The pattern of tuberculous meningitis in the population is different in different areas of the world. In areas with much tuberculosis, tuberculous meningitis usually affects young children. It develops typically 3 to 6 months after the primary tuberculosis infection. By contrast, in areas with less tuberculosis, tuberculous meningitis tends to strike adults. It may follow a primary infection but, more frequently, is due to reactivation of an old focus of tuberculosis that had been dormant, sometimes for many years.
Tuberculois meningitis begins insidiously with a gradual fluctuating fever, fatigue, weight loss, behavior changes, headache, and vomiting. This early phase is followed by neurologic deficits, loss of consciousness, or convulsions. A dense gelatinous exudate (outpouring) forms and envelops the brain arteries and cranial nerves. It creates a bottleneck in the flow of the cerebrospinal fluid, which leads to hydrocephalus. The development of arteritis and infarctions of the brain can cause hemiplegia or quadriplegia.
A high index of suspicion is essential to diagnose the disease because early diagnosis is the key to a satisfactory outcome. If tuberculous meningitis is seriously suspected, treatment should start immediately. Treatment involves chemotherapy to control and eradicate the infection, management of hydrocephalus and elevated intracranial pressure, and immunomodulation with corticosteroids (cortisone-like drugs such as prednisone).
The World Health Organization (WHO) recommends a two-month intensive course of isoniazid, rifampin, pyrazinamide, and ethambutol followed by 4 months of isoniazid and rifampin. Elevated intracranial pressure can be life-threatening. The hydrocephalus may require placement of a ventriculoperitoneal shunt. The use of the corticosteroid dexamethasone improves survival in patients over 14 years of age but probably does not prevent severe disability.