This chapter presents a discussion on tuberculous meningitis. Tuberculous meningitis presents as either a subacute or a chronic meningitis, characterized by fever, headache, night sweats, and malaise, or a fulminant meningoencephalitis with coma, raised intracranial pressure, seizure activity, and stroke. In children, tuberculous meningitis occurs during primary infection with Mycobacterium tuberculosis. In adults, tuberculous meningitis does not occur during the course of primary infection, but rather from endogenous reactivation of infection in caseous tuberculous foci adjacent to the subarachnoid space that developed during hematogenous spread of tubercle bacilli in the course of an earlier primary infection, usually pulmonary tuberculosis. Meningitis is the result of the discharge of bacilli and tuberculous antigens into the subarachnoid space. It is not known what causes the growth and rupture of caseous lesions, but immunological mechanisms most likely have a role. The differential diagnosis of tuberculous meningitis includes those diseases that cause this combination of symptoms with a cerebrospinal fluid (CSF) lymphocytic pleocytosis and a mildly decreased glucose concentration. A person becomes infected with M. tuberculosis when they inhale aerosolized droplet nuclei containing tubercle bacilli. Hydrocephalus is the most common abnormality on neuroimaging and often progresses during the course of the disease. The chapter discusses practical management and adjunctive therapy.
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