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.
- Progressive multifocal leukoencephalopathy produces subacute progressive focal or cognitive deficits with white-matter lesions that usually have little mass effect; immune restoration is the central treatment.
- Primary central nervous system lymphoma can resemble toxoplasmosis, often with fewer enhancing lesions, profound immunosuppression and cerebrospinal-fluid Epstein-Barr-virus signal, but tissue may be required.
- Tuberculous meningitis tends to cause basal meningeal enhancement, cranial neuropathies, hydrocephalus, infarcts and low cerebrospinal-fluid glucose; obtain adequate volume for mycobacterial tests.
- CMV ventriculoencephalitis or polyradiculopathy occurs mainly with very low CD4 counts and can produce confusion, cranial signs, urinary retention and rapidly progressive lower-limb weakness.
- Always consider ordinary bacterial meningitis, HSV or VZV encephalitis, abscess and sepsis alongside opportunistic disease; immunosuppression may remove fever and cerebrospinal-fluid pleocytosis.
- Antiretroviral therapy should not be started or restarted on an improvised timetable: early immune recovery helps many infections but increases lethal intracranial inflammatory risk in cryptococcal or tuberculous meningitis.
- Coordinate HIV or transplant specialists, microbiology, neurology, neuroradiology and pharmacy because drug interactions, marrow toxicity, renal injury and immune-reconstitution syndromes commonly determine outcome.
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.
- Start syndrome-directed empirical treatment for bacterial meningitis, HSV encephalitis or a life-threatening opportunistic infection when delay is more dangerous than reduced microbiological yield.
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.Monitor blood count, liver and renal function, rash, crystalluria and sulfonamide allergy; major antiretroviral and prophylaxis decisions need HIV-pharmacy review.
Liposomal amphotericin B plus flucytosineInduction doses and duration follow current BHIVA cryptococcal-meningitis guidance, weight, kidney function and local antifungal access.Amphotericin causes renal potassium and magnesium loss, while flucytosine causes marrow and hepatic toxicity; therapeutic monitoring does not replace active intracranial-pressure management.