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OCT测量黄斑区神经节细胞复合体厚度在高度近视眼中的应用进展

Application progress of OCT measurement for ganglion cell complex thickness in high myopic eyes

来源期刊： 眼科学报 | 2023年3月 第38卷 第3期： 274-286 发布时间：2023-03-01 收稿时间：2023/3/24 11:21:59 阅读量：7431
作者：
范圆媛,
谢平,
胡仔仲,
关键词：
黄斑区神经节细胞复合体高度近视光学相干断层扫描视网膜神经纤维层
ganglion cell complex high myopia optical coherence tomography retinal nerve fiber layer
DOI：
10.12419/j.issn.1000-4432.2023.03.12
近视防控已经上升到我国国家战略层面，高度近视引起的视神经病变会损害视功能，但在临床上常常被忽视。OCT可以非侵入、高分辨率、快速以及可重复地定量视网膜各层厚度，是评估高度近视相关视神经病变的有力工具。由于高度近视常合并视盘和盘周的改变，视神经纤维层厚度的定量常出现误差。近年来，学者开始聚焦于黄斑区神经节细胞复合体(ganglion cell complex,GCC)厚度的研究，但其在高度近视眼中的变化规律尚不统一。该文针对近年来高度近视眼黄斑区GCC的测量规范、诊断价值、变化规律等进行综述，以期提高眼科医师对高度近视视神经病变的重视和研究水平。
Myopia prevention and control has risen to the national strategic level in China. Optic neuropathy caused by high myopia can damage visual function, but it is often ignored in clinical practice Optical coherence tomography (OCT) characterized by non-invasiveness, high resolution, rapid, and repeatable quantifying the thickness of each layer in the retina has emerged as a powerful tool for evaluating high myopia related optic neuropathy. Due to the changes in and near the optic disc in high myopia, errors often occur in the quantification of the thickness of the optic nerve fiber layer. In recent years, researchers have gradually focused on the study of the thickness of ganglion cell complex (GCC), but the regularity of its changes in high myopia is not yet unified. This article reviews the measurement specifications, diagnostic values, and change rules of GCC in the macular region of high myopia in recent years, in order to improve the attention and research level of ophthalmologists on high myopia optic neuropathy.
    近视是造成视力损伤的最主要原因，也是世界上第二大致盲性眼病，已成为威胁公共健康的全球性问题[1]。我国人群的近视问题尤为严峻，30岁以上人群中近视患病率达26.7%，其中高度近视的患病率为1.8%[2]，提升近视防控水平、提高近视视网膜病变的早诊早治能力已被列为“十四五全国眼健康规划”的重点内容。高度近视通常指屈光度超过-6.0 D的屈光不正，随着近视度数的加深和眼轴的拉长，后巩膜葡萄肿、黄斑劈裂、视网膜脱离、脉络膜萎缩、新生血管生成、漆裂纹、青光眼等诸多病理性近视并发症的发病风险升高[3]。越来越多的证据表明，随着眼轴增长，盘周视网膜神经纤维层(retinal nerve fiber layer, RNFL)厚度也显著变薄[4, 5]，这是高度近视发生神经病变的直接证据。
    视网膜神经节细胞(retinal ganglion cells,RGCs)是视网膜信号传递的重要神经元，其功能损伤或者数量减少会影响视觉信号转导。有研究[6]表明，RGCs至少损伤25%~35%才会出现视野的改变，所以早期监测RGCs变化对于提示神经损害有重要临床意义。RNFL由RGCs的轴索汇聚而成，是反映视神经损害的常用指标，然而盘周RNFL的厚度易受到血管、血流等非神经组织的影响[7]，加之高度近视患者可能合并视盘及盘周改变、固视功能受损，结果常不准确。随着光学相干断层扫描(optical coherence tomography,OCT)技术的飞速发展，相比传统的时域扫描(time-domain OCT,TD-OCT)，频域扫描(spectral-domain OCT,SD-OCT)的轴向分辨率攀升至3 ~ 6 μm，扫描速率达26 000 ~ 27 000 A-Scans/s，分层更准确，能够更加精确、定量地在体获取视网膜各层厚度。最新一代的扫频扫描(swept-source OCT,SS-OCT)使用激光扫频光源，较之SD-OCT(840 nm)有更长的波长(1050~1060 nm)，允许光束穿透视网膜色素上皮层，更好地获取视网膜和脉络膜脉管系统的图像，故而具备更高的灵敏度、成像速度和信噪比。得益于OCT对视网膜结构的精确分层，黄斑区神经节细胞复合体(ganglion cell complex,GCC)厚度作为一种新的评估神经损伤的指标应运而生。
    黄斑区含有约一半的RGCs，是视网膜内多层RGCs排列的唯一区域[8]，可达8~10层。基于黄斑区RGCs密度高、胞体大、个体变异小的特点，监测该区RGCs的变化是评估高度近视神经退行性病变的理想手段。GCC由内丛状层(inner plexiform layer,IPL)、神经节细胞层(ganglion cell layer,GCL)、神经纤维层(retinal nerve fiber layer,RNFL)这3层结构组成，分别代表RGC的树突、胞体以及轴突，其厚度能更加直观、独立地反映RGC的退化和轴突损伤[9]。近年来，利用黄斑区GCC厚度来监测高度近视性视神经病变的研究[10-11]不断推陈出新，但对于GCC的改变规律尚无一总结性论述，为此，本文针对GCC在高度近视眼中的测量规范、诊断及鉴别诊断价值，以及其与眼球血流、结构、功能之间的联系做一综述，以期为高度近性视神经病变的诊治提供思路。

