Bipolar Disorder: A Biological Overview

bipolar disorder: A Biological Overview

Bipolar disorder is one of the most complex and difficult to treat of the major mood disorders. There are several different forms of the illness. Some bipolar I disorder patients exhibit alternating episodes of mania and depression, while other sufferers show less florid periods of mania, a state called hypomania that alternates with depression. These sufferers are said to exhibit a less severe form of the illness, called bipolar II disorder ("Bipolar disorder," 2007, NIH). Susie, given her delusions during periods of mania, seems to exhibit bipolar I features in her manifestation of the disorder. She shows full-blown mania, and exhibits the manic symptoms of elevated mood, over-activity sleeplessness, overconfidence, paranoia, and impaired judgment. Mania is what distinguishes bipolarity from the mood disorder of depression. "A single manic episode is sufficient for the diagnosis of bipolar illness" (Belmaker 2004).

Regarding its biological basis, in both forms of bipolar disorder, the evidence regarding the influence of neurotransmitters is both frustrating and conclusive. It is conclusive in the sense that, like all of the major mood disorders, there is a very clear link between neurotransmitters in the brain existing in a state of imbalance and the development of the disorder. Exactly how this imbalance functions remains mysterious in this illness. Some studies have suggested that a low or high level of a specific neurotransmitter such as serotonin or dopamine may be the cause. Serotonin is the 'feel good' chemical often in a state of deficit in depressed patients, and anti-depressant medications inhibit the ability of the body to soak up serotonin, and thus increase the levels of this chemical. Dopamine is the 'thrill seeking' chemical often present in too great an abundance in the brains of schizophrenics. Yet other studies of bipolar patients "indicate that an imbalance of these substances is the problem, i.e., that a specific level of a neurotransmitter is not as important as its amount in relation to the other neurotransmitters (Read 2007:1).

Despite its physical component, bipolar disorder is not like inheriting blue or brown eyes. "Linkage studies have identified markers, which have been replicated in more than one study, particularly on chromosomes 18 and 22. However, no single locus has been consistently replicated, and the contribution of any identified locus appears small. Progress in genomic medicine offers the hope that specific genes that confer an elevated risk of bipolar illness will be found" (Belmaker 2004). In other words, it cannot be predicted that a child will definitely have the disorder, based on a genetic test, but genes clearly influence the tendency to develop the disorder, particularly under periods of intense stress. Families of persons with bipolar disorder also seem more likely to have a mood disorder than the relatives of those who do not have bipolar disorder, as in the case of Susie. "Approximately 50% of patients with bipolar illness have a family history of the disorder" (Belmaker 2004).

Note that this tendency is not only specific to bipolarity, but to any mood disorder. In the case of Susie, the mood disorder was not bipolarity, but depression. To determine the extent of the genetic influence upon this disorder, scientists have compared tendencies to exhibit the disorder in twin studies. Studies of twins indicate that if one twin has a mood disorder, an identical twin is about three times more likely than a fraternal twin to have a mood disorder as well and in bipolar disorder specifically, the tendency for both twins to have the disorder is 80% higher for identical twins, versus only 16% higher for fraternal twins. Scientists thus call this tendency a "genetic vulnerability" to inherit depression (Read 2007:1)

Biologically, bipolarity is not caused by brain damage although there is mounting evidence that the brains of bipolar patients look different from those without mood disorders. A 2000 study in the American Journal of Psychiatry that the brains of patients with bipolar disorder contain 30% more cells that send signals to other brain cells, suggesting that the extra signal-sending cells may lead to a kind of over-stimulation, causing the rapid shifts of extreme moods characteristic of the disease (Read 2007:1). However, whether the disease causes the different brain configuration or the extra cells causes the disorder still remains a mystery.

To add to the mystery of treating this illness, because bipolar disorder has two distinct mood components, that of mania, and that of depression, treating it with medication can be especially difficult. Patients with bipolar disorder usually must remain on some form of medical treatment for the duration of their lives, and often different treatment plans must be prescribed, and medications must be readjusted depending on whether a patient is in a depressive or manic phase. For example, for patients on lithium, other medications are frequently added to the patient's course of treatment to specifically address the effects of the mania or depression ("Bipolar disorder," 2007, NIH).

Anti-psychotic drugs are used to treat particularly resistant manic episodes, while antidepressants that raise serotonin levels are used to treat the depressive phase of the illness. Atypical antipsychotic medications are also sometimes prescribed to treat mania, and evidence suggests clozapine may be helpful as a mood stabilizer for people who do not respond to lithium or anticonvulsants, because they lower dopamine levels.