A Personal Experience of Learning About Bipolar Disorder

Biology 202
1999 First Web Reports
On Serendip

A Personal Experience of Learning About Bipolar Disorder

Debbie Plotnick

For a later chapter of this story, see a brief autobiographical essay by Ashley Plotnick.

 

My daughter Ashley, an engaging, highly intelligent, beautiful and artistically talented teenager, suffers from a life threatening genetic illness. It is an illness of extremes with a high, some estimates are as much as 20%, mortality rate. It is sometimes, as with my daughter, difficult to treat. It is always difficult for those so afflicted and their families. The contemporary nomenclature for this disease is Bi-Polar Disorder (1). But I prefer the more descriptive, no longer politically correct name, Manic Depression.

Most of us understand the dangers inherent in depression and its associated high risk of suicide. Over the last three years my daughter has employed some of the most common methods. She has cut her forearms twice, fifteen and twenty stitches respectively. And one evening she swallowed a week's worth of her prescribed medications (over one hundred pills) leaving her mother to find her, the next morning, much to her surprise and disappointment alive, and covered in vomit and excrement. But what is not as commonly known is that as precarious as depression can be the manic phase is equally as perilous.

Mania (1) consists of racing thoughts, grandiose delusions and marked lack of judgement. Unlike in the depressive phase it is hard to envision or anticipate the life threatening behaviors in which those so afflicted might engage. My daughter has many times; as is so typical in a manic phase, lost all sense of danger and for example attempted to walk alone at night for miles along a highway. It is also very common in this phase for manic-depressives, as has my daughter, to turn to street drugs (2).

But most of my daughter's experiences with street drugs, which were attempts to self-medicate, and her use of hallucinogens (2) have occurred in the least common and most difficult to treat manifestation of this disorder, the "mixed phase" (4). This is where a form of mania where the person is extremely anxious, hostile and self-destructive called dysphoria (4), occurs simultaneously with the suicidal tendencies of the depressed state. Closely related to the mixed phase, and also among the symptoms experienced by my daughter, is that which is known as "rapid cycling (3). This is defined as "four or more complete mood cycles within a year's time, and some rapid-cyclers can complete a mood cycle in a matter of days--or, more rarely, [as has my daughter] in hours" (3) (2).

Rapid cycling (3), as well as other forms of pharmacologically induced hypomania/mania (5), as my family has learned, can be the direct result of the use of antidepressant medications. Over the course of four years and approximately 30 different psychoactive pharmacidicals my daughter's experiences have been illustrative of how the use of one medication often leads directly to the use of others. And we have seen many of the numerous problems that can be medication induced.

Such experiences began after several months of working with a psychologist and no discernable change in the profound depression which gripped my then 13-year-old daughter. She was referred to her first psychiatrist who prescribed the antidepressant medication Nortriptyline (6). This led directly to her diagnoses as Bipolar. Within hours of her first dose, Ashley began to exhibit the classic symptoms of mania (1). This "phase flipping reaction" is a common when an antidepressant without a mood stabilizer is given to those who are bipolar (5).

Thus began my education into the often-delicate balancing and imprecise guesswork inherent in the use of psychiatric drugs. And also led to my quest to comprehend the mechanisms of said substances. In order to understand how these drugs were developed and how they work several very basic facts about neuron-physiology are required. The first of which is that chemicals called neurotransmitters, such as serotonin, epinephrine, and norepinephrine, are that which the psychoactive drugs act upon. Secondly, the purpose of neurotransmitters is to conduct chemical messages between brain cells (called neurons) because the physiology of the brain is such that neurons don't touch. And that the spaces between neurons are called synapses. It is also essential to know that once neurotransmitters are released, by what is called the pre-synaptic neuron, they are cleared from the synapse and thus stop affecting the cell to which the message is sent (the post-synaptic neuron) after a very brief time. One process by which this clearing occurs is by using another chemical. An example of such a chemical is the enzyme monoamine oxidase. There is also another method by which a synapse is cleared of neurotransmitters. This process is where neurotransmitters are taken back into the cell of origination, the pre-synaptic neuron, and is called uptake or reuptake.

