Nishi Niigata Chuo National Hospital

Niigata-shi, Japan

Nishi Niigata Chuo National Hospital

Niigata-shi, Japan
Time filter
Source Type

Onishi H.,Niigata University of Health and Welfare | Sugawara K.,Niigata University of Health and Welfare | Yamashiro K.,Niigata University of Health and Welfare | Sato D.,Niigata University of Health and Welfare | And 5 more authors.
Brain and Behavior | Year: 2013

The detailed time courses of cortical activities and source localizations following passive finger movement were studied using whole-head magnetoencephalography (MEG). We recorded motor-related cortical magnetic fields following voluntary movement and somatosensory-evoked magnetic fields following passive movement (PM) in 13 volunteers. The most prominent movement-evoked magnetic field (MEF1) following active movement was obtained approximately 35.3 ± 8.4 msec after movement onset, and the equivalent current dipole (ECD) was estimated to be in the primary motor cortex (Brodmann area 4). Two peaks of MEG response associated with PM were recorded from 30 to 100 msec after movement onset. The earliest component (PM1) peaked at 36.2 ± 8.2 msec, and the second component (PM2) peaked at 86.1 ± 12.1 msec after movement onset. The peak latency and ECD localization of PM1, estimated to be in area 4, were the same as those of the most prominent MEF following active movement. ECDs of PM2 were estimated to be not only in area 4 but also in the supplementary motor area (SMA) and the posterior parietal cortex (PPC) over the hemisphere contralateral to the movement, and in the secondary somatosensory cortex (S2) of both hemispheres. The peak latency of each source activity was obtained at 54-109 msec in SMA, 64-114 msec in PPC, and 84-184 msec in the S2. Our results suggest that the magnetic waveforms at middle latency (50-100 msec) after PM are different from those after active movement and that these waveforms are generated by the activities of several cortical areas, that is, area 4 and SMA, PPC, and S2. In this study, the time courses of the activities in SMA, PPC, and S2 accompanying PM in humans were successfully recorded using MEG with a multiple dipole analysis system. © 2013 The Authors. Published by Wiley Periodicals, Inc.

Sasagawa M.,Nishi Niigata Chuo National Hospital
Seishin shinkeigaku zasshi = Psychiatria et neurologia Japonica | Year: 2012

Epilepsy is a common episodic neurological disorder and is often accompanied by mental, psychiatric, and physical disorders; therefore, a comprehensive treatment, including seizure control, is needed to treat it. Epilepsy patients need frequent seizure preventive treatment, which is likely to induce medication dependence. This paper presents a report on the social resources involved in epilepsy treatment. "Services and Support for Persons with Disabilities Acts" is applicable to epilepsy patients and provides public compensation for psychiatric outpatient treatment, enabling disabled persons to apply for disability pension to support their living and medical expenditures. The Mental Health Welfare Notebook is issued to provide welfare services for the disabled, and it plays an important role in promoting employment of disabled persons. The welfare services for the disabled are diverse, ranging from home-based services to services aiding the disabled to step out of their homes, go to day care centers, or pay for house rent. The details of the welfare services for the disabled are available on the homepage of the website for the Ministry of Health, Labour and Welfare. The roles of physicians involve maximizing social resources in coordination with psychiatric social workers, aiming for normalization of disabled persons so that they are able to live comfortably in the community.

Kameyama S.,Nishi Niigata Chuo National Hospital | Masuda H.,Nishi Niigata Chuo National Hospital | Murakami H.,Nishi Niigata Chuo National Hospital
Epilepsia | Year: 2010

