Abstract
The neurobiology of bipolar affective illness can be described in a model with structural and functional components, which also address the role of stressors, coping mechanisms, and psychophysical disposition. More data exist on depressive than on manic patients or on patients switching from one clinical pole to the other. Structural and functional chronobiological alterations appear to play a major role in the pathophysiology of bipolar illness. From an anatomical view, neurobiological abnormalities are primarily confined to limbic-striatal-pallidal-thalamocortical circuits. The whole cascade of neural signaling is changed starting from neurotransmitters and neuromodulators to receptor-mediated intracellular signal transduction targeting nuclear gene expression. Transnosological factors such as suicidal tendency appear to essentially modulate those changes. Replicated data on decisive neurobiological differences between bipolar and unipolar affective disorders are currently not yet available.
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