Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Department of Molecular Neurobiology, Moscow, Russia.
Cephalalgia. 2021 Mar;41(3):353-365. doi: 10.1177/0333102420970172. Epub 2020 Nov 8.
Growing evidence shows a critical role of network disturbances in the pathogenesis of migraine. Unilateral pattern of neurological symptoms of aura suggests disruption of interhemispheric interactions during the early phase of a migraine attack. Using local field potentials data from the visual and motor cortices, this study explored effects of unilateral cortical spreading depression, the likely pathophysiological mechanism of migraine aura, on interhemispheric functional connectivity in freely behaving rats.
Temporal evolution of the functional connectivity was evaluated using mutual information and phase synchronization measures applied to local field potentials recordings obtained in homotopic points of the motor and visual cortices of the two hemispheres in freely behaving rats after induction of a single unilateral cortical spreading depression in the somatosensory S1 cortex and sham cortical stimulation.
Cortical spreading depression was followed by a dramatic broadband loss of interhemispheric functional connectivity in the visual and motor regions of the cortex. The hemispheric disconnection started after the end of the depolarization phase of cortical spreading depression, progressed gradually, and terminated by 5 min after initiation of cortical spreading depression. The network impairment had region- and frequency-specific characteristics and was more pronounced in the visual cortex than in the motor cortex. The period of impaired neural synchrony coincided with post-cortical spreading depression electrographic aberrant activation of the ipsilateral cortex and abnormal behavior.
The study provides the first evidence that unilateral cortical spreading depression induces a reversible loss of functional hemispheric connectivity in the cortex of awake animals. Given a critical role of long-distance cortical synchronization in sensory processing and sensorimotor integration, the post-cortical spreading depression breakdown of functional connectivity may contribute to neuropathological mechanisms of aura generation.
越来越多的证据表明，网络紊乱在偏头痛发病机制中起着关键作用。先兆期单侧的神经系统症状表明偏头痛发作早期半球间相互作用被破坏。本研究采用视觉和运动皮层的局部场电位数据，探讨单侧皮质扩散性抑制（偏头痛先兆的可能病理生理机制）对自由活动大鼠大脑半球间功能连接的影响。
采用互信息和相位同步测量方法，评估单侧皮质扩散性抑制诱导后，自由活动大鼠双侧大脑半球同源运动和视觉皮层局部场电位记录中的功能连接的时间演变。假刺激皮质。
皮质扩散性抑制后，大脑皮层视觉和运动区域的半球间功能连接出现明显的宽带丧失。半球分离始于皮质扩散性抑制去极化阶段结束后，逐渐进展，并在皮质扩散性抑制开始后 5 分钟终止。网络损伤具有区域和频率特异性特征，在视觉皮层比运动皮层更为明显。神经同步受损的时期与皮质扩散性抑制后同侧皮层的电异常激活和异常行为相吻合。
该研究首次提供证据表明，单侧皮质扩散性抑制可导致清醒动物大脑皮层的功能连接可逆丧失。鉴于远距离皮质同步在感觉处理和感觉运动整合中的关键作用，皮质扩散性抑制后功能连接的中断可能有助于先兆发生的神经病理学机制。
