Tubercular meningitis (TBM) is the most severe manifestation of central nervous system tuberculosis and remains a major cause of morbidity and mortality in tuberculosis-endemic regions.[1] India bears the highest global burden of tuberculosis, contributing nearly 27% of worldwide cases, with an estimated 2.8 million cases annually.[2] Among extrapulmonary forms, TBM is particularly devastating due to its insidious onset, diagnostic difficulty, rapid progression, and high risk of neurological sequelae or death if treatment is delayed.[3,4] Diagnosis of TBM is challenging because only few cases have typical clinical characteristics feature are often nonspecific and overlap with other causes of meningitis.[5] In resource-limited settings, restricted access to advanced diagnostics further delays treatment initiation.[6] Conventional cerebrospinal fluid (CSF) microbiological tests have low sensitivity, necessitating reliance on clinical features, biochemical CSF parameters, and neuroimaging.[7] The burden is further compounded by HIV co-infection, malnutrition, and socioeconomic factors, which contribute to severe disease and poor outcomes.[8,9] TBM survivors frequently suffer long-term neurological and cognitive sequelae, particularly children, leading to significant socioeconomic burden. [10,11] Although typical CSF findings include lymphocytic pleocytosis, elevated protein, and low glucose, substantial variability exists, and their correlation with disease severity, radiological features, and outcomes remains inadequately defined, particularly in the Indian context. [12–16] Neuroimaging plays a critical role in diagnosis and prognostication. While CT is widely used, MRI provides superior sensitivity for detecting basal meningeal enhancement, infarcts, and tuberculomas. However, the relationship between CSF biochemical abnormalities and radiological findings is not fully understood.[17] Therefore, the present study was undertaken to analyze the spectrum of CSF findings in tubercular meningitis and to evaluate their correlation with clinical severity, radiological characteristics, and outcomes, with the aim of improving early risk stratification and prognostication.

This cross-sectional study was carried out in the Department of Medicine, F. H. Medical College & Hospital, Agra, over a period of 18 months. All patients admitted with a diagnosis of tuberculous meningitis (TBM) during the study period were evaluated for inclusion. A total of 73 patients were enrolled. Eligibility Criteria: Inclusion criteria: 1. Patients > 10 years of age. 2. Patients satisfying diagnostic criteria of TBM. 3. Willing to participate in study. Exclusion criteria: 1. The patients below 10 years of age. 2. Pregnant or lactating women. 3. Those with malaria, septic, fungal or carcinomatous meningitis, head injury, brain tumor, primary renal, hepatic or cardiac failure, endocrinal disorders, malignancy, or any condition limiting the life expectancy to 1 year. (Encephalopathy / meningitis due to other causes. 4. Not willing to participate in the study. Ethical Considerations Ethical clearance was obtained prior to commencement of the study. Written informed consent was taken from all participants or their legal guardians. Confidentiality and anonymity were strictly maintained. No additional investigations were performed solely for research purposes, and all patients received standard treatment according to existing clinical guidelines. Diagnostic Criteria and Disease Staging The diagnosis of TBM was based on a combination of essential clinical criteria and supportive laboratory and radiological findings. Essential criteria included symptoms and signs of meningitis persisting for more than five days. Supportive criteria included characteristic cerebrospinal fluid (CSF) findings, neuroimaging features on computed tomography (CT) or magnetic resonance imaging (MRI), and evidence of tuberculosis at extra-central nervous system sites. Definite TBM was confirmed by detection of acid-fast bacilli, positive CSF culture, or polymerase chain reaction for Mycobacterium tuberculosis. Disease severity was categorized into Stage I, Stage II, or Stage III based on neurological status and Glasgow Coma Scale scores. LJ media composition: LJ medium is an egg-based, selective solid medium widely used for the isolation and cultivation of Mycobacterium tuberculosis and other mycobacteria. [18-21] It supports slow-growing mycobacteria while inhibiting contaminating flora due to the presence of malachite green. Sterilization is achieved by inspissation at 80–85°C for approximately 45 minutes on three consecutive days, which allows coagulation of the egg proteins while preserving essential nutrients. [20, 22] The inoculated medium is incubated at a temperature of 35–37°C. Growth of M. tuberculosis typically appears as rough, tough, buff-colored colonies. Visible colonies generally develop within 2–8 weeks, reflecting the slow-growing nature of the organism. [19,21,22] Table 1: Standard Composition of Lowenstein–Jensen Medium (per 