Brain Lesions

Central Nervous System Tuberculosis

Author: John M. Leonard
• Source: Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition , pp 283-292
Publication Date : January 2011
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• Abstract:
  

  Central nervous system (CNS) tuberculosis (TB) is among the least common yet most devastating forms of human mycobacterial infection. Conceptually, clinical CNS infection is seen to comprise three categories of illness: subacute or chronic meningitis, intracranial tuberculoma, and spinal tuberculous arachnoiditis. The sequence of events that leads to clinical neurologic illness begins with the hematogenous dissemination of Mycobacterium tuberculosis that follows primary pulmonary infection or late reactivation TB elsewhere in the body. The continued proliferation and coalescence of tubercles result in larger caseous foci. Such lesions, if located adjacent to the ependyma or pia, may subsequently rupture into the subarachnoid space, producing meningitis. This conceptual understanding of the pathogenesis of tuberculous meningitis (TBM) is derived from the observations of Rich and McCordock, who performed meticulous autopsy examinations of TBM patients dying at the Johns Hopkins Hospital during the early part of the last century. The key to the diagnosis in most instances rests with the proper interpretation of the spinal fluid cellular characteristics and chemistries combined with the demonstration of mycobacteria in the cerebrospinal fluid (CSF) by stained smear or culture. The nucleic acid-based amplification technique, based on PCR, is a new and effective method for the rapid detection of specific bacterial DNA in clinical specimens. Late sequelae include cranial nerves (CN) palsies, gait disturbance, hemiplegia, blindness, deafness, learning disabilities, dementia, and various syndromes of hypothalamic and pituitary dysfunction.