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褪黑素敏感性在偏头痛发作间期光过敏中占主导地位。

Melanopsin hypersensitivity dominates interictal photophobia in migraine.

机构信息

Centre for Vision and Eye Research, Institute of Health and Biomedical Innovation, Queensland University of Technology (QUT), Brisbane, Queensland, Australia.

School of Optometry and Vision Science, Queensland University of Technology (QUT), Brisbane, Queensland, Australia.

出版信息

Cephalalgia. 2021 Feb;41(2):217-226. doi: 10.1177/0333102420963850. Epub 2020 Oct 12.

DOI:10.1177/0333102420963850
PMID:33040593
Abstract

PURPOSE

To define the melanopsin and cone luminance retinogeniculate pathway contributions to photophobia in healthy controls and migraineurs.

METHODS

Healthy controls and migraineurs were categorized according to the International Classification of Headache Disorders criteria. Photophobia was measured under full-field illumination using electromyography in response to narrowband lights spanning the melanopsin and cone luminance action spectra. Migraineurs were tested during their interictal headache-free period. Melanopsin-mediated post-illumination pupil responses quantified intrinsically photosensitive Retinal Ganglion Cell (ipRGC) function.

RESULTS

A model combining the melanopsin and cone luminance action spectra best described photophobia thresholds in controls and migraineurs; melanopsin contributions were ∼1.5× greater than cone luminance. In the illumination range causing photophobia, migraineurs had lower photophobia thresholds (∼0.55 log units;  < 0.001) and higher post-illumination pupil response amplitudes ( = 0.03) than controls.

CONCLUSION

Photophobia is driven by melanopsin and cone luminance inputs to the cortex via the retino-thalamocortical pathway. In migraineurs, lower photophobia thresholds reflect hypersensitivity of ipRGC and cone luminance pathways, with the larger and prolonged post-illumination pupil response amplitude indicative of a supranormal melanopsin response. Our findings inform artificial lighting strategies incorporating luminaires with low melanopsin excitation and photopic luminance to limit the lighting conditions leading to photophobia.

摘要

目的

定义健康对照者和偏头痛患者的黑视蛋白和视锥细胞亮度视网膜神经节细胞通路对视光恐惧症的贡献。

方法

根据国际头痛疾病分类标准,将健康对照者和偏头痛患者进行分类。在全视野照明下,使用肌电图测量窄带光对光恐惧症的反应,这些光跨越黑视蛋白和视锥细胞亮度作用光谱。偏头痛患者在无头痛的间歇期进行测试。量化内在光敏性视网膜神经节细胞(ipRGC)功能的光后瞳孔反应来测量黑视蛋白介导的光后瞳孔反应。

结果

一个结合黑视蛋白和视锥细胞亮度作用光谱的模型最好地描述了对照组和偏头痛患者的光恐惧症阈值;黑视蛋白的贡献比视锥细胞亮度高约 1.5 倍。在引起光恐惧症的照明范围内,偏头痛患者的光恐惧症阈值较低(约 0.55 个对数单位; < 0.001),光后瞳孔反应幅度较高( = 0.03)。

结论

光恐惧症是由黑视蛋白和视锥细胞亮度输入到大脑皮层的视网膜-丘脑-皮质通路驱动的。在偏头痛患者中,较低的光恐惧症阈值反映了 ipRGC 和视锥细胞亮度通路的超敏性,较大且持续时间较长的光后瞳孔反应幅度表明黑视蛋白反应异常。我们的发现为包含低黑视蛋白激发和视亮度的人工照明策略提供了信息,以限制导致光恐惧症的照明条件。

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