1 高度近视的神经损伤病理机制

    近视的病理机制涉及多种遗传和环境因素，其形态学上主要表现为眼轴延长。眼轴延长的机制被认为是一种基于视力反馈的眼球自我调节，与大脑无关[12]。当眼球屈光系统的成像焦点位于视网膜之后时，视网膜尤其是周边部受到外界的光刺激的总和，按照视网膜-RPE-脉络膜-巩膜的信号传导顺序引发眼球壁和内容物的顺应性改变，使得眼轴拉长以适应后移的焦点，从而外界图像可以清晰地落在视网膜上。从分子层面出发，视网膜感光细胞首先接收到屈光不正的光刺激，但视网膜具体如何判断眼睛处于近视还是远视状态，尚无完整理论解释。有一种猜测为视网膜通过分析光谱中不同波长的光的组成来解锁失焦信号[13]，因为外界光谱成分的改变[14-15]、视锥细胞光色素基因的突变[16]、中波长光敏感性/长波长光敏感性视锥细胞比例的变化均会影响屈光状态。另外，经过多种神经信号转导通路，RPE上的受体与信号蛋白结合，合成和释放各类生长因子，如胰岛素样生长因子、转化生长因子、血管内皮生长因子等，同时RPE的液体交换和离子运输功能也受到影响。而脉络膜收到眼轴延长的信号后，一方面厚度变薄，干扰视黄酸循环，另一方面也会分泌因子促进巩膜胶原分解，导致巩膜变薄，延展性变好而稳定性变差。巩膜则由于脉络膜薄变和毛细血管受损，血氧供给不足，分泌低氧诱导因子-1α(hypoxia-induced factor-1α,HIF-1α)引发下游细胞因子层级反应，重又促进巩膜外基质解构和重塑[17]。
    多项研究表明高度近视患者出现青光眼样视神经病变的风险增加，传统的解释包括：1)眼轴变长，视盘及其周围的巩膜拉长、变薄，视神经筛板明显变薄[18]；2)视神经和Brunch膜之间出现间隙，RNFL与Brunch膜、脉络膜距离变大，视盘周围视网膜缺乏支撑，仅剩RNFL，加上眼轴延长导致的筛板处加大的剪切力，相同眼压水平下视网膜RGC和RNFL更易受损[19]；3)巩膜厚度与筛板的稳定性相关，同时脉络膜又是供给筛板营养的重要元件，眼轴拉长后，筛板的稳定性下降、视盘血流灌注不足[19]；4)高度近视诱发小梁网的损伤，增加房水回流阻力[20]，使得眼内压升高，从筛板通过的神经纤维因此受到直接挤压。以上因素使得高度近视眼对眼压损害的抵抗力降低，易出现视网膜神经纤维和视盘的病理性损害，而即使是眼内压处于正常范围内的高度近视眼，由于眼球总体容积的扩大，在相同眼压下RNFL所承受的眼压也较实际值高[20]。
    随着对近视和青光眼机制的研究深入，出现了相关蛋白和基因水平对于高度近视眼为何更容易发生青光眼损害的新理论[19, 21]：1)升压基因学说：高度近视与青光眼都对糖皮质激素(激素)均呈现出高眼压反应，激素对小梁细胞的破坏作用被认为是其中的主要机制。小梁皮质激素诱导反应蛋白(trabecular meshwork induced glucocorticoid response protein,TIGR)是激素的高反应受体，广泛表达于睫状体和小梁组织，在TIGR基因即myocilin(MYOC)基因缺陷或者环境变化时表达增加，阻塞小梁网从而致使眼压升高。但此学说尚且缺乏强有力的证据证明MYOC基因的多态性在高度近视人群中的影响。2)胶原学说：高度近视与青光眼都可能与自身免疫系统失衡有关，且在病理状态上相似，均为胶原病变。3)遗传分子相关性机制：高度近视与青光眼均可能与基质金属蛋白酶及其抑制剂的基因表达失调、亮蛋白聚糖基因缺陷相关，也都存在前房可溶性CD44在房水中的含量偏高、E选择素持续升高的现象，前者会引发细胞外基质代谢异常，后者则会影响小梁网的结构和功能，印证了前两种学说的同时，这些遗传分子能否作为高度近视和青光眼之间的枢纽，还需进一步探索。