1000 mL) [ 18-22] Components Approximate quantity Function Fresh hen’s eggs ~750 mL Provide protein, lipids, and solid consistency after coagulation Monopotassium phosphate (KH₂PO₄) 2.4g Buffering agent; maintains pH Magnesium sulfate (MgSO₄) 0.24 g Supplies magnesium ions for enzymatic activity Magnesium citrate 0.6g Provides magnesium and stabilizes medium L-asparagine 3.6 g Nitrogen source for mycobacterial growth Glycerol 12ml Carbon source; enhances growth of M. tuberculosis (omitted for M. bovis) Malachite green 0.025–0.04 g Inhibits growth of contaminating bacteria Data Collection and Investigations Detailed clinical data were recorded at admission using a structured proforma. CSF analysis included cell count, differential count, protein, glucose levels, acid-fast bacilli smear, and culture in selected cases. CSF was classified as typical when cell count ranged from 50–500/mm³, protein levels were 50–500 mg/dL, and glucose was ≤50% of the corresponding blood glucose level. Cranial CT or MRI was performed in all patients at admission, with follow-up imaging undertaken when clinically indicated, particularly in cases of neurological deterioration or suspected paradoxical reactions. Outcome Assessment CSF parameters were correlated with clinical staging, radiological findings, and clinical outcomes at three months. Paradoxical responses to antitubercular therapy, including development or progression of hydrocephalus, tuberculomas, infarcts, or new neurological deficits, were documented clinically and radiologically. Paradoxical reaction (PR) in tuberculosis (TB) is defined by a clinical or radiological worsening of pre-existing tuberculous lesions or the development of new lesions, in patients receiving anti-tuberculous medication who initially improved on treatment. This syndrome has been recognised for some time and, although it is often self-limiting, its potential to cause serious morbidity and, on occasion, death, is increasingly being recognised. Although the exact mechanisms are not understood it is most likely that PR is due to an abnormal immune response or reconstitution of the immune system. [23] Paradoxical reactions are more commonly observed in extrapulmonary TB, particularly lymph node and central nervous system involvement, and are also frequently seen in patients with HIV after starting antiretroviral therapy (immune reconstitution inflammatory syndrome). [23, 24] Statistical Analysis: Data were entered into Microsoft Excel and analyzed using SPSS version 21.0. Continuous variables were expressed as mean ± standard deviation or median with interquartile range, while categorical variables were presented as frequencies and percentages. Appropriate statistical tests were applied, and a p-value <0.05 was considered statistically significant

Table 1: Demographic and Clinical Profile of TBM Patients (n = 73) Parameter Category n (%) Age group (years) 11–20 11 (15.1) 21–30 20 (27.4) 31–40 19 (26.0) 41–50 13 (17.8) >50 10 (13.7) Mean age ± SD (years) 34.09 ± 12.6 Sex Male 42 (57.5) Female 31 (42.5) Residence Rural 46 (63.0) Urban 27 (37.0) Duration of symptoms < 2 weeks 19 (26.0) 2–4 weeks 34 (46.6) > 4 weeks 20 (27.4) TB contact history Present 22 (30.1) HIV co-infection Present 6 (8.2) Graph 1: BMRC Grade Seventy-three patients with tuberculous meningitis were included in the study. The mean age was 34.09 ± 12.6 years, with the highest frequency in the 21–30-year age group. Males predominated (57.5%), and most patients were from rural areas (63%). According to BMRC grading, Grade II disease was most common (38.4%), followed by Grade I (32.9%) and Grade III (28.7%). Nearly half of the patients presented within 2–4 weeks of symptom onset, while TB contact history and HIV co-infection were present in 30.1% and 8.2% of cases, respectively. CSF analysis demonstrated typical inflammatory features of tuberculous meningitis. Elevated cell counts with lymphocytic predominance were observed in the majority of patients. CSF protein levels were raised in 89% of cases, while reduced glucose levels were seen in 74%. ADA levels were elevated in over four-fifths of patients. CSF culture was positive in 16.4% of cases, whereas GeneXpert/PCR showed higher positivity (42.5%), indicating superior diagnostic yield of molecular testing. Table 2: Baseline CSF Characteristics in TBM Patients (n = 73) CSF Parameter Mean ± SD / n (%) Range Cell count (cells/mm³) 180 ± 95 30–450 Lymphocyte (%) 85 ± 10 60–100 Protein (mg/dL) 145 ± 60 50–320 Glucose (mg/dL) 35 ± 15 10–60 ADA (U/L) 18 ± 6 8–35 CSF appearance Clear – 35 (48%) — Hazy – 28 (38%) — Xanthochromic – 10 (14%) — CSF culture (MTB) Positive – 12 (16.4%) — GeneXpert/PCR Positive – 31 (42.5%) — Table 3: Correlation of CSF Parameters with Clinical Severity (Modified BMRC Stage) CSF Parameter Stage I (n=21) Stage II (n=28) Stage III (n=24) p-value (I–III) Cell count (cells/mm³) 130 ± 60 170 ± 70 220 ± 110 0.0002* Protein (mg/dL) 120 ± 40 140 ± 50 180 ± 70 0.0002* Glucose (mg/dL) 42 ± 10 36 ± 12 28 ± 14 0.000003* ADA (U/L) 14 ± 5 18 ± 