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Tuberculous Meningitis


Tuberculous meningitis (TBM) develops in 2 steps. Mycobacterium tuberculosis bacilli enter the host by droplet inhalation. Localized infection escalates within the lungs, with dissemination to the regional lymph nodes. In persons who develop TBM, bacilli seed to the meninges or brain parenchyma, resulting in the formation of small subpial or subependymal foci of metastatic caseous lesions, termed Rich foci.

The second step in the development of TBM is an increase in size of a Rich focus until it ruptures into the subarachnoid space. The location of the expanding tubercle (ie, Rich focus) determines the type of CNS involvement. Tubercles rupturing into the subarachnoid space cause meningitis. (See Pathophysiology.)

Currently, more than 2 billion people (ie, one third of the world’s population) are infected with tuberculosis (TB), of which approximately 10% will develop clinical disease. The incidence of central nervous system (CNS) TB is related to the prevalence of TB in the community, and it is still the most common type of chronic CNS infection in developing countries.

Despite great advances in immunology, microbiology, and drug development, TB remains among the great public health challenges. Poverty; lack of functioning public health infrastructure; lack of funding to support basic research aimed at developing new drugs, diagnostics, and vaccines; and the co-epidemic of HIV continue to fuel the ongoing epidemic of TB. (See Epidemiology.)

TBM is a very critical disease in terms of fatal outcome and permanent sequelae, requiring rapid diagnosis and treatment. Prediction of prognosis of TBM is difficult because of the protracted course, diversity of underlying pathological mechanisms, variation of host immunity, and virulence of M tuberculosis. Prognosis is related directly to the clinical stage at diagnosis. (See Prognosis.)

TBM may have an acute presentation. Sometimes it may present with cranial nerve deficits, or it may have a more indolent course involving headache, meningismus, and altered mental status. The prodrome is usually nonspecific, including headache, vomiting, photophobia, and fever. The duration of presenting symptoms may vary from 1 day to 9 months. (See Clinical Presentation.)

TBM continues to pose a diagnostic problem. A high index of clinical suspicion is absolutely essential. TBM should be a strong consideration when a patient presents with a clinical picture of meningoencephalitides, especially in high-risk groups. Diagnostic confusion often exists between TBM and other meningoencephalitides, in particular partially treated meningitis. TBM must be differentiated not only from other forms of acute and subacute meningitis but also from conditions such as viral infections and cerebral abscess. (See Diagnosis.)

The diagnosis of TBM cannot be made or excluded solely on the basis of clinical findings. Tuberculin testing is of limited value. Variable natural history and accompanying clinical features of TBM hinder the diagnosis. Spinal tap carries some risk of herniation of the medulla in any instance when intracranial pressure (ICP) is increased (eg, TBM), but if meningitis is suspected, the procedure must be performed regardless of the risk. CNS imaging modalities lack specificity but help in monitoring complications that require neurosurgery. (See Workup.)

Prompt treatment is essential; death may occur as a result of missed diagnoses and delayed treatment. Antimicrobial therapy is best started with isoniazid, rifampin, pyrazinamide; addition of a fourth drug is left to local choice. The optimal duration of antimicrobial therapy is unclear. The benefits of adjuvant corticosteroids remain in doubt: their use in adults is controversial, though they may be indicated in the presence of increased ICP, altered consciousness, focal neurological findings, spinal block, and tuberculous encephalopathy.

In patients with evidence of obstructive hydrocephalus and neurological deterioration who are undergoing treatment for TBM, placement of a ventricular drain or ventriculoperitoneal or ventriculoatrial shunt should not be delayed. Prompt shunting improves outcome, particularly in patients presenting with minimal neurological deficit. (See Treatment and Management.)

New research avenues include research into vaccine design, mechanisms of drug resistance, and virulence determinants. Rapid sensitivity testing using bacteriophages considers the problem of drug resistance.

Go to Meningitis, Meningococcal Meningitis, Staphylococcal Meningitis, Haemophilus Meningitis, Viral Meningitis, and Aseptic Meningitis for more complete information on these topics.

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