The development of antidepressant medications came about because of two accidental discoveries. In the 1950's researchers noted that a sizable percentage (15%) of people who were treated with an anti-hypertension medication, became depressed. This particular drug was known to deplete the class neurotransmitters called monoamines. And secondly, a correlation was made about patients who had tuberculosis and who also suffered from depression. It was found that their depression was relived when they were given an anti-tuberculosis drug that was known to inhibit the neuronal breakdown of monoamines by the enzyme monoamine oxidase. "Together these findings implied that abnormally low levels of monoamines in the brain could cause depression" (7).

Several years later the tricyclic antidepressants were developed. They prevent the process of reuptake of norepinephrine and serotonin. Both of these substances have been shown to be deficient in the brains of those who are depressed (7). The tricyclics, and the new class of "designer drugs," called Selective Serotonin Reuptake Inhibitor (SSRI) such as Prozac (9) (which impacts only serotonin), have effects upon mood because they increase the time that these neurotransmitters remain in the synapses (7).

Ashley's experiences with medications began with the second oldest class of neuro-active drugs, the tricyclic antidepressants and progressed through almost all of the antidepressants currently in use. The choice to begin with tricyclics was motivated by the fact that more was known about their long term effects in adolescents than the oldesr types of drugs the MAOI's and the newest, the SSRI's.(9)

Within a year Ashley had a new psychiatrist. He had very little concern for long term effects and began an aggressive array of drug use. Ashley's experiences with MAOI's were especially frightening. She never experienced the common and potentially life threatening rapid rise in blood pressure associated with these drugs (9) (10). However, she did, because she withdrew too quickly (and of her own accord), experience with both Parnate (10) and Nardil (11) hallucinations and other psychotic symptoms.

For reasons previously noted, the very beginning of Ashley's experiences with antidepressant medications necessitated the concurrent quest for a mood stabilizer. Lithium (12) is the mood stabilizer of first choice because it is highly effective for about 70% to 80% of people in controlling mood swings and mania and, unlike the other psychoactive substances, is a naturally occurring element (13). However, while lithium is very effective, the difference between a therapeutic dose and toxic one is very small (12). Things such as a large amount of perspiration caused by exercise, or a change in fluid balance, can increase the incidence of side effects such as nausea, vomiting, dizziness and tremors. This makes lithium especially hated by teens. And so her doctor moved her on to the other, and not originally designed as such, mood stabilizers.

Another of history's long series of serendipitous events lead to the discovery that epileptic patients who were also manic-depressive and took anticonvulsant medications, experienced a stabilization of their moods. Ashley had several long periods on the most commonly used drug of this type, divalproex sodium (Depakote) (13). She also, very briefly (one week), was on another anti-convolsant called carbamazepine (Tegretol) (14). Her brief experience on Tegretol, resulted in a quite unpleasant reaction. She experienced for a full week hives that covered her entire body. We also all learned, from this experience that that a manic-depressive person on steroids can be especially difficult. Unfortunately, this event did not prove to be the last adverse experience Ashley would have with Tegretol. Several years, and many drug combinations later, in an attempt, as she explained, "to not kill herself, merely get "f***ed up,"she purchased from another adolescent a substance that she believed to be the tranquilizer Zanex. Ashley's bad judgement and the other kid's dishonesty resulted in a three day stay in the local hospital's cardiac unit as Ashley experienced another well known side effect of Tegretol "associated with suppression of phase 4 depolarization of the heart muscle fiber"(14).

For several long periods Ashley took Depakote (13) in an unsuccessful attempt to control her moods. And throughout this time we were vigilant about the ever-present threat of serious side effects. These include liver damage and abnormalities in white blood cell and platelets counts. This necessitates periodic blood monitoring of valproatic acid levels (14). She also had several long periods where she took the anti-psychotic drug Zyprexa (15). This drug like many of the other psycho-active agents prescribed outside of the intended usage recently received " a non-approval letter from the United States Food and Drug Administration for use of Zyprexa (olanzapine) in the treatment of acute manic or mixed episodes associated with bipolar disorder" (16).

