Synopsis
Use immune status, tempo, imaging and cerebrospinal-fluid evidence to distinguish opportunistic neurological infections, start syndrome-appropriate treatment, and time antiretroviral or immune therapy safely with specialists.
- The differential is shaped by the type and depth of immune impairment, antiretroviral or prophylaxis history, transplant medicines, neutropenia, corticosteroid exposure, geography and previous latent infections.
- In advanced HIV, cerebral toxoplasmosis often causes headache, fever, focal deficit or seizure with multiple ring-enhancing lesions, frequently involving basal ganglia, although imaging is not diagnostic by itself.
- Cryptococcal meningitis typically causes subacute headache, fever and cognitive slowing; neck stiffness may be absent and raised opening pressure is a major cause of visual loss and death.
Key red flags
Rapid flaccid leg weakness, saddle sensory change, areflexia and sphincter dysfunction in profound immunosuppression is an urgent cauda-equina-like opportunistic syndrome.
Investigation priorities
Quantify immune risk and establish whether virological failure or previously undiagnosed HIV is present.
Management branches
An immunosuppressed person develops new neurological symptoms.
- Stabilise airway and seizures, record antiretroviral and immunosuppressive medicines, CD4 or neutrophil history, prophylaxis, travel, exposures and symptom tempo.
- Obtain urgent contrast brain imaging before lumbar puncture when headache, focal signs, seizure or impaired consciousness makes a mass lesion plausible.
Key medicines
Pyrimethamine, sulfadiazine and folinic acidUse the current BHIVA weight-based loading and maintenance regimen under specialist care; folinic acid accompanies pyrimethamine throughout marrow-toxic exposure.
Liposomal amphotericin B plus flucytosineInduction doses and duration follow current BHIVA cryptococcal-meningitis guidance, weight, kidney function and local antifungal access.