CLINICAL SYISTDKOMES 301 



the case of Graves' disease which years later presents a typical picture of 

 myxedema. It, however, cannot suffice for the coexistence for months or 

 years of a group of symptoms which are explained on the basis of hyper- 

 thyroidism and another group of symptoms attributed to hypothyroidism. 



Klose has no doubt that exophthalmic goiter and the hypothetical 

 hyperthyroidism are qualitatively different; he believes that Basedow's 

 disease and iodin poisoning are probably the same, but does not think 

 that the "lod-Basedow" complex of Kocher is identical with iodin-thy- 

 roidismus as has been suggested by Kevilliod, Jaunin and Kocher. Klose 

 from his own experiments accepts as a working hypothesis that exoph- 

 thalmic goiter is a chronic poisoning from a false or masked iodin com- 

 pound which is more closely related to the inorganic iodin than to the 

 thyreoglobulin. To this theoretical substance he has given the name of 

 Basedow-iodin to distinguish it from the thyreoglobulin of the normal 

 gland. 



Further, Plummer (a) has noted the presence of a considerable group 

 of toxic non-hyperplastic goiters presenting a variable histopathology some- 

 times degenerative in type. Many of these cases have been wrongly 

 diagnosed by the clinician as exophthalmic goiter. The principal charac- 

 teristics of this group according to both Plummer and his surgical asso- 

 ciates Judd and Balfour are briefly as follows : 



(1) Its chronicity; an average developmental period of over fourteen 

 years as compared with one averaging nine months in the hyperplastic 

 toxic goiter of Graves' disease. 



(2) The relative absence of acute toxic symptoms, diarrhea, tachy- 

 cardia, etc. 



(3) The absence of exophthalmos. 



(4) The slow development of chronic cardiovascular changes. 



This is really the toxin-generating adenomatous thyroid producing 

 what Kocher calls the goiter heart. Although differing from exophthalmic 

 goiter it is quite possible in the opinion of Judd that the same symptoms 

 are produced by the same agent or toxin. The thyroid glands of the 

 thyrotoxic type vary considerably ; a patient who has only a small adenoma 

 of the thyroid may have a very marked toxemia ; other thyrotoxic patients 

 may have a general diffuse colloid enlargement with small adenomata dis- 

 tributed throughout the gland. The enlargement is of the colloid adenom- 

 atous type; in some instances the colloid predominates, in others the 

 adenomata. The degree of intoxication seems to coincide with the amount 

 of degeneration in the adenomata and the surrounding thyroid tissue. 

 Exophthalmos is never seen accompanying the purely thyrotoxic gland. 

 The thyrotoxic patient has no definite tremor, though there is often nerv- 

 ousness during exhaustion. The pulse is that of a dilated and damaged 

 heart and usually there is a marked increase in blood pressure. There is a 

 theory that in thyrotoxic goiter the symptoms are produced by the absorp- 



