Spectral ERG Analysis of Hypersensitivity to Light in Traumatic Brain Injury

脑外伤患者光敏感性的光谱视网膜电图分析 摘要 脑震荡引起的对光过敏或创伤性光痛可能是一个终生衰弱的问题 在数百万轻度创伤性脑损伤（mTBI）病例中，没有电流 解释这种持续性光敏感的疼痛，以前没有脑外伤影响的报告。 视网膜处理我们建议采用光适应视网膜电图（ERG）的光谱分析 响应作为强度和波长的函数，以评估对视网膜的意外损伤。 并确定其视网膜细胞来源。我们的初步数据显示，从明视到 暗视b波在光性脑外伤中的存在，这意味着视锥细胞对视杆细胞的抑制 在正常条件下运行，这种抑制被脑外伤的影响所阻断， 光敏感性增强的病例。这些新的见解，以以前未知的视网膜 创伤性光痛的机制提示疼痛性光敏感性的主要病因是 由AII无长突细胞介导的视杆细胞抑制，导致视杆细胞在较高的光照水平下过度激活。 将在一个完整的研究中评估mTBI中光敏感性增强的视杆过度激活的新假设， 全视野ERG作为波长和光适应水平的函数的范围研究。 充分表征联合视杆细胞和视锥细胞ERG波形的既定成分 通路反应，复杂的ERG波形将通过神经分析建模进行分析 该方法将表征来自每个主要视网膜处理水平的ERG成分， 它们在各种刺激条件下的相互作用。特别是，我们将跟踪a波，b波 视杆和视锥光感受器系统的明视负反应（PhNR）作为一个函数 对照组和mTBI的光波长和光适应水平作为光痛水平的函数。在 此外，黑视素系统的作用将根据细胞的光谱灵敏度进行评估。 持续的瞳孔大小，以评估瞳孔大小在诱导 创伤性光痛，因此不能补偿所观察到的视杆敏感性的变化。 神经分析模型将允许计算任何程度的有效控制ERG波形 光强度设置，为记录的ERG波形的精确规格提供基线 由于mTBI的影响而发生的变化。光适应视网膜电图的相关波形变化 波形将提供一个强大的非侵入性诊断生物标志物的痛苦的光敏感性 创伤性光痛和mTBI的持续视网膜效应。神经分析建模方法将 提供了一种用于分析视网膜疾病中ERG波形变化的增强方法， 将军

Spectral ERG analysis of hypersensitivity to light in traumatic brain injury Abstract Concussion-induced hypersensitivity to light, or traumatic photalgia, can be a lifelong debilitating problem for upwards of 60% of the millions of mild Traumatic Brain Injury (mTBI) cases. There is no current explanation for the pain of this persistent light sensitivity and no previous report of brain trauma affecting retinal processing. We propose to employ spectral analysis of light-adapted electroretinographic (ERG) responses as a function of intensity and wavelength to assess unsuspected damage to the retina of the human eye and determine its retinal-cell source. Our preliminary data show a shift from a photopic to a scotopic b-wave in photalgic brain trauma, which implies both that there is rod suppression by cones operating under normal conditions and that this suppression is blocked by the effects of the brain trauma in the cases of enhanced light sensitivity. These novel insights into the previously unknown retinal mechanisms of traumatic photalgia suggest that a primary etiology of the painful light sensitivity is loss of rod suppression mediated by AII amacrine cells, causing overactivation of the rods at higher light levels. The novel hypothesis of rod overactivation in enhanced light sensitivity in mTBI will be evaluated in a full- scope study of the full-field ERG as a function of wavelength and light adaptation level. To fully characterize the established components of the ERG waveforms of the conjoint rod and cone pathway responses, the complex ERG waveforms will be analyzed by a neuroanalytic modeling approach that will characterize the ERG components from each of the main retinal processing levels and their interactions across the range of stimulus conditions. In particular, we will track the a-wave, b-wave and photopic negative response (PhNR) of both the rod and the cone photoreceptor systems as a function of both light wavelength and light adaptation level for controls and mTBI as a function of photalgia level. In addition, the role of the melanopsin system will be assessed in terms of the spectral sensitivity of the sustained pupil size to assess the hypothesis that pupil size is not affected under conditions that induce traumatic photalgia, and hence does not compensate for the observed changes in rod sensitivity. The neuroanalytic model will allow the effective control ERG waveform to be computed for any degree of photalgic intensity setting, providing a baseline for precise specification of the recorded ERG waveform changes due to the effects of the mTBI. The correlated waveform changes in the light-adapted ERG waveforms will provide a powerful non-invasive diagnostic biomarker for the painful light sensitivity of traumatic photalgia and the persistent retinal effects of mTBI. The neuroanalytic modeling approach will provide an enhanced methodology for the analysis of ERG waveform changes in retinal diseases in general.