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We retrospectively evaluated clinical features and outcomes in children treated for tuberculous meningitis (TBM) at Hasan Sadikin Hospital, Bandung, Indonesia, during 2011-2020. Among 283 patients, 153 (54.1%) were <5 years of age, and 226 (79.9%) had stage II or III TBM. Predictors of in-hospital death (n = 44 [15.5%]) were stage III TBM, hydrocephalus, male sex, low-income parents, seizures at admission, and lack of bacillus Calmette-Guérin vaccination. Predictors of postdischarge death (n = 18 [6.4%]) were hydrocephalus, tuberculoma, and lack of bacillus Calmette-Guérin vaccination. At treatment completion, 91 (32.1%) patients were documented to have survived, of whom 33 (36.3%) had severe neurologic sequelae and 118 (41.7%) had unknown outcomes. Predictors of severe neurologic sequelae were baseline temperature >38°C, stage III TBM, and baseline motor deficit. Despite treatment, childhood TBM in Indonesia causes substantial neurologic sequelae and death, highlighting the importance of improved early diagnosis, better tuberculosis prevention, and optimized TBM management strategies.

Tuberculosis (TB) is the leading cause of death from a single infectious agent, with approximately 1.2 million deaths reported in 2023. While TB primarily affects the lungs, it can also spread to other organs, where it is classified as extrapulmonary TB. Tuberculous meningitis (TBM) is the most severe form of extrapulmonary TB, affecting 1–5% of TB cases. Delayed diagnosis contributes to its high mortality and severe neurological complications, with approximately 10% of affected individuals dying or suffering permanent neurological damage. When combined with adjunctive therapy, early detection and treatment can significantly improve survival outcomes. Currently, many studies have identified potential biomarkers of TBM; however, to date, there is no clear consensus on the markers altered in TBM. Hence, we conducted a systematic review aimed at identifying metabolites and proteins that are significantly altered in TBM when compared with healthy controls. Three databases — PubMed, Scopus, and Web of Science — were scanned by two independent reviewers for potential articles that met our inclusion and exclusion criteria. After quality assessment, 17 studies were included, comprising a total of 963 participants (healthy control, n  = 576; TBM, n  = 387). Metabolites and proteins identified as being significantly altered across studies included alanine, isoleucine, myo-inositol, valine, arachidonate 5-lipoxygenase (ALOX5), apolipoprotein B (APOB), and glial fibrillary acidic protein (GFAP), which were detected in serum, urine, brain tissue, and cerebrospinal fluid samples. These markers have potential diagnostic value for TBM. However, further validation is needed to determine their specificity to reliably distinguish TBM from other neurological infections, which could improve early diagnosis and patient outcomes in TBM.

We developed and validated a diagnostic scoring system for tuberculous meningitis (TBM) using 13 laboratory parameters, comparing tuberculous meningitis (TBM) and non-tuberculous meningitis (non-TBM). This study enrolled patients diagnosed with meningitis. We retrospectively collected and analyzed demographic data (gender, age) and cerebrospinal fluid (CSF) parameters, including biochemical profiles and white blood cell counts with differential analysis. Variable selection was performed using least absolute shrinkage and selection operator (LASSO) regression. The dataset was randomly divided into a training set and a validation set. A diagnostic prediction model was developed using logistic regression in the training set, with nomograms constructed to visually demonstrate the diagnostic relationships. Decision curve analysis (DCA) was employed to assess the clinical utility of the model. Finally, the diagnostic performance of the model was evaluated in the validation set. A total of 254 patients with meningitis were included in this study. LASSO regression analysis identified four predictive variables: CSF glucose, CSF chloride, CSF protein and CSF mononuclear cells proportion. These parameters were incorporated into a logistic regression model, with weighted factors generating a diagnostic score. A score of ≥ 3 was suggestive of TBM with a sensitivity of 76.10% and a specificity of 84.10%, and the area under the curve (AUC) values was 0.86 (95% CI 0.81-0.91). Both calibration curves and DCA validated the robust performance of model. We developed and validated a clinically applicable diagnostic model for TBM using routinely available and low-cost CSF parameters. Our findings demonstrated that this scoring system provided reliable TBM diagnosis, particularly in countries and regions with limited microbial and radiological resources.

