Neuropsychiatric alterations and neurocognitive performance in HIV/AIDS: A response to C. Bungener and R. Jouvent

Abstract

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).