Clinical Neurology最新文献_第9页

[Dystypia in a patient with subcortical ischemic stroke]. [皮层下缺血性中风患者的肌张力障碍]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-17 DOI: 10.5692/clinicalneurol.cn-001904

Wakana Yamamoto, Yuichiro Inatomi, Minoru Matsuda

引用次数: 0

[A case of bilateral middle cerebellar peduncle infarction with hot cross bun sign]. [双侧小脑中梗塞伴热十字包征一例]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-17 DOI: 10.5692/clinicalneurol.cn-001897

Daisuke Kuzume, Yuko Morimoto, Satoshi Tsutsumi, Masahiro Yamasaki, Naohisa Hosomi

{"title":"[A case of bilateral middle cerebellar peduncle infarction with hot cross bun sign].","authors":"Daisuke Kuzume, Yuko Morimoto, Satoshi Tsutsumi, Masahiro Yamasaki, Naohisa Hosomi","doi":"10.5692/clinicalneurol.cn-001897","DOIUrl":"10.5692/clinicalneurol.cn-001897","url":null,"abstract":"A 71-year-old man with hypertension and diabetes mellitus presented to our hospital because he felt lightheaded. Diffusion-weighted images (DWI) on brain MRI showed high signal lesions in the left cerebellar hemisphere and the right pons. The diagnosis of cerebellar infarction was made, but he refused treatment. One month later, he came to our hospital because his body leaned to the left. Neurological examination revealed dysarthria and cerebellar truncal ataxia. An electrocardiogram showed atrial fibrillation. DWI on brain MRI showed high signal lesions in the bilateral cerebellar hemispheres and middle cerebellar peduncles (MCP). Dabigatran 300 ‍mg/day was administered for cardiogenic cerebral embolism. On the 12th day of onset, he was transferred to a rehabilitation hospital. At 72 years old, T2*-weighted images on brain MRI showed hot cross bun sign (HCBs) in the pons. We considered that HCBs were caused by antegrade or retrograde degeneration (or both) of pontine infarcts and bilateral MCP infarcts in the pontine cerebellar tract. It seemed preferable to use T2*-weighted images or proton density-weighted images rather than T2-weighted images to detect HCBs. When HCBs is detected, it should be noted that HCBs can be caused by bilateral MCP infarcts in addition to multiple system atrophy.","PeriodicalId":39292,"journal":{"name":"Clinical Neurology","volume":" ","pages":"190-193"},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139900561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Altered antibody titers in patients with neuromuscular diseases after high-dose intravenous immunoglobulin therapy]. [大剂量静脉注射免疫球蛋白治疗后神经肌肉疾病患者抗体滴度的改变]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-17 DOI: 10.5692/clinicalneurol.cn-001895

Wataru Shiraishi, Yukiko Inamori, Ayano Matsuyoshi, Tetsuya Hashimoto

引用次数: 0

[Blood-brain barrier breakdown and autoimmune cerebellar ataxia]. [血脑屏障破坏与自身免疫性小脑共济失调症］

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-23 DOI: 10.5692/clinicalneurol.cn-001932

