THREE factors contribute to the unsatisfactory results that have been obtained in the treatmerit of tuberculous meningitis during the streptomycin era: mechanical obstruction of the circulatory channels of the cerebrospinal fluid by tuberculous exudate; the inability of antimicrobial agents to penetrate avascular tissue and reach tubercle bacilli buried therein; and the necessity of prolonged intrathecal therapy that may, of itself, produce local obstructions in the subarachnoid space by repeated irritation and trauma of the meninges. It is generally conceded that all the newer measures devised to counteract these effects — namely, anticoagulants,1 intrathecal injection of tuberculin,2 , 3 fibrinolytic enzymes 4 , 5 and neurosurgical . . .
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Shane et al. (1953) studied this question.
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