The science of migraine.
The science of migraine.
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DOI：
10.3233/ves-2012-0433
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Rauch SD
中科院分区：
文献类型：
--
作者：
Burstein R;Jakubowski M;Rauch SD
偏头痛的主要症状是头痛。在本文中，我们回顾了这种疼痛的神经生物学，因为它是目前所理解的。近年来，我们发现，在单次偏头痛发作过程中，感知硬脑膜疼痛信号的神经元网络迅速变化，并且发作的治疗是一个移动的目标。我们发现，如果疼痛在开始后10-20分钟内没有停止，网络中的第一组神经元，即位于三叉神经节的神经元，会发生分子变化，使它们对头部内部变化的压力高度敏感，这就解释了为什么偏头痛会抽搐，并因弯腰和打喷嚏而恶化。我们发现，如果疼痛在60-120分钟内没有停止，网络中的第二组神经元，即位于三叉神经脊束核的神经元，会发生分子变化，使它们从依赖第一组神经元从硬脑膜接收的感觉信号转变为独立状态，它们自己成为头痛的疼痛发生器。当这种情况发生时，患者注意到梳头、洗澡、触摸眶周皮肤、剃须、戴耳环等变得疼痛，这种情况称为皮肤异常性疼痛。基于这种情况，我们最近发现，如果在皮肤异常性疼痛和中枢致敏建立之前给予药物治疗，使偏头痛患者无痛的成功率显著增加。从活性依赖性到活性非依赖性的中枢致敏的分子转变以及我们最近的结论，曲坦类药物能够破坏外周和中枢三叉神经血管神经元之间的通信（而不是直接抑制外周或中枢神经元），解释了其临床效果。我们过去五年的临床和临床前研究结果都表明，在急性偏头痛发作的治疗中使用早期治疗方法可能具有短期和长期优势。
The cardinal symptom of migraine is headache pain. In this paper we review the neurobiology of this pain as it is currently understood. In recent years, we discovered that the network of neurons that sense pain signals from the dura changes rapidly during the course of a single migraine attack and that the treatment of an attack is a moving target. We found that if the pain is not stopped within 10–20 minutes after it starts, the first set of neurons in the network, those located in the trigeminal ganglion, undergo molecular changes that make them hypersensitive to the changing pressure inside the head, which explains why migraine headache throbs and is worsened by bending over and sneezing. We found that if the pain is not stopped within 60–120 minutes, the second group of neurons in the network, those located in the spinal trigeminal nucleus, undergoes molecular changes that convert them from being dependent on sensory signals they receive from the dura by the first set of neurons, into an independent state in which they themselves become the pain generator of the headache. When this happens, patients notice that brushing their hair, taking a shower, touching their periorbital skin, shaving, wearing earrings, etc become painful, a condition called cutaneous allodynia. Based on this scenario, we showed recently that the success rate of rendering migraine patients pain-free increased dramatically if medication was given before the establishment of cutaneous allodynia and central sensitization. The molecular shift from activity-dependent to activity-independent central sensitization together with our recent conclusion that triptans have the ability to disrupt communications between peripheral and central trigeminovascular neurons (rather than inhibiting directly peripheral or central neurons) explain their clinical effects. Both our clinical and pre-clinical findings of the last five years point to possible short- and long-term advantages in using an early-treatment approach in the treatment of acute migraine attacks.