The pathology and pathogenesis of tuberculous encephalopathy and myeloradiculopathy: a comparison with allergic encephalomyelitis

Abstract

The pathology and pathogenesis of tuberculous encephalopathy are reviewed. They confirm the findings in a smaller series previously published. The main features were: (1) diffuse brain edema and myelin pallor in the majority of specimens; (2) microvascular distension or necrosis with perivascular macrophage reaction and greater demyelination; (3) focal glial nodules in the white matter; (4) less frequently, hemorrhagic lesions in the presence of mild-to-moderate tuberculous meningitis (TM), but in the virtual absence of the commoner brain-damaging mechanisms. Focal demyelinating lesions in the nerve roots are now added to the above pathology in the brain in some of the cases of spinal tuberculous meningitis. In addition, a picture similar to that in human postinfectious allergic or experimental allergic encephalomyelitis (EAE) has emerged. The spinal cords from one case of the former condition and from four animals with EAE are described to illustrate this similarity. The pathogenesis of tuberculous encephalopathy and myeloradiculopathy is believed, as before, to be due to delayed hypersensitivity, i.e., cell-mediated immunity (CMI) to tuberculoprotein. Experimental confirmation of this demyelination as a nonspecific consequence of CMI to various forms of tubercle bacillus proteins has recently been published. In a proportion of our cases, where two episodes of TM had occurred, the possibility of a hypersensitivity reaction to the brain's own myelin protein is also considered.