Cerebral tuberculosis: Understanding pathogenesis and improving early diagnosis
image: lasma metabolomic analysis in active tuberculosis patients and healthy controls. (A) PCA score plot of active TB patients (n = 36) and HCs (n = 44) based on metabolomic data. (B) OPLS-DA score plot of TB patients (n = 36) and HCs (n = 44) based on metabolomic assay. (C) Permutation and prediction tests were performed to validate the OPLS-DA classification model by using metabolomic data. (D) Heatmap of 15 amino acid contents in the plasma from active TB patients and HC derived from 1H NMR assay. (E) Relative concentrations of four amino acids (mean ± SEM) in TB and HCs. (F) OPLS-DA score plot of active TB patients (n = 36) and HCs (n = 44) by using 4-aminobenzoate, phenylalanine, serine and threonine. (G) Permutation and prediction test to validate the OPLS-DA classification model by using 4 amino acids. Data were presented as mean ± SEM. ∗∗∗, P < 0.001
Credit: Yong Li, Cheng-cheng Yao, Ping Ji, Hui-yu Wang, Shu-jun Wang, Ying Wang, Qi-jian Cheng, Lu Xia, Ying-ying Chen.
Cerebral tuberculosis (CTB), a severe and often fatal form of central nervous system (CNS) tuberculosis, poses significant diagnostic and treatment challenges. This narrative review in LabMed Discovery explores the complex pathogenesis of CTB, which typically begins with hematogenous spread of Mycobacterium tuberculosis from a primary site—often the lungs—to the brain. Once in the CNS, the bacteria can cause granulomatous inflammation, leading to complications like tuberculous meningitis, tuberculomas, and vasculitis. The clinical presentation of CTB is notoriously variable and non-specific, ranging from fever and headache to altered mental status, seizures, and focal neurological deficits, which often results in delayed diagnosis and high mortality.
The article systematically reviews available diagnostic tools, emphasizing their respective strengths and limitations. Neuroimaging techniques like CT and MRI can reveal characteristic features such as meningeal enhancement, hydrocephalus, or intracranial masses, while cerebrospinal fluid (CSF) analysis typically shows lymphocytic pleocytosis, elevated protein, and low glucose. However, none of these findings are definitive. The review highlights molecular diagnostics—especially GeneXpert MTB/RIF—as valuable tools that improve sensitivity and speed, yet their availability remains limited in high-burden, low-resource settings. The authors underscore the urgent need for improved diagnostic strategies and clinical vigilance, particularly in endemic regions, to initiate timely treatment and reduce neurologic sequelae. Overall, the article serves as a vital reference for clinicians, microbiologists, and public health experts tackling one of tuberculosis’s most devastating manifestations.