4. What can be said of treatment? A few favorable results have been reported after intraspinous therapy (Swift-Ellis). Too little work has been done with systematic treatment of juvenile neurosyphilis, both paretic and non-paretic, to permit important conclusions at this time.
5. How can we explain the infection of this sibling whereas the others, both younger and older, escaped? It would seem that we would have to discard the hypothesis of a congenital infection and consider that it was acquired accidentally during the lifetime of the patient. Considering the prevalence of syphilis it is rather to be wondered that more such cases of “innocent” infection do not occur in children. We may recall how many instances of juvenile gonorrhea occur. In a case as this where the symptoms calling attention to syphilis necessarily occur so long after the original infection it is practically impossible to trace the origin of the infection.
The diagnosis of JUVENILE PARESIS is often easy.
Case 36. Theresa Mullen, an under-sized girl of 12 years, presented a remarkable appearance due to congenital amputations of the fingers and toes. She lay in bed, drivelling and making unintelligible cries. It appeared that the patient weighed about 12 pounds at birth and was very fat; that she had been fed on condensed milk, had survived cholera infantum, whooping cough, and, as the parents said, “two kinds of measles.”
Theresa had gone to school at 5 years, reaching the third grade at the age of 9; but at this time, she began to lose ground and was put in a class for backward children. Moreover, at about this time, the teachers noticed spells of causeless laughter and meaningless twisting back and forth. Theresa would also scream at night, looking about the room; once, rising and crying, “Take him away, that black thing,” though no appropriate object was present. There had been little or no complaint of headache. Theresa had been deteriorating for some time, and for a year past had been having increased difficulty in walking. For two months the child had not spoken intelligible words; for the last week, she had been incontinent.
The diagnosis was almost obvious from the manual and pedal deformities taken in connection with the saddle-back deformity of the nose. It was interesting in connection with the contentions of W. W. Graves, that the scapulae were scaphoid in type.
Accordingly, the history given by the parents seemed consistent enough. The parents were both 36 years of age, having married at 23. The first pregnancy was a miscarriage at two months, of unknown cause. Theresa came next; thirdly, came a miscarriage at three months; fourthly, a girl, who is not strong or well physically, has suffered much from headaches and sore throat, but is fairly bright. The fifth pregnancy resulted in a boy, who is bright but of under-size. Three more pregnancies resulted in miscarriage.
Taking into account the above-mentioned physical characteristics, the personal history, and the family history of Theresa, the diagnosis could hardly be in doubt even in the absence of a lack of pupillary reaction to light on the right side, infantilism of genitalia, positive W. R.’s of serum and spinal fluid, positive globulin, and excess albumin, 34 cells per cmm. and the paretic type of gold sol reaction which were found.
The prognosis of this case appears to be rapid deterioration, terminating in death within a few months. Now and again, however, some such cases spontaneously improve. Such a case as that of Theresa Mullen is always disheartening in itself but suggests the social value of Wassermann tests in the other members of the family. The other children of the Mullen family proved to be suffering also from syphilis, since their blood sera all showed a positive W. R.
1. What is the characteristic age of onset in Juvenile Paresis? An impression has prevailed in some quarters that the typical onset of juvenile paresis is in the adolescent years, and Clouston’s first case (1877) developed in a boy of 16. Thierry’s 58 cases, developing from the 8th to the 20th year, averaged 14 years of age at onset. Mott’s 22 cases from the 8th to the 23d year, averaged 17 years at onset. According to Clouston, juvenile paresis develops most often at puberty (15 to 17 years). It is sometimes claimed that cases developing symptoms early live longer, and that juvenile cases developing symptoms after the 20th year run a short course. For a case developing in the 5th year, see John Friedreich, Case No. 77.