4 22 ± 7 0.000059* A progressive worsening of CSF abnormalities was noted with increasing BMRC stage. CSF cell count, protein, and ADA levels increased significantly from Stage I to Stage III, while CSF glucose showed a significant decline with advancing disease. These findings indicate a strong association between CSF inflammatory markers and clinical severity in TBM. Table 4: CSF Biochemistry in Relation to Radiological Findings (n = 73) Radiological Feature Protein (mg/dL) Mean ± SD Glucose (mg/dL) Mean ± SD p-value Basal exudates 165 ± 55 32 ± 11 NS Hydrocephalus 155 ± 60 30 ± 14 NS Tuberculomas 138 ± 50 34 ± 13 NS Infarcts 175 ± 70 28 ± 10 NS Meningeal enhancement 135 ± 45 32 ± 12 NS Patients with radiological abnormalities such as basal exudates, hydrocephalus, infarcts, tuberculomas, and meningeal enhancement showed higher mean CSF protein and lower glucose levels compared to those without these findings. However, these differences were not statistically significant, suggesting limited discriminatory value of CSF biochemistry for individual radiological features. Paradoxical reactions occurred in 16 patients and were associated with significantly higher CSF protein levels. Although ADA levels were higher and glucose levels lower in this group, these differences were not statistically significant. This suggests that increased CSF inflammatory activity may play a role in paradoxical reactions. Table 5: CSF Findings and Paradoxical Reaction (n = 73) Paradoxical Reaction n Protein (mg/dL) ADA (U/L) Glucose (mg/dL) p-value Present 16 170 ± 45 20 ± 4 30 ± 11 0.04* Absent 57 140 ± 60 17 ± 6 36 ± 15 — Table 6: CSF, Radiological Predictors and Outcome at 6 Months. Variable Adjusted OR 95% CI p-value Low CSF glucose (<30 mg/dL) 3.2 1.5–7.0 0.005* High CSF protein (>160 mg/dL) 2.8 1.3–6.1 0.009* ADA >20 U/L 2.1 1.0–4.5 0.04* Stage III TBM 4.5 1.8–11.2 0.001* MRI infarcts 3.9 1.4–10.5 0.008* Low CSF glucose, elevated CSF protein, increased ADA levels, advanced BMRC stage, and MRI-detected infarcts were identified as independent predictors of poor outcome. Among these, Stage III disease was the strongest predictor. These results emphasize the prognostic significance of both CSF biochemical severity and radiological complications in tuberculous meningitis.

Tuberculous meningitis (TBM) remains the most devastating manifestation of extrapulmonary tuberculosis, with high rates of neurological sequelae and mortality despite appropriate therapy. Early identification of disease severity and prognostic markers is therefore essential. Cerebrospinal fluid (CSF) analysis continues to play a central role in TBM diagnosis and monitoring, reflecting the underlying inflammatory and pathological processes within the central nervous system. The present study evaluated the spectrum of CSF abnormalities in TBM and explored their associations with clinical severity, radiological findings, paradoxical reactions, and outcomes. The demographic profile of our cohort showed a young mean age with male predominance, consistent with earlier reports from endemic regions [5,25,26]. Unlike many adult-only hospital-based studies, the inclusion of children and adolescents reflects the broader disease burden in rural and mixed populations. The distribution of Modified BMRC stages at presentation was comparable to previous studies [5], although a higher proportion of Grade I cases suggested earlier presentation, particularly among younger patients. Baseline CSF analysis revealed predominantly clear or mildly hazy appearances, in line with previous literature [27-31]. While a clear appearance remains the most frequent macroscopic finding, the presence of hazy or xanthochromic CSF in a substantial proportion of patients underscores the dynamic inflammatory changes occurring during TBM. These findings reaffirm that gross CSF appearance alone is insufficient to exclude disease activity and must be interpreted alongside biochemical and cellular parameters. Marked abnormalities in CSF cell count, protein, glucose, and ADA levels were observed in the majority of patients, strongly supporting the diagnosis of TBM. The predominance of lymphocytes reflects the T-cell–mediated immune response characteristic of TBM and has been consistently demonstrated across multiple studies [27,32-36]. Although microbiological confirmation remains limited due to the paucibacillary nature of the disease, molecular techniques such as GeneXpert improved diagnostic yield, consistent with earlier reports. A key finding of this study was the clear association between worsening CSF abnormalities and increasing clinical severity. Patients in higher BMRC stages demonstrated significantly elevated CSF cell counts, protein, and ADA levels, along with progressively reduced glucose concentrations. Similar correlations between deranged CSF parameters and advanced disease stages have been reported previously [37,31,36,38,39]. These findings suggest that CSF biochemical markers may serve as useful adjuncts for early severity stratification, even though