this sector of the brain or disruption of its network. These disruptions may be caused by accidents, pharmacology (alcohol intakes or other drugs), or genetic disorders such as Alzheimer's disease or Schizophrenia. While there are no known way to prevent Alzheimer's disease from effecting the brain there are, however, ways to slow normal aging in the brain and to put off losing brain function and memory. These include keeping alcohol intake to a minimum, exercising the memory by using sharpening skills and memory games, and consciously trying hard to remember important details.
References
1)Washington University.
2)Albert, Marilyn S.: Harvard Hahoney Neuroscience Institute Letter, "On the Brain," Vol. 2..
3)Nadel and Moscovitch. "Memory Consolidation, Retrograde Amnesia and the Hippocampal Complex..
3)Nadel and Moscovitch. "Memory Consolidation, Retrograde Amnesia and the Hippocampal Complex..
4) The Symptoms of Alzheimer's. .
5) Greenwood. .
6) Alzheimer's Secondary Victims. .
8) Determining the Cause of Memory Loss in the Elderly .
9)Stress tied to Memory Loss .
10)11) University of Kuopio, Series Reports, Department of Neurology .
| Electroconvulsive Therapy: Why is it Effective? A Name: Cass Barne Date: 2002-05-12 20:20:04 Link to this Comment: 2079 |
Reported for the first time in the 18th century, was the use of convulsive therapy. Psychiatrists observed that after spontaneous epileptic seizure the psychiatric conditions of patients improved. Previously, in the sixteenth-century, Paracelsus, a Swiss physician and alchemist gave camphor by mouth to produce convulsions and to cure lunacy. Originally, the induced convulsions treated severe catatonic stupors and schizophrenia. Today we know the convulsions are secondary to grand mal seizures in the brain, and that the seizure is the primary therapeutic agent of electroconvuslive therapy (ECT). Metrazol and Cardiazol later replaced Camphor because of its rapid onset. The extremely unpleasant sensations led investigators to seek alternative methods and electroconvulsive therapy was born. Electrical stimulation first tested epileptic seizures on dogs and pigs, and its first treatment helped a delusional, hallucinating homeless man diagnosed with schizophrenia in 1938. After chronic administration of ECT, the patient fully recovered.
The introduction of ECT to the United States created a burst of therapeutic optimism in psychiatry. Psychiatrists used ECT experimentally on patients with major mental disorders. This led to its current use for Major Depression. A negative stigma has remained since movies like One Flew Over the Cuckoo's Nest stress the abuse of ECT: "The Shock Shop, Mr. McMurphy . . . might be said to do the work of the sleeping pill, the electric chair and the torture rack. It's a clever little procedure, simple, quick, nearly painless it happens so fast, but no one ever wants another one. Ever".
The idea that all the Doctor has to do is "push the button" and hope for the best, while prolonging the electric shock for hours at a time, to increase the effectiveness, instills the fear that ECT will be a horrific traumatic experience with brain damage and severe side effects. It is possible that this may have existed in the times of asylums as a form of punishment, but today, doctors are more careful and familiar with the equipment to produce positive effects.
However, there still remains controversy. There remains controversy because some experience more negative effects than they do positive effects. Negative results include side effects, relapse, and possible death. On the other hand, the positive result is an immediate anti-depressant effect despite the possible side effects and relapse. Some argue however, "There is no controversy about the indications for ECT and its efficacy in alleviating severe mood disorders, not about the safety of the procedure when properly done" (2). There are those who argue that ECT is brain-damaging or brain-disabling, but research has not been able to find tangible evidence on long-term brain changes when properly administered.
What remains unknown is why electroconvulsive therapy is effective. A plethora of studies show the neurochemical correlates of this treatment and its relation to the anti-depressant effect, yet none are conclusive. Richard Abrams has studied ECT for years and discusses a wide variety of reasons for its effectiveness in his revised edition of Electroconvulsive Therapy. For a person who has studied this treatment for 50 years, he concludes that there is nothing more to say about ECT's mechanism of action than he did when ECT was first widely used.
Electroconvulsive therapy is "the induction of a seizure (fit) for therapeutic purposes by the administration of a low frequency electrical stimulus shock" (1). Why does a seizure, which creates random activity in the brain, able to relieve depression and other mental conditions? What does the electricity do to one's brain? Abrams' interpretation of its effectiveness, partially based on his own work and the interpretations of many other researchers, is that "the mechanism of the anti-depressant effect remains unknown and probably involves several interacting neurotransmitters. It seems that ECT affects various neurotransmitters and neuromodulators and that the interactions among these systems result in the neuroendocrine changes observed following an ECT course" (2).
Researchers, such as Abrams, believe that ECT changes the inactive neurotransmitter systems involved those suffering from depression. However, this claim is unsatisfying because of its vagueness, and is most likely due to the fact that the etiologies of these "disorders" are unknown. Furthermore, ECT has merits when used for a wide range of depressive disorders, notably psychotic depression and bipolar disorder, as well as catatonia (mental numbness), schizophrenia, and schizoaffective disorders (3). There are several plausible reasons as to why these mental conditions result, but they are too generalized and vague. In addition, there exists no coherent generalized neurochemical theory of action of ECT, although it remains efficacious for these states. Moreover, since the mode of action is unknown in these mental states, the discovery of the mechanism of ECT is that much more difficult to assess.
The most common neurotransmitter systems involved in depression are the dopamine, norepinephrine, and serotonin systems. These systems are also involved in other psychiatric conditions, and include a long list of neurochemical correlates. It ranges from endorphins, enkephalins and prolactin, to GABA, glutamate and acetylcholine correlates. All of these systems in some way or another are involved in the behavioral manifestations of psychiatric illness, yet researchers do not know which systems are more involved with depression, than depression with psychosis. If this is unknown, then certainly the mechanism of action will not make sense, especially if there are multitudes of chemicals involved. The excessive amount of possible neurochemical correlates makes it difficult to sort out which chemicals are normal and which relate to the mental illness. Complexity of the system doubles when illnesses become comorbid.
The etiology of major depression for instance, hypothesizes it occurs because of a lack of activity in neurotransmitter systems (dopamine, norepinephrine, serotonin) (5) Some argue that the ECT-induced seizures create an upsurge of activity in the brain, and therefore increase any or all of these neurotransmitters, resulting in an elevated mood (4). For the other mental conditions, such as schizophrenia, ECT increases the prefrontal cortex activity, which may be low in these patients (1). For those in a catatonic state, ECT revives their stupor. How? Researchers do not know. Their best hypothesis or guess would say, 'Electrical stimulation in the brains of catatonics, creates more activity in the brain. This neuro-stimulation and activation may have allowed for involuntary communication within the brain, and therefore the automatic reconnection of the mental processes, and ultimate recovery'. Clearly, this is just as vague as 'ECT induces activity in the areas of the brain that are inactive in those who are depressed', or schizophrenic. If science knew the mechanism of these psychiatric conditions, then the mode of action for ECT would not be as vague. Similarly, if science knew the action of ECT, the mechanisms for psychiatric conditions of which ECT is effective could be insightful as well.
ECT is arguably superior to all other forms of treatment, especially for depression (6). Nevertheless, none of the studies tells us why. If there was a coherent theory for each of these mental conditions, which psychiatry and society labels illness, then the mechanism of action of ECT would be something more than a generalized statement about the reactivation of the brain and increase in neurotransmitter systems.
It is possible that chronic ECT administration is effective because it changes gene expression in those suffering from a mental health condition, but none of the literature discusses this in detail. ECT may strengthen the second messenger systems in these people and allow for a re-alteration in gene expression, which serves to increase neurotransmission and create an anti-depressant effect or "anti-schizophrenic effect". Furthermore, relapse in these people may occur because the ECT treatment ends, and what was once re-altering these genes, is no longer. Ending treatment may cause re-re-alteration in genes that serves to bring the patient back to his original state of depression.
We must assume that the brain's activity manifests itself in behavior concerning these mental conditions. For example, the reason we know anti-depressant medication works, is because it induces activity in the neurotransmitter systems that are low. One concludes therefore, that a dopamine agonist, which increases dopamine activity and has a positive effect on mood, must be lacking in a person with severe depression. Hence, this treatment becomes effective. The same goes for ant psychotic drugs as well. Presumably, if these medications (SSRI's, tricyclic anti-depressants, psychotropics) work for depression and schizophrenia for instance, then ECT must have the same mechanism of action. Clearly, some studies show this, while others do not. It follows the general rule of halves. In half of the subjects, ECT shows an increase of these systems, and in the other half, ECT does not increase activity. So why does it work? Aside from "spotty" memory loss, "transient" cognitive impairment and possible death from ECT, which is not very scientifically credible (2), there is no conclusive evidence for the effectiveness of ECT. Yet, it is a widely used treatment and has far higher success rates than any other form of treatment, including sham ECT (2).
.
The fact of the matter is that we do not understand ECT's mode of action. But then, we are no worse off with regard to ECT than in our lack of understanding of the mode of action of psychoactive drugs, or behavior modification, or psychoanalysis, or psychotherapy. Max Fink, M.D., an expert on ECT states, and commentator in Abrams' book states, "I believe we actually know more about the effects of induced seizures in man than we do about the effects of psychoactive drugs, and a concerted effort at research into the mode of action of ECT would be particularly rewarding in our understanding of mood disorders, psychosis, brain function, and behavior" (2).
Agreeable? Yes. If science knew more about the action of ECT then it would certainly help in understanding the mechanisms involved in the conditions for which it works. However, if the field knows more about the effects of seizures on psychiatric conditions than drugs, the literature does not examine it. Moreover, if the field knows more about why ECT is effective, it is not discussed either. The book, designed for clinicians, researchers, students, administrators, and patients, does discuss "possible neurochemical correlates". Even then, the chemicals overlap from mental condition to mental condition, and from person to person. Therefore, science still does not know what takes place in the brain to account for its effectiveness. Research knows that it is effective, but not how or why.
There must be other observations to make better sense of ECT treatment. Perhaps there is a final common pathway for all of these neurochemical correlates, and discovering this would lead to the answer of why electricity helps patients. If neurotransmitters went to one area of the brain, the end of this pathway, then plausibly ECT may activate this area. This would lead to an effective treatment. ECT may activate gene replication and create cells that were once not there. Although unlikely, perhaps ECT alters just one mutated gene that caused the mental illness. Brain activation with ECT may switch the mutation, in the end helping the patient. As one can see, it is hard to come up with plausible explanations of why this treatment is effective. It would make sense to find out why the diseases take place, then examine the treatment. However, one way is not better than the other is since discovery would lead to insight in both cases.
The interpretations of the efficaciousness of ECT do not fit very well into the problem of these mental conditions. This is because there is not a "depression gene" or any other. There is not one system serving as the culprit of this "illness". If there is no firm theory for depression, or schizophrenia than how does one expect there to be a profound interpretation of ECT? Abrams put it well when he said "modern theories of the action of ECT- even as formulated by sophisticated investigators...have not surpassed in conceptual elegance the 18th century claim that things burned because they contained phlogiston; ECT awaits its Lavoisier" (2). Indeed, ECT awaits its father of psychopharmacology, so does depression, and every other mental illness. How long are we going to sit on the idea that the effects of ECT are unknown and that it probably involves several neurotransmitter and neuromodulator systems acting together? Research must continue to study the mechanisms of action of ECT and severe mental illness in hopes of coming to a definitive conclusion about why they occur, and how treatment is effective.
1)Electroconvulsive therapy for schizophrenia
2) Abrams, R. (1997). Electroconvulsive Therapy. (3rd ed.). New York: Oxford University Press.
6)All about ECT- Electroconvulsive Therapy
| D Name: Jenny Mary Date: 2002-05-13 14:12:04 Link to this Comment: 2081 |
The mysterious nature of déjà vu does not only lie in the experience itself, but in its definition. The sole unity of truth is the direct French translation - 'already seen.' In general, the phenomena can be summed up as experiencing the past in the present. It is "an uncanny feeling or illusion of having already seen or experienced something that is being experienced for the first time." (3) The déjà vu experience is puzzling because it often leaves people disoriented and searching for explanations. In fact, it is a fairly common occurrence with 70% (a higher rate is reported between the ages of 15 and 25) of the population reporting that they have felt déjà vu at some point in their lives. (2) The frequency of the experience has left specialists scrounging for information. There is an evident absence of truth, as expressed through varying opinions from psychologists, scientists, neurobiologists and spiritual healers. The nature? The cause? No one seems to be pointing to a definite answer. Some widely discussed causes appear to point to the brain's temporal lobes, past memory, wish fulfillment or temporarily mismatched connections in the brain.
Emile Borac who was greatly interested in psychic phenomena first utilized the term déjà vu. (3) The connotation used refers to the past, while the nature of the experience is clearly positioned in the present reality. It is ambiguities such as these that spark debate over the nature of the actual déjà vu experience. Hence several definitions of déjà vu have arose, all emphasizing different aspects of the experience. Arthur Funkhouser, Ph.D. and Vernon Neppe, M.D., Ph. D. have performed extensive research on the various types of déjà vu.
Funkhouser seeks to clarify déjà vu and remove it from inaccurate associations. He claims that there are three forms of déjà vu: déjà vecu, déjà senti, and déjà visite. Déjà vecu is most similar to the widely acknowledged definition of déjà vu. It is the feeling that the present scenario has been experienced in the past - the details are identical and it is possible to predict what will happen next. While in the midst of déjà vecu, the detail of the experience is astounding, and the person is conscious that the present scenario conforms to their memory of it. (5) Déjà senti is best described an act of reminiscing, triggered by a thought or a voice. It is distinguished from déjà vecu by the following: 1. it is primarily a mental occurrence, 2. there are no existing precognitive aspects where the person has the ability to foretell an action and 3. it often times escapes the person's memory afterwards. (5) Déjà visite, unlike the other forms of déjà, is overtly physical or geographical. The experience is associated with a location, familiar inanimate objects, or a particular situation. Commonly it is experienced as the feeling of a location seeming familiar, despite the fact that it is, in the present, a new experience. Furthermore, Funkhouser adds to the phenomena of déjà vu by mentioning that it is possible to experience the interplay of all three forms of déjà vu and other phenomena exist, which closely resemble this synthesis.
Vernon Neppe, defines déjà vu as "any subjectively inappropriate impression of familiarity of the present experience with an undefined past." Concurrently, Neppe classifies déjà vu into 21 different types falling under 7 phenomenological classifications of experience: disorder of memory, disorder of ego state, an ego defense, a temporal perceptual disturbance, a recognition disorder, a manifestation of epileptic firing, and a subjective paranormal experience. (6) The theoretically, the argument is premised on the experience being dependent on the definition. Neppe's definitions, in contrast to Funkhouser's, heavily rely on the theoretical causes of déjà vu's clinical manifestations to dictate their description.
Despite the several means of defining déjà vu, explanations of the causes remain uniformly elusive. A scientific reading of the experience maintains that déjà vu is related to memory. The divided specialization of experience in the brain: the frontal lobes are tied to the future, the temporal lobes are concerned with the past and the limbic system deals with the present. (4)Regular function of all parts, under a normal state of consciousness, will only trigger sensory responses in accordance with the time frame being targeted. In this area of the brain are the hippocampus (part of the limbic system) associated with short-term memory and the parahippocampal cortex (on the surface of the brain, along the bottom of the temporal lobes) associated with long-term memory. Often, upon proper functioning, there is seamless integration between the past, present and future. However, when excessive communication between short-term and long-term memories occurs, the present may begin to feel like the past. (4) When perceptions of the present are incorrectly filtered through the memory system of the parahippocampal gyrus and its neocortical connections (responsible for recognizing memories from the past), the present moment will feel like a past memory. Since the memory system is responsible for judgments of familiarity, the faulty, isolated activity results in a momentary scene being given the characteristics of familiarity, which would ordinarily be in conjunction with a conscious recollection. (1) While the seemingly scientific explanation may debunk déjà vu's phenomenological reputation, the phenomenon is found in the fact that the miscommunication is completely isolated. Parts of the brain structure involved in memory retrieval (prefrontal cortex, hippocampus), function normally while the isolated activity in the memory system is occurring. (1)
Déjà vu has been linked to schizophrenia and temporal lobe epilepsy (TLE) to explain causality. The link to TLE appears to be significantly stronger, as déjà vu appears in the aura of temporal lobe epilepsy. An instance of déjà vu can occur right before a temporal lobe epileptic attack or during the seizure between convulsions. (7) The prevalence of déjà vu in society, however, discredits the notion that déjà vu is attributed to TLE because the experience is undergone by masses of people, not solely epileptics.
Yet another discussed cause of déjà vu appears to be the emergence of memories of past lives to the present life. Parapsychologists support this hypothesis as being connected to wish fulfillment from the past life in the present. This particular reasoning is highly debated because it can't be proved, disproved or investigated. It remains a matter of faith. However, Algorithmic Reincarnation is most consistent with the theory of reincarnation and predicts that memories are unable to pass from one life to the next. A set of signals, instead, can be transferred to reflect states of consciousness. (4)
Treatment for déjà vu is dependent on the individual response of the person. Some people become terrified, while other find it exciting in its surrealism. "As with all other altered state experiences, most people who enjoy it think of the experience in spiritual terms, and those who don't, think about it in psychological terms." (4) While the experience of déjà vu in itself remain harmless, if the activity from the hippocampus (subscribing to a neurobiological explanation for causation) were to transfer to the amygdala; the structure that emotionally overwhelms consciousness in the present state, it is likely that déjà vu can yield a sense of fear. The advice commonly given for fear of déjà vu is to seek professional help from a psychologist, epileptologist, etc. For people who react positively to déjà vu, meditation and further spiritual exploration of the experience is suggested. The goal, therefore, of the meditation, which would focus in the here and now, would be to emphasize the present reality of déjà vu, as opposed to focusing on the familiar perception of the past. (4) Aside from the spiritual approach, there seem to be few recommended treatments for déjà vu because it is not classified as a disorder, or condition. It is only by association with temporal lobe epilepsy, schizophrenia, bipolar disorder, and other similar conditions that it acquires a symptomatic quality.
Déjà vu, in all respects, is considered a phenomenon from definition to treatment. It occupies a realm of altered states and varied realities. The fascinating nature of déjà vu is precisely that it is inexplicable. Funkhouser's definitions are helpful in differentiating seemingly similar experiences of déjà vu, thus giving the opportunity to disseminate the varied forms past references. The references triggered by déjà vu may often feel increasingly familiar, prompting people to seek less scientific explanations for causality, such as dreams, familiar objects. This sort of commonsensical action is the epitome of a person's reaction to the equating of the brain to behavior. The possibility is unreal, too vast to comprehend. Déjà vu accurately symbolizes these qualities. A glimpse of a familiar object in the present is often too simple, too common of an occurrence to trace back to proper brain functioning. Déjà vu and similar everyday phenomena promote exploration of states of consciousness. People's nature is to seek explanations and reasons for every aspect of their lives. Mysterious phenomena thus serve as catalysts for educating people about reality and at times, the inexplicable. It would be greatly beneficial if déjà vu caused people to examine their existence and their emotional and psychological relationship with memory. The cause of déjà vu may be fully attributed to brain function, but in pondering metaphysical causes, people who experience déjà can come to channel and better understand their states of consciousness.
1)The Jornal of Neuropsychiatry and Clinical Neuro Sciences, on the Science Direct website, Déjà vu: possible parahippocampal mechanisms
2) BBC UK website, Déjà Vu
3)Skeptic's Dictionary, Definition of déjà vu
4)The experience of Déjà Vu in clinical and spiritual terms
5)Three types of Déjà Vu, Arthur Funkhouser's classifications
6)Pacific Neuropsychiatric Institue website, Neppe Déjà Vu Resrach and Theory
7) 'How Stuff Works' Question of the Day, What is Déjà Vu?
| My Adventure with Corticosteroids: A Chiaroscuro E Name: Beverly We Date: 2002-05-13 15:23:35 Link to this Comment: 2082 |
"I can breathe! In less than twenty-four hours I am practicing the flute with the kind of breath control I've been missing for months. And all it took was one day and sixty milligrams of prednisone! ...I feel a little shaky and weird, but I can play the flute! But now it is three days later. It is the middle of the night. I'm squinting into the mirror in the bathroom. Only seventy-two hours into my prednisone therapy and my face is definitely spreading. I'm already turning into a pumpkin." (2). I understand what Eugenia Zuckerman meant. I was also on prednisone.
Corticosteroids (9) are wonderful-terrible-wonderful drugs. They make you crazy. (I was in psychotherapy.) They increase your appetite and increase your weight. (I was always hungry.) They put your nervous system on high alert. (I was nervous and frightened, my hands were shaky, and one eyelid twitched.) They produce edema. (My face and ankles swelled.) They cause insomnia, (I stayed up most of the night watching old movies on television.) Moreover, they give you the "gift" of boundless energy. (I bounced off the walls.)
I was obsessed with cleaning my house, (my house was never cleaner), my hair became brittle, my skin became dry, my nails became soft, and my beautiful singing voice became "different." All of these changes came from one drug, prednisone (3).
Corticosteroids are a group of anti-inflammatory drugs similar to the natural corticosteroid hormones produced by the cortex of the adrenal glands. These drugs work by a variety of mechanisms including decreasing the density of mast cells along mucosal surfaces, decreasing chemotaxis and activation of eosinophils, decreasing cytokine production by lymphocytes, monocytes, mast cells, and eosinophils, inhibiting the metabolism of arachidonic acid and other mechanisms.
The terrible side of this drug is that is has these many negative effects. The wonderful side of the drug, though, is its effectiveness in stopping autoimmune response. It stopped the symptoms of my new visitor: my incessant, debilitating, truly unpleasant, life threatening constant companion, Inflammatory Bowel Disease.
IBD is only one of many autoimmune diseases that can come into your life and change it forever. Autoimmune disease is a politically correct visitor, showing no preference for gender, race, age, religion or national origin. It also has no favorite places. It can attack almost any organ in the body, including the nervous system, the gastrointestinal system, connective tissue, joints, eyes, blood, blood vessels, skin, kidney, lungs, and the endocrine system (4). In all these diseases the underlying mechanism is the same: the body's immune system becomes misdirected, attacking the very organs that it was supposed to protect (4).
The word "auto" is Greek for self. The immune system is a complicated network of cells and cell components (molecules) that normally work to defend the body and eliminate infections caused by bacteria, viruses, and other invading microbes. With an autoimmune disease, the body's immune system mistakenly attacks itself, targeting the cells, tissues, and organs of a person's own body. A collection of immune system cells and molecules at a particular organ, called a target site, is broadly referred to as an inflammation (5).
Corticosteroids are in a class of drugs called immunosuppressants, drugs that inhibit the body's immune system's ability to fight infection (5). These drugs are sometimes used for the control of such autoimmune reactions as allergies, skin rash, asthma attack, or even severe laryngitis. These kinds of episodes require a fast controlling agent to calm the attack; with episodes such as these, corticosteroids use is of short duration, and does not do much damage. Sometimes, however, these episodes indicate that serious disease is present. When the disease is autoimmune, doctors prescribe anti-inflammatory agents, the ever-wonderful/terrible corticosteroids. For my illness, my doctor prescribed Deltasone, a more refined version of the generic drug, prednisone (3), (7).
My doctor, Franz Goldstein, told me not to read the PDR, The Physician's Desk Reference, because the list of dangerous side effects would upset me (8). "What was worse", I wondered, "knowing about the dangerous side effects of this drug or not knowing?" I decided that if I was going to learn how to live with this disease, I must trust my doctor. I did not do any research of my own. I just needed to be told that I would survive.
I came to Dr. Goldstein after being under the care of another physician, Dr. R., whose manner was abrasive, who did not take time to answer my questions, who had started me on medication that did not help me, as I got sicker every day. Dr. Goldstein put me into the hospital, attached me to several IV's filled with corticosteroids, glucose and potassium, and soon the symptoms began to subside. I became hopeful. I wasn't going to die.
Ulcerative Colitis, my form of IBD, is a nasty illness, causing a breakdown in the digestive tract (6). The physical symptoms are debilitating, but the feelings of hopelessness and sorrow that set in before diagnosis are even worse. Every day, I waited to feel better, and every day I felt worse than the day before. It is hard to accept that your body is failing, that what is happening is out of your control. No amount of bed rest and tea and toast will make the symptoms go away, or the fear subside. What was happening to me? Would I get well without medical intervention? Would I need surgery? What was this incapacitating illness? What was the cause?
Inherited genes, together with the way the immune system responds to certain triggers or environmental factors, may influence the development of an autoimmune or immunopathic disease (5). Some immunopathic diseases are known to begin or worsen in the presence of a trigger such as a viral infection. When I was a new mother, 23 years old, I developed a virus, was hospitalized with severe abdominal pain and a fever of "unknown origin," After many tests, I was sent home without a diagnosis. Whatever it was, was gone. I got well. The human body is resilient; homeostasis is a wonder. Ten years later, however, I became ill with different symptoms. After exhaustive testing, I was diagnosed with IBD. Was there a connection between the earlier virus and the new disease? Yes. Viruses can act as a trigger mechanism when there is a genetic predisposition to immunopathic disease. Family members with autoimmune disease may inherit and share a set of abnormal genes, although they may develop a different autoimmune disease (5).
My adventure with prednisone lasted for 8 years, and, although life became more normalized, it never became normal. Corticosteroid medication saves lives, by inhibiting the body's tendency to attack its own tissue. Quite soon, symptoms subside and normal functioning of the target organ resumes. However, as bad as the physical side effects of this medication are, the emotional side effects may be worse.
The mind and body work together. In a healthy state, the balance of the two is a wonder. The I-function comes into play (or it doesn't) in a synchronized ballet, where the mind and body send action potential signals, inputs and outputs, and reafferent loop systems. When all is working well, streams of neurotransmitters go to all the right receptors, keeping the body in a state of homeostasis, so that it can receive and distribute appropriately all these neuro chemicals. When disease strikes, however, the system changes, the signals get crossed or deleted or multiplied, and the body begins to break down or fall apart.
When medication is used to correct an illness, side effects might be physical or emotional, depending on the drug. With this medication, both the body and brain are seriously affected by unpleasant and sometimes dangerous side effects. The side effects normally associated with most FDA approved drugs are relatively standard and predictable; they could include: dry mouth, rash, gastrointestinal symptoms, blurred vision, sodium retention, these annoyances influence a patient's decision to continue or discontinue a medication. Sometimes, the pharmacist will advise the patients to ride out the side effects for the length of time that they need to be on the drug.
With corticosteroids the side effects are more serious. In addition to the non-life-threatening symptoms I mentioned earlier, such as increased appetite, insomnia, and edema (especially in the face), prednisone also carries with it some dangerous side effects as well. These include bone thinning (osteoporosis), hypertension, muscle problems, hip joint deterioration, glaucoma, cataracts, increased blood sugar, kidney involvement, delayed wound healing, decreased ability to fight infection, increased sensitivity to the sun and increased fat deposits, which compromise the heart (7). It is better not to read the PDR when you are first put on corticosteroids. My doctor gave me good advice.
Although I could not do much about the physical side effects that might occur, I could do something about the emotional roller coaster. My emotional symptoms included insomnia, fear, nightmares, anxiety, trembling hands, and huge mood swings that would cause me to cry with little provocation. My understanding and sympathetic Dr. Goldstein told me that psychotherapy might help me to learn to live with the strictures and emotional burdens of this disease. So I made an appointment with a psychiatrist.
The mind/brain is an amazing entity. With the help of a mild tranquilizer, my psychiatrist taught me relaxation techniques and I attended scheduled sessions of cognitive behavior talk therapy once or twice a week. I began to read about the disease and the medication, to learn how I could control it, rather than have it control me. After the initial shock of the illness started to dissipate, I was grateful for two things. First, that the prednisone worked and my symptoms were under control, and, second, that with the help of a wonderful support system, my family, I began to reorganize my thinking so that I was not only a "sick person."
My adventure with prednisone ended in 1987 when the prednisone was no longer able to control the symptoms of my Inflammatory Bowel Disease. My doctor, fearing a risk of color cancer, and anticipating additional years of prednisone side effects, recommended extensive surgical intervention.
This surgery brought with it a new set of emotional problems, but, ironically, the psychological lessons I had learned during my prednisone years prepared me to adapt to and accept life conditions that often cause despair and depression.
What I learned from prednisone is the difference between chiaroscuro and real life. In chiaroscuro painting, the artist creates the illusion of depth with alternating patterns of light and dark (1). During my first years on prednisone, my life was alternating patterns of light and dark, wonderful days or terrible days, painful days or euphoric days, hopeful days or desperate days.
As my therapy progressed, however, I learned that I was not just a person defined by the light and dark of the drug; rather, I am a three dimensional person, not a two-dimensional illusion of reality.
I began to resume my life. I could go to the movies again. I could do the marketing by myself. I could travel to Europe with my husband. My children were seeing their mother return.
2) Bookshelf: Coping with Prednisone (Zuckerman & Ingelfinger) ,
3) Deltasone (Prednisone) - Side Effects & Warnings ,
4) Autoimmune Disease the Facts (National Women's Health Information Center) ,
5) Understanding Autoimmune Disease (National Institute for Autoimmune Disease) ,
6) Ulcerative Colitis (National Digestive Diseases Information Clearinghous) ,
7) Prednisone: Good Guy - Bad Guy (TransWeb) ,
8) Drug Information (PDR.net) ,
9) Allergy Glossary (Health on the Net Foundation) ,
WWW Sources
1) Encyclopedia Britannica "chiaroscuro" ,
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| Stress: The Breakdown of Mental Health and Stabili Name: Joan Stein Date: 2002-05-13 17:55:47 Link to this Comment: 2083 |
Progress has always been an essential component in modern society. At times it is equivalent to success, learning, and overall growth. In the field of science, progress is measured by comparisons to what was known before, what is known now, and what can be known in the future. Therefore, one could say that much progress was made in the field of science in terms of understanding the functions of the human brain and some of its behavior. It seems that as each new day passes, something new is discovered about the brain, whether it be a new mental or physiological brain condition, or merely a link and clue to one of the vast number of questions the world has considering the human brain and behavior. These discoveries and answers are becoming more and more important and imperative due to the fact that the overall population seems to becoming more and more emotionally fragile and more subject to several cerebral ills such as depression, anxiety, hysteria, and clinical insanity.
A good question to ask is whether or not the overall population seems to be suffering more mental and cerebral ills, or that it is merely a result of more cases being reported and more statistics calculated. But if it is true that the number of people suffering from conditions or types of behavior which hinder their ability to go on with their everyday lives, what is the cause? And when we find the cause, what is the cure? Or how will society as a whole handle it?
