36 GENERAL PART 



These infectious processes may spread to the ductless gland from the neigh- 

 borhood, they may affect the acini of the pancreas through the ducts and 

 involve the insular apparatus by contiguity; in most cases, however, the 

 infection follows by the hematogenous route. In many cases in which the 

 infectious process involves many ductless glands at a time and causes de- 

 struction (multiple ductless glandular sclerosis), a congenital or acquired 

 predisposition of the ductless glandular system is perhaps present. Also 

 chronic intoxications, as alcoholism, poisoning by the toxin of goiter, etc., 

 may damage single or several ductless glands. Furthermore, tumors that 

 proceed from parts in the neighborhood or from the ductless gland itself may 

 destroy the functionating tissue. Again, in many ductless glands, purely 

 functional disturbances on a nervous basis are possible, analogous to those 

 hyposecretions that occur in glands with external secretion. The possi- 

 bility of a functional Addison's disease was long ago discussed by v. Neusser. 

 A like supposition seems to me debatable for the chromaffin tissue or for 

 the pancreatic insular apparatus. Nor would trophic degenerations of the 

 ductless glands be impossible. 



A greater importance should be ascribed to nervous influences in the 

 pathogenesis of the diseases of hyperfunction. The pathologico-anatomical 

 correlate of hyperfunction is hyperplasia, or in ductless glands of definite 

 morphological structure, of adenoma formation. The latter is found in 

 the disease of hyperfunction of the glandular hypophysis, of the thyroid 

 gland, and the suprarenal cortex; while in the sexual glands sarcoma toid 

 tumors are more often found. Hyperplasia of the chromaffin tissue is found 

 in the hypertonic diathesis. Even where, however, the adenoma formation is 

 most common, indeed constant, can a nervous cause of the hyperfunction not 

 always be precluded. In peracute Basedow's disease, the entire symptom- 

 complex and the swelling of the thyroid gland can develop in a few hours; here 

 we cannot well blame the adenoma formation, as it is very much more likely 

 that in such cases the adenoma formation sets in at some later stage of 

 the disease. Such cases and the fact that many symptoms of Basedow's 

 disease, for instance the marked exophthalmos, can hardly be produced by 

 hyperthyroidization have led certain authors back to the conception of the 

 older French authors, according to which Basedow's disease was regarded 

 as a vegetative neurosis and in which many of the symptoms of the Basedow's 

 were considered as coordinated with the hyperthyroidism. According to 

 this we might distinguish Basedow's disease as a hyperthyrosis from the 

 symptom-complex of hyperthyroidism. Whether such views are to be ap- 

 plied to the adenomata of the hypophysis and suprarenal cortex can hardly 

 be decided at the present time. As far as severe diabetes is concerned, we 

 can hardly get away from the assumption of a hyperfunction, whether it be 

 secondary or primary. In Chapter XIII the opinion will be advocated that 

 the entire apparatus regulating sugar metabolism (central projection-fields, 



