ASPD blunts the effects of HIV and antiretroviral treatment on event-related brain potentials
ASPD blunts the effects of HIV and antiretroviral treatment on event-related brain potentials
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DOI：
10.1159/000089917
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发表时间：
2006-01-01
影响因子：
3.2
通讯作者：
Shanley, JD
中科院分区：
文献类型：
--
作者：
Bauer, LO;Shanley, JD
一些研究表明，抗逆转录病毒疗法减少了艾滋病毒/艾滋病对大脑功能的不利影响。然而，很少有研究探讨共病精神障碍的作用，限制恢复的幅度。本研究探讨了存在与不存在这样一种障碍反社会人格障碍（ASPD）对脑功能的影响，在HIV-1血清阴性对照组（n = 68）和HIV-1血清阳性患者接受（n = 26），与不接受（n = 71），抗逆转录病毒治疗。脑功能的主要依赖措施是P300事件相关电位的振幅，潜伏期和地形图。ANCOVA显示ASPD的显著主效应以及ASPD与HIV-1/治疗状态之间的相互作用。与ASPD阴性组相比，ASPD参与者的额叶P300振幅显着降低。更重要的是，进一步的分析表明，ASPD减弱了未经治疗的HIV/ AIDS患者P300的下降以及抗逆转录病毒治疗患者P300的改善。结果表明，抗逆转录病毒治疗对HIV-1血清阳性伴ASPD患者的P300改善最小。抗逆转录病毒药物疗效的缺乏很难用药物依从性差来解释。对治疗的反应减弱更可能与预先存在的神经生理学衰减有关，该神经生理学衰减局限于艾滋病毒/艾滋病和抗逆转录病毒治疗发挥最大作用的相同大脑区域。版权所有（C）2006 S. Karger AG，巴塞尔。
Several studies have demonstrated that antiretroviral therapy diminishes the adverse effects of HIV/AIDS on brain function. Yet, few studies have examined the role of comorbid psychiatric disorders in limiting the magnitude of recovery. The present study examined the effects of the presence versus absence of one such disorder antisocial personality disorder ( ASPD) - on brain function in an HIV-1 seronegative control group ( n = 68) and in HIV-1 seropositive patients receiving ( n = 26), versus not receiving ( n = 71), antiretroviral treatment. The primary dependent measures of brain function were the amplitude, latency, and topography of the P300 event-related potential. ANCOVA revealed a significant main effect of ASPD as well as an interaction between ASPD and HIV-1/treatment status. Participants with ASPD exhibited a significant decrement in frontal P300 amplitude in comparison to the ASPD-negative groups. More importantly, further analyses showed that ASPD blunted the decrement in P300 accompanying untreated HIV/ AIDS as well as the improvement in P300 accompanying antiretroviral treatment. The results suggest that P300 is minimally improved by antiretroviral therapy among HIV-1 seropositive patients with comorbid ASPD. The lack of antiretroviral efficacy is not easily explained by poor medication compliance. The diminished response to treatment is more likely related to a pre-existing neurophysiological decrement localized to the same brain regions where HIV/AIDS and antiretroviral treatment exert their maximal effect. Copyright (C) 2006 S. Karger AG, Basel.