Tbe development of cutaneous allodynia during a migraine attack - Clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine
Tbe development of cutaneous allodynia during a migraine attack - Clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine
复制标题
DOI：
10.1093/brain/123.8.1703
复制
发表时间：
2000-08-01
期刊：
影响因子：
14.5
通讯作者：
Yarnitsky, D
中科院分区：
文献类型：
--
作者：
Burstein, R;Cutrer, MF;Yarnitsky, D
最近，我们发现，大多数偏头痛患者表现出皮肤异常性疼痛的内部和外部的疼痛涉及的地区时，检查在一个充分发展的偏头痛发作。在这份报告中，我们研究的方式，皮肤异常性疼痛的发展，通过测量疼痛阈值在头部和前臂双边在几个时间点在偏头痛发作的42岁男性。在头痛之前，他经历了视觉、感觉、运动和言语先兆。头痛期间，他出现了对照片、声音和气味的恐惧，恶心和呕吐，咳嗽或移动头部使头痛加重，刮胡子、梳头或触摸头皮时皮肤疼痛。在没有偏头痛和偏头痛发作后1，2和4小时，他的疼痛阈值之间的比较显示了以下内容。(i)1小时后，机械和冷异常性疼痛开始在同侧头部，但不是在任何其他网站。(ii)2小时后，这种异常性疼痛增加的同侧头部和蔓延到对侧头部和同侧前臂，（iii）4小时后，热异常性疼痛也检测到，而机械和冷异常性疼痛继续增加。这些临床观察结果表明，该患者三叉神经血管疼痛通路上发生了以下沿着事件。(i)在他的外周伤害感受器最初激活后几分钟，它们变得敏感;这种敏感性可以介导颅内过敏的症状。(ii)来自外周伤害感受器的一连串脉冲激活了二级神经元，并启动了它们的敏化作用;这种敏化作用可以介导同侧头部皮肤异常性疼痛的发展。(iii)来自致敏的二级神经元的一连串脉冲激活并最终致敏三级神经元;这种致敏可以介导对侧头部和同侧前臂在2小时点的皮肤异常性疼痛的发展，在同侧头部出现异常性疼痛后超过1小时。这种解释要求在中枢致敏作用出现之前，尽早使用针对外周伤害性感受器的抗偏头痛药物。如果中枢致敏发展，治疗的基本原理是抑制它，因为目前可用的药物，旨在抑制中枢致敏是无效的，这项研究强调需要开发他们治疗偏头痛。
Recently, we showed that most migraine patients exhibit cutaneous allodynia inside and outside their pain-referred areas when examined during a fully developed migraine attack. In this report, we studied the way in which cutaneous allodynia develops by measuring the pain thresholds in the head and forearms bilaterally at several time points during a migraine attack in a 42-year-old male. Prior to the headache, he experienced visual, sensory, motor and speech aura. During the headache, he experienced photo-, phono- and odour-phobia, nausea and vomiting, worsening of the headache by coughing or moving his head, and cutaneous pain when shaving, combing his hair or touching his scalp. Comparisons between his pain thresholds in the absence of migraine and at 1, 2 and 4 h after the onset of migraine revealed the following. (i) After 1 h, mechanical and cold allodynia started to develop in the ipsilateral head but not in any other site. (ii) After 2 h, this allodynia increased on the ipsilateral head and spread to the contralateral head and ipsilateral forearm, (iii) After 4 h, heat allodynia was also detected while mechanical and cold allodynia continued to increase. These clinical observations suggest the following sequence of events along the trigeminovascular pain pathway of this patient. (i) A few minutes after the initial activation of his peripheral nociceptors, they became sensitized; this sensitization can mediate the symptoms of intracranial hypersensitivity. (ii) The barrage of impulses that came from the peripheral nociceptors activated second-order neurons and initiated their sensitization; this sensitization can mediate the development of cutaneous allodynia on the ipsilateral head. (iii) The barrage of impulses that came from the sensitized second-order neurons activated and eventually sensitized third-order neurons; this sensitization can mediate the development of cutaneous allodynia on the contralateral head and ipsilateral forearm at the 2-h point, over 1 h after the appearance of allodynia on the ipsilateral head. This interpretation calls for an early use of anti-migraine drugs that target peripheral nociceptors, before the development of central sensitization. If central sensitization develops, the therapeutic rationale is to suppress it. Because currently available drugs that aim to suppress central sensitization are ineffective, this study stresses the need to develop them for the treatment of migraine.