Biological Theories of Manic-Depression ?
Q.Like every mental illness, there is no definitive evidence concerning the etiology of manic-depression, also known as bipolar disorder. The disorder is characterized by alternating periods of depression and mania and occurs in 1% of the population. The depressive episodes can range in severity from dysthymia to major depressive episodes. The major depressive episodes are classified as periods of at least two weeks in length during which sadness, lethargy, insomnia or excessive sleep, increase or decrease in appetite, hopelessness, and suicidal ideation or suicide attempts are present. Dysthymia is the milder form of depression, during which suicidal ideation and attempts are not present. Manic episodes are of at least two weeks in duration and are characterized by euphoria, flight of ideas, grandiose delusions, pressured speech, increased activity, and insomnia.
A.Much of the existing body of knowledge concerning the causes of manic-depression points to genetics. Many scientists have isolated single genes to which they believe manic-depression can be attributed; however, very few agree on which gene it is. Egeland (1987) announced that she and her colleagues had found a gene that provided a strong diathesis toward manic-depression on chromosome 11. Two different groups of researchers (Detera-Wadleigh et al., 1987 and Hodgkinson et al., 1987) found no connection between the same gene and manic-depression, which led to the theory that more than one gene may be responsible for the disorder. At the same time, Baron et al. (1987) announced they had found a genetic link between manic-depression and a different gene. Both Baron and Egeland later stated that their findings may be inconclusive ((1)). In 1993, Bredbecka et al. announced that the gene for manic-depression is on the X-chromosome; the next year Berrettini et al. (1994) reported to have found the gene that contributes to the disorder on chromosome 18 and Straub et al. (1994) reported it to be on chromosome 21. McMahon et al. (1995) found evidence to suggest that manic-depression was more likely to be inherited from mothers than from fathers, proposing that the gene for the disorder would be different in women and men. At the same time, Stine (1995) published a paper supporting the theory that the gene for manic-depression is on chromosome 18. Gershon's research found that cases of manic-depression in which there is a connection to chromosome 18 was not present in cases where the disorder seemed to be inherited from the mother. In 1997, Nurnberger stated that he and his colleagues found evidence that points to as many as eight different chromosomes that may contain genes for manic-depression, hypothesizing that the various genes may work in different combinations ((2)); this might explain the different manifestations of manic-depression. Recently, Stine reported that there are "three or four locations that look about equally promising for finding manic-depression genes," one of them chromosome 18. His research also seems to support Gershon's; Stine believes that a predisposition from chromosome 18 is present only if inherited from the father ((3)). Another common theory of the etiology of manic-depression is neurochemical malfunctions in the brain. If indeed manic-depression has its origins in biology, something yet to be proven, and given the theories that suggest neurotransmitter dysfunctions in depression, perhaps the best solution to finding the cause of manic-depression would be to investigate a chemical basis of the disorder. It seems as if the best areas in which to start would be the same neurotransmitters that have thus far been implicated in depression and the areas affected by medications which alleviate symptoms of manic-depression. The most widely used medication to treat manic-depression today is lithium carbonate, an alkali salt. Lithium began to be utilized in the treatment of manic-depression approximately fifty years ago and yet no one knows exactly how it works ((4)), although it is known to be effective for approximately 67% of individuals with manic-depression. It has no known biological function and is not metabolized by the body; it is excreted in its whole form by the kidneys. One theory suggests that it alters membrane excitability by partially substituting for sodium. Another hypothesis is that it is an antagonist at calcium binding sites; this arose from findings that show low calcium levels in the cerebrospinal fluid of depressed individuals and high levels in manic individuals (Feldman et al., 1997). However, lithium is also used in the treatment of major depressive disorder, without manic episodes, as an adjunct to antidepressants. It has also been shown to have prophylactic effects for both depressive episodes and manic episodes in manic-depressive individuals. If lithium blocks calcium from binding at cell membranes and therefore decreases the amount of calcium available, it would not seem possible that it would aid in preventing depression, based on the aforementioned evidence from Feldman et al. Only vague theories exist concerning how lithium affects neurotransmitters; some researchers believe lithium promotes the uptake of serotonin and norepinephrine at the postsynaptic synapse, while others believe it decreases norepinephrine and dopamine activity.
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