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W. R. INGRAM, Ph.D.; C. FISHER, Ph.D.; S. W. RANSON, M.D.

Arch Intern Med. 1936;57(6):1067-1080.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The experimental production of diabetes insipidus in a large series of cats has been reported, and the various phases of the problem of the etiology of this condition have been discussed in a series of recent publications.¹ It is sufficient for the present to state that polyuria of long duration has always been found, in our experience, in association with lesions of the hypothalamus placed so as to interrupt the bundle of unmyelinated fibers which runs from the nucleus supra-opticus down the infundibular stalk into the pars posterior of the hypophysis. In these cases atrophy of the supra-optic nucleus and of the pars nervosa has been a striking feature of the changes observed at autopsy. The development and course of the polyuria in cats are characteristic. Usually, although not always, the operation is followed by the immediate onset of a transient polyuria, which subsides after from one to four . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO

From the Institute of Neurology, Northwestern University Medical School.

Footnotes
This work was aided by a grant from the Rockefeller Foundation.

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