Skip to content

HIV encephalopathy

Summary

fleuron

  • HIV encephalopathy is a neurocognitive disorder caused by HIV infection of the central nervous system
  • Characterised by progressive cognitive decline, motor dysfunction, and behavioural changes
  • Neuroimaging typically shows cerebral atrophy and white matter abnormalities1

Pathophysiology

  • Direct infection of CNS by HIV, crossing the blood-brain barrier via infected monocytes
  • Neuronal damage caused by:
    • Viral proteins (e.g., gp120, Tat)
    • Inflammatory mediators released by infected glial cells
    • Oxidative stress and mitochondrial dysfunction
  • Disruption of the blood-brain barrier, leading to increased permeability

Demographics

  • Affects 15-50% of HIV-infected individuals
  • Risk factors:
    • Advanced HIV disease (low CD4 count, high viral load)
    • Older age
    • Co-infections (e.g., hepatitis C)
    • Substance abuse

Diagnosis

  • Clinical presentation:
    • Cognitive impairment (memory, attention, executive function)
    • Motor dysfunction (gait disturbance, tremor)
    • Behavioural changes (apathy, depression)
  • Neuropsychological testing
  • CSF analysis:
    • Elevated protein levels
    • Presence of HIV RNA
  • Exclusion of other causes (e.g., opportunistic infections, tumours)

Imaging

  • MRI findings:
    • Cerebral atrophy (cortical and subcortical)
    • White matter hyperintensities on T2-weighted and FLAIR sequences
    • Bilateral, symmetrical involvement of periventricular and deep white matter
    • Corpus callosum thinning
  • Advanced imaging techniques:
    • DTI: Reduced fractional anisotropy in white matter tracts
    • MR spectroscopy: Decreased N-acetylaspartate, increased choline and myo-inositol
  • FDG-PET:
    • Reduced glucose metabolism in subcortical and cortical regions

panels-1 panels-2 panels-3

  • Patient who had been non-compliant with antiretroviral therapy presented with cognitive impairment.
  • MRI showed a transient diffuse encephalopathy with swelling.
  • On the follow-up imaging, the leukoencephalopathy regressed and brain volume had decreased.

panels-1

  • A 50-year-old patient presented with cognitive impairment.
  • A new diagnosis of HIV was made on admission.
  • MRI showed patchy diffuse white matter hyperintensity without enhancement in both cerebral hemispheres that spared the subcortical U fibres (red arrows).
  • Following CSF analysis to exclude other causes and a follow-up scan 1 month later that showed no changes, the findings were ascribed to HIV encephalopathy.

Treatment

  • Antiretroviral therapy, which can improve the leukoencephalopathy; the key is excluding opportunistic infection and lymphoma

Differential diagnosis

Differential Diagnosis Distinguishing Feature
Progressive Multifocal Leukoencephalopathy (PML) Asymmetric, subcortical white matter lesions with scalloped margins; no enhancement in classic PML
Toxoplasmosis Ring-enhancing lesions in basal ganglia and at grey-white matter junction; restricted diffusion in centre
Primary CNS Lymphoma Periventricular or corpus callosum homogeneously enhancing mass; marked diffusion restriction
CADASIL / Small vessel disease Anterior temporal pole and external capsule involvement; subcortical lacunar infarcts
HSV Encephalitis Asymmetric haemorrhagic temporal lobe and insular FLAIR hyperintensity with diffusion restriction

  1. B Brew. The clinical spectrum and pathogenesis of HIV encephalopathy, myelopathy, and peripheral neuropathy. 1994. Current opinion in neurology - Open in new tab. ↩