TY - JOUR
T1 - Corpus callosal involvement is correlated with cognitive impairment in multiple system atrophy
AU - Hara, Kazuhiro
AU - Watanabe, Hirohisa
AU - Bagarinao, Epifanio
AU - Kawabata, Kazuya
AU - Yoneyama, Noritaka
AU - Ohdake, Reiko
AU - Imai, Kazunori
AU - Masuda, Michihito
AU - Yokoi, Takamasa
AU - Ogura, Aya
AU - Tsuboi, Takashi
AU - Ito, Mizuki
AU - Atsuta, Naoki
AU - Niwa, Hisayoshi
AU - Taoka, Toshiaki
AU - Maesawa, Satoshi
AU - Naganawa, Shinji
AU - Katsuno, Masahisa
AU - Sobue, Gen
N1 - Funding Information:
Funding KH reports Grants from the Ministry of Education, Culture, Sports, Science and Technology (Grant number JP 15K19484). He also reports a salary from Nagoya University. HW reports Grants-in-Aid from the Research Committee of Central Nervous System Degenerative Diseases by the Ministry of Health, Labour, and Welfare and from the Integrated Research on Neuropsychiatric Disorders project carried out under the Strategic Research for Brain Sciences by the Ministry of Education, Culture, Sports, Science, and Technology of Japan. He also reports a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan (Grant number 80569781) and a Grant-in-Aid for Scientific Research on Innovative Areas (Brain Protein Aging and Dementia Control) (26117002) from MEXT. He reports a salary from the Brain and Mind Research Center, Nagoya University. EB reports Grants-In-Aid for Scientific Research (KAKENHI number 26350993) funded by the Japan Society for the Promotion of Science and a salary from the Brain and Mind Research Center, Nagoya University. KK reports no disclosures. NY reports no disclosures. RO reports no disclosures. KI reports no disclosures. MM reports no disclosures. TY reports no disclosures. AO reports no disclosures. TT reports Grants from the Japan Society for the Promotion of Science (Grant number JP16K19507), GlaxoSmithKline, and Novartis. He also reports a salary from Nagoya University. MI is funded by a Grant-in-Aid from the Ministry of Education, Culture, Sports, Science and Technology of Japan. NA is funded by a Grant-in-Aid from the Ministry of Education, Culture, Sports, Science and Technology of Japan. HN reports no disclosures. TT reports no disclosures. SM reports no disclosures. SN reports no disclosures. MK is supported by KAKENHI Grants from MEXT/JSPS, Japan (nos. 17H04195 and 16K15480); Grants from the Japan Agency for Medical Research and Development (nos. 17ek0109221h0001, 16dk0207026h0001, and 15ek0109165); and a Grant from the Naito Foundation. GS reports KAKENHI Grants from MEXT/JSPS, Japan (nos. 26117001); Grants from the Japan Science and Technology Agency; Grants from the Japan Agency for Medical Research and Development (AMED) (nos. 15ek0109025, 15ek0109048, and 15ek0109165); and Grants from the Ministry of Welfare, Health, and Labor of Japan.
Funding Information:
Acknowledgements This research is partially supported by a Grant-in-Aid from the Research Committee of Central Nervous System Degenerative Diseases by the Ministry of Health, Labour, and Welfare, Integrated Research on Neuropsychiatric Disorders project carried out by SRBPS and a Grant-in-Aid for Scientific Research on Innovative Areas (Brain Protein Aging and Dementia Control 26117002) from the MEXT of Japan, Integrated Research on Neuropsychiatric Disorders carried out under the Strategic Research Program for Brain Sciences, Scientific Research on Innovative Areas (Comprehensive Brain Science Network), and Integrated Research on Depression, Dementia and Development Disorders by the Strategic Research Program for Brain Sciences from the Japan Agency for Medical Research and Development, AMED.
Publisher Copyright:
© 2018, Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2018/9/1
Y1 - 2018/9/1
N2 - Objective: We examined the anatomical involvement related to cognitive impairment in patients with multiple system atrophy (MSA). Methods: We examined 30 patients with probable MSA and 15 healthy controls. All MSA patients were assessed by the Unified MSA-Rating scale and Addenbrooke’s Cognitive Examination-Revised (ACE-R). We classified 15 MSA patients with ACE-R scores > 88 as having normal cognition (MSA–NC) and 15 with scores ≤ 88 as having cognitive impairment (MSA–CI). All subjects underwent 3 T MRI scanning and were investigated using voxel-based morphometry and diffusion tensor imaging. Results: Both the MSA–NC and MSA–CI patients exhibited cerebellar but not cerebral atrophy in voxel-based morphometry compared to controls. In contrast, tract-based spatial statistics revealed widespread and significantly decreased fractional anisotropy (FA) values, as well as increased mean diffusivity, radial diffusivity, and axial diffusivity in both the cerebrum and cerebellum in MSA–CI patients compared to controls. MSA–NC patients also exhibited similar involvement of the cerebellum but less extensive involvement of the cerebrum compared with the MSA–CI patients. In particular, FA values in MSA–CI patients were significantly decreased in the anterior part of the left corpus callosum compared with those in MSA–NC patients. The mean FA values in the left anterior part of the corpus callosum were significantly correlated with total ACE-R scores and subscores (memory, fluency, and language) in MSA patients. Conclusions: Decreased FA values in the anterior corpus callosum showed a significant correlation with cognitive impairment in MSA.
AB - Objective: We examined the anatomical involvement related to cognitive impairment in patients with multiple system atrophy (MSA). Methods: We examined 30 patients with probable MSA and 15 healthy controls. All MSA patients were assessed by the Unified MSA-Rating scale and Addenbrooke’s Cognitive Examination-Revised (ACE-R). We classified 15 MSA patients with ACE-R scores > 88 as having normal cognition (MSA–NC) and 15 with scores ≤ 88 as having cognitive impairment (MSA–CI). All subjects underwent 3 T MRI scanning and were investigated using voxel-based morphometry and diffusion tensor imaging. Results: Both the MSA–NC and MSA–CI patients exhibited cerebellar but not cerebral atrophy in voxel-based morphometry compared to controls. In contrast, tract-based spatial statistics revealed widespread and significantly decreased fractional anisotropy (FA) values, as well as increased mean diffusivity, radial diffusivity, and axial diffusivity in both the cerebrum and cerebellum in MSA–CI patients compared to controls. MSA–NC patients also exhibited similar involvement of the cerebellum but less extensive involvement of the cerebrum compared with the MSA–CI patients. In particular, FA values in MSA–CI patients were significantly decreased in the anterior part of the left corpus callosum compared with those in MSA–NC patients. The mean FA values in the left anterior part of the corpus callosum were significantly correlated with total ACE-R scores and subscores (memory, fluency, and language) in MSA patients. Conclusions: Decreased FA values in the anterior corpus callosum showed a significant correlation with cognitive impairment in MSA.
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U2 - 10.1007/s00415-018-8923-7
DO - 10.1007/s00415-018-8923-7
M3 - Article
C2 - 29974207
AN - SCOPUS:85049566947
VL - 265
SP - 2079
EP - 2087
JO - Deutsche Zeitschrift fur Nervenheilkunde
JF - Deutsche Zeitschrift fur Nervenheilkunde
SN - 0340-5354
IS - 9
ER -