Retinopathy of prematurity (ROP) is a neurovascular disease that affects prematurely born infants and is known to have significant long term effects on vision. We conducted the studies described herein not only to learn more about vision but also about the pathogenesis of ROP. The coincidence of ROP onset and rapid developmental elongation of the rod photoreceptor outer segments motivated us to consider the role of the rods in this disease. We used noninvasive electroretinographic (ERG), psychophysical, and retinal imaging procedures to study the function and structure of the neurosensory retina. Rod photoreceptor and post-receptor responses are significantly altered years after the preterm days during which ROP is an active disease. The alterations include persistent rod dysfunction, and evidence of compensatory remodeling of the post-receptor retina is found in ERG responses to full-field stimuli and in psychophysical thresholds that probe small retinal regions. In the central retina, both Mild and Severe ROP delay maturation of parafoveal scotopic thresholds and are associated with attenuation of cone mediated multifocal ERG responses, significant thickening of post-receptor retinal laminae, and dysmorphic cone photoreceptors. These results have implications for vision and control of eye growth and refractive development and suggest future research directions. These results also lead to a proposal for noninvasive management using light that may add to the currently invasive therapeutic armamentarium against ROP.

早产儿视网膜病变 (ROP) 是一种影响早产儿的神经血管疾病，已知会对视力产生显着的长期影响。我们进行本文所述的研究不仅是为了更多地了解视力，也是为了了解 ROP 的发病机制。 ROP 发病与视杆细胞感光外节的快速发育伸长同时发生，促使我们考虑视杆细胞在这种疾病中的作用。我们使用无创视网膜电图 (ERG)、心理物理和视网膜成像程序来研究神经感觉视网膜的功能和结构。早产儿数年后，ROP 成为一种活跃疾病，杆状光感受器和感受器后反应发生显着改变。这些改变包括持续的视杆细胞功能障碍，并且在 ERG 对全场刺激的反应和探测视网膜小区域的心理物理阈值中发现了受体后视网膜的代偿性重塑的证据。在视网膜中央，轻度和重度 ROP 均会延迟中心凹旁暗视阈值的成熟，并与视锥细胞介导的多焦点 ERG 反应减弱、感受器后视网膜层显着增厚以及视锥细胞感光细胞变形相关。这些结果对视力以及眼睛生长和屈光发育的控制具有影响，并提出了未来的研究方向。这些结果还提出了使用光进行无创治疗的建议，这可能会增加目前针对 ROP 的侵入性治疗手段。