THEORETICAL CONCLUSIVE CONSIDERATIONS 567 



tion; there is much for the thought, however, that the violent conditions of 

 excitation in the vegetative nervous system may be of significance for the 

 genesis of a nervous glycosuria. 



For the assumption of a nervous glycosuria there are brought about 

 symptoms that indicate a disease of the pons, cerebellum, and medulla ob- 

 longata, perhaps also Circumstances that can bring about an irritation of the 

 splanchnics or the great sympathetic ganglia either directly or by circuitous 

 routes; especially, trien, severe neuralgias. Further we have to turn our 

 especial attention to the behavior of the vegetative nervous system and the 

 influencing of the glycosuria through the psyche. In many cases we can 

 perhaps carry out the test for adrenalin glycosurias (in the aglycosuric con- 

 dition) or Lowi's reaction; high-grade polyuria as well as simultaneously 

 existing hypertonia speak for the nervous form or for a marked associated 

 involvement of the nervous system. 



Finally, as to the thyrogenic form, naturally we must take pains to 

 detect synchronous systems of hyperthyroidism. I would mention that in 

 all the cases of true thyrogenic glycosuria that I have seen, the eye symptoms 

 were at most indicated. But tremor, sweats, and mononucleosis of the blood 

 were always present. A higher degree of glycosuria speaks well against the 

 purely thyrogenic origin. Fat stools with strikingly good splitting of the fat 

 and abundant soap-contents speak for the thyrogenic glycosuria. The diag- 

 nosis would be assured, if with the retrogression of the hyperthyroidism 

 (spontaneously or by means of Rontgen illumination, etc.), the glycosuria 

 disappeared altogether, and if now strong loading of the carbohydrate 

 metabolism no longer led to elimination of sugar. 



To close with some therapeutic points of view. In pancreatogenic dia- 

 betes the difficult feature of 'the treatment up to the present lies in the diet, 

 which purposes to avoid [the functionating of] the diseased organ. This 

 is brought about by limitation, or even by temporary complete withdrawal 

 of the supply of carbohydrates and by simultaneous limitation of the supply 

 of proteins. Also in cases with ketonuria, an abundant supply of fat should 

 be avoided. The patient should be made free of sugar, and when possible, 

 maintained sugar-free. There often occurs in such cases a restoration of 

 the insular apparatus; if later than the investigation shows that the assim- 

 ilatory ability has significantly increased, carbohydrates should again be 

 administered at times in order to avoid permanent poverty in glycogen. The 

 great significance of v. Noot -den's oat-meal treatment lies in the fact that in 

 an individual under-nourished with carbohydrates large quantities of gly- 

 cogen are administered as an increment. Thus is often explained the wonder- 

 ful action on the ketonuria. The catabolism becomes limited. In the severe 

 forms the complete withdrawal of carbohydrates is not possible perma- 

 nently, as the complete absence of glycogen increases the formation of 

 ketone bodies entirely too markedly. Here we must try to restrict the gly- 