2 黄斑区GCC的测量设备、参数和放大率问题

    目前，市场有多款商用OCT系统，诸如Cirrus HD-OCT(Carl Zeiss Meditec,美国)、Spectralis OCT(Heidelberg Engineering,德国)、RTVue FD-OCT(Optovue,美国)、Topcon 3D-OCT(Topcon,日本)、Swept-source DRI OCT(Topcon,日本)。除了最后一种是基于SS-OCT的系统，其余都是基于SD-OCT。GCC厚度是常用的黄斑测量参数，不同设备的扫描范围也不一样，此处以RTVue FD-OCT为例，GCC程序扫描以中心凹颞侧0.75~1 mm为中心的7 mm×7 mm方形区域，计算黄斑6 mm直径内的GCC厚度、GCC的局部丢失容积(focal-loss volume,FLV)及整体丢失容积(global-loss volume,GLV)[22]。FLV代表测得的GCC厚度与正常人数据库GCC厚度的差异，反映局部GCC厚度的变异；GLV表示受检者黄斑区整体GCC厚度与正常人数据库GCC厚度相比较薄变的情况，反映弥漫性损伤，可以有效区分病情严重程度，用于病情随访。Cirrus HD-OCT则可以提供另一种测量神经节细胞-内丛状层(ganglion cell-inner plexiform layer,GCIPL)厚度的算法，测量的是以黄斑中心凹为中心，长短轴分别为4.8 mm×4.0 mm和1.2 mm×1.0 mm的两个横向椭圆形之间的环形区域[9]。
    既有的OCT光学系统使用固定的眼轴长度进行扫描，但在高度近视眼，眼轴的拉长会产生投射伪影或放大效应，后者导致横向测量错误[23-24]。黄斑直径约5.5 mm，而视网膜不同区域的GCL厚度不同，如果不加以矫正，扩大的扫描范围将周边视网膜计入黄斑GCC平均和分区厚度，将会使测量结果大大减小。针对上述情况，临床上可使用Littmann公式消除光学放大效应[23, 25]：t=0.01306×(χ–1.82)×p×s(其中t为实际参数值，χ为被测量眼的眼轴长度，p为OCT系统的光学放大系数，s为OCT测量参数值)。有研究[26]显示，光学放大效应矫正前后的GCC与眼轴之间的关系发生改变，矫正后的GCC厚度与眼轴长度呈正相关关系。Chang等[27]使用带有内置矫正程序的RS-3000(Nidek,日本)OCT系统测量高度近视眼的GCC厚度时，假阳性率低于未矫正的Cirrus HD-OCT组，后者容易导致青光眼病变的过度诊断。尽管有研究证明，不同SD-OCT设备间在测量GCC厚度时比较差异无统计学意义[28]，但RS-3000 SD-OCT除了内置的光学放大效应矫正程序，还额外有一套针对眼轴在26~29 mm之间高度近视眼的备选数据库，使其在评估高度近视眼时拥有更加令人满意的特异度[29]。因此，在使用光学成像检测GCC时，光学放大效应和设备技术差异是需要纳入考量的方面。
    TD-OCT由于扫描速率慢等问题，逐渐被灵敏度、特异度更高的SD-OCT和SS-OCT取代。为了比较后两种扫描技术的测量值是否具有一致性，Lee等[30]和Yang等[31]使用SD-OCT和SS-OCT分别测量了正常人群和青光眼人群中GCIPL的厚度，SD-OCT所得数据均高于SS-OCT。而针对近视，特别是高度近视人群，刘莎莎的研究[32]也得到了相同的结论，这可能与SS-OCT宽场扫描造成的图像失真以及拍摄过程中的屈光补偿有关。该研究还发现SD-OCT测量GCIPL的假阳性率为 16.09%，高于SS-OCT的9.20%，但二者比较差异并无统计学意义。所以，即使SS-OCT具备更高的特异度，也不能完全取代SD-OCT。

