# Basal Ganglia Ischemic Stroke as Sentinel Sign for Pediatric Tuberculous Meningitis in an Immunocompetent Child: A Case Report

## TL;DR

A previously healthy child developed severe neurological symptoms from tuberculous meningitis, diagnosed after basal ganglia stroke and confirmed with imaging and lab tests.

## Contribution

Highlights basal ganglia ischemic stroke as a rare but critical sign of pediatric TBM in immunocompetent children.

## Key findings

- Basal ganglia infarction on MRI was a key indicator of TBM despite negative initial tests.
- Clinical improvement was observed after 16 months of anti-tuberculosis treatment and supportive care.
- Emphasizes the need for early TB therapy in cases with neurological deterioration and epidemiological risk factors.

## Abstract

Background: Tuberculous meningitis (TBM) is the most severe manifestation of tuberculosis in children, with high mortality rates and long-term neurological sequelae. Early diagnosis is challenging due to its nonspecific symptoms and insidious onset. Case Presentation: An 8-year-old previously healthy male, fully vaccinated, presented with a two-week history of fever, headache, vomiting, and abdominal pain. Cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis, elevated protein, and low glucose levels, while multiplex polymerase chain reaction (PCR) testing for bacteria and viruses yielded negative results. Brain computed tomography (CT) revealed mild ventricular dilation and pansinusitis. Empirical antibacterial and antiviral therapy were initiated; however, the patient subsequently experienced neurological deterioration, including cranial nerve deficits and hemiparesis. Brain magnetic resonance imaging (MRI) demonstrated acute infarctions of the basal ganglia, raising suspicion for TBM. Repeated CSF sampling and Xpert MTB/RIF assay confirmed infection with Mycobacterium tuberculosis. Anti-tuberculosis treatment was initiated in combination with adjunctive corticosteroids, anticonvulsant and anticoagulant therapies, and supportive care, including neurosurgical intervention for hydrocephalus. After 16 months of treatment, the patient showed clinical improvement but sustained left-sided hemiparesis, visual impairment, and cognitive deficits. Conclusions: This case highlights the diagnostic challenges of pediatric TBM in immunocompetent and Bacillus Calmette–Guérin (BCG)-vaccinated children, particularly in the presence of initially negative microbiological findings. It emphasizes the importance of maintaining a high index of clinical suspicion and the crucial supportive role of neuroimaging findings, as well as the earlier initiation of empirical TB therapy especially when epidemiological plausibility exists. Early recognition and intervention remain critical to reducing morbidity and mortality associated with this devastating disease.