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光环和头痛:在转化模型中的关系和差距。

Aura and Head pain: relationship and gaps in the translational models.

机构信息

Department of Neurology and Algology, Gazi University Faculty of Medicine, Besevler, 06510, Ankara, Turkey.

Neuropsychiatry Center, Gazi University, Besevler, Ankara, Turkey.

出版信息

J Headache Pain. 2019 Sep 3;20(1):94. doi: 10.1186/s10194-019-1042-8.

DOI:10.1186/s10194-019-1042-8
PMID:31481015
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6734357/
Abstract

Migraine is a complex brain disorder and initiating events for acute attacks still remain unclear. It seems difficult to explain the development of migraine headache with one mechanism and/or a single anatomical location. Cortical spreading depression (CSD) is recognized as the biological substrate of migraine aura and experimental animal studies have provided mechanisms that possibly link CSD to the activation of trigeminal neurons mediating lateralized head pain. However, some CSD features do not match the clinical features of migraine headache and there are gaps in translating CSD to migraine with aura. Clinical features of migraine headache and results from research are critically evaluated; and consistent and inconsistent findings are discussed according to the known basic features of canonical CSD: typical SD limited to the cerebral cortex as it was originally defined. Alternatively, arguments related to the emergence of SD in other brain structures in addition to the cerebral cortex or CSD initiated dysfunction in the thalamocortical network are proposed. Accordingly, including thalamus, particularly reticular nucleus and higher order thalamic nuclei, which functions as a hub connecting the visual, somatosensory, language and motor cortical areas and subjects to modulation by brain stem projections into the CSD theory, would greatly improve our current understanding of migraine.

摘要

偏头痛是一种复杂的脑部疾病,其急性发作的起始事件仍不清楚。用一种机制和/或单一解剖部位来解释偏头痛的发生似乎很困难。皮质扩散性抑制(CSD)被认为是偏头痛先兆的生物学基础,实验动物研究提供了可能将 CSD 与介导偏侧头痛的三叉神经神经元激活联系起来的机制。然而,CSD 的一些特征与偏头痛头痛的临床特征不匹配,并且 CSD 向有先兆偏头痛的转化存在差距。对偏头痛头痛的临床特征和研究结果进行了批判性评估;并根据经典 CSD 的已知基本特征,根据一致和不一致的发现进行了讨论:最初定义的仅限于大脑皮层的典型 SD。或者,提出了除大脑皮层之外的其他脑结构中 SD 的出现或丘脑皮质网络中 CSD 引发的功能障碍的相关论点。因此,包括丘脑,特别是网状核和高级丘脑核,作为连接视觉、躯体感觉、语言和运动皮质区域的枢纽,受脑干投射到 CSD 理论中的调制,将极大地提高我们对偏头痛的理解。

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本文引用的文献

1
Reduced Short-Latency Afferent Inhibition Indicates Impaired Sensorimotor Integrity During Migraine Attacks.偏头痛发作期间感觉运动整合受损,表现为短潜伏期传入抑制减少。
Headache. 2019 Jun;59(6):906-914. doi: 10.1111/head.13554. Epub 2019 May 20.
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Early focal brain injury after subarachnoid hemorrhage correlates with spreading depolarizations.蛛网膜下腔出血后早期局灶性脑损伤与扩散性去极化有关。
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Aura in Cluster Headache: A Cross-Sectional Study.集群性头痛中的光环现象:一项横断面研究。
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Spreading depolarization in acute brain injury inhibited by ketamine: a prospective, randomized, multiple crossover trial.氯胺酮抑制急性脑损伤中的扩散性去极化:一项前瞻性、随机、多次交叉试验。
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Thalamic Lesions and Aphasia or Neglect.丘脑病变与失语症或忽视症。
Curr Neurol Neurosci Rep. 2018 May 23;18(7):39. doi: 10.1007/s11910-018-0844-4.
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