Computed tomograms (CT) from 204 cases of premature and full term infants were studied. 1) In 70 infants of hyaline membrane disease, primary apnea and asymptomatic transient hypoglycemia and hypocalcemia, without any abnormal CT findings such as intracranial hemorrhage, periventricular lucency was found in 65 cases (93%) and a wide extracerebral space of the temporal lobes was found in 60 cases (86%) before 44 weeks of gestation. A wide interhemispheric fissure was found in 11 cases of extremely premature infants before term. Periventricular lucency and a wide extracerebral space of temporal lobes may not be the result of the intracranial pathological changes, but they may represent a stage of brain development. 2) In 204 cases, intracranial hemorrhage was found in 39 cases ; intra ventricular 14 cases, subependymal 2 cases, intracerebral 4 cases, subarachnoid 19 cases. CT was useful in evaluating the site and extent of hemorrhage. Among 14 cases of intraventricular hemorrhage, 9 cases with massive hemorrhage died and 2 cases had developmental retardation. Other intracranial pathologic changes included hydrocephalus (17 cases), arachnoid cyst (3 cases), and agenesis of corpus callosum (1 case).
Diffuse low density of the cerebral cortex was found in 8 cases. Two cases died and 5 cases had developmental retardation. Early ventricular dilatation was found in 19 cases, 2 with intravfouricular hemorrhage and 5 with diffuse low density of the cerebral cortex. Among them 11 cases had developmental retardation.
Neurological prognosis was poor in infants with massive intraventricular hemorrhage, diffuse low density of the cerebral cortex and early ventricular dilatation.

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In eight patients with GTS (six males and two females), ranging from 7 to 14 years, the secretion of growth hormone (GH), prolactin (PRL) and thyroid stimulating hormone (TSH) was investigated.
1) GH: Two of 8 patients with GTS revealed no response (peak GH level≤5ng/ml) to insulin, 3 patients borderline response (5ng/ml±peak GH level±10 ng/ml), and other 3 patients normal response (10 ng/ml≤peak GH level). In 3 patients, the time of peak GH level was delayed. In all patients with GTS, the response of GH to insulin loading was followed as the mean baseline GH level; 0.15±0.40ng/ml (mean±S. D.), the mean peak GH level ;9.55±5.28 ng/ml, and ΔGH (peak GH level minus baseline GH level);9.40±5.47 ng/ml. As compared with the values of 8 age and sex matched controls (the mean baseline GH level: 2.02± 2.23 ng/ml, the mean peak GH level 28.04±19.83 ng/ml, and ΔGH 26.02±19.21 ng/ml), the mean peak GH level of GTS was significantly low (P±0.05 student t-test). Four (no response; 2, and borderline response; 2) of 5 patients with no or borderline response to insulin loading were studied by the intravenous drip infusion of L-arginine (0.5 g/kg). Two of 4 patients showed normal response. One of 2 patients, who were no response to insulin loading, was no response, and other one borderline response.
2) PRL: All patients but one revealed the normal response of PRL to intravenous injection of TRH. In one, the low response of PRL was observed. In two, the delayed response of PRL was observed.
3) TSH: The secretion of TSH which was examined in 2 patients was normal in response.
4) In 4 of 5 patients who were no or borderline response to insulin loading, the secretion of GH during sleep was investigated, and in two, PRL, too. The episodic secretion and sleep enhancement of GH and PRL were seen during sleep. However, the peak level of GH secretion did not always agree with the state of the slow wave sleep.
From the above results, it was suggested that the latent endocrinological dysfunction exists in some patients with GTS.

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The effects of experimental intrauterine growth retardation on subsequent fetal development, especially with respect to brain development, were studied in two groups of New Zealand white rabbits. The parameters investigated include wet weight, protein, DNA, protein/DNA, and the structure protein in myelin.
Experimental ischemia and subsequent fetal malnutriton were induced in the experimental group by litigation of spiral arterioles according to the method of Marthens and Harel. The results were that the brains in the malnurished fetuses revealed a significant decrease in weight, DNA, and protein content compared with those in the control group. However, there was no significant difference in the mean cell size index (protein/DNA) between the experimental group and the control group. DM-20 protein, proteolipid protein (PLP), and basic protein (BP) were present in all stages of development in both groups, although, unlike the experimental group, there was a gradual increase in the amount of these proteins in myelin from the 26 th to the 30 th day of gestation in the control group. On the other hand, high molecular weight proteins in myelin decreased more rapidly in the control group than in the experimental group during this same period of gestation. Experimental ischemia also caused a significant decrease in liver glycogen in the experimental group but not in the control group.
It was concluded that an inhibition of protein synthesis in the vulnerable period of brain development could lead to changes in brain structure, defects in cell growth, and failure in myelination.

