Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Pain. 2013 Dec;154 Suppl 1:S44-53. doi: 10.1016/j.pain.2013.07.021. Epub 2013 Jul 25.
Scientific evidence supports the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation, and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory, and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. Data supporting the activation and sensitization of the trigeminovascular system include the progressive development of cephalic and whole-body cutaneous allodynia during a migraine attack. In addition, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex.
科学证据支持偏头痛病理生理学涉及大脑兴奋性的遗传改变、颅内动脉扩张、三叉血管通路的反复激活和敏化，以及易感个体的结构和功能变化的观点。从感觉先兆、发作期和发作间期对视觉、听觉和嗅觉刺激的超敏反应以及下行抑制性疼痛通路的激活减少的临床和临床前研究中得出了大脑兴奋性改变的证据。支持三叉血管系统激活和敏化的证据包括偏头痛发作期间头部和全身皮肤痛觉过敏的逐渐发展。此外，结构和功能改变包括皮质下白质病变、参与处理感觉信息的皮质区域增厚以及皮质扩散性抑制诱导的皮质神经可塑性变化。在这里，我们回顾了三叉血管通路及其被皮质扩散性抑制激活的最新解剖学数据，以及偏头痛型畏光的神经基质的新认识，以及脑干、下丘脑和大脑皮层对三叉血管通路的调制。
