Experiint-ntal < )iK'rati<jns on tlit- riiuitary !-•) 



his experimental results conform to his clinical observations. Helievinjj 

 that leeonciliation was not possible, lie was tempted to throw over his 

 experimental results in favour of the clinical evidence that was in conflict 

 with them. 



It will, I think, be sutticient to call atleution to the chief perjilexity 

 which Cu shine; was called upon to face. As we have seen, the if.sults 

 of his experimental work indicate that dystrophia adiposo-j^enitalis 

 is due to anterior lobe insufhciency. But in his clinical experience Cushing 

 found, as already mentioned, that the (m\y symptom of the syndrome 

 dystrophia adiposo-genitalis relieved l>y anterior l(;be extract was 

 the .subnormal temperature. While, on the other hand, thf low blood- 

 pressure, and the carbohydrate tolerance — and, as far as I can understand 

 from his later writings, the genital dystrophy — were mitigated by posterior 

 lobe extract. In view, then, of these clinical observations, how was it 

 possible to attribute this syndrome to the experimental removal of portions 

 of the pars anterior, as Gushing himself and others had done ( Cushing 

 solved the (juestion by rejecting his experimental results. 



The results I have obtained after clamping and separation of the stalk 

 appear to explain the paradoxes. Such an operation could only interfere 

 with the blood-supply of the whole organ ; and, if the infundibulin does 

 pass directly into the third ventricle, stop this source of .supply. 



It is, however, hardly possible tliat the pars posterior and its secretion 

 has anything to do with the matter, for all recent investigators are agreed 

 that the posterior lobe can be removed without producing any symptom 

 whatsoever. Further, since I found it possible to remove large portions of 

 tlie pars anterior and the entire pars posterior without causing dystrophia 

 adiposo-genitalis, but was able to produce this syndrome by clamping 

 and separating the stalk, it is obvious that interference with the blood- 

 supply to the pituitary produces the condition. There seems little reason 

 to doubt, then, that this syndrome is primarily produced by insufficiency 

 of the pars anterior ; but it appears certain that the only sure way to etiect 

 this is to interfere with the blood-supply. If this is done we find the 

 cells of the pars anterior become shrunken, atrophic, and discrete — a 

 state of affairs \vhich is always found in the human subject afflicted 

 with dystrophia adiposo-genitalis. 



It is now necessary to consider how the foregoing statements can be 

 reconciled with the facts that removal of the posterior lobe causes no 

 symptoms, yet infundibulin relieves some of the symptoms— the lowered 

 blood-pressure and the carbohydrate tolerance— in dystrophia adiposo- 

 genitalis. 



I have long held (1913(3)) that to explain these facts we must look upon 

 the pituitary as one organ and not two. Further, from the clinical and 

 experimental evidence of this syndrome, and from other evidence w^hich I 

 need not detail here, it is probable that the view of Herring (190S (13)) 

 concernincr the determination of the secretion of the pars posterior solely 



