Electrophysiological study of neurologically asymptomatic HIV1 seropositive patients.

EEGs, brainstem auditory evoked potentials (BAEPs) and auditory event-related potentials (ERPs) were recorded from 33 individuals infected with the human immunodeficiency virus, type 1 (HIV1+ patients: 13 CDC Class II or III; 20 Class IV). All were neurologically asymptomatic, non-demented, and had a past history of intravenous drug abuse. Sixteen age- and sex-matched normals and 10 HIV1- former drug addicts served as controls. Half of the HIV1+ and HIV1- subjects displayed mild EEG anomalies and, except for one HIV1+ patient, BAEPs were normal in both groups. ERPs were normal in all HIV1- subjects but anomalous (longer latencies of components P2, N2, P3; reduced amplitude of P3) in 9 HIV1+ patients (27%), the incidence of such anomalies being higher for Class IV than Class II/III patients. Auditory ERPs proved the most sensitive and specific of these electrophysiological procedures in detecting subclinical central nervous system involvement in HIV1 infection.

Electrophysiologic study of HIV-1 + patients without signs of peripheral neuropathy.

HIV-1 seropositive patients have a high frequency of nervous system diseases, and asymptomatic abnormalities are frequently detected. We studied 124 neurologically asymptomatic HIV-1 seropositive subjects and 23 normal control subjects by nerve conduction studies. No alterations were detectable in the asymptomatic stages of infection (CDC groups II and III), while subclinical peripheral nervous system (PNS) impairment was detected in symptomatic HIV-1 stages (CDC group IV). Specifically, in CDC group IV we observed a reduction in the motor conduction velocity of the deep peroneal nerve and the median nerve, and a similar reduction of the sensory conduction velocity of the sural nerve. There were no differences of the amplitude and area of the muscular response or of the sensory nerve action potential. As our patients did not present clinical or laboratory evidence for a toxic-dismetabolic etiology, our data indicate a progressive myelin damage more directly related to HIV-1 infection. This subclinical finding may have importance for the progression of the disease in the PNS.

Peripheral and central nervous system anomalies in HIV-1 infection: an electrophysiological study.

This study explored the neurophysiological changes in 87 HIV1+ (20 AIDS, 24 ARC, 24 LAS and 19 AC) patients showing no clinical evidence of neurological impairment. Tracing somatosensory responses by recording SEPs from upper and lower limbs, we found a slowing of both peripheral and central nerve conduction. Peripheral alterations occurred in virtually all patients of the AIDS group. Central anomalies, confined largely to the lower spinal cord, manifested themselves only during the later stages of the disease (ARC and AIDS) and then only in about half of our sample. More marked neurotropic varieties of HIV1 may account for these differences. We feel that SEP studies can serve to reveal pre-clinical NS involvement in HIV1+ subjects and should be included among research strategies aimed at tracing the evolution of AIDS.

Neurological involvement in group iv HIV-positive patients. Neurophysiological and clinical data.

Spinal and cortical SEP responses were recorded during tibial and median nerve stimulation in 58 HIV+ subjects (8 IV/C1, 24 IV/C2 & IV/A, 11 III and 15 II), all asymptomatic from a neurological point of view. The electrophysiological features were compared with clinical assessment and serum HIV markers for purposes of prognosis and therapy. In group IV we observed a slowing of conduction along the afferent pathway in the spinal tracts and afferent ways to the cortex. The major part of the delay occurred in the mid and lower medullary tract. These results agree with neuropathological finding from post-mortem examination in AIDS pts.