Full Name:  Michelle Tahmoush
Username:  mtahmoush@aol.com
Title:  Prozac -- the Toxic Miracle Drug
Date:  2002-02-25 13:56:06
Message Id:  1150
Paper Text:


Biology 202
2002 First Paper
On Serendip

America's society has turned to an aggressive means to treat the overwhelming numbers of people who suffer from depression -- antidepressant medication. "The National Institute of Mental Health... has estimated that almost 10 million Americans are seriously depressed and that a total of 14 million will suffer from it during their lifetimes" (7). Taking psychiatric drugs such as Prozac has become trendy. People no longer covertly take antidepressants, but discuss their medications openly as if there were nothing wrong with chemically altering one's brain. This is partly due to how psychiatrists propose the necessity of Prozac and other such drugs. Psychiatrists explain that Prozac will counteract the low levels of serotonin by inhibiting the loss of this neurotransmitter. The low levels of serotonin are said to be the cause of the depression, thus Prozac remedies this disease for certain people. Supposedly, with only a few side effects exhibited in a mere fraction of the patients taking Prozac, happiness can be in one's grasp. Prozac is idealized in this fashion as a euphoric drug. In reality, Prozac harmfully changes one's brain chemistry with no guarantees of reducing one's depression. Society has ignorantly euphemized this toxic drug as the cure of depression because of faulty trial studies, the understatement of the potential adverse reactions, and the neglect of patients prescribed Prozac.

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"

2) "The Dark Side of Prozac"

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

Full Name:  Raquel P. Deering
Username:  rdeering@brynmawr.edu
Title:  Progressive Supranuclear Palsy: A Neurophysiological Report
Date:  2002-02-25 14:35:41
Message Id:  1152
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

2)Yahoo Health

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.

Full Name:  Balpreet Bhogal
Username:  bbhogal@brynmawr.edu
Title:  Physical Brain Abnormality a Possible Cause of Schizophrenia
Date:  2002-02-25 16:18:45
Message Id:  1156
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Michele Drejka
Username:  mdrejka@brynmawr.edu
Title:  Adderall, Ritalin, AD/HD, and Abuse
Date:  2002-02-25 18:03:47
Message Id:  1162
Paper Text:


Biology 202
2002 First Paper
On Serendip

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,


5)Assessment of Adult AD/HD,

6)ADD Drug Abuse Rising,

7)Overdiagnosis Unlikely,

8) Self-Test for AD/HD,

Full Name:  Kathryn Fong
Username:  kfong@brynmawr.edu
Title:  Bipolar Disorder
Date:  2002-02-25 19:44:31
Message Id:  1169
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Caitlin O'Keefe
Username:  cokeefe@brynmawr.edu
Title:  Schizophrenia
Date:  2002-02-25 20:35:15
Message Id:  1171
Paper Text:


Biology 202
2002 First Paper
On Serendip

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”,

2)“Ask the Experts”,

3)“The Role of Dopamine Receptors in Schizophrenia”,


Full Name:  Amy Cunningham
Username:  acunning@brynmawr.edu
Title:  Reliving the Nightmare: Post-Traumatic Stress Disorder
Date:  2002-02-25 20:48:37
Message Id:  1173
Paper Text:


Biology 202
2002 First Paper
On Serendip

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) Cal State-Chico website on serotonin.

6)Anxiety Disorders Treatment Target: Amygdala Circuitry" from the ADAA 18th annual

Full Name:  Tara Monika Rajan
Username:  trajan@brynmawr.edu
Title:  What is Addiction, and What Causes it?
Date:  2002-02-25 22:52:45
Message Id:  1178
Paper Text:


Biology 202
2002 First Paper
On Serendip

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.


1)The Neurobiology of Addiction

2)The Opiate Receptor

3)Heroin Addiction

4)The Genetics of Alcoholism

5)Cocaine Addition Links

6)Psychology Abstracts

Full Name:  Nicole Pietras
Username:  npietras@brynmawr.edu
Title:  Drug Addiction: A Brain Disease?
Date:  2002-02-25 23:10:53
Message Id:  1182
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Sarah Eberhardt
Username:  idy3176@yahoo.com
Title:  The bipolar brain and the creative mind
Date:  2002-02-25 23:32:26
Message Id:  1183
Paper Text:


Biology 202
2002 First Paper
On Serendip

“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?


1) Kaysen, Susanna. Girl, Interrupted. Vintage Books: New York, 1993.

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

6)The Serendip webpage, an article entitled “Creativity and Psychopathology”

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

Full Name:  Sook Chan
Username:  schan@brynmawr.edu
Title:  Dissociative Identity Disorder: How Many Personalities Do You Have?
Date:  2002-02-25 23:38:15
Message Id:  1184
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Tiffany Vaughan
Username:  taildogv@hotmail.com
Title:  Did it Already Happen, or is it Happening Now?
Date:  2002-02-26 00:51:17
Message Id:  1189
Paper Text:


Biology 202
2002 First Paper
On Serendip

"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)Mental Health, definition of amnesia.
2)Amnesia, description of retrograde and anterograde amnesia.
3)Question of The Day, lists types of amnesia and explains retrograde and anterograde amnesia.
4)Memory,explanation of memory.