Summary Purpose: To topographically localize the ictogenic zone within hypothalamic hamartomas (HHs) and the symptomatogenic zone for gelastic seizure (GS), we analyzed data from both interictal and ictal single photon emission computed tomography (SPECT). Methods: Ictal SPECT was performed immediately after GS onset in 21 patients with HH (aged 2-36 years, mean 13.8 years) who underwent stereotactic radiofrequency thermocoagulation (SRT). SPECT data were statistically analyzed by means of subtraction ictal SPECT coregistered to magnetic resonance imaging (MRI) (SISCOM) and statistical parametric mapping (SPM). Topographic localization of ictal hyperperfusion areas was evaluated. Results: SISCOM obtained in 27 studies demonstrated ictal hyperperfusion in the HH interface zone in 16 studies of 13 patients (hot HH group). In these patients, HHs were significantly larger than those without hyperperfusion of HH in 11 studies of 8 patients (21.4 ± 10.3 vs. 12.3 ± 7.3 mm in diameter, p < 0.05, t-test). In all patients and in the hot HH group, SPM group analysis of individual differences between interictal and ictal data revealed significantly (p < 0.001) hyperperfused areas in the ipsilateral hypothalamus, mediodorsal (MD) nucleus of the thalamus and putamen, bilateral pontine tegmentum, and contralateral inferior semilunar lobule of the cerebellum. There was no hyperperfusion in the mammillothalamocingulate pathway. Discussion: The present study confirmed that ictogenesis occurs in the HH interface zone, which should accordingly be the target for SRT. We suggest that a thalamopontocerebellar circuit plays an important role for stereotypical and automatic symptomatogenesis of GS and that the hypothalamus and MD nucleus of the thalamus are potentially involved in epileptic encephalopathy. © 2010 International League Against Epilepsy.

Onishi H.,Niigata University of Health and Welfare | Oyama M.,Niigata University of Health and Welfare | Soma T.,Niigata University of Health and Welfare | Kirimoto H.,Niigata University of Health and Welfare | And 3 more authors.
Clinical Neurophysiology | Year: 2011

Objective: To investigate the projection of muscle afferents to the sensorimotor cortex after voluntary finger movement by using magnetoencephalography (MEG). Methods: The movement-evoked magnetic fields (MEFs) after voluntary index-finger extension were recorded by a 204-channel whole-head MEG system. Somatosensory-evoked magnetic fields (SEFs) were recorded after motor-point stimulation was applied to the right extensor indicis muscle by using a pair of wire electrodes. Results: The MEF waveforms were observed at 35.8 ± 9.7. ms after movement onset (MEF1). The most concentrated SEFs were identified at 78.7 ± 5.6. ms (M70), and the onset latency of M70 was 39.0 ± 5.5. ms after motor-point stimulation. The mean locations of the equivalent current dipoles (ECDs) of MEF1 and M70 were significantly medial and superior to that of N20m elicited by median-nerve stimulation. The ECD locations and directions of both MEF1 and M70 were concordant in the axial, coronal and sagittal planes. Conclusions: MEF1 and M70 might be elicited by muscle-afferent feedback following muscle contraction. In addition, these ECDs may be located in area 4. Significance: Motor-point stimulation is a useful tool for confirming the projection of muscle-afferent feedback to the sensorimotor cortex after voluntary movement. © 2010 International Federation of Clinical Neurophysiology.

Takahashi H.,Niigata University | Kakita A.,Niigata University | Tomikawa M.,Nishi Niigata Chuo National Hospital | Okamoto K.,Niigata University | Kameyama S.,Nishi Niigata Chuo National Hospital
Neuropathology | Year: 2013

We studied a frontal lobe subcortical cystic tumor that had been resected from a 13-year-old girl with a 3-year history of intractable partial seizure. Currently, more than 13 years after surgery, the patient remains recurrence-free and has no neurological deficits. Histological examination showed that the tumor was non-infiltrating and paucicellular with a mucinous matrix, and consisted of fairly uniform small cells with round to oval nuclei. Within the mucinous matrix, the tumor cells were often arranged in pseudorosettes around small blood vessels. Mitotic activity and necrosis were absent, with a Ki-67 labeling index of <1%. Based on the immunohistochemical and ultrastructural findings, the constituent tumor cells were considered to be those of oligodendroglioma, including mini-gemistocytes and gliofibrillary oligodendrocytes. No neuronal elements were identified. Features of cortical dysplasia (FCD Type 1) were evident in the cortex covering the lesion. The surrounding white matter also contained a significant number of ectopic neurons. The entire pathological picture appeared to differ somewhat from that of ordinary oligodendroglioma (WHO grade II). Considering the clinical and pathological features, the present unusual oligodendroglioma appeared to represent a previously undescribed form of oligodendroglioma (WHO grade I) lying within the spectrum of dysembryoplastic neuroepithelial tumor (DNT; WHO grade I). Simultaneously, the present oligodendroglioma also raises the question of whether or not oligodendrocyte-like cells of DNTs truly show neurocytic differentiation. © 2013 Japanese Society of Neuropathology.

