SUMMARY

Summary Page 1–4. The introduction gives a brief historical survey of cerebral palsy and an account of the various investigations of the frequency of the disease. Page 5–6. The material is based on anamnestic information and on clinical examinations of 370 children suffering from cerebral palsy. Page 7–10. To illustrate the etiology of the disease, data are presented. The material shows a male predominance, 60 % against 40 % of females. A predominance of first‐born children is statistically significant (52.7 %). Page 11. Possible genetic causal factors: Among the 370 patients familial occurrence on possible genetic basis was reported in siblings of two families. In two cases, cerebral malformations were demonstrated. Page 12. Other prenatal factors: There was no increase of maternal morbidity, nor was there information of possible external factors that might have caused injury to the fetus during the pregnancy. Malformations known to be thus caused were not demonstrated in any case. Page 13–22. Natal factors: Information regarding the course of birth showed pathologic birth in 43.8 %, protracted birth and breech presentation being the most common forms. In 47 % of the children, information suggested perinatal asphyxia and/or symptoms of cerebral injury. In 26 children (7 %) the information pointed to kernicterus in the neonatal period. 28.2 % of the patients were prematures (birth weight under 2500 gms). As many as 49 % of the patients with bilateral spasticity were prematures, and of these a relatively large percentage had very low birth weight. Pathologic birth was less frequent among the prematures than in the total number of cases (25%). On the other hand, the material also shows a statistically significant increase in the number of large babies with birth weight over 4 000 gms. The percentage of normal birth weights (2500–‐4000 gms) thus is considerably lower than in a normal population (55% as against normally 80–‐85%). The material includes 25 pairs of twins. In 15 cases, the other twin was healthy, in 6 cases it was stillborn. In two pairs of twins both children had cerebral palsy. Page 23. Postnatal factors: In 18 cases (5%) there was information of postnatal cerebral infection or other cerebral injury that might be the presumed cause of their cerebral palsy. Page 24–36. The etiological conclusions to be drawn from these data are discussed. They do not indicate an essential etiological importance of hereditary genetic factors or external fetal injuries in the organogenetic period to the development of cerebral palsy. But several conditions point to a dominant etiological importance of perinatal brain injuries. In a comparatively small group these cerebral injuries are due to kernicterus. It is pointed out that kernicterus is not rare in prematures without blood‐group incompatibility, and the possibility is suggested that mild cases of kernicterus may occur, undiagnosed in the neonatal period, leading to cerebral palsy. Reference is made to animal experiments, autopsy findings, and clinical observations that point to deep‐seated anoxemic cell lesions and hemorrhages in connection with birth as the main cause of cerebral palsy. The frequent occurrence of prematurity and clinical symptoms of asphyxia/cerebral hemorrhage in this study supports the view, but cannot be considered definite evidence. More significant is the great number of pathologic deliveries and the demonstrated predominance of children with birth weight over 4000 gms. It must be presumed that the same cerebral injuries which cause perinatal mortality, when of sublethal degree are also responsible for cerebral palsy. The prophylaxis of cerebral palsy must be aimed at preventing these injuries. In about 5% of the patients the disease probably was due to infective, anoxemic, or vascular injuries during infancy after the neonatal period. Page 37–40. Some remarks on the diagnosis of cerebral palsy. Page 41–47. The classification of the clinical types of cerebral palsy is described. The type division in the present study is the following. Uncomplicated spasticity (56.7%) with the subgroups of spastic hemiparesis (24%) and spastic diplegia (32.6%). Uncomplicated athetosis (14.3%). Uncomplicated ataxia (6.5%). The remaining 22.4% of the patients, not referable to any of these types, but presenting a predominant mixture of pyramidal and extra‐pyramidal symptoms, were collected into a special group. Page 48–60. Pneumoencephalography was made of 105 of the 370 patients. In 79 the examination permitted an evaluation of the ventricular system. 16 % were found to be normal. 