Predicting cerebral infarction in tuberculous meningitis and its prognostic significance

Although tuberculous meningitis (TBM) is a major infectious cause of cerebral infarction in low-middle-income countries, its pathophysiology and predictive factors remain under-explored. This prospective study aimed to identify baseline predictors of cerebral infarction in TBM and evaluate its impact on in-hospital outcomes. Of the 186 patients enrolled (median age 33 years, 51.6% male), 43.0% (n = 80) had cerebral infarction. The majority of infarctions (71.3%) were multiple, with the primary locations being cortical areas (30.3%), basal ganglia and thalamus (23.0%), other subcortical regions (22.4%), brainstem (13.2%), and cerebellum (11.2%). Infarctions were predominantly associated with the perforators and cortical branches of the middle cerebral artery, superior cerebellar artery, and posterior cerebral artery. Independent baseline predictors of infarction included elevated blood pressure at admission, shorter illness duration, low Glasgow coma scale, and hydrocephalus. Neuroimaging features of inflammation (e.g., basal exudates, meningeal enhancement, or vasculitis), cerebrospinal fluid analysis abnormalities, and pre-existing cardiovascular risks did not predict infarction. In-hospital mortality was higher in patients with infarction (20.0%) compared with those without (12.3%), with advanced TBM (stage 3) being a strong predictor of mortality among patients with infarction. The study's major limitations include data from a single tertiary care center, absence of post-discharge follow-up, and limited utilization of magnetic resonance angiography and vessel wall imaging. Our findings highlight the potential role of raised intracranial pressure in the pathogenesis of TBM-related infarction, as indicated by associations with elevated blood pressure at admission, hydrocephalus and low Glasgow coma scale.