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Higher rates of alcohol use have been reported in HIV+ individuals
compared to the general population. Both heavy alcohol use and HIV
infection are associated with increased risk of neuropsychological (NP)
impairment. We examined effects of heavy active alcohol use and HIV on
NP functioning in a large sample of community-residing HIV+ individuals
and HIV− controls. The four main study groups included 72
HIV− light/non-drinkers, 70 HIV− heavy drinkers
(>100 drinks per month), 70 HIV+ light/non-drinkers, and 56 HIV+
heavy drinkers. The heavy drinking group was further subdivided to
assess effects of the heaviest levels of active alcohol use (>6
drinks per day) on NP functioning. A comprehensive NP battery was
administered. Multivariate analysis of covariance was employed to
examine the effect of HIV and alcohol on NP functioning after adjusting
for group differences in age and estimated premorbid verbal
intellectual functioning. The analyses identified main effects of heavy
drinking and HIV on NP function, with greatest effects involving the
contrast of HIV+ heavy drinkers and the HIV− light drinkers.
Synergistic effects of heaviest current drinking and HIV infection were
identified in analyses of motor and visuomotor speed. Supplementary
analyses also revealed better NP function in the HIV+ group with
antiretroviral treatment (ART) and lower level of viral burden, a
finding that was consistent across levels of alcohol consumption.
Finally, heavy alcohol use and executive functioning difficulties were
associated with lower levels of self-reported medication adherence in
the HIV+ group. The findings suggest that active heavy alcohol use and
HIV infection have additive adverse effects on NP function, that they
may show synergistic effects in circumstances of very heavy active
alcohol use, and that heavy drinking and executive functioning may
mediate health-related behaviors in HIV disease. (JINS, 2005,
HIV infection often results in MRI-detectable brain
atrophy and white matter signal hyperintensities (WMSHs).
Magnetic resonance images were obtained from 31 HIV+ male
patients and 10 high-risk controls. Variation within the
HIV+ group on neuropsychological (NP) impairment and stage
of systemic disease were relatively independent, allowing
examination of the relative association of MRI measures
with NP impairment versus with systemic stage
of disease. HIV+ patients compared to high-risk controls
evidenced global atrophy, reduced caudate nuclei volume,
and a trend to gray matter volume loss but no difference
in white matter volume or in WMSHs. These effects were
progressive with CDC clinical stage such that patients
at CDC stage A had values very close to those of controls,
while patients at CDC stage C had the most abnormal values.
In contrast, the relationship between these MRI variables
and severity of NP impairment was much less dramatic, with
the mildly to moderately impaired HIV+ subjects showing
MRI volume effects greater than or equal to those of the
severely impaired HIV+ subjects. These results suggest
that MRI-detectable brain atrophy secondary to HIV infection
is not the primary substrate underlying the progressive
NP impairment in HIV disease. (JINS, 1997, 3,
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