Takeo Hashimoto

Vascular architecture in white matter of neonates: its relationship to periventricular leukomalacia.

Abstract. Arterial and venous structures in the deep white matter of the developing brain were examined by postmortem angiography. About the anterior horn, body and trigon of the lateral ventricle, ventriculopetal arteries reached the deep white matter and branched out to form an abundant network of small arterioles (hypervascular zone) particularly in premature brain, thus indicating the tentative border zone between ventriculofugal and petal arteries not to be hypovascular. A deep draining group of medullary veins converged at different zones in the deep white matter, becoming large to form a large converging zone, and finally drained into a subependymal vein. A fan-shaped draining area of the converging group of veins corresponded well to the area of periventricular leukomalacia (PVL) with edema and hemorrhage. About the occipital horn and inferior horn of the lateral ventricle, transcerebral veins were abundant and PVL was rarely seen. The pathogenesis of PVL could not be fully explained by border zone infarct. An alternative pathogenesis of PVL is considered the following: 1) circulatory disturbance of the deep draining group of veins occurs, 2) edema with or without venous hemorrhage follows, 3) edema fluid and hemorrhage compress abundant arterioles in the deep white matter with 4) consequent coagulation necrosis.

Cranial MRI of neurologically impaired children suffering from neonatal hypoglycaemia

Background. Metabolic disturbances such as anoxia and hypoglycaemia are important in causing maldevelopment of the neonatal brain. While there have been some pathology studies of the effects of neonatal hypoglycaemia on brain development, reports of MRI findings in such infants have been rare. Objectives. To describe the MRI findings in neurologically handicapped children who had suffered from neonatal hypoglycaemia and to evaluate the relationship between the neurological impairment and neonatal hypoglycaemia. Materials and methods. We retrospectively evaluated the MRI findings in eight full-term infants with neonatal symptomatic hypoglycaemia who later exhibited neurological handicap. The age at which the MRI scans were obtained ranged from 9 months to 8 years 10 months (mean 4 years 1 month, median 4 years). Results. The most striking findings were prolonged T1 weighting and T2 weighting in the parieto-occipital periventricular deep white matter in six patients, suggesting abnormal or delayed myelination. Dilatation of the lateral ventricles, especially of the trigones, was observed in five patients in whom the distance between the posterior horns of the lateral ventricles and the adjacent sulci was reduced. The volume of white matter relative to grey matter was reduced in two patients. In addition, four patients exhibited cerebral cortical atrophy, mainly in the occipital lobe. Conclusions. These findings suggest that neonatal hypoglycaemia may cause delayed or abnormal myelination, especially in the parieto-occipital, periventricular, deep white matter, and may cause cerebral cortical atrophy, especially in the occipital lobe.

Germinal matrix hemorrhage of venous origin in preterm neonates

The rupture point of germinal matrix hemorrhage in premature neonates was examined by postmortem angiography. Thirteen cases of germinal matrix hemorrhage were injected via artery (four cases), vein (five cases), and both artery and vein simultaneously (four cases). Only material injected via vein leaked into the hemorrhage, which was confirmed by stereomicroscopic and histologic examination. This study suggests that germinal matrix hemorrhage is venous in origin.

Thirty-One Autopsy Cases of Trisomy 18: Clinical Features and Pathological Findings

The clinical features and morphological findings in 31 Japanese infants with trisomy 18 are presented. The majority were small-for-date infants. There was no sex predominance in our series, as opposed to male:female ratios of 1:3 reported in the literature. The average age at death was greater in females than in males. Cardiovascular anomalies were consistently present; ventricular septar defect and patent ductus arteriosus being the most common malformations. Various other internal malformations including the Arnold-Chiari malformation were observed.

Neonatal subdural hematoma secondary to birth injury: clinical analysis of 48 survivors

In order to evaluate the treatment and prognosis of subdural hematoma in neonates, we analyzed 48 survivors in the 3-year period January 1979 to December 1981. Based on the CT findings, the hematomas were grouped into four types according to location: type I, localized around the posterior interhemispheral fissure (25 cases, 52%); type II, extending from the posterior interhemispheral fissure to the hemispheric convexity (5 cases, 10%); type III, extending from the incisura to the posterior fossa (15 cases, 31%); and type IV, subdural hematoma accompanied by intracerebral hemorrhage (3 cases, 7%). Intracranial pressure was measured via the anterior fontanel in 13 cases. In 10 cases of extensive hemorrhage, the pressure exceeded 200 mm H2O. The age of the patients was from 0 to 7 days. There were 36 mature (75%) and 12 premature (25%) infants. The mothers were primiparous in 27 cases (56%). Fetal presentation was cephalic in 38 cases (79%), in 10 of which (21%) suction delivery was performed, and breech in 11. The fundus oculi was examined in 32 cases. Retinal hemorrhage was noted in 12 cases; it did not correlate with the type of hematoma or the intracranial pressure. Operations were performed in 13 cases; 1 of type I, 4 of type II, 5 of type III, and 3 of type IV. Functional prognoses were found to be as follows: type I, normal 15, abnormal 4, undetermined 6; type II, normal 4, abnormal 1; type III, normal 13, abnormal 1, undetermined 1; type IV, normal 1, abnormal 2 cases.

