Survival of Retinal Ganglion Cells After Damage to the Occipital Lobe in Humans is Activity-Dependent

This dataset accompanies the following published paper:

Schneider C., Prentiss E., Busza A., Matmati K., Matmati N., et. al. (2019). Survival of retinal ganglion cells after damage to the occipital lobe in humans is activity dependent. Proceedings of the Royal Society B: Biological Sciences, 286(1897) pp: 20182733. doi: 10.1098/rspb.2018.2733

Abstract:Damage to the optic radiations or primary visual cortex leads to blindness in all or part of the contralesional visual field. Such damage disconnects the retina from its downstream targets and, over time, leads to trans-synaptic retrograde degeneration of retinal ganglion cells. To date, visual ability is the only predictor of retinal ganglion cell degeneration that has been investigated after geniculostriate damage. Given prior findings that some patients have preserved visual cortex activity for stimuli presented in their blind field, we tested whether that activity explains variability in retinal ganglion cell degeneration over and above visual ability. We prospectively studied 15 patients (4 females, mean age = 63.7 years) with homonymous visual field defects secondary to stroke, 10 of whom were tested within the first 2 months after stroke. Each patient completed automated Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and spectral-domain optical coherence tomography of the macula. There was a positive relation between ganglion cell complex thickness in the blind field and early visual cortex activity for stimuli presented in the blind field. Furthermore, residual visual cortex activity for stimuli presented in the blind field soon after the stroke predicted the degree of retinal ganglion cell complex thinning 6 months later. These findings indicate that retinal ganglion cell survival after ischemic damage to the geniculostriate pathway is activity-dependent.7/6/2020 - Sub-14_Ses-01 .events files updated with the correct information (they were empty before).

本数据集伴随以下已发表的论文：

施奈德（C. Schneider）、普伦蒂斯（E. Prentiss）、布斯扎（A. Busza）、马特马蒂（K. Matmati）、马特马蒂（N. Matmati）等人（2019）。人类枕叶损伤后视网膜神经节细胞的存活与活动依赖性。英国皇家学会B类学报：生物科学，第286卷（1897号），第20182733号。DOI：10.1098/rspb.2018.2733

摘要：视觉辐射或初级视觉皮层的损伤会导致对侧视野的全部或部分失明。此类损伤切断了视网膜与其下游目标之间的联系，并随着时间的推移，导致视网膜神经节细胞的跨突触逆行性退化。迄今为止，视觉能力是唯一已被研究作为视神经束损伤后视网膜神经节细胞退化的预测因子。鉴于先前的研究发现，一些患者在盲视场中呈现的刺激中保留了视觉皮层活动，本研究旨在检验这种活动是否能够解释除视觉能力之外视网膜神经节细胞退化的变异性。我们对15名（其中女性4名，平均年龄为63.7岁）因中风导致的同侧视野缺损的患者进行了前瞻性研究，其中10名患者在中风后前2个月内接受了测试。每位患者完成了自动化亨氏视野测试、功能磁共振成像下的视网膜拓扑映射以及黄斑的光学相干断层扫描。盲视场中神经节细胞复合体厚度与盲视场中呈现的刺激的早期视觉皮层活动之间存在正相关关系。此外，中风后不久在盲视场中呈现的残余视觉皮层活动预测了6个月后的视网膜神经节细胞复合体变薄的程度。这些发现表明，在缺血性损伤视神经束后视网膜神经节细胞的存活是活动依赖性的。2020年7月6日 - Sub-14_Ses-01 .events 文件已更新为正确信息（之前为空）。