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Research Article

Predicting cerebral infarction in tuberculous meningitis and its prognostic significance

ORCID Icon, ORCID Icon, ORCID Icon & ORCID Icon
Received 07 Jan 2024, Accepted 18 Apr 2024, Published online: 17 May 2024
 

Abstract

Aim: Tuberculous meningitis (TBM) often causes cerebral infarction, but its predictive factors are not well understood. Methods: Patients aged ≥13 years admitted with TBM were enrolled prospectively. Cerebral infarction was diagnosed using magnetic resonance imaging. Results: Of 186 patients, 80 (43%) had infarction. Most infarctions were multiple and located in the cortical areas, basal ganglia and subcortical regions. Independent predictors of infarction at admission included high blood pressure, short illness duration, low Glasgow coma scale and hydrocephalus. Neuroimaging inflammation signs, cerebrospinal fluid analysis abnormalities and pre-existing cardiovascular risks did not predict infarction. In-hospital mortality was higher in TBM with infarction, particularly in those with advanced TBM (stage 3). Conclusion: Baseline parameters of raised intracranial pressure predict cerebral infarction in TBM.

Summary points
  • 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.

Supplemental material

Supplemental data for this article can be accessed at https://doi.org/10.1080/17520363.2024.2347194

Acknowledgments

Authors thank Mrs Sunaina Verma for her help in statistics.

Author contributions

A Aggrohiaa: data curation (main), drafted the manuscript (supporting). V Bhatia: data curation (supporting), revised the manuscript (supporting). A Saroch: data curation (supporting). AK Pannu: conceived the idea (main), data curation (supporting), methodology (main), drafted the manuscript (main), revised the manuscript (main), supervised the project (main).

Financial disclosure

The authors have no financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Competing interests disclosure

The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, stock ownership or options and expert testimony.

Writing disclosure

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The authors state that they have obtained appropriate institutional review board approval (No.: INT/IEC/2022/SPL-1151) and/or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations.

In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.

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