中脑导水管周围灰质网络在癫痫和偏头痛交互影响中的作用

癫痫与偏头痛的交互影响关系受到越来越多的重视。中脑腹侧导水管周围灰质（vPAG）作为下行抑制性痛觉调节的关键核团，其功能受损是偏头痛的重要病理原因。新近研究表明vPAG的兴奋冲动能够激活脑桥的脚桥核（PPN），后者的激活则有显著的抗癫痫作用。结合癫痫和偏头痛的发病理论及其交互作用关系，我们假说：慢性癫痫发作致vPAG神经元脱失和功能受损，痛觉抑制减弱，引发偏头痛，同时致vPAG-PPN兴奋传导下降，从而导致癫痫发作加重；反之，偏头痛反复发作致vPAG受损，恶化偏头痛，同时致vPAG-PPN兴奋传导下降，也导致了癫痫发作的加重。本研究应用立体定向核团毁损、神经逆向示踪、脑电、脑场电位及行为记录的方法，观察癫痫和偏头痛/痛觉过敏所致vPAG结构及vPAG-PPN连接强度受损及其反馈效应，初步明确vPAG-PPN传导通路在癫痫和偏头痛交互影响中的作用，为未来癫痫和偏头痛的共治探索一新的方向。

The interacting relationship between epilepsy and migraine is attracting more and more attention. Dysfunction of the midbrain ventrolateral periaqueductal gray (vPAG), a key structure of descending inhibitory modulation of pain, is one of the major pathogenic events in migraine. Recent studies indicate that the excitatory transduction from vPAG can activate the pedunculopontine nucleus (PPN) whose activation has a significant anti-epileptic effect. In combination with the fact of the interacting relationship between epilepsy and migraine and the pathogenic theories of them, we raise the following hypothesis: In chronic epilepsy, recurrent attacks of seizures lead to neuronal loss and function disturbance of the vPAG, resulting in attenuation of the inhibitory pain modulation and thus causing the susceptibility of migraine headache attacking. Simutaneously, the neuronal loss and function disturbance of the vPAG lead to the weakening of the PPN-activating signal from the vPAG and thus causing the susceptibility of seizure attacking. Conversely, the neuronal loss and function disturbance of the vPAG caused by recurrent attacks of migraine headaches will deteriorate the migraine headache attacking, and will simutaneously facilitate the seizure attacking due to the weakened PPN-activating signal from the vPAG structurely and functionaly impaired by the chronic headache attacks. In the current study, measures of stereotactic lesion to specific gray nucleus, neural fiber retrograde tracing, electroencephalogram and behavior recording, imaging technique are employed to investigate the neuronal injury in the vPAG, the impairment of the connectedness between vPAG and PPN and their retroaction on epileptic seizure as well as on migraine/hyperalgesia, preliminarily clarifying the role of the vPAG-PPN pathway in the interacting relationship between epilepsy and migraine, and thus exploring a novel direction for future co-treatment of epilepsy and migraine.