Early and extensive spinal white matter involvement in neuromyelitis optica

Shotaro Hayashida, Katsuhisa Masaki, Tomomi Yonekawa, Satoshi Suzuki, Hiwatashi Akio, Takuya Matsushita, mitsuru watanabe, Ryo Yamasaki, Toshihiko Suenaga, Toru Iwaki, Hiroyuki Murai, Jun-Ichi Kira

研究成果: ジャーナルへの寄稿記事

7 引用 (Scopus)

抄録

Objectives: Studies of longitudinally extensive spinal cord lesions (LESCLs) in neuromyelitis optica (NMO) have focused on gray matter, where the relevant antigen, aquaporin-4 (AQP4), is abundant. Because spinal white matter pathology in NMO is not well characterized, we aimed to clarify spinal white matter pathology of LESCLs in NMO. Methods: We analyzed 50 spinal cord lesions from eleven autopsied NMO/NMO spectrum disorder (NMOSD) cases. We also evaluated LESCLs with three or fewer spinal cord attacks by 3-tesla MRI in 15 AQP4 antibody-positive NMO/NMOSD patients and in 15 AQP4 antibody-negative multiple sclerosis (MS) patients. Results: Pathological analysis revealed seven cases of AQP4 loss and four predominantly demyelinating cases. Forty-four lesions from AQP4 loss cases involved significantly more frequently posterior columns (PC) and lateral columns (LC) than anterior columns (AC) (59.1%, 63.6%, and 34.1%, respectively). The posterior horn (PH), central portion (CP), and anterior horn (AH) were similarly affected (38.6%, 36.4% and 31.8%, respectively). Isolated perivascular inflammatory lesions with selective loss of astrocyte endfoot proteins, AQP4 and connexin 43, were present only in white matter and were more frequent in PC and LC than in AC (22.7%, 29.5% and 2.3%, P corr = 0.020, and P corr = 0.004, respectively). MRI indicated LESCLs more frequently affected PC and LC than AC in anti-AQP4 antibody-seropositive NMO/NMOSD (86.7%, 60.0% and 20.0%, P corr = 0.005, and P corr = 0.043, respectively) and AQP4 antibody-seronegative MS patients (86.7%, 73.3% and 33.3%, P corr = 0.063, and P corr = 0.043, respectively). PH, CP and AH were involved in 93.3%, 86.7% and 73.3% of seropositive patients, respectively, and in 53.3%, 60.0% and 40.0% of seronegative patients, respectively. Conclusions: NMO frequently and extensively affects spinal white matter in addition to central gray matter, especially in PC and LC, where isolated perivascular lesions with astrocyte endfoot protein loss may emerge. Spinal white matter involvement may also appear in early NMO, similar to cerebral white matter lesions.

元の言語英語
ページ(範囲)249-265
ページ数17
ジャーナルBrain Pathology
27
発行部数3
DOI
出版物ステータス出版済み - 5 1 2017

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Neuromyelitis Optica
Aquaporin 4
Spinal Cord
Horns
Antibodies
Astrocytes
Multiple Sclerosis
White Matter
Pathology
Connexin 43

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Pathology and Forensic Medicine
  • Clinical Neurology

これを引用

Early and extensive spinal white matter involvement in neuromyelitis optica. / Hayashida, Shotaro; Masaki, Katsuhisa; Yonekawa, Tomomi; Suzuki, Satoshi; Akio, Hiwatashi; Matsushita, Takuya; watanabe, mitsuru; Yamasaki, Ryo; Suenaga, Toshihiko; Iwaki, Toru; Murai, Hiroyuki; Kira, Jun-Ichi.

:: Brain Pathology, 巻 27, 番号 3, 01.05.2017, p. 249-265.