Shimizu T.,Nishi Niigata Chuo National Hospital
Japanese Journal of Clinical Radiology | Year: 2015

We reviewed chest CT findings of 198 patients who had asbestos exposure and followed up CT examination between 2006 and 2013. In this retrospective study, 15 patients ranging in age from 60 to 74 years (mean 66.6 years) were diagnosed with rounded atelectasis (18 lesions in 15 patients). Two lesions were localized in upper lobes (2/18), 5 were in middle lobe (5/18), and 11 were in lower lobes (11/18). Fourteen lesions were localized at right side (14/18), and 4 were at left side (4/18). The size of them ranged from 17 to 44 mm (mean 27 mm). Diffuse pleural thickening was found in all patients (15/15), pleural plaque in 5 patients (5/15), pleural calcification in 14 patients (14/15), pleural effusion in 13 patients (13/15). In one patient, rounded atelectasis appeared in the same timing as the appearance of the pleural effusion during the follow-up period. There was no lesion increased in size during the follow-up period.

Yamazaki S.,Niigata City General Hospital | Ikeno K.,Niigata City General Hospital | Abe T.,Niigata City General Hospital | Tohyama J.,Nishi Niigata Chuo National Hospital | Adachi Y.,Matsue Medical Center
Pediatric Neurology | Year: 2011

Hemiconvulsion-hemiplegia-epilepsy syndrome involves sudden and prolonged unilateral seizures, followed by transient or permanent hemiplegia and epilepsy during infancy or early childhood. Some patients with familial hemiplegic migraine and demonstrating the S218L mutation in CACNA1A experience severe attacks with unilateral cerebral edema after trivial head trauma. We report on a 5-year-old Japanese girl presenting with hemiconvulsion-hemiplegia-epilepsy syndrome after infection with parvovirus B19. Magnetic resonance imaging performed 2 days after admission revealed cerebellar atrophy and marked hyperintensity in the left hemisphere on T 2-weighted and diffusion-weighted imaging. Magnetic resonance angiography performed 7 days after admission demonstrated obliteration of the left proximal middle cerebral artery in the acute phase. However, this finding was not evident on brain angiography performed 25 hours after magnetic resonance angiography. Genetic analysis of familial hemiplegic migraine revealed a heterozygous S218L mutation in CACNA1A. Taken together, these results suggest that vasospasms of cerebral vascular smooth muscle, with possible cortical spreading depression, may have caused the hemiconvulsions and hemiplegia in the left hemisphere. This case report is the first, to the best of our knowledge, to associate CACNA1A with hemiconvulsion-hemiplegia-epilepsy syndrome and familial hemiplegic migraine, and to suggest that similar pathogenic mechanisms may underlie these two disorders. © 2011 Elsevier Inc. All rights reserved.

Kameyama S.,Nishi Niigata Chuo National Hospital | Masuda H.,Nishi Niigata Chuo National Hospital | Shirozu H.,Nishi Niigata Chuo National Hospital | Ito Y.,Nishi Niigata Chuo National Hospital | And 2 more authors.
Clinical Neurophysiology | Year: 2016

