This complication occurs in 15% of AIDS patients usually in patients with a CD4 count below 200/mms. The early reports of evidence of cognitive abnormalities in HIV positive asymptomatic individuals have been discounted by large cohort studies using clinical, neuropsychological, MRI and neurophysiological methods of assessment. The clinical picture is of a variably progressive dementia with psychomotor slowing and impairment of memory.
The diagnosis is one of exclusion of other infective or neoplastic aetiologies by brain imaging and CSF examination. Although there is a correlation between the CSF HIV RNA viral load and the severity of dementia, there is too much overlap for use as a diagnostic test. A neuropsychological assessment is also helpful. MRI shows cortical atrophy and diffuse or patchy white matter high signal on T2-weighted images.
The underlying pathophysiological mechanisms are unclear but HIV is usually isolated from the microglial cells and astrocytes rather than neuronal cells. Productive infection of the macrophages and microglia with the release of cytokines such as TNF results in neuronal damage.
Since the introduction of zidovudine and subsequently HAART the incidence of HIV-associated dementia has progressively declined. However, more recently there is concern that the CNS may become a sanctuary for HIV, since most of the newer drugs penetrate the CNS poorly.
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