研究成果: ジャーナルへの寄稿記事

@article{7005d0425a3742c196ed5f390a6a4094,
title = "Early and extensive spinal white matter involvement in neuromyelitis optica",
abstract = "Objectives: Studies of longitudinally extensive spinal cord lesions (LESCLs) in neuromyelitis optica (NMO) have focused on gray matter, where the relevant antigen, aquaporin-4 (AQP4), is abundant. Because spinal white matter pathology in NMO is not well characterized, we aimed to clarify spinal white matter pathology of LESCLs in NMO. Methods: We analyzed 50 spinal cord lesions from eleven autopsied NMO/NMO spectrum disorder (NMOSD) cases. We also evaluated LESCLs with three or fewer spinal cord attacks by 3-tesla MRI in 15 AQP4 antibody-positive NMO/NMOSD patients and in 15 AQP4 antibody-negative multiple sclerosis (MS) patients. Results: Pathological analysis revealed seven cases of AQP4 loss and four predominantly demyelinating cases. Forty-four lesions from AQP4 loss cases involved significantly more frequently posterior columns (PC) and lateral columns (LC) than anterior columns (AC) (59.1{\%}, 63.6{\%}, and 34.1{\%}, respectively). The posterior horn (PH), central portion (CP), and anterior horn (AH) were similarly affected (38.6{\%}, 36.4{\%} and 31.8{\%}, respectively). Isolated perivascular inflammatory lesions with selective loss of astrocyte endfoot proteins, AQP4 and connexin 43, were present only in white matter and were more frequent in PC and LC than in AC (22.7{\%}, 29.5{\%} and 2.3{\%}, P corr = 0.020, and P corr = 0.004, respectively). MRI indicated LESCLs more frequently affected PC and LC than AC in anti-AQP4 antibody-seropositive NMO/NMOSD (86.7{\%}, 60.0{\%} and 20.0{\%}, P corr = 0.005, and P corr = 0.043, respectively) and AQP4 antibody-seronegative MS patients (86.7{\%}, 73.3{\%} and 33.3{\%}, P corr = 0.063, and P corr = 0.043, respectively). PH, CP and AH were involved in 93.3{\%}, 86.7{\%} and 73.3{\%} of seropositive patients, respectively, and in 53.3{\%}, 60.0{\%} and 40.0{\%} of seronegative patients, respectively. Conclusions: NMO frequently and extensively affects spinal white matter in addition to central gray matter, especially in PC and LC, where isolated perivascular lesions with astrocyte endfoot protein loss may emerge. Spinal white matter involvement may also appear in early NMO, similar to cerebral white matter lesions.",
author = "Shotaro Hayashida and Katsuhisa Masaki and Tomomi Yonekawa and Satoshi Suzuki and Hiwatashi Akio and Takuya Matsushita and mitsuru watanabe and Ryo Yamasaki and Toshihiko Suenaga and Toru Iwaki and Hiroyuki Murai and Jun-Ichi Kira",
year = "2017",
month = "5",
day = "1",
doi = "10.1111/bpa.12386",
language = "English",
volume = "27",
pages = "249--265",
journal = "Brain Pathology",
issn = "1015-6305",
publisher = "Wiley-Blackwell",
number = "3",

