Fein G, Biggins C A, MacKay S
Department of Psychiatry, University of California, San Francisco, USA.
Biol Psychiatry. 1995 Feb 1;37(3):183-95. doi: 10.1016/0006-3223(94)00119-N.
Both alcohol and human immunodeficiency virus (HIV) infection have been shown to produce central nervous system (CNS) morbidity in frontal brain 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 that occurs when novel nontarget stimuli are presented in the midst of a target detection paradigm. Four groups of subjects were compared: HIV+ alcohol abusers, HIV+ light/nondrinkers, HIV- alcohol abusers, and HIV- light/nondrinkers. The alcohol abuser and light/nondrinker HIV+ groups were matched on percent CD4 lymphocytes, insuring that the results reflected specific CNS effects and were not a result of differences between the groups in the degree of systemic immune suppression. Alcohol abuse and HIV infection had at least additive effects on P3A latency, consistent with alcohol abuse worsening the effect of HIV disease on frontal cortex function. Post-hoc analyses suggested that concomitant alcohol abuse results in the effects of HIV infection on P3A latency becoming manifest earlier in the HIV disease process.
酒精和人类免疫缺陷病毒（HIV）感染均已被证明会导致额叶脑区出现中枢神经系统（CNS）病变。本研究使用听觉P3A诱发电位，探究了酗酒是否会使HIV感染所致的CNS病变（影响额叶皮质功能方面）进一步加重。P3A代表一种定向反应，当在目标检测范式中呈现新的非目标刺激时，额叶皮质上的反应最为强烈。研究比较了四组受试者：HIV阳性酗酒者、HIV阳性少量饮酒者/不饮酒者、HIV阴性酗酒者以及HIV阴性少量饮酒者/不饮酒者。酗酒组和少量饮酒/不饮酒的HIV阳性组在CD4淋巴细胞百分比上相匹配，以确保结果反映的是特定的CNS效应，而非两组间全身免疫抑制程度差异导致的结果。酗酒和HIV感染对P3A潜伏期至少具有累加效应，这表明酗酒会使HIV疾病对额叶皮质功能的影响恶化。事后分析表明，同时存在酗酒情况会使HIV感染对P3A潜伏期的影响在HIV疾病进程中更早显现出来。
