THE PITUITARY BODY 



body were carefully studied anatomically to determine how 

 the lesions found could be correlated with animals' symp- 

 toms. As a result of this study, the authors have reached 

 the following conclusions:^ (i) diabetes insipidus is due to a 

 deficiency of pars neuralis secretion, presumably the vaso- 

 pressor principle; (2) the secretion of the pars neuralis is 

 not formed and liberated unless at least one supraoptic nu- 

 cleus is functionally active and connected with the pars 

 neuralis. The fibers from the supraoptic nuclei to the pars 

 neuralis appear to be efferent. If the tract(s) is interrupted, 

 the nerve cells of the nuclei degenerate. The anatomical 

 changes in the hypothalamic-hypophysial region accompany- 

 ing diabetes insipidus may be due to {a) a lesion causing 

 destruction of both supraoptic nuclei, ((^) a lesion interrupt- 

 ing the tract fibers arising from both nuclei as in the tuber 

 cinereum or the stalk, or (c) destruction or removal of the 

 pars neuralis; lesions (a) or (^) are followed by atrophy of 

 the pars neuralis. (3) The pars tuberalis and probably the 

 pars intermedia are of no significance in the genesis and main- 

 tenance of diabetes insipidus; and, finally, (4) the pars 

 glandularis probably is important or essential, if pronounced 

 diabetes insipidus occurs. 



The relationship of hypothalamic nuclei to the pituitary 

 as well as the most convenient position in which suprapitui- 

 tary lesions can be placed to produce diabetes insipidus are 

 illustrated in Figures 27 (cat) and 4 (monkey). Destructive 

 lesions of the mammillary bodies or of nuclei other than the 

 supraoptic nuclei (such as the paraventricular nuclei, the 

 ventrolateral hypothalamic nuclei, etc.) are not followed by 

 diabetes insipidus. 



Farr, Hare, and Phillips (1937), using cats, have confirmed 

 the observations of Ranson and his colleagues. In reports 

 of the anatomical changes in 4 human cases of diabetes in- 



^ The conclusions refer to the experiments of Fisher, Ingram, and Ranson. The 

 authors do not hold that other mechanisms for producing diabetes insipidus — espe- 

 cially in other animals — do not exist. 



(280I 



