BECAUSE meningitis is the primary cause of death from tuberculosis in children (2), diagnosis is urgent. If only the parameters of tuberculin skin test, contact history, and organism identification are used, antituberculous therapy may often be withheld. Associated pneumonia, split sutures, hydrocephalus, and cerebral arterial changes also indicate tuberculous origin of sterile meningitis. Pneumonia without calcification has been reported in 43 to 75 per cent (2, 10) of children with tuberculous meningitis. This is not necessarily characteristic in pattern. Adenopathy, calcification, miliary disease, or pleural effusion has been present in fewer patients. These findings are especially significant when meningitis is the presenting manifestation of tuberculosis. Acheson and Smith (1) and Foltz and Sheehy (5) have noted that major degrees of hydrocephalus are characteristic of the more severe cases, and that it carries a poor prognosis. In tuberculous meningitis studied by pneumoencephalography, hydrocephalus has been reported in 40 to 68 per cent (13, 5) of pediatric patients. The hydrocephalus is usually communicating, with the block at the sylvian and interpeduncular cisterns, but obstruction has also been described at the aqueduct (8), at the foramen of Magendie and Luschka (13), and at two levels (5). Spasm or narrowing about the internal carotid artery bifurcation has been described by Greitz (6) and Lehrer (8). Intracranial calcification has not been found until fifteen months after the onset of meningitis (11). Patients with Tuberculous Meningitis The 14 patients of this report were hospitalized at St. Louis Children's Hospital or Barnes Hospital between 1956 and 1967. Six were Negro, 8 Caucasian, 5 female, and 9 male. Five were between eleven months and twenty-four months of age, 6 were between four and seven years of age, and 3 adults were twenty-one, thirty-three, and sixtv-six years old. Chest radiographs were obtained on 13 patients. Pneumonia was present in 9, and in 4 of these there was also hilar adenopathy and in another apical pleural thickening. In 1 patient only hilar adenopathy was noted radiographically, although pneumonia was present at autopsy (Fig. 1). A calcified 5 mm parenchymal nodule was observed in another infant, whose hilar lymph nodes later became enlarged and calcified during antituberculous therapy. The only 2 chest examinations failing to indicate possible active pulmonary disease were in adults. Skull examination disclosed split sutures in 6 patients: aged eleven months, one, one, two, four, and seven years. The sutures were closed in 7 patients aged four, five, six, seven, twenty-one, thirty-three, and sixty-six years. In 3 patients with closed sutures air studies showed dilated ventricles. The hydrocephalus was of the communicating type in 2 cases (Fig. 2), with air reaching the sulci in a third.