3 高度近视眼黄斑区GCC的变化规律

3.1 高度近视黄斑区GCC厚度与眼轴、屈光度的关系

    表1罗列了近年来关于黄斑区GCC与眼轴和屈光度的关系。笔者在PubMed数据库上以关键词“high myopia+ganglion cell complex”全文搜索获取23篇文章，选取研究对象为高度近视人群、研究指标包含眼轴和(或)屈光度的英文文献。同时，笔者在万方医学网检索“神经节细胞复合体高度近视”，选取研究对象为高度近视人群、研究指标包含眼轴和(或)屈光度的中文文献。此外，笔者还利用文献关联链接以及文献中提到的其他文献补充了部分内容。由于近年来关于高度近视中黄斑区GCC厚度与眼轴和屈光度的研究不多，故未予以时间限制，所列举文章最早发表时间可追溯至2011年。理论上，随着近视程度的加重，即眼轴增长和屈光度加深，视网膜、脉络膜、巩膜受到牵拉延伸，RGCs数目不变，形态被拉长，分布趋于稀疏，厚度会随之下降。许多研究[33-37]已证实GCC厚度受眼轴和屈光度的影响：GCC厚度与眼轴长度呈负相关关系，而与屈光度呈正相关。Takeyama等[38]还提出眼球轴向长度每增加1 mm，GCC厚度就会相应平均减少1.62 μm。然而，当眼轴增长尚未或者超过一定限度时，这种相关性会消失。Sezgin Akcay BI等[35]研究低度近视组时发现GCC厚度与眼轴在统计学上无相关性，这可能因为在近视发展早期视网膜尚无神经病理损伤，GCC厚度较为稳定。王伟伟等[39]则发现，随着眼轴增长超过28 mm，GCC厚度与眼轴的相关性也会消失，其原因可能是眼球扩张到一定程度后，脉络膜视网膜缺血、缺氧导致RGCs的减少趋于稳定。另外，光学放大效应是需要考虑的因素，Wu等[40]利用Bennett公式校正后显示黄斑区GCC厚度与眼轴无相关性，引发新的争议。最新的一项荟萃分析收集了47项研究12 223眼的数据，比较了正视眼、近视眼、远视眼各层视网膜厚度，在排除了未经光学放大系数矫正的数据后，发现高度近视组中的GCC、GCIPL的厚度皆低于正视眼组，而在中度近视组中，平均GCC厚度也比正视眼组低[11]。目前，关于中低度近视与正视眼之间的比较十分缺乏，期待更多的对比性研究来关注中低度近视是否合并GCC厚度的薄变。
    黄斑不同区域的GCC厚度随眼轴变化的程度也有差异。既往研究并没有发现中心凹区域内层或全层视网膜厚度与近视程度相关[41,42,46]，这可能归因于后极部玻璃体对黄斑区视网膜的向心性牵拉和内层视网膜组织水肿[46]。GCIPL厚度排除了中心凹区域的影响，仍旧显示出其与眼轴的负相关及与屈光度的正相关性[32,43,44]，与前述研究结论相同。目前已有研究证实GCC在中心凹上方和下方区域一致薄变[11, 47]，但在鼻侧和颞侧的改变情况则争议较大。Seo等[43]、刘莎莎等[32]结果显示鼻侧GCC随近视加重而薄变的程度并不如颞侧明显，可能鼻侧黄斑更靠近眼球后极部，受到拉伸强度稍弱。但赵雨晴等[46]调整了屈光状态、眼轴、年龄、性别等因素后，发现GCC厚度仅在中心凹周围区与屈光度呈正相关，且仅有旁中心凹区鼻侧象限与眼轴呈负相关。鉴于研究中常用RTVue FD-OCT观察GCC厚度，仅能获得平均、上方和下方GCC厚度，不如Cirrus HD-OCT能够获得各个象限的平均值，迄今关于鼻颞侧GCC厚度随近视程度的改变无法达成一致，尚需进一步研究。