A possible theory is to look at the correlation between the rate of growth and process in modern society and the stress level of the average individual. Another question to ask is what exactly is the role stress plays in an individual's overall health, both physically and mentally? Could it be a key factor in this sudden uprising of mental ailments and the loss of many people's emotional and mental balance and stability?
There are numerous studies linking stress with a multitude of health problems, many with a neurobiological connection. One of the biggest things stress takes it's toll upon is the immune system. The impact of stress on physical health is clearly evident, as it has been reported that ninety percent of all doctor's visits are due to stress-related ailments and stress-related disorders. Chronic acute stress leads to a shift in the balance of one's biochemistry, one symptom being suppressed serotonin.(1) It has become common knowledge that most clinically diagnosed cases of depression are treated with serotonin drugs, believing that the cause of the depression is a lack of that cerebral hormone. Depression appears to be one of the conditions that is on the rise and is given specific attention by the scientific and psychological community.
There is a specific way in which the body responds to stress. Doctor's call this reaction General Adaptation Syndrome (GAS). The process itself has the potential to enter several stages, depending on how the individual responds and reacts to certain levels of stress. When the stress is first triggered, the brain initiates 1400 different responses, including the dumping of a variety of chemicals into the blood stream. Usually it is adrenaline or some kind of chemical, which gives the body a boost of energy to temporarily give it the ability to withstand whatever is happening at the moment. This is the first stage of GAS, also known as the "fight or flight response". The body will go back to normal once the source of the stress is removed. However, if the stress source is not removed the body will go onto stage two of GAS, called "resistance or adaptation". The body goes into a longer lasting protection mode, including the raising of blood sugar levels and blood pressure to provide sustained energy. The adrenal cortex of the brain also gets involved by producing hormones called corticosteroids. If the body uses this defense mechanism for too long, it can lead to disease and a weakening of the immune system. The third and final stage is exhaustion. The body has run out of its reserves of energy and immunity. It is at this stage where the mental, physical, and emotional resources suffer greatly. Everything drops, blood sugar levels, adrenals get depleted, all systems shut down and the body collapses. Usually this leads to a decreased stress tolerance for later on, progressive mental and physical exhaustion, and illness.
This chain of reaction cycle is a cleverly designed mechanism for survival for humans, but continual stress early in life can disrupt it. For some, even when the source of stress is removed the process will continue. The brain, specifically the hypothalamus, will continue signaling the adrenals to produce the cortisol hormones. This exhausts the stress mechanism and leads to fatigue and depression. These continually high levels of cortisol has been shown to suppress the immune system, adding evidence to the theory that stress and depression have a negative effect on the immune system.(2) An activity or reaction, which involves some brain activity, especially a strain on brain activity has the potential to damage other areas. The suppressed serotonin and overload of cortisol are a clear and rational explanation for the possibility of depression to arise in the individual suffering from intense, chronic stress.
There are physiological side effects specifically on the brain itself due to stress. A study at Stanford shows that a prolonged flow of stress hormones can actually cause shrinking in certain brain areas, particularly in the hippocampus, which plays a major role in memory. Therefore it is no unusual for people with prolonged stress to experience forgetfulness and have difficulty learning.(3) Stress-induced structural changes in brain regions such as the hippocampus, due to an overflow of stress hormones such as cortisol, have clinical ramifications for disorders such as depression, post-traumatic stress disorder and individual differences in the aging process. Abnormalities of the stress system activation have been shown in behavioral syndromes such as melancholic depression. The stress response is central to resistance to behavioral syndromes,(4) therefore it's easy to see how constant exposure to stress and the wearing down of the system itself can make someone clearly more susceptible to developing symptoms of, and even becoming completely enveloped in, clinical depression.
The constructs of our society make it difficult for most to handle their stress in the way the body naturally does. The innate impulse is to either run from the situation which is causing the stress or fight it. Take for example a situation where one individual, a boss, is yelling at one of his employees. The employee goes through the natural, GAS response and probably either wishes to run away or hit the yelling boss with everything he has. Of course the employee does neither of these or risk losing his job. Therefore, it is the body itself that has to deal with it, using and burning up a lot of energy because all in all there is nothing that can be done in response to the reaction from the stress. The fact that people in today's society cannot, without putting themselves socially at risk, do or react in the way that nature intended leads to a more damaging effect from stress. Evidently the lack of damage from the outside is balanced out by the potential damage on the inside.
A contributing factor to the ever-growing plague of stress is from mother to child. New research shows that prenatal stress could significantly influence development of the brain and organization of behavior in fetus. Because stress affects many of the body's systems— nervous, cardiovascular, endocrine and immune— there is good reason to believe that severe emotional stress could cause defects in the fetus, especially during the first trimester of pregnancy when development occurs at the fastest rate. In women who are exposed to severe stress and anxiety, this effect is caused by reduced blood flow through the arteries that feed the uterus. Usually, the cranial nerve crest, a structure of cells that is thought to contribute to the development of the head and face in a fetus, gets affected. According to Dr Vivette Glover, research head of a study linking obstetrics, pediatrics, psychology and psychiatry, experiment on animals shows that maternal, fetal, or neonatal experience can set the stress responses of the developing offspring for life. If true, in human beings this could predispose children to have behavioral problems, such as hyperactivity, or cause them to suffer from depression in later life.(5)
A hypothesis that could easily be made is that the way our society has progressed leads to lives filled with complexity and incredibly high levels of stress. Since humans are not able to deal and process the reactions of stress in the nature that was originally intended, and the fact that many of the sources of stress simply do not go away (for example: work, family, relationships, the environment), stress has in a way become an epidemic of it's own. The physiological and psychological effects are knocking people off their delicate balance and raising the levels of anxiety and depression amongst the population. Perhaps evolution will take hold and those with brains and systems more well adapt to handling this relatively new level of stress will flourish, making our society stronger. Or it could have a reverse effect, making society weaker in the process. Hopefully stress and it's harmful effects will be brought to attention more by the scientific community and as a whole society will do something about it or risk suffering from the potential set backs.
1)Physiological Effects of Stress
2)Holistic-online
3)http://www.brainsource.com/stress_&_health.htm
4)Neurobiology of Stress
4)http://www.lifepositive.com/Mind/psychology/stress/symptoms-of-anxiety.asp
| Can't Help Falling in Love Name: Nicole Pie Date: 2002-05-14 00:11:50 Link to this Comment: 2084 |
Wise men say only fools rush in/ but I can't help falling in love with you/ Shall I stay/ would it be a sin/If I can't help falling in love with you/ Like a river flows surely to the sea/ Darling so it goes/ some things are meant to be/ take my hand, take my whole life too/ for I can't help falling in love with you/ Like a river flows surely to the sea/ Darling so it goes/ some things are meant to be/ take my hand, take my whole life too/ for I can't help falling in love with you/ for I can't help falling in love with you –Elvis Presley (1)
Elvis may have been wise before his time, because research has found out that you cannot "help falling in love". (1) Many recording artists sing about love and how you cannot help the way you feel about someone when you are in love. Many researchers have done studies to find out what happens within the brain when you are in love and the results are interesting. Before one can understand the emotion of love, one must look at emotions themselves and what they do within the brain.
Emotions:
Emotions are defined as "stereotypic patterns of the body, which are triggered by the central nervous system in response to distinct external environmental situations or to the recollection of memories related to such situations." (2) In other words, this means the emotions are the way the nervous system reacts to different situations one might find themselves in. In order to survive, emotional responses must be present. (2) "Whenever an emotion is triggered, a network of brain regions (traditionally referred to as the limbic system) generates a pattern of stereotypic outputs, which ultimately induce a biological response of the body." (2) These stereotypic outputs are what humans call emotions. They are predictable responses to certain situations, for instance when a person is in a sad situation, they will cry and feel depressed or if a person is in a happy situation, they will laugh and smile. These responses are because "specific circuits of the emotional motor system have evolved to both generate this stereotypic emotional facial response, as well as instantaneously recognize it when it occurs in somebody else." (2) This holds true for people in love, when you see someone in love you can tell because their face tells all.
What is Love Psychologically Speaking?:
Most people experience at least once in their lifetime, most people experience "love" more than that, but it is not true love it's more being in love with being in love. However, "the emotion of love is essential for bonding between individuals." (2) This bond of love allows for humans to reproduce which leads to the continuation of the species. Love also allows for companionship, which gives a person gratification and a feeling of purpose in life, because they have other people to take care of, who has a special meaning to the other person. Along with love come some behavioral responses to this emotion. " 'Early love is when you love the way the other person makes you feel... mature love is when you love the person as he or she is.' It is the difference between passionate and compassionate love." (7) Most people when they first fall in love, feel great passion for the other person, as well as feeling playful, giddy, and are preoccupied with thoughts of the one they love. (3), (7) Love is a very selfish emotion, because all of the feelings one feels when they are in love are self-gratifying. "Along with the exhilaration of infatuation and the warm, cozy comfort of attachment, love creates and reinforces the self. People's sense of who they are is strongly affected by whom they love and whom they perceive as loving them." (3) When people are in mature, compassionate love, they feel that they must protect the one they love and will do anything for the one they love, which makes "the lover obtain a strong sense of gratification and identity" (3) as well as making self-sacrifices give them a sense of a reward. When a person is in mature love, intimacy, passion and commitment are all present, which gives the person a feeling of feeling one with the person they are in love with. However, love is not only makes psychological responses occur, but biological responses occur also.
Is Love an Addiction?: Biologically Speaking:
Your lights are on, but you're not home/ Your mind is not your own/ Your heart sweats, your body shakes/ Another kiss is what it takes/ You can't sleep, you can't eat/ There's no doubt, you're in deep/ Your throat is tight, you can't breathe/ Another kiss is all you need/ Whoa, you like to think that you're immune to the stuff, oh yeah/ It's closer to the truth to say you can't get enough, you know you're/ Gonna have to face it, you're addicted to love/ You see the signs, but you can't read/ You're runnin' at a different speed/ You heart beats in double time/ Another kiss and you'll be mine, a one track mind/ You can't be saved/ Oblivion is all you crave/ If there's some left for you/ You don't mind if you do/ Whoa, you like to think that you're immune to the stuff, oh yeah/ It's closer to the truth to say you can't get enough, you know you're/ Gonna have to face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Your lights are on, but you're not home/ Your will is not your own/ You're heart sweats and teeth grind/ Another kiss and you'll be mine/ Whoa, you like to think that you're immune to the stuff, oh yeah/ It's closer to the truth to say you can't get enough, you know you're/ Gonna have to face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love/ Might as well face it, you're addicted to love
–Robert Palmer (9)
Robert Palmer might have been just writing a song, but there is a basis for saying someone is addicted to love. The feeling of love begins with an infatuation phase and then turns into the attachment phase when the two people become more involved with each other. (3) In the infatuation phase, a person feels exhilaration when they see the person, an intense passion for the person and a yearning to see their lover. (3) "The euphoria or elation that accompanies infatuation can cause lovers to crave 'staying in love'." (3) Along with a heightened nervous system, there are hormones that are released.
One of these hormones is dopamine, which is also a hormone that is involved with addictive behavior. (3) When a person feels in love, they are activating their pleasure centers in the brain, which are rich in dopamine and blood flow is elevated. (8) Since dopamine is the hormone that makes a person feel an "erotic high" when they see their lover, (5) eventually the person will become addicted to feeling that "erotic high" and when it is taken away, they will go through withdrawal. Dopamine also causes a person's heart to race; pupils to dilate and a slight perspire. (4) Since dopamine is a natural endorphin, which acts like heroin or morphine when someone takes those drugs, it causes the body to respond by relaxing the body and kills pain in high doses but in low doses it cause the body to feel unpleasant, which could be related to the depressed feeling when someone falls out of love or loses a lover. (6) (7) Also, when there is a continue presence of a lover, there is a gradual increase of dopamine, which also cause the horrible feeling when we lose a lover. (7)
Dopamine is also related to obsessive-compulsive disorder, which makes love biochemically similar to obsessive-compulsive disorder. (4) When people have obsessive-compulsive disorder, there is an increased blood flow, which leads to abnormal amounts of platelet cells, which is also present when someone is in love. (4)
Another hormone involved with the feelings of love is phenylethylamine (PEA), which is also a natural endorphin that affects mood and attachment. "One study of 33 people who were 'happily attached and feeling great' found that all had increased PEA levels." (3) Researchers have also found that high levels of PEA increases sex drive and is believed that this might be the hormone of libido. (4) The body also becomes tolerant of PEA like dopamine once the body has been exposed to it for long periods of time. (3)(7)
The last hormone involved with love is oxytocin, which is also an endorphin and has an opiate-like effect. (5) "Oxytocin is another chemical that has recently been implicated in love. Produced by the brain, it sensitizes nerves and stimulates muscle contraction. Scientists speculate that oxytocin might encourage cuddling between adult women and men." (7) Since oxytocin acts as a natural tranquilizer, it allows for a woman to become more sensitive to other's feelings when present. (6) Oxytocin is released during sexual experiences as well as when lovers touch, because it activates cell-surface proteins in the nucleus accumbens, in the brain, which causes the release of dopamine. (3) So with this release of dopamine, the person feels a euphoric high.
Now to answer the question asked, is love an addiction? I believe love is a type of addiction, not necessarily love itself but the feelings that arise when a person is in love. When a person is in love, the pleasure parts of the brain are activated by the hormones released dopamine, PEA and oxytocin. Since all three of these hormones are natural endorphins, they must act like amphetamines do on the brain. Since these hormones are acting like drugs do on the brain, the brain must become tolerant to these hormones and when the couple breaks up, there must be a withdrawal period. In life, both of these phenomenons occur. The longer a couple is together their brains become tolerant to the hormones being released, which causes the euphoric feeling to not be felt as strong or not even felt at all, so when this happens the couple could still be in love, but their love changes from a passionate love into a more committed love where the two people love each other for who they are. If the two people are not truly in love, they might break up and when this happens, the brain stops having it's doses of dopamine, PEA and oxytocin, so the brain goes through withdrawal, which is why when you lose a lover you feel sad and depressed. These symptoms are a lot like being addicted to drugs, so therefore the people who think they are addicted to love, might really be, but they are really addicted to the feelings and hormones released during being in love.
1)Elvis Presley's Can't Help Falling In Love
2)The Neurobiology of Stress and Emotions
3)What is Love, Medically Speaking?
4)Love is All in Your Head—Or is it in Your Genes?
6)Can't Do Without Love: What Science Says About Those Tender Feelings
7)The Right Chemistry
8)Beauty of Love is a Beast for Scientists
| Double Trouble: Dual Diagnosis Name: Adria Robb Date: 2002-05-14 16:59:00 Link to this Comment: 2088 |
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| Double Trouble: Dual Diagnosis -- Individuals Sim Name: Adria Robb Date: 2002-05-14 17:11:35 Link to this Comment: 2089 |
In this day in age, there are many diseases that one can contract. Sometimes a person contracts a disease because it was contagious, and others because they are genetically prone to it. Still others contract diseases and disorders in ways that are not clear to doctors and medical researchers.
In recent years, alcoholism and substance abuse have been labeled as diseases because of new research findings that doctors have discovered regarding the biological and psychological factors causing someone to become an alcoholic or a substance abuser. Anyone who has a friend of family member who suffers from any form of substance abuse knows the extreme difficulty of helping the suffering individual seek help and recover. The same goes for individuals suffering from a mental illness.
In the past two decades doctors have discovered that at least 50 percent of mental ill individuals in this country also suffer from either alcoholism or substance abuse. (4) Some studies indicate that this percentage translates to 7.2 million individuals between the ages of 18 and 54 are suffering from both a substance abuse problem and a mental illness. (2) These numbers are simply staggering. Many of these numbers apply to the adolescent demographic in particular, who the National Alliance for the Mentally Ill (NAMI) say are most prone to having a mental illness "...that may in fact lead to self-medicating with street drugs and alcohol." (1) NAMI's fact sheet on Dual Diagnosis also states that mental health professionals are discovering Dual Diagnosis in such high rates that they have come to expect that individuals with a substance abuse problem will also have a previously undiagnosed mental illness. These mental illnesses range from Attention Deficit Disorder to Bipolar Disorder and everything in between. (1)
The problem with Dual Diagnosis patients, however, is the fact that they typically seek treatment for one problem and not the other. What makes things more difficult is that most substance abusers and alcoholics do not seek help at all. For the Dual Diagnosis patients that do seek treatment for alcoholism, let's say, do not then get treated for another underlying illness like depression. Doctors, psychiatrists and other mental health care professionals are hard at work in implementing effective treatment programs for these special patients, which I will discuss later. (1)
Another complicating issue Dual Diagnosis individuals face is the fact that often the patient will use one disorder to mask the other from his or herself as well as their friends, families, co-workers, and health care providers. This causes some difficulty in diagnosing someone as having two disorders. There is also the specific issue of diagnosing the teenage population. Most people are keenly aware of the fact that teenagers are hard to figure out due to their fluctuating moods and hormones. "How can [we] separate the normal mood variations of a fifteen year old teenager from certain Bi-polar disorders? When substance use or abuse is present, with resulting mood fluctuation, the variables become staggering," says a counselor in an article for About.com. (5)
Dual Diagnosis patients are more prone to relapse of either their substance abuse problem or their mental illness and they are also more prone to commit suicide and be violent. (1) Relapse often occurs because both problems the individual is suffering from were not treated in a manner that addresses both problems simultaneously. This is also something that I will examine later on. Studies have also found that Dual Diagnosis individuals have a high rate of sexual abuse experience as well (as either victim or perpetrator). (5)
As I conducted research on the World Wide Web on Dual Diagnosis, almost every site I visited on the subject had a link to a page authored by Kathleen Sciacca, M.A. Sciacca is both founder and director of Sciacca Comprehensive Service Development for Mental Illness, Drug Addiction and Alcoholism (MIDAA), based in New York. Among other accomplishments, Sciacca has written books and articles (many of which are available her website), is a touring lecturer, and leader in the development of effective treatment programs for individuals with Dual Diagnosis. She began her work in the 1980s and helps to train other mental health care workers in treating these special patients. (3)
According to research done by Sciacca, there were several programs instated in the early 1980s around the US that were working to treat the dually diagnosed patient. The programs tried what most mental health care professionals believe is best for Dual Diagnosis individuals, which is to treat both of their illnesses simultaneously rather than have the patient attend one 12-Step program and psychiatric therapy at the same or different times. One person with two problems does not mean two different treatments; the whole person needs to be treated at the same time. Although these types of patients are not often heard of in mainstream society, Sciacca cites an article in TIME Magazine in the 1980s that a reporter wrote after hearing about one the new treatment programs being developed. That, Sciacca says, was the first time Dual Diagnosis was mentioned on a national level in the popular media. (3)
The early treatment programs took "A "non-confrontational" approach to denial and resistance, involving acceptance of all symptoms [of the patient]...." (3) Not being confrontational or accusatory of patients with alcohol or substance abuse problems especially is key to effectively reaching out to these patients. With so many stigmas in society about drug and alcohol abusers, and the lack of knowledge in general about chemical abuse as a disease and not just a 'problem' or choice, makes most patients feel like seeking treatment means admitting they are wrong or bad. Sciacca explains that many mental health care workers also do not understand and recognize alcoholism and chemical dependency as a disease, and this hinders treatment of such patients. Therefore a comprehensive treatment program for Dual Diagnosis individuals must recognize both diagnoses as diseases that the patient does not have control over. (3, 1)
Some components of the Sciacca's model for treatment include, day programs in clinics, residential programs, and support/therapeutic group work. She cites that many patients find discussing their chemical abuse and mental illness problems in a group setting with others who share similar problems, helps a Dual Diagnosis individual to see in others what is going on inside of them. Another component of the program is incorporating Alcoholics Anonymous and other such groups into the treatment. Most Dual Diagnosis patients find that programs like AA are ineffective for them. However, Sciacca has found that brining in speakers from groups like AA to join group therapy discussions is very effective and helpful to patients. Through group discussion, one on one time with a therapist, and other activities in the program, a patient comes to understand his or herself as having multiple problems that can be treated simultaneously. Sciacca also stresses communication between all therapists and psychiatrists working with a given patient in order that comprehensive treatment will occur. (3)
The difficulty of living with a mental illness is extreme, as is the difficulty of living with a chemical dependency. Both problems are diseases with both biological and psychological causes and symptoms. Treatment is more difficult if an individual is dually diagnosed with both problems. But treatment is possible. From models developed by Kathleen Sciacca and other mental health care professionals, simultaneous treatment of both disorders appears to be the best method for recovery as a Dual Diagnosis individual. For a condition that applies to so many millions of people in the United States alone, it is a wonder that more outreach and treatment programs have not been established to help such patients. But with more awareness of the disorder by the general population, it will become easier to identify multiple problems in an individual family member or friend, and aid them in seeking treatment.
Resources Cited:
1) National Alliance for the Mentally Ill (NAMI), general information on Dual Diagnosis
2) The Dual Diagnosis Pages , Dual Diagnosis Conference Reports
3) Kathleen Sciacca's website , leading resource on treatment methods and program sites
4) National Alliance for the Mentally Ill , Fact Sheet on Dual Diagnosis
5) About.com article on Dual Diagnosis
For Further Information:
7) Dual Recovery Anonymous , an AA-style support ring
| Repressed Memory Name: Kathryn Fo Date: 2002-05-14 21:10:42 Link to this Comment: 2091 |
If someone asks me, "Where were you on September 11, 2001?" I would be able to give that person an accurate answer. It seems impossible to ever forget the events of that day. How could one forget such a traumatic day? It seems like life changing events would stay with a person forever. However, there are many victims of, let's say, child abuse that cannot remember the actual abuse. The memories of such horrors have been erased so there is no recollection of the events. Being a skeptic, I am not sure if I would be able to forget such horrific events. Repressed memories can also be recovered, through therapeutic treatment. It seems odd how people can forget certain traumas, but still able to remember others. How does memory actually work, and how can one selectively repress certain memories?
Memory and the I-function seem to be closely related. Memory allows individuals to store and retrieve information gained from previous experience. It can then be used to predict human response to certain stimuli. Optic neurons often "make things up as it goes along". The I-function relies on memory in order to do this. Memory is used to perform tasks such as comprehension and production of language, reasoning, and recognition of declarative. Memory is also necessary for skill acquisition. Different models of memory have been proposed. One is that there is a limited capacity for the amount of information that can be stored. Memory can decay, and the longer a memory has been stored and not used, the less available it will be. As new information enters the memory, it may be harder to access other information and cognitive system seems to be less efficient (2).
Memory consists of three basic functions: encoding, storage, and retrieval. Encoding is the actual formation of memory. It is an active process which screens out certain materials, and allowing only selective material to be encoded. It is thought that all materials are registered, but only certain ones are retained in memory (3). The more distracting and useless messages are screened out. The encoding of the memory can be affected by how much attention is devoted to the message. Encoding can be done at three different levels. The first is the structural level of encoding, which focuses most on the physical characteristics and structures. This is the shallowest level of encoding. The second is phonetic encoding, which focuses more on words and the sounds of words. The third, and deepest level, is semantic encoding, which emphasizes the meaning of the message. Encoding works in association with other processes. It is part of elaboration, or associating the message with other information. It also works with vision and visual stimuli. Visual images can add more depth on what is being remembered. Memory is also self-referent, which allows the individual to decide how the material is relevant to his or her life. This message that has been encoded is called an engram, which will lie dormant until it is retrieved (4).
After the memory is formed, it must be retained and stored. There are three stages to memory storage: sensory storage, short-term storage, and long-term storage. Sensory storage is allows the individual to store the sensory image for a short duration of time, a couple of seconds, just enough time to gain perception of the image. Short-term memory can last for about 20-30 seconds, without rehearsal of the information, for example, remembering a phone number after looking at it. It is a working memory as long as the rehearsal of the information is continued, and the short term memory can be maintained. There is limited amount of storage space for short-term memory, and to increase capacity, information can be blended together. Short-term memory can be lost by simple decay and displacement. Long-term memory is thought to be permanent. Long term memories are not forgotten; only the mode of retrieval is lost. This can be seen with flashbulb memories, when a vivid recollection of a certain event can be remembered. It is also seen with hypnotic aided, or recovery of memory, when a certain memory can be unearthed with the aid of therapy. However, because the memories are never 100% accurate, it is possible that long-term memory is in fact not permanent. Information from the short-term memory can be shifted into long-term memory. This can be done with repetitive rehearsal of the information or with the significance of the information that is being rehearsed. If the information is important enough, it can shift from short-term to long-term memory (4).
Once memories are stored, they need to be retrieved at appropriate times. Memory retrieval is a process that relies on the cues and stimuli from the environment. Usually it is helpful for the individual to be in the same context as he or she was when the memory was formed in order to retrieve it. The original mood that the individual was in may also help in retrieval of the memory. Sometimes memory retrieval may be inaccurate because the memories can be misconstrued in the mind (1).
The physiological mechanisms of memory are still being discovered. It is thought that the memory process depends on "synaptic tagging" or "late heterosynaptic reinforcement", which describes the interaction between synaptic inputs to a neuron. When the brain forms a memory, it is strengthening the neurons that participate when encoding for the memory. The different changes at the synapse and their interaction with the neurotransmitters account for different memories. Patients with Alzheimer's disease are shown to have a depletion of the neurotransmitters acetylcholine and glutamate (5). When a person forgets something, the connection between the neuronal networks has been lost (4).
Memory can also depend on the coordinated expression and the specific regulation of certain genes. Different genes encode for different proteins. The encoding of the different proteins is important for the formation, modulation, and plasticity of the synapse. The connection between genetics and memory is still not completely understood, and research is being done for better understanding (5).
Memory is a very complex mechanism, which is not always accurate. That is why it is difficult to rely on the words of different eye witnesses of the same crime. Usually, each different witness remembers something different. The mind is capable of repressing memory as well. The mind is able to subconsciously forget a certain event, usually traumatic events, as a defense mechanism. These repressed memories can be recovered; however, there is much controversy behind that. Many argue that recovered memories are not always accurate (1).
Memory repression is done through a dissociation process. The dissociation process is an active process which causes the conscious and subconscious to split in the active experience. The active experience is like the I-function, it is the neural structure that operates all internal and external sensory inputs, and regulates behavior, learned processes, and memory. Dissociation can be done both automatically and voluntarily. One can automatically repress noise or sound. For example, when one is reading and concentrating, he or she is able to not hear the noise in the background. One can also voluntarily repress a thought or memory. One can avoid thinking about a certain memory or message. It is still in the memory, but the dissociation process keeps it from going into the consciousness, and remains in the subconscious (7).
The memories that are repressed can be recovered, though there is much controversy in that. This is because many patients who go through repressed memory therapy also end up with False Memory Syndrome. This is when the patient remembers something that did not even happen. A false image is planted into the mind, and is accepted as truth. However, there are positive results of repressed memory therapy. It allows the person to recover and face the pressed memories, whatever they may be. This is believed that it is the only way a healthy psychological state can be obtained (6).
Repressed memory therapy can be done using different techniques, some in combination with others. These techniques include hypnosis, group therapy, visualization, dream work, and suggestion by the therapist. These techniques help patients remember the traumatic events. One of the controversial issues with repressed memory therapy is concluding that any abuse has in fact been done. It is the therapist who decides whether any abuse, or other traumatic events, has actually occurred, and their decisions are not always accurate. This is how false memories are planted. All the techniques listed above essentially put the patient back to the time of when the abuse happens, or when the therapist believed that is happened, and allows the patient to relive the trauma (6).
The reliability of the recovered memory is still uncertain. Sometimes, the patient may combine pieces of dreams and reality together to fabricate an image is accepted as a truth. Often, in group therapy, patients experience communal reinforcement of delusion. People in groups often encourage the fabrication of outrageous stories. Groups nourish the birth of fantasies that are farfetched. Therapists also encourage patients to talk extensively about their childhood, background, etc to try to make conclusions of abuse. Patients are often praised for it, and if a patient is hesitant, the therapist may conclude that the patient is in denial, or needs more recovery therapy. Furthermore, some memories are forgotten not because they are repressed, but because either the person was rendered unconscious during the trauma, the brain was damaged due to the trauma, or the person was too young to remember the trauma (6).
As mentioned before, even if memories are repressed, it may not be intentional. Some people choose to deliberately forget some traumatic experience. Memories can be forgotten due to a weak neural connection that was formed during the time of the experience or the brain did not encode for the memory (6). However, it can consciously be forgotten as well. Earlier, it was said that memories are able to decay and replaced. If a person chooses to forget a certain memory, he or she can just stop thinking about it. With time, the memory will fade and be replaced with other memories (2).
The idea of memory repression makes us review the idea of I-function. The I-function is based on experience, good or bad. Some of the actions of the nervous system are based largely on the I-function. So when someone has repressed memories, does that mean that the I-function is defective, or is there something even higher than the I-function that controls memory? This also makes me think about the control that we have over our thoughts and mind. I would like to think that I have total control of my mind, but the idea of unconsciously repressing memories makes me uneasy. How does the brain know which memories should be repressed? Is repressing more detrimental than actually remembering them? Being able to face traumatic experiences, and move on seems healthier than repressing them. I do not quite fully understand why the brain would repress memories in order to protect the person. The mind is a web of mysteries, and memory repression is just on thread of the web.
| Repressed Memory Name: Kathryn Fo Date: 2002-05-14 21:11:26 Link to this Comment: 2092 |
If someone asks me, "Where were you on September 11, 2001?" I would be able to give that person an accurate answer. It seems impossible to ever forget the events of that day. How could one forget such a traumatic day? It seems like life changing events would stay with a person forever. However, there are many victims of, let's say, child abuse that cannot remember the actual abuse. The memories of such horrors have been erased so there is no recollection of the events. Being a skeptic, I am not sure if I would be able to forget such horrific events. Repressed memories can also be recovered, through therapeutic treatment. It seems odd how people can forget certain traumas, but still able to remember others. How does memory actually work, and how can one selectively repress certain memories?
Memory and the I-function seem to be closely related. Memory allows individuals to store and retrieve information gained from previous experience. It can then be used to predict human response to certain stimuli. Optic neurons often "make things up as it goes along". The I-function relies on memory in order to do this. Memory is used to perform tasks such as comprehension and production of language, reasoning, and recognition of declarative. Memory is also necessary for skill acquisition. Different models of memory have been proposed. One is that there is a limited capacity for the amount of information that can be stored. Memory can decay, and the longer a memory has been stored and not used, the less available it will be. As new information enters the memory, it may be harder to access other information and cognitive system seems to be less efficient (2).