>From Ashley's point of view, approved for use in her condition, or not, the most difficult side effect, from both Depoke and Zyprexa, that she experienced was unremitting fatigue. This led to, in spite of great protestations from her mother, the psychiatrist prescribing the amphetamine Adderal. And also because a major symptom of depression is sleep disturbance (17), Ashley regularly took an often-changing line-up of sleeping pills.

As medication changes became frequent the concept that "antidepressants poop out and require a change and/or the use of augmentation drugs to increase their activity"(18) became evident. The combination of symptoms and side effects resulted in the situation that between the ages of 15 and almost 17, Ashley was a severely depressed, mixed-phased, rapid-cycling manic-depressive who used drugs to go to sleep, wake or stay up, and who regularly changed mood stabilizers and antidepressants. The situation became such that Ashley was taking eight or ten medications simultaneously. It became difficult to know which were the effects of her illness and which were the problems caused by the use of psychoactive agents.

While, being bipolar is a difficult truth for Ashley and our family to face, the diagnosis came as little surprise (7) (9). My father is so afflicted and causes those around him also to suffer from his to date untreated sever form of bipolar illness. And I have a milder form of the illness called cyclothymia (1). Currently several members of my family, (my father, daughter, and I) are participants in a genetic study of Bipolar Illness and Schizophrenia in Ashkenazic Jews (those of eastern European descent) being conducted at Johns Hopkins University. And yes, Ashley sometimes, especially in a manic phase and because she is an adolescent, does blame me for "giving her this disease." And because I'm a mother, therefore receptive to guilt, I do blame myself for having the mistaken assumption that nurture (homebirth, prolonged breastfeeding and lots of love) could overcome nature (genetics). Research has shown the family history seems to have an influence on the onset of the earliest symptoms (17). "The more family members have a depressive disorder, the more often this is a bipolar disorder, the greater the chances that a child will BP and the earlier one will see BP symptoms {Smeraldi et al, 1982};{Strober & Carlson, 1982}" (17). Some estimates place the chances of developing this disease for those with first degree relatives so affected up to 25% for bipolar and 41% for unipolar (depression only) (17). The exploration of my own family did bear this out. I discovered a preponderance of depressive and manic-depressive artists. This phenomenon has been document by Dr. Kay Redfield Jamison (19) who purports that a high degree of "creativity" often accompanies this illness.

Ashley's feelings of inadequacy and the cognitive difficulties that resulted from her use of so many medications left her unable to regularly attend school and with no interest in her work with stained-glass and ceramics. Late last year, after her third hospitalization in as many months, it became clear that radical changes were required. Contact with the National Institutes of Mental Health circuitously and serendipitously lead to a consultation with the person who is considered "the expert" in mood disorders in children and adolescents. In a bit of good fortune this person Dr. Elizabeth Weller (5), can be found at Children's Hospital in Philadelphia, just 40 minutes from our home. Dr. Weller proposed another hospitalization in order to provide Ashley safe environment for withdrawing from eight of the ten medications that she was taking.

Having had her fill of psychoactive substances, Ashley expressed a desire to try another long-standing treatment, Electroconvulsive Therapy (ECT). It is not clearly understood why ECT is effective. However, it is successful in a large percentage of cases of depression and mania that have been shown to be drug resistant. While over the course of the 45 years that ECT has been employed, its administration has become much less violent and dangerous. Today, ECT is administered under general anesthesia, in conjunction muscle-relaxants, and no longer poses the once high risk of compression fractures (21). However, what it does do is to put enough electricity into the brain to produce a seizure and accompanying convulsions. This is because almost 60 years ago it was discovered that depressed epileptics' moods were improved after suffering a seizure. And while broken bones are no longer a problem, ECT patients must now contend with the effects, and potential side effects of the accompanying drugs, of grogginess and short term (and perhaps long term) memory impairment (21).

