PATHOLOGY AND PATHOGENETIC MECHANISMS IN NEUROTUBERCULOSIS

Abstract

The mechanisms and the changes described herein typically begin with a dense basal meningeal exudate often resulting from a "Rich focus" along the basal surface of the cerebrum or ventricular ependyma. In the interpeduncular fossa, when the exudate is copious, among other structures the proximal parts of the optic nerves and of the internal carotid arteries are seen surrounded and compressed by the exudate. This exudate is made up of small and large mononuclear cells, including epithelioid cells, which also act as macrophages and may fuse to form Langhans' giant cells. Further extension of this exudate along small proliferating blood vessels into the brain substance constitutes a border zone encephalitis with the development of focal and diffuse ischemic brain changes due to vasculitis. Entrapment and occasional arteritic occlusion of larger arteries, such as the middle cerebral in the Sylvian fissures, results in infarction. Blockage of the basal subarachnoid cisterns around the midbrain and pons by the dense basal exudate or narrowing of aqueduct and third ventricle by a small tuberculoma causes consequent hydrocephalus. Development of many or one large focal granuloma (i.e., tuberculoma) occurs in the cerebrum, cerebellum, and/or brain stem. Similar pathogenetic mechanisms produce tuberculous spinal meningitis myeloradiculopathy that may be secondary to or occur before cranial tuberculous meningitis. More extensive damage to the white matter may occur together with the infrequent onset of perivascular demyelination on the basis of a hypersensitivity reaction to tuberculoprotein (i.e., "allergic tuberculous encephalopathy"). Finally, there may be a part played by NO in the production of the vascular and perivascular inflammatory central nervous system changes and a role for the the potential beneficial action of corticosteroids, especially in cases of tuberculous encephalopathy.