Chapter 18 : Central Nervous System Tuberculosis

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Central Nervous System Tuberculosis, Page 1 of 2

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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 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.

Citation: Leonard J. 2011. Central Nervous System Tuberculosis, p 283-292. In Schlossberg D (ed), Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817138.ch18

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Brain Lesions
Magnetic Resonance Imaging
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Image of Figure 1.
Figure 1.

Computerized axial tomogram for a patient with TBM. Note the enlarged ventricles and effacement of sulci, indicating raised intracranial pressure.

Citation: Leonard J. 2011. Central Nervous System Tuberculosis, p 283-292. In Schlossberg D (ed), Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817138.ch18
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Image of Figure 2.
Figure 2.

MRI of the same patient as for Fig. 1 . (A) After contrast enhancement, showing two dense, bilateral inflammatory masses (tuberculomas) in the region of the thalamus; (B) T-2 weighted image showing inflammatory edema and possible ischemic changes of vasculitis in the basal region of the temporal lobe (arrowhead).

Citation: Leonard J. 2011. Central Nervous System Tuberculosis, p 283-292. In Schlossberg D (ed), Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817138.ch18
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Generic image for table
Table 1.

Presenting symptoms and signs of TBM

Citation: Leonard J. 2011. Central Nervous System Tuberculosis, p 283-292. In Schlossberg D (ed), Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817138.ch18
Generic image for table
Table 2.

Differential diagnosis of TBM

Citation: Leonard J. 2011. Central Nervous System Tuberculosis, p 283-292. In Schlossberg D (ed), Tuberculosis and Nontuberculous Mycobacterial Infections, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817138.ch18

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