SAMUKAWA Makoto
Department of Medicine | Lecturer |
Last Updated :2024/12/04
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J-Global ID
Research Keyword
- Migraine Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Guillain-Barré syndrome Myasthenia Gravis
■Career
Career
- 2018/04 - Today Kindai University HospitalDepartment of NeurologyAssistant professor
- 2015/04 - 2018/03 Kindai University HospitalDepartment of Neurologyassistant professor
- 2014/04 - 2015/03 Kindai University HospitalDepartment of Neurologyassistant professor
- 2009/03 - 2010/04 Kindai University HospitalDepartment of Neurologyassistant professor
- 2007/04 - 2009/03 Kindai University Hospital総合医学教育研修センター初期臨床研修医
Educational Background
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■Research activity information
Award
- 2021/10 日本神経摂食嚥下・栄養学会学術集会 第16・17回日本神経摂食嚥下・栄養学会学術集会優秀演題賞
- 2017/07 近畿大学医学会 近畿大学医学会賞
Electrophysiological assessment of Guillain-Barré syndrome with both Gal-C and ganglioside antibodies; tendency for demyelinating type受賞者: 寒川 真 - 2015/07 近畿大学医学会 Kinki daigaku igakukaisho
Clinical features in Guillain-Barré syndrome with anti-Gal-C antibody受賞者: Makoto Samukawa - 2013/11 The Japanese Society for Neuroimmunology Best Poster Award of The 25th Annual Meeting of the Japanese Society fo Neuroimmunology
JPN international_society受賞者: Makoto Samukawa - 2013/07 近畿大学医学会 Kinki daigaku igakukaisho
A Case of Severe Neurotoxicity Associated With Exposure to 1-Bromopropane, an Alternative to Ozone-Depleting or Global-Warming Solvents受賞者: Makoto Samukawa
Paper
- Takamichi Sugimoto; Shigeaki Suzuki; Akiyuki Uzawa; Takemori Yamawaki; Masayuki Masuda; Naoya Minami; Naoki Kawaguchi; Tomoya Kubota; Masanori P Takahashi; Yasushi Suzuki; Genya Watanabe; Shingo Konno; Takashi Kimura; Makoto Samukawa; Kei Ishizuchi; Hiroyuki Akamine; Yosuke Onishi; Manato Yasuda; Yuriko Nagane; Hirofumi Maruyama; Hiroyuki Murai; Kimiaki UtsugisawaJournal of the neurological sciences 464 123154 - 123154 2024/07INTRODUCTION/AIMS: The common presentations of statin intolerance are muscle-specific symptoms. Although statins are one type of drug reported to cause myasthenic worsening, myasthenic worsening has not been recognized as statin intolerance. The purpose of the present study is to investigate in a large cohort the safety profiles of statins in patients with myasthenia gravis (MG). METHODS: A total of 1710 consecutive patients with MG who visited sites associated with the Japan MG registry 2021 group between April and October 2021 were reviewed. Statin-associated myasthenic worsening was defined as worsening of any myasthenic symptoms on statin use and improvement of the symptom by stopping the statin or by undertaking additional treatment with patient and doctor confirmation. RESULTS: Among the 400 patients who used statins, 8 (2%) patients experienced statin intolerance and 6 (1.5%) patients experienced myasthenic worsening. No patients developed MG on the statin. Ptosis was a main symptom of myasthenic worsening in 4 (67%) patients. Atorvastatin was used in all patients with statin-associated myasthenic worsening. The symptoms of statin intolerance and statin-associated myasthenic worsening were improved within 2 months and 3 months, respectively, in all patients by cessation of statin use. DISCUSSION: Regarding statin-associated myasthenic worsening, prevalence was low, and severity was mild; with cessation of statin use, symptoms improved within a few months, and outcomes were generally good. Although statins can be used in MG patients with little concern, statin-associated myasthenic worsening should be noted in addition to the classical statin intolerance associated with statin use.
- Shigeaki Suzuki; Akiyuki Uzawa; Yuriko Nagane; Masayuki Masuda; Shingo Konno; Tomoya Kubota; Makoto Samukawa; Kei Ishizuchi; Daiki Tokuyasu; Hideo Handa; Manato Yasuda; Naoki Kawaguchi; Takashi Kimura; Yasushi Suzuki; Takamichi Sugimoto; Naoya Minami; Masanori P Takahashi; Hiroyuki Murai; Kimiaki UtsugisawaNeurology. Clinical practice 14 (3) e200276 2024/06BACKGROUND AND OBJECTIVES: Efgartigimod, which has been well tolerated and efficacious in individuals with generalized myasthenia gravis (MG), is available in Japan not only for the treatment of anti-acetylcholine receptor-positive (AChR+) but also anti-muscle-specific receptor tyrosine kinase (MuSK+) and seronegative generalized MG. We report details of the use of efgartigimod for generalized MG in clinical practice in Japan. METHODS: We included patients with generalized MG in the 2021 survey of Japan Myasthenia Gravis Registry (JAMG-R) study group who received an initial cycle of efgartigimod between May and September 2022. We defined "responders" as patients who achieved a score ≥2 points for MG activities of daily living (MG-ADL) in the first treatment cycle. The MG composite and the Revised scale of the 15-item Myasthenia Gravis-Quality of Life scale (MG-QOL15-r) were also evaluated. RESULTS: Of 1,343 JAMG-R patients, 36 (2.7%) started efgartigimod (female 68%, age 53 years). Their serologic profiles were as follows: AChR+, n = 19 (53%); MuSK+, n = 6 (17%); and seronegative, n = 11 (31%). Twenty-six patients (72%) had refractory MG. There were 81 cycles of efgartigimod during the 26-week observation in 34 patients (average, 2.4 cycles). The mean interval between cycles was 5.9 weeks. A continuous 4-weekly infusion of efgartigimod was performed in 65 (80%) of 81 cycles. In the first cycle, the MG-ADL score of the 34 patients decreased significantly from 10.5 ± 4.3 to 6.9 ± 5.1 (p = 0.003). Similarly, the mean MG composite and MG-QOL15-r decreased from 18.4 ± 13.6 to 11.8 ± 9.6 (p = 0.004) and from 19.2 ± 6.3 to 14.2 ± 8.3 (p = 0.007), respectively. Twenty-one (62%) patients were responders. Therapeutic responses were observed in the subsequent cycles. The duration of effectiveness of efgartigimod was varied among the responders; 4 responders had only a single effective cycle. Significant improvement was observed in the MuSK+ patients. Prednisolone dose of 7 patients was reduced. Our examination of the patients' postintervention status revealed that 6 patients achieved minimal manifestations. COVID-19 occurred in 5 patients. We failed to detect clinical or laboratory findings associated with responders. DISCUSSION: Efgartigimod can be considered for the treatment of patients with generalized MG who do not achieve minimal manifestations, with a broad flexibility of patient selection and treatment schedules.
- Akiyuki Uzawa; Shigeaki Suzuki; Satoshi Kuwabara; Hiroyuki Akamine; Yosuke Onishi; Manato Yasuda; Yukiko Ozawa; Naoki Kawaguchi; Tomoya Kubota; Masanori P Takahashi; Yasushi Suzuki; Genya Watanabe; Takashi Kimura; Takamichi Sugimoto; Makoto Samukawa; Naoya Minami; Masayuki Masuda; Shingo Konno; Yuriko Nagane; Kimiaki UtsugisawaBMC neurology 24 (1) 139 - 139 2024/04 [Refereed]
BACKGROUND: Non-motor symptoms in myasthenia gravis (MG) are rarely confirmed. Although there are some small cohort studies, a large-systemic survey has not yet been performed. METHODS: We investigated the incidence and clinical characteristics of patients with MG who had taste disorders and alopecia using data of 1710 patients with MG enrolled in the Japan MG Registry 2021. RESULTS: Among them, 104 (6.1%) out of 1692 patients and 138 (8.2%) out of 1688 patients had histories of taste disorders and alopecia, respectively. Among the patients with MG, taste disorders were significantly more common in women, those with severe symptoms, refractory MG, or thymoma-associated MG, and were less common in those with ocular MG. The taste disorders often occurred after the onset of MG and often responded to MG treatments. Alopecia was more common in MG patients with a history of bulbar palsy and thymoma, and it often occurred before the onset of MG and sometimes responded to MG treatments. Multivariate logistic regression analysis revealed taste disturbance was associated with worst quantitative MG score and thymoma-associated MG; and alopecia was associated with thymoma-associated MG. CONCLUSION: Clinicians should be aware of the non-motor symptoms in MG, especially in patients with severe myasthenic symptoms and thymoma-associated MG. - Daiki Tokuyasu; Shigeaki Suzuki; Akiyuki Uzawa; Yuriko Nagane; Masayuki Masuda; Shingo Konno; Tomoya Kubota; Makoto Samukawa; Takamichi Sugimoto; Kei Ishizuchi; Munenori Oyama; Manato Yasuda; Hiroyuki Akamine; Yosuke Onishi; Yasushi Suzuki; Naoki Kawaguchi; Naoya Minami; Takashi Kimura; Masanori P Takahashi; Hiroyuki Murai; Kimiaki UtsugisawaAnnals of clinical and translational neurology 2024/04OBJECTIVE: Eculizumab and ravulizumab are complement protein C5 inhibitors, showing efficacy and tolerability for patients with anti-acetylcholine receptor-positive (AChR+) generalized myasthenia gravis (gMG) in phase 3 clinical trials and subsequent analyses. The purpose of the present study was to evaluate the clinical significance of eculizumab and switching to ravulizumab for refractory AChR+ gMG patients in the real-world experience. METHODS: Among the database of Japan MG registry survey 2021, we studied AChR+ gMG patients who received eculizumab. We also evaluated these patients who switched from eculizumab to ravulizumab. Responder was defined as an improvement of at least 3 points in MG-ADL. We performed a questionnaire of preference between eculizumab and ravulizumab. RESULTS: Among 1,106 patients with AChR+ gMG, 36 patients (3%) received eculizumab (female 78%, mean age 56.0 years). Eculizumab was preferentially used in severe and refractory MG patients. The duration of eculizumab treatment was 35 months on average. MG-ADL improved from 9.4 ± 4.9 to 5.9 ± 5.1, and 25 (70%) of the 36 gMG patients were responders. Postintervention status was markedly improved after the eculizumab treatment. Of 13 patients who did not continue eculizumab, 6 showed insufficiencies. Early onset MG was most effective. However, 15 patients switching from eculizumab to ravulizumab kept favorable response and tolerability. Questionnaire surveys showed preference for ravulizumab over eculizumab. INTERPRETATION: Eculizumab and switching to ravulizumab showed to be effective for refractory AChR+ gMG patients in clinical settings.
- Atsushi Terayama; Motoi Kuwahara; Keisuke Yoshikawa; Yuko Yamagishi; Makoto Samukawa; Shoko Yamashita; Kyohei Onishi; Tomoya Nagano; Chikao Tatsumi; Junko Ishii; Michi Kawamoto; Takashi Tokashiki; Shoko Deguchi; Kentaro Deguchi; Atsushi Ishida; Yasuhiko Baba; Shigeki Yamaguchi; Susumu Kusunoki; Yoshitaka NagaiJournal of neurology 2024/04BACKGROUND AND PURPOSE: Takotsubo cardiomyopathy (TCM) is a serious autonomic complication of Guillain-Barré syndrome (GBS). However, the association between TCM and GBS has not been investigated in detail. We investigated the characteristics of GBS patients with TCM (GBS-TCM). METHODS: Clinical features and anti-ganglioside antibody between the GBS-TCM patients and 62 classical GBS patients without TCM as control patients were compared. RESULTS: Eight GBS-TCM patients were identified, in whom TCM was diagnosed at a mean of 6.5 [range 3-42] days after the onset of GBS. The age at onset of GBS was elder in the GBS-TCM patients than in the control GBS patients (76.5 [56-87] vs. 52 [20-88] years, p < 0.01). Notably, cranial nerve deficits, particularly in the lower cranial nerves, were observed in all GBS-TCM patients (100% vs. 41.9%, p < 0.01). Additionally, the GBS-TCM patients showed a higher GBS disability score at nadir (5 [4-5] vs. 4 [1-5], p < 0.01), and lower Medical Research Council sum scores at admission and nadir (37 [30-44] vs. 48 [12-60] at admission, p < 0.05, and 20 [12-44] vs. 40 [0-60] at nadir, p < 0.05, respectively). Mechanical ventilation was more frequently required in the GBS-TCM patients (62.5% vs. 11.3%, p < 0.01). Three GBS-TCM patients were positive for anti-ganglioside antibodies. CONCLUSIONS: TCM occurred at a relatively early phase of GBS. The characteristics of GBS-TCM were the elder, lower cranial nerve involvements, severe limb weakness, and respiratory failure.
- Hirano M.; Samukawa M.; Isono C.; Kusunoki S.; Nagai Y.Heliyon. 12 (10) e23407 - e23407 2024/01 [Refereed]
- Manato Yasuda; Akiyuki Uzawa; Satoshi Kuwabara; Shigeaki Suzuki; Hiroyuki Akamine; Yosuke Onishi; Yukiko Ozawa; Naoki Kawaguchi; Tomoya Kubota; Masanori P Takahashi; Yasushi Suzuki; Genya Watanabe; Takashi Kimura; Takamichi Sugimoto; Makoto Samukawa; Naoya Minami; Masayuki Masuda; Shingo Konno; Yuriko Nagane; Kimiaki UtsugisawaJournal of neuroimmunology 385 578241 - 578241 2023/11 [Refereed]
This study included 51 patients with muscle-specific kinase antibody-positive myasthenia gravis (MuSK-MG) from a Japanese multicenter survey to examine clinical features and outcomes. Median onset age was 37 years and female predominance was observed. All patients developed generalized symptoms and almost all (50/51) patients had bulbar symptoms. About half of the patients met the criteria for refractory MG. The refractory group had a lower age of onset, higher severity scores, and higher maximum daily doses of oral prednisolone compared to the nonrefractory group. The outcomes for MuSK-MG patients in Japan are not favorable, indicating the need for more aggressive treatment. - Makito Hirano; Motoi Kuwahara; Yuko Yamagishi; Makoto Samukawa; Kanako Fujii; Shoko Yamashita; Masahiro Ando; Nobuyuki Oka; Mamoru Nagano; Taro Matsui; Toshihide Takeuchi; Kazumasa Saigoh; Susumu Kusunoki; Hiroshi Takashima; Yoshitaka NagaiScientific reports 13 (1) 17801 - 17801 2023/10Cerebellar ataxia, neuropathy, and vestibular areflexia syndrome (CANVAS) has recently been attributed to biallelic repeat expansions in RFC1. More recently, the disease entity has expanded to atypical phenotypes, including chronic neuropathy without cerebellar ataxia or vestibular areflexia. Very recently, RFC1 expansions were found in patients with Sjögren syndrome who had neuropathy that did not respond to immunotherapy. In this study RFC1 was examined in 240 patients with acute or chronic neuropathies, including 105 with Guillain-Barré syndrome or Miller Fisher syndrome, 76 with chronic inflammatory demyelinating polyneuropathy, and 59 with other types of chronic neuropathy. Biallelic RFC1 mutations were found in three patients with immune-mediated neuropathies, including Guillain-Barré syndrome, idiopathic sensory ataxic neuropathy, or anti-myelin-associated glycoprotein (MAG) neuropathy, who responded to immunotherapies. In addition, a patient with chronic sensory autonomic neuropathy had biallelic mutations, and subclinical changes in Schwann cells on nerve biopsy. In summary, we found CANVAS-related RFC1 mutations in patients with treatable immune-mediated neuropathy or demyelinating neuropathy.
