Keith, Haddow M.

THE TUBERCLE bacillus is the most common cause of lymphadenitis with caseous necrosis. Such a condition in the cervical region, while less frequent than in previous decades, still occurs occasionally. While other agents, for example, Coccidioides, Histoplasma, Brucella, Pasteurella and Miyagawanella, are known to produce a similar histopathologic reaction, they are not commonly associated with lesions in the cervical lymph nodes, especially in children. Therefore the finding of acid-fast bacilli in such lesions has generally been considered bona fide evidence of tuberculosis, although previous reports from this clinic indicate that such is not necessarily true. It is recognized that there are other acid-fast bacilli, such as the lepra and smegma bacilli, which may or may not cause disease. In 1944 Gellerstedt reported seven cases of tuberculoid skin lesions due to atypical acid-fast bacilli. He considered these to be due to exogenous infection with acid-fast bacilli differing from the organisms found in tuberculosis, and he considered them as possibly saprophytic organisms. In 1948 MacCallum and co-workers reported six cases of skin lesions due to acid-fast organisms that were not Mycobacterium tuberculosis. The lesions did not contain tubercle follicles, giant cells or caseous material. The name "Mycobacterium ulcerans" was applied to these organisms by Australian workers. In 1954 Linnell and Nordén described skin lesions that occurred in 80 boys and girls who used a certain swimming pool in a Swedish town. The etiologic organisms were acid fast, differed from those described by MacCallum and associates and were not lepra bacilli. Guinea pigs injected with these organisms presented no evidence of lesions after 7 weeks.

Four groups of children were studied over periods of 1 to 14 years. Group 1 included 402 children who had been born after prolonged labor. Follow-up studies were made of 321 of the 402 children. Twelve children (3.7%) were noted to have convulsions, but only one child had a recurring convulsive disorder (epilepsy). The remainder had so-called febrile convulsions. No other persistent neurologic difficulties were found. Group 3 included 236 children who had asphyxia (anoxia) or delayed respiration at birth. Follow-up data were available on 180 children. The only resulting neurologic difficulties noted were febrile convulsions in two children. None had persistent convulsive disorders (epilepsy). Group 5 included 124 babies whose mothers had had toxemia of pregnancy. Fourteen were stillborn or died in early infancy. Four of the remaining 110 (3.6%) had a febrile convulsion at some time, but to our knowledge persistent convulsions did not develop. Groups 2 and 4 were control groups and included a total of 633 children, who were born after relatively short uncomplicated deliveries. Follow-up data were available for 498 of the children; among them 16 children (3.2%) had convulsions at some time, and 13 of the 16 had convulsions at some time between the ages of 8 and 14 years. No other persistent neurologic conditions were found. Four children had recurring convulsive disorders and four others had a single convulsion or occasional convulsion of unknown etiology. Eight others had so-called febrile convulsions. No other persistent neurologic conditions were found. The findings of the present study reinforce the conclusions in the previous report from this clinic—that prolonged labor, asphyxia, or delayed respiration at birth did not cause any neurologic abnormality in children who survive the early months of life, and that convulsions of any type are not commoner among children who had difficulty at birth than among children who did not have difficulty at birth.

A study was made of the electroencephalograms of 50 children who had proved neoplasms of the brain. In 9 of 12 children who had tumors of the cerebral cortex, the localization afforded by the EEG was correct. In 8 children who had supratentorial tumors of or near the brain stem no localizing or consistent electroencephalographic pattern was observed. In 21 (70%) of 30 children who had tumors of the posterior fossa a bilateral abnormality was observed in the EEG recorded from the occipital region or occipital and contiguous regions. It is acknowledged that the abnormality found in this last group also is found occasionally in conditions other than in brain tumors of the posterior fossa. These conditions usually can be excluded by use of the history and other laboratory aids. Electroencephalography in the study of brain tumors in children should not be considered as an infallible test but rather as a diagnostic aid to be used and evaluated with the help of a clinical history and other diagnostic and laboratory aids.

