Human immunodeficiency virus-associated dementia: review of pathogenesis, prophylaxis, and treatment studies of zidovudine therapy.

Abstract

Human immunodeficiency virus (HIV)-associated dementia (HIVD) has been reported in up to 15% of HIV-infected adult patients. Although the pathogenesis of HIVD remains unclear, HIV probably plays an important role in the syndrome, as evidenced by the correlation between cerebrospinal fluid (CSF) HIV load and neuropsychological functioning. Although a large number of antiretrovirals are used to treat HIVD, zidovudine is the best studied. Zidovudine therapy has been associated with reduced levels of HIV RNA in CSF, fewer HIV-related changes in brain tissue at autopsy, and time-limited improvements in neurological function among AIDS and HIVD patients. More recent studies have investigated the penetration into CSF of other antiretrovirals, including protease inhibitors, and the clinical efficacy of abacavir in the treatment of dementia. HIV encephalopathy may occur in 30%-60% of children with AIDS and causes significant disability. Zidovudine has been associated with improved neuropsychological functioning in children with progressive encephalopathy, but optimum dosing levels, duration of effect, and prophylactic potential remain to be demonstrated.