Current developments in spinal cord injury research.
Current developments in spinal cord injury research.
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DOI：
10.1016/s1529-9430(01)00029-8
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发表时间：
2002-03-01
期刊：
影响因子：
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通讯作者：
Gorden, Carey
中科院分区：
文献类型：
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作者：
Carlson, Gregory D;Gorden, Carey
背景情况：神经科学的最新进展为预防和治疗脊髓损伤（spinal cord injury，SCI）的毁灭性影响打开了希望之门。目的：强调目前对创伤性SCI机制的理解，提供有关急性脊髓损伤患者最先进护理的信息，并探索未来旨在保护和重建神经的治疗方法。有关创伤性SCI的神经病理生理学的文献提供了一个选择性的概述，重点是药物治疗和创伤后的实验策略，旨在改善神经保护和晚期neuroregenerative repair.METHODS：一百五十四个同行评议的基础科学和有关SCI的临床文章进行了审查。引用的文章被选择的相对优点和贡献的基础上，目前的理解SCI神经病理生理学，神经再生，和临床SCI治疗patterns.RESULTS：更好地了解的病理生理学和早期治疗脊髓损伤的病人，导致死亡率持续下降，减少急性住院和并发症的发生率，更快速的康复和重返社会。进行性神经损伤由继发性损伤机制的组合引起，包括缺血、生化改变、细胞凋亡、兴奋性毒性、钙蛋白酶蛋白酶、神经递质积累、脂质过氧化/自由基损伤和炎症反应。实验研究表明，最终的创伤后神经功能缺损不仅是最初的冲击力的结果，而是这些力量和继发的时间依赖性事件，随后不久的初始impacts.CONCLUSIONS：实验研究继续提供一个更好的理解创伤性SCI后的病理生理事件的复杂的相互作用。未来的方法将涉及旨在阻断进行性中枢神经系统损伤的多种机制和促进神经再生的策略。
BACKGROUND CONTEXT: Recent advances in neuroscience have opened the door for hope toward prevention and cure of the devastating effects of spinal cord injury (SCI).PURPOSE: To highlight the current understanding of traumatic SCI mechanisms, provide information regarding state-of-the-art care for the acute spinal cord-injured patient, and explore future treatments aimed at neural preservation and reconstruction.STUDY DESIGN/SETTING: A selective overview of the literature pertaining to the neuropathophysiology of traumatic SCI is provided with an emphasis on pharmacotherapies and posttraumatic experimental strategies aimed at improved neuropreservation and late neuroregenerative repair.METHODS: One hundred fifty-four peer-reviewed basic science and clinical articles pertaining to SCI were reviewed. Articles cited were chosen based on the relative merits and contribution to the current understanding of SCI neuropathophysiology, neuroregeneration, and clinical SCI treatment patterns.RESULTS: A better understanding of the pathophysiology and early treatment for the spinal cord-injured patient has led to a continued decrease in mortality, decreased acute hospitalization and complication rates, and more rapid rehabilitation and re-entry into society. Progressive neural injury results from a combination of secondary injury mechanisms, including ischemia, biochemical alterations, apoptosis, excitotoxicity, calpain proteases, neurotransmitter accumulation, lipid peroxidation/free radical injury, and inflammatory responses. Experimental studies suggest that the final posttraumatic neurologic deficit is not only a result of the initial impaction forces but rather a combination of these forces and secondary time-dependent events that follow shortly after the initial impact.CONCLUSIONS: Experimental studies continue to provide a better understanding of the complex interaction of pathophysiologic events after traumatic SCI. Future approaches will involve strategies aimed at blocking the multiple mechanisms of progressive central nervous system injury and promoting neuroregeneration.