Degeneracy: Its Causes, Signs and Results

by Eugene S. Talbot

As the subjects of the deeper degeneracies associated with cleft-palate usually perish in early infancy, the nutritive degeneracies are most frequently found associated with cleft-palate in adult life. The mouth in the vertebrates does not agree in character with the invertebrate mouth. The mouth has grown in proportion to evolution in the lower vertebrates. It is larger, however, in proportion in the human embryo than in the adult. In this it agrees with the general lower type of the human face. The human chin is at first retreating, and does not become distinctly prominent until the fifth month of fœtal life. The nose separates from the mouth toward the end of the second month. It is at first short and broad and resembles at three months the type of some of the lower negro races. When the nose is separated from the mouth a partition forms between the cavities of the nose and the mouth, later supplemented by the true palate, which divides the mouth into an upper respiratory passage and a lower digestive passage. This palate is partly composed of bone and partly of flesh. The fleshy part ends in what is called the uvula. This is very subject to abnormalities, as has been pointed out by C. L. Dana; it is a very frequent mark of degeneracy. Dickens noticed the uvular tone of voice in young thieves, due to deformity of the uvula.

Cleft palates are comparatively rare in proportion to other forms of nutritive degeneracy. Palatal embryology casts light on the causation. At a very early period of fœtal life a series of clefts appear on each side of the cephalic extremity, separated by rods of tissue called branchial arches. The clefts communicate with the alimentary canal. These various clefts have usually coalesced about the ninth and tenth week of fœtal life, but occasionally this coalescence fails or is incomplete. This leads to various deformities, the chief of which are cleft palate and hare-lip. Cleft palate has been known to affect several members of the same family, and to occur in the offspring of the affected members. There are instances of the transmission of this deformity from an affected pug-bitch to her offspring. If it were possible to practise selective breeding in man as in dogs a race of men with hare-lips and cleft palates could probably be produced.[201]

FIG. 31.

Cleft palate may be divided into two classes, congenital and acquired, acquired cleft palate being the result of disease either inherited or acquired, but only affecting the part after birth. Congenital cleft palate is divisible into two kinds, complete and partial; complete when the fissure extends the entire length, from the uvula to and including the anterior alveolar process and even the lips (Fig. [31]), partial when only a small part of the structure is involved. Thus the cleft may extend through the anterior alveolar process, involving the incisive bone only, which is very rare; when present single or double hare-lip almost invariably coexists. I have observed in practice six cases where a small portion of the interior alveolar process was involved, with the jaw and one or two teeth. The hard palate only may be involved to the extent of a small fissure, or the whole palate may be wanting. The soft palate only may contain the cleft, or simply the uvula. Cases are on record in which the non-development of the intermaxillary bones produces fissures in the lip. A priori, cleft palate is an evident expression of hereditary defect. Langdon Down found a constant relation between brain deformity, cleft palate, and deformed vaults.

In a case cited elsewhere,[202] three members of one family had cleft palate; one 17 years old, the other 30, and the third 35. The first and last are women, the other a married man with a family, who have no trace of the father’s deformity. In these cases no instance of cleft palate could be found either among the ancestors or the collateral branches of the family.

Another family has a remarkable history. G. H. C., born 1853, perfect; L. C., born 1855, single hare-lip and cleft palate; J. F. C., born 1856, perfect; F. W. C., born 1860, double hare-lip and cleft palate; H. E. C., born 1868, perfect. The paternal grandmother also had cleft palate.

Knecht found that 5 per cent. of 1,200 criminals examined had cleft palate. Fourteen per cent. of the prostitutes examined by Pauline Tarnowsky had cleft palates. Langdon Down, among congenital idiots, found only a half per cent. of cleft palates. Grenzer found only nine cases in 14,466 children, or one in 1,607. I examined 1,977 feeble-minded children without finding a single case. In 207 blind only one case was observed. In 1,235 deaf mutes two cases were found. The percentage among the defective classes, while not large, is, undoubtedly, much larger than among normal individuals.

A keeper of the Zoological Gardens in Philadelphia observed cleft palate in the mouths of lion cubs born in the gardens. Cleft palates were also observed in a number of pups born in Buffalo. Dr. Ogle found that 99 per cent. of the lion cubs born in the London Zoological Gardens had cleft palates. He claims that this is due to the artificial diet, as the result of enforced captivity. Similar results observed in other gardens in Europe are charged to feeding the mothers with meat without bone, as feeding with the whole carcass of small animals greatly diminished these deformities. It would seem that if cleft palate is due to this cause other bony structures should also be involved, and, as a matter of fact, many of the lions born in captivity are rickety. Cleft palate has been observed among dogs, sheep, goats, &c. The question, therefore, whether domesticity here does not play the alleged part of civilisation in man can be solved only by a knowledge of the frequency of the condition among wild animals of the same genus. It is evident that, in dealing with the question of ætiology, the influence of shock on the mother’s nervous system cannot be excluded in the cases charged to feeding.