Espinosa-Sanchez Juan M, Lopez-Escamez Jose A
Otology and Neurotology Group CTS495, Human DNA Variability Department, GENYO Centre for Genomics and Oncological Research Pfizer - University of Granada - Junta de Andalucia , Granada , Spain ; Department of Otolaryngology, Hospital San Agustin , Linares , Spain.
Otology and Neurotology Group CTS495, Human DNA Variability Department, GENYO Centre for Genomics and Oncological Research Pfizer - University of Granada - Junta de Andalucia , Granada , Spain ; Department of Otolaryngology, Hospital de Poniente , El Ejido , Spain.
Front Neurol. 2015 Feb 6;6:12. doi: 10.3389/fneur.2015.00012. eCollection 2015.
Vestibular migraine (VM) is a common disorder in which genetic, epigenetic, and environmental factors probably contribute to its development. The pathophysiology of VM is unknown; nevertheless in the last few years, several studies are contributing to understand the neurophysiological pathways involved in VM. The current hypotheses are mostly based on the knowledge of migraine itself. The evidence of trigeminal innervation of the labyrinth vessels and the localization of vasoactive neuropeptides in the perivascular afferent terminals of these trigeminal fibers support the involvement of the trigemino-vascular system. The neurogenic inflammation triggered by activation of the trigeminal-vestibulocochlear reflex, with the subsequent inner ear plasma protein extravasation and the release of inflammatory mediators, can contribute to a sustained activation and sensitization of the trigeminal primary afferent neurons explaining VM symptoms. The reciprocal connections between brainstem vestibular nuclei and the structures that modulate trigeminal nociceptive inputs (rostral ventromedial medulla, ventrolateral periaqueductal gray, locus coeruleus, and nucleus raphe magnus) are critical to understand the pathophysiology of VM. Although cortical spreading depression can affect cortical areas involved in processing vestibular information, functional neuroimaging techniques suggest a dysmodulation in the multimodal sensory integration and processing of vestibular and nociceptive information, resulting from a vestibulo-thalamo-cortical dysfunction, as the pathogenic mechanism underlying VM. The elevated prevalence of VM suggests that multiple functional variants may confer a genetic susceptibility leading to a dysregulation of excitatory-inhibitory balance in brain structures involved in the processing of sensory information, vestibular inputs, and pain. The interactions among several functional and structural neural networks could explain the pathogenic mechanisms of VM.
前庭性偏头痛（VM）是一种常见疾病，遗传、表观遗传和环境因素可能都对其发病有影响。VM的病理生理学尚不清楚；然而在过去几年中，多项研究有助于了解VM所涉及的神经生理途径。目前的假说大多基于对偏头痛本身的认识。迷路血管的三叉神经支配以及这些三叉神经纤维的血管周围传入终末中血管活性神经肽的定位证据支持了三叉神经血管系统的参与。三叉神经 - 前庭蜗反射激活引发的神经源性炎症，随后内耳血浆蛋白外渗和炎症介质释放，可导致三叉神经初级传入神经元持续激活和致敏，从而解释VM症状。脑干前庭核与调节三叉神经伤害性传入输入的结构（延髓头端腹内侧、导水管周围灰质腹外侧、蓝斑和中缝大核）之间的相互连接对于理解VM的病理生理学至关重要。虽然皮层扩散性抑制可影响参与处理前庭信息的皮层区域，但功能神经成像技术表明，由于前庭 - 丘脑 - 皮层功能障碍，前庭和伤害性信息的多模态感觉整合及处理出现失调，这是VM潜在的致病机制。VM的高患病率表明，多个功能变异可能赋予遗传易感性，导致参与感觉信息处理、前庭输入和疼痛处理的脑结构中兴奋 - 抑制平衡失调。多个功能和结构神经网络之间的相互作用可以解释VM的致病机制。