ECT is often a therapy of last resort. One reason is that it requires a large number of treatments that virtually render the patient incapable of functioning for several days following each session. But, because of our geographic location, the doctors at Children's hospital were able to recomend an alternative. They referred Ashley to Dr. Marty Szuba, a professor of psychiatry at the University of Pennsylvania. Dr. Szuba and his staff are conducting clinical studies using a relatively new tool that is offering new possibilities for therapies for some of the most troubling of brain dysfunctions. This technique is called Transcranial Magnetic Stimulation or TMS (22) (23).

TMS is a new non-invasive and non-violent method for causing brain stimulation. It works through the principal of induction. A small electrical current is passed through a coil of wire that is placed on or near a person's scalp. The resultant magnetic field, not electricity, which is produced by an alternating current of electricity, is conducted through the skull. By changing the magnetic field over time (pulsing the electrical current), and because the properties of electricity and magnetism are reciprocal, the magnetic energy is converted it into electrical current. The pulsing or oscillating magnetic field thus causes charged particles (ions) in and around the neurons in the brain to become excited. These charged ions then depolarize thus producing an electrical flow. Because TMS is delivered via a small hand-held device it allows for stimulation of only the part of the brain where depression is occurs. This is believed to be "the dorsal lateral pre-frontal cortex. The area slightly above the temple and behind the forehead" (22). Use of this technique has shown to be as effective ECT (22). The best explanation, that I have heard, as to why TMS and ECT are effective in treating both depression and mania came from. Dr. Szuba. He explained that procedures "reset the neurons in the brain." (20). But a significant difference is that TMS treatments are given, without the need for drugs, to patients while they sit in a chair. It takes only 20 minutes and there appear to be no side effects.

Presently, in spite of all that she has experienced over the last four years, Ashley is much improved, under the care of a new psychiatrist and on a program of only lithium and cognitive psychotherapy. However, she is considering, if her mania and/or depression so warrant, becoming a participant in a study conducted by Dr. Szuba of the use of TMS on adolescents.

Thanks to:

My daughter Ashley, who gave permission for me to explore and expound upon my version of her story.

My husband Mike for proof-reading and for his explainations on conductivity

And to Professor Grobstein for allowing me to further my understanding on topics of great personal as well as educational importance to me.

 

WWW Sources

1)Mining Co - Bipolar Page

2)Mental Health Glossary

3)Mood Swing

4)Rapid Cycling

5)Psychiatric Times

6)Mining Company - Drug Terms

7)Scientific American - June 1988

8) Psychiatric Times

9)Mining Company - Depression - SSRIs

10)MetalHealth.com

11)MetalHealth.com - Drugs

12)MedHelp - Lithium

13)Helpline - Depakote

14)MetalHealth.com - Drugs

15)Zyprexa

16)MetalHealth.com - Drugs

17)Depression - Family Links

18)DrugLink

19)Suicide & Depression Bookstore

20)Personnal Interview

21)Electroconvulsive Therapy

22)U of P News Release

23)TMS Resources

 

 

Continuing conversation (to contribute your own observations/thoughts, post a comment below) 01/08/2006, from a Reader on the Web Ashley has been through the ringer. I was 22 before I had a major manic episode and was hospitalized in nyc. I have bipolar I and have had 2 major episodes so far and I am now 54. I have never been fooled into thinking that this is not a life threatening disease and I manage the illness by living simply. When I was 22 after my episode lithium worked wonders. I find now that I am older an no longer able to take lithium because of diabetes insipidus I am on depakote and abilify along with tegretol. I also see an acupuncturist on a regular basis, someone who I trust and is now familiar with my illness. You might want to suggest this to Ashley. I also see a psychiatrist who I have been working with a longer time.

 

 

I graduated from Bryn Mawr in 1997, so good to see this forum online. I, too, am bipolar. I have been hospitalized twice and undergone 8 or 9 ECT sessions. I am now beginning to see the unofortunate side effect of ECT induced mania. It is so disappointing because my earlier ECT treatments only lifted me out of the horrible place of depression and left me on the shores of life again. I am curious about the TMS treatments. I have had bad reactions to the overwhelming majority of drugs to treat bipolar disorder, hence the ECT. Best of luck to you and your daughter. Keep writing! ... SB, 3 may 2006