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Volume 29, Issue 2
Displaying 1-12 of 12 articles from this issue
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[in Japanese]1997 Volume 29 Issue 2 Pages 90
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDownload PDF (149K) -
Tohru Seki1997 Volume 29 Issue 2 Pages 91-99
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe efficacy and side effects of various antiepileptic drugs (AEDs), especially pyridoxine, ACTH and valproate sodium (VPA), in the treatment of West syndrome were reviewed.
ACTH remains to be the most effective treatment for West syndrome. However, there are significant adversive effects with prolonged ACTH therapy. The efficacy of pyridoxine at the dose of 40-50 mg/ kg/day is less encouraging, but there are no serious adversive effects, as opposed to ACTH.
Some reports have indicated the possible efficacy of VPA in regular, large (40-100 mg/kg/day) and very high (100-300 mg/kg/day) doses. However, in patients under the age of 2 years, monotherapy using VPA in lower doses should be employed to minimize the risk of VPA-induced adversive effects, such as fatal hepatic toxicity.
Consequently, a safer and more effective treatment is required.
We have reported a pilot study on combination therapy with high-dose pyridoxine phosphate (40-50 mg/kg/day) and low-dose ACTH (0.01 mg/kg/day) in 25 children with West syndrome, mainly on the basis of neurochemical analysis of the ictal epileptic spasms.
The response rate was similar to those achieved with high- dose ACTH, but a quicker cessation of spasms was obtained with the combination therapy than ACTH monotherapy. Transient increases in liver enzymes occurred in 50%, but none of the patients developed more serious side effects.
Further study is required to determine the efficacy of this combination therapy.View full abstractDownload PDF (1148K) -
Morimi Shimada, Takehiko Okuno1997 Volume 29 Issue 2 Pages 100-101
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSCortical dysplasias caused by the destruction of neuron production and migration have been recognized as relatively common neuropathological findings among the children with intractable epilepsy and mental and/or physical handicaps.
Together with various environmental factors, an increasing number of gene abnormalities have recently been identified as a cause of cortical dysplasias. However, the processes from the gene abnormality to the development of cortical dysgenesis remain unknown.
In this symposium, the pathology, pathogenesis and MRI manifestation of neuronal migration disorders as well as intimate correlation with intractable epilepsy and neurosurgical treatment for this disorder, were reviewed by six experts.View full abstractDownload PDF (257K) -
Shinji Fushiki1997 Volume 29 Issue 2 Pages 102-107
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSCortical malformations such as cortical dysplasia and heterotopia constitute the underlying pathology of epilepsy and mental retardation. It is thus important to elucidate the pathogenesis of these migration disorders from the neuropathological viewpoint based upon animal experiments. In this review, I describe the experiment in which low-dose prenatal X- or γ-irradiation was performed at the mid-gestational period of mice or rats. Low-dose irradiation as low as 150 mGy induced decelerated migration of cortical neurons during the embryonic period together with a changed pattern of cell adhesion molecule, N-CAM. In addition, the effect of radiation remained at least up until 3-week postnatal as disorganized neuronal allocation with respect to the birthdate. With time of further maturation in the neocortex, however, the architecture, in terms of the pattern of distribution of the labeled neurons, returned closely to that found in non-irradiated control animals. Considering the fact that the number of labeled cells per unit cortical area decreased considerably from 3-week to 8-week postnatal, it is conceivable that apoptotic cell death might have occurred in aberrantly placed neurons.
Recent progress of molecular genetical approach to human hereditary neurodevelopmental diseases is briefly reviewed, since it greatly contributes to our understanding on the pathogenesis of neuronal migration disorders.View full abstractDownload PDF (867K) -
Yoshihiro Tsutsui, Akira Mizutani1997 Volume 29 Issue 2 Pages 108-114
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe have analyzed 60 autopsy cases of cerebral palsy (CP) at the Aichi Prefectural Colony. The weight of the CP brains was distributed most frequently between 60 to 70% of normal brain weight. Coronal thin sections of the whole brains through the mammillary bodies were made using a large-sized microtome and stained with hematoxylin-eosin (HE) and Kliiver-Barerra (KB) stains. Macroscopically, CP brains were classified into microgyria-pachygyria type (45 cases), thin cerebral mantle type (10 cases), hydrocephalus type (3 cases), and lissencephalic type (2 cases). Macroscopic image analysis was performed using the KBstained whole brain sections from the microgyria-pachygyria type CP brains, as well as 9 brains of control cases with non-neurological diseases and 4 brains with Fukuyama congenital muscular dystrophy (FCMD). The CP brains showed narrowed white matter with dilated ventricules compared with the controls. Microscopic analysis showed that ectopic grey matter (about 16%), and disorganization of the cerebral cortex (about 50%), and neuronal depletion (about 50%). These findings suggest that some of the CP brains resulted from disturbance of neuronal migration.View full abstractDownload PDF (13348K) -
Nobutaka Arai, Masaya Oda1997 Volume 29 Issue 2 Pages 115-122
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA variety of brain malformative lesions, resulting mainly from abnormalities in neuronal migration, have been recently highlighted with increasing knowledge on surgical pathology of intractable epilepsy. In this article, a wide spectrum of pathology in and around the neuronal migration period are reviewed. Morphological changes of lissencephalies, polymicrogyria, microdysgenesis and focal cortical dysplasia were described, as well as some problems in the classification of malformative brains.View full abstractDownload PDF (15684K) -
Takehiko Okuno, Takehiko Okuno, Michimasa Matsuo, Toshiaki Higa, Haruo ...1997 Volume 29 Issue 2 Pages 123-128
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSRecent progress in magnetic resonance imaging (MRI) has sucessfuly visualized neuronal migration disorders (NMDs) without autopsy.
