PRENTISS: POLYDACTYLISM IN MAN AND DOMESTIC ANIMALS. 309 
digit ts produced, but simply a variation in the structure of the pollex, 
hallux, and minimus. It would seem, therefore, that it is this tendency 
of the 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 the duplicated claws of arthropods and the 
doubled horns of sheep. Polydactylism according to Fackenheim (’88) 
is often correlated with abnormality by defect. 
None 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;” the 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. 
6b. 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. Weismann’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 that 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 
