Abstract
According to the original catecholamine hypothesis of affective disorder [1], mania was thought to be due to an overactivity within central noradrenergic (and possibly dopaminergic) pathways. But in recent years dopamine (DA) has emerged as being of relatively greater importance. The first hint that this might be the case came from the report that fusaric acid, a DA hydroxylase inhibitor, exacerbated the condition [2]. We went to examine this possibility further by studying the effects of pimozide, a relatively specific dopamine (DA) receptor blocking compound in five patients presenting with a florid manic illness [3]. The results were encouraging; all five patients improved within three days. We concluded that our finding was consistent with the idea that mania results from overactivity of central DA pathways. The same year Gerner et al [4] came to a similar conclusion on the basis of their finding that piribedil, a DA receptor agonist, precipitated manic episodes in a predisposed individual, while pimozide ameliorated them.
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