Imaging description

Tuberculosis of the central nervous system (CNS) accounts for 2% of HIV-negative and 19% of HIV-positive patients infected with pulmonary tuberculosis [1]. It is thought to be due to reactivation of a dormant “Rich focus” due to primary pulmonary tuberculosis [2,3]. Tuberculous meningitis (TBM) (Fig. 38.1), considered a medical emergency, is a common manifestation of CNS tuberculosis, presenting with meningeal inflammation, basal exudates, vasculitis, and hydrocephalus [4,5].

Basal exudates or meningeal inflammation may not be apparent on non-contrast CT or MRI; only possible hydrocephalus or patchy multifocal vasculitis may be seen; however, intense basilar leptomeningeal enhancement is seen on post-contrast studies [1,5,6]. Depending on the stage of response of the immune system, a parenchymal granuloma may or may not exhibit caseating necrosis [1]. A solid non-caseating granuloma (Fig. 38.2) appears as a solid isodense and isointense T1 signal mass-like lesion with a characteristic hypointense T2 signal and solid or complete ring enhancement [1,6,7]. Due to a cell-mediated delayed hypersensitivity reaction, the core undergoes a coagulative and liquefactive necrosis called caseation [1]. A caseating tuberculous granuloma (Fig. 38.3) with necrotic center exhibits a central hyperintense T2 signal within a hypointense T2 signal lesion and peripheral rim enhancement.