some studies have reported inconsistent correlations [15]. When analysed in relation to neuroimaging findings, CSF protein and glucose levels showed limited association with individual radiological abnormalities. This observation supports the concept that radiological changes represent structural and vascular consequences of disease, whereas CSF biochemistry reflects active inflammatory and metabolic processes that may evolve independently [40,41]. Nevertheless, certain radiological features—particularly basal exudates, hydrocephalus, and infarcts—were significantly associated with more pronounced CSF derangements, reinforcing their combined diagnostic and prognostic relevance [43,44]. Notably, patients who developed paradoxical reactions exhibited significantly higher CSF protein and ADA levels with lower glucose concentrations, indicating an exaggerated inflammatory response. While paradoxical reactions are well recognized in TBM [45,46] detailed associations with CSF biochemical changes remain poorly documented. The clinical or radiological worsening of pre-existing tuberculous lesions, or the appearance of new lesions, after initiation of appropriate anti-tubercular therapy (ATT), despite good adherence and initial improvement, [47,23]. This reaction is closely related to effective drug therapy rather than treatment failure. Rapid killing of Mycobacterium tuberculosis by first-line drugs such as isoniazid and rifampicin leads to the release of mycobacterial antigens and cell wall components, which trigger an exaggerated host inflammatory response [47,24]. The reaction is therefore considered immune-mediated. In patients with HIV infection, initiation of antiretroviral therapy (ART) along with ATT may result in immune restoration, causing an intensified inflammatory response against residual mycobacterial antigens, a condition known as tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) [24]. High bacillary load, extrapulmonary disease, low baseline CD4 count, and cytokine overproduction (e.g., TNF-α, interferon-γ) are important contributing factors [23,24]. Before diagnosing a paradoxical reaction, drug resistance, poor compliance, malabsorption, and secondary infections must be excluded [47,23]. Our findings therefore contribute novel evidence suggesting that CSF parameters may help identify patients at risk of paradoxical worsening, although conflicting results have been reported [15]. Outcome analysis at six months demonstrated that severe CSF abnormalities at baseline were strongly associated with deterioration and mortality. Elevated CSF protein and ADA levels, reduced glucose concentrations, and higher culture positivity rates were significantly more frequent among patients with poor outcomes. These findings are consistent with previous studies linking adverse outcomes to severe CSF biochemical disturbances and microbiological positivity [48-53]. Multivariate analysis further identified low CSF glucose, high CSF protein, elevated ADA levels, advanced BMRC stage, and cerebral infarcts as independent predictors of poor outcome. These results align with earlier reports emphasizing the prognostic value of CSF parameters and disease stage at presentation [52-55]. Collectively, the findings highlight the importance of early, comprehensive CSF evaluation combined with clinical and radiological assessment to guide risk stratification and management in TBM. In conclusion, this study demonstrates that CSF biochemical and cellular abnormalities correlate closely with clinical severity, paradoxical reactions, and long-term outcomes in TBM. Although individual CSF parameters may not fully predict radiological patterns, their combined assessment provides valuable prognostic information. These observations support a multimodal approach incorporating CSF analysis, neuroimaging, and clinical staging to improve early prognostication and therapeutic decision-making in tuberculous meningitis.

Cerebrospinal fluid (CSF) biochemical parameters in tubercular meningitis demonstrated a significant correlation with clinical severity, radiological findings, and treatment outcomes. Elevated CSF cell counts, protein, and adenosine deaminase levels, along with reduced glucose, were associated with advanced disease stage and poorer prognosis. Radiological features such as cerebral infarcts and basal exudates were linked to more severe CSF abnormalities, while paradoxical reactions reflected persistent inflammatory activity despite ongoing therapy. On multivariate analysis, low CSF glucose, high protein levels, elevated ADA, Stage III disease, and the presence of infarcts emerged as independent predictors of poor outcomes. Overall, CSF profiling serves as a valuable adjunct for early risk stratification and prognostication in tubercular meningitis, enabling timely therapeutic escalation, informed surgical decisions, and potentially improved long-term neurological outcomes. The only existing indication of CSF is to confirm exclude meningitis.

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