This condition, which is essentially a self-limited meningitis, is observed with some frequency in countries where tuberculosis is prevalent. The CSF shows a modest pleocytosis in some, but not all, cases, a normal or elevated protein content, and normal glucose levels. Headache, lethargy, and confusion are present in some cases and there are mild meningeal signs. Lincoln, who was the first to call attention to this syndrome, believed it to be a meningeal reaction to an adjacent tuberculous focus that did not progress to frank meningitis.
These are tumor-like masses of tuberculous granulation tissue, most often multiple but also occurring singly, that form in the parenchyma of the brain and range from 2 to 12 mm in diameter (see Fig. 31-4). The larger ones may produce symptoms of a space-occupying lesion and periventricular ones may cause obstructive hydrocephalus, but many are unaccompanied by symptoms of focal cerebral disease. In the United States, tuberculomas are rare; in developing countries, however, they constitute from 5 to 30 percent of all intracranial mass lesions. In some tropical countries, cerebellar tuberculomas are the most frequent intracranial tumors in children. Because of their proximity to the meninges, the CSF often contains a small number of lymphocytes and increased protein (serous meningitis), but the glucose level is not reduced. True tuberculous abscesses of the brain are rare except in HIV patients. In two of our patients who presented with a brainstem tuberculoma, there was a serous meningitis that progressed to a fatal generalized tuberculous meningitis.
The spinal cord may be affected in a number of ways in the course of tuberculous infection. In addition to compressing spinal roots and cord, causing spinal block, the inflammatory meningeal exudate may invade the underlying parenchyma, producing signs of posterior and lateral column and spinal root disease. Spinal cord symptoms may also accompany tuberculous osteomyelitis of the spine with compression of the cord by an epidural abscess, a mass of granulation tissue (Pott disease, “Pott paraplegia”), or, less frequently, by the mechanical effects of angulation of the vertebral column. Pott disease, a tuberculous osteomyelitis of the spine that leads to compression of vertebral bodies and a highly characteristic kyphotic deformity at the thoracic or upper lumbar level, is discussed in Chap. 42.
Treatment of Central Nervous System Tuberculous Infections
The treatment of tuberculous meningitis consists of the administration of a combination of four drugs—isoniazid (INH), rifampin (RMP), ethambutol (EMB), and/or pyrazinamide (PZA) for the first 2 months. Some regimens omit the last drug but recent recommendations from various U.S. societies prefer the four-drug combination. An alternative regimen is INH, PZA, high-dose RMP, and moxifloxacin. All of these drugs have the capacity to penetrate the blood–brain barrier, with INH and PZA ranks higher than the others in this respect. Resistant strains of tuberculous organisms are emerging, requiring the use of second-line drugs. It has been pointed out that individuals from certain regions have high rates of INH, and sometimes EMB-resistant organisms. In these cases of multidrug resistance, ethionamide (ETA) must be added as a fifth drug. Antibiotics must be given for a prolonged period, 9 to 12 months if first-line treatment has been given (although it may not be necessary to give all 3 or 4 drugs for the entire period).