PEDIATRIC CENTRAL NERVOUS SYSTEM TUBERCULOSIS: A CROSS-SECTIONAL HOSPITAL-BASED STUDY

Central nervous system (CNS) tuberculosis (TB), particularly tuberculous meningitis (TBM), represents the most severe and life-threatening form of infection caused by Mycobacterium tuberculosis. It is associated with high rates of mortality and long-term neurological disability, despite advances in anti-tubercular therapy and intensive care management. TBM contributes disproportionately to tuberculosis-related deaths and remains one of the most devastating manifestations of extrapulmonary TB [1].

 

The burden of CNS tuberculosis is especially significant because of its aggressive clinical course and delayed diagnosis. Even with appropriate treatment, mortality rates may exceed 50%, and a substantial proportion of survivors are left with permanent neurological sequelae. These include cognitive impairment, developmental delay in children, seizures, hydrocephalus, motor deficits, and cranial nerve palsies, which significantly affect quality of life and long-term functional outcomes [2]. A large number of cases remain undiagnosed or are diagnosed late, particularly in resource-limited settings, leading to poor outcomes due to delayed initiation of therapy [3].

 

In children, CNS tuberculosis often arises following recent primary infection, typically acquired through close household contact with an infectious adult case. Young children, especially those under five years of age, represent a highly vulnerable group due to their immature immune system and higher risk of progression from primary TB infection to disseminated disease, including CNS involvement. The epidemiology of pediatric CNS TB is not well defined in many regions, particularly in developing countries, where underreporting, limited diagnostic facilities, and lack of systematic surveillance contribute to gaps in knowledge [4].

 

The pathogenesis of TBM involves hematogenous dissemination of Mycobacterium tuberculosis from a primary pulmonary focus to the meninges and brain parenchyma, leading to the formation of Rich foci. Rupture of these foci into the subarachnoid space results in intense inflammatory response, causing basal meningitis, vasculitis, infarctions, and hydrocephalus. These pathological processes explain the wide spectrum of clinical manifestations and severe neurological complications associated with CNS TB [5].

 

Early diagnosis of CNS tuberculosis remains challenging due to its non-specific clinical presentation in the early stages, which often mimics other forms of meningitis. Delay in recognition and treatment initiation is strongly associated with poor neurological outcomes. Therefore, early identification of clinical patterns, radiological findings, and cerebrospinal fluid characteristics plays a crucial role in improving prognosis.

 

Given the high morbidity, mortality, and diagnostic challenges associated with pediatric CNS tuberculosis, there is a need for detailed clinical and epidemiological studies. Understanding the spectrum of disease presentation in children can aid in early diagnosis, timely management, and reduction of long-term neurological sequelae. In this context, the present study aims to analyze CNS tuberculosis among children in a cross-sectional setting.

Aim and Objectives

Aim

To study the clinical, radiological, and laboratory profile of central nervous system (CNS) tuberculosis among children in a tertiary care setting.

 

Objectives

1.      To describe the clinical spectrum of CNS tuberculosis in pediatric patients.

2.      To analyze the common presenting symptoms and neurological signs in children with CNS tuberculosis.

3.      To evaluate cerebrospinal fluid (CSF) and neuroimaging findings associated with CNS tuberculosis.

 

 

Table 1 – Demographic and contact profile: The majority of cases occurred in the youngest age group, 0–5 years (56.9%), indicating that young children are particularly vulnerable to severe, disseminated forms of TB affecting the central nervous system — likely related to their immature cell-mediated immunity, which predisposes to hematogenous spread of mycobacteria beyond the lungs. A mild male predominance was observed (55.4% vs 44.6%). Socioeconomic distribution showed that the large majority of children belonged to the lower middle, upper lower, and lower strata combined (80%), reflecting the well-established link between poverty, overcrowding, undernutrition, and increased risk of TB exposure and progression to severe disease. A history of contact with a known TB case was present in 60% of children, highlighting the important role of household or close-contact transmission in pediatric CNS TB; the substantial 40% without an identifiable contact history may reflect under-detection of source cases in the community or limitations in contact tracing, and emphasizes the need for more thorough screening of household and close contacts.

 

Table 1:Age,gender,socioeconomicstatusandhistoryofcontactdistributionamongthestudysubjects

 

Table2:DistributionofcasesaccordingtotypeofCNStuberculosis

 

Table 2 – Type of CNS tuberculosis: Tubercular meningitis (TBM) was overwhelmingly the most common presentation, accounting for more than two-thirds of cases (67.7%), consistent with TBM being recognized as the most frequent and most severe neurological manifestation of tuberculosis in children. Tuberculous encephalopathy was the second most common form (18.4%), a presentation often attributed to a hypersensitivity reaction to tuberculoprotein and typically seen in younger infants, which aligns with the predominance of the 0–5 year age group in this cohort. The remaining forms — TB vasculopathy (6.3%), CNS tuberculoma (4.6%), tuberculous brain abscess (1.5%), and Pott's spine with paraplegia (1.5%) — were relatively uncommon, together making up less than 15% of cases, but represent clinically important variants that should be considered in children presenting with focal neurological deficits, spinal symptoms, or atypical features.

