Virtually all mycobacterial infections of the central nervous system (CNS) are caused by Mycobacterium tuberculosis. Infection begins with inhalation of infectious particles, with hematogenous dissemination soon thereafter. The main target of organism deposition is the reticuloendothelial system. The brain and meninges, not part of that system, receive relatively few mycobacteria. T-cell–mediated immunity reaction is induced within 4 weeks after infection.

A tubercle forms at the site of immune response to mycobacterium. This consists of macrophages and lymphocytes surrounding a necrotic caseous center. The subsequent illness course is a function of host immunologic capacity and poorly defined genetic factors. At best, small caseous foci are completely eliminated, leaving no residua of infection except a positive tuberculin skin test. Less efficient host response results in larger caseous foci, which harbor viable mycobacteria with the potential to cause reactivated disease if the host’s immune status lessens.

If the host immunity is impaired, primary tubercles continue to grow, the caseous center liquefies, organisms proliferate, and the tubercle ruptures, discharging organisms and their antigenically potent products into surrounding tissues. When these events occur within the brain and meninges, tuberculous (TB) meningitis results. Specific CNS syndromes are a function of the original location of the infecting tubercle:70

  • Foci located on brain surface or ependyma can rupture into subarachnoid space or the ventricular system to cause meningitis.
  • Foci deep within brain parenchyma can enlarge to form tuberculomas or, more rarely, TB abscesses.

As with other forms of tuberculosis, the incidence of tuberculosis in the CNS is greatly increased in human immunodeficiency virus (HIV)–infected patients.77 In fact, in some HIV populations, TB meningitis is the most common CNS infection.

Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (

Reviewed By: 
Steven C. Schachter, MD
Monday, March 1, 2004