表 1 黄斑区 GCC* 厚度与眼轴、屈光度间的关系
Table1 The association between the thickness of GCC in macular region and AL,SE

20230324114330_1708.png

续表

20230324114417_3902.png

续表

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3.2 高度近视黄斑区GCC厚度与视盘及盘周改变的关系

    已有研究证明，近视人群中黄斑区GCC厚度与盘周RNFL厚度同时减少，呈正相关关系[34]。这是可以理解的，因为二者都位于眼球后极部，同时受到眼轴拉长所产生的机械牵拉而薄变。赵雨晴[46]则发现GCL和IPL都在中心凹周围区和旁中心凹区随近视程度增加而显著变薄，在厚度变化地形图上的薄变区域几乎同步，同区域的RNFL变化却不明显，提示黄斑区GCC厚度减少的主要原因是GCL和IPL厚度的减少。Shoji等[48]将盘周RNFL与黄斑区GCC厚度之比作为研究指标，发现正视眼组比值大于1而高度近视眼组比值小于1，且差异有统计学意义，说明高度近视时RNFL的薄变主要发生在盘周区域，且变化率不如黄斑区GCC稳定。
    此外，一项在低龄人群中的研究表明，杯盘比越大、视盘或盘沿面积越小，黄斑区GCC厚度越小[47]。但鉴于儿童群体生长发育的特殊性，另一项在成年近视人群中的研究更具说服力，其研究结果提示GCC与前房深度、视盘大小以及中央角膜厚度无关[33]。但总的而言，近视人群中黄斑区GCC改变与视盘及盘周改变等的研究较少，与高度近视相关的眼底结构性改变诸如脉络膜萎缩、视盘倾斜、视盘鼻侧牵引、后巩膜葡萄肿等的相关性也缺乏数据支持，有待临床进一步研究。