Memory consists of three basic functions: encoding, storage, and retrieval. Encoding is the actual formation of memory. It is an active process which screens out certain materials, and allowing only selective material to be encoded. It is thought that all materials are registered, but only certain ones are retained in memory (3). The more distracting and useless messages are screened out. The encoding of the memory can be affected by how much attention is devoted to the message. Encoding can be done at three different levels. The first is the structural level of encoding, which focuses most on the physical characteristics and structures. This is the shallowest level of encoding. The second is phonetic encoding, which focuses more on words and the sounds of words. The third, and deepest level, is semantic encoding, which emphasizes the meaning of the message. Encoding works in association with other processes. It is part of elaboration, or associating the message with other information. It also works with vision and visual stimuli. Visual images can add more depth on what is being remembered. Memory is also self-referent, which allows the individual to decide how the material is relevant to his or her life. This message that has been encoded is called an engram, which will lie dormant until it is retrieved (4).
After the memory is formed, it must be retained and stored. There are three stages to memory storage: sensory storage, short-term storage, and long-term storage. Sensory storage is allows the individual to store the sensory image for a short duration of time, a couple of seconds, just enough time to gain perception of the image. Short-term memory can last for about 20-30 seconds, without rehearsal of the information, for example, remembering a phone number after looking at it. It is a working memory as long as the rehearsal of the information is continued, and the short term memory can be maintained. There is limited amount of storage space for short-term memory, and to increase capacity, information can be blended together. Short-term memory can be lost by simple decay and displacement. Long-term memory is thought to be permanent. Long term memories are not forgotten; only the mode of retrieval is lost. This can be seen with flashbulb memories, when a vivid recollection of a certain event can be remembered. It is also seen with hypnotic aided, or recovery of memory, when a certain memory can be unearthed with the aid of therapy. However, because the memories are never 100% accurate, it is possible that long-term memory is in fact not permanent. Information from the short-term memory can be shifted into long-term memory. This can be done with repetitive rehearsal of the information or with the significance of the information that is being rehearsed. If the information is important enough, it can shift from short-term to long-term memory (4).
Once memories are stored, they need to be retrieved at appropriate times. Memory retrieval is a process that relies on the cues and stimuli from the environment. Usually it is helpful for the individual to be in the same context as he or she was when the memory was formed in order to retrieve it. The original mood that the individual was in may also help in retrieval of the memory. Sometimes memory retrieval may be inaccurate because the memories can be misconstrued in the mind (1).
The physiological mechanisms of memory are still being discovered. It is thought that the memory process depends on "synaptic tagging" or "late heterosynaptic reinforcement", which describes the interaction between synaptic inputs to a neuron. When the brain forms a memory, it is strengthening the neurons that participate when encoding for the memory. The different changes at the synapse and their interaction with the neurotransmitters account for different memories. Patients with Alzheimer's disease are shown to have a depletion of the neurotransmitters acetylcholine and glutamate (5). When a person forgets something, the connection between the neuronal networks has been lost (4).
Memory can also depend on the coordinated expression and the specific regulation of certain genes. Different genes encode for different proteins. The encoding of the different proteins is important for the formation, modulation, and plasticity of the synapse. The connection between genetics and memory is still not completely understood, and research is being done for better understanding (5).
Memory is a very complex mechanism, which is not always accurate. That is why it is difficult to rely on the words of different eye witnesses of the same crime. Usually, each different witness remembers something different. The mind is capable of repressing memory as well. The mind is able to subconsciously forget a certain event, usually traumatic events, as a defense mechanism. These repressed memories can be recovered; however, there is much controversy behind that. Many argue that recovered memories are not always accurate (1).
Memory repression is done through a dissociation process. The dissociation process is an active process which causes the conscious and subconscious to split in the active experience. The active experience is like the I-function, it is the neural structure that operates all internal and external sensory inputs, and regulates behavior, learned processes, and memory. Dissociation can be done both automatically and voluntarily. One can automatically repress noise or sound. For example, when one is reading and concentrating, he or she is able to not hear the noise in the background. One can also voluntarily repress a thought or memory. One can avoid thinking about a certain memory or message. It is still in the memory, but the dissociation process keeps it from going into the consciousness, and remains in the subconscious (7).
The memories that are repressed can be recovered, though there is much controversy in that. This is because many patients who go through repressed memory therapy also end up with False Memory Syndrome. This is when the patient remembers something that did not even happen. A false image is planted into the mind, and is accepted as truth. However, there are positive results of repressed memory therapy. It allows the person to recover and face the pressed memories, whatever they may be. This is believed that it is the only way a healthy psychological state can be obtained (6).
Repressed memory therapy can be done using different techniques, some in combination with others. These techniques include hypnosis, group therapy, visualization, dream work, and suggestion by the therapist. These techniques help patients remember the traumatic events. One of the controversial issues with repressed memory therapy is concluding that any abuse has in fact been done. It is the therapist who decides whether any abuse, or other traumatic events, has actually occurred, and their decisions are not always accurate. This is how false memories are planted. All the techniques listed above essentially put the patient back to the time of when the abuse happens, or when the therapist believed that is happened, and allows the patient to relive the trauma (6).
The reliability of the recovered memory is still uncertain. Sometimes, the patient may combine pieces of dreams and reality together to fabricate an image is accepted as a truth. Often, in group therapy, patients experience communal reinforcement of delusion. People in groups often encourage the fabrication of outrageous stories. Groups nourish the birth of fantasies that are farfetched. Therapists also encourage patients to talk extensively about their childhood, background, etc to try to make conclusions of abuse. Patients are often praised for it, and if a patient is hesitant, the therapist may conclude that the patient is in denial, or needs more recovery therapy. Furthermore, some memories are forgotten not because they are repressed, but because either the person was rendered unconscious during the trauma, the brain was damaged due to the trauma, or the person was too young to remember the trauma (6).
As mentioned before, even if memories are repressed, it may not be intentional. Some people choose to deliberately forget some traumatic experience. Memories can be forgotten due to a weak neural connection that was formed during the time of the experience or the brain did not encode for the memory (6). However, it can consciously be forgotten as well. Earlier, it was said that memories are able to decay and replaced. If a person chooses to forget a certain memory, he or she can just stop thinking about it. With time, the memory will fade and be replaced with other memories (2).
The idea of memory repression makes us review the idea of I-function. The I-function is based on experience, good or bad. Some of the actions of the nervous system are based largely on the I-function. So when someone has repressed memories, does that mean that the I-function is defective, or is there something even higher than the I-function that controls memory? This also makes me think about the control that we have over our thoughts and mind. I would like to think that I have total control of my mind, but the idea of unconsciously repressing memories makes me uneasy. How does the brain know which memories should be repressed? Is repressing more detrimental than actually remembering them? Being able to face traumatic experiences, and move on seems healthier than repressing them. I do not quite fully understand why the brain would repress memories in order to protect the person. The mind is a web of mysteries, and memory repression is just on thread of the web.
| "The Truth is Out There" Name: Asra Husai Date: 2002-05-14 22:51:35 Link to this Comment: 2093 |
Murders', rapists, robbers, con artists, terrorist, kidnappers, and the list could go on. They bring fear and disgrace to a town. They are a part of society that we would like to get rid of. Even though the number of crimes has been declining in the past few years, ideally we as a society would like it to continue to decline to zero, but realistically we would be happy with a low crime rate. There are a number of technologies that facilitate the conviction of suspects such as DNA testing, lie detector testing, fingerprinting, hypnosis, forensic study, etc. Of course, there is always a bit of discrepancy with the accuracy of each of these technologies.
However, a very recent development called Brain fingerprinting, is taking a big step towards eliminating that margin of error. Dr. Lawrence Farwell, a Director and Chief Scientist at the Human Brain Research Laboratory in Fairfield, Iowa first introduced brain fingerprinting. Brain fingerprinting serves a similar purpose as that of the lie detector testing device, but claims to be 100% accurate unlike the lie detector, which is nearly 100% accurate. Brain fingerprinting determines whether the crime was committed or not and the results are not affected by anxiety, nervousness, or lying, since it simply measures if the information is stored in the brain (2).
Since the brain is the archive to a human's life story, storing all of the memories, the brain cannot lie, whereas the person can verbally lie. Taking images and words that are irrelevant and relevant to the crime are shown to the suspect by flashing them on a computer screen. Electrical brain responses are measured non-invasively through a patented headband equipped with sensors (1). Memory and encoding related multifaceted electroencephalographic response (MERMER) is the name for the specific brain wave, P300, which is brought forth when the brain recognizes significant information. As Iona Miller, Graywolf Swinney, and John Penkert's studies show that P300 waves can be observed in relation to the journeys to determine if psychologically significant imagery will trigger this objective sign of recognition (6). Thus if a crime was committed by the suspect undergoing brain fingerprinting, the brain will have a recollection of the crime and when a relevant image or word to the crime flashes on the screen, P300 will be emitted and detected by the computer analyzing data.
Dr. Farwell believes this new tool will be the next lie detector and benefit the society greatly. He has done several research studies funded by government agencies such as FBI, CIA, and the U.S. Navy (3). After what happened on September 11th, government agencies are looking to invest in brain fingerprinting technologies and use them to detect terrorists and anyone who has participated in the planning, training, and support activities essential to carrying out the terrorist act (5). It can also identify terrorists before they strike because they have the critical information about the organization, training, and planning of the terrorist act. Other benefits to brain fingerprinting are finding politicians who tell the truth during campaigns, detecting honesty in meeting contractual obligations, but I think it would be best implemented for determining facts in murder or kidnapping cases.
For instance, Terry Harrington, 41 years old, was convicted of murdering a retired police captain in 1977. Twenty-five years later, Dr. Farwell conducted the brain-fingerprinting test on Harrington and another key-witness, who claimed to have been riding with Harrington when they went to steal the car (7). For Harrington, brain fingerprinting had shown no recollection of the car theft or the killing of the police captain and the witness's testimony was proven false and the witness later retracted the testimony stating that he only incriminated Harrington because he was told that, if he failed to testify against the accused, that he himself would be charged with the murder (7). Therefore, Harrington's lawyers required for a new trial based on newly discovered evidence. However, the judge rejected to motion for a new trial because he didn't feel brain fingerprinting technology had had enough study done, but did admit the brain fingerprinting technique into evidence. This didn't stop Harrington's lawyers from appealing the case to the Iowa Court of Appeals. Clearly this a great tool for the wrongly accused, but this raises concerns about a citizen's privacy rights.
For example, if you were traveling to Saudi Arabia, Afghanistan, Pakistan, India, or any country that the United States is potentially threatened by and upon your return to the U.S., the government officials require you to be brain fingerprinted. Personally, I know I would feel violated and scared to know what they would find out about me as a person. How do I know if they are only testing to detect terrorists? What if I did a thorough research on terrorism and terrorist acts and wrote my thesis on it? Should I be worried that my recognition and positive response to the images and words label me as a terrorist or a potential threat to the society?
If the government allows for the random screening of travelers to take place, then they may begin to screen random people in public places such as tourist attractions, movie theaters, shopping malls, etc. Private businesses and big corporations may find brain fingerprinting a useful tool in detecting what a person knows at a job interview. This is poses a threat to interviewees who may not want to reveal their religion, sexual orientation, past criminal records, or anything that they wish to keep confidential.
Another problem with brain fingerprinting that should be taken into consideration is brain fingerprinting an alleged witness. An innocent bystander may have witnessed a crime and therefore has the same memories as the criminal. How does brain fingerprinting distinguish between a criminal's and a witness's memories? Dr. Farwell argues that his technology can only tell you what the brain has recorded as a sequence of events and if the witness did not commit the crime, the brain will not have a memory of it. Sexual harassment cases or rape cases would definitely be questionable as to the degree of validity. Both of these cases deal with issues of intent and brain fingerprinting cannot be of any help, but it can be used to find out if both of the parties involved have the same alibi.
After thoroughly thinking about the positive and negative aspects of brain fingerprinting, I feel as though more research needs to be done before it can be used. Dr. Farwell only mentions a test done on FBI agents. His device was able to detect 17 FBI agents out of 21 people tested (4). Even though Dr. Farwell claims to have 100% accuracy, Peter Rosenfeld, a professor of psychology at Northwestern University, does not see how he is getting 100% accuracy. Rosenfeld himself is getting about 80% correct from conducting a similar brainwave study (4). He believes the subjects used for Dr. Farwell's study may have become use to the test and the type of images and words appearing on the screen. Thus there is ambiguity in how the device was tested and who should be used as controls for the experiment.
However, the most disturbing issue that I find with brain fingerprinting is human rights. I agree with most of Dr. Farwell's points and his technology, but I am concerned about the future of human rights and the right to privacy. If this device becomes a standard tool in court cases, airports, and government buildings, then there is no telling what the limitations of its application will be in the future.
Other studies are being conducted on the brain and its relationship with the "act of lying." Dr. Daniel Langleben and Dr. Ruben Gur from University of Pennsylvania are studying the brain's behavior during deception. Their study is called "Functional Magnetic Resonance Imaging (fMRI) of the Brain During Deception" and fMRI is used as a kind of lie detector (4). Subjects are put inside an MRI machine, which measures blood flow to various regions of the brain (4). This piece of equipment has allowed researchers to identified the anterior cingulated cortex, which is located a few inches behind the forehead, and the left premotor cortex, which is located near the ear, as regions that become activated when the subjects are lying (4). These areas of the brain become activated when the "act of lying" is happening. This machine as well brings forth similar problems that brain fingerprinting faces. People can convince themselves into thinking that they are telling the truth, which defeats the purpose of fMRI. Gur and Langleben both suggest further testing of fMRI in order to have a better understanding of this machine.
Both the Brain fingerprinting technology and fMRI are very recent developments in the scientific world and add to the understanding of the human brain and behavior. According to Dr. Farwell and other scientists, the P300 brain wave is responsible for recognizing imagery and words, which means that the person has a memory of it. When a subject has seen an image or words that he/she remembers and there is a positive response of the P300 brain wave. This tells analysts that the subject's brain, which does not lie, has seen it before. The same line of thinking goes for Gur and Langleben's research on the fMRI machine. This device is slightly different in that it identifies if the "act of lying" occurs when the subject is asked a question. This instrument will detect activation in a certain area of the brain to recognize lying. Since both of these technologies have similar purposes, they bring similar benefits as well as similar concerns to the society.
Thus, scientists see brain fingerprinting and fMRI as technologies benefiting the society in a great way such as exonerating the wrongly accused, convicting the guilty, and protecting the nation against terrorism. Then again, both of these technologies can be easily abused. If Dr. Farwell's claim of 100% accuracy does prove to be true by other scientists and if Gur and Langleben's fMRI machine is perfected, then these machines could be used to determine religion, sexual orientation, or anything a citizen wishes to keep private, which is a violation of human right to privacy.
As with every other new discovery in the scientific world, there will always be debate as to the validity of the research and of the machine it self as well as creating ethical and moral issues. No matter how many experiments are done, there will always be risks. The question is where do we draw the line? With science, there is no end as to how far we will go to play "God." Therefore, the most important thing to remember as scientist is that "With great powers comes a great responsibility," as best put by Spiderman's uncle.
1)Brain Fingerprinting, A Brief Study of the Technology
2)Health Watch- A View of the Criminal Mind
3) Brainwave Sensor Touted as Tool in Counter-Terrorism
5) Brain Fingerprinting: A New Paradigm in Counter terrorism
| Schizophrenia, A Matter of Perception Part 2: Real Name: Sook Chan Date: 2002-05-15 03:31:47 Link to this Comment: 2094 |
What is reality? To many, reality is the ability to validate a sensory experience with another sensory experience, for example, when one is able to touch what he sees, then that something is real. Yet, our perception, the collection of all our sensory inputs formatted into the framework of the mind, is unreal. A blue box is not really blue, but consists of waves transmitted to our visual receptors. What sounds like music is really a collection of vibrations, and smells are really different molecules interacting with our nasal receptors. Our perception does not correctly reflect the true identity of an object. The electromagnetic waves absorbed and transmitted off an aggregate of mass, manifests itself as a blue cube, and all our visual limitations allows us to see is a blue cube. If reality were defined as the existence of an object as we perceive it, then reality is unreal. There are many errors to the human experiences and the human mind because mankind needs the affirmation that information and facts are either right or wrong. Once upon a time, the world was the center of the universe, with mankind standing at its' pedestal. Even when evidence was present, it took many years before people then learned to accept a new form of thinking. So what we view as real and right today, may just be a summary waiting to be replaced. Yet, are we ready to accept a new reality?
Perception in itself varies greatly from one individual to another. No two people are the same, and no two people have the same fine tunings that discriminate the sensory environment. What our environment presents to our sensory receptors differs from what our brain presents to our perception. When presented with a painting of a blue cube, one person might notice the different textures of the paint and the background, while another might focus on the dimensions of the cube. As these images are transmitted to the brain, the schemata that is accessed by this input also varies from one individual to another. Jo may see the color blue and remember the time her father bought her a blue bike, bringing her back to happy childhood memories. The color blue may send a shiver down Bob's spine as he remembers the blue vodka bottle his alcoholic and abusive father used to drink. Where does one draw the line between reality and perception? And how does one determine which reality is more real?
We perceive the world around us through our sensory systems. However, there is no real format by which to generalize different individual's perceptions. When a stimulus from the external world is sent to the brain, it formats and contextualizes the information into something familiar and sensical based on the individual's schemata. So what happens when one's train of thought is fragmented and one's brain is unable to organize these fragments into a comprehensible pattern? Imagine if at times, your experiences become a slide show, fragments of experiences that do not come together. This is, in fact, how many people suffering from schizophrenia describe their experience (1). Schizophrenia is one of the most severe psychopathologies present today. Its causes are still vague, and the symptoms vary across a large spectrum. However, two generalized grouped of symptoms have been identified for schizophrenics: positive symptoms, and negative symptoms. Negative symptoms include lack of activity, anhedonia, and loss of interest. Positive symptoms include disorganized speech, hallucinations, and delusional experiences (1).
Individuals with schizophrenia experience many problems with combining and associating their different sensory inputs. They have a false sense of reality and are unable to interpret the context and of situations and the difference between reality and imaginary. Schizophrenics are also unable to provide context to fresh sensory experiences due to their inability to access old memories and schemata (2). Many schizophrenics remark that their surroundings seem unreal and their external sensory environment are altered from what they previously experienced. It has been reported that schizophrenics often receive their environmental surroundings in fragments of sensory input. Their perceptions lack chronology and order, and maybe, their perception does not fully represent reality. This results in visual and auditory hallucinations and impairments with information processing
"Everything is in bits. You put the picture up bit by bit into your head. It's like a photograph that is torn to bits in your head" (2).
Two types of hallucinations are commonly experienced by Schizophrenics: auditory and visual. Auditory hallucinations come in a form of voices speaking to the individual, commenting on his actions, music, and voices of others conspiring. Schizophrenics are often portrayed as a crazy man talking to himself. However, auditory hallucinations are valid and it is understandable as to why they occur so commonly amongst schizophrenics. As mentioned before, the sensory input of schizophrenic individuals, including sight and sound, are sent as fragments, with no chronology or order, to the brain. Normally, what we see and what we hear come together to the brain. However, there is a possibility that if what is heard and what is seen are sent as separate fragments, the brain conjures and fills in pieces of information that are missing. Auditory hallucinations may result from the brain's expectation of sounds associated with fragments of images received by the brain. This is a result of conditioning; the expectation that a certain image would be associated with a certain sounds (3). Auditory hallucinations activate an area of the brain known as the Heschl's gyrus, the same region involved in the perception of hearing (4). However, in a study done, the Heschl's gyrus was also activated when schizophrenic participants were asked to imagine a sound or voice (4). This indicates the possibility that auditory hallucinations result from an external stimulus, and so, schizophrenic auditory hallucinations do not generate internal stimuli differently from non schizophrenic individuals. They merely interpret external stimuli differently. An error in circuitry from within the brain regions may impair the processing of sensory input from the external environment. Also, there is a possibility that the "voices" they hear of people talking to them are their own conscious, automatic thoughts and inner speech perceived as external. This is probable occurence as there are many reports of auditory hallucinations by people who are placed in solitary confinement or isolation (5).
Visual hallucinations in schizophrenia involve animals, figures, or a delusional religious character. In the latter stages of the disorder, visual hallucinations may be accompanied with auditory hallucinations (6). Hallucinations and delusions are secondary conditions to the distortion of reality (6). One might say that hallucinations and delusions exists from the inability to correctly rationalize confusing situations from random fragments of information.
Schizophrenics also experience cognitive failures in information processing. Common knowledge and social interactions no longer have precise meanings to them. They fail in areas of social intuition and automaticity of social interactions (6). This is also characterized by deficits in memory tasks that engage prefrontal and medial temporal systems, both of which are abnormal in these patients (7). In a study, monkeys were administered with the drug phenycylidine to recreate the dopaminagenic activities of a schizophrenic's brain. The monkeys were presented with a transparent cube with a banana inside and a small hole at one of the faces. It was found that when the opening was turned away from the monkey, it kept grabbing for the banana in the cube, even though their hands kept banging into the cube wall. Researchers associated this cognitive impairment to the abnormal dopamine levels in the brains of these monkeys (9).
"I miss the natural way of taking things for granted" (8).
Patients with schizophrenia process irrelevant information that intrudes into their consciousness and causes distractibility. During a psychotic episode, the cognitive defect plays a major part. They are unable to organize inputs into a larger picture to provide context. Hence, schizophrenics fail to control the contents of their consciousness (2). The main question is what is the cause of this distractibility and flawed perception?
The prefrontal cortex and the hippocampus are the brain structures that are believed to be impaired in schizophrenic individuals (5). The prefrontal cortex elicits responses guided by internalized knowledge that include one's schemata and memory. The hippocampus stores memory and allows for its retrieval. It is the structural framework that provides the brain with a sense of context by binding together sites in the neocortex that represents the correct contextual framework (5). A strong correlation has been found between the prefrontal cortex physiological activation and the reduced hippocampus volume in schizophrenic subjects.
Much of the neurobiology of schizophrenia remains unknown. However, effective anti-hallucinating, anti-psychotic drugs such as clozapine target the dopamine receptors of the brain, indicating a possibility that dopamine D4 receptors may be a critical site of action (1). It has been summarized that the brain fills in the missing pieces of our sensory environment, making us see things that may not be there. A schizophrenic individual's brain is unable to correctly retrieve stored past experiences to format a current experience into context. Hence, the brain starts afresh, with no prior training of how to fill in the different fragments of sensory input. Schizophrenics experience an impaired sense of reality because as the brain is sticking the fragments of experiences together, it fills in pieces that are not there, making the individual believe in things that are out of context and out of reality.
"My perception of the world seemed to sharpen the sense of strangeness in things. In the silence and immensity, each object was cut off by a knife ... spaced off from other things. If you move it's frightening. The picture you had in your head is still there but it's broken up. If I move there's a new picture that I have to put together again." (2).
Are the perceptions of individuals suffering from schizophrenia unreal? If reality is defined as the "norm" way of viewing things, then yes. However, who is to say which and who's reality is real? One question that arises is that schizophrenia is substantially a genetically predisposed disorder. If this is the case, why is the gene coding for schizophrenia still so prominent? It has been identified that traits that underlie schizophrenia are found in many people who are not ill and who are among the most creative and succesfull members of society (10). These genes have been maintained in the gene pool by natural selection because of their beneficial effects of enhancing creativity (7). To quote David Horrobin, author of The Maddness of Adam and Eve: How Schizophrenia Shaped Humanity, "Without the genes which in combination cause schizophrenia we would be like Neanderthals or Homo Erectus-large brained, clever, but lacking that lust for change and creative spark that have so dramatically distinguished our species from our immediate predecessors." (7). It is because Schizophrenics have the gift to view things in a different light and angle, with no inhibitions and past paradigms standing in their way, that Schizophrenics are able to be creative. This creativity stems not from imagined visions or sounds, but from the reception of the external environment in a different manner. So remember, just because something isn't stored in your memory, does not mean that something is unreal or inexistent. To answer an age old question, when the tree falls in a forest far away, we do not hear the sound it makes, but the sound vibrations still exists.
References:
(1)What happens to the body and brain of individuals with schizophrenia?
(2) Context and Cognition in Schizophrenia
(3)What causes them?
(4) Hearing voices
(5)Impaired recruitment of the hippocampus during conscious recollection in schizophrenia
(6)Cerebral activity associated with auditory verbal hallucinations
(7)The missing link
(8) Cause identified in Schizophrenic Hallucinations
(9)Schizophrenia clues from monkeys
(10)Eccentric Origins of Creativity
| Neurobiological Effects of Medicinal Marijuana Name: Alisa Alex Date: 2002-05-16 02:53:44 Link to this Comment: 2098 |
After conducting extensive research on the different neurobiological effects of medicinal and recreational marijuana, my original question concerning the difference of its effects were still left unanswered. I realized that through discovering the components found in marijuana, logical conclusions could possibly be made answering my original question about the neurological effects of medicinal marijuana verses recreational marijuana. Almost all of the studies conducted about marijuana neglect to address the issue I chose to present in this paper. The sites found give extensive research of the plant, Cannibus Sativa, and active component of the plant, THC. Questions of THC and the effects of this component became the focus of my research which I concluded would lead to the answers I originally sought in my previous paper.
THC, delta-9 tetrahydrocannibinol, is the chemical in the marijuana plant that produces the various effects of the drug. THC is produced in the epidermal glands of the leaves, stems, and the bracts that support the flowers of the marijuana plant. (1) The strength of this element in the plant depends on the different conditions the plant is subjected under. Various climate changes change the degree of effectiveness of THC such as humidity, temperature and sunlight. THC has been proven to affect the transferring of pain in the brain and that it "interacts with the brain's endogenous opioid system, an important system for the medical treatment of pain. (2) THC is absorbed by receptors in the brain that interact with the element, causing the body and mind to react in various ways. There are two types of receptors in the brain that play a role in the effects of marijuana.
CB1, CB2 and anandamide, a substance naturally produced by the body that acts at the cannabinoid receptor and has effects similar to those of THC. The CB1 receptor is found primarily in the brain and mediates the psychological effects of THC. The CB2 receptor is associated with the immune system; its role remains unclear. (2)
THC and other cannabinoids found in marijuana have been found to affect the control of pain, movement and memory. Most of the experiments conducted concerning marijuana have been done on animals and through the research, scientists were able to discover that there is a dependency and withdrawal effect from the use of marijuana but not nearly as sever with other drugs.
The experiments conducted of the drug have been done to differentiate the effects of the two different types of THC and its affects on the brain. Delta-8 and Delta-9 are the two types of THC that produce the neurobiological and psychological effects of marijuana. (3) Delta-9 is much more abundant in marijuana than delta-8 which is why more studies have been conducted regarding the substance. It has also been concluded that since there is more of delta-9 THC, the effects of the drug is largely due to delta-9. When delta-9 THC is inhaled, it reacts with the receptor which then affects the neurons in the brain. The effects in the brain only take place after it binds with the receptors. Binding to a receptor triggers an event or a series of events in the cell that results in a change in the cell's activity, its gene regulation, or the signals that it sends to neighboring cells. (4) Another key tool involves identifying the receptor protein and determining how it works. Which this key information, scientists are able to locate where the components of marijuana effects the receptors in the brain. Signals are sent to the receptors to make them visible once binding has occurred. This is how scientists are able to see where the drug binds to the receptors, which will lead them to where the drug has its greatest effects in the brain. Because THC is mostly a fatty substance, it is easily absorbed by cell membranes therefore entering into the blood faster. (4) Through this process, tracing THC's activity becomes clearly visible.
When marijuana is taken at a specific dosages, in a monitored environment, subjects suffering form various illnesses have be noted to benefit from the drug. Most patients seek marijuana to elevate the pain. THC binding with particular receptors effects nerves that are affected due to certain illnesses. Recent research has made it clear that CB1 receptor agonists act on pathways that partially overlap with those activated by opioids but through pharmacologically distinct mechanisms. (5) Research on cannabinoid biology offers new insights into clinical use, especially given the scarcity of clinical studies that adequately evaluate the medical value of marijuana. For example, despite the scarcity of substantive clinical data, basic science has made it clear that cannabinoids can affect pain transmission and, specifically, that cannabinoids interact with the brain's endogenous opioid system, an important system for the medical treatment of pain. (2)
Institutions nationally have conducted studies on the use of medicinal marijuana on disease stricken patients. The Institute of Medicine published a journal on the use of marijuana and the effects it as a recreational drug and medicinal drug. Because the substance, when used medicinally, is monitored/controlled, the psychological effects on the patient is slightly different, and its effects also vary depending on the type of the disease the patient is suffering from. A complete report done by the National Academy of Sciences details the psychological effects of recreational and medicinal marijuana. In the 20th century, marijuana has been used more for its euphoric effects than as a medicine. Its psychological and behavioral effects have concerned public officials since the drug first appeared in the southwestern and southern states during the first two decades of the century. (6)
When marijuana is taken without regulation of the intake, the effects are quite similar. Those taking the drug, whether recreationally or medicinally experience similar effects. Marijuana has been linked to psychological dependence but not proven to be physically addictive.
"Many users describe two phases of marijuana intoxication: initial stimulation, giddiness and euphoria, followed by sedation and pleasant tranquility. Mood changes are often accompanied by altered perceptions of time and space and of one's bodily dimensions. The thinking process becomes disrupted by fragmented ideas and memories. Many users report increased appetite, heightened sensory awareness and pleasure. Negative effects can include confusion, acute panic reactions, anxiety attacks, fear, and a sense of helplessness and loss of self-control." (7)
Some researchers conclude that constant recreational use of marijuana in high doses can cause lung cancer, respiratory problems and brain impairment. Those advocating the use of medicinal marijuana argue that because it will be controlled by the doctor administering the drug, there isn't a chance of psychological addiction or any other problems believed to be connected with marijuana use.
The main difference between medicinal marijuana and recreational marijuana is the quality of the drug. (8) Purchasing recreational marijuana can subject the user to various side effects due to the purity of the product. Because marijuana is an illegal drug, products sold outside government regulation are subjected to various types of additives to just for profit. These additives can cause serious side-effect in the brain. Because much research on marijuana and the effects of THC on the brain have been conducted, medicinal marijuana is provided in a controlled environment and the product given is of the highest quality. The controlled environment includes careful monitoring of the substance.
Because patients are already suffering from illness such as those listed below, the neurobiological effects, through studies conducted of these patients, have only served to help them.
