中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (9): 907-908.doi: 10.4103/1673-5374.133130

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

雷电和电击伤致迟发性神经损伤机制:神经元死亡、血管坏死抑或脱髓鞘?

  

  • 收稿日期:2014-05-07 出版日期:2014-05-20 发布日期:2014-05-20

Delayed neural damage induced by lightning and electrical injury: neural death, vascular necrosis and demyelination?

Andrew D. Reisner   

  1. Forensic Diagnostic Center of District Nine, PO Box 126, Byesville, OH, 43723-0126, USA
  • Received:2014-05-07 Online:2014-05-20 Published:2014-05-20
  • Contact: Andrew D. Reisner, Psy.D., Forensic Diagnostic Center of District Nine, PO Box 126, Byesville, OH, 43723-0126, USA, forensicd9@gmail.com.

摘要:

20世纪30年代初,研究者们开始了解雷电和电击伤后的迟发性神经变性综合征现象,但至今科学家们对其中所涉及的机制仍然知之甚少。最早的理论是电击损伤通过损伤血管内皮细胞可造成血管结构性损害。近来有证据表明谷氨酸过度刺激可以带来有害的自由基,而一些自由基可从脂质中获得。根据这一事实,雷电和电击损伤后可发生迟发性脱髓鞘综合征,而当未检测到血管损伤时,可通过过度电刺激在富含脂质的髓鞘细胞直接造成有害自由基的现象进行判断。来自美国第九区法医诊断中心的Andrew D. Reisner博士对皮质醇升高、谷氨酸过度刺激与破坏性自由基形成影响进行了分析,并解释了这两种形式的迟发性神经损伤。而关于电击伤假说,目前仍旧不能明确是否会立即导致与迟发性神经损伤有关。

Abstract:

The phenomenon of delayed neurodegenerative syndromes following lighting and electrical injury has been know since the early 1930’s, but to the present day the mechanisms involved have been poorly understood. An initial theory is that the electrical insult causes damage to the vascular structures feeding the spinal cord via damage to vascular endothelial cells. There is evidence suggesting that glutamatergic overstimulation can bring about damaging free radicals and that some of these free radicals can be derived from lipids. Using this evidence, it has been suggested that in cases where delayed demyelinating syndromes occur following electrical and lightning injury, and when vascular damage has not been detected, the electrical overstimulation may create damaging free radicals directly in the lipid-rich myelin cells. Dr. Andrew D. Reisner, who comes from Forensic Diagnostic Center of District Nine in USA, reviewed the literature on the effects of cortisol elevation, glutamatergic over-stimulation, and formation of destructive free radicals, and explanations for both forms of delayed neurological damage were offered. With regard to the electroporation hypothesis, it is unclear as to whether electroporation would cause immediate versus delayed neurological damage.