PDF(Pubmed)
Abstract：
To quantify interictal photophobia in migraine with and without aura using reflexive eye closure as an implicit measure of light sensitivity and to assess the contribution of melanopsin and cone signals to these responses.
Participants were screened to meet criteria for 1 of 3 groups: headache-free (HF) controls, migraine without aura (MO), and migraine with visual aura (MA). MO and MA participants were included if they endorsed ictal and interictal photophobia. Exclusion criteria included impaired vision, inability to collect usable pupillometry, and history of either head trauma or seizure. Participants viewed light pulses that selectively targeted melanopsin, the cones, or their combination during recording of orbicularis oculi EMG (OO-EMG) and blinking activity.
We studied 20 participants in each group. MA and MO groups reported increased visual discomfort to light stimuli (discomfort rating, 400% contrast, MA: 4.84 [95% confidence interval 0.33, 9.35]; MO: 5.23 [0.96, 9.50]) as compared to HF controls (2.71 [0, 6.47]). Time course analysis of OO-EMG and blinking activity demonstrated that reflexive eye closure was tightly coupled to the light pulses. The MA group had greater OO-EMG and blinking activity in response to these stimuli (EMG activity, 400% contrast: 42.9%Δ [28.4, 57.4]; blink activity, 400% contrast: 11.2% [8.8, 13.6]) as compared to the MO (EMG activity, 400% contrast: 9.9%Δ [5.8, 14.0]; blink activity, 400% contrast: 4.7% [3.5, 5.9]) and HF control (EMG activity, 400% contrast: 13.2%Δ [7.1, 19.3]; blink activity, 400% contrast: 4.5% [3.1, 5.9]) groups.
Our findings suggest that the intrinsically photosensitive retinal ganglion cells (ipRGCs), which integrate melanopsin and cone signals, provide the afferent input for light-induced reflexive eye closure in a photophobic state. Moreover, we find a dissociation between implicit and explicit measures of interictal photophobia depending on a history of visual aura in migraine. This implies distinct pathophysiology in forms of migraine, interacting with separate neural pathways by which the amplification of ipRGC signals elicits implicit and explicit signs of visual discomfort.
Participants were screened to meet criteria for 1 of 3 groups: headache-free (HF) controls, migraine without aura (MO), and migraine with visual aura (MA). MO and MA participants were included if they endorsed ictal and interictal photophobia. Exclusion criteria included impaired vision, inability to collect usable pupillometry, and history of either head trauma or seizure. Participants viewed light pulses that selectively targeted melanopsin, the cones, or their combination during recording of orbicularis oculi EMG (OO-EMG) and blinking activity.
We studied 20 participants in each group. MA and MO groups reported increased visual discomfort to light stimuli (discomfort rating, 400% contrast, MA: 4.84 [95% confidence interval 0.33, 9.35]; MO: 5.23 [0.96, 9.50]) as compared to HF controls (2.71 [0, 6.47]). Time course analysis of OO-EMG and blinking activity demonstrated that reflexive eye closure was tightly coupled to the light pulses. The MA group had greater OO-EMG and blinking activity in response to these stimuli (EMG activity, 400% contrast: 42.9%Δ [28.4, 57.4]; blink activity, 400% contrast: 11.2% [8.8, 13.6]) as compared to the MO (EMG activity, 400% contrast: 9.9%Δ [5.8, 14.0]; blink activity, 400% contrast: 4.7% [3.5, 5.9]) and HF control (EMG activity, 400% contrast: 13.2%Δ [7.1, 19.3]; blink activity, 400% contrast: 4.5% [3.1, 5.9]) groups.
Our findings suggest that the intrinsically photosensitive retinal ganglion cells (ipRGCs), which integrate melanopsin and cone signals, provide the afferent input for light-induced reflexive eye closure in a photophobic state. Moreover, we find a dissociation between implicit and explicit measures of interictal photophobia depending on a history of visual aura in migraine. This implies distinct pathophysiology in forms of migraine, interacting with separate neural pathways by which the amplification of ipRGC signals elicits implicit and explicit signs of visual discomfort.
