Brazerol Jacqueline, Iliev Milko E, Höhn René, Fränkl Stephan, Grabe Hilary, Abegg Mathias
*Department of Ophthalmology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland †Department of Ophthalmology, University Medical Center Mainz, Mainz, Germany.
J Glaucoma. 2017 May;26(5):423-429. doi: 10.1097/IJG.0000000000000633.
Macular optical coherence tomography (OCT) analysis can be used for quantitative measures of optic nerve atrophy at a location far from the optic nerve head. This recently led to the finding of microcystic macular edema (MME), that is vacuolar inclusions in the macular inner nuclear layer, in some glaucoma patients. The involvement of individual retinal layers is yet unclear in glaucoma. In this study we systematically investigated glaucoma-induced changes in macular layers to evaluate whether glaucoma-associated damage extends beyond the macular ganglion cell layer.
We included 218 consecutive patients and 282 eyes with confirmed primary open-angle glaucoma or pseudoexfoliation glaucoma, and macular OCT in a cross-sectional observational study. Eyes were screened for presence of MME. Thickness of individual retinal layers was determined using a semiautomatic segmentation algorithm. Peripapillary nerve fiber layer thickness and mean defect in visual field testing were extracted from OCT and medical records, respectively. Results were compared with a small group of eyes with no apparent glaucoma.
We found MME in 5 eyes from 5 primary open-angle glaucoma patients and 3 eyes of 3 pseudoexfoliation glaucoma patients (2.8%). MME was confined to the inner nuclear layer in a perifoveal ring and was associated with thinning of the ganglion cell layer and thickening of the macular inner nuclear layer. Glaucoma eyes without MME showed a significant inverse correlation of inner nuclear layer thickness with glaucoma severity.
Glaucomatous damage leads to a gradual thickening of the inner nuclear layer, which leads to MME in more severe glaucoma cases. These changes, along with nerve fiber loss and ganglion cell loss, may be summarized as glaucoma-associated retrograde maculopathy.
黄斑光学相干断层扫描(OCT)分析可用于对视神经乳头远侧部位的视神经萎缩进行定量测量。最近,这一技术在一些青光眼患者中发现了微囊性黄斑水肿(MME),即黄斑内核层中的液泡状包涵体。青光眼患者中各视网膜层的受累情况尚不清楚。在本研究中,我们系统地研究了青光眼引起的黄斑层变化,以评估青光眼相关损害是否超出黄斑神经节细胞层。
在一项横断面观察性研究中,我们纳入了218例连续的确诊为原发性开角型青光眼或剥脱性青光眼的患者及282只眼睛,并进行了黄斑OCT检查。筛查眼睛是否存在MME。使用半自动分割算法确定各视网膜层的厚度。分别从OCT和病历中提取视乳头周围神经纤维层厚度和视野检查中的平均缺损。将结果与一小群无明显青光眼的眼睛进行比较。
我们在5例原发性开角型青光眼患者的5只眼中和3例剥脱性青光眼患者的3只眼中发现了MME(2.8%)。MME局限于中心凹周围环的内核层,与神经节细胞层变薄和黄斑内核层增厚有关。无MME的青光眼眼的内核层厚度与青光眼严重程度呈显著负相关。
青光眼性损害导致内核层逐渐增厚,在更严重的青光眼病例中导致MME。这些变化,连同神经纤维丢失和神经节细胞丢失,可概括为青光眼相关的逆行性黄斑病变。