Photophobia: shared pathophysiology underlying dry eye disease, migraine and traumatic brain injury leading to central neuroplasticity of the trigeminothalamic pathway.

Photophobia: shared pathophysiology underlying dry eye disease, migraine and traumatic brain injury leading to central neuroplasticity of the trigeminothalamic pathway.
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畏光症:共同的病理生理学基础干眼病,偏头痛和创伤性脑损伤,导致中枢神经可塑性的三叉丘脑途径。

DOI:
10.1136/bjophthalmol-2020-316417
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发表时间:
2021-06
期刊:
The British journal of ophthalmology
影响因子:
--
通讯作者:
Galor A
Galor A
中科院分区:
其他
文献类型:
--
作者:
Diel RJ;Mehra D;Kardon R;Buse DC;Moulton E;Galor A

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畏光是一种潜在的衰弱症状,常见于干眼病(DE)、偏头痛和创伤性脑损伤(TBI)。我们通过PubMed检索英文文章对文献进行了回顾,重点关注畏光症如何与DE、偏头痛和脑外伤的共同病理生理学有关。DE、偏头痛和脑外伤是普通人群中的常见疾病,通常并存,并以畏光为症状。在这三种情况下,外周和中枢神经系统成分的神经失调与各种动物模型和人类的恐光有关。神经肽降钙素基因相关肽(CGRP)的活性增强与畏光密切相关。目前治疗恐光症的方法包括保护眼睛免受特定波长影响的眼镜,肉毒杆菌毒素,以及抑制CGRP及其受体。尽管使用了这些疗法,但许多人仍有持续性的恐光症状,因此,需要开发新的疗法。DE、偏头痛和脑外伤患者畏光症状的存在提示了共同的三叉神经丘脑病理生理机制,神经肽CGRP介导的中枢神经可塑性和超敏反应可以解释这一现象。持续性畏光患者应考虑针对神经通路(即口服神经调节剂、经皮神经刺激)的治疗策略,特别是对其症状不能通过传统疗法控制的DE患者。
Photophobia is a potentially debilitating symptom often found in dry eye disease (DE), migraine and traumatic brain injury (TBI). We conducted a review of the literature via a PubMed search of English language articles with a focus on how photophobia may relate to a shared pathophysiology across DE, migraine and TBI. DE, migraine and TBI are common conditions in the general population, are often comorbid, and share photophobia as a symptom. Across the three conditions, neural dysregulation of peripheral and central nervous system components is implicated in photophobia in various animal models and in humans. Enhanced activity of the neuropeptide calcitonin gene-related peptide (CGRP) is closely linked to photophobia. Current therapies for photophobia include glasses which shield the eyes from specific wavelengths, botulinum toxin, and inhibition of CGRP and its receptor. Many individuals have persistent photophobia despite the use of these therapies, and thus, development of new therapies is needed. The presence of photophobia in DE, migraine and TBI suggests shared trigeminothalamic pathophysiologic mechanisms, as explained by central neuroplasticity and hypersensitivity mediated by neuropeptide CGRP. Treatment strategies which target neural pathways (ie, oral neuromodulators, transcutaneous nerve stimulation) should be considered in patients with persistent photophobia, specifically in individuals with DE whose symptoms are not controlled with traditional therapies.
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