314 BENSON A. COHOE 



adrenal) deficiency, hypoadrenalism, hypoepinephry, and hypoadrenia. 

 Sajous(a) regards the term hypoadrenia as preferable to the more gen- 

 erally used hypoadrenalism, in that the latter term is misleading as con- 

 veying the impression of an habitual insufficiency of the gland. The term 

 hypoadrenia appears to have become well established in the literature. 



The first step in the recognition of a clinical syndrome associated 

 with arrested function of the gland was rendered possible by the observa- 

 tion on the part of physiologists and pathologists of certain clinical phe- 

 nomena following suprarenal extirpation in animals, or the production 

 of lesions in the gland substance by means of mechanical injury, or by 

 the injection of certain bacterial and chemical toxins. Brown-Sequard(a) 

 first established the vital importance of the organs. Among the symp- 

 toms produced by extirpation, he noted muscular weakness, convulsions, 

 delirium and coma. 



Hultgren and Andersson made a careful study of the symptoms pro- 

 duced by extirpation. They noted that no ill effects were apparent, ex- 

 cept loss of appetite, during the first few days following the operation, 

 but that shortly before death the animals became stupid and apathetic, 

 the tempterature fell, and the prostration became extreme. Cardiac weak- 

 ness, dyspnea, and occasionally convulsions, were also observed. Strehl 

 and Weiss found, in addition to muscular weakness and a low temperature, 

 a fall in blood pressure following extirpation, an observation which was 

 confirmed by JMoore and Purinton(c) and others. Gastro-mtestinal dis- 

 turbances have also been described by several observers, A loss of appetite 

 was commonly noted, and in some instances increased peristalsis and 

 diarrhea (]STothnagel(&), Tizzoni). 



Various theories have been advanced as to the cause of death follow- 

 ing extirpation of the glands. Alezais and Arnaud, as a result of animal 

 experimentation, concluded that the suprarenal glands, though still func- 

 tioning in the adult, are not indispensable for life, and that a lesion of the 

 gland may cause death by affecting the nervous system. Abelous and 

 Lang'lois (d) observed toxic symptoms resembling those of curare poison- 

 ing (a progressive paralysis beginning in the hind limbs and becoming 

 general before death), after the destruction of the adrenals of frogs by 

 cauterization. They believed that death resulted from the accumulation of 

 toxic substances in the blood, which the adrenal glands normally remove. 

 'Battelli(c), from a special study of circulatory conditions following extir- 

 pation, regarded cardiac failure as the cause of death. With the discovery 

 of the internal secretion of the gland (epinephrin), it appeared plausible 

 to explain the fatal effects of suprarenal extirpation on the basis of epi- 

 nephrin deficiency in the circulating blood. Elliott (a), having demon- 

 strated that the effect of epinephrin injection is exactly equivalent to stim- 

 ulation of the sympathetic nervous system, has suggested that suprarenal 

 deficiencv results from the loss of some substance necessary to maintain 



