290 BENSON A. COHOE 



doses, or secreted by the glands during splanchnic stimulation, greatly 

 improved the activity of fatigued muscles. On the whole, it would appear 

 that the results of physiological research offer greater justification for at- 

 tributing the asthenia to an epinephrin deficiency than is the case with 

 the other symptoms of the disease. The adherents of the antitoxic theory 

 of the disease explain the myasthenia as resulting from the toxic effects 

 of muscular poisons, which the suprarenal in its normal state destroys. 



The gastro-intestinal symptoms are generally regarded as arising from 

 a disturbance of the cortical function. Another suggestion has been of- 

 fered, that they are due to the irritation or paralysis of the abdominal 

 sympathetic nervous system, especially of the nervus splanchnicus. 



The arterial hypotension has been very generally ascribed to the 

 epinephrin deficiency of the circulating blood (hypoepinephrlnemia). 

 Recent physiological investigations have, however, tended to show that 

 the circulating blood does not contain sufficient epinephrin to exercise any 

 influence of a hypertensive nature, and, indeed, to cast doubt upon the 

 existence of a true epinephrinemia. Moreover, it has been demonstrated 

 that epinephrin in small doses produces a fall in blood pressure. It ap- 

 pears evident that this widely accepted explanation of the hypotension is, 

 in the light of experimental research, no longer tenable. 



The nervous disturbances of the milder form have been regarded as 

 due to chromaphil deficiency, while the more severe nervous manifesta- 

 tions have been attributed to a disturbed cortical function. The neuralgic 

 pains (perirenal, epigastric) have been thought to be caused by pressure 

 or irritation of the sympathetic nervous structures. 



The hypothermia has been explained on the basis of low blood pres- 

 sure. Another possible explanation has recently been offered by 

 Cramer (c) who has attempted to show that the so-called thyroid-supra- 

 renal apparatus is a factor in regulating the body temperature. In the 

 absence of epinephrin discharge, a decreased glycogenolysis takes place. 

 The validity of this hypothesis has not been confirmed. 



In conclusion it may be emphasized that such interpretations of the 

 symptoms of the disease are as yet purely theoretical, and must remain 

 so until we acquire a more precise knowledge of the physiology of the 

 suprarenal glands. Vincent (g), from the viewpoint of the physiologist, 

 has recently voiced the opinion that the symptoms of Addison's disease can 

 in no way be explained by the accumulated results of investigations in com- 

 parative anatomy and experimental physiology of the suprarenal glands. 



Symptomatology. In the typical case of the disease, the onset is 

 extremely insidious, and the course essentially chronic. The clinical 

 picture of the outspoken Addisonian syndrome, with its triad of cardinal 

 symptoms asthenia, gastro-intestinal disturbances, and melanoderma 

 develops slowly. The patient, who may or may not have been weakly 

 from youth, begins to tire readily on slight exertion, and evinces a grow- 