摘要：
使用反射性闭眼作为光敏感性的隐式量度来量化有或无先兆的偏头痛的发作间畏光，并评估黑视素和视锥信号对这些反应的贡献。
对参与者进行筛选，以满足3组中的1组标准：无头痛（HF）对照组，无先兆偏头痛（MO），与视觉先兆偏头痛（MA）。如果MO和MA参与者认可发作和发作间畏光，则将其包括在内。排除标准包括视力受损，无法收集可用的瞳孔测量，以及头部外伤或癫痫发作史。参与者观察了选择性靶向黑视素的光脉冲，锥体，或在记录眼轮匝肌肌电图（OO-EMG）和眨眼活动期间它们的组合。
我们研究了每组20名参与者。MA和MO组报告对光刺激的视觉不适增加(不适等级，400%对比度,与HF对照(2.71[0,6.47])相比,MA:4.84[95%置信区间0.33,9.35];MO:5.23[0.96,9.50])。OO-EMG和眨眼活动的时程分析表明，反射性闭眼与光脉冲紧密耦合。MA组对这些刺激有更大的OO-EMG和眨眼活性(EMG活性，400%对比度：42.9%Δ[28.4，57.4]；眨眼活动，400%对比度：11.2%[8.8,13.6])与MO(肌电图活性，400%对比度:9.9%Δ[5.8,14.0];眨眼活动,400%对比度：4.7%[3.5，5.9])和HF控制(EMG活动，400%对比度：13.2%Δ[7.1，19.3]；眨眼活动，400％对比：4.5％[3.1，5.9]）组。
我们的研究结果表明，内在光敏视网膜神经节细胞（ipRGC），整合黑视素和视锥信号，在疏光状态下为光诱导的反射性眼睛闭合提供传入输入。此外，我们发现发作间畏光的内隐和外显之间的分离取决于偏头痛的视觉先兆病史。这意味着不同的病理生理学形式的偏头痛，与单独的神经通路相互作用，ipRGC信号的放大会引起视觉不适的隐含和明确迹象。
对参与者进行筛选，以满足3组中的1组标准：无头痛（HF）对照组，无先兆偏头痛（MO），与视觉先兆偏头痛（MA）。如果MO和MA参与者认可发作和发作间畏光，则将其包括在内。排除标准包括视力受损，无法收集可用的瞳孔测量，以及头部外伤或癫痫发作史。参与者观察了选择性靶向黑视素的光脉冲，锥体，或在记录眼轮匝肌肌电图（OO-EMG）和眨眼活动期间它们的组合。
我们研究了每组20名参与者。MA和MO组报告对光刺激的视觉不适增加(不适等级，400%对比度,与HF对照(2.71[0,6.47])相比,MA:4.84[95%置信区间0.33,9.35];MO:5.23[0.96,9.50])。OO-EMG和眨眼活动的时程分析表明，反射性闭眼与光脉冲紧密耦合。MA组对这些刺激有更大的OO-EMG和眨眼活性(EMG活性，400%对比度：42.9%Δ[28.4，57.4]；眨眼活动，400%对比度：11.2%[8.8,13.6])与MO(肌电图活性，400%对比度:9.9%Δ[5.8,14.0];眨眼活动,400%对比度：4.7%[3.5，5.9])和HF控制(EMG活动，400%对比度：13.2%Δ[7.1，19.3]；眨眼活动，400％对比：4.5％[3.1，5.9]）组。
我们的研究结果表明，内在光敏视网膜神经节细胞（ipRGC），整合黑视素和视锥信号，在疏光状态下为光诱导的反射性眼睛闭合提供传入输入。此外，我们发现发作间畏光的内隐和外显之间的分离取决于偏头痛的视觉先兆病史。这意味着不同的病理生理学形式的偏头痛，与单独的神经通路相互作用，ipRGC信号的放大会引起视觉不适的隐含和明确迹象。
