Episodic migraine (EM)

发作性偏头痛(EM)是最常见的神经系统疾病，影响12%的成年人口。 阳性和阴性的神经系统症状可能出现在头痛之前或伴随头痛，但偏头痛的疼痛可能会在没有任何征兆的情况下发生。许多自主神经、胃肠、躯体感觉和认知变化伴随着偏头痛，加剧了EM的影响和负担。影像和神经生理学研究证实受累于皮质、皮质下、脑干以及中央和周围三叉神经结构。有效的治疗方法出现得很慢，而且数量也很少。EM是共病的 患有情绪障碍以及一系列复杂的持续性疼痛状况(CPPC)，包括IBS、FM、WS和TMD。外周和中枢敏感化发生在发作期间，而定量感觉测试在发作之间通常是正常的。诱发电位显示两次发作之间的习惯性降低。尽管已确定家族性偏瘫偏头痛的基因，但这与神经胶质和突触功能的改变有关 在这种情况下，还没有在普通偏头痛中发现任何基因。EM在炎症性/免疫性疾病患者中的患病率增加，有时与深部白质的结构变化有关。EM在一些患者中变得慢性，从而导致大脑结构发生永久性变化，从而有助于疼痛识别和调制。我们认为，EM与其他CPPC包括FM、IBS、W S和TMD具有共同的行为、表型和遗传因素。此外，我们预计这些因素将预测可测试的皮质反应的变化。我们的目标是全面描述一大群EM患者的特征。我们已经组建了一个多学科的研究团队，他们拥有神经学、止痛药、神经生理学、口腔面部疼痛和牙科、遗传学、心理生理学、心理学、生物统计学和流行病学方面的专业知识。这些被提议的目标将从以下方面为EM的潜在机制提供一致的证据：1)EM中与其他CPPC共同观察到的心理社会特征；2)对感觉刺激的反应特征和适应；以及3)影响疼痛、感觉加工和心理特征的候选基因。这一证据将指导基于机制的治疗EM和其他普遍的、致残的和痛苦的疾病的发展。

Episodic migraine (EM) is the most prevalent neurologic disorder, affecting 12% of the adult population. Positive and negative neurological symptoms may precede or accompany head pain though the pain of migraine may ensue without warning signs. Autonomic, gastrointestinal, somatosensory and cognitive changes many accompany migraine, compounding the impact and burden of EM. Imaging and neurophysiology studies confirm involvement of cortical, subcortical, brainstem and central and peripheral trigeminal structures. Effective treatments have been slow to emerge and are few in number. EM is co-morbid with mood disorders as well as a host of Complex Persistent Pain Conditions (CPPCs) including IBS, FM, WS and TMD. Peripheral and central sensitization occur during attacks while Quantitative Sensory Testing is typically normal between attacks. Evoked potentials show decreased habituation between attacks. Although genes have been identified for Familial Hemiplegic Migraine, implicating changes in glial and synaptic function in that condition, no gene has been identified in common migraine. EM has an increased prevalence in patients with inflammatory/immunologic diseases and is associated with structural changes in deep white matter at times. EM becomes chronic in some with resultant permanent changes in brain structures subserving pain recognition and modulation. We propose that EM shares behavioral, phenotypic and genetic factors with other CPPCs including FM, IBS, W S and TMD. In addition, we expect that these factors will predict variations in testable cortical responses. Our objective is to fully characterize a large group of patients with EM. We have assembled a multi-disciplinary team of investigators with expertise in neurology, pain medicine, neurophysiology, orofacial pain and dentistry, genetics, psychophyslcs, psychology, biostatistics and epidemiology. The proposed aims will provide converging evidence for the mechanisms underlying EM with respect to: 1) psychosocial profiles in EM commonly observed with other CPPCs; 2) response characteristics and adaptation to sensory stimuli; and 3) candidate genes that influence pain, sensory processing, and psychological profiles. This evidence will guide development of mechanism-based treatments for EM and other prevalent, disabling and painful disorders.