AIDS. Marijuana can reduce the nausea, vomiting, and loss of appetite caused by the ailment itself and by various AIDS medications. (8)
Glaucoma. Marijuana can reduce intraocular pressure, thereby alleviating the pain and slowing -- and sometimes stopping -- the progress of the condition. (8)
Cancer. Marijuana can stimulate the appetite and alleviate nausea and vomiting, which are common side effects of chemotherapy treatment. (8)
Multiple Sclerosis. Marijuana can limit the muscle pain and spasticity caused by the disease, as well as relieving tremor and unsteadiness of gait. (8)
Epilepsy. Marijuana can prevent epileptic seizures in some patients. (8)
Chronic Pain. Marijuana can alleviate the chronic, often debilitating pain caused by myriad disorders and injuries. (8)
The positive affects of medicinal marijuana documented through the case studies done of patients who used the drug as treatment to help elevate the pain and other side effects due to their illness. THC fast absorption into the blood stream leads to the immediate relief sought by the sick. Research has only concluded that medicinal marijuana because of its pure content and type of subject receiving the drug creates the difference from recreational marijuana use. Only long-term research can show concrete long-term effects of marijuana use. The short-term usage of the drug is helping many cope with their illness, it is because of these effects doctors, patients, and medicinal marijuana supporters rally for legal use of the drug in America. Many who rally for legal use of the drug do so because the statistics fail to prove any long-term psychological effects even when used recreationally.
1)National Academy Press
2)National Academy Press
3)National Academy Press
4)National Academy Press
5)National Academy Press
6)National Academy Press
7)The Effects of Marijuana
8)Medical Marijuana Briefing Paper
| Preemies and Pain: More Than Just a Memory Name: Alyson Dym Date: 2002-05-16 23:49:52 Link to this Comment: 2100 |
"Ouch!!" Ordinarily, that word elicits a predictable response. However, is that response one that is unilaterally perceived? The topic of pain endurance is one that is often discussed. It is understood that the feeling of discomfort is something abhorrent to all people, and is intrinsic at birth. While most people assume that the level of torment is comparable in all people, scientists have recently begun exploring the possibility that pain tolerance may be greatly dissimilar among individuals.
Recently, in class, we have wondered how anyone could be sure that pain is felt to the same degree in all people. It is a fact that all humans feel pain due to the presence of pain receptors. When confronted with a stimulus, the nerves send signals to the brain, which interprets the signals as discomfort. We know that others feel pain because we are able to communicate with one another. If something hurts a person, that individual is able to say, "Ouch, that hurts."
While the majority of humans are able to express their discomfort, there is one group that does not have that luxury. Because babies are unable to speak, and subsequently communicate their feelings, we automatically assume they feel no pain. Because of this situation, there has long been a debate concerning babies and their threshold of pain. People recognize that babies signal their pain in a variety of ways, including crying and contorted facial gestures. Although scientists might deem these reactions as mere reflexes because they have no definitive measure of the infant's pain threshold, most doctors believe that a newborn feels pain. This tenet is due to the existence of a completed nervous system. If people are at the mercy of their systems, and this is why they feel pain, it would make sense that an infant, with a complete nervous system, would feel the same way.
Nevertheless, until ten years ago, it was not acknowledged that premature, or even, unborn children feel pain because people believed that their nervous systems were too immature to function properly (2). Because of this, it was acceptable practice in the past for doctors to operate on premature babies without anesthesia because they thought that, even if the babies felt pain, they would not suffer any long-term damage (1). However, now studies have shown that not only do unborn, premature, and newborn infants feel pain, their sensitivity to pain is likely to be much greater and more prolonged than that of a regular adult (2).
Babies have unique sensory systems, which contain pain-signaling mechanisms that disappear with age. This special wiring causes the newborns to not only feel pain sooner, but also to experience more detrimental physiological effects due to the painful stimuli. We would like to think that every individual feels pain in the same manner. However, the conclusions reached through research indicate that infants can experience pain differently than adults even when the same stimulus is present. Furthermore, the perception of pain can be different between regular newborns and premature infants. In premature children, the mechanism that comes with age, allowing older individuals to dampen down the pain, does not function properly (3). This means that babies who are born prematurely end up feeling pain like newborns when they are adults: the pain is at a greater magnitude than normal.
When a baby is born prematurely, its nervous system may or may not be developed fully. However, the tools needed to feel pain do function because the spino-thalamic system, the network that coveys pain in humans, is connected by the 20th week of gestation (5). However, the mechanism needed to reduce the pain naturally is not. In newborns, nerve pathways that carry pain-inhibiting messages from the brain stem to the spinal cord mature later than other parts of the system. The nerve fibers start to grow from the brain stem down the spinal cord early during the fetus's life, but they do not extend into the branches of the nervous system and do not begin to function until after a normal birth (3).
As a result of this loss of ability to reduce the feeling of pain, the effects of pain last a lifetime for premature children. Not only does this special system function improperly, but also painful stimuli cause a child's developing nervous system to grow more of the nerve cells that carry pain sensations to the brain. Scientists have found more nerve endings that transmit pain signals in animals that had been born prematurely. Later in life, these same animals appear more sensitive and exhibit greater responses to pain that their normal counterparts (4).
One of the reasons why I am so fascinated by these findings is because I was born two months prematurely. Growing up, I questioned whether everyone felt pain in the same way, because I firmly believed that somehow I felt it differently than the rest of my family. Like most premature babies, when I was born I was faced with operations, blood transfusions and countless needle injections to check my blood levels. Every two hours, the search for a viable vein began. Because my mother was too ill to visit me in the hospital, it became something my dad endured. My mom recalls my dad coming back from visiting me in the ICU one evening, more distraught than usual. Although it had become a common occurrence for the doctor to stick a needle into my paper thin skin forty or fifty times, this day was different. Ordinarily, I would cry as the prodding took place. One this particular evening, I showed no emotion as I was stuck 46 times in my head, toes, heels, and fingers. My parents feared I had succumbed to autism, because even though I had reacted to the pain at first, I now seemed indifferent to it. They were concerned that, because the pain had become so unbearable, I had gone into a private place within myself.
When I was young I would not let my mother brush my hair. I ran around looking like a very disheveled young lady, but it was too painful to have someone comb through the rat's nest piled on top of my head. Any type of contact with my skull caused me great anguish. I also had to keep my feet covered at all times due to their sensitivity and feeling of cold. My fingers became something that had a unique connection to my soul. They were a source of solace, artistic expression, and constant sensitivity. It was only after reading an article on premature infants that I realized why those three areas held such significance for me. They were the places were I was bombarded with needles as an infant. Although I do brush my hair now, it is still a somewhat painful experience for me. I use many special solutions and a special brush just to make the experience less painful. Trips to the hairdresser are filled with dread, knowing the affect it will have on my tender scalp. I never understood why brushing one's hair was not as painful to other people as it was to me. What made my reactions so much more extreme than that of my sister or my friends'?
I believe the recent studies support how I behaved as a young girl and furthermore how I still react today. It has been proposed that more pain, and sensory receptors form in areas where distress is experienced soon after birth. It would, therefore, make sense that due to the repeated painful stimuli to my head, heels, and fingers, I have developed more sensory receptors in these areas. If I did develop more nerve endings in addition to the ones receptive to pain, then I would feel all things, including pain, to a greater extent than someone with a normal amount of receptors. Additionally, if the system that is responsible for decreasing the pain signals does not work properly, then I would feel greater pain than the average person.
Like many preemies born around the same time, anesthesia was not used on me. Doctors thought that premature babies would not be able to handle the powerful drug as well as babies born after full term. Besides, many times preemies are born under stress and need operations immediately. It is understandable that doctors would perform operations without proper anesthesia, due to the life threatening situations that often occur. The reasoning was that the infant would have no recollection of the pain endured and, therefore, would suffer no lasting harm. However, researchers now understand that the memory of pain is not the only outcome from these past practices. These tiny bodies sustain physical alterations in response to their pain that last the child's lifetime (1).
It is reasonable to question how severe the pain really is. When I was about three years old, I went to the doctor's office to receive a shot. I kicked, I screamed, but eventually the doctor administered the shot while 4 nurses held me down. Was I scared of the shot because it was so painful or was I just frightened because of my memories of needles as a baby? If it was a phobia as the result of pain in the past, it can be dismissed because the actual experience of the pain is not that great. However, if my nervous system was permanently changed as the result of the stimuli as a baby, then the pain from the needle would be greater and it is understandable why I would be so scared.
My parents believed my pain to be perceived, rather than real. Although I always knew the distress I felt was not something I had fabricated, I can now find studies that substantiate my beliefs. When I said a mere bump hurt really badly, it was not just my perception of pain, but rather a universal one.
One of the most important aspects of scientific findings is the opportunity they give us to compare our experiences with those of others. People need to realize that everyone's sensations are unique: while something may feel merely discomforting to one person, it may be tortuous to another. If it is possible for a human's capacity for pain to be changed as a result of experiences as an infant, imagine what other mechanisms used to define one's reality can be changed as well.
Some people argue that it is possible to separate the mind's action from that of the body. I believe that the scientific findings I have detailed, lead to an even stronger argument toward the brain equaling that of behavior. People only feel and respond to pain due to the presence of nerve receptors and special mechanisms. If these mechanisms were not present, the person would not "feel" any pain even though the stimulus would be the same. A greater feeling of pain is directly correlated to the presence of more pain receptors and an improperly functioning pain reducer. Therefore, mind and body are intertwined. Our mental reality is at the mercy of our physiological reality, which is totally dependent on the functioning of our body's nervous system.
1)Detroit News Website, has a good article about premature infants and pain
2)The Unborn Child Does Feel Pain, great website of facts given by anti-abortion groups
3)New-Born Babies Feel Pain Quicker and Longer, another good article
4)ABC News Website, "Early Pain May Rewire Brain" good article about premature babies' sensitivity to pain and other related articles
5)Anti-Abortion Website, Abortion and the Unborn Baby: The Painful Truth, overview of how unborn and premature children feel pain
6)University of Minnesota Website, Good diagrams of developing fetus
7)AbortionFacts.com, A great website with many articles and findings on the unborn fetus, premature children, and regular newborns and pain
8)PsycPort News Website, Infant pain experience may linger. Another news report on another study on preemies that undergo painful procedures.
9)Medical Research Council, gives reliable facts on how infants can feel pain
10)NEW ENGLAND JOURNAL OF MEDICINE, Vol. 317 No 21 (19 Nov. 1987): Pages 1321-1329, Pain And Its Effects in the Human Neonate and Fetus
| Preemies and Pain: More Than Just a Memory Name: Alyson Dym Date: 2002-05-16 23:49:55 Link to this Comment: 2101 |
"Ouch!!" Ordinarily, that word elicits a predictable response. However, is that response one that is unilaterally perceived? The topic of pain endurance is one that is often discussed. It is understood that the feeling of discomfort is something abhorrent to all people, and is intrinsic at birth. While most people assume that the level of torment is comparable in all people, scientists have recently begun exploring the possibility that pain tolerance may be greatly dissimilar among individuals.
Recently, in class, we have wondered how anyone could be sure that pain is felt to the same degree in all people. It is a fact that all humans feel pain due to the presence of pain receptors. When confronted with a stimulus, the nerves send signals to the brain, which interprets the signals as discomfort. We know that others feel pain because we are able to communicate with one another. If something hurts a person, that individual is able to say, "Ouch, that hurts."
While the majority of humans are able to express their discomfort, there is one group that does not have that luxury. Because babies are unable to speak, and subsequently communicate their feelings, we automatically assume they feel no pain. Because of this situation, there has long been a debate concerning babies and their threshold of pain. People recognize that babies signal their pain in a variety of ways, including crying and contorted facial gestures. Although scientists might deem these reactions as mere reflexes because they have no definitive measure of the infant's pain threshold, most doctors believe that a newborn feels pain. This tenet is due to the existence of a completed nervous system. If people are at the mercy of their systems, and this is why they feel pain, it would make sense that an infant, with a complete nervous system, would feel the same way.
Nevertheless, until ten years ago, it was not acknowledged that premature, or even, unborn children feel pain because people believed that their nervous systems were too immature to function properly (2). Because of this, it was acceptable practice in the past for doctors to operate on premature babies without anesthesia because they thought that, even if the babies felt pain, they would not suffer any long-term damage (1). However, now studies have shown that not only do unborn, premature, and newborn infants feel pain, their sensitivity to pain is likely to be much greater and more prolonged than that of a regular adult (2).
Babies have unique sensory systems, which contain pain-signaling mechanisms that disappear with age. This special wiring causes the newborns to not only feel pain sooner, but also to experience more detrimental physiological effects due to the painful stimuli. We would like to think that every individual feels pain in the same manner. However, the conclusions reached through research indicate that infants can experience pain differently than adults even when the same stimulus is present. Furthermore, the perception of pain can be different between regular newborns and premature infants. In premature children, the mechanism that comes with age, allowing older individuals to dampen down the pain, does not function properly (3). This means that babies who are born prematurely end up feeling pain like newborns when they are adults: the pain is at a greater magnitude than normal.
When a baby is born prematurely, its nervous system may or may not be developed fully. However, the tools needed to feel pain do function because the spino-thalamic system, the network that coveys pain in humans, is connected by the 20th week of gestation (5). However, the mechanism needed to reduce the pain naturally is not. In newborns, nerve pathways that carry pain-inhibiting messages from the brain stem to the spinal cord mature later than other parts of the system. The nerve fibers start to grow from the brain stem down the spinal cord early during the fetus's life, but they do not extend into the branches of the nervous system and do not begin to function until after a normal birth (3).
As a result of this loss of ability to reduce the feeling of pain, the effects of pain last a lifetime for premature children. Not only does this special system function improperly, but also painful stimuli cause a child's developing nervous system to grow more of the nerve cells that carry pain sensations to the brain. Scientists have found more nerve endings that transmit pain signals in animals that had been born prematurely. Later in life, these same animals appear more sensitive and exhibit greater responses to pain that their normal counterparts (4).
One of the reasons why I am so fascinated by these findings is because I was born two months prematurely. Growing up, I questioned whether everyone felt pain in the same way, because I firmly believed that somehow I felt it differently than the rest of my family. Like most premature babies, when I was born I was faced with operations, blood transfusions and countless needle injections to check my blood levels. Every two hours, the search for a viable vein began. Because my mother was too ill to visit me in the hospital, it became something my dad endured. My mom recalls my dad coming back from visiting me in the ICU one evening, more distraught than usual. Although it had become a common occurrence for the doctor to stick a needle into my paper thin skin forty or fifty times, this day was different. Ordinarily, I would cry as the prodding took place. One this particular evening, I showed no emotion as I was stuck 46 times in my head, toes, heels, and fingers. My parents feared I had succumbed to autism, because even though I had reacted to the pain at first, I now seemed indifferent to it. They were concerned that, because the pain had become so unbearable, I had gone into a private place within myself.
When I was young I would not let my mother brush my hair. I ran around looking like a very disheveled young lady, but it was too painful to have someone comb through the rat's nest piled on top of my head. Any type of contact with my skull caused me great anguish. I also had to keep my feet covered at all times due to their sensitivity and feeling of cold. My fingers became something that had a unique connection to my soul. They were a source of solace, artistic expression, and constant sensitivity. It was only after reading an article on premature infants that I realized why those three areas held such significance for me. They were the places were I was bombarded with needles as an infant. Although I do brush my hair now, it is still a somewhat painful experience for me. I use many special solutions and a special brush just to make the experience less painful. Trips to the hairdresser are filled with dread, knowing the affect it will have on my tender scalp. I never understood why brushing one's hair was not as painful to other people as it was to me. What made my reactions so much more extreme than that of my sister or my friends'?
I believe the recent studies support how I behaved as a young girl and furthermore how I still react today. It has been proposed that more pain, and sensory receptors form in areas where distress is experienced soon after birth. It would, therefore, make sense that due to the repeated painful stimuli to my head, heels, and fingers, I have developed more sensory receptors in these areas. If I did develop more nerve endings in addition to the ones receptive to pain, then I would feel all things, including pain, to a greater extent than someone with a normal amount of receptors. Additionally, if the system that is responsible for decreasing the pain signals does not work properly, then I would feel greater pain than the average person.
Like many preemies born around the same time, anesthesia was not used on me. Doctors thought that premature babies would not be able to handle the powerful drug as well as babies born after full term. Besides, many times preemies are born under stress and need operations immediately. It is understandable that doctors would perform operations without proper anesthesia, due to the life threatening situations that often occur. The reasoning was that the infant would have no recollection of the pain endured and, therefore, would suffer no lasting harm. However, researchers now understand that the memory of pain is not the only outcome from these past practices. These tiny bodies sustain physical alterations in response to their pain that last the child's lifetime (1).
It is reasonable to question how severe the pain really is. When I was about three years old, I went to the doctor's office to receive a shot. I kicked, I screamed, but eventually the doctor administered the shot while 4 nurses held me down. Was I scared of the shot because it was so painful or was I just frightened because of my memories of needles as a baby? If it was a phobia as the result of pain in the past, it can be dismissed because the actual experience of the pain is not that great. However, if my nervous system was permanently changed as the result of the stimuli as a baby, then the pain from the needle would be greater and it is understandable why I would be so scared.
My parents believed my pain to be perceived, rather than real. Although I always knew the distress I felt was not something I had fabricated, I can now find studies that substantiate my beliefs. When I said a mere bump hurt really badly, it was not just my perception of pain, but rather a universal one.
One of the most important aspects of scientific findings is the opportunity they give us to compare our experiences with those of others. People need to realize that everyone's sensations are unique: while something may feel merely discomforting to one person, it may be tortuous to another. If it is possible for a human's capacity for pain to be changed as a result of experiences as an infant, imagine what other mechanisms used to define one's reality can be changed as well.
Some people argue that it is possible to separate the mind's action from that of the body. I believe that the scientific findings I have detailed, lead to an even stronger argument toward the brain equaling that of behavior. People only feel and respond to pain due to the presence of nerve receptors and special mechanisms. If these mechanisms were not present, the person would not "feel" any pain even though the stimulus would be the same. A greater feeling of pain is directly correlated to the presence of more pain receptors and an improperly functioning pain reducer. Therefore, mind and body are intertwined. Our mental reality is at the mercy of our physiological reality, which is totally dependent on the functioning of our body's nervous system.
1)Detroit News Website, has a good article about premature infants and pain
2)The Unborn Child Does Feel Pain, great website of facts given by anti-abortion groups
3)New-Born Babies Feel Pain Quicker and Longer, another good article
4)ABC News Website, "Early Pain May Rewire Brain" good article about premature babies' sensitivity to pain and other related articles
5)Anti-Abortion Website, Abortion and the Unborn Baby: The Painful Truth, overview of how unborn and premature children feel pain
6)University of Minnesota Website, Good diagrams of developing fetus
7)AbortionFacts.com, A great website with many articles and findings on the unborn fetus, premature children, and regular newborns and pain
8)PsycPort News Website, Infant pain experience may linger. Another news report on another study on preemies that undergo painful procedures.
9)Medical Research Council, gives reliable facts on how infants can feel pain
10)NEW ENGLAND JOURNAL OF MEDICINE, Vol. 317 No 21 (19 Nov. 1987): Pages 1321-1329, Pain And Its Effects in the Human Neonate and Fetus
| Phobias and the Brain Name: Miranda Wh Date: 2002-05-17 02:10:15 Link to this Comment: 2104 |
You are in an airport waiting for your plane to arrive. You've never flown before, and are more terrified than you can ever remember being. Everyone has told you the supposedly comforting statistics - "millions of planes take off each day and there's only a handful of crashes," "flying is safer than driving." You know rationally that there is no reason to be so scared, but regardless your heart is racing, your palms are sweating, and you're light-headed. Simply the thought of being up in the air, out of control, makes you feel faint. Finally the flight attendant announces that your plane has arrived. But as all the other passengers line up to get onboard, you grab your luggage and walk straight out of the airport, with every step feeling more and more relieved. What is this feeling of anxiousness? Why can't you get rid of it even though you consciously know that it is irrational? What is it caused by? How can it be prevented or lessened?
What you experienced in the airport is a phobia. A phobia is the sensation of extreme fear "when it is not justified by the presence of any real danger or threat, or by any rational cause, and when it is accompanied by a systematic avoidance of the situations that lead to it." (1) A phobia is brought on by a specific stimulus or situation, for example, insects, heights, crowds, or the dentist. Presentation with the fear-inducing stimulus causes a severe anxiety response with very apparent and specific physical manifestations, such as a rapid heartbeat, shortness of breath, trembling, and sweating. Most individuals suffering from phobias are able to recognize that their fear is fundamentally irrational, yet nonetheless go through great lengths to avoid any contact with the given stimulus. (2) Somewhere between 5.1% and 12.5% of Americans have experienced some sort of phobia. (3) Women are two to three times as likely to have phobias than men. There are three basic kinds of phobias: agoraphobia (fear of situations in which escape may be difficult), social phobia, and specific phobias. The DSM-IV has separated phobic stimuli into four basic categories: animal, situational, blood injury, and nature-environment. (3)
Though the experience of phobias is relatively common and their physical characteristics are generally well understood, there is no real consensus on the neurobiological basis of phobias. Instead, there are currently several different models and theories that work to try to understand how and why phobias occur in the human brain. Most hypotheses regarding phobias take a different approach, from biological to psychoanalytic to evolutionary. Is there one model that seems "less wrong" or more satisfying in our efforts to understand the biology of phobias? Using the various models, how do phobias seem to come about? How does thinking about phobias add to our understanding of the brain and behavior?
The classical conditioning model was one of the first theories used to describe phobias. Many years ago, scientists observed that one could willingly elicit a fear response in an animal or human through systematic teaching. For example, if every time a rat is presented with a low buzzing noise, it is electrically shocked, eventually, when it hears the noise alone (with no shock), it will exhibit symptoms of fear. (3) Scientists used to think that people were similarly conditioned to fear the phobic stimulus. In other words, individuals at some point in their lives experienced a negative event with their phobia and so learned to fear it. Though ostensibly a good explanation for the exaggerated fear response exhibited in phobic individuals, with closer scrutiny, this theory proves to be problematic.
Most people do not recall having an initial negative interaction or trauma associated with their phobia. Similarly, there are many cases in which patients have, without a doubt, never come in contact with their phobic stimulus. For example, many people who have flying phobias have never actually been on a plane. In fact, almost half of all phobic people have never had a painful experience with the object of their fear. (4)) In addition, a very small number of stimuli comprise the majority of phobias. In the same way, not all individuals who are presented with a fear-inducing stimulus develop phobias. (3))
Others believe that phobias exist because of evolutionary development to avoid danger in order to improve survival. There are several stimuli that are shared by the most phobic people (heights, insects, crowds, etc.) These phobias, with a couple of exceptions, relate more closely to pre-technological societies. Thus, some scientists, such as Martin Seligman, believe that people are inherently "prepared" to fear certain objects. ((5))) In other words, our phobias relate closely to the perils of our ancestors, as through natural selection, those who feared the dangerous stimulus survived while those who didn't, died off. Prepared fears appear to be very easily conditioned. Some scientists, such as LeDoux, believe that preparedness and the ease of conditioning are the result of certain preexisting neurological connections that exist evolutionarily. These connections are turned on with relative ease.
The most convincing evidence in support of the evolutionary model of phobias is provided by fear conditioning experiments using rhesus monkeys. Wild rhesus monkeys fear snakes while domestic rhesus, unless conditioned, do not. In the experiment, domestic rhesus monkeys are shown a video in which peers respond fearfully to both snakes (fear-relevant stimuli) and flowers (neutral stimuli). When exposed to the two stimuli, the monkeys all exhibited a fear response to snakes but not to flowers. (6) Thus it seems that there is a pre-existing pathway that causes the fear of snakes to be easily turned on by simple conditioning. Interestingly, if this hypothesis holds true, we must have an altered concept of phobias and phobic individuals. Phobias are clinically defined as irrational fears. Yet, evolutionarily, they appear to be extremely realistic, having their roots in very real dangers. Nonetheless, all evidence regarding the evolutionary preparedness hypothesis remains largely speculative.
Many people have turned to the brain in order to understand the biological circuitry behind phobias. The amygdala, an almond shaped nuclear complex that is located in the dorsomedial portion of the temporal lobe, has been proved to be intricately tied in with the brain's perceptions of fear. A portion of the amygdala known as the lateral nucleus is particularly responsible for fear responses. The amygdala receives afferent projections from such areas as the olfactory system, the hypothalamus, the cerebral cortex, and the brain stem. It projects efferent signals to the dorsal thalamus, the cerebral cortex, and brain stem. (7)) There are many more circuits leading from the amygdala to the prefrontal cortex than the other way around, causing us to have so little control over our fears.
LeDoux proposed a hypothesis regarding fear conditioning and the brain that has been well accepted by the science community. There are two separate neurological pathways that account for the ability of animals to be conditioned to fear objects. The two circuits, both activated by a conditioned stimulus, have different functions and destinations in the brain. One pathway leads from the sensory thalamus to the amygdala and the other pathway goes through the sensory cortex. The former provides rapid, imprecise information in order to ensure a quick response if necessary. It allows for the formation of emotional memories in the amygdala. (3)) The latter pathway (from the sensory cortex) takes more time, but generates a more detailed understanding and representation to the amygdala. This pathway permits the brain to liken one situation to a previous encounter in order to respond most effectively. This circuit is tied with the hippocampus in order to form clear fear-related memories. Thus, in theory, the two pathways should work together to create the most accurate and rapid response to danger. (8))
But what goes wrong in the pathways of phobic individuals? Why do their brains seem to react to harmless situations as if they were lethal? Is this phenomenon explicable using this model? Changes in the processing abilities of the amygdala may have a profound effect on the processing of fear. "Lesions of the amygdalar central nucleus interfere with every measure of controlled fear, including physiological and behavioral responses." (9)) There is evidence that amygdala and hypothalamic damage may be the cause of phobias. For example, phobic children are born with a decrease in the activation of the neurons in their amygdala and hypothalamus. Abnormalities in the hippocampus and the medial prefrontal cortexes may also be the cause of phobias. Damage to the hippocampus has a strong effect on memory, and thus could cause an individual to incorrectly remember a fearful event. The medial prefrontal cortex is associated with the phenomenon of extinction, the weakening of a fear response to a conditioned stimulus over time. Thus, damage to this region could allow for the persistence of a fear response for years after an initial encounter with the stimulus (even when the individual is repeatedly shown that the stimulus is in fact harmless).
Genetics may also play a role in the formation of phobias. There is recent evidence that phobias might be linked to a mutation in chromosome 15. This defect may make people more susceptible to developing phobias. It is thought that phobic individuals are born with the mutation, but it doesn't manifest itself until later in life. (10)) Personality traits may also play a role in the formation of phobias. On the other hand, some believe that phobias are the result of one's culture. Some phobias are much more prevalent in some societies than others. For example, a person is much more likely to suffer from agoraphobia in the United States than in Mongolia. Similarly, only Japanese suffer from a phobia called taijin kyofusho, the fear of offending others through one's social incapability. (4))
There are various ways to go about treating phobias. One of the most effective cures is behavior therapy (otherwise known as exposure therapy.) In behavior therapy, a patient and therapist systematically confront the feared stimulus until the patient becomes desensitized to it. One type of exposure treatment is called flooding. Flooding is a therapeutic technique in which the phobic individual is exposed to their feared object or situation for an extended period of time. Eventually, the fear response will fade as the person sees the irrationality behind their phobia. Another method is called modeling, a technique in which a patient watches another person face their phobia and thus vicariously learns that their phobia is truly harmless. Many therapists also use relaxation and hypnosis to cure their patients of phobias. Relaxation training involves teaching the patient to be aware of the physical symptoms of their phobia (increased heart rate, muscle tension, etc.) and to, if possible, eliminate them. Another form of treatment is cognitive therapy, a technique in which people are taught to "think differently." Patients are made aware their fears are unrealistic, harmful, and meaningless. (11)
More recently biomedical drugs have been commonly used to control the panic and lessen the anxiety of phobias. Some medications are used to lessen the physical responses associated with phobias. Benzodiazepine anti-anxiety agents, such as Xanax and Valium, are used in short-term situations to treat phobias. Doctors also prescribe beta-blockers to diminish the performance-inhibiting fear response. Other common phobia treatment drugs include serotonin specific reuptake inhibitors (Prozac, Paxil, Zoloft) along with other antidepressants. (12)) Interestingly, in a study done on the brains of patients who underwent various forms of phobia treatments, both biomedical drugs and behavioral therapy alter brain functioning in the exact same way, as the two treatments caused a decreased blood flow in the amygdala and the hippocampus. (13))
In the future, scientists should try to gain more concrete, biological knowledge about the origins of phobias in order to produce the most effective treatment possible. Doctors should make use of imaging techniques, such as MRIs, CT scans, and PET, in order to better understand the brains of phobic patients and see if there are actual differences between phobic and non-phobic individuals. In addition, neurobiologists might conduct research to better understand the processes by which phobias come into existence, in particular the interaction of a vulnerable brain and a particular experience that coalesce into a phobia. By doing so, it may be possible to come up with forms of prevention, not just treatments.
Though these different models and treatments of phobias do not allow for a conclusive or single biological understanding, they do bring up some very important questions about the brain. Each model seems to indicate differing brain functions and pathways that cause phobias. Thus the question of what exactly makes a phobia happen remains unanswered. But it is quite possible that phobias exist in different people for different reasons. Therefore, perhaps is it most accurate to understand phobias through seeing a coexistence of all the different models. Phobias are very much related to the issue of brain and behavior. There seems to be a clear parallel between the pathways in the brain and a person's behavior. It is clear that phobias originate in the brain yet they resonate loudly in the body, strongly influencing one's behavior. But at the same time, in some treatments, for example flooding, alterations in patients' behavior cause clear changes in brain functioning. For me, this helps prove that the brain and behavior are one and the same.
1)Phobias: When Fear is a Disease
2)American Psychiatric Association, a comprehensive look at the different kinds of phobias
3) Fyer, Abbey J. Current Approaches to Etiology and Pathophysiology of Specific Phobia. Society of Biological Psychiatry, 1998.
4)The Phobia List Categories
5)Website that Deals With Preparedness
6)Evidence for Preparedness Theory
7)Anatomy of FearThe Biology Related to Fear and the Amygdala
8) Ledoux, Joseph. Fear and the Brain: Where Have We Been, and Where Are We Going? Society of Biological Psychiatry, 1998.
9)Personality Correlates to Memory Change
10)The Link Between Phobias and Genetics
11)A Page of Various Treatments for Phobias
12)General Information of Phobias
| The K+ Channel Revisited Name: Gabrielle Date: 2002-05-17 08:55:42 Link to this Comment: 2105 |
Many scientists enter the field of neuroscience with a desire to understand how the human brain functions to create our actions. Some take a large approach and study reactions to stimulus in live animals. This approach leaves us still wanting to know about things that aren't a result of an outside stimulus. Other scientists take the minimalist approach and start by studying the exact mechanisms of individual cells of the brain. But, what good does that do us for everyday life? There is also the approach of taking our knowledge of behavior from diseases of the brain. Would we have thought about how our brain regulates our moods if it weren't for the fact that some people experience depression, in which the regulation of mood goes amiss? Many of the disease have led us to a deep understanding of the chemical interactions in our brain and body. At a very broad level, and ignoring religious discussions, we can say that every part of our existence is a result of chemical interactions. Besides giving us our substance, chemistry also gives us a mode of communication throughout our bodies. In our brain a large chemical component is that of the action potential that is conducted along a neuron as a result in the changing permeability of the cell.
