Christensen M D, Hulsebosch C E
Department of Anatomy and Neurosciences, University of Texas Medical Branch, Galveston 77555-1069, USA.
J Neurotrauma. 1997 Aug;14(8):517-37. doi: 10.1089/neu.1997.14.517.
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 stimuli. 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.
脊髓损伤（SCI）常常导致感觉异常，尽管采取了多种干预措施，但这些感觉异常对临床治疗仍难以奏效。SCI后治疗感觉异常的策略之所以失败，是因为缺乏对SCI后引发慢性疼痛机制的关注。本文将概述SCI患者群体中慢性疼痛的发生情况。此外，还将介绍一种脊髓损伤后慢性中枢性疼痛的哺乳动物模型。该模型的特征是出现机械性和热性痛觉过敏，通过测量公认的伤害性测试阈值来证明，即爪部退缩反应伴随着与有害刺激体验一致的行为变化。此外，还测量了伴随着与接收有害刺激一致的姿势和行为变化且涉及脊髓上通路的发声反应。还使用Basso、Beattie和Bresnahan（BBB）旷场测试量表对运动功能进行了测试和评分。我们的数据表明，SCI后，引发爪部退缩（屈肌反射）或发声的机械性和热性刺激的体感阈值存在显著差异，且伴随着复杂的行为变化。这些变化代表了机械性和热性痛觉过敏的发展。为了确定感觉反应改变的潜在机制，我们使用电生理技术来确定伤害性背角神经元对周围刺激的兴奋性是否增加，这可通过对自然体感刺激的反应增加来证明。所呈现的数据支持脊髓半切术后背角神经元中枢敏化的发展。这为SCI后机械性和热性痛觉过敏的发展提供了一种机制。本文还讨论了关于SCI后中枢性疼痛状态发生的假说以及改善疼痛状态的治疗干预措施。
