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有或无中枢性疼痛的脊髓损伤患者对局部辣椒素的反应

Reaction to topical capsaicin in spinal cord injury patients with and without central pain.

作者信息

Finnerup Nanna B, Pedersen Louise H, Terkelsen Astrid J, Johannesen Inger L, Jensen Troels S

机构信息

Danish Pain Research Center and Department of Neurology, Aarhus University Hospital, Norrebrogade 44, DK-8000 Aarhus, Denmark.

出版信息

Exp Neurol. 2007 May;205(1):190-200. doi: 10.1016/j.expneurol.2007.01.026. Epub 2007 Feb 6.

DOI:10.1016/j.expneurol.2007.01.026
PMID:17346705
Abstract

Central neuropathic pain is a debilitating and frequent complication to spinal cord injury (SCI). Excitatory input from hyperexcitable cells around the injured grey matter zone is suggested to play a role for central neuropathic pain felt below the level of a spinal cord injury. Direct evidence for this hypothesis is difficult to obtain. Capsaicin, activating TRPV1 receptors on small sensory afferents, induces enhanced cellular activity in dorsal horn neurons and produces a central mediated area of secondary hyperalgesia. We hypothesized that sensory stimuli and capsaicin applied at and just above the level of a spinal cord injury which already is hyperexcitable, would cause enhanced responses in patients with central pain at the level of injury compared to patients without neuropathic pain and healthy controls. Touch, punctuate stimuli, cold stimuli and topical capsaicin was applied above, at, and below injury level in 10 SCI patients with central pain below a thoracic injury, in 10 SCI patients with a thoracic injury but without neuropathic pain, and in corresponding areas in 10 healthy control subjects. The study found increased responses to touch at injury level compared to controls (p=0.033) and repetitive punctuate stimuli above and at injury level compared to controls and pain-free SCI patients (p<0.04) but not an increased response to capsaicin in patients with central pain. These results suggest that SCI patients with below-level pain have increased responses to some but not all sensory input at the level of injury.

摘要

中枢性神经病理性疼痛是脊髓损伤(SCI)常见的一种使人衰弱的并发症。损伤灰质区周围的兴奋性过高细胞的兴奋性输入被认为与脊髓损伤平面以下感觉到的中枢性神经病理性疼痛有关。这一假说的直接证据很难获得。辣椒素可激活小感觉传入神经上的TRPV1受体,诱导背角神经元的细胞活性增强,并产生中枢介导的继发性痛觉过敏区域。我们推测,在已经兴奋性过高的脊髓损伤平面及以上施加的感觉刺激和辣椒素,与无神经病理性疼痛的患者和健康对照相比,会使有中枢性疼痛的患者在损伤平面出现增强的反应。对10例胸段损伤以下有中枢性疼痛的SCI患者、10例有胸段损伤但无神经病理性疼痛的SCI患者以及10例健康对照者的相应区域,在损伤平面上方、损伤平面处及损伤平面下方施加触觉、点状刺激、冷刺激和局部辣椒素。研究发现,与对照组相比,损伤平面处对触觉的反应增强(p = 0.033),与对照组和无疼痛的SCI患者相比,损伤平面及损伤平面上方对重复性点状刺激的反应增强(p < 0.04),但中枢性疼痛患者对辣椒素的反应并未增强。这些结果表明,有损伤平面以下疼痛的SCI患者在损伤平面处对某些但并非所有感觉输入的反应增强。

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