Meningitis is an inflammatory condition affecting the meninges surrounding the brain and spinal cord. Meningitis can be triggered by various factors, including infectious agents like viruses and bacteria and non-infectious contributors such as cancer or head injuries. The impact of meningitis on the central nervous system involves disruptions in the blood–brain barrier, cellular infiltrations, and structural alterations. The clinical features that differentiate between tuberculous meningitis (TBM) and non-tuberculous meningitis (NTM) are discussed in this review and aid in accurate diagnosis. The intricate interplay of reactive oxygen species, ferroptosis, and reactive nitrogen species within the central nervous system reveals a promising field of research for innovative therapeutic strategies tailored to TBM. This review highlights the alternative treatments targeting oxidative stress-induced TBM and ferroptosis, providing potential avenues for intervention in the pathogenesis of this complex condition.

Background: Lumboperitoneal shunt is a known procedure for communicating hydrocephalus. Being an extracranial procedure, it can also be utilized in normal-sized ventricles. Objective: To report our experience of lumboperitoneal shunt done with a minimal follow-up of 12 months with an emphasis on patient selection, technique, and complication avoidance. Methods: This was a retrospective analysis of patients who underwent LP shunt during October 2014-October 2019 at the authors' institute. Inclusion criteria were patients with communicating hydrocephalus due to tubercular meningitis, normal pressure hydrocephalus, idiopathic intracranial hypertension, and postoperative refractory cerebrospinal fluid leaks. Data were collected for demographics, Glasgow coma scale and Glasgow outcome scale, vision, gait, memory, urinary incontinence, failed attempts, and complications. Results: A total of 426 patients underwent the LP shunt procedure. The commonest indication was tubercular meningitis followed by idiopathic intracranial hypertension and normal pressure hydrocephalus. Age ranged from 16 to 72 years. There were 255 male and 171 female patients. The mean follow-up was 41 ± 8 months. Overall, 301 patients (70.6%) had neurological improvement. Shunt-related complications occurred in 112 (26.29%) patients, of which shunt block was the commonest. Other complications were infection in 17 (3.9%) patients and extrusion in four (0.9%) patients. Transient postural headache was seen in 46 (10.7%) patients, which gradually improved. Conclusion: Lumboperitoneal shunt was found to be a safe and effective treatment in appropriately selected communicating hydrocephalus patients. A meticulous technique reduces the complication rate.

Paroxysmal autonomic instability with dystonia syndrome (PAIDS) is a rare and life-threatening complication of neurologic diseases. We report the case of a 20-year-old male with acute severe brain damage from tuberculous meningitis, who eventually developed paroxysmal episodes of spontaneous and inducible tachycardia, tachypnea, hypertension, and decerebrate posturing. We diagnosed the patient as suffering from paroxysmal autonomic instability with dystonia syndrome. The unavailability of morphine and the prohibitive cost of prolonged fentanyl use led to a trial of gabapentin, clonazepam, and propranolol for the patient, resulting in symptom resolution. Brain injury causes dysfunction of autonomic centers leading to paroxysmal autonomic instability with dystonia syndrome. Management includes minimizing stimulation and pharmacotherapy with preventive and abortive medications. Alternatives like gabapentin, propranolol and clonazepam were effective in treating the paroxysmal episodes, proving that they may have a role in resource limited settings. PAIDS requires urgent recognition and treatment to prevent further complications and death.

Background The defining feature of the cerebrospinal fluid (CSF) collected from infants and children with tuberculous meningitis (TBM), derived from an earlier untargeted nuclear magnetic resonance (NMR) metabolomics study, was highly elevated lactic acid. Undetermined was the contribution from host response (L-lactic acid) or of microbial origin (D-lactic acid), which was set out to be determined in this study. Methods In this follow-up study, we used targeted ultra-performance liquid chromatography–electrospray ionization–tandem mass spectrometry (UPLC–ESI–MS/MS) to determine the ratio of the L and D enantiomers of lactic acid in these CSF samples. Results Here we report for the first time that the lactic acid observed in the CSF of confirmed TBM cases was in the L-form and solely a response from the host to the infection, with no contribution from any bacteria. The significance of elevated lactic acid in TBM appears to be that it is a crucial energy substrate, used preferentially over glucose by microglia, and exhibits neuroprotective capabilities. Conclusion These results provide experimental evidence to support our conceptual astrocyte–microglia lactate shuttle model formulated from our previous NMR-based metabolomics study — highlighting the fact that lactic acid plays an important role in neuroinflammatory diseases such as TBM. Furthermore, this study reinforces our belief that the determination of enantiomers of metabolites corresponding to infectious diseases is of critical importance in substantiating the clinical significance of disease markers.