3.3 高度近视合并青光眼时黄斑区GCC厚度的变化

    越来越多的研究提示近视和青光眼之间的相关性，在青光眼中近视的患病率增加，而近视也是原发性开角型青光眼(primary open-angle glaucoma,POAG)的高危因素[49]。高度近视时眼球结构的改变、眼底血流的变化、视网膜代谢受损等使视盘更加容易凹陷，对损害耐受性降低，而眼压的升高会改变眼球的屈光状态，进一步加重近视的程度，因而早期诊断高度近视合并POAG在临床上有重要意义。然而，高度近视患者的视杯改变、视盘倾斜、鼻侧牵引、后巩膜葡萄肿等表现常常会掩盖青光眼的早期损害，若合并视功能损害，对视力下降也并不敏感，且POAG眼压升高不显著，均增加了高度近视合并POAG的诊断难度。
    盘周RNFL厚度分析也是目前OCT在诊断青光眼中广泛使用的参数，对于黄斑区GCC与盘周RNFL的关系研究有助于延伸GCC的应用范围。两者都在青光眼早期病变时出现厚度减少[50- 51]，不仅在数值上呈正相关关系[52, 53]，而且在空间分布特征上，GCIPL缺损区在形状上表现为RNFL缺损区同侧的弓形延伸[54]。已知高度近视时黄斑区GCC厚度的变化率比盘周RNFL厚度更加稳定，故而当高度近视合并GCC厚度明显变薄时，应特别警惕青光眼的可能[39] 。黄斑区RGCs收集的信号通过上下侧弓形排列的轴突汇入视盘处的视神经，GCC厚度的下降因此也影响盘周RNFL厚度。也有人认为黄斑区GCC厚度的改变继发于RNFL的变化，因为在RNFL较薄的区域，视网膜的厚度出现老年性退化的程度更低[55]。目前已发表的文献大部分为横断面研究，关于GCC与RNFL减少的时间顺序或是二者是否为等比率减少有待于前瞻性研究补充说明。
    有研究发现黄斑区GCC和盘周RNFL的受试者曲线下面积在高度近视组和低中度近视组间比较差异有统计学意义，提示二者诊断高度近视的能力存在差异[35]，而在检测高度近视是否合并青光眼时，相对于盘周RNFL，黄斑GCC厚度具有类似甚至更好的青光眼性病变的检测能力[48, 56-62]。这是因为GCC不易受年龄、性别、眼轴长度的影响[63-64] ，拥有良好的可重复性[65]。实际上，在青光眼人群中，GCC本身就具备探查视野前青光眼和早期青光眼的能力[66-67]。不过也应注意到，由于黄斑内仅有约50%的RGCs存在(而视盘周边区域含有100%的视网膜节细胞轴突)，如果剩余50%位于黄斑区外的RGCs受到影响，则黄斑GCC扫描方案将无法发现青光眼的损害，对GCC广泛丢失的晚期青光眼疾病的诊断能力有限，检测严重青光眼损害的能力低于RNFL[68-69]。此外，关于不同年龄阶段GCC厚度的正常值数据虽然已有报道[70-72]，但针对非青光眼性高度近视眼的GCC数据尚无经典的研究结果[28]，这一部分的缺失大大限制了GCC厚度在诊断高度近视合并青光眼时的应用。
    GCC厚度与眼轴的关联使得OCT测量时仍需考虑光学放大效应所导致的误差，而且近视和青光眼发生发展中都伴随了GCC厚度的减少。为了进一步弥补这种缺陷，有学者选择了FLV和GLV作为鉴别诊断的参数，他们认为，单纯性眼轴增长时，GLV升高而FLV不变，后者在合并青光眼时出现下降[59-60]。但也有研究发现两者都随眼轴增长而增长[35, 39, 62]，因而FLV的可靠程度存在争议。Kita等[73, 74]则引入了神经节细胞复合体与外层视网膜厚度比(ganglion cell complex/outer retinal layer,G/O)和神经节细胞复合体与黄斑区总视网膜厚度比(ganglion cell complex/total retinal layer,G/T)的概念，证明G/O和G/T随青光眼严重程度的加重而变小，在近视眼人群中却与眼轴延长和屈光度均无关[38, 62]，即说明这两个值不随近视的加重而改变。通过对G/O和G/T的观察和随访，有助于临床医师判定GCC厚度的变化是由近视本身所导致的还是合并了青光眼病变后发生的。

