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。 阳性和阴性神经症状可能先于或伴随头痛，尽管偏头痛的疼痛可能在没有警告信号的情况下发生。自主神经、胃肠、躯体感觉和认知变化许多伴随偏头痛，加重了EM的影响和负担。影像学和神经生理学研究证实皮质、皮质下、脑干和三叉神经中枢及外周结构受累。有效的治疗方法出现缓慢，而且数量很少。EM共病 患有情绪障碍以及一系列复杂持续性疼痛状况（CPPC），包括IBS、FM、WS和TMD。在发作期间发生外周和中枢致敏，而定量感觉测试通常在发作之间正常。诱发电位显示攻击之间的习惯性下降。虽然家族性偏瘫性偏头痛的基因已被鉴定，涉及神经胶质和突触功能的变化， 在这种情况下，普通偏头痛中没有发现基因。EM在炎性/免疫性疾病患者中的患病率增加，有时与深部白色物质的结构变化相关。EM在某些情况下成为慢性的，从而导致大脑结构的永久性变化，从而有助于疼痛识别和调节。我们认为EM与其他CPPC包括FM、IBS、WS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层反应的变化。我们的目标是充分描述一个大的EM患者群体。我们已经组建了一个多学科的研究团队，他们具有神经病学，疼痛医学，神经生理学，口腔颌面疼痛和牙科学，遗传学，心理学，心理学，生物统计学和流行病学的专业知识。提出的目标将为EM的潜在机制提供以下方面的会聚证据：1）与其他CPPC一起观察到的EM中的社会心理特征; 2）对感觉刺激的反应特征和适应;以及3）影响疼痛，感觉处理和心理特征的候选基因。这一证据将指导EM和其他流行的、致残的和疼痛的疾病的基于机制的治疗的发展。

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.