Development of moyamoya disease after non-herpetic acute limbic encephalitis: A case report

被引:7
作者
Takahashi, Yasuhiro [1 ]
Mikami, Takeshi [1 ]
Suzuki, Hime [1 ]
Komatsu, Katsuya [1 ]
Yamamoto, Daisuke [2 ]
Shimohama, Shun [2 ]
Houkin, Kiyohiro [3 ]
Sugita, Shintaro [4 ]
Hasegawa, Tadashi [4 ]
Mikuni, Nobuhiro [1 ]
机构
[1] Sapporo Med Univ, Dept Neurosurg, Sapporo, Hokkaido, Japan
[2] Sapporo Med Univ, Dept Neurol, Sapporo, Hokkaido, Japan
[3] Hokkaido Univ, Grad Sch Med, Dept Neurosurg, Sapporo, Hokkaido, Japan
[4] Sapporo Med Univ, Dept Surg Pathol, Sapporo, Hokkaido, Japan
基金
日本学术振兴会;
关键词
Autoimmune disease; LGI1; Limbic encephalitis; Quasi-moyamoya disease; RNF213; GENE; ASSOCIATION; ANTIBODIES;
D O I
10.1016/j.jocn.2018.04.042
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
We report a case of moyamoya disease (MMD), which developed after non-herpetic acute limbic encephalitis (NHALE) associated with anti-leucine-rich glioma-inactivated 1 (LGI1) antibody. The patient's mother had a history of MMD. No vascular lesions were identified at the time of the NHALE. Nine years later, the patient visited our hospital due to memory disturbances and repeated transient ischemic attacks affecting the right limb. Diffusion-weighted magnetic resonance imaging revealed scattered areas of signal hyperintensity, and the patient was ultimately diagnosed with MMD based on angiography. Revascularization surgery was performed on the left side, where cerebral blood flow was impaired on I-123-N-isopropyl-p-iodoamphetamine single photon emission computed tomography. Postoperatively, the patient was discharged with a normal neurological examination. NHALE associated with LGI1 antibodies is an autoimmune disease. Although autoimmune disease is the most frequent finding other than atherosclerosis in quasi-MMD, this is the first report of NHALE associated with anti-LGI1 antibodies mimicking quasi-MMD. Inflammation and angiogenesis may contribute to the development of MMD, in addition to genetic background. (C) 2018 Elsevier Ltd. All rights reserved.
引用
收藏
页码:250 / 253
页数:4
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