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From the Departments of Neurosciences (Dr. Iragui and J. Kalmijn), and Ophthalmology (Drs. Plummer, Sample, and Freeman), University of California San Diego School of Medicine, and the Veterans Affairs Medical Center (Dr. Iragui), San Diego, CA; and the Department of Ophthalmology (Dr. Trick), Henry Ford Health Sciences Center, Detroit, MI.
Supported by the Veterans Affairs Research Service and grants 4 P50 MH45294, EYO7366, and EYO8208.
Received November 14, 1995. Accepted in final form April 16, 1996.
Address correspondence and reprint requests to Dr. Vicente J. Iragui, Neurophysiology Laboratory (7740), UCSD Thornton Hospital, 9300 Campus Point Drive, La Jolla, CA 92037-7740.
Retinal microangiopathy associated with HIV infection is usually asymptomatic and escapes detection unless funduscopic examination is performed when evanescent cotton-wool spots are present. The aim of this study was to assess retinal and optic nerve/retrochiasmal function in HIV infection by means of electrophysiologic techniques that are sensitive to the detection of subclinical visual impairment. We studied transient and steady state pattern electroretinograms (PERGs) and pattern-reversal visual evoked potentials (PVEPs) in 21 HIV-negative controls and 33 HIV-positive subjects (16 with CD4 >or=to 200/mL and 17 with CD4 < 200/mL) without visual symptoms or infectious retinopathy. HIV-positive subjects with CD4 >or=to 200/mL had reduced amplitude of the transient PERG P1 potential, but no other latency or amplitude abnormalities. The HIV-positive group with CD4 < 200/mL had reduced P1 transient PERG amplitude, as well as latency delay of the transient PVEP. These findings suggest that HIV infection is associated with subclinical retinopathy and that, when severe immunosuppression occurs, both retinopathy and optic nerve/retrochiasmal dysfunction are present. Transient PERGs are more sensitive measures of visual system disease in HIV infection than are steady state responses.
NEUROLOGY 1996;47: 1452-1456
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