Cerebrovascular complications of tuberculous meningitis are common, and may represent its most serious legacy. They present in clinically diverse ways, and continue to develop during the initial stages of treatment. Magnetic resonance imaging is the imaging modality of choice in detecting brain infarcts, typically revealing multiple or bilateral lesions in the territories of the middle cerebral artery perforating vessels. Vessel pathology appears to be a consequence of its immersion in the local inflammatory exudate. Infiltrative, proliferative and necrotising vessel pathologies have been described, but the relative contributions of each and of luminal thrombosis to brain damage remain unclear. There is some evidence that vasospasm may mediate strokes early in the course of the disease and proliferative intimal disease later strokes. Anti-tuberculous chemotherapy appears to be relatively ineffective in preventing vascular complications, perhaps suggesting an immune mechanism. However, a preventive role for corticosteroids remains to be proven. Study of the molecular pathogenesis of TBM vasculopathy is in its infancy. This review focuses in particular on pathogenetic aspects of tuberculous cerebrovascular disease, with a view to its future targeted prevention.