ALCOHOL-ABUSE AND HIV-INFECTION HAVE ADDITIVE EFFECTS ON FRONTAL-CORTEX FUNCTION AS MEASURED BY AUDITORY-EVOKED POTENTIAL P3A LATENCY

Both alcohol and human immunodeficiency virus (HIV) infection have bee n shown to produce central nervous system (CNS) morbidity in frontal b rain regions. The degree to which the CNS morbidity in HIV infection, as it affects frontal cortex function, may be preferentially increased by alcohol abuse was examined using the auditory P3A evoked potential . The P3A indexes an orienting response, maximal over frontal cortex t hat occurs when novel nontarget stimuli are presented in the midst of a target detection paradigm. Four groups of subjects were compared: HI V+ alcohol abusers, HIV+ light/nondrinkers, HIV- alcohol abusers, and HIV- light/nondrinkers. The alcohol abuser and light/nondrinker HIV+ g roups were matched on percent CD4 lymphocytes, insuring that the resul ts reflected specific CNS effects and were not a result of differences between the groups in the degree of systemic immune suppression. Alco hol abuse and HIV infection had at least, additive effects on P3A late ncy, consistent with alcohol abuse worsening the effect of HIV disease on frontal cortex function. Post-hoc analyses suggested that concomit ant alcohol abuse results in the effects of HIV infection on P3A laten cy becoming manifest earlier in the HIV disease process.