Biomedical subjects

M Fukumizu

Publications and source records attributed to M Fukumizu.

27 records · Page 2Linked to original sources

PubMed1995

Neonatal posthemorrhagic hydrocephalus: neuropathologic and immunohistochemical studies.

A neuropathologic study was undertaken to examine associated brain damage in patients with fetal and neonatal posthemorrhagic hydrocephalus (PHH). In PHH the association of periventricular leukomalacia and pontosubicular necrosis was not increased, but that of cerebellar subarachnoid hemorrhage and olivo-cerebellar pathology was significantly increased. All patients with the olivocerebellar pathology exhibited associated cerebellar subarachnoid hemorrhage and loss of Purkinje cells. Ferritin-positive glia were increased in the molecular layer of most patients, and glial fibrillary acidic protein-positive glia and/or fibers were increased in the molecular layer, granular layer, and white matter in older infants. Neonates with PHH had more severe brain lesions than those with only intraventricular hemorrhage. At 2 weeks of age in PHH, the ventricular wall displayed hemosiderin deposits and nodular gliosis, with ependymal cell loss and subependymal rosette formation. These findings may be closely related to the underlying pathogenesis and neurologic sequelae of PHH.

Brain Stem↗

PubMed1994

Neuropathology and immunohistochemistry of the brain-stem in neonates with congenital hydrocephalus: comparative studies between aqueductal stenosis and Arnold-Chiari malformation.

Neuropathological and immunohistochemical studies were done on the brain-stem of neonates who had congenital hydrocephalus with aqueductal stenosis or Arnold-Chiari malformation (ACM). The infants with aqueductal stenosis showed heterogeneity in their clinicopathological findings while the infants with ACM were relatively similar in neuropathological findings. There were prominent astrogliosis, decreased immunoreactivity with antisera to tyrosine hydroxylase and myelin basic protein in the periaqueductal area, and an increased reactivity with antiserum to substance P in the tegmentum of most patients with aqueductal stenosis and other malformations. In ACM, there was little gliosis in the tegmentum and periaqueductal area and minimal immunoreactivity of tyrosine hydroxylase, myelin basic protein and substance P. In both groups of cases, the cells in the periaqueductal region differ in neurotransmitter/neuromodulator immunoreactivity and degree of myelination reflecting a difference possibly in their maldevelopment.

Arnold-Chiari Malformation↗

PubMed1994

[Pathology of congenital aqueductal stenosis and posthemorrhagic hydrocephalus].

The brain stem of children with congenital aqueductal stenosis or posthemorrhagic hydrocephalus were examined histologically and immunohistochemically. Congenital aqueductal stenosis occurs in various stages of CNS development, and is associated with microdysplasia and maturational abnormalities including astrogliosis, loss of neurons (tyrosine hydroxylase reactivity) and decreased myelination (myelin basic protein reactivity) in the periaqueductal gray matter. In Arnold-Chiari type II malformation there are few dysplasias, and poor development of glial and neural components in the periventricular brainstem. On the other hand, there are marked astroglial proliferation and defects of neural fibers in the periaqueductal area in children with posthemorrhagic hydrocephalus. Fibrous proliferation in aqueduct makes stenosis, and its pathogenesis seems to be caused by edema, ependymal cell desquamation, microglial proliferation and astrogliosis in parts of hemosiderin deposition. Thus, different CSF circulation disturbance and neural transmission disorder of the brainstem may develop with occurrence time, etiology or secondary complication of hydrocephalus.

Arnold-Chiari Malformation↗

PubMed1993

Phasic muscle activity during REM sleep in infancy-normal maturation and contrastive abnormality in SIDS/ALTE and West syndrome.

The generation of phasic muscle activity during REM sleep is regulated by the brainstem. We proposed two sleep indices for phasic muscle activity during REM sleep, and examine their usefulness in assessing normal brainstem maturation and functional brainstem impairment during infancy. One - the dissociation index (DI) - seems to reflect maturation of the tonic inhibitory system functioning during REM sleep, and the other - % body movements in REMs bursts (%BMs-R) - to reflect that of the phasic one. In normal infants, DI showed a gradual, linear and significant increase with age, whereas %BMs-R showed a gradual and significant decrease with age. In infants with sudden infant death syndrome (SIDS) and one who had experienced apparent life-threatening events (ALTE), the DI values were lower than those in controls, although %BMs-R values were identical in the controls. In contrast, DI was variable in infants with West syndrome (WS), while %BMs-R exceeded normal values. The tonic inhibitory system seemed to be specifically involved in SIDS and ALTE, but the phasic inhibitory one in WS. Anatomical differences between these inhibitory systems are also discussed.

