LONG LATENCY EVENT-RELATED POTENTIALS IN PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS

Long latency auditory evoked potentials were recorded in 55 homosexual men infected with human immunodeficiency virus (HIV). Forty‐one of these patients were asymptomatic from the infection and 14 had clinical signs of illness. Nine of the symptomatic patients were demented and 8 (6 of whom were demented) met other diagnostic criteria for acquired immunodeficiency syndrome (AIDS). Cerebral responses were recorded from Fz, Cz, and Pz electrode placements referred to linked mastoids and averaged separately to rare (2,000 Hz) and frequent (1,000 Hz) tones presented in a pseudorandom sequence. Electroencephalography (EEG) was performed in 54 of the patients and magnetic resonance imaging (MRI) or computed tomography (CT) was done in 14 (13 of whom were symptomatic from the infection). The latency of N1, P2, N2, and P3 components was delayed in HIV‐positive patients compared to normal and this was particularly so for the N1, N2, and P3 components. These changes were more marked in those patients who were symptomatic from their infection, especially in those who were demented. They were, however, present to a lesser degree even in asymptomatic (Class II) patients. Thus, 78% of the demented patients and 28% of nondemented patients had a delay in latency of at least one of the evoked potential components beyond the upper limit of our normal population. By contrast, the EEG was normal in all patients with asymptomatic HIV infection and most symptomatic patients, although 5 patients in this latter group had mild generalized slowing. MRI and CT findings were similarly nonspecific, particularly in the nondemented group. Our findings suggest that long latency auditory evoked potentials may be particularly useful in the evaluation of HIV‐infected patients, possibly permitting the early recognition of HIV encephalopathy and identifying those patients with a worse prognosis or in need of more aggressive management; perhaps, also, recording these potentials will permit the course of this disorder, and its response to therapy, to be followed. Copyright © 1990 American Neurological Association