Sánchez-del-Río González Margarita
Hospital Ruber Internacional, 28034 Madrid, Espana.
Rev Neurol. 2013 Dec 1;57(11):509-14.
Although our knowledge of which systems are activated during migraine is reasonably complete, why the system is activated remains unknown. Incorporating the findings obtained in studies on pain in general has allowed a more integrated model to be generated. According to this new model, there is an anatomical substrate consisting in a complex framework of pain that is made up not only of the trigeminovascular system (end pathway) but of a number of networks that are in turn connected to one another, like the neurolimbic, the ascending and descending modulatory system. This complex network is responsible for modulating and conveying nociceptive signals. In patients with migraine, hyperexcitability of this framework is conditioned by genetic and epigenetic alterations. Epigenetic changes are chemical modifications affecting chromatin, which modulates the activity of genes without modifying the DNA sequence, and which are capable of modulating the expression of genes involved in a number of different aspects, such as plasticity, system excitability, memory of pain or moods. In turn, the presence of external factors (such as environmental changes or alcohol) and internal factors (such as hormones or sleep disorders) contribute to activate this loaded anatomical substrate, resulting in the attack of migraine.
尽管我们对于偏头痛发作时哪些系统被激活的认识已经相当完整,但该系统为何被激活仍然未知。整合从一般疼痛研究中获得的发现,有助于构建一个更完整的模型。根据这个新模型,存在一个由复杂疼痛框架构成的解剖学基础,该框架不仅由三叉神经血管系统(终末通路)组成,还包括许多相互连接的网络,如神经边缘系统、上行和下行调节系统。这个复杂的网络负责调节和传递伤害性信号。在偏头痛患者中,这个框架的过度兴奋由遗传和表观遗传改变所决定。表观遗传变化是影响染色质的化学修饰,它在不改变DNA序列的情况下调节基因活性,并能够调节涉及许多不同方面的基因表达,如可塑性、系统兴奋性、疼痛记忆或情绪。反过来,外部因素(如环境变化或酒精)和内部因素(如激素或睡眠障碍)的存在促使这个负荷过重的解剖学基础被激活,从而引发偏头痛发作。