These paralytic appearances may manifest themselves suddenly, in one night, or gradually. In the upper extremities hereditary-syphi litic bone diseases always give the picture of flaccid paralysis, in the lower extremities that of the spastic type.
The skull in hereditary infantile syphilis may present four types of changes: 1. Simple rachitic changes which manifest themselves in softening of the bone in the squamous portions, and along the sutures, and are not distinguishable from ordinary rachitic changes, especially from craniotabes. These frequently occur during the first few months of life.
2. Abnormal protuberance of the frontal and parietal eminences with striking hardness of the cranial bones and of the sutures, clue to an early periosteal hyperostosis of these bones. This occurs during the first few months of life but is not so frequent in early infancy as the preceding type.
3. Periosteal swelling and rarefaction of the bone in isolated or extensive areas, due to a specific inflammatory involvement of the cranial bones. This is the rarest syphilitic lesion of the skull bones during the earliest period of life, and is characterized by areas of wast ing (caries sicea) surrounded by walls of hone.
4. Hydrocephalus. In earliest childhood this is, in a good many cases, caused by hereditary syphilis. The latter can produce inflam matory changes in the meninges and plexuses, and even lead to disease of the intracranial vessels, simulating tuberculous meningitis. quently, a specific diffuse periostitis of the inner surface of the cranial bones is the starting point for a meningitis. Specific hydrocephalus of infancy has a superficial resemblance to rachitic pseudohydrocephalus, but can be distinguished from it. In a large number of eases syphi litic hydrocephalus is curable by the use of iodides and mercury.
A close relationship exists bet ween hereditary syphilis and rachitis.
Among children afflicted with hereditary syphilis, rachitis is some what more frequent than among those that are free from this disease. Rickets begins earlier in syphilitic children, has a more rapid course, but only rarely leads to a high degree of bone deformity.
The circumference of the skull in infants with hereditary syphilis is greater during the whole of the first than in those that are nor mal because of the greater bone formation at the centres of growth of the squamous bones due to specific excitation. During the first half
year it exceeds that of rachitic children, and only during the second half year of life are the skulls of rachitic children larger than those of children with hereditary syphilis. As a consequence there is a peculiar shape to the upper surface of the cranium, characterized by the prominence of the frontal and parietal eminences, while between the latter there is a more or less well marked furrow. This cranial anomaly, called caput natiforme by Parrot, can only then, with certainty, be laid to heredi tart' syphilis, when it is well developed during the first few months of life and is associated with an abnormal hardness of the skull bones and with a relatively small fontanelle; the same shape occurs also in the heads of rachitic children who are free from syphilis, during the second and third year of life.
If the caput na-tiforme is associated with microcephalus without well marked rachitic changes in the thorax and extremities, this speaks absolutely for hereditary syphilis. On the other hand, the combina tion of a high degree of rachitic deformity of the extremities and this form of head almost positively excludes a syphilitic origin, because we know from experience that syphilitic children only exceptionally be come severely rachitic.
Liver syphilitic disease of the liver in infancy differs but little anatomically from the changes previously discussed that occur in the fretus and the newborn child, except that syphilomatous nodules, considerable induration and constriction of large portions of parenchyma by contracted interstitial cell infiltration, together with diffuse cell proliferation, are all met more frequently.
The manifestations in the liver may be either a fresh diffuse interstitial process which causes the organ to increase in size while remaining soft, or an indurative inflammation with connective tissue proliferation and palpable increase in inconsistency. A termination in cirrhotic contraction is not found in infancy. Likewise I could never demonstrate any considerable degree of ascites in hereditary syphilis of the liver in infancy, while in later childhood icterus as well as ascites are common in this condition.