ASPD blunts the effects of HIV and antiretroviral treatment on event-related brain potentials.

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.