The axons of our neurons are the pathway for the communication that exists in our nervous system. This communication takes the form of an electric signal, also called an action potential. The action potential occurs due to a change in voltage across the membrane of the axon. The change in voltage is achieved by a change in the permeability of the neurons to the ions, Na+, Ca+, and K+.(1)The cell starts with a large concentration of potassium ions, K+, inside the cell, and a large concentration of sodium ions, Na+, outside the cell.
The action potential propagates down the axon due to openings and closing of different channels allowing changing of the permeability to the differing ions (10). Channels are proteins that span the membrane of the axon. These proteins have a structure so that they can be allow ions to flow through pores that are only open at the appropriate times. Some of the channels are opened and closed by other chemicals, while some are initiated by a change in the membrane potential. The phase, opened or closed, controls the permeability of the cell, and therefore the possibility of an action potential. Each channel has a very distinct role in which ions it allows in and out of a cell. Channels are called by the ion that they primarily let through. One of the most impressive aspects of these channels is the precision under which they operate. If they didn't all of our functions would not occur with the ease that we experience.
A potassium channel works to let in only potassium ions. Yet, sodium ions are smaller, and intuition would say that they would get in without a problem through a pore, which is big enough to allow potassium through. The selection occurs in the central of the pore. The helices that the channel is composed of have enough space between them to hold exactly 2 potassium atoms (11). Only one Na+ ion gets in for every 10,000 K+ ions. At the same time that the channel is very selective it also allows the K+ to flow through at almost the exact same rate as diffusion, 108 ions per second. This precision is beyond our human understanding, yet contained within our own person. See a picture (11). Our cells are smarter than we can ever imagine being?
Based on their amino acid sequence, all K+ channels turn out to have a very similar structure and basis of function. Potassium channels are not unique to any organism or cell. A particular K+ channel, which is greatly studied, is the voltage-gated potassium channel. This means that the channel opens in response to a certain voltage difference that occurs across the membrane. The channel is closed when the cell is at rest. Following inactivation the channel opens via a complicated mechanism, which scientists are still trying to decipher(7)(8). The specific voltage is that which occurs after the Na+ channel has opened and allowed a significant amount of Na+ to be released from the cell. So, the K+ channel is induced to an open state by a depolarization of the membrane potential. The K+ channel opens at the beginning of the repolarization, or after the depolarization has almost reached its peak. The opening of this channel allows K+ ions to flow outside of the membrane of the cell, bringing the voltage of the cell back down to its normal level. The K+ returns to the inside of the cell through a pump that exchanges it for Na+ so that there is little voltage change.
Knowing the structure of the voltage dependant K+ channel was the one of the first steps scientists took towards understanding the channel. Scientists have defined the subunits as being S1-S6. The S1-S4 lie on the outer side of the pore, and influence the pore defining helices, S5 and S6. These two pore-defining units are those that are common to all K+ channels Near the center of the channel is a water-filled cavity where some drugs, such as TEA, bind to block activation(3). This core is very important, because it is where the potassium channels are selectively filtered. Much potential for further work lies within this core. It may be possible that different variations on the K+ channel have slightly different structures within the pore that could lead to important drug interactions. Ideally the brain's K+ channels could be enhanced, for treatment of disease such as Alzheimer's, without affecting other K+ channels.
A portion of S4 is positively charged, and the change in the membrane potential change moves this portion, possibly even to the other side of the membrane. The closed state of the channel is more stable than the open state due to a series of hydrogen bonds in the protein structure (8). This is why such a strong energy change, such as the depolarization of the cell or interaction with another molecule is necessary to change the structure of the channel. The helix probably rotates around its inner axis, and slightly out of the membrane at an angle. This motion is comparable to that of a corkscrew which opens as if it had petals. The S4 is also in very close proximity to the pore-forming segments, S5 and S6. S4 connects directly to the S5. This is still being evaluated, but the current proposal is that the torque in the S4 is translated directly to S5 and indirectly to S6. This seems very probable because the gating of channels that aren't voltage-gated rely on a twisting in S6 to open the channel. The other possibilities are that the S4 rotates the pore-defining helices in a way similar to the way that gears work, or that it moves outward from the protein complex, opening the channel by a pushing action (5). Channels that aren't voltage-gated contain similar apparatus that respond to other changes in their environment, such as the appearance of another protein, or ion.
There are many differences that are recognizable between voltage-gated and non-voltage-gated channels. These differences help understand how the voltage-gated channel works. We have already discussed the fact that there are additional helices on the voltage-gated channels, and that there are minute differences in the structure of the pore-defining helices. Another important structure in a channel is the "residues" that line the helices. Residues are the amino acids that reside on the transmembrane surface (5). In non-voltage gated channels that residues only interact with the lipids of the membrane that surrounds them. In voltage-gated channels these residues also interact with the additional helices (2). This is beneficial because these residues can possibly show where the interactions are between the different helices. Mutants of the residues have been studied to see which ones change the voltage-sensing domain (2). . Some mutations have no or little affect, while some eliminate gating altogether.
I feel that it is important to note how quickly the world of knowledge on our K+ channels is changing. Just 2 years ago scientists were frustrated and confused about these channels a href="#2">(2), and now they are being used as a guide for studying other ion channels, and pore openings a href="#3">(3). There have been multiple experiments done to determine the structure of the channel through x-ray crystallography, flourometry, and mutagenesis a href="#2">(2) a href="#4">(4). The picture has been almost perfected. Mutations have been done to determine structures that have a big influence on the voltage sensing and gating properties of the channel. For example, Li-Smerin et al. did a series of 37 mutations on the pore residues that led to two groups that they call the major impact and the minor impact residues a href="#2">(2). They were defined as being major or minor depending on how great of an affect the mutation had on the functionality of the resulting channel. When the major residues were mapped on the structure the scientists could make references as to what kind of contribution the original residue had. This information can define where the important structures are for making drugs that interact with these pores.
Eventually there will be a lot of helpful medical advances coming out of the knowledge of this channel works. Many diseases, from depression to Alzheimer's could possibly be affected by further knowledge of the ion channels. Recently researchers found that a genetic mutation in mice caused a selectivity decrease in the K+ channel which resulted in Alzheimer's like symptoms a href="#12">(12). This could have very strong potential for further implications. Further knowledge about the deficit in Alzheimer's can aid us in understanding what the normal flexibility of the brain is a href="#14">(14). We know so far that this protein, which is invisible to the naked eye, may hold our potential for learning. Mutations to the protein alter its response to voltage changes, and therefore the potential to propagate an action potential. The possibilities are endless, and the knowledge is fast approaching. But, it is without a question that the K+ channel is inescapable in its importance to our behavior and existence.
1)Serendip Notes, Some notes are available from the class on the Neurobiology of Behavior which discuss Action Potentials.
2)A Localized Interaction Surface for Voltage-Sensing Domains on the Pore Domain of a K+ Channel
4)Reconstructing Voltage Sensor-Pore Interaction from a Fluorescence Scan of a Voltage-Gated K+ Channel
5)Taking Apart the Gating of Voltage-Gated K+ Channels
6)Reconstructing Voltage Sensor-Pore Interaction from a Fluorescence Scan of a Voltage-Gated K+ Channel
7)Tight Steric Closure at the Intracellular Activation Gate of a Voltage-Gated K+ Channel.
10)Lights, Camera, Action Potential, A site made for children that has great descriptions and visuals of an action potential.
11)3-D Image of Potassium Channel
12)Potassium Channels: Molecular Defects, Diseases, and Therapeutic Opportunities
13)The Structure of the Potassium Channel: Molecular Basis of K+ Conduction and Selectivity
| Alzheimer's Disease: Implications for the notion o Name: Kornelia K Date: 2002-05-17 09:21:44 Link to this Comment: 2106 |
If we accept that the brain's ability to "fill in the blanks" about each experience we have, then we can conclude that our past is indeed partially our own brain's creature. However, there are still some norms created by people that define certain experiences as normal and others as not. What happens when a person starts to behave ab-normally? How is his/her brain filling the blanks in a different manner? To discuss this subject we would discuss the most common form of dementia among old people, the Alzheimer's disease.
Dementia is a brain disorder, a loss of intellectual function (thinking, remembering, reasoning), which substantially affects a person's ability to carry out daily activities. Alzheimer's disease (AD), a form of progressive, irreversible dementia with no known cause or cure, first described in 1906 by Dr. Alois Alzheimer, causes damage to the parts of the brain that control thought, memory and language. The consequences of the disease in terms of the patient's lifestyle are often times confused with the natural syndromes of aging. However, AD is not a normal part of aging.
The processes which occur in an AD patient are still extensively researched. Nerve cells in the regions controlling the above mentioned faculties are lost and certain neurotransmitters' performance is damaged. The two most affected types of brain cells by AD are neuritic plaques and neurofibrillary tangles. While some neuritic plaques are commonly found in brains of elderly people, they appear in excessive numbers in the cerebral cortex of Alzheimer patients. Neurofibrillary tangles are twisted remnants of a protein called tau, found inside brain cells and crucial for maintaining proper cell structure and function (5)
As a result normal thinking and memory is harmed due to the disrupted communication between the different neuron cells. Thus, the ability of the person to participate in normal interaction with other people is severely damaged. (3)
The experiencing of the world and the way the patient reacts to it is radically influenced by this unhealthy interaction within the brain. The initial symptoms involve mild forgetfulness of recent events, activities or familiar people/things. In the process of development of the disease, skills acquired throughout the life of the patients such as brushing the teeth, easting with a fork and a knife are forgotten; thoughts are very unclear, and behavior becomes unable to be subordinated to normal human life norms. All the clues the brain has learned so as to be able to fill in the blank in everyday life have been forgotten. (3)
The symptoms of the disease are predominantly behavioral – agitation, anxiety, depression or sleeplessness, in general mood swings a feeling of withdrawnness. (1)
Main characteristics are personality changes, impairment of judgment (4)
Plaques and tangles develop in the brain, leading to the death of brain cells. The rate of progression can vary from 3 to 20 years with the final stage being common to all – a complete incapability of taking care of oneself. There is a list of warning signs developed by researchers that are used as base for judgment of resemblance of a medical condition to AD and the potential further examination this could prompt. Among the major signs, as formulated by researchers, are memory loss affecting job skills, difficulty performing familiar tasks, problems with language, disorientation to time and place, problems with abstract thinking, misplacing things, changes in mood and behavior, and subsequent changes in personality, loss of initiative. All this signals pertain to the essence of a personal identity and thus show the
Age is one of the greatest risk factors for dementia, affecting one in twenty people over the age of 65, and one in five over the age of 80. Another equally debated cause might be with genetic origin, genetic predisposition or abnormal protein build-up in the brain, as well as environmental toxins. (4)
However, the effect of inheritance seems to be very small, so that the possibility of developing Alzheimer if a parent or a relative has the dementia, is slightly higher than if you had no cases of the disease in your immediate family. (1)
After extensive investigation it has been found that people with Down's syndrome who succeed in surviving until their 50s are likely to develop AD. (2)
Other similar coincidences have been examined about people who have experienced severe head injuries, such as boxers, have a greater chance of developing AD.
Similar to Parkinson's disease, there has not been found yet a cure for Alzheimer's. The treatments that could ameliorate the condition have been acting upon delaying the onset of the symptoms. Another direction of treatment has been maintaining the level of acetylcholine, a neurotransmitter essential for processing memory and learning, in the brain which seems to decrease in patients with AD. However, all of these attempts only try to stabilize the symptoms for a limited period of time. (1)
What is one of the most intriguing aspects of studying the Alzheimer's disease is the effect it has upon a person's memory, experience and behavior. We talked a lot about the relationship between brain and behavior, whether they mean the same thing, and if not what is their mutual relationship. Looking at the specific symptoms and results of Alzheimer, we witness a complete eradication of prior learning experience, inability to perform or understand activities which have used to be essential for the person's existence, personally confusion, impaired judgment. And the processes that have harmed the normal functioning of the brain with no doubt, affect this outcome. So if your identity, your personality, your soul even, is argued to be something external to the biological processes happening in the body, how would such a theory or approach account for effects of diseases as this one. An argument is that memory loss is a natural part of aging. However, the symptoms of Alzheimer's disease have consequences different than just simple lapses of memory. Patients have difficulty executing all processes which they have learned throughout their life - communication, learning, thinking, reasoning. It involves destruction of brain cells as supposed to pure aging. This provokes the question of the extent to which yourself, everything you associate as being your personality, your memories, your knowledge, is vulnerable and how everything that defines a "self" could be destroyed.
1) Alzheimer's Society information sheet
2) About Alzheimer's Disease – Symptoms, Risk factors, etc.
3) Alzheimer's Disease Fact Sheet.
4) Alzheimer's Association
5) Neurology Forum
| How is our I-Function related to Impulsive Behavio Name: Lauren Wel Date: 2002-05-17 10:35:46 Link to this Comment: 2107 |
What are impulses? We experience impulses every day. Why are you wearing your orange shirt today? Why did you pick a salad for dinner instead of steak? Why did you drive one route to work as opposed to another? I suppose some people are more spontaneous than others, but can impulses be called sporadic? Uncontrolled? Are they valid choices you have made - or are impulses something we do not realize we are powerless to? Can we choose to say certain things? Do we have any choices? Who, or what rather, is in control?
Some people have impulses that are not conducive to the decorum of society. Some people cannot explain their need, their impulse, to shout obscenities, to make strange faces at strangers, or to excessively mimic others around them. Tourette's Syndrome is one example of a disorder that causes a person to be overwhelmed by impulses to say and do things that they cannot control. Do impulses have varying degrees? And can some people more efficiently control these impulses, or channel the impulsive thoughts into something other than actions? Is our behavior conducive to the ability to monitor numerous impulses of all degrees? And I wonder what role I-function plays in behavior, if behavior is explained in terms of controlled impulses.
I wrote my last paper on obsessive-compulsive disorder (OCD) and the implications that this disorder has on our understanding of the I-function. OCD patients are overwhelmed by the impulse to do certain actions or rituals that calm their fears. These fears might be of germs, heights, strangers, or something less common. OCD sufferers are treated by attempts to help the patients teach themselves to overcome their impulses that relieve their unfounded fears. The question that arises is how the OCD sufferer can be aware of their unrealistic and unprecedented fears, but cannot control their impulsive behavior? We are not conscious of the blind spot when our brain 'fills in' the empty area created by the blind spot, and thus have no control over our blind spot. However, OCD patients are aware of their brain's autonomous control over their behavior that causes obscure actions and thoughts that are typical of OCD patients. The I-function is not involved in the blind spot, but is it or is it not involved in OCD behaviors? How can the OCD patient be aware of what is going on, but not be able to control himself? Surveys show that eighty percent of the American population experiences violent and upsetting thoughts, which are speculated to occur due to automatic associations produced by the brain (10). Can we control any of our thoughts? Are we all as helpless as OCD patients, but we just are upset by this fact to a lesser degree than OCD patients seem to be? Are these thoughts impulses which are an integral part to being human?
One can bring bodily processes under conscious control with biofeedback. Biofeedback may be defined as the technique of using equipment (usually electronic) to reveal to human beings some of their internal physiological events, normal or abnormal, in the form of visual and auditory signals in order to teach them to manipulate these otherwise involuntary or unfelt events by manipulating and displaying signals (11). This is an interesting concept when thinking about OCD patients, and also persons without a specific mental disorder. The ability to incorporate the I-function into facets of the human body's working is unimaginably amazing and unprecedented. The things that you do not normally know are going on in your body can become conscious and controlled through the help of mechanics and computers, what could be the implications of this? Even in the field of athletics, biofeedback plays a very important role, because people have discovered that proper training methods and the appropriate instrumentation can remove mental blocks preventing one from achieving higher performance. Biofeedback trainers have worked with ice figure skaters, marksmen, hockey players, gymnasts, runners at all levels, often at the elite olympic level. Biofeedback is the most direct method to change the biofield (both brain and body-field) and thereby improve physiological and psychic conditions permanently (psycho-neuro-cybernetics) (11). Have we, as intelligent beings, surmounted the boundries of our own consciousness and created an ability to allow our I-functions to reach beyond natural thresholds?
There are many kinds of impulses, on both macro and micro levels. On the most basic scale, impulses can be described in physics textbooks as relating to forces and momentum. Physics defines impulses as either instant and permanent or instant and impulsive. Instant and permanent forces are summed during integration. Instant and impulsive forces get reset to zero after occurring (12). Physics seems to claim "impulsive" as pulsating and non-cumulative; this does not take into account the cause of the force that is pulsating. There are impulse magnets that are made of a coil of wire that is non-magnetic when it is not charged, but when an electrical charge is sent through it, it creates a magnetic field. The electrical charge is "pulsed" or sent through the coil for a very short time via a capacitor bank (3). This is a magnet that impulsively attracts metal objects - it is not consistent. However, in terms of human beings, impulsive behavior is not so much displayed as "pulsating," but more so as intermittent and unmethodical. Impulsive behavior can be observed, but we cannot yet understand the source that is "pulsed or sent through the coil." For example, we do not know the cause of OCD, or why some people react differently than others to the same stimulus.
Cybernetics is a part of science that has attempted to understand and explain, and model with computer networks, the relation between input and output. The feedback system of the human neural system is complicated, and if more well understood can possibly offer a better understanding of human impulses. According to cybernetics, the human brain and nervous system coordinate information to determine which actions will be performed. Control mechanisms for self-correction in machines also serve a similar purpose. This principle, known as feedback, is the fundamental concept of automation. One of the basic beliefs of cybernetics is that information can be statistically measured in accordance with the laws of probability. Purposive behavior in humans or in machines requires control mechanisms that maintain order by counteracting the natural tendency toward disorganization (9). Computer networking has modeled the feedback mechanisms that are the basis of our own behavior, but our individual configurations are not well understood. Is creating hypothetical parallels between neural and computer programs able to aid in our understanding of automation, the involvement of I-function, and impulsive behavior? Computers do not have I-functions, so this may be a hopeless attempt at systematizing the basic human condition.
When you think of impulsive behavior, do you imagine it as being a good thing or a bad thing? I was very surprised that most of the places that "impulsive behavior" is discussed, whether in written work or conversation, is usually with a negative connotation. If impulsive behavior is not in accordance with society's norms, such as with a mental disorder, it is discussed with either pity or condescension. Why is it that impulsive, or unfounded, behavior is so immoral? Is it the fear that people have for the unknown? Or is it the fear that they themselves could possibly one day lose control of their impulses and become like those with so-called disorders? It can not be explained why Tourette's Syndrome patients can not suppress their impulsive tics and shouts. Even religion shows dissention towards impulses - and deems them as evil. As stated in the Old Testament, 6:5, God sees that the problem with man is his 'yetzer' ("impulse" in Hebrew), and 'yetzer mahshevet libo' (literally "the impulse of his heart's thoughts" in Hebrew). Here the Bible addresses itself to the psychological basis of the human condition, restating the classic philosophic problem; how could a good God create evil? The Bible only hints at the problem, namely that the qualities with which God found it necessary to endow humans for them to carry out their tasks included impulses that humans could not control. The political implications of this are extraordinarily important. Man is not naturally good but, as Freud put it, a bundle of impulses in desperate need of expert management. If God cannot control man's prior actions through what He has implanted within human beings, then any effort to establish a political framework for humanity must be based on this reality. Evil impulses must be recognized as inevitable and arrangements must be instituted for their management (7). Therefore, religion requires a person to be the best that they can be in managing evil impulses. But how can all impulses be evil? Impulses are the basis of human behavior and if every behavior was censored out of fear of evil, what would the human race become?
There are many attempts to not only understand what causes a person to behave upon impulses, but there are facets in life that try to control these impulses. Yoga and mediation are some forms of control. Instead of relying on and being moved by the normal human impulses, one seeks contact with the soul deep within and acts from that center with its guidance. In effect one suspends and offers up one's own impulses, feelings, understanding and will power so that a higher impulsion, truer knowledge and more powerful will can act through one. By this means the seeker gradually comes more in contact with a higher power and the higher power enters into and takes hold of his entire inner life and all one's outer circumstances (8). Turning one's energies inward and focusing on perception of one's inner thoughts and feelings seems to be one method that works for some people to control impulsive thoughts and behaviors. I think that prayer and religion work in this same way, in a calming manner to the human race. But I cannot help but wonder, what is the great societal need to manage one's own inclinations and impulses? Are they dangerous? Evil? A form of weakness? Does impulsive behavior show a loss of control of our I-function?
Some impulses, such as artistic impulses, are not weaknesses. Musicians and artists create their works of art based on impulses that they learn to appreciate and become more aware of. Art schools encourage students to become more aware of their own tastes, inclinations, impulses and passions (6). Also, following one's inclinations, or "gut feeling" about a person or a situation can be advantageous to successfully surviving that situation. This borders more on natural instinct, but I think that impulsive behavior must have an instinctual basis because neither instinctual behavior nor impulsive behavior seem to involve the I-function. These behaviors occur without thought, almost automatically. Do we need our I-function for survival then? If instinctual and impulsive behaviors occur everyday without our own forethought, with out our conscious I-function aiding in our decisions, then what is the purpose of our I-function? If impulses and instinctual behaviors occur almost intrinsically, to what degree can we change or alter our responses - or can we at all if the I-function isn't naturally involved?
One example of a weak impulse is that of addiction. These addictive cravings are, in reality, spontaneous nerve impulses. Even in the longer term, overwhelming cravings are outside the addict's control. The overwhelming craving for drugs or alcohol that endlessly defeats addicts is in reality a neurological impulse - and they have absolutely no control over the craving when it is triggered. All they know is that they want, need, and feel that they MUST have the drug. This "desire," this craving, is not a free choice (4). The rat's nerve impulse to use cocaine has nothing to do with free will. He will chose to have cocaine until death. This shows that impulsive behavior is independent of free will, and thus also free of I-function involvement.
Another impulse that displays weakness includes the followers of fad diets. The typical first impulse of those attempting to solve a weight problem is to start a diet, and the newer the diet the better. This almost never works permanently. While weight is usually lost by dieting, it rarely stays off, because its causes have not been eliminated In order to improve our mood we crave carbohydrates, which increases the serotonin level in the brain. However, when this is coupled with poor impulse control the problems are compounded (5). Can impulse dieter's help their weakness for over eating and trying fad diets?
Our society thrives on toying with people's impulses. The next time you are in a supermarket, take notice of the lighting, music and store displays. The goal of the supermarket is to keep you there as long as possible. Market research estimates that approximately $1.89 is spent for every minute a consumer is in the store. Techniques such as the physical location of store items, displays, and slowing down the shopper with lighting and familiar music will entice the shopper to spend more. The most common staples in the American diet are bread and milk. Ever notice that the milk and bread are at opposite sides of the grocery store? By stocking those items farther apart the shopper is exposed to more impulse shopping and spends more (1). There is great power in initiating a wanted impulse buying response with specific selected triggers chosen by advertising companies. Advertising companies have mastered the techniques that make the buyer most susceptible to buying. The advertising companies create situations where I-functions would not have time to affect the decision to buy. Items that are on sale are most likely at the end of the aisle so the shopper will be more likely to put them into the shopping cart. Lack of I-function seems to be a pre-requisite for impulse behavior.
What is notably interesting is our society's legal definition of impulses. In 1929, the Supreme Court case Smith v. United States introduced the "Irresistible Impulse Test," which emphasized an "uncontrollable impulse" to commit the crime, creating a new type of mental state that could be identified as insane. Can the presence of certain abnormal mental conditions remove blame from the offender? And how can the courts or any qualified doctor accurately determine if someone is legally "insane"? This also presents an interesting moral consideration of accountability-who is held accountable for what crimes, and who defines accountability? The irresistible impulse had to be strong enough that the offender could not stop himself even though he knew the act was wrong. How could the offender do such a thing when they indeed have an I-function? Is there some sort of abnormality in their I-function? Could they possible be aware of the malice they were demonstrating, and not be able to willfully stop? Because of these skeptical questions, many states are hostile to the insanity defense. In fact, in three states (Montana, Idaho and Utah) the insanity defense has been abolished. However, recently the insanity defense, though not widely used, has gained much notoriety in recent cases like Hinkley, the Unabomber, and even Lorena Bobbitt. The 1984 Insanity Defense Reform Act defines the legally insane individual as one that, "as a result of a severe mental disease or defect, is unable to appreciate the nature and quality or wrongfulness of his acts."(2). This alteration of the insanity defense occurred because of the skepticism surrounding this 1984 trial involving the guilt of Hinkley. Hinkley pleaded guilty by reason of insanity to his attempted assassination of Reagan in 1982. The skepticism following his pardon ensued the alteration of the insanity plead. The new 1984 Insanity Defense Reform Act makes it impossible for the I-function to have been involved in the offender's malicious action. Now, a person has to prove that they had no conscious knowledge of the consequences of their deed - that it not only was an uncontrollable impulse, but that the deed was also done incoherently.
Human impulsive behavior is something that seems to be instinctual, and without the involvement of the I-function. Impulses are a part of everyone's behavior, some of which you are conscious of, and some that you aren't. The question is, how can you be aware of your impulses when they occur without any conscious consideration on your part? And if science can alter our ability to control and understand our human impulses, how is this evolving our own I-function?
1)The marketing of food and diets in America.
3)National High Magnets Field Labratory.
4)Addiction: It's a Neurological Disorder.
5)Dieting Impulses Lead to Weight Loss Blind Alleys.
7)Noah, The Basic Flaw in Human Impulses.
| Pedophilia and Sexual Deviance: A Social or Biolog Name: Porsha Gau Date: 2002-05-17 11:21:22 Link to this Comment: 2108 |
Pedophilia is one of a group of psychological disorders called paraphilias, which are disorders of sexual attraction and include such deviant behaviors as exhibitionism, voyeurism, sexual masochism and sexual sadism. They are considered illnesses if they cause problems for the person having the urges or for others. Pedophilia is considered one of the most dangerous of these disorders because sex with a child is always criminal and exploitive. Although the term is popularly used to describe adults who are sexually drawn to children, it technically refers to urges toward pre-pubescent boys and girls (5).
The onset of paraphilic sexual interest usually occurs before the age of 18. The average age for the onset of nonincestuous homosexual pedophilia is 18.2 and 21.1 for nonincestuous heterosexual pedophilia (2).
The clinical evaluation of pedophiles reveals them to be a diverse group. They differ educationally, vocationally, religiously, and socio-economically. They vary in the amount of force or aggression used in their pedophilic acts. They also vary in the many different causes that lead to the development of their sexual problem.
For some child molesters, their sexual acting out can be explained by the presence of a psychosis or an organic brain deficit. Individuals with a history of closed or open head injuries and individuals with a diagnosis of schizophrenia may become sexually aggressive because of their unique mental disorder or because of their brain injuries. For example, there are recorded brain damaged individuals who molest children because of impaired intellectual functioning. Their pedophilic behavior is not the result of a primary sexual disorder but of an organic disorder.
No single explanation can account for all the different pathways leading towards pedophilia. Any theory of pedophilia must be multifaceted and account for the wide range of behaviors, fantasies, and organic factors that may play a role in the development of this disorder. A comprehensive theory of pedophilia must refer to psychological, familial, environmental, social, genetic, hormonal, organic, and biological factors.
Psychological theories address only those aspects of the emotional congruence, sexual arousal, blockage, and disinhibition found in pedophilia that are independent of organic causes. These theories include such diverse perspectives as psychoanalysis, social learning theory, and family systems. While it is argued that a single perspective cannot explain the complex phenomena of pedophilia, this does not mean the the psychological theories are irrelevant. Rather, an integrated approach the combines several different approaches is best(5).
Psychoanalytical theories look at deviant sexual behavior as stemming from early childhood trauma. This trauma, which may take the form of sexual or physical abuse, leaves the child in a state of overstimulation, confusion, separation anxiety, and rage. Feeling helpless, out of control, and powerless, this victim may, in turn, act out as a way of re-creating the original trauma and attempting to master the anxiety associated with it. This psychic mechanism is called a repetition compulsion.
Or, this victim may identify with the aggressor, that is, he or she may identify with the abusing adult and then act out sexually with a younger child. Identifying with the aggressor would enable the person to defend against the unwanted feelings of helplessness and powerlessness. The sexual acting out with children or makes the individual feel alive and vital; it reestablishes a feeling of control, dominance, and power, and allays the anxiety associated with the childhood trauma.
However, this is only an illusory feeling of having solved an earlier childhood conflict. The feelings of dominance, control, power and being alive soon dissipate and the reenactment has to be repeated. Because the molester's attempts at mastery and problem-solving are illusory, he/she must molest over and over again (1).
Family system theories stress the role of unresolved intergenerational family dynamics on specific family members. It is argued that deviant sexuality is learned within the family. It first arises within the nuclear family and then is unconsciously transferred in family lines. Individual members can be 'targeted' to act out family conflicts.
For example, an unconscious conflict which is unacceptable to a parent may be encouraged in a child. A parent's unconscious wish to act out sexually with children may be repressed or pushed out of consciousness because of the fear of punishment. These unresolved wishes may be projected onto a child who is vulnerable. In the context of subtle family communications, the child may be passively of actively encouraged to act out those parental wishes. In this way, parents can both repress the forbidden sexual impulse and act it out through their child's behavior (1).
Typically, family system theories focus on communication patterns within a family and regard the sexual symptom of an one family member as being influenced by the specific communication patterns of that family. These family patterns exercise a powerful influence on the child.
Behaviorism and social learning theories stress the importance of learning our behavior. For example, a child may have had sex experiences with other children or adults which were prolonged. Sexual excitement, event when it is the result of abuse, is pleasurable. Pleasure is a strong, positive reinforcer of behavior and, thus, such sexual experiences have a high probability of becoming learned behavior and/or of becoming generalized to other sexual behavior (2).
At the same time, a child who has been sexually assaulted by an adult or another child may experience a tremendous guilt over these early sexual experiences. This guilt is likely to be associated in the child's mind with sexual curiosity and sexual pleasure. The child is then vulnerable to distressing symptoms because of the internal conflict of guilt versus pleasure associated with normal sexuality. When the child becomes an adult, this internal conflict, and the resulting ambivalence, may take the form of sexually acting out with children (1).
This psychological approach, stressing the psychic, social and environmental factors that give rise to child molestation, must never lose sight of the importance of biological factors. These factors acknowledge the importance of organic issues, especially brain pathology.
The search for a biological explanation of pedophilia is compelling and has attracted many researchers. The central question its: What effect does the brain have on perverse sexual behavior? Can deviant sexual behavior be attributed to brain illness or damage? This is an important question, the answer to which might link sexually deviant behavior to brain disease or abnormalities. Research in this area has taken several paths as well, linking certain kinds of brain damage and especially hormonal problems to sexual deviance.
