CNS tuberculosis can occur as meningitis (the most common form), intracranial tuberculomas or spinal tuberculous arachnoiditis. It usually occurs following dissemination after primary infection (in children and young adults) or during reactivation as part of miliary TB.
The prevalence of CNS tuberculosis is high in regions with a high incidence of TB. It accounts for 1% of all cases of tuberculosis and 6% of all cases of extrapulmonary tuberculosis in immunocompetent individuals. 80% of TB meningitis occurs in patients with HIV infection.
If untreated, most patients with TB meningitis die within 5-8 weeks of the onset of illness.
Phases of TB Meningitis
Phase
Description
Prodrome (2 – 3 weeks)
Gradual onset of malaise, lassitude, headache, low-grade fever and personality change
Meningitic phase
Pronounced neurologic features such as meningismus, protracted headache, vomiting, lethargy, confusion, cranial nerve and long-tract deficits and hydrocephalus
Paralytic phase
Illness accelerates rapidly leading to stupor and coma, seizures, and hemiparesis.
Pathophysiology
Primary infection or latent reactivation of tuberculosis
Bacillemia (Mycobacterium tuberculosis in blood) spreads to the central nervous system
Scattered tuberculomas are established in the brain, meninges or adjacent skull/spine
Proliferative arachnoiditis at the base of the brain (fibrous mass involving cranial nerves and other structures)
CNS vasculitis leading to thrombosis and infarction commonly in the basal ganglia, cerebral cortex, pons and cerebellum
Communicating hydrocephalus due to inflammation of the basilar cisterns which impairs CSF circulation and resorption. Tuberculomas and exudates may also obstruct outflow through the aqueducts.