SINCE Putnam and Merritt's discovery in 1937 of diphenylhydantoin sodium (Dilantin® sodium), many other drugs for treatment of seizures have been studied and used clinically. The most satisfactory undoubtedly has been trimethadione (Tridione®) (1945), which is extremely useful in the control of attacks of petit mal in children. Anticonvulsant drugs may be conveniently grouped in several major categories: 1) barbiturates, 2) hydantoins, 3) oxazolidinediones, 4) succinimides and 5) miscellaneous. Of the barbiturates, phenobarbital (phenylethylbarbituric acid) and Mebaral® or mephobarbital (methylphenylethylbarbituric acid) are best known and their use antedated the discovery of Dilantin® sodium. The newest member of this group is metharbital, or Gemonil® (5, 5-diethyl-1-methylbarbituric acid) which has been used since 1950. It is said to be beneficial mainly against seizures caused by organic disease of the brain, especially when used in combination with Mebaral® There are few factual data in the more recent literature to substantiate this.

Forty cases of disease of the central nervous system, characterized by several episodes and disseminated lesions, with onset in childhood and clinically typical of multiple sclerosis, were studied. The disease as it occurs in children does not appear to differ clinically from the disease as observed in adults, in respect to mode of onset, symptoms, physical findings, and changes in the spinal fluid. In the Mayo Clinic series, however, almost twice as many girls as boys were affected. A pediatrician confronted with a child showing evidence of scattered neurologic deficits that remit, particularly a disturbance of vision and co-ordination, should consider the possibility of multiple sclerosis.

Among 4,464 births which took place during a period of four years, 1944 through 1947, there were 57 infants who had demonstrable neurologic lesions. Six of the 57 died with conclusive evidence of gross intracranial hemorrhage due to trauma. None of the six had been subjected to "difficulties of labor," five having had spontaneous births and one having been born by breech delivery which was not considered difficult. Twenty-two other infants died within a few minutes after birth or after intervals of days or weeks. Twenty of these had gross lesions of such type that injury at birth or difficulties during delivery definitely could not be considered the cause of death. The other two probably had injuries due to difficulties of birth but one had hydrocephalus which may have been the cause and not the result of the injury. Of the remaining 22 infants who survived for nine months or more, 13 had gross neurologic abnormalities. Two of the remaining nine were subjected to difficulty during birth. One had bilateral brachial palsy and one had two convulsive seizures. Both were quite normal at 1 year and at 15 months of age, respectively. Six of the nine had muscle twitchings or convulsions, but were well after intervals of seven months to 4½ years. These children must be observed for many years to determine what their future course may be. The remaining child had multiple congenital abnormalities and experienced convulsions. Among the 57 infants, there were only five who had frankly difficult births. Two recovered completely. One died with a subdural hematoma, one with hydrocephalus and intraventricular hemorrhage, and one after attacks of cyanosis. Delivery in the last case was a "difficult breech," but necropsy showed evidence of anoxia with no hemorrhage. It seems reasonable to conclude that difficulties during delivery had comparatively little to do with persistent neurologic abnormalities in most of the infants who survived. A survey was made to determine the relationship of prolonged labor, asphyxia and delayed respiration to the occurrence of trauma and, thereby, neurologic lesions of the infant. As might be expected, prolonged labor appeared to increase the risk of intracranial injury and death of the infant. However, if the infants survived, there was little or no abnormality in subsequent development and no increase in neurologic disturbances, at least during the first few years of life. More children had convulsive disorder in the "normal" or control group than in the group of those subjected to prolonged delivery. The same held true among the infants who were asphyxiated, that is, there were more who had convulsive disorder in the control group than among those who were asphyxiated. There were more deaths and more abnormal infants among those who were asphyxiated, but these included a considerable number of premature infants, many of them being not viable. If the infants survived the neonatal period, they developed normally, or at least no more abnormalities were noted among those who were asphyxiated than among the controls. Anoxia caused by delay in respiration did not have a serious prognosis in those infants who survived the neonatal period. Even a delay of 11 to 15 minutes, while fatal in 2 instances, did not appear to cause any abnormality, at least during the first four years of life, in the infants who survived.