Given the low sensitivity of existing CSF tests for detecting TB
and the slow growth of M. tuberculosis in culture, antituberculous
treatment is often initiated empirically. Treatment is more
complex for multidrug-resistant TB (MDR TB; resistant to
isoniazid [INH] and rifampicin) and extensively drug-resistant
TB (resistant to INH, rifampin, fluoroquinolones, capreomycin,
kanamycin, and amikacin). In a study of 1614 patients with
positive CSF cultures, the presence of isoniazid resistance was
associated with 2.1 times higher risk of death [71]. Determining
the prevalence of drug resistance is extremely important for
guiding initial therapy, especially when sensitivities are pending
or not feasible [72].
Monitoring TB medication levels in blood or CSF is rarely
necessary except in patients with treatment failure, known malabsorptive
states, or those who are receiving cycloserine and
develop adverse CNS effects. Intrathecal treatment is not the
standard of care, but successful use of intrathecal levofloxacin
and amikacin for MDR TB has been reported [73].
The use of corticosteroids is widely accepted as adjuvant
therapy for CNS TB, particularly for TB meningitis, as well as
for CNS TB-associated IRIS (see below) [66]. A meta-analysis of
7 randomized controlled trials concluded that ‘‘corticosteroids
should be used routinely in HIV-negative people