Is there a relationship between hormones and pedophilia?
Pedophilia is mostly seen in males, and it has been shown that male sex drive and male aggression are mostly regulated by the male hormone testosterone. It has been suggested that there is a direct relationship between male hormone levels and aggression/sexuality, although the relationship is not that simple (4).
It has also been suggested that catecholamines and serotonin may play a role in the pathophysiology of paraphilias. Catecholamines are compounds occurring naturally in the body that serve as hormones or as neurotransmitters in the sympathetic nervous system. The catecholamines includes such compounds as epinephrine (adrenaline), norepeinephrine, and dopamine. Epinephrine and norepeinephrine are secreted principally by the medulla of the adrenal gland, and norepeinephrine is also secreted by some nerve fibers. Secretions of these hormones is stimulated when and animal is excited or scared, and causes such things as heightened heart rate, increase in blood sugar, increased blood flow, and changes to prepare for an emergency (3).
An experiment was conducted to measure epinephrine and norepeinephrine concentrations in the normal men and in pedophiles. The results showed a significantly greater concentrations of the catecholamines: epinephrine and norepeinephrine, in the pedophilic men. There was an especially high concentration of epinephrine in these paraphilic subjects. There is evidence that points towards a positive relationship between catecholaminergic activities and peripheral sympathoadrenal system activation. So, the results suggest that pedophilia may be caused by an increased peripheral sympathoadrenal activity, in connection with increased catecholaminergic activation. The peripheral side of the nervous system is that which carries impulses to the central nervous system from sensory end organs in peripheral tissue. The Sympathoadrenal system deals with igniting the 'fight or flight' condition in the body. This study showed that the increased presence of epinephrine may lead to greater activity in the sympathoadrenal system (3).
Other experiments have tested groups of pedophiles using newer technologies of imaging the brain to reveal abnormalities, such as the MRI and PET scans. There have not been any outstanding or consistent results from these experiments.
Overall, there is no biological conclusive evidence suggesting the real reasons for pedophilia, and the answer continues to lie in the combination of the before mentioned theories. Until there is more conclusive neurobiological evidence, the evidence has to manifest itself in behavior of the pedophiles.
Power and control are critical factors for the pedophile. The child is pliant and yielding, unlike an adult who may be rigid and unyielding. The child can be coerced and brought under control through simple requests and demands; the child will yield to the adults power and control because he or she still lacks autonomy and self-initiative to that extent. If the adult is in a more influential role such as a priest, coach or teacher, the child is particularly vulnerable.
For a pedophile, the emotional congruence factor is critical. The perpetrator is often developmentally arrested and may be at the same pyschosexual age as his victims. The pedophile may emotionally and sexually identify with the child who becomes his or her victim. Pedophiles may even engage in sexual acts appropriate to their arrested pyschosexual age such as just showing or touching (1).
During the sexual molestation, the aggressor's thinking is disturbed. Many sex offenders speak of the molestation as taking place in a hypnotic-like trance from which they awaken only after orgasm. This trance seems to be the mind's way of separating the rage from consciousness. Some researchers argue that this behavior may be the result of damage to the frontal and temporal lobes of the brain, leading to poor judgment, blunted anxiety, and impulsivity. Moreover, the disappearance of sexually motivation fantasies in the post-ejaculatory phase suggest even more strongly the link between the body's hormonal system and cognition (4).
Pedophilia remains an aggressive act. The perpetrator's apparent lack of awareness of this aggressive component in the relationship is akin to disavowal or denial and it is a delusional suspension of reality. Such persons may rationalize their molestation as serving a caretaker or parental role, performing and educational function, or providing friendship.
The establishment of and aggressive relationship give the perpetrator, as has been suggested, power, control, and dominance over the child and provides a connection to a real individual in order to overcome feelings of isolation and loneliness. During the "courtship" phase, the perpetrator disguises the aggression in order to coerce the child into participating in the "game" or "play".
The child's adoring or admiring attitude, or the teenager's idealization, is critical to the deception. This adoration and admiration feeds the narcissistic grandiosity of the perpetrators, provides them with a modicum of self-esteem, and confirms their self-image as loving and caring. Essentially, the victim unwittingly provides the pedophile with and important narcissistic balance to an otherwise depleted and depressed personality. The sexual encounter seems to provide a feeling of cohesion to a psyche which is in danger of disintegrating.
Given the perpetrator's obvious lack of self-assertion, psychosexual and psychosocial immaturity, and inability to form gratifying peer relationships, the child is an ideal object for sexual exploitation. Because the abuser lacks genuine empathy and connectedness to others, the child is viewed as a pliable object that can be persuaded to relate sexually to the adult.
The issue still remains as to whether pedophilia is an actual disorder within the chemical norm of the body and the brain, or whether it is simply deviance from a social norm. How are social norms defined? There have been many, many pedophiles discovered, and pedophilic acts occur every day. As atrocious as it may sound, could pedophilia and sexual afflictions like it be present more commonly and perhaps normally than our society allows?
| Post Traumatic Stress Disorder: A Response to Sexu Name: Sujatha Se Date: 2002-05-17 11:49:38 Link to this Comment: 2109 |
Sexual Assault described in technical terms is defined as any sort of sexual activity between two or more people in which one of the people involved is involved against his or her will. (3) The description of "against his or her will" extends to varying degrees of aggression, ranging from indirect pressure to a direct physical attack. According to the Crime Victim Research and Treatment Center 1.3 adult women are sexually assaulted in the United States every minute. (1) Of these assaults 84% of the attacks occur by someone the victim knows. The Senate Judiciary Committee the United States sighted the United States as having the highest rate of sexual assaults per capita in the world. (1) Unfortunately the majority of sexual assaults that occur against women go unreported. Only 31% of sexual assaults that occurred in 1996 were reported to law enforcement authorities. (1) The problem of sexual assault is increasing. In the year 2000 the number of sexual assaults against women had increased by 16.5%. (1) A woman's reaction to sexual assault can vary. Feelings of guilt, being ashamed, intense anger, and denial are common. In addition a woman can feel stigmatized by those around her and her community.
A question to look at is how victims of sexual assault deal with the trauma that they have experienced. The assaults often times have psychological repercussions. In addition a woman can develop health problems. These health problems can develop as varying degrees of depression, anxiety, and clinical stress. An issue to look at is how much control a victim of sexual assault has over her reaction. How much control can a woman have over repressing her emotions? How much of control does a woman have over her physical response to trauma? Furthermore what is the relationship between the mind and body? If a woman tries to repress her psychological response, does she develop a physical reaction? One type of disorder that develops among many women who have experienced sexual assault is called Post Traumatic Stress Disorder or PTSD. While the exact symptoms, and the length that PTSD lasts varies, the disorder is found among many victims of sexual assault.
The symptoms of Post Traumatic Stress Disorder vary. They can include an increased level of anxiety, which can result in difficulty sleeping, concentrating, and an exaggerated response to noise. PTSD can affect a woman who has experienced sexual assault ability to remember past events, in particular events associated with her assault. (2) PTSD can cause feelings of detachment and numbness, as well as a desire to avoid anything that the victim might associate with her assault. While doctors have been able to identify the symptoms in many victims of sexual assault the exact cause of the disorder is still questioned. Is the disorder the body's response to trauma? If so what relationship exists between the symptoms associated with PTSD as trauma? A strong correlation has been found between sufferers of PTSD and poor health. (3) PTSD can lead to depression and sickness. PTSD if not treated can also indirectly cause accidents that can affect a victim's health. These accidents can be the result high levels of anxiety, of a lack of ability to focus, and a lack of ability to respond.
Post Traumatic Stress Disorder can develop in two different forms, Complex Traumatic Stress Disorder and Acute Traumatic Stress disorder. (3) Complex PTSD, also known as Disorder of Extreme Stress is found among victims who have been exposed to prolonged traumatic circumstances. (3) Acute PTSD is found among victims who have been exposed to short-term trauma or isolated incidents of trauma. One question to ask is how does PTSD affect the brain? Sufferers of PTSD have been found to have abnormal levels of hormones that help the body respond to stress. Biologically victims of trauma can respond biologically by having lower levels of cortisone and increased levels of epinephrine and norepinephrine. (4) In addition the function of the thyroid, and the transmission of serotonin and opiates, is affected. Serotonin affects he transmission of messages between nerve cells. (1) The release of opiates is a way that the body blocks its response to pain. (4)
Post Traumatic Stress Disorder affects the body's ability to remember and its ability to express emotion. Studies done on the brains of victims of sexual assault have suggested that suffering a trauma can affect the hippocampus. (4) The hippocampus is a part of the brain that is involved in recalling memory and emotion. Scientists are now questioning whether the change in the hippocampus is responsible for flashbacks that can occur in sufferers of PTSD. (4) In addition to changes in the hippocampus, victims of sexual assault experience an increased level of release of corticotropin. This release is responsible for triggering the body into responding to stress. The result to a release of high levels of corticotropin can be a startled response. (4)
Treatment for Post Traumatic Stress Disorder can be approached from two directions: through psychological therapy, and through the use of medicine. Because doctors and scientist have yet to fully understand PTSD and how it affects the body, treatment approaches are limited. The psychological treatment approach to PTSD can include Cognitive-behavior therapy (CBT). (3) CBT works to change the emotions that a victim of trauma feels. This is done through re-exposure to feelings associated with the trauma, followed by an analysis of the response. Through re-exposure therapists CBT can readjust a victim's behavioral response to the trauma that they experienced. CBT includes teaching a victim how to deal with the anxiety and stress that they experience. (3) The medicinal approach to treating Post Traumatic Stress Disorder includes the prescription selective serotonin reuptake inhibitors (SSRIs). SSRIs work to correct the imbalance of serotonin in a trauma sufferer. (3) Overall the best method for the treatment of PTSD has proven to be a combination of both psychological therapy, and pharmacotherapy. This suggests that there is a direct relationship between the mind and body in their response to trauma. It also leads us to question the specific effects that trauma can have on a victim psychologically and physically. If a victim represses her psychological reaction, does that affect the way she will respond physically?
What affect does an environment have on a victim's response to trauma? Do woman who feel that they are in a supportive environment recover quicker than woman who feel isolated? What correlation can be found between the high rate of sexual assaults against women in the United States and the number of cases of PTSD diagnosed? If women who have been sexually assaulted felt that they could express their trauma more openly in American society, their recovery would be faster. The feelings of being stigmatized, feeling ashamed, and feeling guilt are reactions imposed upon victims of sexual assault by the communities that they live in. Furthermore if more efforts were made to prevent sexual assault against women in the first place were made, the number of Post Traumatic Stress Disorder Cases would decrease. As more is learned about the implications that the environment can have on a victim of trauma, as well as the relationship between the mind and body, more can be learned about treating Post Traumatic Stress Disorder.
1) Sexual Assault Crisis and Support Center
3) Informational website on PTSD
| Migraines: A Personal Perspective on a Complex Dis Name: Priya Puja Date: 2002-05-17 12:02:41 Link to this Comment: 2110 |
If I can only make it to my bed, I'll be fine. My head hurts terribly. I would do anything
to stop the pain. I've taken three extra strength Tylenols and the pain hasn't diminished
at all. My head is spinning. Ever so often, the world around me turns dim and then
bright. I close my eyes. I need to lie down, but I am driving. I feel nauseous. The pain
that started on one side of my head is spreading as it pulsates. I squeeze my head and rub
my temples, but the pain remains. I wish for a lobotomy. I wish somebody could stop
the pain. I'm home. I run to my room. I tie a rag tightly around my head. It doesn't
help. I press my head against a wall. I feel like vomiting again. I know relief is coming
soon. I pass out. I am a Migraineur, and have been ever since I can remember.
1)
Migraine headaches are a type of vascular headache that affects 28 million Americans, 75
percent of whom are women 1)
Institute of Health, a good source of general information on migraine headaches.
Annually, migraines cost the American taxpayers $13 billion in missed work and reduced
productivity 1)
Institute of Health, a good source of general information on migraine headaches.
Migraines are not a disorder unique to overworked Americans. In fact, the World Health
Organization identified migraine among the world's top 20 leading causes of disability
name="2">2)
articles about migraine headaches. According to the World Health Organization, aside
from the physiological experience of the headache for the individual whom it affects,
there exists the "burden" of the migraine. In particular, this burden includes "the
economic and emotional difficulties that family experiences as a result of migraine"
name="2">2)
articles about migraine headaches. According to one report, migraine headaches account
for 1.4% of total years of life lost due to disability in both sexes of all ages
name="2">2)
articles about migraine headaches. Despite all this data, migraines are not considered by
many to be a legitimate medical problem.
Migraine headaches, as previously noted, are not unique to Americans, nor are they an
exclusively modern disorder. In fact, there exists a rich body of historical literature that
demonstrates the progression of mankind's knowledge of the headache from the "magical
to the molecular level" 3)
Neurology, provides a historical perspective on topics related to neurology. Five
thousand years ago, Mesopotamian physicians were not in the practice of precisely
diagnosing different types of headaches. This can be attributed to their acceptance of
"supernatural pathophysiologic properties" 3)
Neurology, provides a historical perspective on topics related to neurology. In
particular, they viewed headaches as a disease caused by the evil spirit Tiu. Many of the
treatments used in ancient times were based on dealing with evil spirits. For example in
ancient Egypt, a clay effigy of a sacred crocodile was bandaged to the head of the
sufferer. If this treatment, along with praying, did not bring relief to the sufferer, then
trephination was practiced. This process involved the "releasing of the evil spirit through
a hole gouged in the skull by a trephine" 3)
Neurology, provides a historical perspective on topics related to neurology. The
next step in mankind's evolving knowledge of headaches was the recognition that
particular types of headaches existed.
Hippocrates classified the migraine as a specific kind of headache. Unlike the
Mesopotamians, he did not attribute migraine to evil spirits, but rather to an "imbalance
of natural forces in the body" 3)
Neurology, provides a historical perspective on topics related to neurology.
According to Hippocrates, migraine headaches were caused by the rise of vapors from the
liver to the head. This view of migraine pathophysiology persisted until the 17th century
when Thomas Willis revolutionized thinking about "megrim". More specifically, he
attributed migraine headaches to nerves themselves and to the congestion of blood
vessels, rather than to the ascent of vapors. The recognition that migraine headaches
result from cranial vasodilatation, although not immediately accepted, did eventually lead
to changes in migraine treatment. In particular, treatment involving the opening of the
skull and the use mercury to drain vapors was phased out and replaced by more
pharmaceutically based treatment.
Migraines are unilateral (felt on one side of the head) in about 60% of migraine sufferers,
and the associated pain is typically described as throbbing in nature
name="4">4)
provides information on all types of headaches. Although the brain itself lacks pain
receptors, the meninges (membranes that surround the brain), blood vessels, and bony
anatomy of the head have a complex system of nerve branches that respond to pain
name="8">8)
comprehensive look at migraine headaches. Migraine headaches differ from other types
of headaches in that they are potentially disabling and are associated with various
combinations of symptoms. Severe pain, nausea, vomiting, and sensitivity to light, sound
or odor are only a few of the possible migraine-related symptoms. In fact, nausea occurs
in up to 90% of patients and vomiting occurs in about one third of Migraineurs
name="5">5)
Forest University Baptist Medical Center, lecture notes of a professor at the medical
school. Although the precise step-by -step pathophysiology of migraine headaches is still
unclear, there exists a general consensus that blood flow change in the brain is key to
understanding the origin of migraine headaches. More specifically, it has been suggested
that individuals who suffer from migraine headaches have blood vessels that overreact to
various triggers due to an inherited abnormality in blood vessel regulation
name="1">1)
Institute of Health, a good source of general information on migraine headaches.
According to the current theory on migraines, the nervous system responds to a trigger
such as stress by creating spasms in the nerve-rich arteries at the base of the brain. These
spasms constrict several arteries and result in a reduction in the amount of blood flowing
to the brain. At the same during which this vasoconstriction is occurring, platelets, blood
clotting factors, clump together in a process that promotes the release of the
neurotransmitter serotonin. Serotonin serves to further constrict arteries and reduce blood
and oxygen to the brain. In response to the reduced oxygen supply, the trigeminal nerve
stimulates specific arteries around the brain dilate. The vasodilatation spreads and
eventually affects the neck and scalp arteries. The dilation of these arteries triggers the
release of pain producing chemicals called prostaglandins. These in turn activate specific
blood cells and cause them to release substances that cause inflammation, swelling and
sensitivity to pain. These physiological changes serve to stimulate pain-sensitive
nociceptors and result the throbbing pain that is commonly associated with migraines.
1)
Institute of Health, a good source of general information on migraine headaches
Migraine is a genetically based disorder. According to one study, individuals who have
one parent who is a Migraineur have a 50% chance of having migraine headaches
name="6">6)
suffer from migraine headaches. At least 7 genes contribute to the events that lead to
migraine headaches 5)
Forest University Baptist Medical Center, lecture notes of a professor at the medical
school. One of these genes, located on chromosome 19, has recently been implicated in
familial hemiplegic migraine, a severe form that is coupled with paralysis
name="6">6)
suffer from migraine headaches. Not all migraines are associated with paralysis. As
such, it is important to distinguish between the migraine subtypes. In particular, there are
four main migraine subtypes?migraine without aura, migraine with aura,
opthalmoplegic migraine, and retinal migraine. Of these, the two most common subtypes
are migraine with aura and migraine without aura.
Migraine with aura, also known as a classic migraine, is one in which an aura occurs 20
to 40 minutes before the headache starts 7)
School. An aura is a single symptom or set of symptoms that a Migraineur experiences
prior to the onset of a headache. The aura may consist of visual disturbances, numbness
in parts of the body, motor weakness, dizziness, vertigo, abdominal symptoms, ringing in
ears, speech disturbance, and/or olfactory hallucinations. The most common auras are
visual and involve flashing lights, wavy lines, or brief vision loss. The end of the aura
marks the beginning of a throbbing or pulsating headache on one side of the head. The
headache may be accompanied by the previously mentioned symptoms of nausea,
vomiting, sensitivity to light (photophobia), or sound (phonophobia), and it may spread to
both sides of the head 7)
School. The duration of the headache can vary from one hour to one to two days.
Migraine without aura, also known as a common migraine, affects a larger number of
patients than the classic migraine. Individuals who suffer from common migraines have
the same headache as those who suffer from a classic migraine. However, they do not
experience the very obvious warning sign of an aura.
Beyond the physiological and genetic underpinnings of the disorder, migraine headaches
are brought about by various trigger mechanisms. Trigger mechanisms fall into two main
categories: uncontrollable and controllable 6)
suffer from migraine headaches. Triggers vary amongst individuals, and they often work
in combination. Controllable triggers include foods, certain activities, and medications.
Uncontrollable triggers relate to environmental stimuli. Factors related to emotional
well-being can also act as triggers, and can not be classified by controllable vs.
uncontrollable dichotomy. Common triggers include:
-Food- caffeinated foods and beverages, alcohol, dairy products, monosodium
glutamate (MSG), soy sauce, garlic, certain fruits, smoked meats
-Emotions- stress, anger, depression, anxiety, and sudden excitement
-Environmental stimuli- sudden changes in temperature, barometric pressure, or
altitude; strong odors (especially perfumes); loud noises; bright lights or glare
-Activities- riding in a car, plane; intense exercise; changes in sleep patterns;
skipping a meal
-Medications- vitamin supplements, nonprescription pain relievers, certain medicines
for high blood pressure and heart disease, certain birth control pills and hormone
supplements 7)
Medical School
Migraine is a disorder that leads to the heightening of one's senses, and as a result a
Migraineur is more sensitive to his or her environment 6)
suffer from migraine headaches. For example, it is known that weather patterns serve as
trigger for migraines in many patients. A recent study entitled "The Effects of Weather
on the Frequency and Severity of Migraine Headaches" concluded that: "wind from the
southeast was shown to be associated with more attacks than wind from any other
direction" 6)
suffer from migraine headaches.
Another very common uncontrollable trigger amongst women is the menstrual cycle.
Migraine often develops around the time of the first menstrual period, menarche, and is
related to falling levels or reduced availability of estrogen 6)
suffer from migraine headaches. In fact, a recent study involving female students at
Belgrade University found that both migraine and nonmigraine headaches were worse
during menstruation 2)
articles about migraine headaches. In addition, researchers found that both types of
menstrually related headaches occurred around the first day of menstruation. These
findings suggest that menstrual migraines occur during peak fluctuation in estrogen
levels. This relation of migraine to menstruation occurs in only 14% of women sufferers
4)
provides information on all types of headaches. In fact, in 60% of women there is no
definitive association between the two 4)
provides information on all types of headaches. In addition, other hormonally related
events?pregnancy, breastfeeding, and menopause?are also linked with changes in
headache frequency and severity 4)
provides information on all types of headaches.
The use of medication to treat migraine can be divided into two categories: abortive
treatment and prophylactic or preventive treatment 8)
comprehensive look at migraine headaches. Medications used to treat acute migraines
include analgesics, serotonin, receptor medications, triptans, ergots and antiememtics.
Preventive treatment includes the usage of beta-blockers, antidepressants, valproate, and
calcium channel blockers.
I am a Migraineur. I suffer from the classic migraine. My aura involves visual
disturbances. Specifically, everything in my field of vision becomes incredibly bright,
and then dark. My migraines always lead me to experience the symptoms of throbbing
pain, nausea and vomiting. Vomiting is more often, than not followed by fainting. An
hour or two later I wake up from these episodes physically exhausted. Fortunately, I've
never experienced migraine symptoms for longer than a few hours.
I started getting my headaches at a very young age. In fact, I have vivid elementary
school memories of having to go to the nurse's office, and wait for my mother as the pain
in my head grew unbearable. My mother is a Migraineur as well. As such, she had
plenty of helpful tips on how to deal with the disorder. Over the years, I've noticed many
changes in the triggers and in the frequency of my migraines. In particular, as a child the
consumption of certain dairy products often led me to experience migraines. Today, I
don't react the same way to dairy products, but skipping meals, standing outside in the
sunlight, and changes in barometric pressure remain as primary migraine triggers for me.
Although I still have the occasional random migraine, my migraines are less frequent and
tend to cluster around the days of my menstrual cycle. I feel as though I finally have the
vocabulary to understand my disorder, and as such, I feel empowered to overcome it.
References
Institute of Health, a good source of general information on migraine headaches
2)
articles about migraine headaches
3)
Neurology, provides a historical perspective on topics related to neurology (3)
4)
provides information on all types of headaches
5)
Forest University Baptist Medical Center, lecture notes of a professor at the medical
school
6)
suffer from migraine headaches
7)
School
8)
comprehensive look at migraine headaches
| Picture Smart:Spatial Reasoning and Its Role in Co Name: Cindy Zhan Date: 2002-05-17 13:08:34 Link to this Comment: 2113 |
There are many theories about the nature of intelligence. The formal definition of intelligence is "the capacity to acquire and apply knowledge." One aspect or kind of intelligence, according Dr. Howard Gardner, founder of the multiple intelligence theory, is spatial intelligence(1). Spatial intelligence is one amongst eight kinds of intelligence. The most common description of spatial intelligence is the ability to be able to recreate one's visual experience and reasoning about shape, measurement, depiction and navigation.
Spatial intelligence might be one of less familiar kind of intelligence, however it has wide implications in many academic and professional disciplines. It is extremely important in disciplines such as mathematics and computer science. Spatial Intelligence also accounts for the thinking process of engineers, architects, designers, sculptors and inventors. This paper is an over all comprehension of spatial reasoning and why it is important in learning and problem solving, it is an investigation into what spatial reasoning is and its role in learning and cognition. This paper will also address the neurobiology of spatial reasoning and discuss the specific areas and organization of the brain that accounts for spatial intelligence.
There are many theories and models attempting to define spatial reasoning. The first model is called the MV/PD model. According to this model, spatial representation consist of two parts. The first is a metric diagram, which includes quantitative information and provides a substrate, which can support perceptual-like processing. The second part of the model is termed place vocabulary, which makes explicit qualitative distinction in shape and space relevant to the current task (2). Therefore, spatial reasoning is not just visualization of objects and space but also the ability to take qualitative information and then transformation them to spatial representations so that it can be better understood.
Spatial reasoning is useful in physics, math and computer science and can be applied to different industries. Engineers use graphs to express complex relationships, such as temperature-entropy or pressure volume plots, Often these graphs are sketches, intended to convey qualitative information about the shapes of curves and relative magnitudes rather than precise numerical values(2). Therefore, spatial reasoning is an essential part of the thinking process of scientist and engineers because they need to understand and interpret qualitative information in graphs and models in order to gain critical understanding of the problems at hand.
What exactly is the process through which humans use spatial reasoning to solve problems?
Another theory addressing spatial intelligence is called the mental model theory,
developed by Johnson-Laird and Byrne. According to the mental model theory, first, the person constructs a mental model of the premises of the problem. Second, the person draws a conclusion from the model that is informative. The model helps to extract information that is not directly asserted by the premises. Third, the participant tries to construct another alternative model to try and contradict the initial one, if they cannot construct an alternative model, then they take the first one to be correct(3). According to the mental model theory, reasoning is guided by a 'search for counter –examples procedure." However, if the search of counter examples takes too much working memory capacity, then the process of searching for counter examples to get the right answers will come to a halt. Also, the mental model theory predicts that problem difficulty increases as the number of different possible mental models increases.
To illustrate how mental models can be used to solve a problem and why the problem difficulty increases as the number of different possible model increases, consider these two problems.
Problem one:
1. A is on the right of B
2. C is on the left of B
3. D is in front of C
4. E is in front of B.
What is the relationship between D and E?
Problem two:
1. B is on the right of A.
2. C is on the left of B.
3. D is in front of C.
4. E is in front of B.
What is the relationship between D and E?
Both of the problem is expressed in the same number of expressions however, there is only one model for the first problem which looks like this. C B A
D E
However, for the second problem there are two models: C B A and A C B
D E D E
For the second problem the answer is the same, D is on the left of E regardless of the models. However, according to the result from studies on subjects trying to solve both problems, 70% of participants get the first one right where as only 46% get the second right. This result is consistent with the mental model theory and its prediction that the problem gets more difficult if there the number of possible model increases.
According to the last two paragraphs, spatial intelligence is an essential part of how we absorb and process problems. If this is true, then would it make sense to say that spatial reasoning has an overall effect on intelligence or IQ? IQ, or intelligence quotient is found to have a direct correlation with RT, which is the decision time. The equation for RT is RT=mx+c. This equation is called Hick's law, according to equation, IQ is proportional to the slope m, which is a representation of the processing speed; m is lower in individuals with higher IQ(4). A challenge to this idea is that slope relates only weakly to IQ and that the absolute RT correlates better to IQ. This implies that IQ correlates better with choice RT or the c intercept. Studies had also shown that when the choices or stimulus is increased in complexity and spatial representations of the choices, the Hick's equation can produce the same correlation of IQ to RT without having to focus on just m, the processing speed. Therefore, it is reasonable to conclude that spatial effect added to the experience has a significant influence on RT and in turn also on IQ and that "effects of spatial attention requirements on choice RT may provide a better measure of intelligence than just measuring the processing speed (4)."
Now we know that spatial reasoning is significant to the way we learn and has a direct relationship in reference to intelligence, it is also important to look into the brain and the specific region of the brain that accounts for spatial intelligence. In order to detect the area of the brain that is responsible for spatial awareness scientists conduct studies on individuals who are deficient in spatial detection. When four individual with left lesion and another four with right lesion were asked to replicate a model of a house. Drawings of the right-lesion individuals show spatial disorganization, left hemisphere neglect and lack of perspective(5). This study indicates that spatial awareness is probably a function of the right hemisphere of the brain.
A recent article in nature confirms this presumption. According to the article, at first the area of the brain though to be responsible for spatial awareness is the posterior parietal lobe. However, by studying individuals with "pure" spatial defection rather than spatial defection along with deficiencies in other areas indicates that spatial awareness is " largely confined to the right superior temporal cortex, a location topographically reminiscent that of language on the left (6)
Since the brain needs to process problems involving space and dimension, it is not absurd to say that the functional brain structure can be described in geometric terms. In the book Brain Theory: Spatio-temporal aspects of brain function, the author argues that the brain exist primarily in space and the function of the brain, especially in the "front end" or visual system, can be viewed and understood geometrically(7). This notion of the brain as a geometry engine demonstrates that the way information is processed in the brain adheres to the structure of the brain. The brain is not purely logical and linear, therefore, when data or information is passed through it, it does not solved the problem in linear steps, it makes more sense to perceive the brain as an organ that naturally stores the information in different areas and then constructs models from the data and correlates different data according to the models in order to derive an answer or solution.
So far we've discuss spatial intelligence and its role in cognition and problem solving, we also discuss the neurobiological aspects of spatial reasoning and found out what areas of the brain accounts of spatial awareness. At the beginning of the paper, spatial intelligence is only one kind of intelligence, however, as I found out more about the topic, I am convinced that spatial reasoning is not separate from other kind of intelligence but is a part of many thinking processes. No matter what the problem at hand is, it always helps to use spatial representation such as pictures, graphs models and metaphors, if not written physically, than envisioned mentally to better understand the problem and come to a valid conclusion. As I finish this paper, I begin to view the multiple intelligence theory in a different light, instead of perceiving spatial intelligence or any other kind of intelligence as completely different entities unrelated to each other, I start to ponder the possibility that intelligence is consisting of all kinds of thinking processes that are interrelated and interactive to prompt the individual to absorb and process information in the most efficient way.
| Chronic Fatigue Syndrome and Nervous System Involv Name: Natasha Gj Date: 2002-05-17 13:26:41 Link to this Comment: 2115 |
Upon concluding my neurobiology course, I spent some time reflecting on what I've learned about the nervous system and its functions. I thought about how much progress has been made in the last couple of decades alone in defining and understanding certain aspects of neuronal functions, and must admit that I am very impressed. However, there is still so much we don't know about this area, and nowhere has this notion proved more true than in my exploration of Chronic Fatigue Syndrome. As will soon be clear, this disease is highly debilitating and can greatly lower the quality of an individual's life, yet to date there are no definite findings about the etiology of this illness. But even more importantly, this illness shows the importance of understanding and being able to assess the different workings of our nervous system and its complex nature. Unfortunately, the study of this same disease also shows the human inability to yet do so.