Objective: In patients with hemifacial spasm, stimulation of a branch of the affected facial nerve elicits an abnormal response in the muscles innervated by another branch. We tested the hypothesis that this anomaly results from lateral spread of impulses from one motor axon to another at the site of the nerve compression by the offending artery. Methods: In a preoperative study of 21 patients, we delivered a series of stimuli, in short increments, successively distally along the temporal branch of the facial nerve to record abnormal muscle responses from the orbicularis oculi and mentalis muscles. In intraoperative monitoring of 10 patients during microvascular decompression, we monitored propagating nerve action potentials with a handheld electrode placed on the facial nerve 3 mm distal to the vascular compression site. Results: With incremental shifts of stimulating points distally, the latency of abnormal muscle responses increased by 0.3 ± 0.1 ms/cm. This finding implicates the antidromic motor impulse as the trigger for lateral spread. The nerve action potentials recorded during surgery comprised the initial antidromic signal followed by one or more additional peaks. The latter immediately abated, together with abnormal muscle responses, after microvascular decompression. Thus, the secondary peaks must represent the orthodromic impulses generated by ephaptic transmission. An average inter-peak interval of 1.1 ms between the first and secondary peaks is consistent with the estimated conduction time from the stimulation point to the site of vascular compression but not to the facial nucleus and return. Conclusion: An abnormal muscle response results from lateral spread of impulses between motor axons at the site of vascular compression rather than at the facial nucleus. Significance: This study establishes the mechanism of lateral spread responsible for abnormal muscle responses and contributes to the understanding of pathophysiology underlying hemifacial spasm. © 2016 International Federation of Clinical Neurophysiology.

Nakashima M.,Yokohama City University | Saitsu H.,Yokohama City University | Takei N.,Niigata University | Tohyama J.,Nishi Niigata Chuo National Hospital | And 16 more authors.
Annals of Neurology | Year: 2015

Objective: Focal cortical dysplasia (FCD) type IIb is a cortical malformation characterized by cortical architectural abnormalities, dysmorphic neurons, and balloon cells. It has been suggested that FCDs are caused by somatic mutations in cells in the developing brain. Here, we explore the possible involvement of somatic mutations in FCD type IIb. Methods: We collected a total of 24 blood-brain paired samples with FCD, including 13 individuals with FCD type IIb, 5 with type IIa, and 6 with type I. We performed whole-exome sequencing using paired samples from 9 of the FCD type IIb subjects. Somatic MTOR mutations were identified and further investigated using all 24 paired samples by deep sequencing of the entire gene's coding region. Somatic MTOR mutations were confirmed by droplet digital polymerase chain reaction. The effect of MTOR mutations on mammalian target of rapamycin (mTOR) kinase signaling was evaluated by immunohistochemistry and Western blotting analyses of brain samples and by in vitro transfection experiments. Results: We identified four lesion-specific somatic MTOR mutations in 6 of 13 (46%) individuals with FCD type IIb showing mutant allele rates of 1.11% to 9.31%. Functional analyses showed that phosphorylation of ribosomal protein S6 in FCD type IIb brain tissues with MTOR mutations was clearly elevated, compared to control samples. Transfection of any of the four MTOR mutants into HEK293T cells led to elevated phosphorylation of 4EBP, the direct target of mTOR kinase. Interpretation: We found low-prevalence somatic mutations in MTOR in FCD type IIb, indicating that activating somatic mutations in MTOR cause FCD type IIb. © 2015 American Neurological Association.

Watanabe T.,Nishi Niigata Chuo National Hospital
Kyobu geka. The Japanese journal of thoracic surgery | Year: 2010

Of 897 patients who underwent operation for lung cancer between April 1996 and March 2010, 57 patients underwent pulmonary resection for 2nd primary lung cancer. There were 44 men and 13 women. The average age at the 2nd operation was 71. The initial pulmonary resection was lobectomy in 49 patients, segmentectomy in 4 and wedge resection in 4. The 2nd pulmonary resection was lobectomy in 10 patients, segmentectomy in 12 and wedge resection in 35. Preoperative stage of the 2nd primary lung cancer was IA in 43, IB in 13 and IIB in 1. Postoperative stage was IA in 38, IB in 10, IIA in 1, IIB in 3, IIIA in 2 and IIIB in 3. Surgical complications occurred in 4, but there were no perioperative deaths. The 5-year survival rate for 2nd primary lung cancers was 59.9%. The 5-year survival rate for patients treated with wedge resection was 71.1%. The 5-year survival rate of the patients with p-stage IA was 72.7%, and that for patients with p-stage IB or more advanced diseases was 32.9%. We conclude that an aggressive surgical approach for a 2nd primary lung cancer is effective and is linked with good outcome if the tumor is detected at stage IA, when the possible cure by performing wedge resection is promissing.

Loading Nishi Niigata Chuo National Hospital collaborators
Loading Nishi Niigata Chuo National Hospital collaborators