Hydrocephalus, secondary to disturbed CSF flow and absorption.Vasculitis with endarteritis and infarcts.Leptomeningitis, epididymitis, choroid plexitis, encephalitis, and later pachymeningitis with basal and opticochiasmatic arachnoiditis.This MTB bacilli so released produce an intense, cytokine-mediated host inflammatory response, leading to following This lead to seeding of the meninges or ependyma with multiple small granulomatous foci or tubercles (Rich focus) that may proliferate, coalesce and caseate and finally rupture into the subarachnoid space before the onset of meningitis. PathophysiologyĬNS-TB begins with either the hematogenous dissemination of MTB following primary lung infection or the late reactivation of TB. Despite the advances in diagnosis and management, CNS–TB still carries high mortality of 15 to 40%, especially in children. The incidence of reported TB rose 9.4% in 2021 (2.37) compared with 2020 (2.16). Since 2010, TB incidence has fallen by 2 to 3% every year, especially in 2020, probably due to the pandemic mitigation efforts, travel restrictions, or delayed or missed TB diagnoses.
An estimated 9272 cases of CNS-TB were diagnosed in the US in 2016. They may account for 20 to 30% of all intracranial space-occupying lesions. Tuberculomas are seen mostly in India and parts of Asia. 70 to 80% of cases of CNS-TB present as TBM. It accounts for 5 to 8% of extra-pulmonary tuberculosis (EPTB) in immunocompetent hosts. CNS-TB is reported in 1 to 2% of individuals with active TB. It has been estimated that 25 to 30% of the human population is infected with MTB. Infection is primarily acquired through airborne aerosols from infective individuals. Humans are the only hosts or reservoirs known for MTB. The etiological contribution of the other four species of MTB-complex in causing CNS-TB is not determined. It is alcohol and acid-fast bacillus, stained using the Ziehl-Neelsen/Auramine-rhodamine/Kinyoun stains. Mycobacterium tuberculosis (MTB) is the organism responsible for CNS-TB. Untreated or unrecognized TBM may cause death within 5 to 8 weeks of the onset of the disease.
Multiple factors determine the prognosis, the most important being the clinical stage of TBM at initial presentation. Treatment efficacy depends upon how early it is instituted. The diagnosis and management of CNS-TB may be complicated by drug resistance, immune reconstitution inflammatory syndrome, and human immunodeficiency virus (HIV) coinfection. A 4-drug regimen of isoniazid, rifampin, pyrazinamide, and ethambutol with adjunctive corticosteroid reduces morbidity and mortality. A strong clinical suspicion is enough to start prompt anti-tubercular therapy. CNS-TB is frequently complicated by vasculitic infarcts, cranial nerve palsies, multiple neurological deficits, and hydrocephalus. Īdvanced radiological imaging techniques are usually of great assistance in making presumptive diagnoses. Identifying Mycobacterium tuberculosis in CSF by staining, culture methods, and molecular analysis is confirmatory but may be challenging. Besides the clinical clues, diagnostic indicators in cerebrospinal fluid (CSF) include mononuclear pleocytosis, low sugar values, and high protein concentrations. The diagnosis is fraught with challenges and is often delayed due to the varied and non-specific presentation. It presents as a subacute to chronic meningitis with disease severity commensurate with the duration of illness.
Of these, TBM predominates, causing 70 to 80% of the infections. Neurological tuberculosis (TB) or central nervous system tuberculosis (CNS-TB) may take three clinic-pathological forms: a diffuse form of tubercular meningitis (TBM), a focal form as tuberculoma, and spinal arachnoiditis also referred to as TB radiculomyelitis. Mycobacterium tuberculosis is responsible for 5.9% of community-acquired CNS infections worldwide.
This activity reviews the early identification and management of CNS-TB and highlights the importance of interprofessional team members in coordinating well to enhance outcomes in patients with CNS tuberculosis. CNS tuberculosis (CNS-TB) carries high morbidity and mortality among all forms of TB. TBM develops either due to rupture of subependymal or meningeal tubercular foci or through the hematogenous route. This may take the form of either tubercular meningitis (TBM), tuberculoma, or spinal arachnoiditis. One of the catastrophic manifestations of extrapulmonary TB (EPTB) is the affection of the central nervous system (CNS). Tuberculosis (TB) is a prevalent worldwide infection.
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