NMDs are observed in the patients with hydranencephaly, porencephaly, cerebellar hypoplasia, agenesis of corpus callosum, agenesis of septum pellucidum and holoprocencephaly.
Miller-Dieker syndrome, Fukuyama-type congenital muscular dystrophy, Walker- Warburg syndrome, hypomelanosis of Ito, congenital rubella syndrome, toxoplasmosis, Zellweger syndrome and other diseases are also associated with lissencephaly, pachygyria and polymicrogyria.
Neuroimagings of illustrative cases with NMDs were shown here.View full abstractDownload PDF (7606K) -
Kosaburo Aso, Sachie Nakashima, Kazuyoshi Watanabe1997 Volume 29 Issue 2 Pages 129-133
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe retrospectively studied 32 patients who had cortical dysplasia and epilepsy. Cortical dysplasia was classified into diffuse cortical dysplasia (8 patients), bilateral localized cortical dysplasia (5), unilateral diffuse cortical dysplasia (2), and focal cortical dysplasia (17). The onset of epilepsy was younger in patients with more widespread lesions. At the onset, patients with bilateral lesions generally had symptomatic generalized epilepsy, while those with unilateral cortical dysplasia tended to have symptomatic localization-related epilepsy. In patients with focal cortical dysplasia, however, 4 patients had West syndrome, either at the onset of epilepsy or during the follow up period. Seizure outcome was poor in any type of cortical dysplasia. An evaluation of prognostic factors in patients with focal cortical dysplasia did not show any of statistical significance, including gender, age at onset of epilepsy, psychomotor delay and the presence of high intensity areas in T2-weighted MRI.View full abstractDownload PDF (676K) -
Tadahiro Mihara, Kazumi Matsuda, Takayasu Tottori, Toshiaki Otsubo, Yu ...1997 Volume 29 Issue 2 Pages 134-144
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe conducted corticectomy in twenty-five patients with intractable partial epilepsy due to focal cortical dysplasia (FCD). MRI could not detect FCDs in three patients, interictal SPECT, however, revealed hypoperfusion corresponding to FCDs in two of these patients, while the FCD in one remaining patient was histologically identified in a resected specimen. The location of FCDs was as follows: the frontal lobe in sixteen patients, the temporal in five, the occipital in two, fronto- parietal in one, and the temporo- parietal in one. Prior to the surgery, twenty-one patients underwent invasive long-term intracranial EEG/CCTV monitoring. Of the fourteen patients who were tracked for longer than 2 years following surgery, eleven belonged to Class I according to Engel's criteria, two to Class II, and one to Class We compared intracranial EEG findings (interictal and ictal) between these twenty- one patients and eight patients with frontal lobe epilepsy resulting from different lesions. The results of this comparison, together with the seizure outcome following surgery, indicated that FCD is intrinsically epileptogenic. The invasive long- term monitoring should, as a rule, be performed in all patients with FCDs prior to the corticectomy.View full abstractDownload PDF (1450K) -
Part IlI: Prevalence of Children with Suspected Learning DisabilitiesMadoka Shiota, Tatsuya Koeda, Kenzo Takeshita1997 Volume 29 Issue 2 Pages 145-148
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe prevalence of children with suspected learning disabilities (LD) was investigated. One thousand and eight-hundred- eighty-nine pupils at ordinary elementary classes were evaluated by class teachers. We defined suspected LD as a condition with normal IQ (not less than 70) and low PRS score (not more than 65). Eighteen children (12 boys, 5 girls, and 1 with sex unknown) were considered as suspected LD with this criterion. The prevalence of suspected LD at elementary schools was 0.95%, the lowest figure as compared to those in previous reports. The suspected LD children were studied for the LD type and school grade. Verbal LD was not found, non-verbal LD was found in 6 children, and mixed type in 11. In the study of their school grades, the third grade suspected LD children were the largest. There was a significant decrease in number at higher school grades.View full abstractDownload PDF (452K) -
Part N: A Prospective Study of Children with Risk Factors for Learning Disability at Three Year-Old Screening-Clinical Examinations in 1995Tatsuya Koeda, Madoka Shiota, Kenzo Takeshita1997 Volume 29 Issue 2 Pages 149-154
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe are following children with risk factors for learning disability (LD) at three year- old screening prospectively. In 1995, one child reportedly as normal in 1994 was considered to have a possibility of LD. The complaints of their parents had shifted to underachievement. In several children, their poor social skill in school and family was considered to be more serious in 1995 than in 1994. All children who were clumsy in early childhood showed non- optimal motor co- ordination on minor neurological examinations by Touwen. This suggested that non-temporary neurological impairments led them to LD.View full abstractDownload PDF (751K) -
[in Japanese], [in Japanese]1997 Volume 29 Issue 2 Pages 161-168
Published: March 01, 1997
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDownload PDF (1126K)
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