| 1.
Introduction
One essential criterion for a diagnosis
of bipolar I disorder is a past or present history of a manic episode.
As the investment in these activities becomes excessive, the individual
loses the capacity to behave with reasonable caution and judgment
and to conform to social expectations and norms. When the mood elevation
is of a milder nature, either in severity or in duration, and is unassociated
with a marked impairment in function, an assessment of hypomania rather
than mania is made, resulting in a bipolar II disorder rather than
a bipolar I diagnosis.
Although bipolar illness has traditionally been associated
with a relatively late age at onset, current evidence indicates a
peak age of onset of between 20 and 25 years. Some surveys have indicated
that premorbid symptomatology may start even earlier in adolescence
and, more rarely, in early childhood. Bipolar illness with onset during
childhood or adolescence is commonly misdiagnosed and differentiation
of childhood bipolar disorder from attention-deficit disorder is particularly
difficult.
2. Epidemiology
Multinational studies indicate that
the lifetime risk of bipolar disorder is approximately 1-2%. Depending
on how the phenotype is defined, the concordance rate for bipolar
illness ranges from 65% to 85% in monozygotic twins and is 20% in
dizygotic twins. Bipolar illness occurs in relatives of patients with
bipolar disorder much more frequently than in relatives of patients
with major depression; the rates for depression alone are approximately
the same. Adoption studies show that rates of illness clearly depend
on the risk associated with the biological rather than the adoptive
parents. In general, bipolar probands have more relatives with bipolar
disorder and mood disorder than unipolar probands.
3. Etiology
A. Biochemical Factors: Although
many differences in biochemical indices have been described when patients
with bipolar disorder are compared to normal control subjects, there
is no agreement about which alterations have etiological significance
and which are secondary effects or epiphenomena. Since the "switch"
from depression into mania (and vice versa) can occur in minutes,
attempts have been made to identify biochemical changes that might
be associated with the switch. Specific changes in brain monoamine
neurotransmitter metabolism and receptor function appear to be the
most likely mechanisms.
Electrolyte disturbances have also been found in patients with bipolar
disorders and may represent a defect of cellular membrane function.
In general, sodium retention and potassium and water excretion increase
during depression and decrease during manic intervals. Abnormal calcium
homeostasis has also been reported. A variety of neuroendocrine changes
have also been reported for patients with bipolar disorder who are
in the depressed phase.
Because of pharmacological parallels to temporal lobe epilepsy and
beneficial responses to several anticonvulsant agents, some investigators
have hypothesized that recurrent bipolar mood episodes derive from
an endogenous "kindling" of electrical discharges in limbic
areas of the brain. Others have emphasized patterns in alteration
of circadian rhythmicity.
Thus far, the results of studies in molecular genetics have been inconclusive.
Regions on chromosome 18p and 18q and on chromosomes 4 and 21 have
received the strongest support, although no specific gene has thus
far been isolated for what is most certainly a complex multigenic
disorder.
B. Psychosocial Factors: There is no reliable evidence that
psychosocial factors cause bipolar disorder, although life stresses
may precipitate manic or depressed bipolar states and may in fact
be necessary for the expression of symptomatology in milder bipolar
syndromes. The lifetime prevalence of comorbid substance abuse exceeds
60%. Recent research in biological circadian rhythmicity suggests
that subtle changes in the light-dark cycle (eg, seasonal variations)
are an additional predictor of risk.
4. References:
American Psychiatric Association: Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition, Text Revision. Washington,
DC, American Psychiatric Association, 2000.
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