PRENTISS: POLYDACTYLISM IN MAN AND DOMESTIC ANIMALS. 305 



digit is produced, but simply a variation in the structure of the pollex, 

 hallux, and nmiimus. It would seem, therefore, that it is tins tenJeucy 

 of tlie modified digits to vary which is inherited. 



We know that such digital variations occur also in the offspring of 

 normal individuals, and that they are inherited. Bateson cites the 

 occurrence of such a case in cattle and the formation of a three-toed 

 race thereby. The duplication of appendages is common in the lower 

 animals, and variation is of frequent occurrence in all neomorphic organs. 

 Well-known examples are tlie duplicated claws of arthropods and the 

 doubled horns of sheep. Polydactylism according to Fackenheim ('88) 

 is often correlated with abnormality by defect. 



jSTone of these variations can be attributed to reversion. The law 

 of Mendel, as Bateson and Saunders (:02, p. 150) have pointed out, 

 " applies only to the manner of transmission of a character already 

 existing. It makes no suggestion as to the manner in which such a 

 character came into existence." Bateson regards the polydactyle fowl as 

 "a palpable sport;" tlie usual digital abnormalities of the fowl, the 

 cat, and of man undoubtedly belong to the same class of polydactylous 

 abnormalities. It is possible that reversion may be the primal cause in 

 producing certain of these digital variations, but the present evidence 

 does not warrant a positive statement to that effect. 



h. Germinal Variation. 



This has been regarded as the chief factor in polydactylism by Forster 

 ('61), Darwin ('76), Gegenbaur ('80), Howes ('92), Weismann ('93), 

 Bateson ('94), Wilson ('96), and many others. Weismanu's view ('93, 

 p. 329) is, that excessive nutrition in the cells of the embryo may cause 

 the duplication of a group of determinants which are to form a particular 

 digit; the doubled condition of the determinants might then be in- 

 herited, and thus the inheritance of these digital abnormalities accounted 

 for. This, however, does not explain the changes in position which 

 digital variations in man may undergo in the course of hereditary trans- 

 mission (that is, from fingers to toes). Wilson ('96) attempts to clear 

 up this point by assuming tliat there may be variation in those determi- 

 nants which affect the nutrition of the digital fundament, and that it is 

 the tendency of these determinants to vary which is transmitted, rather 

 than the doubled condition of the digital determinants themselves. 



There is some direct evidence that germinal variation is due to an 

 excess of nutrition. It has been observed by Ercolani ('81) and Boas 

 ('85, '90} that certain polydactyle conditions in the ox and horse 



