start-ver=1.4
cd-journal=joma
no-vol=353
cd-vols=
no-issue=1-2
article-no=
start-page=185
end-page=186
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20156
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Selective disappearance of medial back muscles in a case of myotonic dystrophy type 1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=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.
en-copyright=
kn-copyright=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=DeguchiKentaro
en-aut-sei=Deguchi
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=Myotonic dystrophy type 1
kn-keyword=Myotonic dystrophy type 1
en-keyword=Paraspinal muscles
kn-keyword=Paraspinal muscles
en-keyword=Late onset
kn-keyword=Late onset
END

start-ver=1.4
cd-journal=joma
no-vol=387
cd-vols=
no-issue=15
article-no=
start-page=70
end-page=74
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20184
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Familial and sporadic chronic progressive degenerative parietal ataxia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=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.
en-copyright=
kn-copyright=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DeguchiKentaro
en-aut-sei=Deguchi
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IkeuchiTakeshi
en-aut-sei=Ikeuchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KitaguchiMasataka
en-aut-sei=Kitaguchi
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=2
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=3
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=4
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=5
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=6
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=7
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=8
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=9
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Molecular Genetics, Bioresource Science Branch, Center of Bioresource, Brain Research Institute Niigata University
kn-affil=

affil-num=11
en-affil=Department of Neurology, Baba Memorial Hospital
kn-affil=

affil-num=12
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
en-keyword=parietal ataxia
kn-keyword=parietal ataxia
en-keyword=parietal lobe atrophy
kn-keyword=parietal lobe atrophy
en-keyword=crossed cerebellar diaschisis
kn-keyword=crossed cerebellar diaschisis
en-keyword=MAPT
kn-keyword=MAPT
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=5
article-no=
start-page=e67
end-page=e69
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201305
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A novel familial prion disease causing pan-autonomic-sensory neuropathy and cognitive impairment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MatsuzonoKosuke
en-aut-sei=Matsuzono
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IkedaYoshio
en-aut-sei=Ikeda
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuWentao
en-aut-sei=Liu
en-aut-mei=Wentao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DeguchiShoko
en-aut-sei=Deguchi
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DeguchiKentaro
en-aut-sei=Deguchi
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=

affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=3
en-affil=
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=5
en-affil=
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=
en-keyword=Prion disease
kn-keyword=Prion disease
en-keyword=Novelgene mutation
kn-keyword=Novelgene mutation
en-keyword=2bp deletion in codon 178
kn-keyword=2bp deletion in codon 178
en-keyword=stopcodon at codon 195
kn-keyword=stopcodon at codon 195
en-keyword=Sensoryneuropathy
kn-keyword=Sensoryneuropathy
en-keyword=HSAN
kn-keyword=HSAN
en-keyword=Pan-autonomicfailure
kn-keyword=Pan-autonomicfailure
en-keyword=Familial case
kn-keyword=Familial case
END

start-ver=1.4
cd-journal=joma
no-vol=125
cd-vols=
no-issue=1
article-no=
start-page=69
end-page=71
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Guidelines for the treatment of Parkinson’s disease
kn-title=パーキンソン病の治療ガイドライン
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=倉田智子
kn-aut-sei=倉田
kn-aut-mei=智子
aut-affil-num=1
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=阿部康二
kn-aut-sei=阿部
kn-aut-mei=康二
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　神経内科

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　脳神経内科学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=変異β-アミロイド前駆体蛋白と変異プレセニリン-１の両者を発現したトランスジェニックマウスではリン酸化α-シヌクレインの蓄積が促進される
kn-title=Enhanced Accumulation of Phosphorylated α-Synuclein in Double Transgenic Mice Expressing Mutant β-Amyloid Precursor Protein and Presenilin-1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=倉田智子
kn-aut-sei=倉田
kn-aut-mei=智子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END