Journal Article↗

PubMed1992

Tay-Sachs disease: progression of changes on neuroimaging in four cases.

The neuroradiological findings in four patients with Tay-Sachs disease are described in three phases of the clinical course. The basal ganglia and cerebral white matter show low density on computed tomography and high signal intensity on T2-weighted magnetic resonance imaging in the initial phase. The caudate nuclei are characteristically enlarged and protrude into the lateral ventricles in the first and second phases. The cerebral white matter shows low density on the CT which varies in extent from the second to third phases, and the whole brain becomes atrophic in the last phase. Thus, central nervous system involvement in the disease may begin in basal ganglia as well as in cerebral white matter.

Atrophy↗

PubMed1992

Partial seizures in two cases of metachromatic leukodystrophy: electrophysiologic and neuroradiologic findings.

This report concerns two cases of metachromatic leukodystrophy presenting partial seizures. One was a 2-year-old boy with a late infantile type and the other a 17-year-old girl with a juvenile type. The former had tonic-clonic seizures on the left with concomitant twitching of the left side of the face and adversive conjugate deviation of the eyes. After a while, his interictal sleep electroencephalogram (EEG) showed spikes in the right central area. The second case had hemiconvulsions on the right side, consisting mainly of tonic flexion of the upper limb followed by clonic flexions, and accompanied by adversive conjugate deviation of the head and eyes. Her ictal EEG showed rhythmic 6- to 7-Hz wave bursts in the left frontal area. To this date, no report has given a detailed discussion of the type of seizures and ictal EEG in metachromatic leukodystrophy. In addition, there have been few detailed reports of magnetic resonance imaging (MRI) in the juvenile type. It is interesting that typical partial seizures were observed in a hereditary metabolic disorder characterized by diffuse demyelination of the white matter, and the pathophysiology is discussed here mainly in relation to MRI findings of the case with the juvenile type.

Adolescent↗

PubMed1991

[Pedaling automatism in atypical West syndrome: a case report].

A seven-month-old girl with atypical West syndrome with pedaling automatism was reported. She started to have early infantile epileptic encephalopathy with suppression-burst (EIEE) at age 14 days followed by infantile spasms at 3 months of age. She began to have spasms with automatism at 4 month, mainly consisting of pedaling movements of both feet associated with tonic spasms of upper extremities and writhing of trunk. Ictal EEG showed irregular slow waves with occasional spikes predominantly over the right hemisphere mixed with artifacts. Interictal EEG during sleep showed suppression-burst patterns. Cerebral atrophy and microcephaly were revealed on brain CT, immature myelination on MRI and decreased blood flow in the frontal, temporal, and parietal lobes on the right on PET scan. Pedaling automatism is rare in infancy and its clinical significance was discussed in relation to West syndrome and complex partial seizures.

Age Factors↗

PubMedDate not supplied

Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus.

This immunohistochemical, neuropathological study was performed on the ventricular wall of the brainstem in children with fetal and neonatal posthemorrhagic and congenital hydrocephalus. In posthemorrhagic hydrocephalus (PHH), hemosiderin deposits, nodular gliosis, ependymal cell loss and subependymal rosette formation developed subventricularly after 2 weeks of age. Ferritin-positive reactive microglia were well stained until about 2 weeks of age and thereafter diminished as reactive astrocytosis occurred. In congenital hydrocephalus (CH), the damage to the ventricular wall was less than in PHH at all ages and was associated with only mild astrogliosis. These differences in the neuropathological findings of periventricular regions, consisting mainly of glial reactions between PHH and CH, are due to differences in pathophysiology, and the timing of the insult in both conditions. The differences may be due to the effects of intraventricular hemorrhage and/or rapidly increased intracranial pressure in PHH. These results may have implications for the neurological prognosis in children with PHH.

Biomarkers↗

PubMedDate not supplied

Periaqueductal microdysplasia in children with congenital aqueductal stenosis.

The brainstems of children with aqueductal stenosis (AS) and controls were examined histologically and immunohistochemically. In the periaqueductal area of children with AS, there was astrogliosis, loss of neurons (tyrosine-hydroxylase (TH) reactivity) and decreased myelination (myelin basic protein reactivity). In locus coeruleus, there was a decreased neuronal cell density (TH-positive neurons) in those with AS. In other areas of the brainstem (medial reticular formation), there appeared to be more TH and substance P reactive neurons. These alterations (dysplasia of slight degree) in neurons were more remarkable in children with AS with other identified brain anomalies than in those with only AS, judged by specific immunocytochemical identification of neurons. The periaqueductal astrogliosis and delayed/insufficient myelination suggest secondary damage to this region.

Abnormalities, Multiple↗