Makindo Medical Notes

Tuberculosis may spread to the brain, forming a Rich focus that can rupture into brain tissue.

About

• Insidious onset, often with a subtle presentation. Early diagnosis is critical for effective treatment and to prevent severe complications.

Tuberculous Involvement of the CNS

• Tuberculous Meningitis: Inflammation of the meninges caused by Mycobacterium tuberculosis infection.
• Tuberculomas: Granulomatous masses that act as space-occupying lesions, leading to focal neurological deficits.
• Spinal Arachnoiditis: Inflammation of the spinal arachnoid mater, causing pain, weakness, and potential paralysis.
• TB Arteritis: Vascular inflammation that may lead to stroke-like presentations.
• Hydrocephalus: Common due to impaired CSF flow, causing increased intracranial pressure (ICP).
• Cranial Nerve Involvement: Particularly affecting the VI nerve, often causing cranial nerve palsies.

Aetiology

• Risk factors include recent TB exposure, alcoholism, immunosuppression (e.g., HIV/AIDS), and malnutrition.

Stages

• Stage I: Fully conscious, rational, without focal neurological signs or hydrocephalus.
• Stage II: Confusion, possibly with focal neurological signs.
• Stage III: Comatose, with symptoms like delirium, hemiparesis, or paraplegia.

Clinical Presentation

• Symptoms: Malaise, fever, and headache persisting for 2-3 weeks.
• Signs: Meningism, vomiting, confusion, cranial nerve palsies (especially III and VI), stupor, coma, and seizures.
• Pathophysiology: Often presents as basal meningitis, with optic chiasm involvement and localized vasculitis causing thrombosis and hemorrhage.
• Hydrocephalus: Caused by impaired CSF resorption and flow, which may lead to aqueductal blockage by high-protein CSF.
• Systemic Findings: Lymphadenopathy and splenomegaly in some cases.

Investigations

• Blood Tests: FBC, U&E, LFTs, CRP, and ESR often elevated.
• Mantoux Test: Positive in about 50% of cases, but not definitive.
• CSF Analysis: High protein (1-5 g/L), low glucose, increased lymphocytes (polymorphs may appear initially). Acid-fast bacilli (AFB) staining often negative; cultures may take up to 6 weeks. PCR can expedite diagnosis.
• Imaging:
  • CT Brain: May appear normal early on; later stages show hydrocephalus and basal enhancement from exudates. Tuberculomas might be visible.
  • MRI: Preferred imaging for detailed evaluation, especially of tuberculomas and basal meningeal enhancement.
• HIV Testing: Recommended in all cases due to strong association with immunocompromise.

Management

• Anti-tuberculous Therapy:
  • Initial phase with four drugs: Isoniazid, Rifampicin, Pyrazinamide, and Ethambutol for 2 months, followed by continuation phase with Isoniazid and Rifampicin for at least 7-10 months.
• Steroids: Indicated for patients with raised ICP, cerebral oedema, focal deficits, or hydrocephalus. Consider prednisolone or dexamethasone for 4-8 weeks with tapering.
• Management of Hydrocephalus: Shunting may be necessary in severe cases.
• HAART: Initiate if HIV/AIDS is diagnosed, with careful management to avoid immune reconstitution inflammatory syndrome (IRIS).