CLINICAL HISTORY:
A 40-years-old man who enjoyed good past health, presented with persistent fever, cough, headache and fatigue for 1 week. He later developed confusion. MRI brain (axial T1W, axial T2W, coronal T2W FLAIR, axial & coronal T1W+C) was obtained.
DIAGNOSIS:
TB Meningitis
COMMENT:
MRI brain showed T1W isotense T2W hyperintensities (to CSF) filling up the basal cisterns and sulci in the basal brain region, and is hyperintense on FLAIR sequence, suggestive of presence of proteinaceous exudates. Marked nodular meningeal enhancement is observed on the postcontrast scan, mainly involving the basal cistern and with presence of multiple small rim enhancing lesions scattered diffusely in the intraparenchyaml region as well as in the cisterns, suggestive of caseating granuloma. Overall findings are compatible with tuberculosis meningitis.
Involvement of CNS is seen in approximately 5% of patients with tuberculosis, predisposed in immunocompromised patients, infants and small children. Early diagnosis and treatment with anti-tuberculosis drugs is important to reduce the mobility and mortality.
Tuberculosis meningitis usually results from hematogenous spread. It can also be secondary to rupture or extension of a subependymal or subpial focus (Rich focus) or direct extension from cerebrospinal fluid (CSF) infection.
The typical radiographic feature of tuberculosis meningitis is homogenous meningeal contrast enhancement, particularly noted in the basal cisterns, with some degree of involvement of the interhemispheric and Sylvian Fissures. These findings are most pronounced on gadolinium-enhanced T1W imaging than CT.
The commonest complication of tuberculous meningitis is communicating hydrocephalus, being caused by blockage of the basal cisterns by inflammatory exudates. Other complications of tuberculosis meningitis include non-communicating hydrocephalus due to obstruction by tuberculoma, ischaemic infarcts and cranial nerve involvement. |