The manifestations of tuberculosis are protean, its incidence still great in several parts of the world, and the morbidity and mortality resulting from it disconcerting inspire of modern medications. The incidence of intracranial forms of the disease is likewise high, and the expressions of tuberculous meningitis, or of menJngo-encephalitis as it is rightly called, are also many and varied. While, for instance, the admission rate for tuberculous children at our Paediatric Centre has fallen from about 15~ in 1953 to about 90/0 in 1960 (UDA~I, 1961), the number of annual adminissions was about 400 in 1960 and still remains the same. Of these, some 42o/0 had tuberculous meningitis. During approximately the same period, of the 455 specimens of intra-cranial space occupying lesions studied at the Neuropatho]ogy Unit, 22.50/0 were tuberculomas (DASTUR and IYER, 1961), indicating the other eommou form of neurotuberculosis. This high incidence still remains and tuberculomas are seen to constitute 48.5~ of all brain "tumors" in children under 14 (DAsTV~ et al., 1966, unpublished data). Parenchymal neurotuberculosis secondary to an extension inwards of the leptomeningeal or ependymal inflammatory reaction, or to softening resulting from gross occlusion of the arteries at the base of the brain due to compression in the tuberculous exudate and arteritis, is fairly well known (e. g. WILson, 1940, and DASTu~, 1964, respectively). Quite distinct from these, are cases of tuberculosis, with or without clinical and CSF changes of tuberculous meningitis, which present predominant signs of diffuse cerebral involvement, and which have been recognized earlier (UDA~I, 1958). A brief pathological consideration of this has been presented recently (DAsTuR and UDA~I, 1965), the present communication being a detailed account and discussion.