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In order to investigate the mechanism of the development of the parachute reaction, the authors tried to analyze the effect of the stimulation of touch and proprioceptive sensation on the reaction which was elicited with quick approach of child vertically held in space to the surface of the wall.
The subjects were divided into 3 groups, and each group consisted of 34 normal children from 12 to 15 month of age. The reaction was elicited with quick approach of children vertically held in space to the surface of the wall. In group 1 the reaction was elicited two times continuously on each child. Then the armes of the child were pushed against the wall. Again the reaction was elicited two times continuously. In group 2 the reaction was elicited four times continuously after pushing technique. In group 3 the reaction was elicited four times continuously without pushing technique. The responses of shoulder joint, elbow joint and finger joint were scored respectively as follows: 1; no response, 2; slight response, 3; moderate response, 4; almost complete response, 5; complete response. The average score of each time was compared among each groups.
In group 1 the score significantly increased after pushing technique. The score of first trial of group 2 or second trial of group 2 was significantly higher than that of first trial of group 1 or second trial of group 1 respectively. The score of third trial of group 1 or fourth trial of group 1 was significantly higher than that of third trial of group 3 or fourth trial of group 3 respectively.
The reaction against the wall is not and the same with the parachute reaction, but has the same nature in protective reaction and visual and vestibular stimulation as the parachute reaction. The results indicate that the response of the arm is more facilitated after the stimulation of touch and proprioceptive sensation than only with visual and horizontal vestibular stimulation. Kitahara reported that the positive parachute reaction appeared when children could push themselves circularly or backward in prone position. So we consider the stimulation of touch and proprioceptive sensation on arm as well as visual and vestibular stimulation play the important role in the developmental course of the parachute reaction.

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Acute infantile hemiplegia is caused by various diffuse cerebral disorders. In this report four patients, who seemed to be caused by acute encephalitis or encephalopathy, 8-34 months of age, were described with special reference to the changes in the CT scans of the brain.
The initial CT, taken within 10 days after the onset of the disease, revealed a unilateral and diffuse low density hemisphere, suggesting brain edema secondary to inflammation or ischemia.
Two weeks later the affected hemisphere became atrophic with a dilatation of the lateral ventricle on the same side, and a shift of the midline structure such as falx and the pineal body was also noted. The low density area suggesting gliosis became less conspicuous with the course of the disease.
The follow-up CT after several years showed thickened of calvaria, and dilatation of frontal and ethimoidal sinuses and also of mastoid air cells.
In two cases subdural hematoma was detected in association with brain atrophy 40 days and 6 months later respectively, but thereafter disappered spontaneously.

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Serum phenytoin levels were determined by the GLC technique in 15 epileptic patients, aged 9 to 26 years, taking usual doses of phenytoin for more than 5 years. The levels of this anticonvulsant rose about threefold on 7 to 10 days after adding sulfaphenazo (50 mg/kg daily).
In order to investigate the disappearance curve of serum phenytoin, ¹⁴C-phenytoin was injected intravenously to rats. From these experiments it was found that the disappearance rate of ¹⁴C-phenytoin was markedly prolonged in two rats pretreated with sulfaphenazole (1, 000 mg/kg daily) for 3 days before the experiment, as compared with three control rats. The half-life of ¹⁴C-phenytoin was about 90 minutes in control rats while that in sulfaphenazole pretreated rats was more than 240 minutes.
When the preparation of rat liver microsomes was used in vitro, parahydroxylation of ¹⁴C-phenytoin was inhibited by 44% in the presence of 1 mM sulfaphenazole.
These findings suggest that sulfaphenazole inhibits the activity of enzyme hydroxylating phenytoin and may cause the increase of serum phenytoin levels. Consequently sulfaphenazole should be carefully given to epileptic patients taking usual doses of phenytoin.

