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创伤性脑损伤患者的内在光敏性视网膜神经节细胞驱动的瞳孔反应。

Intrinsically photosensitive retinal ganglion cell-driven pupil responses in patients with traumatic brain injury.

机构信息

University of Houston College of Optometry, 4901 Calhoun Rd, Houston, TX 77004, United States.

University of Houston College of Optometry, 4901 Calhoun Rd, Houston, TX 77004, United States.

出版信息

Vision Res. 2021 Nov;188:174-183. doi: 10.1016/j.visres.2021.07.007. Epub 2021 Aug 2.

DOI:10.1016/j.visres.2021.07.007
PMID:34352476
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8440415/
Abstract

Previous findings regarding intrinsically photosensitive retinal ganglion cell (ipRGC) function after traumatic brain injury (TBI) are conflicting. We examined ipRGC-driven pupil responses in civilian TBI and control participants using two pupillography protocols that assessed transient and adaptive properties: (1) a one second (s) long wavelength "red" stimulus (651 nm, 133 cd/m) and 10 increasing intensities of 1 s short wavelength "blue" stimuli (456 nm, 0.167 to 167 cd/m) with a 60 s interstimulus interval, and (2) two minutes of 0.1 Hz red stimuli (33 cd/m), followed by two minutes of 0.1 Hz blue stimuli (16 cd/m). For Protocol 1, constriction amplitude and the 6 s post illumination pupil response (PIPR) were calculated. For Protocol 2, amplitudes and peak velocities of pupil constriction and redilation were calculated. For Protocol 1, constriction amplitude and the 6 s PIPR were not significantly different between TBI patients and control subjects for red or blue stimuli. For Protocol 2, pupil constriction amplitude attenuated over time for red stimuli and potentiated over time for blue stimuli across all subjects. Constriction and redilation velocities were similar between groups. Pupil constriction amplitude was significantly less in TBI patients compared to control subjects for red and blue stimuli, which can be attributed to age-related differences in baseline pupil size. While TBI, in addition to age, may have contributed to decreased baseline pupil diameter and constriction amplitude, responses to blue stimulation suggest no selective damage to ipRGCs.

摘要

先前关于创伤性脑损伤 (TBI) 后光感受器神经节细胞 (ipRGC) 功能的研究结果相互矛盾。我们使用两种瞳孔描记法协议检查了民用 TBI 和对照参与者的 ipRGC 驱动的瞳孔反应,这些协议评估了瞬态和适应性特性:(1) 持续 1 秒的长波长“红色”刺激 (651nm, 133cd/m) 和 10 个强度递增的 1 秒短波长“蓝色”刺激 (456nm, 0.167 至 167cd/m),刺激间隔为 60 秒,以及 (2) 两分钟的 0.1Hz 红色刺激 (33cd/m),随后是两分钟的 0.1Hz 蓝色刺激 (16cd/m)。对于协议 1,计算收缩幅度和 6 秒后光照瞳孔反应 (PIPR)。对于协议 2,计算瞳孔收缩和扩张的幅度和峰值速度。对于协议 1,对于红色或蓝色刺激,TBI 患者和对照组之间的收缩幅度和 6 秒 PIPR 没有显著差异。对于协议 2,瞳孔收缩幅度随时间对红色刺激减弱,随时间对蓝色刺激增强,所有受试者均如此。收缩和扩张速度在组间相似。与对照组相比,TBI 患者的瞳孔收缩幅度对于红色和蓝色刺激均明显较小,这归因于基线瞳孔大小的年龄相关差异。虽然 TBI 除了年龄之外,还可能导致基线瞳孔直径和收缩幅度减小,但对蓝色刺激的反应表明 ipRGC 没有选择性损伤。

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