Diabetes Insipidus The Role of the Anterior Hypophysis

[N the routine examination of some seven hundred brains, seven were found to have shown the clinical syndrome of diabetes insipidus (Biggart, 1935, 1936, and 1937). Whilst the anatomical findings in these seven cases allow of the interpretation of the pathogenesis of the diabetic syndrome on the basis of the destruction of the (1) supraoptic nuclei, or (2) the supraoptic-hypophyseal tract, or (3) the posterior hypophysis and its epithelial investments, it is a curious and still unexplained observation that polyuria is not found in all cases in which these structures are involved. It seems difficult, for example, for the supraoptic hypophyseal tract to escape in many patients suffering from tumours of the pars tuberalis, and yet many of these do not show the syndrome. Other patients with diabetes insipidus show a diminution in the polyuria, which may eventually entirely disappear, and yet at post-mortem a lesion may be found which, because of its destruction of the supraoptic-hypophyseal system, might well be expected to be associated xvith polyuria. The following case, therefore, because of the site of the lesion, seemed worthy of analysis and report: The patient, Mrs. J. McD., was a woman of fifty-four years of age. One year previously she had a radical mastectomy performed for the removal of a tumour of the left breast. Pathological exanmination of the tissue showed the tumour to be a scirrhous type of carcinoma. Following this operation, she was quite well until one month ago. Since then she has noticed a rapid loss in weight, and .has suffered from pains. These pains are most severe over the back of the neck and over the head. There is no history of any urinary trouble. She has no nocturia, and no frequency. Examination of the patient showed little of note. She was emaciated, with a dry, rather inelastic skin. There was an enlarged gland palpable in the left axilla. Nothing abnormal was noted in the heart, lungs, or abdomen. Two days before death some left facial weakness developed, and examination of the fundus showed some papillcedema. Paresis of the seventh cranial nerve appeared, and the patient gradually became weaker, and died in coma with signs of pulmonary cedema. During her stay in hospital the urinary output in the twenty-four hours varied from ten to fifteen ounces-a definite oliguria. The specific gravity was 1025. There was no sugar and no albumen. Autopsy showed a few lymph-nodes …