- Kazumasa Saigoh; Makito Hirano; Yoshiyuki Mitsui; Itsuki Oda; Atsuko Ikegawa; Makoto Samukawa; Keisuke Yoshikawa; Yuko Yamagishi; Susumu Kusunoki; Yoshitaka NagaiJournal of medical case reports 17 (1) 431 - 431 2023/10BACKGROUND: Huntington's disease is an autosomal dominant inherited disorder characterized by personality changes (such as irritability and restlessness) and psychotic symptoms (such as hallucinations and delusions). When the personality changes become noticeable, involuntary movements (chorea) also develop. The disease is caused by the CAG repeat expansion in the coding region of the HTT gene, and the diagnosis is based on the presence of this expansion. However, there is currently no effective treatment for the progression of Huntington's disease and its involuntary motor symptoms. Herein, we present a case in which memantine was effective in treating the chorea movements of Huntington's disease. CASE PRESENTATION: A 75-year-old Japanese woman presented to the hospital with involuntary movements of Huntington's disease that began when she was 73 years old. In a cerebral blood flow test (N-isopropyl-p-iodoamphetamine-single-photon emission computed tomography), decreased blood flow was observed in the precuneus (anterior wedge) and posterior cingulate gyrus. Usually, such areas of decreased blood flow are observed in patients with Alzheimer's-type dementia. So, we administered memantine for Alzheimer's-type dementia, and this treatment suppressed the involuntary movements of Huntington's disease, and the symptoms progressed slowly for 7 years after the onset of senility. In contrast, her brother died of complications of pneumonia during the course of Huntington's disease. CONCLUSIONS: We recorded changes in parameters such as the results of the N-isopropyl-p-iodoamphetamine-single-photon emission computed tomography and gait videos over 7 years. Treatment with memantine prevented the chorea movement and the progression of Huntington's disease. We believe this record will provide clinicians with valuable information in diagnosing and treating Huntington's disease.
- 鈴木 重明; 鵜沢 顕之; 長根 百合子; 増田 眞之; 紺野 晋吾; 久保田 智哉; 寒川 真; 石鎚 啓; 徳安 大樹; 半田 秀雄; 安田 真人; 川口 直樹; 木村 卓; 高橋 正紀; 村井 弘之; 槍沢 公明神経治療学 (一社)日本神経治療学会 40 (6) S218 - S218 0916-8443 2023/10
- 重症筋無力症における胸腺外悪性腫瘍の合併と免疫チェックポイント阻害薬使用例の検討吉積 一樹; 渡邊 将平; 木村 卓; 久保田 智哉; 鵜沢 顕之; 川口 直樹; 増田 眞之; 紺野 晋吾; 南 尚哉; 寒川 真; 渡辺 源也; 鈴木 靖士; 長根 百合子; 高橋 正紀; 鈴木 重明; 槍澤 公明臨床神経学 (一社)日本神経学会 63 (Suppl.) S251 - S251 0009-918X 2023/09
- Akiyuki Uzawa; Shigeaki Suzuki; Satoshi Kuwabara; Hiroyuki Akamine; Yosuke Onishi; Manato Yasuda; Yukiko Ozawa; Naoki Kawaguchi; Tomoya Kubota; Masanori P Takahashi; Yasushi Suzuki; Genya Watanabe; Takashi Kimura; Takamichi Sugimoto; Makoto Samukawa; Naoya Minami; Masayuki Masuda; Shingo Konno; Yuriko Nagane; Kimiaki UtsugisawaJournal of neurology, neurosurgery, and psychiatry BMJ PUBLISHING GROUP 94 (6) 467 - 473 0022-3050 2023/01BACKGROUND: Early fast-acting treatment (EFT) is the aggressive use of fast-acting therapies such as plasmapheresis, intravenous immunoglobulin and/or intravenous high-dose methylprednisolone (IVMP) from the early phases of treatment. EFT is reportedly beneficial for early achievement of minimal manifestations (MM) or better status with ≤5 mg/day prednisolone (MM5mg), a practical therapeutic target for myasthenia gravis (MG). OBJECTIVE: The current study aimed to clarify which specific EFT regimen is efficacious and the patient characteristics that confer sensitivity to EFT. METHODS: We recruited a total of 1710 consecutive patients with MG who enrolled in the Japan MG Registry for this large-cohort study. Among them, 1066 with generalised MG who had received immunotherapy were analysed. Prognostic background factors were matched in a 1:1 ratio using propensity score matching analysis between patients treated with EFT (n=350) and those treated without EFT (n=350). The clinical course and time to first achieve MM5mg after starting immunotherapy was analysed in relation to treatment combinations and patient characteristics. RESULTS: Kaplan-Meier analyses showed that EFT had a significant effect on the achievement of MM5mg (p<0.0001, log-rank test; HR 1.82, p<0.0001). Notably, EFT was efficacious for any type of MG, and the inclusion of IVMP resulted in earlier and more frequent achievement of MM5mg (p=0.0352, log-rank test; HR 1.46, p=0.0380). In addition, early administration of calcineurin inhibitors also promoted MM5mg achievement. CONCLUSION: Early cycles of intervention with EFT and early use of calcineurin inhibitors provides long-term benefits in terms of achieving therapeutic targets for generalised MG, regardless of clinical subtype.
- Akiyuki Uzawa; Shigeaki Suzuki; Satoshi Kuwabara; Hiroyuki Akamine; Yosuke Onishi; Manato Yasuda; Yukiko Ozawa; Naoki Kawaguchi; Tomoya Kubota; Masanori P Takahashi; Yasushi Suzuki; Genya Watanabe; Takashi Kimura; Takamichi Sugimoto; Makoto Samukawa; Naoya Minami; Masayuki Masuda; Shingo Konno; Yuriko Nagane; Kimiaki UtsugisawaNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics SPRINGER 20 (2) 518 - 523 1933-7213 2023/01The efficacy of intravenous high-dose methylprednisolone (IVMP) in ocular myasthenia gravis (MG) has not been fully established. This study aimed to elucidate the effects of early intervention with IVMP for achieving the therapeutic targets (minimal manifestations [MM] or MM or better status with prednisolone ≤ 5 mg/day [MM5mg]) in ocular MG. In this observational study, we included a total of 1710 consecutive patients with MG enrolled in the Japan MG Registry in 2021. Of these, 204 patients with ocular MG who received immunotherapy were analyzed. The clinical course and time to first achieve MM or MM5mg after starting immunotherapy were compared between the early IVMP group (treated with IVMP within 3 months of treatment initiation) and the non-early IVMP group. Despite having greater clinical severity before immunotherapy and lower oral prednisolone doses throughout the course, the early IVMP group (n = 55) showed a higher rate of achievement of MM (P = 0.0040, log-rank test; hazard ratio 1.58, 95% confidence interval [CI] 1.13-2.20, P < 0.0001) and MM5mg (P = 0.0005, log-rank test; hazard ratio 1.78, 95% CI 1.27-2.51, P < 0.0001) compared with the non-early IVMP group (n = 149). In conclusion, an early intervention with IVMP is likely to increase the probability of achieving a better long-term outcome and reducing the total dose of corticosteroids in ocular MG.
- MG1 Japan MG registry 2021におけるスタチン不耐の検討杉本 太路; 鈴木 重明; 鵜沢 顕之; 山脇 健盛; 増田 眞之; 南 尚哉; 川口 直樹; 久保田 智哉; 高橋 正紀; 鈴木 靖士; 渡辺 源也; 紺野 晋吾; 木村 卓; 寒川 真; 石鎚 啓; 赤嶺 博行; 大西 庸介; 安田 真人; 長根 百合子; 槍澤 公明神経免疫学 (一社)日本神経免疫学会 27 (1) 133 - 133 0918-936X 2022/10
- SCA8関連筋萎縮性側索硬化症の表現型変異と治療戦略(Phenotypic variation and therapeutic strategy of SCA8-associated amyotrophic lateral sclerosis)Hirano Makito; Takehara Toshiyuki; Murayama Shigeo; Izumi Yuishin; Samukawa Makoto; Matsubara Tomoyasu; Saito Yuko; Saigoh Kazumasa; Nakamura Yusaku; Fukuda Kanji; Kusunoki Susumu; Nagai Yoshitaka臨床神経学 (一社)日本神経学会 62 (Suppl.) S216 - S216 0009-918X 2022/10
- 平野 牧人; 竹原 俊幸; 村山 繁雄; 和泉 唯信; 寒川 真; 松原 知康; 斎藤 祐子; 西郷 和真; 中村 雄作; 楠 進; 永井 義隆神経治療学 (一社)日本神経治療学会 39 (6) S232 - S232 0916-8443 2022/10
- 平野 牧人; 竹原 俊幸; 村山 繁雄; 和泉 唯信; 寒川 真; 松原 知康; 斎藤 祐子; 西郷 和真; 中村 雄作; 楠 進; 永井 義隆神経治療学 (一社)日本神経治療学会 39 (6) S232 - S232 0916-8443 2022/10
- Shigeaki Suzuki; Masayuki Masuda; Akiyuki Uzawa; Yuriko Nagane; Shingo Konno; Yasushi Suzuki; Tomoya Kubota; Takamichi Sugimoto; Makoto Samukawa; Genya Watanabe; Kei Ishizuchi; Hiroyuki Akamine; Yosuke Onishi; Kazuki Yoshizumi; Takafumi Uchi; Itaru Amino; Yuki Ueta; Naoya Minami; Naoki Kawaguchi; Takashi Kimura; Masanori P. Takahashi; Hiroyuki Murai; Kimiaki UtsugisawaClinical and Experimental Neuroimmunology Wiley 1759-1961 2022/10
- Ituki Oda; Daisuke Danno; Kazumasa Saigoh; Johanna Wolf; Norihito Kawashita; Makito Hirano; Makoto Samukawa; Shigekazu Kitamura; Shoji Kikui; Takao Takeshima; Yoshiyuki Mitsui; Susumu Kusunoki; Yoshitaka NagaiNeuroscience research 2022/03We analyzed the clinical symptoms of hemiplegic migraine (HM) and their relevance in four Japanese patients considered to have ATP1A2 mutations as a cause. Sequencing of ATP1A2 was performed using the Sanger method in 43 blood samples from clinically suspected patients with familial HM. Subsequently, algorithm analysis, allele frequency determination, and three-dimensional structure analysis of the recognized variants were performed, and the recognized variants were evaluated. We found four heterozygous missense mutations in ATP1A2 (Case 1: p.R51C; Case 2: p.R65L; Case 3: p.A269P; Case 4: p.D999H), three of which had not been reported to date. These four mutations may also affect the structure of the protein products, as assessed using a three-dimensional structural analysis. In all four cases, the clinical symptoms included visual, sensory, motor, and verbal symptoms and the frequency and duration of headache attacks varied. Additionally, oral administration of a combination of lomerizine hydrochloride and topiramate had a partial effect in three cases. We report four missense mutations in ATP1A2. This report will be useful for the future analysis of mutations and clinical types in Asians, as well as Westerners, with migraine.
- MELASにおける上腸間膜動脈症候群寒川 真; 桑原 基; 西郷 和真; 三井 良之; 楠 進臨床神経学 (一社)日本神経学会 61 (Suppl.) S297 - S297 0009-918X 2021/09
- Rino Inada; Makito Hirano; Nobuyuki Oka; Makoto Samukawa; Kazumasa Saigoh; Hidekazu Suzuki; Fukashi Udaka; Akihiro Hashiguchi; Hiroshi Takashima; Yukihiro Hamada; Yusaku Nakamura; Susumu KusunokiJournal of neurology 268 (8) 2933 - 2942 2021/08BACKGROUND: We intended to clarify the phenotypic and molecular diversities of spinocerebellar ataxia type 2 (SCA2) in Japan. METHODS: DNA was extracted from the peripheral blood of 436 patients, including 126 patients with chronic neuropathy, 108 with amyotrophic lateral sclerosis, and 202 with cerebellar ataxia. We then PCR-amplified and sequenced the ATXN2 gene. The biopsied sural nerves of mutation-positive patients were subjected to light-microscopic and electron-microscopic analyses. Transfection analyses were performed using a Schwann cell line, IMS32. RESULTS: We found PCR-amplified products potentially corresponding to expanded CAG repeats in four patients. Two patients in the chronic neuropathy group had a full repeat expansion or an intermediate expansion (39 or 32 repeats), without limb ataxia. The sural nerve biopsy findings of the two patients included axonal neuropathy and mixed neuropathy (axonal changes with demyelination). Schwann cells harbored either cytoplasmic or nuclear inclusions on electron microscopic examination. Both patients recently exhibited pyramidal signs. In the third patient in the cerebellar ataxia group, we identified a novel 21-base duplication mutation near 22 CAG repeats (c.432_452dup). The transfection study revealed that the 21-base-duplication mutant Ataxin-2 proteins aggregated in IMS32 and rendered cells susceptible to oxidative stress, similar to a CAG-expanded mutant. The fourth patient, with 41 repeats, had ataxia and spasticity. The two patients with cerebellar ataxia also had peripheral neuropathy. CONCLUSIONS: Patients with expanded CAG repeats can exhibit a neuropathy-dominant phenotype not described previously. The novel 21-base-duplication mutant seems to share the aggregation properties of polyglutamine-expanded mutants.
