The findings reported in the Letter to the Editor authored
by Bungener and Jouvent are consistent with results we have
presented here (Castellon et al., 2000) and again underscore
the importance of considering the potentially multifactorial
nature of depression in many neurologic diseases/disorders.
We have suggested, although the idea is hardly a new one, that
depression in HIV/AIDS can be secondary to any of multiple
potential etiologies. For example, it may be a direct central
nervous system (CNS) consequence of infection (i.e., neurochemical
and/or neuropathological changes), a result of increased exposure
to social, medical, and financial stressors secondary to living
with HIV, a reaction to multiple losses (e.g., bereavement,
loss of instrumental capacity), or be an admixture of multiple
etiological factors. The phenomenology of this disruption of
mood, motivation, and affect may differ as a function of
etiology/pathophysiology. We believe that a prominent
amotivation/apathy syndrome may be a more pure manifestation
of the CNS effects of HIV-1 infection than is the more
heterogeneous construct of depression and therefore more closely
associated with other putative measures of CNS integrity (e.g.,
neurocognitive performance).
HIV-1 and the developing central nervous system
