Diabetes insipidus following tuberculous meningitis.

In tuberculous meningitis the site of the maximal infection and of the most dense exudate is the basal cisterns, particularly the cisterna chiasmatis and the cisterna ambiens. This exudate may lead to obstruction of the cerebrospinal fluid pathways, which can be readily demonstrated by pneumoencephalograms (Lorber, 1951). Calcification of this exudate occurs in a large proportion of children who recover from the diseaseand can be shown two or three years after the onset of the meningitis on radiographs of the skull (Lorber, 1952; Lorber, 1958). These lesions are in close proximity to the pituitary gland and the hypothalamic nuclei. They may lead to vascular thromboses and consequently to softening of the adjacent brain substance. Furthermore, the hypothalamic nuclei may suffer as a consequence of the variable degrees of hydrocephalus produced by the obstruction of the cerebrospinal fluid. In view of these very common developments it would be reasonable to expect endocrine sequelae to result from a disturbance of the posterior pituitaryhypothalamic mechanism. Of the endocrine disorders originating in this area diabetes insipidus is one of the best recognized examples. Nevertheless, although by now thousands of patients must have survived tuberculous meningitis, reports of diabetes insipidus occurring as a complication during or after this illness are very few indeed (Table 1) and none of the reports furnished adequate proof of a true diabetes insipidus. All the reported cases had polyuria and polydipsia, and it is possible that full proof of diabetes insipidus was established in some of them by appropriate endocrinological tests, but these were not published. This certainly applies to the patient of Hooft and van Winckel (1957) about whom Professor Hooft kindly supplied fuller details in a personal communication which fully established the diagnosis of true pitressinsensitive diabetes insipidus. It is possible that the 11 cases briefly summarized in Table 1 are an incomplete list. The literature on tuberculous meningitis is so vast now that mention of some cases in papers not specifically dealing with endocrine sequelae or with follow-up studies may have escaped detection. The table does not include a few cases quoted by authors without details or quoting exact references. It is noteworthy that, with one exception (Acheson and Smith, 1958), none of the reported cases was in the British or American literature. No case of diabetes insipidus has developed among 131 surviving children who were treated in the Children's Hospital, Sheffield, and who were followed for two to 10 years after their admission. We have, however, seen and investigated a child through the courtesy of Dr. J. S. Oldham, who referred him to us because of polyuria and polydipsia, and who was proved to have true diabetes insipidus. Case History