- James F. Howard; Vera Bril; Tuan Vu; Chafic Karam; Stojan Peric; Temur Margania; Hiroyuki Murai; Malgorzata Bilinska; Roman Shakarishvili; Marek Smilowski; Antonio Guglietta; Peter Ulrichts; Tony Vangeneugden; Kimiaki Utsugisawa; Jan Verschuuren; Renato Mantegazza; Jan De Bleeker; Kathy De Koning; Katrien De Mey; Annelien De Pue; Rudolf Mercelis; Maren Wyckmans; Caroline Vinck; Linda Wagemaekers; Jonathan Baets; Eduardo Ng; Jafar Shabanpour; Lubna Daniyal; Shabber Mannan; Hans Katzberg; Angela Genge; Zaeem Siddiqi; Jana Junkerová; Jana Horakova; Katerina Reguliova; Michaela Tyblova; Ivana Jurajdova; Iveta Novakova; Michala Jakubikova; Jiri Pitha; Stanislav Vohanka; Katerina Havelkova; Tomas Horak; Josef Bednarik; Mageda Horakova; Andreas Meisel; Dike Remstedt; Claudia Heibutzki; Siegfried Kohler; Sarah Hoffman; Frauke Stascheit; John Vissing; Lizzie Zafirakos; Kuldeep Kumar Khatri; Anne Autzen; Mads Peter Godtfeldt Stemmerik; Henning Andersen; Shahram Attarian; Alexander Tsiskaridze; Csilla Rózsa; Gedeonne Margo Jakab; Szilvia Toth; Gyorgyi Szabo; David Bors; Eniko Szabo; Angela Campanella; Fiammetta Vanoli; Rita Frangiamore; Carlo Antozzi; Silvia Bonanno; Lorenzo Maggi; Riccardo Giossi; Francesco Saccà; Angela Marsili; Tiziana Imbriglio; Giovanni Antonini; Girolamo Alfieri; Stefania Morino; Matteo Garibaldi; Laura Fionda; Luca Leonardi; Shingo Konno; Akiyuki Uzawa; Kaoru Sakuma; Chiho Watanabe; Yukiko Ozawa; Manato Yasuda; Yosuke Onishi; Makoto Samukawa; Tomoko Tsuda; Yasushi Suzuki; Sayaka Ishida; Genya Watanabe; Masanori Takahashi; Hiroko Nakamura; Erina Sugano; Tomoya Kubota; Tomihiro Imai; Suzuki Mari; Ayako MoriThe Lancet Neurology 20 (7) 526 - 536 1474-4422 2021/07Background: There is an unmet need for treatment options for generalised myasthenia gravis that are effective, targeted, well tolerated, and can be used in a broad population of patients. We aimed to assess the safety and efficacy of efgartigimod (ARGX-113), a human IgG1 antibody Fc fragment engineered to reduce pathogenic IgG autoantibody levels, in patients with generalised myasthenia gravis. Methods: ADAPT was a randomised, double-blind, placebo-controlled, phase 3 trial done at 56 neuromuscular academic and community centres in 15 countries in North America, Europe, and Japan. Patients aged at least 18 years with generalised myasthenia gravis were eligible to participate in the study, regardless of anti-acetylcholine receptor antibody status, if they had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (>50% non-ocular), and were on a stable dose of at least one treatment for generalised myasthenia gravis. Patients were randomly assigned by interactive response technology (1:1) to efgartigimod (10 mg/kg) or matching placebo, administered as four infusions per cycle (one infusion per week), repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle. Patients, investigators, and clinical site staff were all masked to treatment allocation. The primary endpoint was proportion of acetylcholine receptor antibody-positive patients who were MG-ADL responders (≥2-point MG-ADL improvement sustained for ≥4 weeks) in the first treatment cycle. The primary analysis was done in the modified intention-to-treat population of all acetylcholine receptor antibody-positive patients who had a valid baseline MG-ADL assessment and at least one post-baseline MG-ADL assessment. The safety analysis included all randomly assigned patients who received at least one dose or part dose of efgartigimod or placebo. This trial is registered at ClinicalTrials.gov (NCT03669588); an open-label extension is ongoing (ADAPT+, NCT03770403). Findings: Between Sept 5, 2018, and Nov 26, 2019, 167 patients (84 in the efgartigimod group and 83 in the placebo group) were enrolled, randomly assigned, and treated. 129 (77%) were acetylcholine receptor antibody-positive. Of these patients, more of those in the efgartigimod group were MG-ADL responders (44 [68%] of 65) in cycle 1 than in the placebo group (19 [30%] of 64), with an odds ratio of 4·95 (95% CI 2·21–11·53, p<0·0001). 65 (77%) of 84 patients in the efgartigimod group and 70 (84%) of 83 in the placebo group had treatment-emergent adverse events, with the most frequent being headache (efgartigimod 24 [29%] vs placebo 23 [28%]) and nasopharyngitis (efgartigimod ten [12%] vs placebo 15 [18%]). Four (5%) efgartigimod-treated patients and seven (8%) patients in the placebo group had a serious adverse event. Three patients in each treatment group (4%) discontinued treatment during the study. There were no deaths. Interpretation: Efgartigimod was well tolerated and efficacious in patients with generalised myasthenia gravis. The individualised dosing based on clinical response was a unique feature of ADAPT, and translation to clinical practice with longer term safety and efficacy data will be further informed by the ongoing open-label extension. Funding: argenx.
- 桑原 基; 福本 雄太; 吉川 恵輔; 寒川 真; 楠 進末梢神経 日本末梢神経学会 31 (2) 286 - 286 0917-6772 2020/12
- 病理学的に確認されたATXN8OS関連筋萎縮性側索硬化症の最初の患者についての報告(The first patient with pathologically-definite ATXN8OS-associated amyotrophic lateral sclerosis)Hirano Makito; Murayama Shigeo; Izumi Yuishin; Samukawa Makoto; Matsubara Tomoyasu; Saigoh Kazumasa; Nakamura Yusaku; Kusunoki Susumu臨床神経学 (一社)日本神経学会 60 (Suppl.) S345 - S345 0009-918X 2020/11
- PNPLA2遺伝子関連中性脂肪蓄積病の臨床像寒川 真; 中村 尚子; 平野 牧人; 森川 みゆき; 坂田 花美; 西野 一三; 井泉 瑠美子; 鈴木 直輝; 黒田 宙; 滋賀 健介; 青木 正志; 楠 進臨床神経学 (一社)日本神経学会 60 (Suppl.) S388 - S388 0009-918X 2020/11
- 免疫チェックポイント阻害薬関連ニューロパチーの解析桑原 基; 福本 雄太; 吉川 恵輔; 寒川 真; 楠 進神経免疫学 (一社)日本神経免疫学会 25 (1) 163 - 163 0918-936X 2020/10
- 平野 牧人; 井上 貴美子; 伊藤 龍生; 寒川 真; 藤村 晴俊; 能勢 和宏; 楠 進; 中村 雄作神経治療学 (一社)日本神経治療学会 37 (6) S223 - S223 0916-8443 2020/10
- Makito Hirano; Chiharu Isono; Makoto Samukawa; Kanji Fukuda; Susumu KusunokiParkinsonism & related disorders 78 98 - 99 2020/09
- Makoto Samukawa; Naoko Nakamura; Makito Hirano; Miyuki Morikawa; Hanami Sakata; Ichizo Nishino; Rumiko Izumi; Naoki Suzuki; Hiroshi Kuroda; Kensuke Shiga; Kazumasa Saigoh; Masashi Aoki; Susumu KusunokiEuropean neurology 83 (3) 1 - 6 2020/06 [Refereed]
Mutations in the PNPLA2 gene cause neutral lipid storage disease with myopathy (NLSDM) or triglyceride deposit cardiomyovasculopathy. We report a detailed case study of a 53-year-old man with NLSDM. The PNPLA2 gene was analyzed according to the reported method. We summarized the clinical, laboratory, and genetic information of 56 patients, including our patient and 55 other reported patients with homozygous or compound heterozygous mutations in the PNPLA2 gene. We found a novel homozygous mutation (c.194delC) in the PNPLA2 gene that resulted in frameshift. The patient suffered from normal-tension glaucoma and pulmonary cysts, symptoms that are relatively common in the elderly but were not previously reported for this disease. Our summary confirmed that Jordan's anomaly, polymorphonuclear leukocytes with lipid accumulation, was the most consistent finding of this disease. Because this disease is potentially treatable, our results may help rapid and correct diagnosis. - 桑原 基; 吉川 恵輔; 森川 みゆき; 稲田 莉乃; 寒川 真; 平野 牧人; 楠 進末梢神経 日本末梢神経学会 30 (2) 335 - 335 0917-6772 2019/12
- 寒冷刺激による頭痛と生体温度変化について西郷 和真; 米島 康平; 木川 和弥; 稲垣 拓武; 長谷川 隆典; 寒川 真; 濱田 征宏; 市橋 珠里; 三井 良之; 楠 進日本頭痛学会誌 (一社)日本頭痛学会 46 (2) 486 - 486 1345-6547 2019/11
- 仲間美奈; 西郷和真; 平野牧人; 濱田征宏; 金城ちなつ; 寒川真; 長谷川隆典; 北口正孝; 三井良之; 巽純子; 田村和朗; 楠進日本遺伝カウンセリング学会誌 日本遺伝カウンセリング学会 40 (3) 95 - 100 1347-9628 2019/10 [Refereed]
脊髄小脳変性症(spinocerebellar ataxia:SCA)は特に小脳性の運動失調症状を主体とする神経変性疾患の総称で、孤発性と遺伝性に大別される。遺伝性SCAのうち90%以上が常染色体優性遺伝を示し、原因遺伝子や臨床的特徴の違いにより40以上もの病型に分類される。疾患頻度は集団により異なるが、比較的頻度の多いSCA31が同定された2009年以降に近畿圏の病型別頻度は調査されていない。本研究では、近畿大学病院脳神経内科にて得られたSCA症例をもとに、近畿圏の病型別頻度を調査したところ、遺伝性SCA80例のうちSCA6が最も頻度が高く44%、次いでMJD/SCA3が12%、SCA31が10%であった。そのほかSCA8、DRPLA、SCA2、SCA1、SCA23、SCA36が認められ、病型未確定は14%であった。本解析を通じて本疾患の遺伝子診断の意義、pre-mutationの取り扱いについて考察したので報告する。(著者抄録) - 高齢で発症した抗neurofascin155(NF155)抗体関連ニューロパチーの1例坂田 花美; 寒川 真; 定金 秀爾; 緒方 英紀; 桑原 基; 竹内 啓喜; 岡 伸幸; 吉良 潤一; 楠 進臨床神経学 (一社)日本神経学会 59 (4) 234 - 234 0009-918X 2019/04
- Charcot-Marie-Tooth disease with a mutation in FBLN5 accompanying with the small vasculitis and widespread onion-bulb formations.Yamagishi Y; Samukawa M; Kuwahara M; Takada K; Saigoh K; Mitsui Y; Oka N; Hashiguchi A; Takashima H; Kusunoki S.J Neurol Sci 410 116623 2019 [Refereed]
- Hirano M; Itoh T; Fujimura H; Inoue K; Samukawa M; Nose K; Sakamoto H; Maekura S; Ueno S; Satou T; Nishioka T; Kusunoki S; Nakamura YJ Neuropathol Exp Neurol. 2019 [Refereed]
Anti-N-methyl-d-aspartate receptor (anti-NMDAR) encephalitis is the most common type of autoimmune encephalitis. The disease predominantly affects women (1:5-1:10), with only 3 reports of autopsy findings in women being published to date. The present study reports findings from the first autopsy performed on a man with anti-NMDAR encephalitis. The patient had some scattered lesions in the limbic system with neuronal loss, gliosis, and microglial activation. The temporal and frontal cortices showed additional patchy demyelination. T-lymphocyte infiltration was detectable in the fusiform gyrus lesion. These findings were partly similar to those reported in female patients. Although clinical differences based on the sex of the patient are reported for this disease, the observed pathological similarities potentially help to establish common therapeutic strategies for all patients. Severe testicular damage was additionally observed in the male patient in this study. Biopsy-proven severe testicular damage was also confirmed in another, previously fertile man who became azoospermic. Moreover, serum follicle-stimulating hormone levels, which often increased in response to disturbed spermatogenesis, were elevated, and testosterone/luteinizing hormone ratio reflecting Leydig cell function was low in all 5 male patients in this study. Overall, these findings suggest similar brain pathology in patients of both sexes and severe testicular damage in male patients. - Yoshikawa K; Kuwahara M; Saigoh K; Ishiura H; Yamagishi Y; Hamano Y; Samukawa M; Suzuki H; Hirano M; Mitsui Y; Tsuji S; Kusunoki SeNeurologicalSci 14 34 - 37 2019 [Refereed]
Spastic paraplegia 30 is a recently established autosomal recessive disease characterized by a complex form of spastic paraplegia associated with neuropathy. Homozygous mutations of KIF1A reportedly lead to hereditary spastic paraplegia or hereditary sensory and autonomic neuropathy type 2 (HSAN2), whereas heterozygous mutations can cause nonsyndromic and syndromic intellectual disability (MRD9). Here we report the case of a 37-year-old female who presented with gait disturbance complicated with moyamoya disease. Results: The patient exhibited hypotonia during infancy, after which intellectual disability, epileptic fits, spastic paraplegia, and cerebellar atrophy occurred. Genetic analysis revealed a novel de novo mutation (c.254C > A, p.A85D) in the motor domain of KIF1A. - 口腔内寒冷刺激における体温変動について西郷 和真; 米島 康平; 長谷川 隆典; 濱田 征宏; 寒川 真; 市橋 珠里; 三井 良之; 楠 進日本頭痛学会誌 (一社)日本頭痛学会 45 (2) 422 - 422 1345-6547 2018/11
- Guillain-Barré症候群寒川 真; 楠 進Clinical Neuroscience (株)中外医学社 36 (9) 1035 - 1038 0289-0585 2018/09 [Refereed][Invited]
- Yuko Yamagishi; Kazumasa Saigoh; Yoshiro Saito; Ikuko Ogawa; Yoshiyuki Mitsui; Yukihiro Hamada; Makoto Samukawa; Hidekazu Suzuki; Motoi Kuwahara; Makito Hirano; Noriko Noguchi; Susumu KusunokiNeuroscience research 128 58 - 62 0168-0102 2018/03 [Refereed]
Parkinson's disease (PD) is difficult to distinguish from progressive supranuclear palsy (PSP) and multiple system atrophy (MSA); in addition, biomarker studies in PD mostly focused on those found in the cerebrospinal fluid, and there are few reports of simple biomarkers identified by blood analysis. Previously, the DJ-1 gene was identified as a causative gene of familial PD. Oxidized DJ-1 protein (oxDJ-1) levels were reported to increase in the blood of patients with unmedicated PD. Therefore, we determined the levels of oxDJ-1 in the erythrocytes of patients with PD, PSP, and MSA using ELISA. The oxDJ-1 levels were 165±117, 96±78, and 69±40ng/mg protein in the PD, PSP, and MSA groups, respectively. The mean level in disease control group was 66±31, revealing significant differences between the PD and PSP groups, the PD and MSA groups, and the PD and disease control groups. Our results indicated that oxDJ-1 levels in erythrocytes can be used as a marker for the differential diagnosis of PD. - 森口幸太; 西郷和真; 山下翔子; 定金秀爾; 柳本諭志; 稲田莉乃; 岡崎真央; 寒川真; 鈴木秀和; 平野牧人; 三井良之; 楠 進大阪てんかん研究会雑誌 大阪てんかん研究会 29 (1) 7 - 9 0918-9319 2018 [Refereed]
ペランパネル(PER)を投与した難治性てんかん8例(男性4例、女性4例、平均45.5歳)を対象とした。知的能力障害を伴った症例が4例あり、幼少期からてんかん発作を認めた。比較的高齢使用例の2例は、特発性血小板減少性紫斑病や、多発血管炎性肉芽腫症を合併した。抗てんかん薬(AED)は、PERを含めて2~4剤(平均3.1剤)であった。併用AEDとして使用されていたのは、バルプロ酸(VPA)4例、レベチラセタム(LEV)3例、ラモトリギン(LTG)3例、カルバマゼピン(CBZ)3例、ゾニサミド(ZNS)2例、ラコサミド(LCM)1例、ガバペンチン(GBP)1例であった。知的能力障害を伴う2例は焦燥感、興奮性等の症状により投与を中止した。知的能力障害を伴わない成人発症てんかん6例は、比較的少量で有効性を認め、ふらつきで減量を要する症例もあったが、薬剤中止はなく忍容性は良好であった。CBZの併用は3例で、うち1例は最大容量に近い10mgまでPERが増量され、CBZにより血中濃度が低下していた可能性が考えられた。 - Hirano M; Samukawa M; Isono C; Saigoh K; Nakamura Y; Kusunoki SNeurol Genet. 4 e252 2018 [Refereed]
- James F. Howard; Kimiaki Utsugisawa; Michael Benatar; Hiroyuki Murai; Richard J. Barohn; Isabel Illa; Saiju Jacob; John Vissing; Ted M. Burns; John T. Kissel; Srikanth Muppidi; Richard J. Nowak; Fanny O'Brien; Jing-Jing Wang; Renato MantegazzaLANCET NEUROLOGY ELSEVIER SCIENCE INC 16 (12) 976 - 986 1474-4422 2017/12Background Complement is likely to have a role in refractory generalised myasthenia gravis, but no approved therapies specifically target this system. Results from a phase 2 study suggested that eculizumab, a terminal complement inhibitor, produced clinically meaningful improvements in patients with anti-acetylcholine receptor antibody-positive refractory generalised myasthenia gravis. We further assessed the efficacy and safety of eculizumab in this patient population in a phase 3 trial. Methods We did a phase 3, randomised, double-blind, placebo-controlled, multicentre study (REGAIN) in 76 hospitals and specialised clinics in 17 countries across North America, Latin America, Europe, and Asia. Eligible patients were aged at least 18 years, with a Myasthenia Gravis-Activities of Daily Living (MG-ADL) score of 6 or more, Myasthenia Gravis Foundation of America (MGFA) class II-IV disease, vaccination against Neisseria meningitides, and previous treatment with at least two immunosuppressive therapies or one immunosuppressive therapy and chronic intravenous immunoglobulin or plasma exchange for 12 months without symptom control. Patients with a history of thymoma or thymic neoplasms, thymectomy within 12 months before screening, or use of intravenous immunoglobulin or plasma exchange within 4 weeks before randomisation, or rituximab within 6 months before screening, were excluded. We randomly assigned participants (1:1) to either intravenous eculizumab or intravenous matched placebo for 26 weeks. Dosing for eculizumab was 900 mg on day 1 and at weeks 1, 2, and 3; 1200 mg at week 4; and 1200 mg given every second week thereafter as maintenance dosing. Randomisation was done centrally with an interactive voice or web-response system with patients stratified to one of four groups based on MGFA disease classification. Where possible, patients were maintained on existing myasthenia gravis therapies and rescue medication was allowed at the study physician's discretion. Patients, investigators, staff, and outcome assessors were masked to treatment assignment. The primary efficacy endpoint was the change from baseline to week 26 in MG-ADL total score measured by worst-rank ANCOVA. The efficacy population set was defined as all patients randomly assigned to treatment groups who received at least one dose of study drug, had a valid baseline MG-ADL assessment, and at least one post-baseline MG-ADL assessment. The safety analyses included all randomly assigned patients who received eculizumab or placebo. This trial is registered with ClinicalTrials.gov, number NCT01997229. Findings Between April 30, 2014, and Feb 19, 2016, we randomly assigned and treated 125 patients, 62 with eculizumab and 63 with placebo. The primary analysis showed no significant difference between eculizumab and placebo (least-squares mean rank 56.6 [SEM 4.5] vs 68.3 [4.5]; rank-based treatment difference -11.7, 95% CI -24.3 to 0.96; p=0.0698). No deaths or cases of meningococcal infection occurred during the study. The most common adverse events in both groups were headache and upper respiratory tract infection (ten [16%] for both events in the eculizumab group and 12 [19%] for both in the placebo group). Myasthenia gravis exacerbations were reported by six (10%) patients in the eculizumab group and 15 (24%) in the placebo group. Six (10%) patients in the eculizumab group and 12 (19%) in the placebo group required rescue therapy. Interpretation The change in the MG-ADL score was not statistically significant between eculizumab and placebo, as measured by the worst-rank analysis. Eculizumab was well tolerated. The use of a worst-rank analytical approach proved to be an important limitation of this study since the secondary and sensitivity analyses results were inconsistent with the primary endpoint result; further research into the role of complement is needed.
