Stroke in tuberculous meningitis (TBM) occurs in 15-57% of patients especially in advance stage and severe illness. The majority of strokes may be asymptomatic because of being in a silent area, deep coma or associated pathology such as spinal arachnoiditis or tuberculoma. Methods of evaluation also influence the frequency of stroke. MRI is more sensitive in detecting acute (DWI) and chronic (T2, FLAIR) stroke. Most of the strokes in TBM are multiple, bilateral and located in the basal ganglia especially the 'tubercular zone' which comprises of the caudate, anterior thalamus, anterior limb and genu of the internal capsule. These are attributed to the involvement of medial striate, thalamotuberal and thalamostriate arteries which are embedded in exudates and likely to be stretched by a coexistent hydrocephalus. Cortical stroke can also occur due to the involvement of proximal portion of the middle, anterior and posterior cerebral arteries as well as the supraclinoid portion of the internal carotid and basilar arteries which are documented in MRI, angiography and autopsy studies. Arteritis is more common than infarction in autopsy study. The role of cytokines especially tumor necrosis factor (TNFα), vascular endothelial growth factor (VEGF) and matrix metaloproteineases (MMPs) in damaging the blood brain barrier, attracting leucocytes and release of vasoactive autocoids have been suggested. The prothrombotic state may also contribute to stroke in TBM. Corticosteroids with antitubercular therapy were thought to reduce mortality and morbidity but their role in reducing strokes has not been proven. Aspirin also reduces mortality and its role in reducing stroke in TBM needs further studies.
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