Ikeda Kensuke, Kiyota Naoki, Kuroda Hiroshi, Sato Douglas Kazutoshi, Nishiyama Shuhei, Takahashi Toshiyuki, Misu Tatsuro, Nakashima Ichiro, Fujihara Kazuo, Aoki Masashi
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Department of Neurology, Tohoku University School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, Japan
Mult Scler. 2015 Apr;21(5):656-9. doi: 10.1177/1352458514551455. Epub 2014 Sep 25.
We report a patient with neuromyelitis optica (NMO) presenting anti-myelin-oligodendrocyte glycoprotein (MOG)-seropositive, in whom biomarkers of demyelination and astrocyte damage were measured during an acute attack. A 31-year-old man developed right optic neuritis followed by longitudinally extensive transverse myelitis, fulfilling the criteria for definite NMO. He was anti-MOG-seropositive and anti-aquaporin-4 seronegative. The myelin basic protein level was markedly elevated whereas glial fibrillary acidic protein was not detectable in cerebrospinal fluid during an acute attack. His symptoms quickly improved after high-dose methylprednisolone therapy. This case suggests that NMO patients with anti-MOG may have severe demyelination in the absence of astrocyte injury.
我们报告了一名视神经脊髓炎(NMO)患者,其抗髓鞘少突胶质细胞糖蛋白(MOG)血清学呈阳性,在急性发作期间对其脱髓鞘和星形胶质细胞损伤的生物标志物进行了检测。一名31岁男性出现右眼视神经炎,随后发生纵向广泛横贯性脊髓炎,符合确诊NMO的标准。他抗MOG血清学呈阳性,抗水通道蛋白4血清学呈阴性。急性发作期间,脑脊液中髓鞘碱性蛋白水平显著升高,而胶质纤维酸性蛋白未检测到。大剂量甲泼尼龙治疗后,他的症状迅速改善。该病例表明,抗MOG的NMO患者在无星形胶质细胞损伤的情况下可能存在严重脱髓鞘。