- 若年頭痛患者における睡眠アンケート調査による関連性について西郷 和真; 竹下 真未; 佐藤 亜美; 濱田 征宏; 寒川 真; 楠 進日本頭痛学会誌 (一社)日本頭痛学会 44 (2) 381 - 381 1345-6547 2017/11
- 再生不良性貧血の同種骨髄移植後に中枢神経原発移植後リンパ増殖性疾患を発症した1例山名 正樹; 寺山 敦之; 森川 みゆき; 寒川 真; 鈴木 秀和; 田崎 貴之; 奥田 武司; 小森 舞子; 井上 宏昭; 楠 進神経免疫学 日本神経免疫学会 22 (1) 123 - 123 0918-936X 2017/10
- 経静脈的免疫グロブリン療法(IVIg)が奏効した抗ミトコンドリア抗体陽性筋炎の1例山名 正樹; 寒川 真; 三井 良之; 西野 一三; 楠 進臨床神経学 (一社)日本神経学会 57 (10) 662 - 662 0009-918X 2017/10 [Refereed]
- Motoi Kuwahara; Makoto Samukawa; Tae Ikeda; Miyuki Morikawa; Rino Ueno; Yukihiro Hamada; Susumu KusunokiJOURNAL OF NEUROLOGY SPRINGER HEIDELBERG 264 (3) 467 - 475 0340-5354 2017/03 [Refereed]
Mycoplasma pneumoniae infection often causes various neurological complications of both the central nervous system (CNS) and the peripheral nervous system. We retrospectively investigated the IgM and IgG antibodies to nine glycolipids [GM1, GM2, GM3, GD1a, GD1b, GD3, GT1b, GQ1b, and Gal-C (galactocerebroside)] and clinical features in neurological diseases associated with M. pneumoniae infection diagnosed in multiple hospitals throughout Japan between September 2010 and March 2012. Of the 46 patients with neurological diseases associated with M. pneumoniae infection, 27 were diagnosed with Guillain-Barr, syndrome (GBS), 2 with Fisher syndrome (FS), 16 with CNS diseases, and 1 with both GBS and CNS disease. Anti-Gal-C IgM and IgG antibodies were most frequently detected (23/46, 50%). Patients with CNS diseases were younger than patients with GBS or FS, and IgM antibodies to Gal-C were more frequently detected in the patients with CNS diseases (41%) than in those with GBS or FS (13%). Of the nine patients who were positive for anti-Gal-C IgM antibody but lacked IgG antibody, we found the class-switch of anti-Gal-C antibody from IgM to IgG in two patients. The IgG antibodies appeared during their recovery phase, and the IgG belonged to the IgG1 subclass. Anti-Gal-C antibodies are closely associated with neurological diseases after M. pneumoniae infection. Particularly, anti-Gal-C IgM antibody is more frequently detected in younger patients affected with CNS involvement. The class-switch from IgM to IgG sometimes occurs in anti-Gal-C antibodies. - Miyuki Morikawa; Motoi Kuwahara; Rino Ueno; Makoto Samukawa; Yukihiro Hamada; Susumu KusunokiJournal of Neuroimmunology Elsevier B.V. 301 35 - 40 1872-8421 2016/12 [Refereed]
We performed a serological investigation using glycoarray in Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and multifocal motor neuropathy (MMN). Antibodies to 10 glycolipids and 45 glycolipid complexes were tested. Anti-GM1/sulfatide and anti-GA1/sulfatide IgG antibodies were common in GBS (20.0% and 19.0%, respectively). Anti-GQ1b/sulfatide IgG antibody was detected in 14.0% of GBS patients. IgG antibodies to antigens containing GQ1b were significantly correlated with ophthalmoplegia in GBS (p < 0.01). IgM antibodies to antigens containing GM1 or GalNAc-GD1a were in 50% and 37.5% of MMN patients, respectively. Glycoarray is efficient for detecting antibodies against numerous glycolipid complexes in immune-mediated neuropathies. - Makoto Samukawa; Motoi Kuwahara; Miyuki Morikawa; Rino Ueno; Yukihiro Hamada; Kazuo Takada; Makito Hirano; Yoshiyuki Mitsui; Masahiro Sonoo; Susumu KusunokiJournal of Neuroimmunology Elsevier B.V. 301 61 - 64 1872-8421 2016/12 [Refereed]
Whether patients who have GBS with antibodies to galactocerebroside (Gal-C) and gangliosides (Gal-C-GS-GBS) more often have demyelinating or axonal neuropathy remains controversial. We assessed the electrophysiological data from 16 patients with Gal-C-GS-GBS based on the two established criteria to clarify this issue. In this largest cohort of Gal-C-GS-GBS, eight patients had demyelinating neuropathy and none exhibited axonal neuropathy on either criterion. These data indicated that antibodies to Gal-C, a myelin antigen, might predominantly be associated with demyelinating neuropathy, even in the presence of concomitant antibodies to gangliosides. - わが国におけるGBSの予後予測マーカーの検討山岸 裕子; 鈴木 秀和; 寒川 真; 桑原 基; 濱田 征宏; 福本 雄太; 山名 正樹; 油原 佳子; 吉川 恵輔; 森川 みゆき; 上野 莉乃; 河合 滋; 岡崎 真央; 西郷 和真; 宮本 勝一; 三井 良之; 楠 進臨床神経学 (一社)日本神経学会 56 (Suppl.) S425 - S425 0009-918X 2016/12
- Makoto Samukawa; Motoi Kuwahara; Miyuki Morikawa; Rino Ueno; Yukihiro Hamada; Kazuo Takada; Makito Hirano; Yoshiyuki Mitsui; Masahiro Sonoo; Susumu KusunokiJOURNAL OF NEUROIMMUNOLOGY ELSEVIER SCIENCE BV 301 61 - 64 0165-5728 2016/12 [Refereed]
Whether patients who have GBS with antibodies to galactocerebroside (Gal-C) and gangliosides (Gal-C-GS-GBS) more often have demyelinating or axonal neuropathy remains controversial. We assessed the electrophysiological data from 16 patients with Gal-C-GS-GBS based on the two established criteria to clarify this issue. In this largest cohort of Gal-C-GS-GBS, eight patients had demyelinating neuropathy and none exhibited axonal neuropathy on either criterion. These data indicated that antibodies to Gal-C, a myelin antigen, might predominantly be associated with demyelinating neuropathy, even in the presence of concomitant antibodies to gangliosides. (C) 2016 Elsevier B.V. All rights reserved. - Miyuki Morikawa; Motoi Kuwahara; Rino Ueno; Makoto Samukawa; Yukihiro Hamada; Susumu KusunokiJOURNAL OF NEUROIMMUNOLOGY ELSEVIER SCIENCE BV 301 35 - 40 0165-5728 2016/12 [Refereed]
We performed a serological investigation using glycoarray in Guillain-Barre syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and multifocal motor neuropathy (MMN). Antibodies to 10 glycolipids and 45 glycolipid complexes were tested. Anti-GM1/sulfatide and anti-GA1/sulfatide IgG antibodies were common in GBS (20.0% and 19.0%, respectively). Anti-GQ1b/sulfatide IgG antibody was detected in 14.0% of GBS patients. IgG antibodies to antigens containing GQ1b were significantly correlated with ophthalmoplegia in GBS (p < 0.01). IgM antibodies to antigens containing GM1 or GaINAc-GD1a were in 50% and 37.5% of MMN patients, respectively. Glycoarray is efficient for detecting antibodies against numerous glycolipid complexes in immune-mediated neuropathies. (C) 2016 Elsevier B.V. All rights reserved. - 睡眠中に頭痛発作にて中途覚醒する頭痛の1例西郷 和真; 濱田 征宏; 油原 佳子; 寒川 真; 三井 良之; 大森 隆; 楠 進日本頭痛学会誌 (一社)日本頭痛学会 43 (2) 319 - 319 1345-6547 2016/10
- Hiroshi Ureshino; Takero Shindo; Hiroyoshi Nishikawa; Nobukazu Watanabe; Eri Watanabe; Natsuko Satoh; Kazutaka Kitaura; Hiroaki Kitamura; Kazuko Doi; Kotaro Nagase; Hiromi Kimura; Makoto Samukawa; Susumu Kusunoki; Masaharu Miyahara; Tadasu Shin-; Ryuji Suzuki; Shimon Sakaguchi; Shinya KimuraCANCER IMMUNOLOGY RESEARCH AMER ASSOC CANCER RESEARCH 4 (8) 644 - 649 2326-6066 2016/08 [Refereed]
The regulatory T cells (Treg) with the most potent immunosuppressive activity are the effector Tregs (eTreg) with a CD45RA -Foxp3(++)CCR4(+) phenotype. Adult T-cell leukemia (ATL) cells often share the Treg phenotype and also express CCR4. Although mogamulizumab, a monoclonal antibody to CCR4, shows marked antitumor effects against ATL and peripheral T-cell lymphoma, concerns have been raised that it may induce severe autoimmune immunopathology by depleting eTregs. Here, we present case reports for two patients with ATL who responded to mogamulizumab but developed a severe skin rash and autoimmune brainstem encephalitis. Deep sequencing of the T-cell receptor revealed that ATL cells and naturally occurring Tregs within the cell population with a Treg phenotype can be clearly distinguished according to CADM1 expression. The onset of skin rash and brainstem encephalitis was coincident with eTreg depletion from the peripheral blood, whereas ATL relapses were coincident with eTreg recovery. These results imply that eTreg numbers in the peripheral blood sensitively reflect the equilibrium between antitumor immunity and autoimmunity, and that mogamulizumab might suppress ATL until the eTreg population recovers. Close monitoring of eTreg numbers is crucial if we are to provide immunomodulatory treatments that target malignancy without severe adverse events. (C) 2016 AACR. - RCVS、片麻痺性片頭痛の両者の病態が考えられ、治療経過中に群発頭痛を呈した一例濱田 征宏; 福本 雄太; 河合 滋; 西郷 和真; 桑原 基; 鈴木 秀和; 寒川 真; 楠 進日本頭痛学会誌 (一社)日本頭痛学会 42 (2) 133 - 133 1345-6547 2015/11
- RCVS、片麻痺性片頭痛の両者の病態が考えられ、治療経過中に群発頭痛を呈した一例濱田 征宏; 福本 雄太; 河合 滋; 西郷 和真; 桑原 基; 鈴木 秀和; 寒川 真; 楠 進日本頭痛学会誌 (一社)日本頭痛学会 42 (2) 133 - 133 1345-6547 2015/11
- Samukawa M; Kusunoki SNihon rinsho. Japanese journal of clinical medicine 73 Suppl 7 367 - 373 0047-1852 2015/09 [Refereed]
- The first Japanese familial case of spinocerebellar ataxia 23 with a novel mutation in the PDYN geneKazumasa Saigoh; Jun Mitsui; Makito Hirano; Mitsuaki Shioyama; Makoto Samukawa; Yaeko Ichikawa; Jun Goto; Shoji Tsuji; Susumu KusunokiPARKINSONISM & RELATED DISORDERS ELSEVIER SCI LTD 21 (3) 332 - 334 1353-8020 2015/03 [Refereed]
