TY - JOUR T1 - Tuberculous meningitis JF - Journal of Neurology, Neurosurgery & Psychiatry JO - J Neurol Neurosurg Psychiatry SP - 289 LP - 299 DO - 10.1136/jnnp.68.3.289 VL - 68 IS - 3 AU - G Thwaites AU - T T H Chau AU - N T H Mai AU - F Drobniewski AU - K McAdam AU - J Farrar Y1 - 2000/03/01 UR - http://jnnp.bmj.com/content/68/3/289.abstract N2 - Uncertainty and doubt dominate all aspects of tuberculous meningitis (TBM). The variable natural history and accompanying clinical features of TBM hinders the diagnosis. Ziehl-Neelsen staining lacks sensitivity and culture results are often insufficiently timely to aid clinical judgement. New rapid diagnostic methods are incompletely evaluated, and many are not suitable for laboratories in low income countries. The duration of chemotherapy for TBM is unclear and the benefits of adjuvant corticosteroids remain in doubt. The only uncomfortable certainties lie in the fatal consequences of missed diagnoses and delayed treatment.This review will discuss the current uncertainties surrounding TBM. More attention will be given to diagnosis and management, as these areas have a direct bearing on patient outcome. About 2000 million people in the world today are infected with tuberculosis,1 but only 10% develop clinical disease. Why some people develop clinical disease remains unclear. The reasons are likely to be multifactorial: inherent not just to the individual person, but to their given population and environment. Before HIV the most important determinant for the development of TBM was age. In populations with high TB prevalence TBM differs from pulmonary, and other extrapulmonary tuberculosis, in that the peak age is from 0–4 years.2 In populations with lower TB prevalence, most cases of TBM are in adults. Risk factors identified for these people are alcoholism, diabetes mellitus, malignancy, and recent corticosteroid use.3-5 Coinfection with HIV now dwarfs these risk factors. HIV increases the lifetime risk of developing clinical TB postinfection to 1 in 3.6 HIV also predisposes to the development of extrapulmonary TB, and in particular TBM,7 a risk which increases as the CD4 count declines.8 The disease constitutes either reactivation of latent infection, or new infection. Evidence from DNA fingerprinting of strains using restriction fragment length polymorphism suggests … ER -