This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

MITCHELL BERNSTEIN, M.D.; MATTHEW T. MOORE, M.D.; DAVID B. FISHBACH, M.D.

Arch Intern Med. 1938;62(4):604-617.

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

Diabetes insipidus as a clinical manifestation has long been a subject of interest and controversy. The latter has resulted in an accumulation of clinical and experimental data which has tended to clarify the concept of the mechanism of diabetes insipidus. A complete review of the literature of the subject of diabetes insipidus would literally inundate the reader with watery references. However, for want of space, reference to several notable surveys, presented from different points of view, will indicate the extent of the literature and serve as source material.

Staemmler,¹ in 1932, in an extensive review of the subject up to that time, presented evidence indicating that isolated lesions involving the posterior and intermediate lobes of the pituitary body or the hypothalamus may lead to diabetes insipidus. Roussy and Mosinger² and Leschke,³ in 1933, in separate reviews showed the evidence favoring the hypothalamic origin of diabetes insipidus. More . . . [Full Text PDF of this Article]

Author Affiliations
PHILADELPHIA

From the Jewish Hospital and from the John L. Eckel Memorial Laboratory of Neuropathology.

Footnotes
Read before the Section on General Medicine of the College of Physicians of Philadelphia, April 25, 1938.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?