Chronic central pain after spinal cord injury
Chronic central pain after spinal cord injury
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DOI：
10.1089/neu.1997.14.517
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发表时间：
1997-08-01
影响因子：
4.2
通讯作者：
Hulsebosch, CE
中科院分区：
文献类型：
--
作者：
Christensen, MD;Hulsebosch, CE
脊髓损伤（SCI）经常导致感觉障碍，尽管有各种干预措施，但临床治疗仍难治。治疗策略的失败是由于缺乏对引起脊髓损伤后慢性疼痛的机制的关注。关于慢性疼痛在脊髓损伤患者群体的发展的文献综述将给出。此外，一个哺乳动物模型慢性中枢性疼痛后脊髓创伤将提出。该模型的特点是机械和热异常性疼痛的发展，正如测量公认的伤害性测试阈值所证明的那样，爪子退缩反应伴随着与有害刺激经验一致的行为变化。此外，还测量了与接受有害刺激相一致的姿势和行为变化以及涉及棘上通路的发声反应。采用BBB （Basso, Beattie, and Bresnahan）开放性测试量表对运动功能进行测试和评分。我们的数据表明，在脊髓损伤后，引起足部退缩（屈肌反射）或发声的机械刺激和热刺激的体感阈值，伴随着复杂的行为变化，都有显著不同。这些变化代表了机械和热异常性疼痛的发展。为了确定改变感觉反应的潜在机制，我们使用电生理技术来确定伤害性背角神经元是否表现出对外周刺激的兴奋性增加，这可以通过对自然体感刺激的反应增加来证明。这些数据支持脊髓半切后背角神经元中枢敏化的发展。这为脊髓损伤后机械和热异常性疼痛的发展提供了机制。讨论了脊髓损伤后中枢疼痛状态发展的假设，以及改善疼痛状态的治疗干预措施。
Spinal cord injury (SCI) frequently results in dysesthesias that have remained refractory to clinical treatments despite a variety of interventions. The failure of therapeutic strategies to treat dysesthesias after SCI is due to the lack of attention given to mechanisms that elicit chronic pain following SCI. An overview of the literature with respect to the development of chronic pain in the SCI patient population will be given. In addition, a mammalian model of chronic central pain following spinal cord trauma will be presented. The model is characterized by the development of mechanical and thermal allodynia, as demonstrated by measuring the thresholds of accepted nociceptive tests, the paw withdrawal responses accompanied by changes in behavior consistent with the experience of noxious stimulis. In addition, vocalization responses that are accompanied by postural and behavioral changes consistent with the receipt of a noxious stimulus and involving supraspinal pathways are measured. Locomotor function was also tested and scored using the Basso, Beattie, and Bresnahan (BBB) open field test scale. Our data indicate that somatosensory thresholds for both mechanical and thermal stimuli that elicit paw withdrawal (flexor reflex) or vocalizations, accompanied by complex changes in behavior, are significantly different following SCI. These changes represent the development of mechanical and thermal allodynia. To determine the underlying mechanism for the altered sensory responses, we used electrophysiological techniques to determine if nociceptive dorsal horn neurons demonstrated increased excitability to peripheral stimulation as evidenced by increased responses to natural somatosensory stimuli. The data presented support the development of central sensitization of dorsal horn neurons after spinal cord hemisection. This provides a mechanism for the development of mechanical and thermal allodynia after SCI. Hypotheses that account for the development of the central pain state after SCI, as well as therapeutic interventions to ameliorate the pain state, are discussed.