Elsevier BV Acta Medica Okayama 0022-510X 353 1-2 2015 Selective disappearance of medial back muscles in a case of myotonic dystrophy type 1 185 186 EN Ryuta Morihara Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science Nozomi Hishikawa Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science Toru Yamashita Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science Kentaro Deguchi Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science Tomoko Kurata Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science Koji Abe Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science Here, we report a unique case of late-onset myotonic dystrophy type 1 in a 64-year-old woman, with selective disappearance of the medial lower back muscles. We compared the clinical features of this patient with those of a cohort of 29 patients with myotonic dystrophy type 1 to clarify the correlation between clinical features and lower back muscle atrophy. After classification into three subgroups according to muscle atrophy pattern, medial muscle atrophy was present in 17.2% of the patients. Affected patients were older at onset than non-affected patients, and limb muscle power and respiratory function decreased with atrophy progression. No potential conflict of interest relevant to this article was reported.

Elsevier BV Acta Medica Okayama 0022-510X 387 15 2018 Familial and sporadic chronic progressive degenerative parietal ataxia 70 74 EN Ryuta Morihara Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Toru Yamashita Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Kentaro Deguchi Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Tomoko Kurata Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Emi Nomura Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Kota Sato Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Yumiko Nakano Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Yasuyuki Ohta Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Nozomi Hishikawa Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Takeshi Ikeuchi Department of Molecular Genetics, Bioresource Science Branch, Center of Bioresource, Brain Research Institute Niigata University Masataka Kitaguchi Department of Neurology, Baba Memorial Hospital Koji Abe Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University Background & objective: Parietal ataxia has been mainly reported as a consequence of acute ischemic stroke, while degenerative parietal ataxia has not been reported. Methods: We investigated clinical characteristics, neuroimaging data, and genetic analysis of patients with cerebellar ataxia plus parietal atrophy. Results: We identified seven patients, including five patients from two families, with chronic progressive cerebellar ataxia due to degenerative parietal atrophy but not stroke. Age at onset of ataxia was 57.6 +/- 6.9 years. All patients showed chronic progressive cerebellar ataxia with severity of ataxic gait > limb ataxia > dysarthria. Patients showed no cognitive dysfunction, muscle weakness, or parkinsonism, and only two patients showed mild sensory disturbances. The seven patients showed lateralized limb ataxia with greater contralateral parietal lobe atrophy by magnetic resonance imaging, and hypoperfusion by single photon emission computed tomography, without any abnormal cerebellar pathology (i.e., crossed cerebellar diaschisis). Pathogenic mutations in the microtubule-associated protein tau gene were not found using two single nucleotide polymorphisms. Conclusions: This is the first description showing unique clinical features of familial and sporadic chronic progressive degenerative parietal ataxia. No potential conflict of interest relevant to this article was reported.

Wiley Acta Medica Okayama 1351-5101 20 5 2013 A novel familial prion disease causing pan-autonomic-sensory neuropathy and cognitive impairment e67 e69 EN Kosuke Matsuzono Yoshio Ikeda Department of Neurology, Okayama University Graduate School of Medicine and Dentistry Wentao Liu Tomoko Kurata Department of Neurology, Okayama University Graduate School of Medicine and Dentistry Shoko Deguchi Kentaro Deguchi Department of Neurology, Okayama University Graduate School of Medicine and Dentistry Koji Abe Department of Neurology, Okayama University Graduate School of Medicine and Dentistry No potential conflict of interest relevant to this article was reported.

岡山医学会 Acta Medica Okayama 0030-1558 125 1 2013 パーキンソン病の治療ガイドライン 69 71 EN Tomoko Kurata Koji Abe No potential conflict of interest relevant to this article was reported.

Acta Medica Okayama 2008 Enhanced Accumulation of Phosphorylated α-Synuclein in Double Transgenic Mice Expressing Mutant β-Amyloid Precursor Protein and Presenilin-1 EN Tomoko Kurata No potential conflict of interest relevant to this article was reported.