- Yukihiro Hamada; Makito Hirano; Motoi Kuwahara; Makoto Samukawa; Kazuo Takada; Jyoji Morise; Keiko Yabuno; Shogo Oka; Susumu KusunokiNEUROSCIENCE RESEARCH ELSEVIER IRELAND LTD 91 63 - 68 0168-0102 2015/02 [Refereed]
Anti-myelin-associated-glycoprotein (MAG) neuropathy is an intractable autoimmune polyneuropathy. The antigenic region of MAG is the human natural killer-1 (HNK-1) carbohydrate. We and others previously suggested that the extension of antibody reactivities to HNK-1-bearing proteins other than MAG was associated with treatment resistance, without statistical analyses. In this study, we established an ELISA method with recombinant proteins to test binding specificities of currently available monoclonal antibodies to MAG and another HNK-1-bearing protein, phosphacan. Using this system, we found the distinct binding specificities of anti-MAG antibody in 19 patients with anti-MAG neuropathy. Their clinical relevance was then determined retrospectively with the adjusted 10-points INCAT disability score (0 = normal and 10 = highly disable). The results showed that strong reactivities of anti-MAG antibodies to phosphacan were significantly associated with treatment resistance or progressive clinical courses, indicating a possible clinical relevance of the binding specificities. (C) 2014 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved. - Shuro Kogawa; Atsushi Nakajima; Syuhei Kobashi; Makoto Samukawa; Susumu KusunokiClinical Neurology Societas Neurologica Japonica 55 (3) 171 - 173 0009-918X 2015 [Refereed]
A 67-year-old man noticed paresthesia in both legs in July 2011. Three days later, he was found on a street where he was unable to stand up. On admission, the deep sensation in both legs was severely disturbed, but their muscle strength remained normal. Cranial nerves and autonomic functions were normal. The deep tendon reflexes were diminished in both legs. Magnetic resonance imaging of the spine was normal. Motor nerve conduction studies revealed normal conduction velocity, amplitude, and F-wave latency. However, sensory nerve conduction studies revealed severe reduction of amplitude in the upper and lower extremities. Cerebrospinal fluid analysis showed normal cell counts but elevated protein levels. Screening for glycolipid antibodies showed a selective increase of galactocerebroside (Gal-C) IgG antibody. We diagnosed him with pure-sensory-type Guillain-Barré syndrome (GBS). We administered intravenous immunoglobulin (IVIG) for 5 days. After IVIG therapy, his gait disturbance improved slightly but the disturbance of deep sensation remained severe and he was transferred to a rehabilitation ward 53 days after admission. To the best of our knowledge, this is the first report of a case of pure-sensory-type GBS with Gal-C antibody alone. This case suggests a close relationship between Gal-C antibody and sensory nerve disturbance. - Mogamulizumab投与に関連した抗ガングリオシド抗体陽性脳幹脳炎(Brainstem Encephalitis with anti-ganglioside antibody associated with mogamulizumab treatment)Ureshino Hiroshi; Shindo Takero; Miyahara Masaharu; Nishikawa Hiroyoshi; Sakaguchi Shimon; Samukawa Makoto; Kusunoki Susumu; Kimura Shinya臨床血液 (一社)日本血液学会-東京事務局 55 (9) 1489 - 1489 0485-1439 2014/09
- Nobutsune Ishikawa; Yoshiyuki Kobayashi; Yuji Fujii; Makoto Samukawa; Susumu Kusunoki; Masao KobayashiPEDIATRIC NEUROLOGY ELSEVIER SCIENCE INC 51 (3) 441 - 443 0887-8994 2014/09 [Refereed]
INTRODUCTION: Postinfectious peripheral neuropathy can be associated with various viral or bacterial infections. Group A beta-hemolytic Streptococcus infection can lead to neurological disorders, which involve predominantly the central nervous system, whereas peripheral neuropathy during childhood is rare. PATIENT DESCRIPTION: We describe a 12-year-old boy who presented with peripheral polyneuropathy associated with Group A beta-hemolytic Streptococcus infection. Anti-GM1 IgM was significantly elevated in his serum during the acute phase, which suggested that it was related with the pathophysiology in this patient. CONCLUSION: Group A beta-hemolytic Streptococcus infection may cause peripheral neuropathy via the autoimmune system and glycolipids. - Makoto Samukawa; Yukihiro Hamada; Motoi Kuwahara; Kazuo Takada; Makito Hirano; Yoshiyuki Mitsui; Masahiro Sonoo; Susumu KusunokiJOURNAL OF THE NEUROLOGICAL SCIENCES ELSEVIER SCIENCE BV 337 (1-2) 55 - 60 0022-510X 2014/02 [Refereed]
Introduction: Guillain-Barre syndrome (GBS) has often been associated with antibodies to glycolipids, such as galactocerebroside (Gal-C), a component of myelin. Whether patients who have GBS with anti-Gal-C antibody (Gal-C-GBS) more often have demyelinating neuropathy or axonal neuropathy remains controversial. Their clinical features have also been unestablished. Methods: We enrolled 47 patients with Gal-C-GBS. Their clinical and electrophysiological data were retrospectively reviewed and compared to 119 patients with CBS without anti-Gal-C antibody (non-Gal-C-GBS). Results: Demyelinating polyneuropathy occurred 4 times more frequently than axonal polyneuropathy in patients with Gal-C-GBS, but without statistical significance compared to patients with non-Gal-C-GBS (2.2:1). Patients with Gal-C-GBS had more frequent sensory deficits, autonomic involvements, and antecedent Mycoplasma pneumoniae (MP) infection than patients with non-Gal-C-GBS. Conclusions: This is the largest study clarifying the clinical and electrophysiological findings that more frequent sensory deficits, autonomic involvements, and antecedent MP infection are associated with Gal-C-GBS. (C) 2013 Elsevier B.V. All rights reserved. - IgMパラプロテイン血症を伴うニューロパチーにおけるHNK-1抗体活性と臨床特徴の関連濱田 征宏; 寒川 真; 桑原 基; 藪野 景子; 森瀬 譲二; 高田 和男; 宮本 勝一; 岡 昌吾; 楠 進臨床神経学 (一社)日本神経学会 53 (12) 1507 - 1507 0009-918X 2013/12
- Samukawa Makoto; Ichihara Gaku; Ueda Masami; Mitsui Yoshiyuki; Oka Nobuyuki; Kusunoki SusumuANNALS OF NEUROLOGY 74 S4 0364-5134 2013/10 [Refereed]
- 寒川真; 塩山実章; 鈴木秀和; 上田昌美; 岡伸幸; 市原学; 三井良之; 楠進産業医学ジャーナル 産業医学振興財団 36 (4) 16 - 21 0388-337X 2013/07症例は43歳男性で、2年前より金属部品洗浄業務に従事していた。右下肢痛に続く左下肢痛、ふらつきの出現で紹介受診し、四肢の異常感覚、疼痛、運動失調を認め、両下肢の温痛覚低下、振動覚消失が認められた。胸部X線・胸腹骨盤造影CT・頸髄MRIで異常所見なく、末梢神経伝導検査で運動神経・感覚神経とも下肢優位に遠位潜時延長、振幅低下、伝導速度低下を認め、精査加療目的に入院した。腓腹神経の生検でときほぐし線維法にて約30%に軸索障害を示唆するmyelin ovoidを認め、エポン包埋標本では大径有髄線維の減少とその10~20%に軸索腫大や消失、myelin ovoidが認められた。詳細な問診で金属紛洗浄剤中に1-Bromopropane(1-BP)の含有が判明し、初診時の残血清検査で血清臭素値の高値を認め、1-BP暴露による中毒性神経障害と判断し、退院の上外来での経過観察とした。徐々に症状は改善し、最終暴露後7ヵ月時点で独歩外出、自転車走行も可能となった。
- Motoi Kuwahara; Hidekazu Suzuki; Makoto Samukawa; Yukihiro Hamada; Kazuo Takada; Susumu KusunokiJOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY BMJ PUBLISHING GROUP 84 (5) 573 - 575 0022-3050 2013/05 [Refereed]
Background LM1 is the predominant glycolipid in human peripheral nerve myelin and antibodies to LM1 and LM1-containing ganglioside complexes are detected in some patients with chronic inflammatory demyelinating polyneuropathy (CIDP). The clinical features of patients with such antibodies have not yet been investigated. Methods Serum antibodies to LM1, a mixture of GM1 and LM1 (GM1/LM1), and that of GD1b and LM1 (GD1b/LM1) were examined in 75 consecutive patients with CIDP. The clinical features of the CIDP patients with such antibodies in the present series and those in the previous reports were investigated and compared with those of antibody-negative patients. Results Of the 75 patients with CIDP, two had antibodies to LM1, three had anti-GM1/LM1 complex antibody, one had anti-GD1b/LM1 complex antibody and two had antibodies to both the GM1/LM1 and GD1b/LM1 complexes. Patients with the LM1-associated antibodies did not have cranial nerve deficits (p<0.05) and exhibited ataxia more frequently than the antibody-negative patients (p<0.01). Conclusion In humans, LM1 is contained more in the dorsal root than in the cranial nerves. The clinical features of CIDP patients with antibodies to LM1 and LM1-containing complexes may be associated with the distribution of the LM1 antigen. LM1-associated antibodies are possible markers for a subclass of CIDP. - 鈴木秀和; 桑原基; 山藤聖子; 寒川真; 濱田征宏; 楠進神経治療学 (一社)日本神経治療学会 30 (2) 173 - 179 0916-8443 2013/03慢性炎症性脱髄性多発ニューロパチー(chronic inflammatory demyelinating polyradiculoneuropathy:CIDP)は、難治性の末梢神経に対する自己免疫性疾患であるが、その病態は未解明の部分が多い。本研究では、2010年のEuropean Federation of Neurological Societies/Peripheral Nerve Society(EFNS/PNS)のCIDP診断基準に基づいてprobable以上であった106例を解析した。抗糖脂質抗体の測定と、ファーストラインの治療である免疫グロブリン大量療法(intravenous immunoglobulins:IVIG)、副腎皮質ステロイド療法の反応性を中心にアンケート調査に基づいて、臨床的解析を行った。抗糖脂質抗体陽性率は8.4%であった。IVIGの有効率は86%、副腎皮質ステロイド療法の有効率は69%であった。髄液中総蛋白が高値(>100mg/dl)であった症例はIVIGもしくは副腎皮質ステロイド療法にて反応性が得られていた。また、少数例での検討であったが、抗糖脂質抗体陽性例は感覚障害が優位である例が多かった。(著者抄録)
