The genetic origin of Dementia ]'ra(-cox s., 



going of symptoms; or where there is a permanent morbid change, lo a 

 suppression ol their function with permanent dissociation. 



We have thus Iwo morphological conditions which will account fcM- 

 undamental disorders, and tlie nature of Ihese disorders \\ill depend 

 upon the cerebral structures affected vvhether in such a way as to produce 

 suppression or suspensión of function. Naturally the nature of the men- 

 tal disorders will also depend upon the localization and the relative inten- 

 sity of the suspensión, or suppression of function of the neurones. 



It is quite probable that there is a hypofunction of the whole of the 

 bodily tissues; there is certainly a diminished vital resista'nce to microbial 

 infections. A large percentage of these cases of Dementia Praecox die 

 of tuberculosis, but my observations show tliat exactly the same neuronic 

 changes can be found in Dementia Praecox that liave died of acute pneu- 

 monía or as in the case of Acute Dementia praecox described without 

 any intercurrent affection to account for death. So that altrough it ig 

 common to find stupor in patients affected with active tuberculosis and 

 although the absorption of toxins may, therefore, have played a part in 

 the production of some ofthe symptoms, yet I have formed the conclu- 

 sión that the essential cause of this disease is an inborn germinal defect. 



In conclussion I would like to express my great apreciation as a 

 neuropathologist in being asked to contribute to a memorial volume in 

 honour of Professor Ramón y Cajal, who by his long pioneer and original 

 researches on the nervous system has done so much to establish and lay 

 the foundations of our present knowledge of its structure and functions. 



I 