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TY - JOUR

T1 - Early and extensive spinal white matter involvement in neuromyelitis optica

AU - Hayashida, Shotaro

AU - Masaki, Katsuhisa

AU - Yonekawa, Tomomi

AU - Suzuki, Satoshi

AU - Akio, Hiwatashi

AU - Matsushita, Takuya

AU - watanabe, mitsuru

AU - Yamasaki, Ryo

AU - Suenaga, Toshihiko

AU - Iwaki, Toru

AU - Murai, Hiroyuki

AU - Kira, Jun-Ichi

PY - 2017/5/1

Y1 - 2017/5/1

N2 - Objectives: Studies of longitudinally extensive spinal cord lesions (LESCLs) in neuromyelitis optica (NMO) have focused on gray matter, where the relevant antigen, aquaporin-4 (AQP4), is abundant. Because spinal white matter pathology in NMO is not well characterized, we aimed to clarify spinal white matter pathology of LESCLs in NMO. Methods: We analyzed 50 spinal cord lesions from eleven autopsied NMO/NMO spectrum disorder (NMOSD) cases. We also evaluated LESCLs with three or fewer spinal cord attacks by 3-tesla MRI in 15 AQP4 antibody-positive NMO/NMOSD patients and in 15 AQP4 antibody-negative multiple sclerosis (MS) patients. Results: Pathological analysis revealed seven cases of AQP4 loss and four predominantly demyelinating cases. Forty-four lesions from AQP4 loss cases involved significantly more frequently posterior columns (PC) and lateral columns (LC) than anterior columns (AC) (59.1%, 63.6%, and 34.1%, respectively). The posterior horn (PH), central portion (CP), and anterior horn (AH) were similarly affected (38.6%, 36.4% and 31.8%, respectively). Isolated perivascular inflammatory lesions with selective loss of astrocyte endfoot proteins, AQP4 and connexin 43, were present only in white matter and were more frequent in PC and LC than in AC (22.7%, 29.5% and 2.3%, P corr = 0.020, and P corr = 0.004, respectively). MRI indicated LESCLs more frequently affected PC and LC than AC in anti-AQP4 antibody-seropositive NMO/NMOSD (86.7%, 60.0% and 20.0%, P corr = 0.005, and P corr = 0.043, respectively) and AQP4 antibody-seronegative MS patients (86.7%, 73.3% and 33.3%, P corr = 0.063, and P corr = 0.043, respectively). PH, CP and AH were involved in 93.3%, 86.7% and 73.3% of seropositive patients, respectively, and in 53.3%, 60.0% and 40.0% of seronegative patients, respectively. Conclusions: NMO frequently and extensively affects spinal white matter in addition to central gray matter, especially in PC and LC, where isolated perivascular lesions with astrocyte endfoot protein loss may emerge. Spinal white matter involvement may also appear in early NMO, similar to cerebral white matter lesions.

AB - Objectives: Studies of longitudinally extensive spinal cord lesions (LESCLs) in neuromyelitis optica (NMO) have focused on gray matter, where the relevant antigen, aquaporin-4 (AQP4), is abundant. Because spinal white matter pathology in NMO is not well characterized, we aimed to clarify spinal white matter pathology of LESCLs in NMO. Methods: We analyzed 50 spinal cord lesions from eleven autopsied NMO/NMO spectrum disorder (NMOSD) cases. We also evaluated LESCLs with three or fewer spinal cord attacks by 3-tesla MRI in 15 AQP4 antibody-positive NMO/NMOSD patients and in 15 AQP4 antibody-negative multiple sclerosis (MS) patients. Results: Pathological analysis revealed seven cases of AQP4 loss and four predominantly demyelinating cases. Forty-four lesions from AQP4 loss cases involved significantly more frequently posterior columns (PC) and lateral columns (LC) than anterior columns (AC) (59.1%, 63.6%, and 34.1%, respectively). The posterior horn (PH), central portion (CP), and anterior horn (AH) were similarly affected (38.6%, 36.4% and 31.8%, respectively). Isolated perivascular inflammatory lesions with selective loss of astrocyte endfoot proteins, AQP4 and connexin 43, were present only in white matter and were more frequent in PC and LC than in AC (22.7%, 29.5% and 2.3%, P corr = 0.020, and P corr = 0.004, respectively). MRI indicated LESCLs more frequently affected PC and LC than AC in anti-AQP4 antibody-seropositive NMO/NMOSD (86.7%, 60.0% and 20.0%, P corr = 0.005, and P corr = 0.043, respectively) and AQP4 antibody-seronegative MS patients (86.7%, 73.3% and 33.3%, P corr = 0.063, and P corr = 0.043, respectively). PH, CP and AH were involved in 93.3%, 86.7% and 73.3% of seropositive patients, respectively, and in 53.3%, 60.0% and 40.0% of seronegative patients, respectively. Conclusions: NMO frequently and extensively affects spinal white matter in addition to central gray matter, especially in PC and LC, where isolated perivascular lesions with astrocyte endfoot protein loss may emerge. Spinal white matter involvement may also appear in early NMO, similar to cerebral white matter lesions.

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