A Personal Experience of Learning About Bipolar Disorder

A Personal Experience of Learning About Bipolar Disorder

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Submitted by SerendipUpdate on Fri, 01/04/2008 - 4:51pm Biology 202

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A Personal Experience of Learning About Bipolar Disorder

Debbie 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 pharmaceuticals 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 relieved 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-convulsant 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).