- Hikaru Sakamoto; Makito Hirano; Makoto Samukawa; Shuichi Ueno; Shunji Maekura; Harutoshi Fujimura; Motoi Kuwahara; Yukihiro Hamada; Chiharu Isono; Keiko Tanaka; Susumu Kusunoki; Yusaku NakamuraEuropean Neurology 69 (1) 21 - 26 0014-3022 2013/02 [Refereed]
Anti-N-methyl-d-aspartate receptor (anti-NMDAR) antibody-associated encephalitis is an immunologic disease characterized by a female preponderance. Males are infrequently affected. The clinical symptoms of affected boys as well as girls have been summarized, and they have some clinical features distinct from those of adults. However, the characteristics of men have been described in only a few reports. We describe in detail four men with anti-NMDAR encephalitis who presented with several clinical features that complicated disease management and recovery, including venous thrombosis, bilateral hippocampal involvement, hypersexuality, and joint contracture. We also report the first detailed clinical information about a male patient who died of this disease. In addition, we summarize the clinical characteristics of five patients previously reported by others. © 2012 S. Karger AG, Basel. - Makoto Samukawa; Makito Hirano; Jun Tsugawa; Hikaru Sakamoto; Emi Tabata; Kazuo Takada; Motoi Kuwahara; Seiko Suzuki; Mari Kitada; Tatsuo Yamada; Hideo Hara; Yoshio Tsuboi; Yusaku Nakamura; Susumu KusunokiNEUROSCIENCE RESEARCH ELSEVIER IRELAND LTD 74 (3-4) 284 - 289 0168-0102 2012/12 [Refereed]
Acute disseminated encephalomyelitis causes multifocal demyelination in the central nerve system. Although this disease generally responds well to steroid therapy, it is occasionally steroid-resistant, leading to poor outcomes. Serological markers of prognosis are currently unavailable. We measured anti-glycolipid antibodies in 25 consecutive patients with acute disseminated encephalomyelitis, and found that four patients were positive for anti-galactocerebroside antibodies. All four patients had a poor response to steroids. We summarize clinical information on these four patients and three similar patients reported previously. This is the first report to describe concomitant involvement of the central nerve system and peripheral nervous system in anti-galactocerebroside antibody-associated acute disseminated encephalomyelitis, consistent with the location of galactocerebroside, and to document a dramatic response to repeated intravenous immunoglobulin therapy after unsuccessful steroid treatment in one patient. (C) 2012 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved. - Makoto Samukawa; Gaku Ichihara; Nobuyuki Oka; Susumu KusunokiArchives of internal medicine 172 (16) 1257 - 60 0003-9926 2012/09 [Refereed]
Health hazard alerts to 1-bromopropane, an alternative to ozone layer-damaging organic solvents, have been issued by some countries. Herein, we report a new case of 1-bromopropane-induced neurotoxicity. A 43-year-old male industrial worker developed muscle weakness, pain, numbness, and gait disturbance. Neurological examination indicated sensory ataxic neuropathy associated with mild impairment of upper motor neurons. He had used 1-bromopropane as a cleaning agent for metal parts at his workplace without appropriate protection. The serum bromide level was elevated at the onset of clinical manifestations. Histopathologic examination of sural nerve biopsy showed axonal damage. Under the tentative diagnosis of 1-bromopropane toxicity, he was kept away from exposure to the solvent. This resulted in gradual improvement of symptoms, recovery of motor function, and resolution of sensory deficits. The diagnosis of 1-bromopropane neurotoxicity in this case was based on details of the work environment, the clinical course, and laboratory and pathologic findings. To our knowledge, this is the first report that describes nerve biopsy findings in a human case. - 寒川真; 鈴木秀和; 市橋珠里; 長谷川隆典; 北口正孝; 三井良之; 楠進神経治療学 (一社)日本神経治療学会 29 (4) 429 - 434 0916-8443 2012/07免疫グロブリン大量静注療法が寛解維持に有効であった抗signal recognition particle(SRP)抗体陽性筋炎の2例を経験した。症例1は33歳女性。X年より筋痛・筋力低下を自覚し当科紹介受診となった。CK上昇と筋生検にて炎症細胞浸潤に乏しい壊死・再生像を観察し、抗SRP抗体陽性で抗SRP抗体陽性筋炎と診断した。ステロイド療法のみでは寛解が得られなかったが、IVIgを追加したところCK低下、筋力の改善が得られた。症例2は56歳女性。Y年頃より歩行困難・筋力低下が出現した。近医にて、著明なCK上昇と筋生検結果より、暫定的に多発筋炎と診断された。ステロイド内服療法にて治療されたが、漸減中による再燃を繰り返したため、Y+6年当科紹介となった。当院で再度施行した筋生検で、炎症細胞浸潤に乏しい壊死・再生像を観察し、抗SRP抗体陽性が判明し抗SRP抗体陽性筋炎と診断した。ステロイド療法のみでは寛解が得られなかったため、IVIgを追加したところ、CK値低下、筋力の改善が得られた。ステロイド漸減中、軽度のCK上昇、筋力低下を認めたため、cyclosporinを併用し寛解が得られている。免疫グロブリン大量静注療法にて寛解維持が得られた抗SRP抗体陽性筋炎の2例について文献的考察とともに報告する。(著者抄録)
- 痙攣発作と精神症状を呈したMorvan症候群の1例楠 進; 寒川 真; 鈴木 秀和; 北田茉里; 塩山 実章; 三井 良之; 中村 雄作大阪てんかん研究会雑誌 大阪てんかん研究会 23 (1) 7 - 14 0918-9319 2012Morvan症候群は、免疫学的機序により中枢神経障害と末梢神経の過剰興奮を来す稀な疾患である。症例の中には胸腺腫、肺小細胞癌などの腫瘍に随伴することがあり傍腫瘍性神経症候群と考えられている。また、一部の症例ではvoltage-gated potassium channelおよびその関連タンパクに対する自己抗体が陽性となる。免疫療法の反応性は良好とされているが、発症様式や臨床経過は多岐にわたり、診断・治療に難渋する症例も存在する。今回、我々は精神症状にて発症し、亜急性の経過で意識障害、痙攣発作が加わり、当初Creutzfeldt-Jakob diseaseが疑われたMorvan症候群の一例を経験した。症例は63歳男性。X年1月頃から緩徐進行性にうつ症状、食思不振、体重減少が出現した。同年5月に近医入院となった。同年8月中旬から亜急性の経過で意識障害、痙攣が加わり、Creutzfeldt-Jakob disease疑いで8月末に当院へ転院となった。神経学診察では高度な意識障害、筋緊張亢進、および全身性に豊富なmyokymiaを観察した。針筋電図で全身に分布するmyokymic dischargeを確認したためMorvan症候群を疑った。ステロイドパルス療法にて意識障害、筋緊張の劇的な改善、myokymic dischargeの消失が得られたが、うつ症状が残存した。その後、意識障害、myokymic dischargeの再燃時に、血漿交換、免疫グロブリン大量静注療法、ステロイドパルス療法、経口ステロイド投与などの免疫療法を行ったが、うつ症状は治療抵抗性であった。長期間継続するうつ症状の原因として、ステロイド精神病を考え、ステロイド漸減したところ、うつ症状の改善が得られた。積極的に腫瘍検索を行ったが腫瘍は認めず、voltage-gated potassium channelおよびその関連タンパクに対する自己抗体は陰性であった。精神症状、意識障害などの中枢神経障害に加え、fasciculation様の下位ニューロン障害を合併する場合は、重要な鑑別診断として、Morvan症候群を念頭に置く必要があると考えられた。(著者抄録)
- 上田 昌美; 豊増 麻美; 大洞 佳代子; 福田 寛二; 鈴木 秀和; 寒川 真; 上野 周一; 市橋 珠里; 楠 進The Japanese Journal of Rehabilitation Medicine The Japanese Journal of Rehabilitation Medicine (公社)日本リハビリテーション医学会 48 (12) 795 - 795 1881-3526 2011/12
- Makoto Samukawa; Makito Hirano; Hikaru Sakamoto; Mari Kitada; Susumu Kusunoki; Yusaku NakamuraMOVEMENT DISORDERS WILEY-BLACKWELL 26 (14) 2572 - 2573 0885-3185 2011/12 [Refereed]
- H. Suzuki; M. Samukawa; M. Kitada; J. Ichihashi; Y. Mistui; K. Tanaka; S. KusunokiEUROPEAN JOURNAL OF NEUROLOGY WILEY-BLACKWELL 18 (11) E145 - E146 1351-5101 2011/11
- Samukawa M; Hirano M; Saigoh K; Kawai S; Hamada Y; Takahashi D; Nakamura Y; Kusunoki SCerebellum. Epub ahead of print [Refereed]
MISC
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- 寒川 真 Progress in Medicine 42- (8) 767 -771 2022/08
- N/AMakoto Samukawa 重症筋無力症/ランバート・イートン筋無力症候群 診療ガイドライン 77 -79 2022/05
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- Samukawa Makoto Neurological Therapeutics 38- (4) 597 -600 2021
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- 寒川 真 神経治療学 37- (6) S164 -S164 2020/10
- 【免疫・炎症疾患のすべて】免疫・炎症疾患各論/神経疾患 慢性炎症性脱髄性多発神経炎(CIDP)寒川 真; 楠 進 日本医師会雑誌 149- (特別2) S270 -S272 2020/10
- 小田いつき; 團野大介; 西郷和真; 西郷和真; 菊井祥二; 木村卓; 平野牧人; 寒川真; 三井良之; 竹島多賀夫; 楠進 日本頭痛学会誌 47- (2 (Web)) 2020
- 平野牧人; 井上貴美子; 伊藤龍生; 寒川真; 藤村晴俊; 能勢和宏; 楠進; 中村雄作 神経治療学(Web) 37- (6) 2020
- 免疫治療で症状の軽快を認めた16歳発症の急性弛緩性脊髄炎の一例寺山 敦之; 山岸 裕子; 柳本 諭志; 寒川 真; 三井 良之; 楠 進 臨床神経学 59- (12) 844 -844 2019/12
- 寒冷刺激による頭痛と生体温度変化について西郷 和真; 米島 康平; 木川 和弥; 稲垣 拓武; 長谷川 隆典; 寒川 真; 濱田 征宏; 市橋 珠里; 三井 良之; 楠 進 日本頭痛学会誌 46- (2) 486 -486 2019/11
- 寒川 真; 寺山 敦之; 森川 みゆき; 山岸 裕子; 楠 進 神経治療学 36- (6) S273 -S273 2019/10
- 意識障害で発症し小細胞肺癌に対する化学療法が奏効した抗SOX1抗体陽性傍腫瘍性辺縁系脳炎の一例寺山 敦之; 山岸 裕子; 寒川 真; 鈴木 慎一郎; 三井 良之; 中川 和彦; 楠 進 臨床神経学 59- (4) 236 -236 2019/04
- 補体を標的とした神経免疫疾患の新規治療寒川 真; 楠 進 Annual Review神経 2019- 113 -122 2019/03
- 西郷和真; 西郷和真; 森口幸太; 森口幸太; 平野牧人; 山下翔子; 定金秀爾; 柳本諭志; 稲田莉乃; 岡崎真央; 寒川真; 鈴木秀和; 三井良之; 楠進 日本神経学会学術大会プログラム・抄録集 60th- (Suppl.) S365 -S365 2019
- 山岸 裕子; 桑原 基; 寒川 真; 鈴木 秀和; 楠 進 末梢神経 29- (2) 298 -298 2018/12
- 我が国におけるGuillain-Barre症候群の特徴 臨床病型,予後予測等山岸 裕子; 鈴木 秀和; 桑原 基; 寒川 真; 楠 進; JGOS study group 臨床神経学 58- (Suppl.) S119 -S119 2018/12
- 口腔内寒冷刺激における体温変動について西郷 和真; 米島 康平; 長谷川 隆典; 濱田 征宏; 寒川 真; 市橋 珠里; 三井 良之; 楠 進 日本頭痛学会誌 45- (2) 422 -422 2018/11
- 脳幹脳炎の併発により急性水頭症に至ったリステリア髄膜炎の1例定金 秀爾; 山下 翔子; 稲田 莉乃; 寒川 真; 楠 進 NEUROINFECTION 23- (2) 204 -204 2018/10
- 寒川真, 楠進 Clinical Neuroscience 36- (4) 456 -459 2018/04
- 寒川真; 谷口佳子; 山岸裕子; 河合滋; 岡崎真央; 濱田征宏; 濱田征宏; 桑原基; 鈴木秀和; 三井良之; 岡伸幸, 楠進 末梢神経 28- (2) 288 -288 2017/12
- 若年頭痛患者における睡眠アンケート調査による関連性について西郷 和真; 竹下 真未; 佐藤 亜美; 濱田 征宏; 寒川 真; 楠 進 日本頭痛学会誌 44- (2) 381 -381 2017/11
- 【腸内フローラと神経・精神疾患】 腸内フローラと神経・精神疾患 Guillain-Barre症候群寒川 真; 楠 進 Clinical Neuroscience 35- (11) 1324 -1326 2017/11
- Makoto Samukawa; Makito Hirano; Kazumasa Saigoh; Susumu Kusunoki ANNALS OF NEUROLOGY 82- S84 -S84 2017/10
- Makito Hirano; Yusaku Nakamura; Kazumasa Saigoh; Makoto Samukawa; Susumu Kusunoki ANNALS OF NEUROLOGY 82- S185 -S185 2017/10
- S. Kusunoki; M. Morikawa; M. Kuwahara; R. Ueno; M. Samukawa; Y. Hamada JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 22- (3) 323 -323 2017/09
- 平野 牧人; 西郷 和真; 寒川 真; 上野 周一; 濱田 征宏; 中村 雄作; 楠 進 日本遺伝カウンセリング学会誌 38- (2) 118 -118 2017/05
- 脊髄炎発症の数年後、同時期に重症筋無力症と視神経炎を発症した症例市川 昌志; 油原 佳子; 寒川 真; 楠 進 臨床神経学 57- (3) 143 -143 2017/03