In the present study of pediatric CNS tuberculosis, a slight male predominance was observed, with males constituting a higher proportion of cases compared to females. Similar gender distribution has been reported in previous pediatric tuberculosis studies, where male preponderance is often attributed to increased exposure, sociocultural factors, and healthcare-seeking behavior differences [6]. However, gender differences in CNS tuberculosis are generally not strongly significant and may vary across populations.

 

Socioeconomic status showed a clear association with disease burden, with the majority of cases belonging to the lower middle (38.5%) and upper lower (33.8%) socioeconomic groups, while only a small proportion (3.1%) belonged to the upper class. This finding highlights the strong relationship between tuberculosis and poverty. Overcrowding, malnutrition, poor ventilation, and limited access to healthcare are well-established risk factors for tuberculosis transmission and progression to severe forms such as CNS involvement [7]. Similar observations have been reported in global TB burden studies, where low socioeconomic conditions significantly increase the risk of both primary infection and disseminated disease [8].

 

A history of contact with tuberculosis was present in 60% of cases, emphasizing the importance of close household exposure as a major risk factor in pediatric CNS tuberculosis. Children, particularly those under 10 years of age, are highly susceptible to progression from primary infection to severe disease due to immature cell-mediated immunity. This finding is consistent with previous studies that identified recent household contact as one of the strongest predictors of pediatric TBM [9].

 

Clinically, tuberculous meningitis (TBM) was the most common presentation, accounting for 67.7% of cases, followed by tuberculous encephalopathy (18.4%). Less common manifestations included TB vasculopathy (6.3%), CNS tuberculoma (4.6%), and tuberculous brain abscess (1.5%). The presence of Pott’s spine with paraplegia in 1.5% of cases reflects disseminated tuberculosis involving multiple systems. These findings are consistent with the known spectrum of CNS tuberculosis, where TBM remains the most frequent and severe form due to hematogenous spread of Mycobacterium tuberculosis to the meninges and subarachnoid space [10].

 

The varied clinical spectrum observed in the present study highlights the diagnostic challenges associated with CNS tuberculosis in children. Early symptoms are often nonspecific, leading to delayed diagnosis and progression to advanced neurological disease. The predominance of TBM in our study aligns with literature indicating that it is the most common CNS manifestation and carries the highest risk of mortality and long-term neurological sequelae [11].

 

Overall, the findings emphasize that pediatric CNS tuberculosis predominantly affects children from lower socioeconomic backgrounds with a history of close contact exposure. The high proportion of TBM underscores the need for early clinical suspicion, prompt neuroimaging, and CSF evaluation for timely diagnosis and management.

The present study highlights that central nervous system (CNS) tuberculosis in children predominantly affects those from lower socioeconomic backgrounds and those with a positive history of tuberculosis contact. Tuberculous meningitis remains the most common clinical presentation, followed by other severe manifestations such as tuberculous encephalopathy, vasculopathy, and tuberculoma.

 

The study emphasizes the wide clinical spectrum of CNS tuberculosis and the diagnostic challenges due to its nonspecific early presentation. The findings underline the importance of maintaining a high index of suspicion in children presenting with prolonged fever, neurological symptoms, and a history of TB exposure.

 

Early recognition through clinical evaluation, neuroimaging, and cerebrospinal fluid analysis is crucial for timely initiation of treatment. Prompt diagnosis and management are essential to reduce morbidity, prevent neurological sequelae, and improve overall outcomes in pediatric CNS tuberculosis.

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2.      Thwaites GE, van Toorn R, Schoeman J. Tuberculous meningitis: more questions, still too few answers. Lancet Neurol. 2013;12(10):999–1010.

3.      World Health Organization. Global tuberculosis report 2023. Geneva: WHO; 2023.

4.      Marais BJ, Gie RP, Schaaf HS, et al. The natural history of childhood intra-thoracic tuberculosis: a critical review of literature from the pre-chemotherapy era. Int J Tuberc Lung Dis. 2004;8(4):392–402.

5.      Donald PR, Schaaf HS. Tuberculous meningitis in children. Clin Infect Dis. 2007;45(10):1277–1284.

6.      Donald PR, Marais BJ, Barry CE 3rd. Age and tuberculosis: implications for transmission and disease progression. Lancet Infect Dis. 2010;10(4):272–283.

7.      Lönnroth K, Jaramillo E, Williams BG, Dye C, Raviglione M. Drivers of tuberculosis epidemics: the role of risk factors and social determinants. Soc Sci Med. 2009;68(12):2240–2246

8.      World Health Organization. Global tuberculosis report 2023. Geneva: WHO; 2023.

9.      Marais BJ, Gie RP, Schaaf HS, et al. The natural history of childhood tuberculosis. Int J Tuberc Lung Dis. 2004;8(4):392–402.

10.   Thwaites GE, van Toorn R, Schoeman J. Tuberculous meningitis: more questions than answers. Lancet Neurol. 2013;12(10):999–1010.

11.   Rock RB, Olin M, Baker CA, Molitor TW. Central nervous system tuberculosis: pathogenesis and clinical aspects. Clin Microbiol Rev. 2008;21(2):243–261.