Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA.
Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA; Department of Population Health, New York University Grossman School of Medicine, New York, NY, USA.
J Neurol Sci. 2020 Dec 15;419:117159. doi: 10.1016/j.jns.2020.117159. Epub 2020 Sep 28.
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.
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.
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.
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.
研究发现,多发性硬化症(MS)患者视交叉后视觉通路的脱髓鞘病变与同型性黄斑神经节细胞/内丛状层(GCIPL)变薄有关。视网膜变薄也可能通过逆行性跨突触变性发生,这是一种在后节视觉通路结构病变导致 GCIPL 通过丘脑突触变薄的过程。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型性半侧黄斑变薄的频率。
对参与正在进行的视觉通路结构和功能观察研究的脱髓鞘疾病(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病[抗-MOG])成年患者进行 OCT 扫描,以分析是否存在半侧 GCIPL 变薄。检查脑 MRI 扫描是否存在后节视觉通路脱髓鞘病变。
在视觉通路研究的 135 名参与者中,5 名患者(3.7%)存在同型性半侧 GCIPL 变薄。11 名患者(8.1%)存在全+半 GCIPL 变薄模式,特征为一只眼出现半侧黄斑变薄,对侧眼出现环形黄斑变薄。除 1 名同型性半侧 GCIPL 变薄患者外,所有患者均存在后节视觉通路脱髓鞘病变;然而,这些病变位于大脑两个半球。
OCT 检查发现的同型性半侧 GCIPL 变薄与视交叉后视觉通路脱髓鞘病变有关,但它似乎是 GCIPL 丧失的一个相对少见的原因。具有这种 GCIPL 模式的患者通常不会抱怨视野缺损。未来的前瞻性和详细 MRI 成像研究可能能够更紧密地将后节视觉通路解剖学适当区域的脱髓鞘病变与同型性半侧黄斑变薄相关联。