- 他の抗糖脂質抗体を伴ったGal-C抗体陽性GBSの臨床的・電気生理学的検討寒川 真; 上野 莉乃; 濱田 征宏; 桑原 基; 平野 牧人; 三井 良之; 楠 進 臨床神経学 56- (Suppl.) S425 -S425 2016/12
- わが国におけるGBSの予後予測マーカーの検討山岸 裕子; 鈴木 秀和; 寒川 真; 桑原 基; 濱田 征宏; 福本 雄太; 山名 正樹; 油原 佳子; 吉川 恵輔; 森川 みゆき; 上野 莉乃; 河合 滋; 岡崎 真央; 西郷 和真; 宮本 勝一; 三井 良之; 楠 進 臨床神経学 56- (Suppl.) S425 -S425 2016/12
- 抗MAG抗体ニューロパチー 抗体affinityの変動と臨床経過濱田 征宏; 桑原 基; 寒川 真; 森瀬 譲二; 堀内 惠美子; 岡 昌吾; 楠 進 臨床神経学 56- (Suppl.) S429 -S429 2016/12
- 濱田征宏; 桑原基; 寒川真; 森瀬譲二; 堀内恵美子; 岡昌吾, 楠進 末梢神経 27- (2) 341 -341 2016/12
- 山岸裕子; 寒川真; 桑原基; 三井良之; 岡伸幸; 橋口昭大; 高嶋博, 楠進 末梢神経 27- (2) 344 -344 2016/12
- 山岸裕子; 鈴木秀和; 寒川真; 園生雅弘; 桑原聡; 野村恭一; 千葉厚郎; 梶龍兒; 神田隆; 海田賢一; 池田修一; 楠進 末梢神経 27- (2) 249 -249 2016/12
- 寒川真; 油原佳子; 桑原基; 三井良之; 岡伸幸, 楠進 末梢神経 27- (2) 338 -338 2016/12
- 睡眠中に頭痛発作にて中途覚醒する頭痛の1例西郷 和真; 濱田 征宏; 油原 佳子; 寒川 真; 三井 良之; 大森 隆; 楠 進 日本頭痛学会誌 43- (2) 319 -319 2016/10
- Susumu Kusunoki; Motoi Kuwahara; Makoto Samukawa; Miyuki Morikawa; Rino Ueno; Yukihiro Hamada ANNALS OF NEUROLOGY 80- S147 -S147 2016/10
- Makoto Samukawa; Motoi Kuwahara; Miyuki Morikawa; Rino Ueno; Yukihiro Hamada; Kazuo Takada; Yoshiyuki Mitsui; Susumu Kusunoki ANNALS OF NEUROLOGY 80- S86 -S87 2016/10
- マイコプラズマ感染に伴う神経疾患と抗糖脂質抗体の特徴桑原 基; 寒川 真; 池田 妙; 森川 みゆき; 上野 莉乃; 濱田 征宏; 楠 進 神経免疫学 21- (1) 146 -146 2016/09
- M. Samukawa; M. Kuwahara; R. Ueno; R. Hamada; K. Takada; M. Hirano; Y. Mitsui; M. Sonoo; S. Kusunoki JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 21- (3) 206 -207 2016/09
- M. Kuwahara; M. Samukawa; Y. Hamada; S. Kusunoki JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 21- (3) 187 -188 2016/09
- グライコアレイを用いた免疫性ニューロパチーにおける血中糖脂質複合体抗体の解析森川 みゆき; 上野 莉乃; 寒川 真; 濱田 征宏; 桑原 基; 楠 進 臨床神経学 55- (Suppl.) S269 -S269 2015/12
- Combinatorial Glycoarrayによる網羅的抗糖脂質複合体抗体の検出 ELISAとの比較桑原 基; 森川 みゆき; 上野 莉乃; 寒川 真; 濱田 征宏; 楠 進 臨床神経学 55- (Suppl.) S269 -S269 2015/12
- 山岸裕子; 寒川真; 桑原基; 三井良之; 岡伸幸, 楠進 末梢神経 26- (2) 356 -356 2015/12
- 寒川 真; 楠 進 検査と技術 43- (12) 1222 -1229 2015/11
- Makoto Samukawa; Keisuke Yoshikawa; Yuko Yamagishi; Shigeru Kawai; Masahiro Okazaki; Toshihiko Shiga; Yukihiro Hamada; Motoi Kuwahara; Hidekazu Suzuki; Yuji Nozaki; Shigeaki Suzuki; Kazumasa Saigoh; Yoshiyuki Mitsui; Ichizo Nishino; Masahiro Funauchi; Susumu Kusunoki ANNALS OF NEUROLOGY 78- S112 -S112 2015/10
- S. Kusunoki; M. Kuwahara; Y. Hamada; M. Morikawa; R. I. N. O. Ueno; M. Samukawa; Y. Mitsui JOURNAL OF THE NEUROLOGICAL SCIENCES 357- E66 -E66 2015/10
- 抗SGPG抗体陰性のIgMパラプロテイン血症を伴うニューロパチーにおける血清学的および臨床的特徴の解析桑原 基; 濱田 征宏; 森川 みゆき; 上野 莉乃; 寒川 真; 楠 進 神経免疫学 20- (1) 126 -126 2015/09
- 寒川 真; 山岸 裕子; 森川 みゆき; 桑原 基; 三井 良之; 北口 正孝; 楠 進 神経治療学 32- (5) 821 -821 2015/09
- 鈴木 秀和; 加藤 茉里; 市橋 珠里; 河合 滋; 寒川 真; 濱田 征宏; 西郷 和真; 三井 良之; 楠 進 神経治療学 32- (5) 768 -768 2015/09
- 寒川 真; 楠 進 日本臨床 73- (増刊7 免疫性神経疾患) 367 -373 2015/09
- S. Kusunoki; M. Kuwahara; Y. Hamada; M. Morikawa; R. Ueno; M. Samukawa; Y. Mitsui JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 20- (2) 176 -177 2015/06
- 鈴木秀和; 桑原基; 濱田征宏; 市橋珠里; 加藤茉里; 寒川真; 岡崎真央; 河合滋; 上野莉乃; 山岸裕子; 森川みゆき; 吉川恵輔; 山名正樹; 福本雄太; 油原佳子; 高田和男; 西郷和真; 宮本勝一; 三井良之; 楠進 日本神経学会学術大会プログラム・抄録集 56th- (Suppl.) 394 -S271 2015
- 寒川真; 吉川恵介; 山岸裕子; 河合滋; 岡崎真央; 志賀俊彦; 濱田征宏; 桑原基; 鈴木秀和; 野崎祐史; 鈴木重明; 西郷和真; 三井良之; 西野一三; 船内正憲; 楠進 日本神経学会学術大会プログラム・抄録集 56th- (Suppl.) 389 -S266 2015
- 西郷和真; 西郷和真; 三井純; 平野牧人; 塩山実章; 寒川真; 市川弥生子; 後藤順; 辻省次; 巽純子; 田村和朗; 楠進 日本人類遺伝学会大会プログラム・抄録集 60th- 262 2015
- インフルエンザウイルス感染後のGuillain-Barre症候群及びFisher症候群桑原 基; 寒川 真; 濱田 征宏; 高田 和男; 楠 進 臨床神経学 54- (Suppl.) S23 -S23 2014/12
- 免疫性神経疾患における抗糖脂質抗体クラススイッチの検討寒川 真; 桑原 基; 上野 莉乃; 濱田 征宏; 高田 和男; 三井 良之; 楠 進 臨床神経学 54- (Suppl.) S107 -S107 2014/12
- 抗GalNAc-GD1a抗体陽性症例における臨床病型の解析濱田 征宏; 上野 莉乃; 寒川 真; 桑原 基; 高田 和男; 三井 良之; 楠 進 臨床神経学 54- (Suppl.) S254 -S254 2014/12
- Febrile infection-related epilepsy syndrome(FIRES)成人例に対する免疫療法の検討鈴木 秀和; 加藤 茉里; 市橋 珠里; 森川 みゆき; 岡崎 真央; 寒川 真; 西郷 和真; 三井 良之; 楠 進 臨床神経学 54- (Suppl.) S65 -S65 2014/12
- Makoto Samukawa; Yukihiro Hamada; Motoi Kuwahara; Kazuo Takada; Makito Hirano; Yoshiyuki Mitsui; Masahiro Sonoo; Susumu Kusunoki ANNALS OF NEUROLOGY 76- S80 -S80 2014/10
- Susumu Kusunoki; Makoto Samukawa; Yukihiro Hamada; Motoi Kuwahara; Kazuo Takada; Makito Hirano; Yoshiyuki Mitsui JOURNAL OF NEUROIMMUNOLOGY 275- (1-2) 9 -9 2014/10
- 寒川真; 山岸裕子; 加藤茉里; 桑原基; 宮本勝一; 楠進 神経治療学 31- (5) 659 -659 2014/09
- 神経疾患における抗GM3抗体の検討桑原 基; 濱田 征宏; 寒川 真; 上野 莉乃; 高田 和男; 楠 進 神経免疫学 19- (1) 154 -154 2014/09
- S. Kusunoki; M. Samukawa; Y. Hamada; M. Kuwahara; K. Takada; M. Hirano; Y. Mitsui JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 19- (3) 272 -272 2014/09
- Y. Hamada; M. Samukawa; M. Kuwahara; Y. Mitsui; S. Kusunoki JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 19- (3) 263 -263 2014/09
- M. Kuwahara; Y. Hamada; M. Samukawa; K. Takada; S. Sonnino; S. Kusunoki JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM 19- (3) 272 -273 2014/09
- 神経疾患における抗GM3抗体の検討桑原 基; 濱田 征宏; 寒川 真; 上野 莉乃; 高田 和男; 楠 進 NEUROINFECTION 19- (2) 218 -218 2014/08
- 寒川 真; 楠 進 日本臨床 別冊- (神経症候群II) 831 -837 2014/03
- Guillain-Barré syndrome (GBS)Makoto Samukawa 別冊日本臨牀 新領域別症候群シリーズ 27- 831 -837 2014/03
- 抗糖脂質抗体とHu抗体が陽性であり小脳失調を主徴とした肺小細胞癌例野倉 一也; 巨椋 義蔵; 加子 哲治; 寒川 真; 楠 進; 田中 惠子 臨床神経学 54- (2) 172 -172 2014/02
- 寒川真, 楠進 日本臨床 別冊- (神経症候群I) 838 -842 2013/12
- 抗galactocerebroside抗体陽性Guillain-Barre症候群の臨床的・電気生理学的検討寒川 真; 濱田 征宏; 桑原 基; 鈴木 秀和; 高田 和男; 三井 良之; 楠 進 臨床神経学 53- (12) 1506 -1506 2013/12
- Guillain-Barre症候群及びFisher症候群におけるGQ1bと交差反応を示す抗GM1/GD1a抗体桑原 基; Mauri Laura; 濱田 征宏; 寒川 真; 高田 和男; Sonnino Sandro; 楠 進 臨床神経学 53- (12) 1535 -1535 2013/12
- 抗ガラクトセレブロシド抗体の関与が疑われた辺縁系脳炎とGuillain-Barre症候群の検討北村 彰浩; 藤田 充世; 垣内 無一; 中西 恵美; 長山 成美; 富岳 亮; 田中 惠子; 寒川 真; 楠 進; 松井 真 臨床神経学 53- (12) 1571 -1571 2013/12
- 寒川真; 平野牧人; 津川潤; 阪本光; 田畑絵美; 高田和男; 桑原基; 山藤聖子; 加藤茉里; 山田達夫; 原英夫; 坪井義夫; 中村雄作; 楠進 末梢神経 24- (2) 333 -334 2013/12
- 抗Gal-C抗体かつ他の抗糖脂質抗体も陽性であったGuillain-Barre症候群の電気生理学的検討寒川 真; 濱田 征宏; 桑原 基; 高田 和男; 三井 良之; 楠 進 神経免疫学 18- (1) 145 -145 2013/11
- 鈴木 秀和; 加藤 茉里; 河合 滋; 上野 莉乃; 寒川 真; 濱田 征宏; 桑原 基; 三井 良之; 岡 伸幸; 楠 進 神経治療学 30- (5) 659 -659 2013/09
- 抗ガラクトセレブロシド(Gal-C)抗体の関与が疑われた辺縁系脳炎の1例北村 彰浩; 藤田 充世; 垣内 無一; 中西 恵美; 長山 成美; 富岳 亮; 田中 惠子; 寒川 真; 楠 進; 松井 真 臨床神経学 53- (9) 767 -767 2013/09
- Susumu Kusunoki; Motoi Kuwahara; Hidekazu Suzuki; Makoto Samukawa; Yukihiro Hamada; Kazuo Takada JOURNAL OF NEUROIMMUNOLOGY 253- (1-2) 29 -29 2012/12
- 非ヘルペス性辺縁系脳炎の頭部MRIにおける初期硬膜病変鈴木 秀和; 北田 茉里; 上野 周一; 寒川 真; 市橋 珠里; 三井 良之; 田中 惠子; 楠 進 臨床神経学 52- (12) 1530 -1530 2012/12
- 寒川真; 筑後孝章; 塩山実章; 加藤茉里; 濱田征宏; 山藤聖子; 桑原基; 上田昌美; 鈴木秀和; 三井良之; 楠進 末梢神経 23- (2) 239 -240 2012/12
- 化学物質による健康障害における労働衛生の軌跡と展望 ブロモプロパンの神経毒性市原 学; 寒川 真 日本職業・災害医学会会誌 60- (臨増) 別96 -別96 2012/11
- 産業化学物質による神経毒性評価 最新の動物実験のヒトにおける毒性評価への応用と可能性 1-ブロモプロパン曝露による神経障害寒川 真 産業衛生学雑誌 54- (臨増) 194 -194 2012/05
- 強皮症にともなう抗NMDA受容体脳炎の1例鈴木 秀和; 寒川 真; 青松 宏美; 三井 良之; 楠 進 臨床神経学 52- (2) 132 -132 2012/02
- locked-in様症状を呈した抗galactocerebroside(Gal-C)抗体陽性ADEMの1例寒川 真; 阪本 光; 平野 牧人; 鈴木 聖子; 桑原 基; 中村 雄作; 楠 進 臨床神経学 52- (2) 133 -133 2012/02
- 本邦におけるバルデー・ビードル症候群の臨床的特徴平野 牧人; 山下 俊英; 生野 恭司; 岩橋 博見; 大石 充; 真野 利之; 石原 立; 田中 一郎; 柳原 恵子; 寒川 真; 阪本 光; 中村 雄作; 楠 進 臨床神経学 52- (2) 138 -138 2012/02
- Makoto Samukawa; Makito Hirano; Hikaru Sakamoto; Mari Kitada; Susumu Kusunoki; Yusaku Nakamura ANNALS OF NEUROLOGY 72- S97 -S97 2012
- Makoto Samukawa; Makito Hirano; Hikaru Sakamoto; Shuichi Ueno; Toshiharu Maekura; Harutoshi Fujimura; Susumu Kusunoki; Yusaku Nakamura ANNALS OF NEUROLOGY 72- S115 -S115 2012
- 多系統萎縮症と抗利尿ホルモン不適合分泌症候群の関連阪本 光; 平野 牧人; 寒川 真; 北田 茉里; 楠 進; 中村 雄作 臨床神経学 51- (12) 1269 -1269 2011/12
- 抗NMDA受容体脳炎連続6症例の検討 臨床的多様性と治療戦略鈴木 秀和; 北田 茉里; 寒川 真; 上野 周一; 市橋 珠里; 三井 良之; 田中 惠子; 楠 進 臨床神経学 51- (12) 1312 -1312 2011/12
- 寒川真; 塩山実章; 鈴木秀和; 上田正美; 岡伸幸; 市原学; 三井良之; 楠進 末梢神経 22- (2) 248 -249 2011/12
- 群発頭痛様発作で発症した中枢神経限局性血管炎の1例西郷 和真; 濱田 征宏; 寒川 真; 桑原 基; 稲次 洋平; 塩山 実章; 三井 良之; 布川 知史; 加藤 天美; 楠 進 日本頭痛学会誌 38- (2) 185 -185 2011/11
- SAMUKAWA MAKOTO; SUZUKI HIDEKAZU; KITADA MARI; MITSUI YOSHIYUKI; NAKAMURA YUSAKU; KUSUNOKI SUSUMU 臨床神経学 51- (10) 795 -795 2011/10
- 回復期に著明な側頭葉萎縮を来した抗NMDA受容体抗体関連脳炎の1例阪本 光; 平野 牧人; 寒川 真; 北田 茉里; 上野 周一; 田中 惠子; 楠 進; 中村 雄作 臨床神経学 51- (10) 792 -792 2011/10
- SAMUKAWA MAKOTO; SUZUKI HIDEKAZU; KITADA MARI; MITSUI YOSHIYUKI; KUSUNOKI SUSUMU; NAKAMURA YUSAKU 神経治療学 28- (5) 556 -556 2011/09
- 北田 茉里; 鈴木 秀和; 寒川 真; 三井 良之; 楠 進; 田中 惠子 神経治療学 28- (5) 539 -539 2011/09
- 多系統萎縮症における抗利尿ホルモン不適合分泌症候群の合併寒川 真; 平野 牧人; 阪本 光; 楠 進; 中村 雄作 自律神経 48- (2) 156 -156 2011/04
- SAKAMOTO HIKARU; HIRANO MAKITO; SAMUKAWA MAKOTO; KITADA MARI; KUSUNOKI SUSUMU; NAKAMURA YUSAKU 日本神経学会学術大会プログラム・抄録集 52nd- 332 2011
- 当院におけるパーキンソン病患者への麦角系ドパミン作動薬使用の現況三井 良之; 塩山 実章; 宮本 勝一; 西郷 和真; 赤松 舞子; 豊増 麻美; 桑原 基; 鈴木 聖子; 寒川 真; 楠 進 臨床神経学 50- (12) 1189 -1189 2010/12
- 寒川 真; 市橋 珠里; 鈴木 秀和; 三井 良之; 楠 進; 長谷川 隆典 神経治療学 27- (3) 397 -397 2010/05
- SAMUKAWA MAKOTO; HIRANO MAKITO; SAKAMOTO HIKARU; KUSUNOKI SUSUMU; NAKAMURA YUSAKU 日本自律神経学会総会プログラム・抄録集 63rd- 182 -182 2010
- 三井良之; 塩山実章; 宮本勝一; 西郷和真; 赤松舞子; 豊増麻美; 桑原基; 鈴木聖子; 寒川真, 楠進 日本神経学会総会プログラム・抄録集 51st- 290 2010
Books and other publications
Lectures, oral presentations, etc.