Brief report: incidence of and risk factors for autistic disorder in neonatal intensive care unit survivors.

We investigated prospectively the incidence of autistic disorder (AD) in the neonatal intensive care unit and the risk factors associated with autistic development. The study population included the 5,271 children at St. Marys Hospital and the diagnosis of AD was performed using DSM-III-R criteria. A total of 36 prenatal, perinatal, and postnatal factors were evaluated in the patients with AD, 57 cerebral palsy (CP), and 214 controls. AD was identified in 18 of the 5,271 children and the incidence was 34 per 10,000 (0.34%). This value was more than twice the highest prevalence value previously reported in Japan. Children with AD had a significantly higher history of the meconium aspiration syndrome (p = .0010) than the controls. Autistic patients had different risk factors than CP.

Dysgenesis of the corpus callosum and associated telencephalic anomalies : MRI

Abstract We analysed the MRI findings in 23 patients with callosal dysgenesis in relation to their associated telencephalic anomalies to investigate the morphological significance of the development of Probsts bundles and the anterior commissure in congenital callosal dysgenesis. We classified callosal dysgenesis into three types: total defect (9 patients), partial defect (7) and hypoplasia (7). Associated anomalies were observed in 15 patients, including migration disorder (8 patients), micrencephaly (5), and lipoma (2). The remaining 8 patients had no associated anomalies. Probsts bundles were not identified in 4 patients with a severe migration disorder. An absent or hypoplastic anterior commissure was observed in 9 of the 16 patients with callosal defect and all 7 of those with callosal hypoplasia. Colpocephaly and keyhole dilatation of the temporal horns were seen in 16 and 21 patients, respectively. Callosal dysgenesis may occur not only through a defect in the callosal anlage, but also from impaired growth of axonal fibres projecting from the cerebral isocortex. Therefore, associated telencephalic anomalies may be responsible for additional features in callosal dysgenesis. Consequently, identification of Probsts bundles and the anterior commissure may be important when assessing cortical development in patients with callosal dysgenesis.

Bilateral cystic nephroblastomas and multiple malformations with trisomy 8 mosaicism

The case of a 16-month-old female infant with bilateral cystic nephroblastomas, Dandy-Walker syndrome, microcephaly, bilateral cataracts, and cerebellar heterotopia is reported. The patients older sister, who had had bilateral cystic nephroblastomas, botryoid sarcoma involving the vagina and urinary bladder, microcephaly, arhinencephaly, and bilateral cataracts, was described in a previous report. Chromosomal study in the present case confirmed trisomy 8 mosaicism (rate of mosaicism, 16 per cent). The familial occurrence and the chromosomal disorder suggest a syndrome involving genetic abnormalities.

Herpes simplex viral infection in human neonates: An immunohistochemical and electron microscopic study

Specimens obtained at autopsy from six neonates with herpes simplex virus (HSV) infections were examined microscopically, electron microscopically, and immunohistochemically. Coagulative necrosis with inclusions was found in the livers and adrenal glands in all cases, as well as in various other organs, including the spleen, bone marrow, lungs, esophagus, tongue, and thymus, in some cases. Distinct hemorrhagic diathesis was found in three cases. No characteristic clinical findings, such as skin rashes or elevated titers of the antibody to HSV, were found, and clinical diagnosis was therefore difficult. In three cases isolation and typing of the causative virus were performed virologically, and type 1 HSV (HSV-1) was identified as the causative virus. Immunohistochemically, the type and distribution of the virus were evaluated in all cases with type-specific antisera to types 1 and 2 (HSV-2) antigens by the peroxidase-antiperoxidase method. In five cases the infections were found to be due to HSV-1 and in only one case to HSV-2. In the placenta in one case of HSV-2 infection, HSV antigen was demonstrated in the chorionic villi. Electron microscopic study confirmed the existence of viral particles in the placenta in that case and, thus, the possibility of a transplacental route of infection.

Detection of the human cytomegalovirus gene in placental chronic villitis by polymerase chain reaction

Placental chronic villitis was observed in 44 cases (2.12%) of 2,073 histologically examined placentas. Infiltrating lymphocytes in chronic villitis were determined by immunohistochemistry to be predominantly helper/inducer T cells. Detection of the cytomegalovirus (CMV) gene was performed on paraffin-embedded sections by polymerase chain reaction (PCR) using two different primers (CMV immediate early gene and CMV late antigen gp 64). Both CMV immediate early gene and late antigen gp 64 gene were detected in one case. Cytomegalovirus late antigen gp 64 gene was observed in only three cases. Among these four cases, the cytomegalic inclusion body was observed only in a single case with light microscopic examination. In two cases generalized CMV infection was manifested during the early infantile period and the patient died of the disease. The other two cases were asymptomatic. Our data suggest that approximately 9% of the cases of chronic villitis are caused by CMV infection, and most of them are difficult to detect morphologically. Detection of CMV gene by PCR using primers, especially late antigen gp 64 gene, is very useful for assessing the cause of placental chronic villitis.