OBJECTIVE Investigations have found associations of homonymous thinning of the macular ganglion cell/ inner-plexiform layer (GCIPL) with demyelinating lesions in the post-chiasmal visual pathway among patients with multiple sclerosis (MS). Retinal thinning may also occur through retrograde trans-synaptic degeneration, a process by which lesions in post-geniculate visual pathway structures lead to thinning of the GCIPL across thalamic synapses. The purpose of our study was to determine the frequency of homonymous hemimacular thinning that occurs in association with post-chiasmal visual pathway demyelinating lesions in patients with MS and other demyelinating diseases. METHODS Adult patients with demyelinating diseases (MS, neuromyelitis optica spectrum disorder [NMOSD], myelin oligodendrocyte glycoprotein antibody disease (anti-MOG)) who were participants in an ongoing observational study of visual pathway structure and function were analyzed for the presence of hemimacular GCIPL thinning on OCT scans. Brain MRI scans were examined for the presence of post-geniculate visual pathway demyelinating lesions. RESULTS Among 135 participants in the visual pathway study, 5 patients (3.7%) had homonymous hemimacular GCIPL thinning. Eleven patients (8.1%) had a whole+half pattern of GCIPL thinning, characterized by hemimacular thinning in one eye and circumferential macular thinning in the contralateral eye. All but one patient with homonymous hemimacular thinning had demyelinating lesions in the post-geniculate visual pathway; however, these lesions were located in both cerebral hemispheres. CONCLUSION Homonymous hemimacular thinning in the GCIPL by OCT is associated with post-chiasmal visual pathway demyelinating lesions but it appears to be a relatively uncommon contributor to GCIPL loss. Patients with this pattern of GCIPL often fail to complain of hemifield visual loss. Future studies with prospective and detailed MR imaging may be able to more closely associate demyelinating lesions in anatomically appropriate regions of the post-chiasmal visual pathways with homonymous hemimacular thinning.

中文翻译：

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OCT 在检测多发性硬化和相关脱髓鞘疾病患者半黄斑神经节细胞层变薄中的作用

目的 研究发现多发性硬化症 (MS) 患者的黄斑神经节细胞/内丛状层 (GCIPL) 同向变薄与视交叉后视觉通路中的脱髓鞘病变有关。视网膜变薄也可能通过逆行跨突触变性发生，这是一个过程，通过这个过程，膝后视觉通路结构中的病变导致跨丘脑突触的 GCIPL 变薄。我们研究的目的是确定 MS 和其他脱髓鞘疾病患者中与视交叉后视觉通路脱髓鞘病变相关的同名半黄斑变薄的频率。方法 患有脱髓鞘疾病（MS、视神经脊髓炎谱系障碍 [NMOSD]、髓鞘少突胶质细胞糖蛋白抗体疾病（抗 MOG）），他们参与了一项正在进行的视觉通路结构和功能的观察性研究，在 OCT 扫描中分析了半黄斑 GCIPL 变薄的存在。检查脑 MRI 扫描是否存在膝后视觉通路脱髓鞘病变。结果 在视觉通路研究的 135 名参与者中，5 名患者 (3.7%) 有同名的半黄斑 GCIPL 变薄。11 名患者 (8.1%) 有整体+一半的 GCIPL 变薄模式，其特征是一只眼睛的半黄斑变薄和对侧眼的圆周黄斑变薄。除了一名患有同向半黄斑变薄的患者外，所有患者的膝后视觉通路都有脱髓鞘病变；然而，这些病变位于两个大脑半球。结论 OCT 引起的 GCIPL 同名半黄斑变薄与视交叉后视觉通路脱髓鞘病变有关，但它似乎是 GCIPL 丢失的一个相对不常见的因素。患有这种 GCIPL 模式的患者通常不会抱怨半场视力丧失。未来的前瞻性和详细 MR 成像研究可能能够将后交叉视觉通路的解剖学适当区域中的脱髓鞘病变与同向半黄斑变薄联系起来。