Synopsis
Recognise subacute tuberculous meningitis, obtain high-volume cerebrospinal-fluid microbiology without trusting a negative rapid assay, start multidrug treatment and corticosteroids promptly, and manage hydrocephalus, infarction and paradoxical inflammation.
- TB meningitis usually evolves over days to weeks with headache, fever, malaise, weight loss, cranial neuropathy or cognitive decline.
- CSF commonly shows lymphocytes, high protein and low glucose, but early neutrophils and immune-suppressed low-cell profiles occur.
- Send a large CSF volume for mycobacterial culture and molecular testing and repeat sampling when initial tests are negative but probability remains high.
- MRI best demonstrates basal enhancement, hydrocephalus, infarction and tuberculoma; chest imaging and sputum can provide an easier culture and susceptibility source.
- Start treatment on clinical probability because smear and rapid molecular sensitivity are limited in paucibacillary CSF disease.
- Use current UK weight-banded rifampicin, isoniazid, pyrazinamide and ethambutol for 2 months followed by rifampicin and isoniazid to complete about 12 months.
- Give adjunctive dexamethasone with a staged taper for TB meningitis unless a specialist contraindication exists.
- Test HIV and coordinate ART timing, rifamycin interactions and immune-reconstitution risk through a TB-HIV team.
Key red flags
Reduced consciousness, papilloedema, repeated vomiting or sixth-nerve palsy raises hydrocephalus and requires urgent neuroimaging and neurosurgical review.
Focal deficit or seizure may reflect basal-artery vasculitis and infarction rather than simple meningeal irritation.
A negative CSF PCR or smear does not exclude TB meningitis and must not postpone treatment when the syndrome is convincing.
Hyponatraemia requires volume assessment because SIADH and cerebral salt wasting have different fluid implications.
Weeks of headache, fever, vomiting, lethargy and weight loss with neck stiffness or cranial neuropathy is a typical presentation.
Worsening headache, sixth-nerve palsy, papilloedema and declining consciousness suggests obstructed CSF flow.
Focal weakness, dysphasia or movement disorder indicates perforator infarction from basal vasculitis.
New focal signs or enlarging lesions after initial treatment may be inflammatory paradox rather than resistance, but both require assessment.
Investigation priorities
Maximise smear, culture and molecular diagnostic yield.
Management branches
Subacute meningitis with low glucose, cranial neuropathy or TB exposure creates significant probability.
- Stabilise physiology, examine cranial nerves and focal neurology and obtain urgent imaging before lumbar puncture when mass effect is plausible.
- Collect high-volume CSF and multiple extraneural specimens for molecular tests, culture and susceptibility before therapy when safe.
- Test HIV and record weight, vision, renal, liver, sodium and all interacting medicines and pregnancy status.
- Start treatment and dexamethasone on probability; do not await culture when delay risks irreversible CNS injury.