3.4 黄斑区GCC厚度与其他因素的关系

    黄斑区GCC厚度与人种相关，健康人眼的GCC厚度在76.6 ~119.8 μm之间[75]，2011年的一项调查发现，非洲人的GCC相对最薄，西班牙人和印度人的GCC相对较厚[76]。
    黄斑区GCC厚度受年龄、性别的影响不大[63]：可能随着年龄增长而有所减少[33, 76]，但在性别之间无明显差异[34,38]。组织学上已经证明，神经节细胞轴突数量的减少导致较大年龄组的RNFL变薄[77]，也许可以从一方面解释GCC厚度随年龄的变化规律。而根据一项针对我国青少年的研究[78]，近视人群中GCC厚度的减少在检眼镜未检测到眼底病变时就已存在，同时GCC厚度也可以指示高度近视是否合并黄斑病变[79]，这提示了GCC纳入近视防控检测的必要性。国内已有收集儿童和青少年正常GCC和RNFL数据的报道[47, 80-81]，但现有的OCT机器都没有建立起针对未成年人正常GCC的数据库，这部分工作需要尽快开展起来。
    眼底血管状态、血流变化与眼底的结构性改变密切相关，一种假说是眼底病变的发生可能遵循着血流微环境改变-结构缺损-功能紊乱的先后顺序，但尚缺乏足够的研究支撑。Milani等[82]、马鑫宇[37] 、Fan等[83]论证了黄斑区GCC越厚，血流密度越大，但最近的2项研究分别进行了多元回归分析和光学误差矫正分析，认为两者无法独立相关[40, 84]。血管微环境损伤可能是眼轴延伸后最早发生的改变，因而血流变化是否影响GCC厚度的独立因素尚待进一步研究。
    GCC厚度的减少与视功能的下降联系紧密，表现为GCC厚度减少带来视网膜光敏感度、最佳矫正视力等功能学指标下降[85-88]。Wu等[40]校正光学放大效应后说明了视功能与GCC并非独立相关，而是受外层视网膜厚度的影响，毕竟视功能的变化，尤其在早期，与外层视网膜(视锥、视杆细胞)更直接相关。此外，现有关于GCC厚度和视觉诱发电位、视网膜电图等其他视功能检查的研究有待填补，这可能是GCC厚度在病变早期尚无功能学改变，因而研究不多的原因。

4 黄斑区GCC应用的局限性

    尽管黄斑区GCC参数相对于RNFL表现出更加优越的诊断能力，临床上应用时仍有一定的局限性。除了高度近视和青光眼，许多其他疾病也会影响到GCC的厚度，如老年性黄斑病变、玻璃体-黄斑界面疾病、视神经病变等。当高度近视患者存在黄斑前膜、黄斑裂孔、黄斑变性等疾病时，RNFL厚度检测则更有优势，结合GCC厚度与RNFL厚度的优点联合分析更为推荐。另外，OCT设备间差异和光学放大效应造成的误差无可避免，正如前文所说，现有的黄斑扫描程序仅覆盖50%的RGCs，无法涵盖剩余50%位于黄斑区外的RGCs的损害，故对GCC广泛丢失的诊断能力有限。

5 结语

    黄斑区GCC厚度的定量为评估高度近视是否合并神经损伤提供了重要的诊断价值和研究指标。鉴于不同OCT设备间的差异、光学放大效应、可能合并的黄斑病变，建议将黄斑区GCC厚度与其他参数结合分析，以提高疾病的诊断率。另外，眼科医师需要重视高度近视性视神经损伤的概念，而黄斑区GCC厚度的随访观测可以为视神经损伤提供客观的指标。在各商业化的OCT机器上，缺少未成年人、不同眼轴(近视度数)的GCC厚度的数据库；临床上，也缺乏对高度近视眼的长期、前瞻性的GCC改变的研究，没有结合人工智能诊疗高度近视视神经病变的尝试，这些都是未来的研究方向。作为近视大国，笔者呼吁眼科医师能够发挥我国近视人口多的优势，开展高度近视视神经病变的临床研究和基础研究，基于人工智能开发更高灵敏度的诊断算法，以提高这类疾病的诊疗效能。

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1、何润田,冯洁,丁天娇等.2型糖尿病患者眼轴长度与糖尿病视网膜病变的相关性分析[J].国际眼科杂志,2023,23(11):1915-1919.
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1、国家自然科学资金青年项目 (81900875)。
This work was supported by National Natural Science Foundation of China (81900875).()
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发布于: 2022-12-01
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