Fumitaka Shimizu

{"title":"[Blood-brain barrier breakdown and autoimmune cerebellar ataxia].","authors":"Fumitaka Shimizu","doi":"10.5692/clinicalneurol.cn-001932","DOIUrl":"10.5692/clinicalneurol.cn-001932","url":null,"abstract":"Autoimmune cerebellar ataxia is a disease entity that affects the cerebellum and is induced by autoimmune mechanisms. The disease is classified into several etiologies, including gluten ataxia, anti-glutamate decarboxylase (GAD) ataxia, paraneoplastic cerebellar degeneration, primary autoimmune cerebellar ataxia and postinfectious cerebellar ataxia. The autoimmune response in the periphery cross-reacts with similar antigens in the cerebellum due to molecular mimicry. Breakdown of the blood‒brain barrier (BBB) could potentially explain the vulnerability of the cerebellum during the development of autoimmune cerebellar ataxia, as it gives rise to the entry of pathogenic autoantibodies or lymphocytes into the cerebellum. In this review, the maintenance of the BBB under normal conditions and the molecular basis of BBB disruption under pathological conditions are highlighted. Next, the pathomechanism of BBB breakdown in each subtype of autoimmune cerebellar ataxia is discussed. We recently identified glucose-regulated protein (GRP) 78 antibodies in paraneoplastic cerebellar degeneration and Lambert-Eaton myasthenic syndrome, and GRP78 antibodies induced by cross-reactivity with tumors can disrupt the BBB and penetrate anti-P/Q type voltage-gated calcium channel (VGCC) antibodies into the cerebellum, thus leading to cerebellar ataxia in this disease.","PeriodicalId":39292,"journal":{"name":"Clinical Neurology","volume":" ","pages":"148-156"},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139973904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[A case of Hashimoto's encephalopathy with acute onset of psychiatric symptoms and diffuse deep white matter lesions on brain MRI]. [一例伴有急性精神症状和脑磁共振成像弥漫性深部白质病变的桥本脑病病例]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-22 DOI: 10.5692/clinicalneurol.cn-001905

Naomi Takahashi, Yukihiro Shikama, Hikaru Kawahara, Yuma Okabe, Masayuki Kurimura, Yasuyuki Ohta

引用次数: 0

[Resting tremor of Parkinson's disease changing into Holmes' tremor by cerebellar hemorrhage: an examination of the pathophysiological mechanism of tremor]. [小脑出血导致帕金森病静止性震颤转变为霍姆斯震颤：震颤的病理生理机制研究]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-22 DOI: 10.5692/clinicalneurol.cn-001936

Masahiro Nakamura, Osamu Isono, Tetsuya Nasu, Yuji Hinuma, Noriko Nakamura

{"title":"[Resting tremor of Parkinson's disease changing into Holmes' tremor by cerebellar hemorrhage: an examination of the pathophysiological mechanism of tremor].","authors":"Masahiro Nakamura, Osamu Isono, Tetsuya Nasu, Yuji Hinuma, Noriko Nakamura","doi":"10.5692/clinicalneurol.cn-001936","DOIUrl":"10.5692/clinicalneurol.cn-001936","url":null,"abstract":"A 71-year-old male who suffered from Hoehn and Yahr stage III Parkinson's disease with bradykinesia, rigidity and a 5-6-Hz tremor at rest in the right extremities was admitted to our hospital due to the sudden onset of vertigo. Right cerebellar hemorrhage was confirmed by CT. The patient's resting tremor in the right extremities disappeared immediately following the cerebellar hemorrhage. Six days later, MRI showed Wallerian degeneration in the cerebello-rubro-thalamic tract. Approximately 5 months later, a 2-3-Hz Holmes' tremor gradually appeared in the right upper extremity. This tremor was improved by increasing L-dopa doses. Case reports of the disappearance of Parkinson's resting tremor and subsequent emergence of Holmes' tremor due to cerebellar lesion are rare. Furthermore, the Wallerian degeneration of the cerebello-rubro-thalamic tract identified on MRI between tremors of the different frequencies is very rare. We hypothesize that the cause of the tremor frequency change was simultaneous damage to the nigro-striatal network and the cerebello-thalamo-cerebral network.","PeriodicalId":39292,"journal":{"name":"Clinical Neurology","volume":" ","pages":"185-189"},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139933399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Cilostazol was effective for capsular warning syndrome during anticoagulant therapy: a case report]. [西洛他唑对抗凝剂治疗期间的囊状警告综合征有效：病例报告]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-17 DOI: 10.5692/clinicalneurol.cn-001927

Ayane Kawatake, Hiroyuki Kawano, Yuko Honda, Yoshiko Unno, Teruyuki Hirano

引用次数: 0

[Recent clinical advances in hereditary spinocerebellar degeneration]. [遗传性脊髓小脑变性的最新临床进展]。

Clinical Neurology Pub Date : 2024-03-22 Epub Date: 2024-02-22 DOI: 10.5692/clinicalneurol.cn-001931

Ichiro Yabe

引用次数: 0

[Embolic stroke due to ascending aortic thrombus in a patient with treatment-resistant ulcerative colitis]. [耐药性溃疡性结肠炎患者升主动脉血栓导致的栓塞性中风]。

