AIDS
Dementia, myelopathy due to HIV infection are AIDS-defining illnesses.
CNS Pathogenesis
HIV enters CNS in primary infection. May produce no symptoms, acute self-limited syndrome, or chronic disorder.
Possible causes: HIV itself, secondary opportunistic infections or neoplasia, metabolic abnormalities, complications of drug therapy, nutritional.
CNS invasion and injury: mechanism not known. In brain, virus infects only microglial cells and macrophages, not neurons, although designated “neurotropic virus” because neurologic disorders are frequent.
Neurologic disorders affect 70% of patients with AIDS; first manifestation of AIDS in 10–20%.
Clinical Syndromes
HIV-related Neurologic Syndromes in Early Infection
Indistinguishable from CNS infection by other viruses: aseptic meningitis, encephalopathy, leukoencephalitis, seizures, transverse myelitis, cranial or peripheral neuropathy, polymyositis, myoglobinuria. Course self-limited, often full neurologic recovery.
CSF abnormalities (pleocytosis up to 200 cells/mm3, oligoclonal bands) differentiate HIV from postinfectious disorders. HIV antibody test sometimes negative because symptoms may precede seroconversion by weeks. Consider p24 antigen and viral load assay if serology negative.
HIV-Related Neurologic Syndromes in Chronic Infection
AIDS Dementia Complex (ADC)
Other terms: HIV encephalitis, HIV encephalopathy.
Severe dementia, behavioral changes; motor disorder. Myelopathy and peripheral neuropathy in 25%. In HIV-positive people, these syndromes are diagnostic of AIDS.
Usually progressive; may be static.
Symptoms
Early: apathy, social withdrawal, diminished libido, slow thinking, poor concentration, forgetful. Psychiatric syndromes: psychosis, depression, mania.
Motor signs: slow movements, leg weakness, gait ataxia.
Advanced stage: akinetic mutism; immobile; global cognitive impairment, urinary incontinence.
Encephalopathy in children: may be static or progressive. Intellectual deterioration, microcephaly, delayed developmental milestones; pseudobulbar palsy; spastic quadriparesis (see also Chapter 168).
Investigations
CSF: normal or mild pleocytosis, high protein content, oligoclonal bands.
CT, MRI: Adults: cerebral atrophy, leukoencephalopathy. Children: also basal ganglia calcification. Pathology: microglial nodules, giant cells, focal perivascular demyelination, gliosis, neuronal loss in frontal cortex. Severity of pathology not always correlated with severity of dementia.
Treatment
Zidovudine (AZT), selegiline, nimodipine: mixed results. Improve, slow dementia, or no effect.
Predictors of dementia: CD4+ count <100 cell/μL, anemia, or AIDS-defining infection or neoplasm (19% to 25% risk in 2 years).
