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Cerebral infarction common in tuberculous meningitis and linked to disease severity and arterial occlusionCould blood thinners or specific treatments make brain strokes worse in severe meningitis?

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Key Takeaway
Recognize that Grade 3 TBM and arterial occlusion mark patients at highest risk for cerebral infarction and new infarcts.

This was a secondary analysis of the ACT-TBM randomized controlled trial, which evaluated adjunctive aspirin or clopidogrel added to standard antitubercular therapy in tuberculous meningitis. The present analysis characterized patterns, associated factors, and predictors of cerebral infarction. Data were drawn from 237 patients enrolled at two tertiary centers in India between 2019 and 2023, with 226 included after excluding 11 with missing imaging or incomplete follow-up. Serial MRI and MR angiography were performed at baseline, 1 month, and 3 months.

Among the 226 analyzed, 84 (37%) developed cerebral infarction. Median age was 26 years (IQR 20-36) and 134 (59.29%) were female. Multiple infarcts were common (78.6% of those affected), with the basal ganglia (72.6%), subcortical white matter (52.4%), and cortex (38.1%) most frequently involved. Arterial occlusion occurred in 61.25% of patients with infarction versus 25.55% without.

In multivariable models, Grade 3 TBM (aOR 3.94; 95% CI 1.19-13.08; p=0.025) and arterial occlusion (aOR 4.43; 95% CI 2.19-8.96; p<0.001) were independently associated with cerebral infarction. Among those with infarction, 32.14% developed new infarcts on follow-up. Modified antitubercular therapy (aOR 3.10; 95% CI 1.18-8.09; p=0.021) and arterial occlusion (aOR 4.23; 95% CI 1.40-12.75; p=0.01) predicted new infarcts, and presence of exudates was associated with arterial occlusion (aOR 2.86; 95% CI 1.08-7.56; p=0.034).

Safety outcomes and adverse events were not reported in this secondary analysis. As a secondary analysis focused on predictors, causal inferences should be restrained; findings support vigilant neuroimaging surveillance and attention to severity and vascular status in TBM.

Imagine a patient fighting a severe infection in the brain's lining. Now imagine that infection also threatens to block blood vessels, leading to strokes. This study looked at 226 patients with tuberculous meningitis in India to understand why some developed these dangerous brain blockages while others did not. The goal was to find warning signs that could help doctors protect vulnerable patients.

The results showed that one-third of the patients suffered from cerebral infarction, a medical term for a stroke caused by blocked blood flow. The study found that having a pre-existing arterial occlusion, or a blocked artery, was strongly linked to developing a stroke. Patients with this blockage were much more likely to have a stroke than those without it. Additionally, the presence of certain fluid collections in the brain was also connected to these blockages.

The researchers also noticed that some patients developed new strokes during the follow-up period. This happened more often in those who received modified tuberculosis treatments or had those arterial blockages. The study did not report specific safety issues like side effects or drug reactions, but it did note that data was missing for a small number of patients. This means the full picture of risk and safety might not be complete yet.

What this means for you:
Certain conditions like blocked arteries increase stroke risk in severe meningitis, urging careful monitoring.

Study Details

Study typeRct
Sample sizen = 61
EvidenceLevel 2
Follow-up1.0 mo
PublishedApr 2026
View Original Abstract ↓
BACKGROUND: Cerebral infarction is a frequent and serious complication of tuberculous meningitis (TBM), contributing substantially to morbidity and mortality. Moreover, studies on infarct patterns and associated factors/predictors remain limited in TBM. ACT-TBM trial (Aspirin or Clopidogrel Therapy in the Treatment of Tuberculous Meningitis) evaluated the efficacy and safety of adjunctive antiplatelet therapy (aspirin or clopidogrel) to standard antitubercular therapy in TBM for the occurrence of stroke or cerebral infarction. Here, we conducted a secondary analysis of the ACT-TBM trial to characterize the patterns, associated factors, and predictors of cerebral infarction in TBM. METHODS: We utilized data of 237 patients from the ACT-TBM randomized controlled trial conducted at 2 tertiary centers in India (2019-2023). Serial magnetic resonance imaging and magnetic resonance angiography were performed at baseline, 1 month, and 3 months in the primary trial. Cerebral infarctions were categorized by size, vascular territory, and number. Multivariable logistic regression models were performed using variables with <0.1 on univariable analysis and clinical relevance. Model estimates are reported as adjusted odds ratios (aORs) with 95% CIs. RESULTS: Of the 237 patients enrolled, 226 were included after excluding 11 with missing imaging or incomplete follow-up data. Among these, 84 (37%) had cerebral infarction. Median age of the entire cohort was 26 years (interquartile range, 20-36), and 134 (59.29%) were females. Multiple infarcts were observed in 66 (78.6%) patients. Most frequent location of infarction was in the basal ganglia (n=61, 72.6%), subcortical white matter (n=44, 52.4%), and cortex (n=32, 38.1%). Arterial occlusion occurred in 49 (61.25%) patients with cerebral infarction versus 35 (25.55%) without (<0.001). In multivariable adjusted models, Grade 3 TBM (aOR, 3.94 [95% CI, 1.19-13.08]; =0.025), and arterial occlusion (aOR, 4.43 [95% CI, 2.19-8.96]; <0.001) were associated with infarction. Among those with infarction, 27 (32.14%) patients (13.17% of the available cohort) developed new infarctions on follow-up. Modified antitubercular therapy (antitubercular therapy; aOR, 3.10 [95% CI, 1.18-8.09]; =0.021) and arterial occlusion (aOR, 4.23 [95% CI, 1.40-12.75]; =0.01) significantly predicted new infarctions. Presence of exudates was associated with arterial occlusion (aOR, 2.86 [95% CI, 1.08-7.56]; =0.034). CONCLUSIONS: Cerebral infarction is common in TBM and associated with disease severity and arterial occlusion. Modified antitubercular therapy predicted new infarcts, while basal exudates were associated with vascular occlusion, highlighting the need for vigilant monitoring and optimized therapeutic strategies.
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