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一氧化碳中毒会导致视神经病变。

Carbon monoxide poisoning causes optic neuropathy.

作者信息

Simmons I G, Good P A

机构信息

Ophthalmology Department, St James' University Hospital, Leeds, UK.

出版信息

Eye (Lond). 1998;12 ( Pt 5):809-14. doi: 10.1038/eye.1998.209.

Abstract

PURPOSE

To describe the electrophysiological and psychophysical effects of carbon monoxide (CO) poisoning on visual function.

METHODS

Three patients are presented who suffered CO poisoning, two due to suicide attempts and one in the course of a road traffic accident. After a full ocular examination, Goldmann visual fields, flash and pattern visual evoked potentials (VEPs) and flash and pattern electroretinograms (ERGs) were tested.

RESULTS

Electrophysiology showed reduced or absent N95 components of the pattern ERG and delayed, reduced VEPs. A positive-negative-positive (PNP) VEP waveform was seen in two cases. In one case, where presentation occurred at an early stage, visual and electrophysiological function was improved with hydroxycobalamine.

CONCLUSIONS

The combination of ERG and VEP findings suggest that CO poisoning can cause a toxic optic neuropathy that may have a similar aetiological mechanism to that in tobacco amblyopia. Early treatment with hydroxycobalamine may be of some benefit.

摘要

目的

描述一氧化碳(CO)中毒对视功能的电生理和心理物理学影响。

方法

报告3例一氧化碳中毒患者,2例因自杀未遂,1例因道路交通事故。在进行全面的眼部检查后,检测了Goldmann视野、闪光和图形视觉诱发电位(VEP)以及闪光和图形视网膜电图(ERG)。

结果

电生理学显示图形ERG的N95成分减少或缺失,VEP延迟、波幅降低。2例出现正负正(PNP)VEP波形。在1例早期就诊的患者中,使用羟钴胺后视觉和电生理功能得到改善。

结论

ERG和VEP的联合检查结果表明,CO中毒可导致中毒性视神经病变,其病因机制可能与烟草性弱视相似。早期使用羟钴胺治疗可能有益。

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