Clinical Neurology Pub Date : 2024-02-23 Epub Date: 2024-01-20 DOI: 10.5692/clinicalneurol.cn-001901

Kenichi Inoue, Toshiyasu Ogata, Takayasu Mishima, Hideki Ishibashi, Fumihito Hirai, Yoshio Tsuboi

{"title":"[Embolic stroke due to ascending aortic thrombus in a patient with treatment-resistant ulcerative colitis].","authors":"Kenichi Inoue, Toshiyasu Ogata, Takayasu Mishima, Hideki Ishibashi, Fumihito Hirai, Yoshio Tsuboi","doi":"10.5692/clinicalneurol.cn-001901","DOIUrl":"10.5692/clinicalneurol.cn-001901","url":null,"abstract":"The patient was a 49-year-old man presenting with recurrent melena due to progressive ulcerative colitis. One day, he developed left lower facial weakness and dysarthria, and the next day, he was transferred to our hospital because of muscle weakness in his left upper and lower extremities. On admission, neurological findings revealed left hemiplegia, including left facial palsy, dysarthria, and left hemispatial neglect. Brain MRI with diffusion-weighted image showed a fresh infarction in the right anterior and middle cerebral artery territory. Contrast-enhanced CT showed thrombus in the ascending aorta in addition to occlusion of the right internal carotid artery, suggesting the diagnosis of cerebral infarction with an embolic source in the aortic lesion. The intra-aortic thrombus disappeared after 48th day of antithrombotic therapy. Laboratory findings revealed elevated blood viscosity, proteinase-3-anti-neutrophil cytoplasmic antibody (PR3-ANCA), and β2GP1-IgG antibodies, suggesting that the cause of the aortic thrombus may be due to elevated blood viscosity and autoantibodies, as well as highly active ulcerative colitis.","PeriodicalId":39292,"journal":{"name":"Clinical Neurology","volume":" ","pages":"93-98"},"PeriodicalIF":0.0,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139513769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Clinical features and pathogenesis of Glial fibrillary acidic protein (GFAP) antibody-associated disorders]. [神经胶质纤维酸性蛋白（GFAP）抗体相关疾病的临床特征和发病机制]。

Clinical Neurology Pub Date : 2024-02-23 Epub Date: 2024-01-27 DOI: 10.5692/clinicalneurol.cn-001925

Akio Kimura

{"title":"[Clinical features and pathogenesis of Glial fibrillary acidic protein (GFAP) antibody-associated disorders].","authors":"Akio Kimura","doi":"10.5692/clinicalneurol.cn-001925","DOIUrl":"10.5692/clinicalneurol.cn-001925","url":null,"abstract":"Glial fibrillary acidic protein (GFAP) antibody-associated disorders (AD) were recently proposed to be immune-mediated neurological disorders. The pathogenesis of GFAP antibody-AD is poorly understood. Pathologically, there is a marked infiltration of large numbers of lymphocytes, including CD8+ and CD4+ T cells, into the meningeal and brain parenchyma, especially around the perivascular areas. GFAP-specific cytotoxic T cells are considered to be the effector cells of GFAP antibody-AD. The common phenotype of GFAP antibody-AD includes meningoencephalitis with or without myelitis. During the clinical disease course, patients present with consciousness disturbances, urinary dysfunction, movement disorders, meningeal irritation, and cognitive dysfunction. The detection of GFAP antibodies in the cerebrospinal fluid (CSF) by cell-based assay is essential for a diagnosis of GFAP antibody-AD. The CSF can be examined for lymphocyte-predominant pleocytosis and elevated protein levels. Brain linear perivascular radial enhancement patterns are observed in about half of GFAP antibody-AD patients. Spinal cord magnetic resonance imaging is used to detect longitudinal extensive spinal cord lesions. Although corticosteroid therapy is generally effective, some patients have a poor prognosis and relapse.","PeriodicalId":39292,"journal":{"name":"Clinical Neurology","volume":" ","pages":"75-84"},"PeriodicalIF":0.0,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139571555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0