So what is Chronic Fatigue Syndrome, or CFS? I would like to be able to explain exactly what CFS is, but true to the nature of what is known about this illness, there is no precise way to describe CFS. Rather, the disease is identified through a number of symptoms (both physical and psychological), including unexplained and persistent fatigue of new or definite onset, concurrent with short-term memory loss, sore throat, tender axillary lymph nodes, muscle pain and unrefreshing sleep, among a number of others, for a duration of at least six months. As is probably evident, the above symptoms, in addition to being signs of CFS, are also the same (or very similar) symptoms experienced in such diseases as Lymes disease and "the flu." There are symptoms that involve the Gastrointestinal Tract (GI), immunological-related symptoms, symptoms of psychiatric disease like depression, sexual malfunction, endocrine dysfunction-basically every system in the body. This is part of the reason why CFS is hard to detect, and is usually chosen as a diagnosis only at the exclusion of all other possible ailments. The other difficulty that lies with diagnosing CFS is that there is no way of measuring the level of a person's fatigue-there is no way for a physician to tell whether a patient complaining of fatigue is experiencing the type of fatigue associated with CFS or he/she is just extremely tired and overworked. Nevertheless, diagnosed or not, it is estimated that about 800,000 Americans suffer from this disorder, whose etiology has yet to be defined (1), (3).
So what? Well, aside from that fact that I like learning and reading about "mystery" illnesses, the reason for my interest in this topic is imbedded in CFS's presumed connection to the nervous system, namely the brain. Many studies have found that patients with CFS, in comparison with healthy control subjects, have a variety of abnormalities of the hypothalamic-pituitary axes. For example, there is reduced hypothalamic production of corticotrophin releasing hormone, leading to diminished pituitary release of ACTH, leading to hypocortisolism. Also, it has been found that the adrenal glands of CFS patients are half the size of adrenals from healthy control subjects. In a study detecting regional cerebral blood flow in CFS, it was found that a deficit in the regional cerebral blood flow in the medial temporal lobe was definite in seven out of the thirteen CFS patients, including the brainstem, left medial temporal lobe, and right medial temporal lobe. Therefore, hypotension-an abnormality in the way the body regulates blood pressure, is a close link to CFS. This condition occurs when the central nervous system's autonomic portion (one controlling heart rate and blood pressure) misinterprets the body's needs during periods of upright posture and sends a message to the heart to slow down and lower blood pressure, which is the opposite of what the body needs at such times (3), (4).
Of course, testing a number of patients through certain methods and then interpreting the information in the context of what that specific test is looking for is quite easy. But what do all these test results mean in the context of CFS-in terms of finding a defining feature that sets CFS apart from all other diseases? The answer here is that no one is quite sure what all of this means. Not all CFS patients exhibit the same symptoms, and not all tests are one hundred percent reliable. However, one this is for certain. The makeup and function of our nervous system is very complex, and not easily studied. Even more importantly, the problem becomes even greater when one realizes that the nervous system is involved in and integral to all other systems of our body. So how do we set everything apart? How do we decide which particular system, or part of a system is malfunctioning? Is there a problem with a particular system, or is the input from several other systems incorrect? In the case of CFS, many systems are malfunctioning-the GI tract, blood pressure control systems, temperature control systems, and weight control systems, and for that reason this disease has been hard to diagnose and define (1), (2), (4).
During my studies of neurobiology, it has been my experience that the best way to understand the entire nervous system is to break it down into the simplest of concepts and work toward understanding the entire system (or perhaps I should say systems) and the way they intertwine, work together and are integral to one another's functioning, while contributing to an enormous amount of complexity. This method has served me well in allowing me to grasp a large amount of information and put it into some kind of order so that it makes sense. However, this approach has its shortcomings. As my exploration and understanding of Chronic Fatigue Syndrome suggests, it is often very difficult, and sometimes impossible, to divide the nervous system into parts, assigning each one a specific function. Rather, often times the systems that we are taught "make up" the nervous system are often indistinguishable from the nervous system itself.
Chronic Fatigue Syndrome is still mostly uncharted territory for most of today's scientists. It is a disease for which there are no definite causes, only a list of definite (although even that is not completely "definite") symptoms. But even though the exploration of this illness proves to be pretty new to many, the study of the nervous system is not. As I see it, this illness, although complex and unexplainable, is giving today's scientists and researchers the chance for further exploration and discovery of our already incredibly evolved, evolving, and extremely complex nervous system.
WWW. Sources:
1)WICFS Home Page, a good site on all perspectives of CFS
2)Wisconsin Institute for CFS, great resource of CFS
3)The Scientist –Genetic and Molecular Mysteries of Sleep are Keeping Researchers Alert, information on sleep disorders in general
4)Harvard Health Publications, News on latest CFS news from Harvard
| Developing and Overcoming Antisocial Personality D Name: Shannon Le Date: 2002-05-17 13:30:28 Link to this Comment: 2117 |
Personality disorders are among the most difficult disorders to be diagnosed and treated in psychology. The highly ingrained behaviors of the disorders, the difficulty in differentiating between normalcy and illness, and the patients lack of understanding and excepting their symptoms as abnormal, are all contributing obstacles of the disorder.
Personality is shaped by experiences during childhood and adolescence as well as genetics. Therefore, children that develop mental disorders are more likely to develop personality disorders as adults. Conduct disorder in children has been highly linked to the development of antisocial personality disorder in adults. The DSM (Diagnostic and Statistical Manual) suggests, but does not require, a history of conduct disorder when making an antisocial personality diagnosis (1). Not only is there a high correlation between people having the disorders, but conduct disorder seems to be a preliminary childhood manifestation of the same underlying malfunctions that are characteristic of the adult disorder, antisocial personality disorder. When looking at the development and causes of antisocial personality disorder it is important to note the symptoms, characteristics, and circumstance of conduct disorder as well.
Conduct disorder, a childhood behavior disorder described by the DSM, is characterized by chronic misbehavior. The children and adolescence often participate in serious physical fighting, alcohol and drug abuse, violation of parental and school rules, vandalizing and setting fires, and many other antisocial behaviors. These children, unless adequately treated, have a 50% rate of becoming involved with drugs and criminal behavior during adolescence. They also have a 75%-85% rate of being chronically unemployed as adults. Many of these children, about 40%, grow up to have antisocial personality disorder (2).
Antisocial personality disorder is a Axis II DSM recognized disorder under the personality disorder category that has earned separation from the acute psychological disorders of Axis I. This is the most common disorder among the personality disorders: between 2.3%-3.3% of the population is diagnosed some time in their lives, it crosses all ethnicity's, and is five times more commonly diagnosed in males than in females. The main symptoms of this disorder are, a tendency to develop maladaptive behaviors that diverge or violate from societal norms, and they have a severe difficulty developing and keeping positive relationships. The characterization of antisocial personality disorder is very similar to that of conduct disorder, but the symptoms are manifested in different ways. These people tend to be cold, uncaring, and can be maliciously cruel at times. They feel very little guilt for their actions, believing they are always faultless. They will often pretend to care and be pleasant until they succeed in getting what they want. They often have extreme personality traits of arrogance, impatient, low tolerance of frustration, and poor impulse control. These characteristics are transient and chronic, often effecting the individual, their family, and the community negatively (3).
The poor impulse control, lack of patience, and uncaring attitude, cause the people with the disorder to have trouble staying in relationships such as marriage. They have difficulty staying employed and doing anything that requires a routine. This extreme personality characteristics is related to criminal activity, violent death due to extreme daring behavior, and suicide attempts (3).
When analyzing this disorder one is likely to wonder, what causes the symptoms of the disorder to develop and how, if at all, the disorder can be overcome? What factors are responsible for 2.3%-3.3% of the population developing these abnormal characteristics and personality extremities to the point of being "disordered?" After much thought and consideration of argumentative suggestions for different causes of the disorder, I have come to the conclusion that it is due to a variation of three main influential factors.
The first influential factor to be discussed that is important in the development of personality disorders, such as conduct disorder and antisocial disorder, is genetic and biological contributions and characteristics that make certain people more likely to develop this disorder than others. There have been many studies done that show ample support for genetic influence in the development of antipersonality disorder. These studies show that criminals with antisocial personality have criminal records more like their biological fathers than their adopted fathers, which supports that the disorder runs in families. Also twins that are identical have a 50% concordance rate of the development of the disorder, as opposed to only a 20% concordance with twins that are not identical (4).
Hormones and neurotransmitters also play a vital role in supporting the biological connection with the disorder. The disordered displaying symptoms of impulsivity and aggression have naturally lower levels of adrenaline in their blood when calm and excited. Adrenaline is a hormone released in higher amounts when the sympathetic system responds to excitable stimuli, such as anxiety, pressure, danger, and joy. Possibly, the variance of this hormone attributes to some symptoms showed by the disordered. The lack of adrenaline, stimulation, might cause the disordered to becomes easily bored and attempt to seek thrills by more dangerous and extreme measures in order to obtain arousal and excitement. This lower hormone concentration also supports reasoning for antisocial and dangerous behavior, because one who is not as stimulated in dangerous situations with fear and anxiety, would feel less aversion to initiating and participating in these situations (5).
Neurotransmitters such as serotonin have been targeted in connection with the disorder. Higher levels of serotonin in the blood have been found in correlation with antisocial personality types. Newborns with a family history of antisocial personality disorder have lower levels of serotonin in the brain at birth than normal infants (AJP CSF). Other findings have also shown that there is decreased serotonin functioning in those with antisocial disorder and those who have high susceptibility to the disorder, but further studies are being done to try and understand the dysfunction (6).
About 60% of children with ADHD (Attention Deficit Hyperactivity Disorder) also develop conduct disorder, and then many of these people go on to develop antisocial personality disorder (1). There are neurological differences in the brains of those with ADHD, deficits in executive functioning. The high comorbidity suggests that there are also differences in the brains of those who develop the personality disorders. Both those diagnosed with ADHD and the personality disorders have a primary deficit in the ability to control impulsiveness and behaviors, which also suggests that the neurological problem may be the same for all of the disorders.
Although, personality disorders are the most difficult of the psychological disorders to treat, there are certain methods used and others in progress by the scientific world today. To treat the biological symptoms, such as low levels of serotonin and the high comorbidity found with ADHD, medications are often prescribed. The most effective drug so far for the disorder is lithium, which decreases the impulsively and hyperactivity of the disordered. Stimulants such as Adderall can be given to treat similar symptoms, and they also increase concentration levels. These drugs have only been approved for treating those with ADHD diagnosis. Antidepressive drugs, such as MAOIs and SSRIs that influence serotonin levels, are starting to be used in the treatment of the disorder. Their efficacy has not been proven to be sufficiently so far by scientific studies (3).
A second influential factor in the development of conduct disorder and antisocial disorder is environmental factors. Psychosocial contributions to the development of these disorders have been supported in numerous studies. Children are heavily influenced from birth and are products of their environment. They learn social skills and coping mechanisms from parental example. Children who have uninvolved parents and that already have genetic predisposition's for the disorders, are more likely to develop antisocial characteristics. Children who have parents that are alcoholic or drug abusers are more likely to be substance abusers themselves. The families with substance abuse have also been found to have poor functioning compared to normal families, and therefore, more children who become disordered. The highest rate of disordered children comes from families that have an antisocial parent that is also a substance abuser (7).
Other environmental contributors to the development of the disorders are teacher and peer groups of the child (3). ADHD is also a good example of supporting environmental influence as well as biological influence. Children with ADHD often have trouble in school because of lack of impulse control and attention span. They are loud and get into trouble, which leads to punishment by the teachers and unpopularity among the other students. This environmental factor furthers the development of even more extreme antisocial behavior, fighting and skipping school, and eventually many of these children are diagnosed with conduct disorder.
Treatment of environmental factors involves attempting to reverse maladaptive cognitive thought developed due to experience. These maladaptive thought processes are very hard to tackle for the antisocial disorder, because a common symptom is the inability of those with the disorder to see their behavior as abnormal. Regardless, it has been found more helpful than not in improving some people with antisocial personality disorder. Treating children through these processes has been proven essential to overcoming the disorder and decreasing the prevalence of antisocial disorder developing later in life. Family counseling and intervention is very helpful as well for children. The maladaptive psychosocial environment can be changed so that the child experiences and learns positive social skills (8).
The third and final contributing factor to whether or not a person develops conduct and antisocial personality disorder, and whether they are able to overcome the disorders, is best described as the unique "I-function" of each individual (9). My comprehension of the I-function is fairly new and incomplete. I can best describe it as the manifestation of consciousness in each individual that is continuously and uniquely effected by the unconscious and unique connectivity's in the brain. The I-function is how one consciously makes decisions and solves problems, but it also is an outlet for all the unconscious products of the brain. I learned in, Dr. Grobstein's, neurobiology class at Bryn Mawr College about the existence of the I-function and about the uniqueness of every individual brain. If the differences in our brains allow for unique ideas and outlooks that make our experiences and ways of thinking unique as well, then I believe some brains can and do develop determination and a will to overcome the antisocial personality disorder, consciously implementing the decisions through the I-function.
Now one may ask how I plan to support the integrity of this rather alternative influential factor for these disorders. Although, I found many theories and studies supporting the importance of psychosocial and biological contributing factors in the development of conduct and antisocial disorder, I found little that answered my initial questions that made me take interest in researching this topic in the first place. These questions included, who overcomes these disorders when the odds are against them, and how do they overcome these other predisposition to antisocial disorders. The foundations of the disorders create a dim outlook because a primary characteristic of the disorder is the person's inability to realize or admit the abnormality of their behaviors. Therefore, it is often difficult to give the person adequate treatment, drugs or psychotherapy, for their symptoms.
I have decided to primarily support the third factor with the very case that struck my interest in the topic. There is a person that I have known all my life who developed conduct disorder by the age eight, worsening in severity of the disorder as he grew into adolescence. He was constantly in trouble and demonstrated nearly every characteristic of conduct disorder including, severe physical fighting, theft and vandalizing property, skipping school, lying, and violation of rules and law for thrills. He eventually did some drugs and became an alcoholic in his adolescence. He was nearly killed several times due to lack of fear and extreme thrill seeking. For instance, he sped at the highest possible speed down a road in the rain at night on a motorcycle. Losing control he hit a telephone pole, which caused him to break many bones in his body, almost killing himself. After several less severe offenses, he was playing with a gun and shot a girl in the head accidentally. The girl lived, stated it was an accident, so he went to jail for a minimal period still believing he just had "bad luck" as opposed to a disorder.
This person has a environmental history of being diagnosed with ADHD, and later antisocial disorder. He was also assumed to have had conduct disorder, although he was not diagnosed during childhood. He comes from a divorced family, with a paternal alcoholic and ADHD history, and had extremely low parental supervision. He was never physically abused in any way. His brain has not been tested for specific abnormalities, but he has many similarities to those that have abnormalities. He refused medication for ADHD, because he did not want to take it. He had severe inability to control impulse and hyperactivity, could not hold a job, and showed extreme low arousal during very disturbing situations.
During the time spent in jail, he somehow made a conscious decision to except the dysfunction of his actions. He then began taking a medication known as Effexor that decreases the re-uptake of serotonin, and is usually prescribed to depressed patients. Even though he was not diagnosed with depression, he claims the medication has been an incredible help to over coming certain symptoms of the disorder. It has decreased his impulsivity, severe temper, and aggression incredibly. He has reformed his way of thinking, treating others, and living life. He is now socially normal can hold a job, and has productive relationships.
From the understanding of antisocial personality disorder so far it seems to be primarily influenced by genetic and environmental causes. The various extremities of the influences highly determine if the third influence, which we will call the I-function, can save the person from the disorder. The genetic, is the most influential and permanent factor, while environment factors run a close second in importance during the development of the disorders. Finally, the I-function demonstrating every human's innate differences is influential if the other two factors are not extreme beyond repair.
If the person is so genetically prone to developing the disorders, with no biological capacity to understand or feel guilt, anxiety, or compassion, then there is little hope that drugs, or any amount of therapy will make the person normal or even safe to live among society. There is also little hope of the brain willing itself to heal if it cannot understand the problem. If there is genetic hope, but the person has consistent negative psychosocial experience due to extremely antisocial environments, then the person will probably not have much hope of overcoming the disorder, but probably more than the former example. I believe the unique I-function, and other differences in the brain that make one different, can possibly bring about determination, a conscious effort to overcome the disorder and predisposition's of genetics and environment influence. However, in cases such as conduct and antisocial personality disorder, the extremities of the other two contributing factors are key to the influence of the I-function.
In order to decrease the chance of a child with conduct disorder or a predisposition for personality disorders from developing antisocial disorder later in life, it is imperative that interventions be made to improve the quality of family functioning and reduce dysfunctional behavior. In order for the child to overcome genetic predisposition's and to learn to behave socially and successfully, the child must be set in a nurturing psychosocial environment and be given any medications that increase that child's ability to develop and function normally. Humans do have a degree of free choice because we are all genetically unique, but chances of escaping the disorders will increase with increased psychosocial and medical help.
The person I referred to earlier had neither early diagnosis of conduct disorder and refused medication for the treatment ADHD. He grew up in a environment that increased the chances of developing antisocial disorder and then did develop the disorder. He showed many symptoms of biological abnormalities. However, somehow he willed himself to change his outlook and began taking the initiative to heal himself. Through these attempts he has been successful at obtaining normalcy. I have learned that some brains have the capacity to heal themselves, but I still do not know what determines which brains make a conscious and unconscious effort to help themselves. This suggests that personal choice has a significant influence on one's ability to correct personality disorders. Along with psychosocial and medical help, these chances can only increase.
The further implications of the brain's ability to overcome genetic and environmental predispositions to disorders are much more important than the scope of this paper. This ability reinforces the idea that even though brain is behavior, brain is also uniquely powerful and creative. The man with antisocial personality disorder had a brain with the ability to overcome all it was accustomed to, in order to help itself adapt and survive.
1)"ADHD" , ADHD comorbidity with conduct and antisocial personality disorder
2)"Antecedents of Personality Disorders in Young Adults.", symptoms of personality disorders
3)"Treatment.", Different treatments for personality disorders
4)
5)"The Neurobiology of Stress and Emotions.", hormone contributors to antisocial personality
6)
7)"Family Functioning and Peer Affiliation in Children of Fathers With Antisocial Personality Disorder and Substance Dependence: Associations With Problem Behaviors.", environmental factors related to the development of antipersonality disorders
8)" Aggression and Transference in Severe Personality Disorders.", characteristics of antisocial personality disorder
9)Serendip Website, I-function
| Lasting Effects of Pain Name: Peffin Lee Date: 2002-05-17 14:21:24 Link to this Comment: 2121 |
Once upon a typical sunny day, Mary, Susie, and Jackie are jumping rope. Unbeknownst to them, as they chant their rhymes, Mikey and Kenny hide in the bushes planning a surprise attack. Just as Mary's little feet barely lift off the ground, the two boys leap towards the girls and push them into the dirt.
"Ouch!!!" they all scream as everyone hits the dirt.
Mary is up on her feet with her knees skinned and bleeding. A smile slowly crept on her face as she tried to hold back a chuckle.
"What's so funny?" asked Mikey, as everyone turned to look at her. "Aren't you supposed to get mad and chase us around?"
Mary shrugs and looks down at her knees.
"Doesn't that hurt?" asks Jackie.
So what exactly does Mary feel when she hurts her knees?
Pain, of course. But, how exactly does she experience it?
Well, inside Mary's tissues lie nociceptors. Nociceptors are specialized sensory nerves that are activated when there is a potential for danger, such as Mary falling to the ground. The stimulation of nociceptors, first, allows large-diameter, myelinated axons to carry rapidly conducted action potentials. This causes the sensation of a sharp, well-localized, pricking or cutting pain. It is then followed by a diffuse burning or aching pain caused by more slowly propagated action potentials that are carried by smaller, less heavily myelinated axons (1).
The action potentials are generated and conveyed to the central nervous system by way of a difference in electrical potential (2). When the threshold potential difference for each nocicpetor is reached, a signal is sent to the central nervous system. As the signal continues to travel to the spinal cord, the medulla, the thalamus, and then the cerebral cortex, it must pass through a series of gates (3). According to the gate theory of pain, the awareness of pain can only get to the brain by passing through a series of gates (Melzack and Hall, 1965). To open a gate, a group of small neurons that form a "pain pool" must reach their threshold. When it is reached, the signal is allowed to be sent higher.
So as Mary and everyone else who falls to the ground, their body is undergoing this awareness of pain.
Kenny is next to stand up.
"Owww, there's sand in my leg," he whimpered unhappily.
"Hey, you pushed us, and now you're crying?" said Mary defiantly, "You are the biggest crybaby ever!"
"I am not!" shouted Kenny.
"Yea you are, I heard your mom tell my mom yesterday! She said you always cry and scream when you fall down!" said Mary.
"That's not true!" said Kenny, "my mom always said I was a premium baby!"
"Premium baby? What's that?" asks Susie.
Jackie and Mary giggle.
"What's so funny?" asks Kenny.
Mikey takes Kenny's arm. "Let's just go home Kenny."
REWIRING OF THE NERVOUS SYSTEM
Up until the mid-1980s, popular belief was that babies did not experience pain. Even the International Association for the Study of Pain (IASP) defined pain in two criteria: "(a) it insists on verbal expression as the only authentic source of evidence for establishing any painful experience, and (b) it suggests that the experience of pain is learned from injuries in early life". This definition excluded non-linguistic beings, thus allowing physicians to perform surgery on infants without anesthesia for many years.
But, recent research shows that infants respond to pain differently than adults in three aspects (6). First, an infant's spinal sensory nerve cells are more excitable than adult's. This means that a harmful stimulus causes greater harm and it's effects last for a longer period of time. Secondly, the individual sensory nerve cells in infants are connected to larger areas of skin. Thus, when they are stimulated, it is hard to determine where exactly the nerve cell effects because a larger area of skin is affected. And finally, infants cannot distinguish between harmful stimulus and light touch. Their body produces the same reflex action to both stimuli.
These differences in processing pain has led to studies that have found pain experienced by newborns may have lasting effects. One such groundbreaking study led by neuroscientist M.A. Ruda of the National Institute of Dental and Craniofacial Research (NIDCR) at the National Institutes of Health (NIH) reported that painful stimuli delivered to rat pups shortly after birth permanently rewired the spinal cord circuits that respond to pain (4). Ruda and her colleagues began with two groups of rat pups. The first group was injected with an irritant (Freud's adjuvant) into the left hind paw when they were one day old, equivalent to that of a 24 week neonate in humans. The second group was injected at fourteen days old, equivalent to that of adolescence in humans. Both groups immediately reacted with shaking, licking of the paw, and occasional vocalization, shortly resulting in skin lesions persisting for 5 to 7 days.
About eight to twelve weeks later, the rat pups', now adults, spinal cords were stained with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to determine the pattern of nerve fibers. The dye stained the pain-sensitive axons and indicated any appearance of new axons formed. Ruda and her colleagues discovered that the rat pups, who received the injection at one day old, had an increase of about 25% more stained axons (5) in the left side of the dorsal horn, corresponding to the side injected. The dorsal horn is the layered structure in the spinal cord that propels pain signals up to the brain. In addition, several spinal segments exhibited an increase in density of axons, specifically the caudal segments.
The increase in pain-sensitive axons can be seen in the adult rats' behavioral response to pain. Once again, the adult rats were injected with an irritant in the left hind paw, then the paw was subjected to heat. The adult rats who had been injected at one day old were much quicker to withdraw their paw than normal rats. These results coincide with the mechanisms of pain. The increased number of activated axons, result in a more intense pain. This accounts for the lower pain threshold experienced by adult rats who had been injected.
The increased sensitivity of pain was only witnessed during a distinct developmental window (5) if the injection was given at one day old to three days old, more neurons are formed. But, as the rat pup increases in age to day fourteen, the physiological and behavioral changes match that of untreated rat pups.
Therefore according to this study, abnormal stimulation during a distinct developmental window can cause changes in the pain circuits. This leads researchers to study the effects of pain on premature infants because they are still considered to be undergoing basic brain development.
FINAL THOUGHTS
The objective of the class was to present "prospects and problems of trying to understand behavior in terms of nervous system function "(7). The study of pain is one type of evidence that can support the belief that brain = behavior. This evidence fits under the category of altering of the nervous system causes variation in behavior. Obviously this can be seen in the long-term effects of rewiring the nervous system, or rather producing more pain-sensitive axons. People who experience such stresses at a critical developmental window, as adults, will be more likely to have problems such as chronic pain and increased pain sensitivity.
The study of pain also leads to a more broad idea that the environment affects the nervous system, thus affecting behavior. The nervous system is not mature at birth. It is still growing and learning, as is the individual. It only makes sense to assume that during development of the nervous system, it will undergo many changes, thereby also causing changes in behavior
2) Information on Pain
4) Ruda, M.A., Ling, Q., Hohmann, A.G., Peng, Y.B., and Tachibana, T. "Althered nociceptive neuronal Circuits After Neonatal Peripheral Inflammation," Science, vol. 289, 28 July 2000, 628-630.
5) Helmuth, Laura. "Neuroscience: Early Insult Rewires Pain Circuits," Science, vol. 289, 28 July 2000, 521-522.
| An Exploration of Creative Traits and Behaviors Name: Melissa Ho Date: 2002-05-17 14:51:28 Link to this Comment: 2122 |
Throughout the years there has been a horrible stereotype that creative people are manic
depressive. Yes, some creative geniuses have had a variety of mental illnesses but, that is not to say that one must be mentally ill in order to be considered creative. Creativity is not the result of a mental illness and, can be found within every human being. There have been studies done showing that creativity can be taught and even enhanced. An individuals subconscious minds and the way in which, it processes information can have an effect on the way that an individual is creative. Strengthing and exercising different parts of the brain can affect creativity, as well. Also, there are different states of mind that can contribute to or hinder the creative process.
How is creativity formed? Creativity is the result of input given to the brain throughout
our lives. Input such as, visual stimulation and contact with other individuals. Anything having to do with the five senses can be considered input. After our brains receive this input it is processed and, in laymen's terms assigned to its designated area and filed way. When we sleep the input that has been filed away is brought to the surface during REM sleep. This sleep cycle is when individuals dream. The information that is brought to the surface, many times is disordered and hectic. Our brain is most creatively active during this sleep cycle. When an individual awakes they may do something creative in response to the information that their brain has processed while asleep.
Does that mean that everyone is creative? No, it does not. Many individuals in our
society have a tendency to drone their way through their lives. These individuals make everyday the same but, there is hope for them yet. Everyone has the potential to be creative. There are even things that an individual can do to enhance their creativity. For every positive there is a negative and, there are also acts and ideals that can hinder an individuals creativity.
What are some of the obstacles that one must overcome in order to be creative? There
are many and, the most common is not believing oneself to be creative. If a person believes themselves to be lacking in creativity they will not pursue creative ways of expressing themselves. Also, if an individual is too busy or involved in a problem they will not be able to find time to focus on a creative endeavor. Individuals that do not allow enough time for relaxation usually will be stressed and their minds will not be able to think creatively because it will be absorbed in the problem at hand.
There are further aspects that hinder creativity within a person that are related to
self-esteem. Examples of such issues are a "fear of criticism and lack of confidence." Self-criticism is another major issue that hinders creativity. If an individual is always telling themselves that others will not like something and that it isn't good enough that is what the result will be. Whenever they present their creative endeavor they will not present it with confidence and enthusiasm. We effect how others respond to us by our demeanor because we are a form of input to them at the time that we are in contact with them and, therefore the individual that has presented the creative work will receive a response that demonstrates a lack of enthusiasm and belief in the project. People must believe in themselves and their ideas in order for others to believe in them. After the individual has received the negative response there is a good chance that they will not pursue it or further creative endeavors of that sort.
Other actions that limit creative actions are routines and, beliefs. Routines have a
tendency to block new creative input. At the time of performing the routine a person is not being exposed to new things and ideas. Creativity is not just for when an individual is creating something. Creativity like many other things in our life is a use it or lose it trait. I realize that the latter of the two seems a bit obscure and contradictory to my earlier statements but, it is not. Having a belief that is too strong limits an individuals "response options" and the way that they receive and process information. Furthermore, an individual may 'filter out' information that is contrary to a belief that is too strong. Tendencies such as a daily routine or too strong of a belief may block an individuals creative potential.
What actions can enhance creativity? The most important action that one can take is to
avoid all aspects which hinder creativity. So, an individual should attempt to add spice to their daily routine even if it is something as simple as brushing their teeth before they take a shower, rather than after. The individual in question could even get daring and brush their teeth while in the shower. I doubt that this action will stimulate the greatest creative creation known to man but, there is only one way to find out. The best piece of advice that I have come in contact with is to "Start small and think big." Through the use of this advice one may target small aspects of their life such as brushing their teeth and taking a shower in order to begin a larger change within their lives, such as an increase in creative output.
More regimented ways of enhancing creativity include but, are not limited to: focusing on
a problem for approximately one half hour before going to bed. The individual should not let the issue come with them to bed. They should stop pondering it whenever they lay down. When the individual wakes in the morning they should rise one half hour before usual and, sit in a quiet space with a notepad and pen documenting all thoughts that enter their mind. The individual should not be critical of their thoughts or even try to sort them out at this point, only document them. The morning seems to be the best time for creative thinking because as human beings we are fresh and, our minds are not cluttered with the trials and tribulations of the day. Also studies have shown that an individual's brain works at a faster rate in the morning, after a good nights sleep, than in the evening. Another, activity that enhances creativity is to write the word happiness in the middle of a sheet of paper and draw lines extending outward from it. At the end of each of these lines an individual should place what happiness means to them. This exercise will stimulate creativity because human beings have an associative memory. This means that one idea may stimulate many others that are in some way related to it. Individuals may continue this exercise with the use of other words and use pictures rather than words as associations to it. A website that may be useful to individuals interested in further exploration of actions stimulating creativity is http://www.athens.net/~merrybeing/CC/index.html. This website offers 52 weekly activities to enhance creativity. The one that I found to be the most compelling is number 44, "Artists and your Art"(Black). In this exercise an individual is asked to find a book that has many pictures on their favorite artist. The individual is asked to flip through the book at first only to enjoy the photos. Then, the individual is asked to mark the pictures that they enjoy the most and, narrow them down to three. The individual is asked to make the assumption that the artist was trying to give them clues about the current challenges and problems through these works. they are then asked to write down what comes to mind; such as s the color, shapes and images that are in the art. Lastly the individual is asked to write down what they discovered through the relation of their problems to the art work. I have recommended it to several people all of whom have felt that it was beneficial to them. The most beneficial thing that an individual can do to enhance their creativity is to take care of themselves. The most known ways of taking care of the human body is a healthy diet consisting of all of the five food groups, exercise, and the proper amount of sleep.
