Restoring function after spinal cord injury

被引:85
|
作者
Becker, D
Sadowsky, CL
McDonald, JW
机构
[1] Washington Univ, Sch Med, Dept Neurol, Spinal Cord Injury Neurorehabil Sect,Restorat Tre, St Louis, MO 63108 USA
[2] Washington Univ, Sch Med, Ctr Study Nervous Syst Injury, St Louis, MO 63108 USA
[3] Washington Univ, Sch Med, Dept Neurol Surg, St Louis, MO 63108 USA
关键词
excitotoxicity; regeneration; rehabilitation; spinal cord injury; stem cell;
D O I
10.1097/01.nrl.0000038587.58012.05
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
BACKGROUND- By affecting young people during the most productive period of their lives, spinal cord injury (SCI) is a devastating problem for modern society. A decade ago, treating SCI seemed frustrating and hopeless because of the tremendous morbidity and mortality, life-shattering impact, and limited therapeutic options associated with the condition. Today, however, an understanding of the underlying pathophysiological mechanisms, the development of neuroprotective interventions, and progress toward regenerative interventions are increasing hope for functional restoration. REVIEW SUMMARY- This study addresses the present understanding of SCI, including the etiology, pathophysiology, treatment, and scientific advances. The discussion of treatment options includes a critical review of high-dose methylprednisolone and GM-1 ganglioside therapy. The concept that limited rebuilding can provide a disproportionate improvement in quality of life is emphasized throughout. CONCLUSIONS- New surgical procedures, pharmacologic treatments, and functional neuromuscular stimulation methods have evolved over the last decades that can improve functional outcomes after spinal cord injury, but limiting secondary injury remains the primary goal. Tissue replacement strategies, including the use of embryonic stem cells, become an important tool and can restore function in animal models. Controlled clinical trials are now required to confirm these observations. The ultimate goal is to harness the body's own potential to replace lost central nervous system cells by activation of endogenous progenitor cell repair mechanisms.
引用
收藏
页码:1 / 15
页数:15
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