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Pathology and pathogenetic mechanisms in neurotuberculosis
D K Dastur1, D K Manghani, P M Udani
1Medical Research Centre, Bombay Hospital, Bombay, India.
Radiologic Clinics of North America
|July 1, 1995
Summary
Tuberculosis affecting the brain begins with basal meningeal exudate, leading to inflammation, ischemia, and granuloma formation. This can cause hydrocephalus, infarction, and neurological damage, with potential roles for nitric oxide and corticosteroids.
Area of Science:
- Neurology
- Pathology
- Infectious Diseases
Background:
- Tuberculous meningitis (TBM) is a severe central nervous system (CNS) infection.
- Understanding the detailed pathological mechanisms of TBM is crucial for effective treatment.
Observation:
- TBM pathogenesis involves basal meningeal exudate formation, rich in mononuclear cells and macrophages.
- Exudate can compress cranial nerves and arteries, leading to ischemia and infarction.
- Inflammation extends into brain parenchyma, causing encephalitis and granuloma (tuberculoma) development.
Findings:
- TBM can result in hydrocephalus due to blocked CSF pathways.
- Vasculitis and arteritic occlusion contribute to ischemic brain changes.
- Tuberculous spinal meningitis and hypersensitivity reactions (allergic tuberculous encephalopathy) can also occur.
Implications:
- Nitric oxide may play a role in CNS inflammation.
- Corticosteroids show potential benefit, particularly in tuberculous encephalopathy.
- Further research into TBM pathogenesis can guide therapeutic strategies.