Other pathologic changes depend on the chronicity of the disease process and recapitulate the changes that occur in the subacute and chronic stages of the other bacterial meningitides (see Table 31-1). Cranial nerves are often involved by the inflammatory exudate as they traverse the subarachnoid space, indeed, far more often than with typical bacterial meningitis. Arteries may become inflamed and occluded, with infarction of brain. Blockage of the basal cisterns frequently results in a meningeal, obstructive hydrocephalus; marked ependymitis with blocking of the CSF in the aqueduct or fourth ventricle is a less-common cause. The exudate occasionally predominates around the spinal cord, leading to multiple spinal radiculopathies and compression of the cord.
Tuberculous meningitis occurs in persons of all ages. Formerly, it was more frequent in young children, but now it is more frequent in adults, at least in the United States. The early manifestations are usually low-grade fever, malaise, headache (more than 50 percent of cases), lethargy, confusion, and stiff neck (75 percent of cases), with Kernig and Brudzinski signs. Characteristically, these symptoms evolve much less rapidly in tuberculous than in bacterial meningitis, usually over a period of a week or two, sometimes longer. In young children and infants, apathy, hyperirritability, vomiting, and seizures are the usual symptoms; however, stiff neck may not be prominent or may be absent altogether.
Because of the inherent chronicity of the disease, signs of cranial nerve involvement (usually ocular palsies, less-often facial palsies or deafness) and papilledema may be present at the time that the infection is recognized (20 percent of cases). Occasionally, the disease may present with the rapid onset of a focal neurologic deficit because of hemorrhagic infarction, with signs of raised intracranial pressure or with symptoms referable to the spinal cord and nerve roots. Hypothermia and hyponatremia have been additional features in several of our cases at the time of discovery of the meningitis.
In approximately two-thirds of patients with tuberculous meningitis there is evidence of active tuberculosis elsewhere, usually in the lungs and occasionally in the small bowel, bone, kidney, or ear. In some patients, however, only inactive pulmonary lesions are found, and in others there is no evidence of tuberculosis outside of the nervous system. As mentioned, among our adult patients, tuberculous meningitis is now seen largely in those with HIV, but also in alcoholics, and in people who have emigrated from Asia, Africa, India, and certain locations in the former Soviet Union. Except for the emergence of drug-resistant organisms, the HIV infection does not appear to much change the clinical manifestations or the outcome of tuberculous meningitis. However, others disagree with this statement, pointing out that the course of the bacterial infection is accelerated in HIV patients, with more frequent involvement of organs other than the lungs. Whether or not HIV infection alters the natural history of tuberculous meningitis, treatment of the HIV infection is of paramount importance and it has been recommended that it should be started within 2 weeks of the onset of antituberculous therapy.
If tuberculous meningitis is untreated, its course is characterized by confusion and progressively deepening stupor and coma, coupled with cranial-nerve palsies, pupillary abnormalities, focal neurologic deficits, raised intracranial pressure, and decerebrate postures; usually, untreated, a fatal outcome follows within 4 to 8 weeks of the onset.