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TEXTBOOK PRESENTATION
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Patients with severe HIV encephalopathy typically have advanced AIDS with a slowly progressive dementia eventually accompanied by motor symptoms.
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Subcortical dementia characterized by cognitive, behavioral, and psychomotor slowing
Prevalence 15–20% in AIDS prior to introduction of ART
40–50% decrease in incidence since the introduction of ART. However, prevalence is rising due to increasing survival.
Severe form of HIV encephalopathy effectively eliminated if treated with ART
Milder deficits still commonly detected by neuropsychological testing
Principal target of HIV virus is perivascular CNS macrophages. Astrocytes may also become infected.
Severe HIV encephalopathy develops late with CD4TL typically < 200 cells/mcL.
Two-fold increased risk in patients aged ≥ 50 years.
Neurotoxicity of HIV may be synergistic with that of cocaine or methamphetamine.
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EVIDENCE-BASED DIAGNOSIS
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History and physical exam
Memory complaints: 70%
Cognitive slowing: 25–30%
Gait difficulty: 45%
Behavioral changes: 10–20%
Seizures: 5–10%
Focal findings uncommon
Laboratory findings
MRI: T2 images with hyperintensities in the deep white matter and basal ganglia without contrast enhancement and/or atrophy; the distribution of lesions is symmetrical in contrast to PML lesions.
CSF
Useful to rule out other infections
Mild CSF leukocytosis and protein elevations may be seen.
CSF HIV RNA levels are not useful because they do not correlate with the severity of HIV encephalopathy.
Cannot diagnose HIV encephalopathy with certainty
Neuropsychological testing useful in evaluating the severity and response to ART
HIV encephalopathy is a diagnosis of exclusion. Diagnostic evaluations serve to exclude other OIs, malignancy, or substance abuse.
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Most patients treated with ART show only partial reversal of neurologic deficits. Early therapy is therefore important.
Elevated levels of CSF beta-microglobulin (suggesting ongoing inflammation) predicted better neurologic recovery with ART.