- 当院で経験した末梢神経障害合併好酸球性多発血管炎性肉芽腫症の臨床像 [Not invited]寒川真; 谷口佳子; 山岸裕子; 河合滋; 岡崎真央; 濱田征宏; 濱田征宏; 桑原基; 鈴木秀和; 三井良之; 岡伸幸, 楠進日本末梢神経学会学術集会プログラム・抄録 2017/07
- トリプレットリピート病遺伝子の中間型アレルを有する患者に対する遺伝カウンセリング [Not invited]平野牧人; 平野牧人; 西郷和真; 寒川真; 上野周一; 濱田征宏; 中村雄作; 楠進日本遺伝カウンセリング学会誌 2017/05
- 再生不良性貧血の同種骨髄移植後に中枢神経原発移植後リンパ増殖性疾患を発症した1例 [Not invited]山名正樹; 寺山敦之; 森川みゆき; 寒川真; 鈴木秀和; 田崎貴之; 奥田武司; 小森舞子; 井上宏昭; 楠進Neuroimmunology 2017
- HNK‐1エピトープを認識するIgM M蛋白を伴うニューロパチー抗体affinityの変化と臨床経過の関連 [Not invited]濱田征宏; 桑原基; 寒川真; 森瀬譲二; 堀内惠美子; 岡昌吾, 楠進日本末梢神経学会学術集会プログラム・抄録 2016/07
- 好酸球性肺炎の治療経過中に免疫性脱髄性ニューロパチーを発症した一例 [Not invited]寒川真; 油原佳子; 三井良之; 岡伸幸, 楠進日本末梢神経学会学術集会プログラム・抄録 2016/07
- 病理学的に血管炎の合併も認めたFBLN5遺伝子の異常によるCharcot‐Marie‐Tooth病の1症例 [Not invited]山岸裕子; 寒川真; 桑原基; 三井良之; 岡伸幸; 橋口昭大; 高嶋博, 楠進日本末梢神経学会学術集会プログラム・抄録 2016/07
- ギラン・バレー症候群の予後予測と治療についての多施設共同研究 [Not invited]山岸裕子; 鈴木秀和; 寒川真; 園生雅弘; 桑原聡; 野村恭一; 千葉厚郎; 梶龍兒; 神田隆; 海田賢一; 池田修一; 楠進日本末梢神経学会学術集会プログラム・抄録 2016/07
- マイコプラズマ感染に伴う神経疾患と抗糖脂質抗体の特徴 [Not invited]桑原基; 寒川真; 池田妙; 森川みゆき; 上野莉乃; 濱田征宏; 楠進Neuroimmunology 2016
- 抗MAG抗体ニューロパチー:抗体affinityの変動と臨床経過 [Not invited]濱田征宏; 桑原基; 寒川真; 森瀬譲二; 堀内惠美子; 岡昌吾, 楠進日本神経学会学術大会プログラム・抄録集 2016
- 他の抗糖脂質抗体を伴ったGal‐C抗体陽性GBSの臨床的・電気生理学的検討 [Not invited]寒川真; 上野莉乃; 濱田征宏; 桑原基; 平野牧人; 平野牧人; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2016
- わが国におけるGBSの予後予測マーカーの検討 [Not invited]山岸裕子; 鈴木秀和; 寒川真; 桑原基; 濱田征宏; 福本雄太; 山名正樹; 油原佳子; 吉川恵輔; 森川みゆき; 上野莉乃; 河合滋; 岡崎真央; 西郷和真; 宮本勝一; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2016
- 単純血漿交換が有効であったGAD抗体低力価陽性小脳性運動失調症の1例 [Not invited]寒川真; 山岸裕子; 森川みゆき; 桑原基; 三井良之; 北口正孝; 楠進神経治療学 2015/09
- 鈴木秀和; 加藤茉里; 市橋珠里; 河合滋; 寒川真; 濱田征宏; 西郷和真; 三井良之; 楠進神経治療学 2015/09
- 遺伝性と考えられる末梢神経障害に血管炎性末梢神経障害を合併した一症例 [Not invited]山岸裕子; 寒川真; 桑原基; 三井良之; 岡伸幸, 楠進日本末梢神経学会学術集会プログラム・抄録 2015/07
- 抗SGPG抗体陰性のIgMパラプロテイン血症を伴うニューロパチーにおける血清学的および臨床的特徴の解析 [Not invited]桑原基; 濱田征宏; 森川みゆき; 上野莉乃; 寒川真, 楠進Neuroimmunology 2015
- 当院で経験した抗signal recognition particle抗体陽性筋症の臨床像 [Not invited]寒川真; 吉川恵介; 山岸裕子; 河合滋; 岡崎真央; 志賀俊彦; 濱田征宏; 桑原基; 鈴木秀和; 野崎祐史; 鈴木重明; 西郷和真; 三井良之; 西野一三; 船内正憲; 楠進日本神経学会学術大会プログラム・抄録集 2015
- Combinatorial Glycoarrayによる網羅的抗糖脂質複合体抗体の検出―ELISAとの比較― [Not invited]桑原基; 森川みゆき; 上野莉乃; 寒川真; 濱田征宏; 楠進日本神経学会学術大会プログラム・抄録集 2015
- 免疫性ニューロパチーの治療反応性予測に基づく有効な治療戦略の構築 LM1抗体陽性GBSの臨床的特徴 [Not invited]楠進; 桑原基; 森川みゆき; 濱田征宏; 上野莉乃; 寒川真; 三井良之免疫性ニューロパチーの治療反応性予測に基づく有効な治療戦略の構築 平成26年度 委託業務成果報告書 2015
- 頭部振戦と頭部MRIにて十字サインとを認めたSCA23の1家系 [Not invited]西郷和真; 西郷和真; 三井純; 平野牧人; 塩山実章; 寒川真; 市川弥生子; 後藤順; 辻省次; 巽純子; 田村和朗; 楠進日本人類遺伝学会大会プログラム・抄録集 2015
- わが国におけるGBSの予後予測マーカー(EGRISおよびmEGOS)の検討 [Not invited]鈴木秀和; 桑原基; 濱田征宏; 市橋珠里; 加藤茉里; 寒川真; 岡崎真央; 河合滋; 上野莉乃; 山岸裕子; 森川みゆき; 吉川恵輔; 山名正樹; 福本雄太; 油原佳子; 高田和男; 西郷和真; 宮本勝一; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2015
- グライコアレイを用いた免疫性ニューロパチーにおける血中糖脂質複合体抗体の解析 [Not invited]森川みゆき; 上野莉乃; 寒川真; 濱田征宏; 桑原基, 楠進日本神経学会学術大会プログラム・抄録集 2015
- 神経疾患における抗GM3抗体の検討 [Not invited]桑原基; 濱田征宏; 寒川真; 上野莉乃; 高田和男; 楠進Neuroinfection 2014/08
- 抗糖脂質抗体とHu抗体が陽性であり小脳失調を主徴とした肺小細胞癌例 [Not invited]野倉一也; 巨椋義蔵; 加子哲治; 寒川真; 楠進; 田中惠子臨床神経学 2014/02
- 神経疾患における抗GM3抗体の検討 [Not invited]桑原基; 濱田征宏; 寒川真; 上野莉乃; 高田和男; 楠進Neuroimmunology 2014
- 楠進; 桑原基; 寒川真; 濱田征宏; 高田和男免疫性神経疾患に関する調査研究 平成25年度 総括・分担研究報告書 2014
- インフルエンザウィルス感染後のGuillain‐Barre症候群及びFisher症候群 [Not invited]桑原基; 寒川真; 浜田征宏; 高田和男; 楠進日本神経学会学術大会プログラム・抄録集 2014
- 鈴木秀和; 加藤茉里; 市橋珠里; 森川みゆき; 岡崎真央; 寒川真; 西郷和真; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2014
- 免疫性神経疾患における抗糖脂質抗体クラススイッチの検討 [Not invited]寒川真; 桑原基; 上野莉乃; 濱田征宏; 高田和男; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2014
- 抗GalNAc‐GD1a抗体陽性症例における臨床病型の解析 [Not invited]濱田征宏; 上野莉乃; 寒川真; 桑原基; 高田和男; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2014
- 抗Gal-C抗体かつ他の抗糖脂質抗体も陽性であったGuillain-Barre症候群の電気生理学的検討 [Not invited]楠 進; 寒川 真; 濱田征宏; 桑原 基; 髙田 和男; 三井 良之第25回日本神経免疫学会学術集会 2013/11 下関 第25回日本神経免疫学会学術集会
- Refractory acute disseminated encephalomyelitis with anti-galactocerebroside antibody [Not invited]楠 進; 寒川 真; 平野 牧人; 阪本 光; 高田 和男; 桑原 基; 鈴木 聖子; 北田 茉里; 中村 雄作; Department of Neurology; Fukuoka University School of Medicine; Department of Neurology; Saga University School of Medicine; Department of Neurology; Fukuoka University School of Medicine; Department of Neurology; Saga University School of Medicine; Department of Neurology; Fukuoka University School of Medicinethe American Neurological Association's 2013 Annual Meeting 2013/10 New Orieans the American Neurological Association's 2013 Annual Meeting
- 鈴木秀和; 加藤茉里; 河合滋; 上野莉乃; 寒川真; 濱田征宏; 桑原基; 三井良之; 岡伸幸, 楠進神経治療学 2013/09
- 抗ガラクトセレブロシド(Gal‐C)抗体の関与が疑われた辺縁系脳炎の1例 [Not invited]北村彰浩; 藤田充世; 垣内無一; 中西恵美; 長山成美; 富岳亮; 田中惠子; 寒川真; 楠進, 松井真臨床神経学 2013/09
- 抗galactocerebsoside抗体陽性で末梢神経障害を合併した急性散在性脳脊髄炎の臨床的特徴 [Not invited]楠 進; 平野 牧人; 阪本 光; 高田 和男; 桑原 基; 山藤聖子; 加藤茉里; 中村 雄作; 寒川 真; 津川 潤; 田畑絵美; 山田達夫; 原 英夫; 坪井義夫第24回日本末梢神経学会学術集会 2013/08 新潟 第24回日本末梢神経学会学術集会
- 抗galactocerebsoside抗体陽性で末梢神経障害を合併した急性散在性脳脊髄炎の臨床的特徴 [Not invited]寒川真; 平野牧人; 津川潤; 阪本光; 田畑絵美; 高田和男; 桑原基; 山藤聖子; 加藤茉里; 山田達夫; 原英夫; 坪井義夫; 中村雄作; 楠進日本末梢神経学会学術集会プログラム・抄録 2013/07
- Guillain‐Barre症候群及びFisher症候群におけるGQ1bと交差反応を示す抗GM1/GD1a抗体 [Not invited]桑原基; MAURI Laura; 濱田征宏; 寒川真; 高田和男; SONNINO Sandro, 楠進日本神経学会学術大会プログラム・抄録集 2013/06 東京 第54回日本神経学会学術大会
- 抗ガラクトセレブロシド抗体の関与が疑われた辺縁系脳炎とGuillain‐Barre症候群の検討 [Not invited]北村彰浩; 藤田充世; 垣内無一; 中西恵美; 長山成美; 富岳亮; 田中惠子; 寒川真; 楠進, 松井真日本神経学会学術大会プログラム・抄録集 2013/06 東京 第54回日本神経学会学術大会
- IgMパラプロテイン血症を伴うニューロパチーにおけるHNK‐1抗体活性と臨床特徴の関連 [Not invited]濱田征宏; 寒川真; 桑原基; 藪野景子; 森瀬譲二; 高田和男; 宮本勝一; 岡昌吾, 楠進日本神経学会学術大会プログラム・抄録集 2013/06 東京 第54回日本神経学会学術大会
- 抗galactocerebroside抗体陽性Guillain-Barre症候群の臨床的、電気生理学的検討 [Not invited]楠 進; 寒川 真; 濱田征宏; 桑原 基; 鈴木 秀和; 高田 和男; 三井 良之第54回日本神経学会学術大会 2013/06 東京 第54回日本神経学会学術大会
- 抗galactocerebroside抗体陽性Guillain‐Barre症候群の臨床的・電気生理学的検討 [Not invited]寒川真; 濱田征宏; 桑原基; 鈴木秀和; 高田和男; 三井良之; 楠進日本神経学会学術大会プログラム・抄録集 2013/01 東京 免疫性神経疾患に関する調査研究班 平成24年度班会議
- 免疫性神経疾患に関する調査研究 ギラン・バレー症候群/フィッシャー症候群(1)抗galactocerebroside抗体陽性Guillain‐Barre症候群の臨床的・電気生理学的検討 [Not invited]楠進; 寒川真; 濱田征宏; 桑原基; 鈴木秀和; 高田和男; 三井良之免疫性神経疾患に関する調査研究 平成24年度 総括・分担研究報告書 2013
- ブロモプロパンの神経毒性 [Not invited]市原学; 寒川真日本職業・災害医学会会誌 2012/11
- Clinical features of CIDP with antibodies to LM1 and LM1 containing ganglioside complexes. [Not invited]楠 進; 桑原 基; 鈴木 秀和; 寒川 真; 濱田 征宏; 高田 和男11th International Congress of Neuroimmunology 2012/11 Boston, USA 11th International Congress of Neuroimmunology
- 非ヘルペス性辺縁系脳炎の頭部MRIにおける初期硬膜病変 [Not invited]鈴木 秀和; 加藤茉里; 上野周一; 寒川 真; 市橋珠里; 三井 良之; 楠 進; 田中惠子第53回日本神経学会学術大会P(2)-275 2012/05 東京 第53回日本神経学会学術大会P(2)-275
- A case of anti-NMDAR encephalitis mimicking diagnosed as cerebral infarction. [Not invited]加藤 茉里; 寒川 真; 三井 良之; 楠 進; 鈴木 秀和; 田中惠子第37回日本脳卒中学会総会 2012/04 福岡 第37回日本脳卒中学会総会
- 強皮症にともなう抗NMDA受容体脳炎の1例 [Not invited]鈴木秀和; 寒川真; 青松宏美; 三井良之; 楠進臨床神経学 2012/02
- locked‐in様症状を呈した抗galactocerebroside(Gal‐C)抗体陽性ADEMの1例 [Not invited]寒川真; 阪本光; 平野牧人; 鈴木聖子; 桑原基; 中村雄作; 楠進臨床神経学 2012/02
- 本邦におけるバルデー・ビードル症候群の臨床的特徴 [Not invited]平野牧人; 山下俊英; 生野恭司; 岩橋博見; 大石充; 真野利之; 石原立; 田中一郎; 柳原恵子; 寒川真; 阪本光; 中村雄作; 楠進臨床神経学 2012/02
- 多系統萎縮症患者における抗利尿ホルモン不適合分泌症候群合併の検討 [Not invited]平野牧人; 上野周一; 寒川真; 阪本光; 楠進; 中村雄作パーキンソン病・運動障害疾患コングレスプログラム・抄録集 2012
- 1‐ブロモプロパン曝露による神経障害 [Not invited]寒川真日本産業衛生学会講演集(CD-ROM) 2012
- 抗NMDA受容体脳炎における男性症例の臨床的特徴 [Not invited]平野牧人; 上野周一; 阪本光; 寒川真; 磯野千春; 楠進; 中村雄作パーキンソン病・運動障害疾患コングレスプログラム・抄録集 2012
- 抗NMDAR抗体陽性脳炎の高次機能障害と機能予後 [Not invited]上田昌美; 豊増麻美; 大洞佳代子; 福田寛二; 鈴木秀和; 北田茉里; 寒川真; 上野周一; 市橋珠里; 楠進Jpn J Rehabil Med 2011/12
- Ciclosporineにより良好な経過がえられた抗NMDAR脳炎の2例. [Not invited]加藤 茉里; 鈴木 秀和; 寒川 真; 三井 良之; 楠 進; 田中惠子第29回日本神経治療学会総会 2011/11 福井 第29回日本神経治療学会総会
- 群発頭痛様発作で発症した中枢神経限局性血管炎の1例 [Not invited]西郷 和真; 濱田 征宏; 寒川 真; 桑原 基; 稲次 洋平; 塩山 実章; 三井 良之; 布川 知史; 加藤 天美第39回 日本頭痛学会総会 2011/11 埼玉 第39回 日本頭痛学会総会
- 回復期に著明な側頭葉萎縮を来した抗NMDA受容体抗体関連脳炎の1例 [Not invited]阪本光; 平野牧人; 寒川真; 北田茉里; 上野周一; 田中惠子; 楠進; 中村雄作臨床神経学 2011/10
- 精神症状が治療抵抗性であったMorvan症候群の一例 [Not invited]寒川真; 鈴木秀和; 北田茉里; 三井良之; 中村雄作; 楠進臨床神経学 2011/10
- Ciclosporineにより良好な経過がえられた抗NMDAR脳炎の2例 [Not invited]北田茉里; 鈴木秀和; 寒川真; 三井良之; 楠進; 田中惠子神経治療学 2011/09
- Morvan症候群2例の治療経験 [Not invited]寒川真; 鈴木秀和; 北田茉里; 三井良之; 楠進; 中村雄作神経治療学 2011/09
- 回復期に著明な側頭葉萎縮を来したNMDA受容体抗体関連脳炎の1例. [Not invited]楠 進; 阪本 光; 平野 牧人; 寒川 真; 北田 茉里; 上野 周一; 中村 雄作; 田中惠子回復期に著明な側頭葉萎縮を来したNMDA受容体抗体関連脳炎の1例。 2011/06 京都 回復期に著明な側頭葉萎縮を来したNMDA受容体抗体関連脳炎の1例。
- 多系統萎縮症と抗利尿ホルモン不適合分泌症候群の関連 [Not invited]阪本光; 平野牧人; 寒川真; 北田茉里; 楠進; 中村雄作日本神経学会学術大会プログラム・抄録集 2011/05 名古屋 多系統萎縮症と抗利尿ホルモン不適合分泌症候群の関連.
- 抗NMDA受容体脳炎連続6症例の検討―臨床的多様性と治療戦略― [Not invited]鈴木秀和; 北田茉里; 寒川真; 上野周一; 市橋珠里; 三井良之; 田中惠子; 楠進日本神経学会学術大会プログラム・抄録集 2011/05 名古屋 第52回日本神経学会学術大会
- 腫瘍非合併抗NMDA receptor 脳炎の3例 [Not invited]鈴木 秀和; 北田 茉里; 寒川 真; 市橋 珠里; 三井 良之; 楠 進; 田中 恵子第11回神経・筋の免疫疾患を考える会 2011/02 大阪 第11回神経・筋の免疫疾患を考える会
- ステロイド療法に抵抗性であったが免疫グロブリン大量療法(IVIg)にて奏効が得られた抗SRP抗体陽性筋炎の2例 [Not invited]寒川真; 市橋珠里; 鈴木秀和; 三井良之; 楠進; 長谷川隆典神経治療学 2010/05
- 当院におけるパーキンソン病患者への麦角系ドパミン作動薬使用の現況 [Not invited]三井良之; 塩山実章; 宮本勝一; 西郷和真; 赤松舞子; 豊増麻美; 桑原基; 鈴木聖子; 寒川真, 楠進日本神経学会総会プログラム・抄録集 2010/05 東京 第51回日本神経学会総会
- 多系統萎縮症における抗利尿ホルモン不適合分泌症候群の合併 [Not invited]寒川真; 平野牧人; 阪本光; 楠進; 中村雄作日本自律神経学会総会プログラム・抄録集 2010