Although the pathophysiology of depression is not fully understood in; eith
er primary depression (i.e., no known neuropathology related to depression)
or secondary depression (i.e., neuropathologic disorder that leads to depr
ession), a number of studies have begun to identify aspects of the pathophy
siology of both primary and secondary depression. This article reviews the
findings of studies examining the pathophysiology of depression following s
troke, Parkinson's disease, or Huntington's disease and compares them to fi
ndings: in primary depression.-Studies examining glucose metabolic rates or
blood flow changes in regional brain areas found that stroke! Parkinson's
disease, and Huntington's disease; as well as primary depression, were all
associated with decreased activity or brain lesions in the orbital frontal
cortex and basal ganglia. There were also abnormalities noted in the basal
temporal lobes, cingulate cortex, and thalamus in some but not all disorder
s. Studies in stroke have also noted depletions of serotonin receptors in l
eft temporal cortex associated with depression.;These findings are consiste
nt with the hypothesis that the pathophysiology of secondary and primary de
pression involves the dysfunction of one or more of the cortical-basal gang
lia-thalamic neuronal loops, This dysfunction may be mediated by decreased
serotonin release. These studies may ultimately lead to more focused and sp
ecific treatments.