Full Name:  Rebecca Roth
Username:  rroth@brynmawr.edu
Title:  Lets all go for a run! ----Does exercise really help the brain?
Date:  2002-02-26 01:12:49
Message Id:  1190
Paper Text:
<mytitle> Biology 202
2002 First Paper
On Serendip

Should I go run a marathon, join a yoga class, or head off to the gym? Is it really worth the time and effort? Afterall, sitting down and watching television can seem just as appealing. Why even bother working out? The reasons to work out may be greater than you think. Physical activity can make you feel good, keep you in shape, keep you healthy, but now researchers also are finding biological evidence that exercise benefits specific brain mechanisms. Just as exercise improves muscle tone and function, it may also have similar effects on the brain.

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.


1)Exercise and the Brain, Society For Neuroscience

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

Full Name:  Asra Husain
Username:  ahusain@brynmawr.edu
Title:  Anorexia and Bulimia Nervosa
Date:  2002-02-26 02:19:48
Message Id:  1191
Paper Text:
<mytitle> Biology 202
2002 First Paper
On Serendip

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)


Works Cited:

1) Abraham, Suzanne. Eating Disorders, the Facts. Oxford University Press, 1992.
2)Anorexia Nervosa/Bulimia: Adolescent Self Image
3)Anorexia and Bulimia Nervosa
4) Scott, Derek. Anorexia and Bulimia Nervosa. New York University Press, 1988.
6) Mitchell, James E. Anorexia Nervosa & Bulimia, Diagnosis and Treatment. University of Minnesota, 1985.
7)Cognitive Behavior Therapy: The Basics
8)Health: Brain chemicals may cause Bulimia

Full Name:  Gabrielle Lapping-Carr
Username:  glapping@brynmawr.edu
Title:  The K+ Channel, A New Hope For a Better Understanding
Date:  2002-02-26 06:05:29
Message Id:  1192
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

3)Potassium Channel Mechanics

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

9)Visual of the K+ Channel

10)Lights, Camera, Action Potential, A site made for children that has great descriptions and visuals of an action potential.

Full Name:  Miranda White
Username:  mcwhite@haverford.edu
Title:  Transient Global Amnesia
Date:  2002-02-26 08:09:59
Message Id:  1193
Paper Text:


Biology 202
2002 First Paper
On Serendip

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.


1)Anterograde amnesia

2)HealthyMe Amnesia

3)E Medicine, Transient Global Amnesia

4)Transient Global Amnesia Case Studies

5)Neuroland, TGA

6)Transient Global Amnesia

7)HealingWell, What Happened to Afterglow

8)Transient Ischemic Attack

9)Basilar Artery Migraine Page

10)The Diencephalon

11)Medial Temporal Lobe

12)The Cognitive and Habit Subsystems , A great image of the anatomy of the brain.

Full Name:  Mary Schlimme
Username:  mschlimm@brynmawr.edu
Title:  The Neurobiological Factors Associated with Depression
Date:  2002-02-26 08:39:40
Message Id:  1194
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Peffin Lee
Username:  plee@brynmawr.edu
Title:  Beauty and the Brain
Date:  2002-02-26 09:20:28
Message Id:  1195
Paper Text:


Biology 202
2002 First Paper
On Serendip

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.


1) BBC News Report

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"

6) Essay by Chris Homan

7) "Food Reward: Brain Substrates of Wanting and Liking"

Full Name:  Amy O'Connor
Username:  aoconnor@brynmawr.edu
Title:  Ecstasy, the Brain and Serotonin (MIA)
Date:  2002-02-26 09:21:00
Message Id:  1196
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

1)Drug Abuse Home Page, a government supported cite, strongly anti-drug, and useful reference

2)NIDA Home Page, a 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.

Full Name:  Jenny Maryasis
Username:  jmaryasi@haverford.edu
Title:  Procrastination: Habit or Disorder?
Date:  2002-02-26 09:25:43
Message Id:  1197
Paper Text:


Biology 202
2002 First Paper
On Serendip

"Procrastination is 'the art of keeping up with yesterday and avoiding today.' "
- Wayne Dyer (6)

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.

1)Physiological and Physical Disorders, Procrastination related to physical disorders and brain lesions

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

Full Name:  Lauren Welsh
Username:  Lauren_welsh@hotmail.com
Title:  Causes of Sexual Dysfunctions
Date:  2002-02-26 09:36:48
Message Id:  1198
Paper Text:


Biology 202
2002 First Paper
On Serendip

"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.


1)Online Dictionary

2)Brain and physiology of emotion

3)Neuroscience of emotions and sexuality



6)Kluver-Bucy Syndrome

7)Limbic System

8)Sexual Dysfunction

9)Sex and states of consciousness

10)Sexual Dysfunction Secondary to Depressive Disorders

11)What causes behavior?

