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Abstract
Neuroimaging studies of major depression have identified neurophysiologic abnormalities
in multiple areas of the orbital and medial prefrontal cortex, the amygdala, and related
parts of the striatum and thalamus. Some of these abnormalities appear mood state-dependent
and are located in regions where cerebral blood flow increases during normal and other
pathologic emotional states. These neurophysiologic differences between depressives
and control subjects may thus implicate areas where physiologic activity changes to
mediate or respond to the emotional, behavioral, and cognitive manifestations of major
depressive episodes. Other abnormalities persist following symptom remission, and
are found in orbital and medial prefrontal cortex areas where postmortem studies demonstrate
reductions in cortex volume and histopathologic changes in primary mood disorders.
These areas appear to modulate emotional behavior and stress responses, based upon
evidence from brain mapping, lesion analysis, and electrophysiologic studies of humans
and/or experimental animals. Dysfunction involving these regions is thus hypothesized
to play a role in the pathogenesis of depressive symptoms. Taken together, these findings
implicate interconnected neural circuits in which pathologic patterns of neurotransmission
may result in the emotional, motivational, cognitive, and behavioral manifestations
of primary and secondary affective disorders.