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甲醇性视神经病变:一项组织病理学研究。

Methanol optic neuropathy: a histopathological study.

作者信息

Sharpe J A, Hostovsky M, Bilbao J M, Rewcastle N B

出版信息

Neurology. 1982 Oct;32(10):1093-100. doi: 10.1212/wnl.32.10.1093.

Abstract

The histopathologic effects of methanol on the optic nerve were studied in four patients. Circumscribed myelin damage occurred behind the lamina cribrosa in each nerve. Axons were preserved. Demyelination also occurred in cerebral hemispheric white matter in one patient. This selective myelinoclastic effect of methanol metabolism is probably caused by histotoxic anoxia in watershed areas of the cerebral and distal optic nerve circulations. Juxtabulbar demyelination may cause optic disk edema in methanol poisoning by compressive obstruction of orthograde axoplasmic flow. Visual loss may be due to disruption of saltatory conduction. Retrolaminar demyelinating optic neuropathy is an early morphologic correlate of visual loss in methanol intoxication.

摘要

对4例患者的视神经进行了甲醇的组织病理学效应研究。每例神经在筛板后均出现局限性髓鞘损伤。轴突得以保留。1例患者大脑半球白质也出现了脱髓鞘。甲醇代谢的这种选择性髓鞘破坏效应可能是由大脑和视神经远端循环分水岭区域的组织毒性缺氧引起的。球后脱髓鞘可能通过正向轴浆流的压迫性阻塞导致甲醇中毒时视盘水肿。视力丧失可能是由于跳跃传导中断所致。筛板后脱髓鞘性视神经病变是甲醇中毒视力丧失的早期形态学相关表现。

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