ESSENTIALS OF DIAGNOSIS
Gradual onset of listlessness and anorexia.
Headache, vomiting, and seizures common.
Cranial nerve abnormalities typical.
Tuberculosis focus may be evident elsewhere.
Cerebrospinal fluid shows several hundred lymphocytes, low glucose, and high protein.
Tuberculous meningitis is caused by rupture of a meningeal tuberculoma resulting from earlier hematogenous seeding of tubercle bacilli from a pulmonary focus, or it may be a consequence of miliary spread.
The onset is usually gradual, with listlessness, irritability, anorexia, and fever, followed by headache, vomiting, convulsions, and coma. In older patients, headache and behavioral changes are prominent early symptoms. Nuchal rigidity and cranial nerve palsies occur as the meningitis progresses. Evidence of active tuberculosis elsewhere or a history of prior tuberculosis is present in up to 75% of patients.
The spinal fluid is frequently yellowish, with increased pressure, cell count 100–500/mcL (0.1–0.5 × 109/L) (predominantly lymphocytes, though neutrophils may be present early during infection), increased protein, and decreased glucose. Acid-fast stains of cerebrospinal fluid are often negative, and cultures also may be negative in 15–25% of cases. Nucleic acid amplification tests are valuable tools that allow for rapid diagnosis although sensitivity is only 68–80%. Chest radiographs often reveal abnormalities compatible with tuberculosis but may be normal. The tuberculin skin testing and interferon-gamma release assays do not distinguish between active and latent tuberculosis and are frequently negative in the presence of CNS infection.
Tuberculous meningitis may be confused with any other type of meningitis, but the gradual onset, the predominantly lymphocytic pleocytosis of the spinal fluid, and evidence of tuberculosis elsewhere often point to the diagnosis. Fungal and other granulomatous meningitides, syphilis, and carcinomatous meningitis are in the differential diagnosis.
Complications of tuberculous meningitis include seizures, cranial nerve palsies, stroke, and obstructive hydrocephalus with impaired cognitive function. These result from inflammatory exudate primarily of the basilar meninges and arteries.
Presumptive diagnosis followed by early, empiric antituberculous therapy is essential for survival and to minimize sequelae. Even if cultures are not positive, a full course of therapy is warranted if the clinical setting is suggestive of tuberculous meningitis.
Regimens that are effective for pulmonary tuberculosis are effective also for tuberculous meningitis (see Table 9–15). Rifampin, isoniazid, and pyrazinamide all penetrate well into cerebrospinal fluid. The penetration of ethambutol is more variable, but therapeutic concentrations can be achieved, and the drug has been successfully used for meningitis. Aminoglycosides penetrate less well. Regimens that do not include both isoniazid and rifampin may be effective but are less reliable and generally must be given ...