demonstrates increased signal relative to cerebrospinal fluid (CSF) on T1-weighted images.
The rim is typically thickest on the cortical aspect and thinnest in its deep aspect, which is a
phenomenon believed to be related to the higher oxygenation of blood flow closer to the gray
matter. A feature that can be used to differentiate late cerebritis from the early capsular stage,
as both demonstrate rim formation, is the phenomenon of “filling in,” in which a 20- to 40-
minute delay on a contrast-enhanced MR will show enhancement in the central portion of the
lesion during late cerebritis, but not once the actual capsule has formed. The center of the
abscess also demonstrates high signal on diffusion-weighted MR imaging, presumably due to
the elevated viscosity of the necrotic material (28,30).
Clinical and Radiologic Diagnosis of CNS Tuberculosis
While isolated involvement of the central nervous system in tuberculosis is rare, CNS
involvement is seen in approximately 5% of cases of tuberculosis, with increased prevalence in
immunocompromised individuals. Infection mostly occurs via hematogeneous spread.
Various forms of cerebral involvement can occur including tuberculous meningitis, cerebritis,
tuberculoma, abscess, or miliary tuberculosis. Tuberculoma (or tuberculous granuloma) is the
most common CNS parenchymal lesion of tuberculosis. The lesions may be solitary or multiple
and can occur anywhere in the brain, although there is a predilection for the frontal and
parietal lobes (31,32).
On CT, the lesions may be round or lobulated, high or low in attenuation, and
enhancement patterns vary from homogeneous to ring enhancing (Fig. 14A and B). The lesions
may also have irregular walls of varying thickness. When chronic, they are associated with
mass effect, surrounding edema, and calcification. The “target sign,” consisting of central
calcification, surrounding edema, and peripheral enhancement, is suggestive of, but not
entirely diagnostic for, tuberculoma. On MR, the lesions are hypointense on T1-weighted
images and hyperintense on T2-weighted images and homogeneously enhance, although once
there is central caseation and necrosis, there is central hypointensity on T1-weighted images
(and hyperintensity on T2-weighted images) and peripheral hyperintensity on T1-weighted
images (and hypointensity on T2-weighted images) as well as rim enhancement (28,32).
Figure 14 (A) Axial CT image of the brain in a male patient demonstrates a round, low-attenuation lesion in the
right temporal lobe (arrow) with surrounding vasogenic edema. (B) After IV contrast administration, the lesion
demonstrates thick peripheral enhancement, which subsequently proved to be a tuberculoma.
Radiology of Infectious Diseases and Their Mimics in Critical Care 87