fMRI Insights into Visual Cortex Dysfunction as a Biomarker for Migraine with Aura.

IF 3.2 Q2 CLINICAL NEUROLOGY
Damian Pikor, Natalia Banaszek-Hurla, Alicja Drelichowska, Mikołaj Hurla, Jolanta Dorszewska, Tomasz Wolak, Wojciech Kozubski
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Abstract

Migraine with aura (MwA) is a common and severely disabling neurological disorder, characterised by transient yet recurrent visual disturbances, including scintillating scotomas, flickering photopsias, and complex geometric patterns. These episodic visual phenomena significantly compromise daily functioning, productivity, and overall quality of life. Despite extensive research, the underlying pathophysiological mechanisms remain only partially understood. Cortical spreading depression (CSD), a propagating wave of neuronal and glial depolarisation, has been identified as a central process in MwA. This phenomenon is triggered by ion channel dysfunction, leading to elevated intracellular calcium levels and excessive glutamate release, which contribute to widespread cortical hyperexcitability. Genetic studies, particularly involving the CACNA gene family, further implicate dysregulation of calcium channels in the pathogenesis of MwA. Recent advances in neuroimaging, particularly functional magnetic resonance imaging (fMRI), have provided critical insights into the neurophysiology of MwA. These results support the central role of CSD as a basic mechanism behind MwA and imply that cortical dysfunction endures beyond brief episodes, possibly due to chronic neuronal dysregulation or hyperexcitability. The visual cortex of MwA patients exhibits activation patterns in comparison to other neuroimaging studies, supporting the possibility that it is a disease-specific biomarker. Its distinctive sensory and cognitive characteristics are influenced by a complex interplay of cortical, vascular, and genetic factors, demonstrating the multifactorial nature of MwA. We now know much more about the pathophysiology of MwA thanks to the combination of molecular and genetic research with sophisticated neuroimaging techniques like arterial spin labelling (ASL) and fMRI. This review aims to synthesize current knowledge and analyse molecular and neurophysiological targets, providing a foundation for developing targeted therapies to modulate cortical excitability, restore neural network stability, and alleviate the burden of migraine with aura. The most important and impactful research in our field has been the focus of this review, which highlights important developments and their contributions to the knowledge and treatment of migraine with aura.

视觉皮质功能障碍作为先兆偏头痛生物标志物的fMRI研究。
先兆偏头痛(MwA)是一种常见且严重致残的神经系统疾病,其特征是短暂而反复的视觉障碍,包括闪烁性暗斑、闪烁性失光和复杂的几何图案。这些情景性视觉现象严重影响日常功能、生产力和整体生活质量。尽管有广泛的研究,潜在的病理生理机制仍然只是部分了解。皮层扩张性抑制(CSD)是神经元和胶质去极化的一种传播波,已被确定为MwA的中心过程。这种现象是由离子通道功能障碍引发的,导致细胞内钙水平升高和谷氨酸过度释放,从而导致广泛的皮层高兴奋性。遗传学研究,特别是涉及到CACNA基因家族的研究,进一步揭示了钙通道失调在MwA发病机制中的作用。神经影像学的最新进展,特别是功能性磁共振成像(fMRI),为MwA的神经生理学提供了重要的见解。这些结果支持CSD作为MwA背后的基本机制的核心作用,并暗示皮层功能障碍持续超过短暂发作,可能是由于慢性神经元失调或过度兴奋性。与其他神经影像学研究相比,MwA患者的视觉皮层显示出激活模式,支持它是疾病特异性生物标志物的可能性。其独特的感觉和认知特征受到皮质、血管和遗传因素的复杂相互作用的影响,表明MwA的多因素性质。由于分子和基因研究与复杂的神经成像技术(如动脉自旋标记(ASL)和功能磁共振成像)的结合,我们现在对MwA的病理生理学有了更多的了解。本文旨在综合现有知识,分析分子和神经生理靶点,为开发靶向治疗方法调节皮质兴奋性,恢复神经网络稳定性,减轻先兆偏头痛的负担提供基础。本综述重点介绍了本领域最重要和最有影响力的研究成果,重点介绍了先兆偏头痛的重要进展及其对先兆偏头痛的认识和治疗的贡献。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neurology International
Neurology International CLINICAL NEUROLOGY-
CiteScore
3.70
自引率
3.30%
发文量
69
审稿时长
11 weeks
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