Neurosurgically relevant aspects of pathology and pathogenesis of intracranial and intraspinal tuberculosis

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Abstract
In view of the persisting high prevalence (though somewhat reduced compared to 20 years ago) of various forms of neurotuberculosis, especially in economically underpriviledged and undernourished urban paediatric populations of the world, some aspects of the neuropathology relevant to neurosurgeons, are briefly presented and discussed. The most conspicuous of these is the development of brain tuberculomas, which act as both space-occupying and inflammatory masses that result in severe oedema or direct destruction of brain parenchyma. The cellular reaction in the border zone of these tuberculomas is identical to that in tuberculous meningitis and consists of specialized large mononuclear cells — the epithelioid cells — which undertake a phagocytic function and also fuse with one another to form giant cells, as seen by both light and electron microscopy. These cells together with others like lymphocytes and plasma cells, also infiltrate the walls of small blood vessels, constituting vasculitis, and these vessels may undergo necrosis, in both the intracranial (mainly basal) and spinal leptomeningeal exudate. The latter is more frequent in young adults than in children, and may be the primary event in the CNS or secondary to extension downwards of the basal meningitis. The quantity and nature of the spinal exudate vary in duration and severity, the more common being extensively “tubular” and subacute, producing radiculopathy and myelopathy by compression of these structures, and rarely infiltration. The damage to the cord, mainly the white matter, occurs through oedema and ischaemia, rather than frank infarction, the larger arteries being rarely involved. The blockage of the intracranial basal cisterns by the adhesive basal meningeal exudate, more so in longdrawn out cases in children who are inadequately treated and the exudate tends to be partly fibrous, results in varying degrees of internal hydrocephalus with consequent damage to cerebral white and then grey matter. The blockage of the aqueduct by the throttling action of the exudate around the brain stem or by tuberculomas in that region, produces the severest forms of internal hydrocephalus, requiring shunting procedures to prevent CSF accumulation.