12)Sexual Dysfunction Following Injury:Time for Enlightenment and Understanding

Full Name:  Adria Robbin
Username:  arobbin@brynmawr.edu
Title:  Walking a Difficult Line: Taking a Look at Borderline Personality Disorder
Date:  2002-02-26 09:48:40
Message Id:  1199
Paper Text:


Biology 202
2002 First Paper
On Serendip

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)

Full Name:  Tina Chen
Username:  tchen@brynmawr.edu
Title:  What is Sleep and the Effects of Sleep Deprivation
Date:  2002-02-26 10:01:36
Message Id:  1200
Paper Text:
What is Sleep and the Effects of Sleep Deprivation Biology 202
2000 First Web Report
On Serendip

What is Sleep and the Effects of Sleep Deprivation

Tina Chen

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!

WWW Sources



3)http://www.nature.com/cgi taf/DynaPage.taf?file=/nature/journal/v403/n6770/full/403655a0_fs.html,


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Full Name:  Porsha Gaughen
Username:  Hairball23@aol.com
Title:  Social Order and Animal Consciousness
Date:  2002-02-26 14:07:09
Message Id:  1212
Paper Text:
The Questions of Animal Consciousness

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.


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

Full Name:  Ms. Cass Barnes
Username:  cassbarnes@hotmail.com
Title:  Intrapsychic Omnipresence in Bodily Symptoms
Date:  2002-02-26 14:24:51
Message Id:  1213
Paper Text:


Biology 202
2002 First Paper
On Serendip

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.


1) The Freud Page

2) Encyclopedia.Com

3) Notes on Neurotic Disorders

4) Pediatric On Call

5) Hypnotizability and traumatic experience

6) Freud, Sigmund. Dora: An Analysis of a Case of Hysteria. New York: Simon & Schuster, 1997.

7) Psychiatric Terminology

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

Full Name:  Alisa Alexander
Username:  aalexand@brynmawr.edu
Title:  Pick's Disease
Date:  2002-02-26 14:31:07
Message Id:  1214
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

3)CANDID Fact Sheets

Full Name:  Cindy Zhan
Username:  qzhan@brynmawr.edu
Title:  The Correlation Between Music and Math: A Neurobiology Perspective
Date:  2002-02-26 14:34:22
Message Id:  1215
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Alisa Alexander
Username:  aalexand@brynmawr.edu
Title:  Pick's Disease
Date:  2002-02-26 14:42:45
Message Id:  1216
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

3)CANDID Fact Sheets

Full Name:  Kornelia Kozovska
Username:  kkozovsk@brynmawr.edu
Title:  Does a split reality exist? Déjà vu as a failure of the brain to put “time stamps” on memories.
Date:  2002-02-26 16:18:47
Message Id:  1217
Paper Text:


Biology 202
2002 First Paper
On Serendip

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

Full Name:  Ashley Farrell
Username:  afarrell@brynmawr.edu
Title:  Attachment and Monogamy as Studied in People and Rodents
Date:  2002-02-26 16:32:54
Message Id:  1219
Paper Text:


Biology 202
2002 First Paper
On Serendip

“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

Full Name:  Erica Carlos
Username:  ecarlos@brynmawr.edu
Title:  Mental Imagery: Can a Figment of Imagination Help Performance?
Date:  2002-02-26 17:01:26
Message Id:  1220
Paper Text:


Biology 202
2002 First Paper
On Serendip

“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

Full Name:  Gavin Imperato
Username:  gimperat@haverford.edu
Title:  Locked-In Syndrome and PVS: Implications for Brain = Behavior
Date:  2002-02-26 20:02:05
Message Id:  1229
Paper Text:


Biology 202
2002 First Paper
On Serendip

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.


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.

Full Name:  melissa hoban
Username:  mhoban@ brynmawr.edu
Title:  Searching for the Location of Creativity
Date:  2002-02-26 20:33:47
Message Id:  1231
Paper Text:


Biology 202
2002 First Paper
On Serendip

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
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.


1) “Toward a Neurobiology of Creativity? Making Connections Between Art, Manic-Depressive Illness, and Frontotemporal Dementia”, by:Diana C. Applegate

2) "Creativity and Psychopathology", by Rachel Friedman, on the Harvard Brain's Website

4) SCIENCE magazine archives "Artistic Creativity and the Brain" Semir Zeki.


6) Metacognitive Musings, by: John Dalton http://serendipstudio.org/local/suminst/bbi01/projects/dalton/

7) Untitled, by: Elaine de Castro

8) Synesthesia: Phenomenology And Neuropsychology - A Review of Current Knowledge by Richard E. Cytowic

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

Full Name:  Aly Dymkowski
Username:  adymkows@brynmawr.edu
Title:  The Link Between Down Syndrome and Alzheimer's Disease
Date:  2002-02-26 21:40:54
Message Id:  1234
Paper Text:


Biology 202
2002 First Paper
On Serendip

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