84 % showed pathologic dilatation of the ventricular system. Two types of pathologic findings were distinguished: those observed in spastic hemiparesis and those seen in all other types of cerebral palsy. In hemiparesis a pathologic finding was frequent (in 15 out of 16 cases). One patient showed normal ventricular system and atrophic changes of the cerebral surface. In the remaining 14 there was dilatation of the ventricular system. Asymmetry of the ventricular system was a regular finding. In 11 cases the changes were bilateral, always with dilatation most marked contralateral to the hemiparesis. In three there was dilatation of the lateral ventricle only on the affected side. Nine of the 14 patients had dilatation also of the third and fourth ventricle. Among all the other types of cerebral palsy, PEG was pathological in 51 of 63 patients. Regardless of the clinical type, the pathologic findings were strikingly uniform, with mainly symmetrical dilatation of the lateral ventricles, and often dilatation also of the third (41 patients) and fourth ventricle (11 patients). The conditions of the sulci on the cerebral surface were estimable in 44 of the examined cases. The shape of the sulci was pathological in 35. The pneumoencephalographic findings seem to suggest that in cerebral palsy there is, besides other processes, possibly a deep‐seated central pathologic process, probably connected with perinatal injury, which is presumed the most important cause of the disease. There is reason to believe that correlation exists between the degree of pneumoencephalographic changes and the degree of motor and mental defects in the patient. The pneumoencephalographic picture in cerebral palsy is strikingly like that seen in epilepsy without neurological symptoms. Page 61–65. It is suggested that organic epilepsy, cerebral palsy, and mental impairment due to cerebral lesions should be considered a pathologic entity, with the same etiology and the same pathologic‐anatomical basis. Intelligence tests were attempted on 212 patients and the intelligence was found normal in 43.9%, I.Q. between 85 and 50 in 21.7%, and under 50 in 34.4%. I.Q. was found the most reduced in the mixed group, the least in athetosis. Page 66–84. Electroencepahlographic examination was made in 223 of the 370 patients. Eighty‐eight (39.4 %) gave no pathologic finding. Thirty‐seven (about 17 %) showed slight general dysrhythmia. In the remaining 98 patients (about 44 %) EEG was distinctly pathological. In the mixed group, clinically the most severe one, EEG was found normal in no less than half the number of those examined. Apart from these cases there was, on the whole, good correlation between the clinical findings and EEG. Thus, in hemiparesis, dysrhythmia usually was found contralateral to the paresis. 82 of the 370 patients (22%) had a history of convulsions. Within the clinical types, convulsions were the most frequent in spastic hemiparesis (34.8 %), the least in ataxia and athetosis (12.5 % and 7.5 % respectively). Sixty‐one of the 82 patients had EEG examination. Six showed normal EEG, and in nine it was pathological without epileptogenic foci; 46 had one or more epileptogenic foci. Epileptogenic foci (spike foci) also were found in 27 patients without manifest convulsive seizures. The location of the epileptogenic foci in the 73 patients were scattered over the whole of the brain, with slight predominance in central and temporal regions. A location in the posterior part of the brain, was predominant in the younger patients. Prematurity, pathologic birth, and symptoms of asphyxia/cerebral hemorrhage in the neonatal period occurred as often in those with convulsions as in the total number of cases. But among patients with epilepsy without cerebral palsy, these conditions were considerably less frequent than in those with cerebral palsy. On the other hand, in epilepsy alone, history of familial occurrence of convulsions is far more frequent than in the convulsion group of cerebral palsy. The I.Q. level, on an average, was considerably lower in the cerebral palsy patients with convulsions than in the cases in general. On the whole, epilepsy in cerebral palsy responds as favourably to anti‐epileptic medicational therapy as do simple epilepsies. In only four patients did the initation of physical treatment appear to induce epileptic seizures. Page 85–88. Strabismus was demonstrated in 53 patients, and centrally conditioned reduction of vision in seven. Definite reduction of hearing was found in 19 patients, mostly in athetoids, in the form of high tone loss. Dysarthria occurred in 80 of 253 patients (31.5%). It was the least frequent in patients with spastic hemiparesis, the most frequent in the athetoids. Page 89–98. The study includes six autopsies. Page 99–101. It is pointed out that although much may be achieved by physical treatment of cerebral palsy patients, the main task in combating the disease lies in prophylaxis.