348 CROWELL. 



salts. Similar cells were also found outside the adrenals especially in the abdo- 

 minal sympathetic. Kohn(22) created the term "chromaffin bodies" for all such 

 cells in and outside of the adrenals and later conceived the term "paraganglia" 

 for such cell accumulations. The number of these paraganglia, or the places 

 where chromaffin cells are found, has been constantly increasing and the boundaries 

 of the chromaffin system are proportionately extended. Thus, they have been 

 found in the inferior mesenteric ganglia ( Zuckerkandl's organ), carotid gland, 

 coccygeal gland, ovary, testis, interventricular septum, aberrant adrenals, and in 

 fact wherever sympathetic nerves are present. The chromaffin of the medullary 

 cells has been found identical with adrenalin, the active substance of the adrenal 

 secretion. 



The importance of these findings was emphasized when Wiesel(26) in 1903 

 propounded the theory that Addison's disease was due to a disease of this chromaf- 

 fin system and perhaps the adrenal, perhaps the extra-adrenal portions of the 

 system were affected in a given case. 



Changes in the sympathetic system had already been described in Addison's 

 disease, and pigmentation of the ganglion cells had been mentioned by Wah- 

 ncau(27) and Babes and Kalindero(28) among others, but it remained for Wiesel 

 to correlate these findings. 



From a careful and minute study of the adrenals and the entire sympathetic 

 system in 5 cases of Addison's disease, all of which had caseous adrenals, the 

 latter investigator propounded his theory. He found changes in the sympathetic 

 nervous system similar to those which had been described by many previous 

 authors, that is, proliferation of the connective tissue of the interstices of nerves, 

 thickening of the walls of the blood vessels, atrophy of the ganglion cells and 

 the formation of pigment and lipochrome in them. However, these he eonsidei'ed 

 as not characteristic of Addison's disease, but rather a purely degenerative 

 process such as occurs with age. He created the term "chromaffin system" to 

 indicate those places where chromaffin cells are found and indicated that this 

 includes the sympathetic nervous system and the adrenal medulla. Addison's 

 disease he conceives as a disease of this chromaffin system which may be attacked 

 at any part either in the sympathetic system or in the adrenal medulla. It con- 

 sists of a progressive atrophy of chromaffin tissue which, as the chromaffin tissue 

 of the adrenal medulla takes part in this degenerative process, spreads secondarily 

 to the cortex. In order that symptoms of the disease may occur, some considerable 

 portion of the chromaffin system must be aft'ected without regard to the exact 

 location; it is not absolutely necessaiy for the adrenal gland to be among the 

 diseased structures, and disease of one portion may be compensated for by 

 hypertrophy of others. He does not attempt to say how many of the ' clinical 

 symptoms are attributable to the involvement of the adrenal cortex and admits 

 that pigmentation of the skin is not accoimted for. 



Karakascheif's(4) conclusions are in direct antagonism to those of Wiesel. 



In 1904 the former reported 2 -cases and quoted 3 others with total atrophy 

 of the adrenal cortex and from his findings concluded that the cortex especially is 

 of importance in Addison's disease, and causes the whole symptom-complex. 

 Microscopically, he found the cortex almost completely desti-oyed and the 

 medulla intact. In his own two cases the coeliac plexus was normal. He re- 

 ported one case of a child 5 months old with an old hsemorrage into the medulla 

 as evidence that the medulla can be completely destroyed without producing 

 Addison's disease. He also quotes Marchand's(ll) case, in which there was exten- 

 sive disease of the solar plexus and upper cervical ganglion without Addison's 

 disease and 6 cases of v. Kahlden'sdS) in which the adrenal medulla was caseous 

 and the coeliac plexus in great part destroyed, without Addison's disease, as 