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More than two years' observation on a 5-year-old boy with muscular symptoms was presented. Onset of the illness was not very clear. It was reported his mental and motor development was retared in infancy, and he was first detected to have elevated serum enzyme at 17 months of age. He was diagnosed as congenital or Duchenne muscular dystrophy, but because of marked inflammatory changes in the biopsied muscle specimen at age 27 months and some difference in clinical feature from any type of muscular dystrophy, treatment with adrenal cortical steroids was decided to start at age 33 months. Immediately after the start of the treatment, serum CPK showed a rapid decrease, and also clinical improvement of the muscular symptoms gradually appeared.
Serum CPK corresponded very sensitively to the dosage of steroids, and at least 1 mg/kg body weight of prednisolone was proven to be necessary to maintain relatively low level of serum CPK, though because of an inhibitory effect on physical development this dosage could not be maintained.
The responsiveness of the symptoms as well as serum CPK and inflammatory muscle changes were considered to support the diagnosis of polymyositis. However, it was not clear whether his mental retardation was also due to the same etiological process as muscular involvement or not. Combination of inflammatory muscular disorder and mental retardation was very rare in contrast to frequent occurrence of mental problems in genetically determined myopathies.
Peculiar findings in muscle biopsy consisted of inflammatory changes of the small blood vessels and marked vascularization in the interstitial spaces. Dilatation of every blood capillaries to individual muscle fibers might be indicative of disturbance in microcirculation within the muscle. Presence of myotube-like structures was probably correlated to regenerating process of muscle fibers.

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The present case is a a newborn baby, who has some congenital malformations of multiple organs. She was delivered by Cesarean section with turbid amnioic fluid in full term. A huge occipital encephalomeningocystocele was noticed without any cerebrospinal fluid leakage. In addition to this anomaly, as external malformations right thumb defect, hyperflexion of right elbow and bilateral pes cavus were demonstrated. As internal malformations, esophageal atresia with esophago-tracheal fistula (Gross C type), defect of the right ulnar bone and systolic murmur at the cardiac apex existed.
Neuroradiological investigations showed that not only the occipital lobes, parietal lobes, temporal lobes but cerebellum and brainstem herniated into the encephalocele, which was compatible with the indings of Arnold-Chiari malformation type 3.
A case with this rare coupled malformations was reported and relevant literature was also reviewed.

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The patient was born weighing 3100 gm after a 38-week gestation to a 30-year-old mother without any complication of pregnancy and delivery, and his head circumference was 36.5 cm at birth. Intraventricular hemorrhage and ventricular dilatation were diagnosed by computed tomography at 24 hours of age. Cerebrospinal fluid obtained by ventricular tap was dark red brown and turbid, and ghost blood red cells were recognized. Methemoglobin peak was found on CSF spectrophotometry and hypoglycorrhachia (CSF/blood glucose ratio was 0.34) was recognized.
From the findings obtained above, it was concluded that intraventricular hemorrhage have occurred in utero and then posthemorrhagic hydrocephalus have developed.

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Computed tomographic findings of tuberculous meningitis and intracranial tuberculoma have been reported by some authors. But there have been no case reports followed up by computed tomography (CT) with regard to the development of intracranial tuberculoma during a course of tuberculous meningitis.
In this report, a case of intracranial tuberculoma observed by serial CT examination during a course of tuberculous meningitis was reported.
A 1-year 8-month-old boy was admitted to our hospital with high fhver, a generalized convulsion and unconsciousness on October 20, 1979. He was diagnosed as having tuberculous meningitis from clinical course, physical findings and laboratory data. He was given SM, INH and RFP. Intial CT on admission showed a low density area in the left internal capsule which seemed to be a cerebral infarction. Postcontrast CT showed a slight enhancement in the left basal and quadrigeminal cisterns. After SM was stopped following the improvement of clinical symptoms and CSF findings, high fever developed again and CT findings became worse. Postcontrast CT on November 27, 1979, showed an extension of abnormal enhancement on the left basal and quadrigeminal cisterns. SM was given again together with EB. Consequently he became afebrile and CSF findings improved steadily. Despite the clinical improvement, the abnormal enhanced area on postcontrast CT enlarged and seemed to be a tuberculoma. At 6th month after initiating treatment, postcontrast CT showed a large tuberculoma surrounded by a low density area at the brain base. A new combination of drugs was started; KM, INH, PAS and TH. One month later, the high density area and surrounding low density area decreased in size on postcontrast CT.
Intracranial tuberculoma is generally known to advance asymptomatically over a long time and this case is not an exception. We could not presume the development of intracranial tuberculoma without CT. This case emphasizes the usefulness of follow-up CT as an evaluation of therapy for tuberculous meningitis.

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