Yuhas Phillip T, Shorter Patrick D, McDaniel Catherine E, Earley Michael J, Hartwick Andrew T E
*OD, MS †OD, PhD ‡OD, MS, FAAO §OD, PhD, FAAO The Ohio State University College of Optometry, Columbus, Ohio (all authors).
Optom Vis Sci. 2017 Jan;94(1):108-117. doi: 10.1097/OPX.0000000000000934.
Photophobia is a common symptom in individuals suffering from traumatic brain injury (TBI). Recent evidence has implicated blue light-sensitive intrinsically photosensitive retinal ganglion cells (ipRGCs) in contributing to the neural circuitry mediating photophobia in migraine sufferers. The goal of this work is to test the hypothesis that ipRGC function is altered in TBI patients with photophobia by assessing pupillary responses to blue and red light.
Twenty-four case participants (mean age 43.3; 58% female), with mild TBI and self-reported photophobia, and 12 control participants (mean age 42.6; 58% female) were in this study. After 10 minutes of dark adaptation, blue (470 nm, 1 × 10 phots/s/cm) and red (625 nm, 7 × 10 phots/s/cm) flashing (0.1 Hz) light stimuli were delivered for 30 seconds to the dilated left eye while the right pupil was recorded. The amplitude of normalized pupil fluctuation (constriction and dilation) was quantified using Fourier fast transforms.
In both case and control participants, the amplitude of pupil fluctuation was significantly less for the blue light stimuli as compared to the red light stimuli, consistent with a contribution of ipRGCs to these pupil responses. There was no significant difference in the mean pupil fluctuation amplitudes between the two participant groups, but case participants displayed greater variability in their pupil responses to the blue stimulus.
Case and control participants showed robust ipRGC-mediated components in their pupil responses to blue light. The results did not support the hypothesis that ipRGCs are "hypersensitive" to light in TBI participants with photophobia. However, greater pupil response variability in the case subjects suggests that ipRGC function may be more heterogeneous in this group.
畏光是创伤性脑损伤（TBI）患者的常见症状。最近有证据表明，对蓝光敏感的内在光敏性视网膜神经节细胞（ipRGCs）参与了偏头痛患者介导畏光的神经回路。这项研究的目的是通过评估瞳孔对蓝光和红光的反应，来检验TBI伴畏光患者的ipRGC功能发生改变这一假设。
本研究纳入了24例轻度TBI且有自我报告畏光症状的受试者（平均年龄43.3岁；58%为女性）以及12例对照受试者（平均年龄42.6岁；58%为女性）。在进行10分钟的暗适应后，对扩张的左眼给予蓝光（470nm，1×10光子/秒/平方厘米）和红光（625nm，7×10光子/秒/平方厘米）闪烁（0.1Hz）光刺激30秒，同时记录右眼瞳孔。使用傅里叶快速变换对标准化瞳孔波动（收缩和扩张）的幅度进行量化。
在病例组和对照组受试者中，与红光刺激相比，蓝光刺激时瞳孔波动幅度明显较小，这与ipRGCs对这些瞳孔反应的作用一致。两组受试者的平均瞳孔波动幅度没有显著差异，但病例组受试者对蓝光刺激的瞳孔反应变异性更大。
病例组和对照组受试者在对蓝光的瞳孔反应中均显示出强大的ipRGC介导成分。结果不支持在有畏光症状的TBI受试者中ipRGCs对光“超敏”这一假设。然而，病例组受试者更大的瞳孔反应变异性表明该组中ipRGC功能可能更具异质性。
