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HIV-1 encephalitis/HIV-1 encephalopathy
HIV-associated neurocognitive disorders
CT
Atrophy
Bilateral periventricular/diffuse WM hypointensities
Basal ganglia, cerebellum, brainstem hypodensity
MR
Diffuse “hazy” hyperintense WM on T2/FLAIR
Nonenhancing (if enhancement present, consider opportunistic infections, immune reconstitution inflammatory syndrome)
HIV has ability to cause neurologic disease
Does not replicate within neural/glial cells
Microglial nodules with multinucleated giant cells
WM pallor early, neocortical infection/atrophy late
Moderate cognitive impairment common despite good virologic response to therapy
Direct HIV infection of brain
Opportunistic infections absent
Cognitive, behavioral, motor abnormalities in 25-70%
Most frequent neurological manifestation of HIV infection
Evidence of “cerebral atrophy” by CT/MR does not indicate AIDS dementia complex in HIV-positive patient
Consider reversible causes 1st (dehydration, malnutrition, protein depletion, alcoholism)
HIV-1 encephalitis/encephalopathy (HIVE)
Direct HIV infection of brain
Opportunistic infections absent
Cognitive, behavioral, motor abnormalities in 25-70%
HIV-associated neurocognitive disorders (HAND) = most frequent neurological manifestations of HIV infection
Moderate cognitive impairment common despite good virologic response to therapy
Best diagnostic clue
Atrophy + bilateral diffuse white matter (WM) abnormalities
Pathology/imaging varies with patient age, acuity of onset
Location
Bilateral periventricular/centrum semiovale WM, basal ganglia, cerebellum, brainstem
Size
Variable, often diffuse
Morphology
Extends to gray-white matter junction
NECT
Children: Atrophy and diffuse WM hypodensity
In utero HIV infection: Characteristic bilateral and symmetrical calcifications in basal ganglia and frontal WM with eventual contrast enhancement
Adults: Normal or mild atrophy, WM hypodensity
No mass effect
CECT
Usually no contrast enhancement
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