Masaaki Uno

Effect of additional auditory and visual stimuli on continuous performance test (noise-generated CPT) in AD/HD children - usefulness of noise-generated CPT

The continuous performance test (CPT) is designed to measure sustained attention quantitatively. Several CPTs are used clinically. We have made changes to the conventional type of visual CPT, by displaying auditory and visual noise along with target or non-target stimuli. By influencing the recognition of the subjects in this way, the changes were intended to increase the sensitivity of detection of inattention and impulsiveness, to make CPT more useful for diagnosis, and to examine the effect of noise on AD/HD children during CPT performance. Its usefulness for AD/HD diagnosis and the reaction of AD/HD children to noise were examined using newly developed computer software. Using this CPT analysis, a significant difference was observed in all measurements, except mean reaction time, between the control and AD/HD groups, showing that it was useful as a supplementary diagnostic method for AD/HD, and was more useful in the younger age group than in the older age group, as the same for conventional CPTs. As compared to no-noise sessions, commission and omission errors both increased significantly in auditory and visual noise sessions. Thus, analyzing the changes in measurements during noise sessions will improve the diagnosis of inattention and combined AD/HD subtypes. Furthermore, it was suggested that analysis of the effects of noise on AD/HD children will benefit their handling in an educational environment. Since omission errors were decreased in AD/HD children by noise during the CPT performance as compared to the control group, noise may induce attention in AD/HD children. The present study presents new findings on the responses to noise of AD/HD children during the CPT.

Age-dependent susceptibility in mumps-associated hydrocephalus: neuropathologic features and brain barriers

Abstract Central nervous system susceptibility to viral infection is often age dependent for unclear reasons. In this study, we examined the age-dependent susceptibility of the brain in mumps virus-induced hydrocephalus in hamsters, and evaluated the relationship between neuropathologic features and brain barriers using glial fibrillary acidic protein and zonula occludentes 1 (ZO-1) immunohistochemistry. In a group intracerebrally inoculated with mumps virus at 2 days of age, pathologic findings such as periventricular edema, ependymal cell loss, and ventricular dilation were more prominent and the distribution of mumps virus antigen was wider than in a group inoculated at 30 days of age. ZO-1-immunoreactive tight junctions in the hydrocephalic brains of the 2-day group were severely damaged in the choroid plexus and ependyma, and in white matter capillaries as early as 3 days after inoculation. These changes were not apparent in the hydrocephalic brains of the 30-day group. Prominent cortical dissemination of virus in the 2-day group was related to underdeveloped perivascular glial foot processes in brain parenchyma. Periventricular edema in the 2-day group was linked to ependymal and blood-brain barrier tight-junction permeability. Our results suggest that tight junctions in the early postnatal period are more immature and fragile than in the adult. We concluded that brain susceptibility in mumps virus-induced hydrocephalus is intimately related to the maturity of brain barriers.

Pathogenesis of cerebellar deformity in experimental Chiari type I malformation caused by mumps virus

We sought to elucidate the pathogenesis of Chiari type I malformation using an experimental model of hydrocephalus produced by inoculating hamsters with mumps virus. Dilatation of the lateral ventricles was detected in all brains inoculated at 2, 10, and 25 days of age. The cerebellum in hamsters inoculated at 2 and 10 days of age showed elongation and flattening of the vermis and protrusion or notching of the uvula. All layers, i.e., the molecular, Purkinje cell, and granular layers, and the white matter were preserved, but had become narrow. Purkinje cells remained normal. Hamsters inoculated at 25 days of age did not develop the cerebellar deformity. Mumps virus antigen was detected in all ependymal cells and in some epithelial cells of the choroid plexus in all hamsters that had been inoculated at 2, 10, or 25 days of age. Results suggest that Chiari type I malformation is caused by two main factors occurring simultaneously, i.e., increasing intracranial pressure and rapid histogenesis of the cerebellar cortex.

Successful Management of Infantile Hepatic Hilar Hemangioendothelioma With Obstructive Jaundice and Consumption Coagulopathy

A 4-month-old boy with benign hemangioma of the porta hepatis is described. Obstructive jaundice and consumption coagulopathy developed, which were treated by percutaneous transhepatic drainage (PTHD), without resection of the tumor or bypass surgery. Because of tumor regression, the patient has remained free of symptoms even after the PTHD tube was removed. Because juvenile hemangioma is a benign tumor and occasional spontaneous regression is known to occur (as in our case and other reports), it is suggested that complete resection or bypass surgery is not necessary for juvenile hemangioendothelioma, even with obstructive jaundice, if bile drainage is adequately maintained.

Tight Junctional Damage in Experimental Mumps-Associated Hydrocephalus

Tight junctions in the central nervous system (CNS) are a major component of brain barriers including the blood‐brain barrier (BBB) and blood‐CSF barrier, which regulate solute entry and protect against invasion by microorganisms. In this study, we examined the breach of tight junctions in mumps virus‐induced hydrocephalic brain in hamsters using antibodies to Laminin B1 chain and zonula occludentes (ZO‐1) immuno‐histochemistry, and evaluated the role of tight junctions in the pathogenesis of hydrocephalus after mumps virus infection.

Congenital Hydrocephalus : Role of Transplacental Myxovirus Infection

The definite etiology in most cases of congenital hydrocephalus still remains unknown. Many studies have been reported on the experimental hydrocephalus induced by viral infection other than TORCH (Toxoplasma, Other agents, Rubella virus, Cytomegalovirus and Herpes simplex type 1 and 2 viruses). Above all mumps virus induces a high frequency of hydrocephalus. Several pediatric cases of hydrocephalus after mumps virus infection have been reported. These cases are thought to be caused by ependymitis due to mumps virus infection. Clinical cases of congenital hydrocephalus possibly caused by intrauterine mumps or influenza virus infection are also accumulating. The definitive evidence of a teratogenic potential for mumps and influenza virus, however, has been obscure yet. Our experimental studies demonstrated that mumps and parainfluenza virus type 3 could induce hydrocephalus by destructive ependymal infection in suckling hamsters. However, the transplacental infection of these viruses was rare. These results show that myxoviruses such as mumps and parainfluenza virus have a strong affinity to ependymal cells, and then they cause resultant ependymal destruction. We suggest that when the placenta is impaired so severely that these viruses are able to pass through the placental barrier, maternal infection would cause the hydrocephalus to the infant.