CNS Tuberculosis

Excerpt

Mycobacterium tuberculosis is responsible for 5.9% of community-acquired CNS infections worldwide. Neurological tuberculosis (TB) or central nervous system tuberculosis (CNS-TB) may take three clinic-pathological forms: a diffuse form of tubercular meningitis (TBM), a focal form as tuberculoma, and spinal arachnoiditis also referred to as TB radiculomyelitis [TBRM]. Of these, TBM predominates, causing 70 to 80% of the infections. It presents as a subacute to chronic meningitis with disease severity commensurate with the duration of illness.

The diagnosis is fraught with challenges and is often delayed due to the varied and non-specific presentation. Besides the clinical clues, diagnostic indicators in cerebrospinal fluid (CSF) include mononuclear pleocytosis, low sugar values, and high protein concentrations. Identifying Mycobacterium tuberculosis in CSF by staining, culture methods, and molecular analysis is confirmatory but may be challenging.

Advanced radiological imaging techniques are usually of great assistance in making presumptive diagnoses. CNS-TB is frequently complicated by vasculitic infarcts, cranial nerve palsies, multiple neurological deficits, and hydrocephalus. A strong clinical suspicion is enough to start prompt anti-tubercular therapy. A 4-drug regimen of isoniazid, rifampin, pyrazinamide, and ethambutol with adjunctive corticosteroid reduces morbidity and mortality. The diagnosis and management of CNS-TB may be complicated by drug resistance, immune reconstitution inflammatory syndrome, and human immunodeficiency virus (HIV) coinfection.

Treatment efficacy depends upon how early it is instituted. Multiple factors determine the prognosis, the most important being the clinical stage of TBM at initial presentation. Untreated or unrecognized TBM may cause death within 5 to 8 weeks of the onset of the disease.