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脊髓损伤后减轻疼痛的细胞和分子方法。

Cell and molecular approaches to the attenuation of pain after spinal cord injury.

作者信息

Eaton Mary J

机构信息

The Miami Project to Cure Paralysis, University of Miami School of Medicine, Miami, Florida 33136, USA.

出版信息

J Neurotrauma. 2006 Mar-Apr;23(3-4):549-59. doi: 10.1089/neu.2006.23.549.

Abstract

Recent experimental research to treat spinal cord injury (SCI) pain has greatly increased our understanding of how such chronic pain might be modulated in the human population. Neuropathic pain is caused by the structural and biochemical changes associated with the peripheral and central nervous system damage associated with nervous system trauma, often leading to an imbalance in endogenous excitatory and inhibitory spinal systems that modulate sensory processing. But current pharmacological therapies are often ineffective over time for the greater number of patients. Although there are a variety of useful surgical and pharmacologic interventions (including electric stimulation, implantable mechanical pumps and a myriad of drugs for pain relief) cell and molecular technologies are a new frontier in pain medicine. These other potential therapeutic agents of pain are based on current and developing treatment strategies elucidated from recent research, especially concerning central spinal sensitization, and the spinal mechanisms that are thought to be the origin and ongoing cause of chronic pain, even when the injury is peripheral in location. Newly developing translational strategies such as molecular agents, viral-mediated gene transfer or cellular transplants to treat chronic pain are being evaluated in a variety of peripheral and central injury models. They seek to address both the causes of neuropathic pain, to interfere with its development and maintenance over time, and give the injured person with pain an improved quality-of-life that allows them to better deal with the larger tasks of daily life and the strenuous rehabilitation that might also improve motor function after SCI.

摘要

近期针对脊髓损伤(SCI)疼痛的实验研究极大地增进了我们对如何在人群中调节这种慢性疼痛的理解。神经性疼痛是由与神经系统创伤相关的外周和中枢神经系统损伤所伴随的结构和生化变化引起的,常常导致调节感觉处理的内源性兴奋性和抑制性脊髓系统失衡。但随着时间推移,目前的药物治疗对大多数患者往往无效。尽管有多种有用的手术和药物干预措施(包括电刺激、植入式机械泵以及大量用于缓解疼痛的药物),细胞和分子技术仍是疼痛医学的一个新领域。这些其他潜在的疼痛治疗药物基于近期研究阐明的当前及正在发展的治疗策略,特别是关于中枢脊髓敏化以及被认为是慢性疼痛起源和持续原因的脊髓机制,即便损伤位于外周部位。诸如分子药物、病毒介导的基因转移或细胞移植等新兴的转化策略正用于治疗慢性疼痛,并在各种外周和中枢损伤模型中进行评估。它们旨在解决神经性疼痛的病因,随着时间推移干扰其发展和维持,提高疼痛患者的生活质量,使他们能够更好地应对日常生活中的各项任务以及可能改善脊髓损伤后运动功能的艰苦康复训练。

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