What behaviors are associated with creative individuals and why? There are many
stereotypes associated with creative individuals that are incorrect. The first that I would like to address is that of mental illness. The reason that this association is made is because all creative individuals have a unique perspective on life and fascinating lifestyles. The reason that creative individuals have such interesting lives is, as I have stated previously, because creativity is not just used within creative works but, in everyday life. One such example is that of Salvador Dali. Dali throughout his life was fascinated death and, had a insatiable craving for sex, money and, fame. These indeed are abnormal behaviors but, then again what is normal. Dali's cravings for sex, money, and, fame are likely related to the feeling experienced when endorphins are released. Endorphins are released when in a state of inspiration. Dali most likely enjoyed the his feelings of inspiration so much that subconsciously he sought out further instant gratification through sex, money and, fame. Many other artists behaviors can be related to this desire for instant gratification found at a time of inspiration. Manic Depressive disorder is also, associated with creativity. I agree with Jamison in her statement that most creative individuals are not emotionally unstable, and emotionally unstable individuals are not necessarily creative.
Traits associated with creative behavior that are more likely are: independence,
self-confidence, enthusiasm, spontaneity, curiosity, idealism, and a wide variety of interests. Furthermore many creative people are risk-takers, enjoy adventure, are high in energy, have a variety of interests and, are somewhat childlike in their playful nature, as described by Robert Alan Black, Ph.D. Creative people have a "carefully and clearly defined set of goals" (Nightingale).
What makes someone that is creative a creative genius? In the development of my
research I found a very interesting and proven test to see if a person is a genius. This test lists 20 characteristics and asks you to evaluate yourself using a scale of 0 to 5. The larger the number that you receive the more apt to being a genius you are. The twenty characteristics that he lists are "Vision, Desire, Faith, Commitment, Planning, Persistence, Learning from mistakes, Subject Knowledge, Mental Literacy, Imagination, Positive Attitude, Auto-Suggestion, Intuition, Mastermind Group (Real), Mastermind Group (Internal), Truth/Honesty, Facing Fears/Courage, Creativity/Flexibility, Love of the Task, Energy (Physical/Sensual/Sexual)." These are indeed a good list of traits to posses and may make an individual apt to do a better job on an assignment but, I have always felt that ambiguous tests such as this tell us only things that we already know about ourselves. This test is a good basis for self-improvement and in my opinion should be regarded as nothing more. There are other more regimented tests available. Some of these tests test for creativity.
Many of them are given to children in elementary school. I personally have never taken
one of these because of my mothers influence and never will. The closest thing to this that I have experienced are the SATs. The reasoning behind my choice to not take these tests is that these tests do nothing good for an individual, and the results are many times quite questionable. First of all if a person scores low especially at a young age they are apt to believe that they are not intelligent. The effect of such a belief will likely, hinder an individuals work drive as well as belief in themselves and their actions. Therefore this individual may not meet their potential or, challenge themselves. The opposite diagnosis from one of these tests is negative as well. If the
individual finds that they are an assumed genius they most likely will not realize that this is merely the potential of being a genius. These individuals will have a similar effect except it will be for different reasons. The reasoning that this individual may experience is that since they are a genius they do not need to try.
I chose to do send a survey via e-mail to 50 of my friends as another form of research.
the survey that was sent is as follows.
As a research document this survey may be filed as an attachment to my final paper and,
displayed on http://serendipstudio.org/bb/neuro/neuro02/ under student web papers. All of your names will be left anonymous. Thank you, Melissa Hoban.
1. What do you feel is your best creative outlet?
2. Where do you feel that you are best able to work creatively?
3. Do you have a favorite creative work of someone other than yourself?
4. If so what is it and why?
5. Do you have a favorite creative work that you have created?
6. If so give a brief description (if it is a writing or something that is easily attached please do so) and, what about it appeals to you?
7. I personally find dance and poetry to be my creative outlets and when creating a piece
sometimes have a feeling of inspiration that through my research has been labeled by many as a spiritualized or dream-like state. Have you experience something similar? and if so would you describe the feeling with the same terms? if not how would you describe it?
8. In my research I have found that many people believe that there are multiple ways of
enhancing creativity. The most commonly known are journals, healthy diet, exercise, new
experiences every day, and relaxation but, there are also many more that are quite specific. Have you ever heard of this idea? How familiar are you with it? Have you ever used any of the tactics listed or otherwise and if so which ones?
9. Following is a list of twenty characteristics devised by Tony Buzan. Please rate yourself by assigning a score of 0 to 5 for each of the qualities.
Vision Desire
Faith Commitment
Planning Persistence
Learning from mistakes Subject Knowledge
Mental Literacy Imagination
My finding were that there are a variety of creative interests that I had not even considered, such as, political writings, embroidery and, doing ones hair. Most of the individuals surveyed felt that they worked best in the morning and by themselves with no distractions. I had not heard of the majority of creative work done by artists other than themselves. Two examples of the artists that I am unfamiliar with and plan to do research on, for my own enjoyment, are the works of Liselotte Erikson and, Frank Zappa. Most of the individuals did not have a favorite creative work of their own. Three-quarters of the surveys said that they had felt the feeling of inspiration
and, had a million different ways to describe it. About 1/10 those surveyed were familiar with the idea that there are things that a person can do in order to enhance their creativity but, those that were not familiar with this idea admitted to having practiced most of the examples given. I have chosen to disregard the last question because many people opted not to answer it and, even many of those that did felt very questionable about its results.
FOR WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY
1)Creativity Challenge Formula,
3) Treisman, A. Features and objects in visual processing. November, 1986.
4) Freeman, W.J. The physiology of perception. February, 1992.
5) Ewert, J.-P. The neural basis of visually guided behavior. March, 1974.
6) Routenberg, A. The reward system of the brain. November, 1978.
7) A.R. Damasio, Descartes' Error, 1994
8) D.C. Dennet, Consciousness Explained, 1991
9) K.R. Jamison, Touched with Fire: Manic Depressive Illness and the Artistic Temperment, 1996
10) V.S. Ramachandran and S. Blakeslee, Phantoms in the Brain: Proving the Mysteries of the Human Mind, 1998
| The consequences of epilepsy Name: Sarah Eber Date: 2002-05-17 15:27:00 Link to this Comment: 2123 |
Epilepsy: Any of various neurological disorders characterized by sudden recurring attacks of motor, sensory, or psychic malfunction with or without loss of consciousness or convulsive seizures (1).
Is epilepsy a purely physical phenomenon? The question is a complicated one. Put simply, the answer should be yes. The psychological trauma sometimes caused by the seizures, however, makes the answer more complex, along with a more troubling trend. In years past epileptics were classed among the mentally ill, and received the same maltreatment as did that unfortunate group of people. Before that they were perceived as having been possessed by evil spirits. But now, in the modern world, we are free of those ignorant superstitions. Aren't we?
Scientifically, epilepsy is the term under which many seizure disorders are grouped. There are four basic types of seizures: petit mal, tonic-clonic (grand mal), simple partial, and complex partial (2). While petit mal seizures consist merely of a short period of immobility and blank staring, occasionally accompanied by brief loss of awareness, tonic-clonic seizures are much more dramatic (2). Also called grand mal seizures, they involve whole-body muscle contractions, loss of consciousness, temporary cessation of breathing, and involuntary biting of the tongue or cheek (2). The simple and complex partial seizures are calmer; the simple includes muscle contractions of a specific part, abnormal sensations, nausea, sweating, flushed skin, and dilated pupils. The complex partial seizure consists of all these symptoms as well as automatism (repeated motions), inappropriate emotions, changes in personality, altered consciousness, and hallucinations of taste or smell (2).
The causes of epilepsy are varied, and one seizure alone doth not an epileptic make. It is only after a repeated pattern of seizures that epilepsy is diagnosed (3). Epilepsy has multiple possible causes (2). Infections such as encephalitis or meningitis, or even complications from AIDS, may trigger seizures, although these are generally more easily treated (2). Developmental problems or genetic defects present at birth trigger seizures as early on in life as infancy (2). Some problems are inherent to the brain, such as degenerative diseases like Alzheimer's, brain injuries, tumors, or brain lesions disrupting normal activity of neurons (2). Others, such as stroke or metabolic problems such as diabetes, have a more indirect effect on the brain's functions (2). Still other epileptics are diagnosed with the mysterious "idiopathic;" causes unknown (2).
Modern medications are quite effective in controlling seizures, and most patients can gain reasonable control over their seizures, or even become seizure-free. Old standbys such as Carbatrol and Phenobarbital are being bolstered by new drugs: Lamictal, Neurontin, Zonegran (4). There are side effects such as drowsiness, dizziness, et cetera, as there are with many medications. (2). The most daunting side effect is perhaps that the doubled risk of neural tube defects in children whose mothers were taking Carbatrol or Depakote during pregnancy (5). However, the incidence of this occurring is only 6-8%, and with careful management a healthy child can easily be born to an epileptic mother. On the whole, then, the phenomenon is scientifically understood and scientifically managed. The situation seems to be under control: diagnose with epilepsy, treat with medications, and that's it. It's a physical solution for a purely physical problem.
Unfortunately, the reality is far different. Many of the old superstitions still stand against those with epilepsy, especially in developing nations, making it impossible for them to live normal lives. In Cameroon, Nepal, and some parts of rural India, those suffering from epilepsy are thought to be possessed by evil spirits and are treated accordingly (6). While some of their "treatments" are merely humiliating, others include beating or starving (6). In some parts of Central America and India during the last five years, of the many suffering patients in psychiatric hospitals – some tied to beds, some without any psychological treatment whatsoever – one-third were committed solely because they had epilepsy (7). With proper medication, many would have been able to live normal lives, according to the medical workers who examined them (7). The United States has not been blameless either, although certainly it has behaved less violently. Until the 1970s, it was perfectly legal to deny epileptics access to public buildings (6). In the UK at that time, a law forbidding those with epilepsy to marry was finally repealed (6). Up until 1980, various states in America also forbade epileptics to marry (6).
When it comes to employment, those whose seizures are controlled by medication are not considered disabled under the Americans with Disabilities Act (8). However, this isn't always completely accurate. Depending on the severity of the seizures, the medication taken can have debilitating effects upon the patient, such as concentration or memory problems, while for some increased need for sleep decreases their productivity (9). Another problem that presents itself is that of transportation: depending on the laws of the state in which the person lives, there may be laws preventing them from obtaining a driver's license due to their epilepsy (9). It is unknown whether it is due to these factors or to actual job discrimination – or a combination of the two – that has such a drastic effect on the employment rate of epileptics. Exact data differs; one study claims that in Germany, Italy, and the United States, 15-20% of people with epilepsy are unemployed and 20% will retire early, while another declares that the unemployment rate for American epileptics is 25% (8). Economic conditions for epileptics in developing countries are so bad that obtaining medication is difficult and can lead to further health problems (10).
This problem, therefore, is not so simply cured. In some contexts, those who cannot control their seizures suffer from more than just the medical consequences. This phenomenon is similar to those who have contracted the AIDS virus: the reaction of their community may be as devastating, or even more so, than the realization of the disease itself. This effect, combined with occasional unexpected effects of medication, lead to a depressive state in many people (9). This problem is magnified by the emotional havoc that epilepsy can wreak upon the brain. Besides the usual turmoil caused by any chronic illness, the "random electricity" of wayward neurons can trigger unexpected and inappropriate emotions before and during some types of seizures (9). Another symptom, sometimes manifesting in simple partial seizures, is that of hallucinations, which if unexpected can lead the patient to worry about their mental health (11). These stresses, combined with anxiety about when the next seizure will occur, can lead to severe depression. The suicide rate for those with epilepsy is much higher than that of the general population, accounting for 7% of deaths, five times the national rate for those who do not have epilepsy (12).
Another problem that presents itself is the phenomenon known as SUDEP: Sudden Unexplained Death in Epilepsy (12). Most patients had a history of grand mal seizures and were found prone in bed, but the cause of death is still mysterious (12). Epilepsy, however, has an unnerving link to death: 42% of deaths in epileptics have been because of their epilepsy (12). Accidents – caused when a seizure occurred while a person was doing something dangerous – made up 8% of deaths for people with epilepsy (12). This phenomenon only serves to add to the stress put on a person diagnosed with epilepsy.
So is epilepsy a fairly simple problem, restricted to the physical? Like many chronic illnesses, the answer proves to be no. A diagnosis of epilepsy, just like a diagnosis of AIDS or cancer, brings along with it a parade of side effects, social problems, and mysteries that are impossible to ignore. The brain is still largely unknown to us, and thus treatments for epilepsy are still imprecise, although they are improving rapidly. More worrying is the fact that, for many, epilepsy is still a mysterious ailment, to be treated by starvation or beatings, or, slightly more moderately, by job discrimination and ostracization. While these are social problems rather than neurological ones, the fact remains that it will be impossible to truly find a solution to epilepsy without both educating of the ignorant and further investigating the mysteries of the brain.
1)Dictionary.com, the entry for epilepsy in a dictionary website
Medline, an entry in a medical encyclopedia regarding epilepsy
3)Medline, an entry in a medical encyclopedia regarding seizures
4)The Epilepsy Foundation, a page charting different epilepsy medications
5)The Epilepsy Foundation, a page answering questions about pregnancy as related to epilepsy
6)The World Health Organization, an information page of the World Health Organization website
7) Solving Mental Health Problems Cpt. 3. World Health Organization 2001.
8)The Epilepsy Foundation, a page discussing the civil rights arguments put forth by various groups of people with epilepsy
9)The Epilepsy Foundation, a page dealing with the secondary problems caused by epilepsy
10)The World Health Organization, a webpage detailing the struggles of people with epilepsy in developing countries
11)The Epilepsy Foundation, a page discussing the impact of epilepsy on the mental health of the patient in both a short-term and long-term context
12)The Epilepsy Foundation, an article discussing epilepsy as a cause of death
| Is There a "Criminal" Brain? Name: Kathryn Ro Date: 2002-05-17 15:56:41 Link to this Comment: 2124 |
Everyone's brain is made up slightly differently, which is good because it provides individual variation. These biological differences can greatly influence how the individual behaves. For example, the frog brain and the human brain look very different structurally and the behaviors exhibited by a frog and a human are very different. Differences in brain structure are not limited to different species, there can be differences within the same species. Wildcats and domestic cats are a good example of this. The visual system of the wild cat and the domestic cat differ in substantial ways. Domestic cats have fewer ganglion cells in the retina and have a smaller lateral geniculate nucleus, which is a part of the thalamus (9). In addition, they have fewer total neurons involved in the visual system of the brain, however the sizes of neurons do not change between the wild and domestic cats (9). It may be possible to explain these changes by looking at "domestication". Through cohabitation with humans, different reproductive and food-search patterns, this process has caused significant changes in the behavior of cats (9). Wildcats are more aggressive and independent than domestic cats, which makes sense since these characteristics are more beneficial to their survival.
Structural brain differences also occur in humans. One significant behavior difference is between men and women. Men tend to be more sexually aggressive and aroused more often. Women are generally more fluent verbally. The suprachiasmatic nucleus is usually about 2.5 larger in the male brain than the female brain and there is a part in the amygdala that is also larger (9). The suprachiasmatic nucleus affects sexual behavior and larger amounts of testosterone cause it to be larger. In females, the corpus callosum and the anterior commissure are larger (9). Both of these structures are responsible for communication between the two hemispheres in the brain. The better communication between the two sides leads to better verbal fluency. These examples show how small differences in the brain can greatly affect human behavior. This means that it is possible that criminals have differences in their brains which cause them to act in socially unacceptable ways.
In order to understand why people act in antisocial ways, one needs to pinpoint which area of the brain controls social behavior. The prefrontal cortex has been thought to have something to do with control of social behavior ever since Phineas Gage's famous accident in 1848 (1). Phineas Gage was a construction foreman who as a result of demolition accident had a tamping rod go into his cheek, through the front part of his brain and out through the top of his head again. He remained conscious through all of this and retained his intelligence and memory. However, the damage to his prefrontal cortex caused Gage's personality to change. He became impulsive, selfish and aggressive, which greatly contrasted the gentle, level-headed personality he possessed before the accident.
The characteristics that Gage exhibited after his accident closely resemble some of the symptoms involved with Antisocial Personality Disorder (1). Some of the symptoms included in the DSM-VI are apathy towards others, a disregard for rights of others, a sense of entitlement, unremorseful, unconscienceable, blameful to others, manipulative, and affectively cold (7). About a 25% of the US inmate population have this disorder (6). A 1992 FBI report said that almost half of the killers of law enforcement officers fit the criteria for antisocial personality disorder (6).
The prefrontal cortex of men who have antisocial personality disorder (ASPD) has 11% less gray matter (1). PET scans, which measure the uptake of glucose to determine the amount of cell activity, have shown that the prefrontal cortex is less active in those with ASPD (8). In one study, 38 murderers were tested; twelve came from bad backgrounds and 26 from good backgrounds. The subjects from good backgrounds showed 5.7% less activity in the medial prefrontal cortex compared to the subjects from bad backgrounds (8). The activity was 14.2% less than the bad background subjects in the right orbital frontal cortex (8).
These results provide a lot of evidence that the brains of those with antisocial personality are different from normal brains. The prefrontal cortex is known to inhibit the limbic system, which is an area of the brain that gives rise to aggressive behavior (8). Adrain Rain describes the prefrontal cortex as an "emergency brake" that prevents people from lashing out in fits of rage (1). The right frontal orbital cortex is involved with fear conditioning, which is the nonconscious process of making an association between socially unacceptable behavior and punishment (8). Fear conditioning is thought to be important in forming the conscience (8). However, since individuals with ASPD seem to lack fear, their emotions often seem blunted. Rain describes it by saying, "While some people have biological systems that make it easy, others have biological systems that make it hard. If you're an individual whose right orbital cortex is not functioning well, you're biologically disadvantaged in developing a conscience (8)."
There have also been many studies done that examine murderer's brains. In one such study, PET scans were again used to determine cell activity in 41 murderers (3). The results showed a lower level of communication between the two hemispheres of the brain. The activity in the corpus callosum, which is the bridge that links the two sides of the brain, was 18% less active than normal (3). This is significant because the left side is usually considered the rational side, and the right side is the irrational side (3). If the bridge that links the two sides isn't very active, then the rational and irrational sides would not be communicating very well. In most people, the left side of the brain has more control, but in murderer's brains neither side rules. The study also showed some evidence that murderer's emotions might be stronger than normal. The PET scans showed increased activity in the thalamus, amygdala, and limbic system by 6% compared to controls (3). All of these areas control basic emotions, such as aggression, sexual desire, and anger, and therefore increased activity in these regions would suggest stronger emotions.
Of course one question that is raised by these differences is whether the brain is different because of genetic reasons or environmental factors. Although the causes of antisocial disorder are unknown, there is some evidence that points to a few possible causes. The first is that it is due to genetics. People who have antisocial fathers are also likely to be antisocial (8). This is also true for people who were not raised by their biological antisocial father. Birth and pregnancy complications also seem to produce ASPD. Fetal Alcohol Syndrome and Heavy Cigarette smoking during pregnancy correlate with conduct disorder (5). Other factors lead exposure and undernourishment (4). It appears that these deficiencies in the child's early developmental stages can create the type of brain damage that leads to ASPD.
The factors that cause these brain differences do not appear to be things that the individual can control. This brings in the question of how accountable are these criminals for their actions. It is fairly clear that the differences in their brains influence how they act, and they could not prevent having these differences, so how much control do they really have over their actions. The reason why these people are punished and held accountable is because people have the power to decide how to act. However there is evidence that suggests that people do not have as much control over their actions as they think. For example, phermones are chemical signals that people emit but are not consciously perceived. The signals can affect how sexually attracted people are to each other yet people do not realize that this is why they are attracted to certain people. This attraction however can affect how this person behaves towards the other person. This feeling of attraction is what provides the motive for how the person responds. However, it is important to point out that the person can respond to this feeling a variety of ways.
It is very likely that criminals may perceive and feel things differently, but it the end it is up to them to decide how to act (1). It may be more difficult for criminals to act in socially responsible ways because their brains cause them to have feelings that contradict these principles, however it can be done. The may brain influence all aspects of behavior, but it doesn't determine behavior. It is important to understand and recognize these differences because it may be able to help prevent crime. If potential criminals are identified and taught how to control their different emotions, it may be possible to prevent hearing about crime everyday on the news.
1)Brain Differences in Antisocials
2)What Lurks Within Murderous Minds?
3)Neural Roots of Murder
4)Crime & Nourishment
5)Prenatal Smoking Linked to Conduct Disorder in Boys
6)Psychopathy and Antisocial Personality Disorder: A Case of Diagnostic Confusion
7)The Psychopath's Brain: Tormented Souls, Diseased Brains
8)Functional Families, Dysfunctional Brains
9)>Different Brains, Different Behaviors
| The Brain as the Primary Sexual Organ Name: Michele Dr Date: 2002-05-28 10:56:00 Link to this Comment: 2135 |
Of all the mysteries of the mind and human behavior, one of the most intriguing may be the concept of sexual drive and the enigma of human orgasm. Since the evolution of humans and primates and presumably far before that time, sexual drive and the desire for sexual release have been an integral part in propagation of species. In an attempt to understand the causes and effects of sexual desire as a means for procreation of a species, it is indispensable to explore the neurobiology of sexual arousal and the brain's reward system, which operates by neurologically pleasurable remuneration in exchange for basic survival and procreative acts on the part of the organism.
The "reward system" is a term given to the brain's technique for subconscious survival of an organism. Simple activities that are necessary for survival such as eating, drinking, or sex, (or even those not necessary, such as drug use/addiction) are rewarded by the brain by the release of pleasure inducing neurotransmitters and neuropeptides. The brain is trained to associate these activities with pleasant feelings, in order to induce the organism to engage in necessary life activities without thought. The reward system is what drives reproduction, through sexual desire and ultimate gratification. Although the climax of the human reproductive act has a multitude of physical results, the trip there is a series of pathways, chemicals, and sensations through the body and most interestingly the brain.
Sexual desire may stem from many different factors - physical or visual stimuli, olfactory stimuli (pheromones or other aphrodisiacs), and most importantly by a complicated neuronal circuitry orchestrating sexual desire from the activity of neurotransmitters, neuropeptides, and central nervous system activity, but also by endocrine factors. While in itself having little to do with neurobiology, the endocrine component of desire fundamentally supports the neurobiological element. Studies relating testosterone, progesterone, and cortisol levels with sexual desire in men and women have been pursued, but results have been somewhat inconsistent, and studies of estrogen levels have shown that estrogen has little effect on the sex drive. However, prolactin, a pituitary hormone stimulating milk production, may have an effect on hypothalamic dopaminergic dysregulation and is known to have inhibitory effects on sexual interest in both males and females (1).
Although experiments so far haven't been very conclusive about the precise mechanisms of prolactin's sexual effects, its effects on dopaminergic regulation are most likely decreasing the dopamine levels if a decrease in interest is observed. This is simply because increases in dopamine levels have been strongly associated with increased sexual arousal, as a function of the reward system. Copulatory behaviors, once begun, were not affected by the dopamine drought, as showed in an experiment with male rats which employed a dopamine antagonist. The initiation of sexual behavior was greatly delayed, as a result of the failure of the reward system to offer any initiative for the rats to begin mating (2). Antipsychotic and various other medications typically lower the dopamine levels in the brain and impair sexual desire, and delay or sometimes entirely inhibit ability to arrive at orgasm. In addition, cocaine works by amplifying dopamine activity, and cocaine is believed to enhance sexual enjoyment. But, in controlled studies of primates, any administration of cocaine higher than a very small dose began to decrease sexual interest (3).
The neurotransmitter serotonin is a tricky one, having an assortment of different subtypes. In general, selective serotonin reuptake inhibitors (SSRIs) prescribed as antidepressants reduce libido, but some serotonin subtypes instigate sexual behaviors and interests, while other subtypes repress them. For example, while activation of a serotonin-2 receptor inhibits sexual desire, the activation of the serotonin-1A receptor has been proven to provoke excitement by experiments showing that sexual gratification is more easily and quickly obtained with its activation (1). The marketing of various SSRIs relies often on the level of sexual side effects that can be expected, which is where the catecholamine neurotransmitter norepinephrine comes onto the scene. Norepinephrine is known to exist naturally at twelve times its normal level in men during orgasm, and has lately been appearing in new antidepressant medications because of its disinclination to suppress sexual function (1). Lastly, a molecule worth mentioning is nitric oxide, which acts as the principle neurotransmitter negotiating blood flow during a sexual experience (4).
Although best known for its role in maternal behaviors, the neuropeptide hormone oxytocin plays an integral part in both sexual interest and orgasm in humans. Oxytocin is secreted by the hypothalamus and stored in the posterior pituitary, until summoned into the bloodstream by maternal necessity or sexual arousal. Oxytocin is presumed to bolster the experience of sexual gratification, with the ventromedial hypothalamus containing high levels of oxytocin receptors and being well known for its relation to sexual behavior (2). Oxytocin levels increase with the first stages of sexual arousal, and continue to increase along with the self-reported level of arousal by the patient. The levels increase dramatically during sexual satiety in males and even more notably in females, with multi-orgasmic females reaching yet higher levels upon successive orgasms (5). In addition, the more intense the orgasm, the higher the oxytocin levels found (2). Oxytocin levels are also unusually high after orgasm (2), fostering affectionate behavior. The association of oxytocin with maternal and loving sexual behaviors along with the commonly higher levels of the neuropeptide found in females seem to make sense of the generalization that females are more affectionate, in both maternal and sexual situations.
The independent influences of these various neuroendocrine and neurotransmitter factors on sexual arousal and the ensuing release are intriguing in their own right, but they interact with the CNS and each other to control the entire sexual experience. If testosterone levels rise in the medial preoptic area of the hypothalamus, nitric oxide production is induced in tissues below the belt. When nitric oxide gets into the bloodstream and flows back up to the brain, it provokes a massive dopamine release (1), resulting in the increasingly pleasurable feeling of rising sexual arousal.
Likewise, if nitric oxide flow to the brain is interrupted, the dopamine release does not occur and sexual arousal makes no progress. By the same token, prolactin increase has a tendency to decrease dopamine production (1), and when the dopamine flood is disrupted, the libido suffers. From these back and forth neurological and endocrine interactions, it's evident that the physiological aspects of sexual arousal rely on the correlation with neurological activity.
Additionally responsible in the interdependence are the sections of the brain and CNS accountable for certain sexual excitement. In the hypothalamus, the medial preoptic area has connections to the limbic system, which is associated with emotion and homeostasis, and quite possibly a component of the elusive I-function. Damages to this area tend to seriously impair male sexual behavior, ability to perform and even identify a possible sexual conquest. In females, damage to this area causes them to avoid male partners altogether (1). The idea of self-identity is a strong factor in selection and recognition of a desired sexual partner, dictating what one sees themselves as, and consequently what one might fancy in a sexual partner. It's possible that the I-function may be so distorted by damage to this area that the subject might avoid a normally acceptable sexual partner.
According to Paul Milgram of the University of Toronto, brain stem and spinal elements operate with a central pattern generator to control sexual response, using ascending pathways that convey sensory information and descending pathways that signal hormonal conditions (2). The amygdala is also crucial in sexual behavior, and displayed its power through several experiments. In one, the entire amygdala was removed from primate brains, resulting in hypersexual to the point of "inappropriate" sexual behavior (2). However, in hamsters, copulatory behavior decreases or disappears entirely with the removal of the medial amygdala (2). The former experiment seems to imply that the neurons of the amygdala may be largely inhibitory rather than excitatory in sexual response. But the latter experiment contradicts this possible presumption, suggesting a potential variability between species.
In the forebrain, experiments have been conducted that apply electrical stimulation to elicit sexual response. Electrical stimulation to the hippocampus produced erections in men, but that is merely a physical response and does not result in sexual satiety or orgasm. However, stimulation to the nucleus accumbens septi, in the anterior region of the forebrain, can cause repeated orgasmic effects in the individual. At Tulane University Medical School in 1972, Dr. Robert G. Heath put depth electrodes into the brains of human mental patients for the first time. Injecting acetylcholine into the septal area gave the patient fantastic enjoyment, both in mood and sexual satisfaction, in certain cases multiple orgasms, the longest of which continued to orgasm for half an hour. The electroencephalogram Heath recorded following the acetylcholine injection showed violent brain activity for the entire thirty minutes, mirroring the type of EEG activity seen in an epileptic seizure (6).
Orgasm accompanying epileptic neural activity is little surprise, because the two are not entirely unrelated. Human epileptic attacks can be preceded by an 'aura' which is sometimes sexually stimulating (2). There was a case of a woman who suffered--if that word can be used in this context--from spontaneous orgasms, or "an internal, ascending feeling indistinguishable from an orgasm" (7). She did not seek medical help until one of the sensations sent her into spasms and unconsciousness. She was found to have a case of epilepsy as a result of tissue damage in the right temporal lobe, where epileptic problems and sexual stimulation both happen to register in women. There have been twenty previous cases of women with an affliction such as this one, brought on by a form of epilepsy, but no similar cases in men (7). This and other male/female orgasmic disparities have led some neurobiologists to speculate that the female orgasm may have evolved differently from the male orgasm, but there is still significant argument that male and female orgasms are the same.
However, in male and female brains alike, the amygdala is related to both seizures and sexual experiences, and contributes heavily to the psychological component of sexual attraction and appetite. The amygdala and the hippocampus work together to produce sexual, dreamlike, religious, etc. types of dreams or hallucinations. The amygdala also works with the hypothalamus, which controls hormonal aspects, to generate the experience of orgasm through enkephalin and endorphin release. With the temporal lobe and hippocampus together, the amygdala can intensify orgasm to be an experience of a "mystical" or "religious" nature, through the generation of rapture, euphoria, and fierce sexual arousal (9). With this function, the hippocampus is thought to have the ability to allow an individual to visualize themselves (9). This type of experience, like the discussion of sexual preference earlier, may build upon an individual's I-function, fabricating the sexual self identity from past intensified experiences or dreams.
The question still remains-- exactly WHAT happens to the brain during sexual excitement and most curiously, the ensuing orgasm? This remains for some part a mystery. We know that human sexual behavior culminates in the release of tension at the peak of excitement, the orgasm, the zenith of human bliss. We have the neurochemical and hormonal symbiosis, the EEG studies relating orgasm and epileptic seizures, the brain localization of sexual function to some extent, and even human examples who can reach a climax without any physical stimulation whatsoever. Reaching a state of sexual satiety is in general a consummation of physical and psychological stimulation, although the combination is not necessary. Direct corporeal stimulation is useful, but not without the erotic state of mind that accompanies it to reach orgasm. With respectful consideration to the fact that a state of sexual satiety can be triggered by neurological and endocrine activity alone, the brain can be confirmed the most powerful libidinous instrument of human sexuality.
1)The Neurobiology of Sexual Function
3)Neurobiology, Neuropharmacology, and Pharmacological Treatment of Compulsive Sexual Behavior
8)Sexual arousal and orgasm in woman: Effects of spinal cord injury
