HIV Neurology
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Direct answer
Neurological disease in HIV comes from the virus itself, from opportunists arriving on schedule with falling CD4 counts, and from antiretroviral toxicity and immune reconstitution. HIV-associated neurocognitive disorder spans asymptomatic impairment to dementia with subcortical features, and distal sensory polyneuropathy is the commonest manifestation. The CD4 count organises the opportunists: toxoplasmosis and cryptococcal meningitis below 100 cells, progressive multifocal leukoencephalopathy at low counts, and cytomegalovirus disease below 50 — with primary central nervous system lymphoma alongside and immune reconstitution after antiretroviral initiation.
What you must remember
- HIV-associated neurocognitive disorder: subcortical cognitive slowing; diagnose by excluding opportunists, depression, intoxication and antiretroviral neurotoxicity; rarer in the antiretroviral era but not absent.
- Distal sensory polyneuropathy: painful stocking-distribution paraesthesiae with absent ankle jerks, from the virus or older antiretrovirals such as stavudine, still encountered in places.
- Cerebral toxoplasmosis: CD4 below 100 with multiple ring-enhancing lesions favouring basal ganglia; treat empirically with pyrimethamine, sulfadiazine and folinic acid — response within two weeks confirms clinically, non-response demands biopsy for lymphoma.
- Cryptococcal meningitis: India carries a large burden; CD4 below 100 with headache and raised pressure, positive antigen and India ink; World Health Organization 2022 guidance endorses single high-dose liposomal amphotericin with flucytosine and fluconazole for one week, with conventional amphotericin-based induction where liposomal drug or flucytosine is unavailable (flucytosine access in India remains variable); therapeutic lumbar punctures save lives; defer antiretrovirals four to six weeks.
- Progressive multifocal leukoencephalopathy: JC virus infection of oligodendrocytes producing non-enhancing white-matter lesions conforming to tracts, confirmed by CSF polymerase chain reaction; immune restoration is the main therapy.
- Cytomegalovirus below 50 cells: retinitis with floaters, lumbosacral radiculomyelopathy with ascending weakness and bladder involvement, and encephalitis; treated with ganciclovir, valganciclovir or foscarnet.
- Primary central nervous system lymphoma: Epstein-Barr-driven single or few deep enhancing lesions with supportive CSF polymerase chain reaction, treated with antiretrovirals plus oncology-directed therapy rather than steroids-first, which obscure the biopsy. Immune reconstitution inflammatory syndrome — paradoxical worsening weeks after antiretrovirals as immunity recovers, dominated by tuberculosis and cryptococcal variants in India — takes corticosteroids when severe while antiretrovirals usually continue.
Common confusion
The ring-enhancing-lesion triad — toxoplasmosis, lymphoma, tuberculoma — is the recurring decision: toxoplasmosis is multiple and basal with prompt empirical-therapy response, lymphoma is fewer, larger and Epstein-Barr-positive, and tuberculoma travels with basal meningitis in India. Cryptococcal and tuberculous meningitis separate on antigen testing and India ink, not gestalt. Cognitive decline is not automatically dementia: depression, efavirenz toxicity and metabolic disease queue first. Immune reconstitution misread as treatment failure leads to blind switches instead of steroids with continued therapy.
Exam-focused takeaway
Organise revision by CD4 strata — below 100 for toxoplasmosis and cryptococcus, below 50 for cytomegalovirus — and by the empiric-then-biopsy algorithm for mass lesions. The cryptococcal numbers carry marks: antiretroviral deferral of four to six weeks and therapeutic lumbar punctures for pressure. Expect an immune reconstitution stem answered by steroids with continued therapy, and a neurocognitive stem answered by exclusion.
Frequently asked questions
At what CD4 count does cryptococcal meningitis occur?
Usually below 100 cells per microlitre; headache in that range warrants antigen testing before it becomes an emergency.
How is cerebral toxoplasmosis managed?
Empirical pyrimethamine with sulfadiazine and folinic acid; clinical and radiological response within two weeks confirms the diagnosis, non-response prompts biopsy.
What causes progressive multifocal leukoencephalopathy?
Reactivation of JC virus infecting oligodendrocytes, producing non-enhancing demyelinating lesions; immune restoration is the mainstay of therapy.
When should antiretrovirals start after cryptococcal meningitis?
After approximately four to six weeks of antifungal therapy, balancing fungal control against immune reconstitution risk.
What is immune reconstitution inflammatory syndrome?
Paradoxical deterioration within weeks of starting antiretrovirals as immunity reacts to latent antigen, classically with tuberculosis and cryptococcus; corticosteroids when severe.