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创伤后头痛的生物标志物和内表型

Biomarkers and Endophenotypes of Post-traumatic Headaches.

作者信息

Kamins Joshua L, Karimi Ramin, Hoffman Ann, Prins Mayumi L, Giza Christopher C

机构信息

Goldberg Migraine Program, Department of Neurology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA.

UCLA Steve Tisch BrainSPORT Program, Department of Neurosurgery, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA.

出版信息

Curr Pain Headache Rep. 2024 Dec;28(12):1185-1193. doi: 10.1007/s11916-024-01255-1. Epub 2024 Aug 13.

DOI:10.1007/s11916-024-01255-1
PMID:39136870
Abstract

PURPOSE OF REVIEW

To review existing literature on biomarkers for post-traumatic headache (PTH).

RECENT FINDINGS

Preclinical models and clinical findings have started to elucidate the biology that underlies PTH. Traumatic brain injury results in ionic flux, glutamatergic surge, and activation of the trigeminal cervical complex resulting in the release of pain neuropeptides. These neuropeptides, including calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide (PACAP), play a key role in the pathophysiology of migraine and other primary headache disorders. Only two studies were identified that evaluated CGRP levels in PTH. Neither study found a consistent relationship between CGRP levels and PTH. One study did discover that nerve growth factor (NGF) was elevated in subjects with PTH. There is no conclusive evidence for reliable blood-based biomarkers for PTH. Limitations in assays, collection technique, and time since injury must be taken into account. There are multiple ideal candidates that have yet to be explored.

摘要

综述目的

回顾有关创伤后头痛(PTH)生物标志物的现有文献。

最新发现

临床前模型和临床研究结果已开始阐明PTH的生物学基础。创伤性脑损伤导致离子通量、谷氨酸能激增以及三叉神经颈复合体激活,从而导致疼痛神经肽释放。这些神经肽,包括降钙素基因相关肽(CGRP)和垂体腺苷酸环化酶激活多肽(PACAP),在偏头痛和其他原发性头痛疾病的病理生理学中起关键作用。仅确定了两项评估PTH中CGRP水平的研究。两项研究均未发现CGRP水平与PTH之间存在一致关系。一项研究确实发现PTH患者的神经生长因子(NGF)升高。尚无确凿证据表明存在可靠的基于血液的PTH生物标志物。必须考虑检测方法、采集技术和受伤后时间的局限性。有多种理想的候选生物标志物尚未得到探索。

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本文引用的文献

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Headache. 2023 Oct;63(9):1240-1250. doi: 10.1111/head.14635. Epub 2023 Oct 5.
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Molecular Mechanisms of Migraine: Nitric Oxide Synthase and Neuropeptides.偏头痛的分子机制:一氧化氮合酶和神经肽。
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Repeat mild traumatic brain injuries (RmTBI) modify nociception and disrupt orexinergic connectivity within the descending pain pathway.
重复轻度创伤性脑损伤 (RmTBI) 会改变痛觉和破坏下行痛觉通路上的食欲素能连接。
J Headache Pain. 2023 Jun 14;24(1):72. doi: 10.1186/s10194-023-01608-y.
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Effect of Voluntary Exercise on Endogenous Pain Control Systems and Post-traumatic Headache in Mice.自愿运动对小鼠内源性疼痛控制系统和创伤后头痛的影响。
J Pain. 2023 Oct;24(10):1859-1874. doi: 10.1016/j.jpain.2023.05.015. Epub 2023 Jun 2.
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Serum Alpha and Beta-CGRP Levels in Chronic Migraine Patients Before and After Monoclonal Antibodies Against CGRP or its Receptor.慢性偏头痛患者在使用 CGRP 或其受体单克隆抗体前后的血清 Alpha 和 Beta-CGRP 水平。
Ann Neurol. 2023 Aug;94(2):285-294. doi: 10.1002/ana.26658. Epub 2023 Apr 21.
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Front Neurol. 2023 Feb 28;14:989974. doi: 10.3389/fneur.2023.989974. eCollection 2023.
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Neurology. 2023 Apr 4;100(14):e1510-e1519. doi: 10.1212/WNL.0000000000206853. Epub 2023 Jan 18.
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