Biomedical subjects

Chihiro Sawai

Publications and source records attributed to Chihiro Sawai.

6 recordsLinked to original sources

PubMed2006

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.

Acoustic Stimulation↗

PubMed2006

Enhanced capacity of epilepsy in brain malformation produced during early development.

This study investigates the clinical features of epilepsy in 20 patients with brain malformation. Epileptic seizures were recognized in 15 patients, 12 of whom had their first seizure by 1 year of age. Partial seizure was the initial seizure type in 10 patients. Epileptic seizures were controlled in only four patients. Patients with holoprosencephaly and lissencephaly had seizure onset by 3 months of age, resulting in the most severe neurologic outcome. Only two patients with porencephaly had epileptic seizures, and in one of those patients the seizures were well controlled. A wide variety of clinical features of epilepsy in patients with brain malformation was found. More immature anomalous brain lesions may be associated with an enhanced capacity of epilepsy and resultant refractory seizures.

Adolescent↗

PubMed2005

Experimental cortical dysplasia following ibotenate administration in hamsters: pathogenesis of microgyria and associated gray matter heterotopia.

The study presented here investigated the pathogenetic relationship among different types of neuronal migration disorders occurring simultaneously in the brain using an experimental model induced by ibotenate in hamsters. In the cerebral cortex, abnormal neuronal arrangement was induced 1 day after ibotenate injection. This brain lesion resulted in microgyria in the rostral portion, focal subcortical heterotopia in the mid-portion, and focal subependymal heterotopia in the caudal portion in the same specimen. Vimentin-immunoreactive radial glial fibers were lacking in the area of disorganized neuronal arrangement, but were detected around the microgyria and the intermediate zone surrounding focal subcortical heterotopia. The focal subependymal heterotopia did not include radial glial elements. Glial fibrillary acidic protein (GFAP)-positive glial reaction was weak in these cortical lesions. We suggest that the occurrence of each type of migration disorder depends on the depth of the cortical lesion, that is, the production of microgyria, focal subcortical heterotopia and focal subependymal heterotopia are closely related to the lesions including the cortical plate, subplate and ventricular zone, respectively.

Animals↗

PubMed2004

High molecular weight microtubule-associated protein 2 over-expression in neuronal migration disorders caused by N-methyl-D-aspartate receptor activation in hamsters.

To evaluate the neuronal cytoarchitectural changes in neuronal migration disorders, the immunohistochemical expression of microtubule-associated proteins (MAPs) was analyzed using the experimental model induced by ibotenate in newborn hamsters. The cortical lesions observed after intracerebral ibotenate injections strongly resembled the following neuronal migration disorders: (1) microgyria; (2) focal subcortical heterotopia; (3) focal subependymal heterotopia; and (4) leptomeningeal glioneuronal heterotopia. Microgyria and leptomeningeal glioneuronal heterotopia had MAP2 (HM-2: high and low-molecular-weight forms of MAP2) immunoreactive dendritic processes or neuronal elements. The high molecular weight isoform of MAP2 (AP-20), which is more characteristic of mature neurons, showed enhanced expression in neurons of focal subcortical or subependymal heterotopia, although MAP1B (AA6: early form of MAP) immunoreactive elements were not detected in these heterotopic areas. We conclude that high molecular weight isoform of MAP2 is closely associated with cytoarchitectural repair and remodeling of neuronal processes, resulting in neuronal heterotopia after NMDA receptor activation.

Animals↗

PubMed2004

Peters' anomaly with bilateral perisylvian polymicrogyria and abdominal calcification.

We report a neonatal case of Peters' anomaly with bilateral perisylvian polymicrogyria and abdominal calcification. The male infant was born after a normal labor. Bilateral central corneal opacities with iridocorneal strands indicated Peters' anomaly. The X-ray and abdominal computed tomography demonstrated multiple calcifications beneath the diaphragma around the liver and the spleen. TORCH serology was negative. Intracranial calcification was not detected. Brain magnetic resonance imaging demonstrated bilateral perisylvian polymicrogyria. Abdominal calcification was suspected to be related to vascular disruption. Bilateral perisylvian polymicrogyria has been thought to result from ischemic events such as intrauterine hypotension or vascular occlusions. Based on these considerations, we conclude that a vascular disruption sequence may an important pathogenetic mechanism of Peters' anomaly.

Abdomen↗

PubMed2004

Radial and tangential neuronal migration disorder in ibotenate-induced cortical lesions in hamsters: immunohistochemical study of reelin, vimentin, and calretinin.

To investigate the mechanisms of radial and tangential neuronal migration disorders, immunohistochemical expressions of reelin, vimentin, and calretinin were examined in brain lesions induced by ibotenate (an agonist of the N-methyl-D-aspartate [NMDA] complex receptor) in hamsters. Thirty-four newborn hamsters were subjected to intracerebral injections of ibotenate, and 12 animals served as the control. These hamsters were examined at 1, 2, 3, 5, and 7 days after injections. The cortical lesions observed after ibotenate injections had a strong resemblance to the following neuronal migration disorders: (1) microgyria, (2) focal subcortical heterotopia, and (3) leptomeningeal glioneuronal heterotopia. In microgyria, the radial glial fibers were sparsely distributed, but in leptomeningeal glioneuronal heterotopia, vimentin-positive fibers extended into this abnormal neural tissue. Calretinin-immunoreactive neurons and fibers were present along the lesion forming the microgyria and abnormal neuronal arrangement. Focal subcortical heterotopia also included a small number of calretinin-expressing neurons originating from the subplate neuronal population. These results imply that the neuronal migration disorders produced by ibotenate show not only the migrational arrest of neurons but also interference from the termination of the migration process. We also suggest that the heterotopic neurons constituting the focal subcortical heterotopia originate in the lateral or medial ganglionic eminence of the ventral telencephalon, probably caused by the abnormal tangential neuronal migration.

Animals↗