Tuberculous Meningitis
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Direct answer
Three weeks of fever and headache, then a sixth nerve palsy — that is the textbook tempo of tuberculous meningitis, a subacute meningitic illness diagnosed on cerebrospinal fluid showing lymphocytic pleocytosis, high protein and low glucose, with confirmation by CBNAAT (GeneXpert MTB/RIF) and culture. Treatment is antitubercular therapy for an extended course with adjunctive corticosteroids, and outcomes hinge on stage at presentation, which makes early suspicion the whole game.
What you must remember
- Tempo is the clue: days to weeks of headache and fever (contrast the hours of pyogenic meningitis and the brief watch of viral), with night sweats, malaise and contact history in many.
- Medical Research Council staging: stage I — no neurological deficit; stage II — cranial nerve palsies, focal deficit or confusion; stage III — coma; mortality climbs steeply by stage, driving the treat-early reflex.
- CSF pattern: lymphocytic pleocytosis (commonly 50–500 cells; early neutrophilic preponderance can mislead), protein raised (often 100–500 mg/dL and higher with spinal block), glucose low (CSF-to-blood ratio below about 0.5); a cobweb coagulum on standing is classical.
- Diagnosis: CBNAAT/GeneXpert MTB/RIF on CSF is the rapid test endorsed under India's National TB Elimination Programme (moderate sensitivity, so a negative result never overrides compatible findings); mycobacterial culture remains reference standard; adenosine deaminase and TB PCR are supportive.
- Neuroimaging: basal meningeal enhancement after contrast, hydrocephalus (communicating more than obstructive), tuberculomas, and ischaemic infarcts of the basal ganglia and internal capsule from arteritis of the lenticulostriate and thalamoperforating vessels.
- Sixth nerve palsy is the commonest cranial nerve involvement (long intracranial course); third, fourth, seventh and eighth follow; vision and hearing are threatened late.
- Treatment: antitubercular therapy — Indian practice commonly uses two months of intensive therapy (HRZE) followed by ten months of continuation (HR), while WHO guidance since 2022 also supports shorter intensive regimens in selected adults — always with adjunctive dexamethasone or prednisolone, which reduces mortality, and pyridoxine cover.
- Manage the complications: hydrocephalus may need CSF diversion, seizures need anticonvulsants, hyponatraemia may be SIADH (also consider cerebral salt wasting), and vision loss demands urgent pressure and inflammatory control.
From suspicion to first-week decisions
A 29-year-old presents with three weeks of evening fever and headache, two days of double vision and one generalized seizure; neck rigidity is mild and he is drowsy but localises. The first fork: pyogenic, viral, tuberculous or fungal — the tempo (weeks), the basal cranial nerve sign and the Indian setting tilt to tuberculous, but the emergency first move is still a CT before lumbar puncture, because TBM's hydrocephalus and tuberculomas raise the herniation stakes. Imaging shows enhancing basal exudates and early communicating hydrocephalus; the LP then returns 180 lymphocytes, protein 220 mg/dL, glucose 28 mg/dL against a blood glucose of 110 — the triad that narrows to tuberculosis, with cryptococcosis the key alternative to exclude by India ink and cryptococcal antigen in an immunosuppressed patient. CBNAAT is sent on the CSF (positive here, with rifampicin susceptibility), sputum and chest radiograph screen for pulmonary source, HIV testing is mandatory. Therapy starts the same day — four drugs plus dexamethasone per standard weight-based dosing, pyridoxine, and an antiepileptic for the seizure — with a low threshold for neurosurgical review of the hydrocephalus. The week-one checklist finishes with hyponatraemia evaluation (SIADH versus salt wasting, because fluid management differs), hearing and vision documentation, and contact screening; the family is counselled that improvement lags weeks behind treatment and that adherence for the full course, not the first fortnight, decides the outcome.
Where students slip
The three numbers students misplace are the CSF cell count (expect lymphocytes in the hundreds, not the thousands of pyogenic disease), the glucose ratio (below about half of blood glucose), and the duration of therapy (months, in contrast to the two weeks of pyogenic meningitis). The second trap is waiting for CBNAAT positivity before treating — its sensitivity is moderate, and in compatible CSF, empirical therapy begins immediately. The third is forgetting the steroids: adjunctive dexamethasone or prednisolone is a mortality-reducing, guideline-endorsed element, not an optional extra; and the infarcts on imaging should be read as arteritic, not as an incidental second disease.
Frequently asked questions
What CSF pattern suggests tuberculous meningitis?
Lymphocytic pleocytosis of roughly 50–500 cells, protein often 100–500 mg/dL or higher, and glucose under half the concurrent blood glucose — with a cobweb clot described classically on standing.
Which rapid test does India's national programme endorse on CSF?
CBNAAT (GeneXpert MTB/RIF), which also detects rifampicin resistance; a negative result does not exclude TBM when the clinical and CSF picture fits.
Why does the sixth nerve palsy occur in TBM?
The abducens nerve has the longest intracranial course and is entrapped by basal meningeal exudate and raised pressure — it is the commonest cranial nerve sign.
Which adjunctive drug reduces mortality in tuberculous meningitis?
Corticosteroids — dexamethasone or prednisolone given with antitubercular therapy, alongside pyridoxine cover for isoniazid.
What causes basal ganglia infarcts in TBM?
Arteritis of the lenticulostriate and thalamoperforating arteries as they traverse the basal exudates, producing ischaemic strokes during the illness.