Tuberculous meningitis

Abstract

Tuberculous meningitis is a severe form of extrapulmonary tuberculosis. The exact incidence and prevalence are not known. In countries with high burden of pulmonary tuberculosis, the incidence is expected to be proportionately high. Children are much more vulnerable. Human immunodeficiency virus-infected patients have a high incidence of tuberculous meningitis. The hallmark pathological processes are meningeal inflammation, basal exudates, vasculitis and hydrocephalus. Headache, vomiting, meningeal signs, focal deficits, vision loss, cranial nerve palsies and raised intracranial pressure are dominant clinical features. Diagnosis is based on the characteristic clinical picture, neuroimaging abnormalities and cerebrospinal fluid changes (increased protein, low glucose and mononuclear cell pleocytosis). Cerebrospinal fluid smear examination, mycobacterial culture or polymerase chain reaction is mandatory for bacteriological confirmation. The mortality and morbidity of tuberculous meningitis are exceptionally high. Prompt diagnosis and early treatment are crucial. Decision to start antituberculous treatment is often empirical. WHO guidelines recommend a 6 months course of antituberculous treatment; however, other guidelines recommend a prolonged treatment extended to 9 or 12 months. Corticosteroids reduce the number of deaths. Resistance to antituberculous drugs is associated with a high mortality. Patients with hydrocephalus may need ventriculo-peritoneal shunting. Bacillus Calmette-Guérin vaccination protects to some degree against tuberculous meningitis in children.

Validation of Thwaites' Diagnostic Scoring System for the Differential Diagnosis of Tuberculous Meningitis and Bacterial Meningitis

“…On the contrary, the BM group typically displayed severe fever with highly elevated total peripheral WBC counts with a left shift, concomitant with CSF neutrophilic pleocytosis. MRI of the brain revealed meningeal enhancement or localized brain abscess (18,19). Despite significant differences between the 2 groups, differentiating between them on the basis of a single clinical symptom or biochemical parameter remains a challenge.…”

Tuberculous meningitis in patients infected with human immunodeficiency virus

“…The microglial cells (the resident macrophages of the brain) are the principal targets of M. tuberculosis. Tumor necrosis factor-alpha released from microglial cells has been shown to play a critical role in the containment of infection, granuloma formation, alteration of blood-brain barrier permeability, and cerebrospinal fluid leukocytosis [1]. Several other cytokines present in the microglia, such as b 2 -integrin (CD-18), interleukin-6, interleukin-1b, chemokine (C-C motif) ligand 2 and chemokine (C-C motif) ligand-5, and chemokine (C-X-C motif) ligand-10, are also involved in the host's defense mechanisms [22].…”

“…Despite adequate chemotherapy, tuberculous meningitis is fatal in up to 50% of the cases. A high frequency of disabling morbidity is observed among survivors [1]. Even in advanced countries, such as the United States, tuberculous meningitis is associated with a high mortality.…”

Nuclear Factor κB Activation Impairs Ependymal Ciliogenesis and Links Neuroinflammation to Hydrocephalus Formation

“…The neuropathological consequences of this increased intracranial pressure are lethal in 20 -50% of patients if left untreated (Poca and Sahuquillo, 2005). Main causes of hydrocephalus are infections and injury of the CNS (e.g., a large proportion of patients with subarachnoid hemorrhages and tuberculous meningitis develop hydrocephalus) (Garg, 2010;Germanwala et al, 2010). During brain development, susceptibility to hydrocephalus formation seems especially high (e.g., in congenital toxoplasmosis) (Mack et al, 1999).…”