辐射诱发的中枢性脱髓鞘,一例罕见的亚急性并发症的报告及文献复习

Christopher R. Trevino, A. Paulino, Vinodh A. Kumar, Nazanin K. Majd, M. Penas-Prado
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摘要

一名患有右额弥漫性星形细胞瘤、异柠檬酸脱氢酶突变型世界卫生组织II级的26岁女性接受了切除和放射治疗(体积调制电弧疗法,30次54 Gy)。放射治疗10周后,她出现左腿无力,脑部磁共振图像显示,接受10-30 Gy治疗的区域内有多灶性急性脱髓鞘性脑损伤。她服用高剂量类固醇后病情好转,随后恢复服用替莫唑胺。她之前没有脱髓鞘疾病的病史。辐射神经毒性的机制包括血管损伤、脱髓鞘以及对神经干细胞和少突胶质细胞的氧化损伤;尽管其病理生理学尚不完全清楚。在没有已知脱髓鞘疾病的情况下发生亚急性脱髓鞘是罕见的,只有四例先前描述过。这种罕见的并发症可以在出现症状时用类固醇成功治疗。如果原发性脑肿瘤放疗后出现新的远处增强病变,当发现不典型的复发时,考虑脱髓鞘是很重要的。
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Radiation-induced central demyelination, report of a rare subacute complication and review of the literature
A 26-year-old woman with a right frontal diffuse astrocytoma, isocitrate dehydrogenase-mutant, WHO Grade II was treated with resection and radiotherapy (54 Gy in 30 fractions by volumetric modulated arc therapy). Ten weeks after radiation, she developed left leg weakness, and a brain magnetic resonance image demonstrated multifocal acute demyelinating brain lesions within regions that received 10-30 Gy. She improved with high dose steroids and subsequently resumed temozolomide. She had no prior history of a demyelinating disorder. The mechanisms of neurotoxicity from radiation include vascular injury, demyelination, and oxidative damage to neural stem cells and oligodendrocytes; though the pathophysiology is not fully understood. Subacute demyelination in the absence of known demyelinating disease is rare with only four cases previously described. This rare complication can be successfully managed with steroids when symptomatic. It is important to consider demyelination if new distant enhancing lesions arise following radiation of a primary brain tumor when findings are atypical for recurrence.
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