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高度近视视神经改变与原发性开角型青光眼的相关性研究进展

Research progress on the correlation between optic neuropathy and primary open-angle glaucoma in high myopia

来源期刊： 眼科学报 | 2023年1月 第38卷 第1期： 45-51 发布时间： 收稿时间：2023/1/17 9:51:07 阅读量：5092
作者：
刘慧,
陈鸣,
关键词：
高度近视开角型青光眼筛板视盘相关性
high myopia open-angle glaucoma lamina cribrosa optic disc correlation
DOI：
10.3978/j.issn.1000-4432.2023.01.04
收稿时间：
 
修订日期：
 
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高度近视(high myopia，HM)作为一种特殊类型的屈光型眼病，不仅会导致进行性、退行性眼底改变，其视神经损伤的患病率也很高。青光眼是全球范围内最常见的一种不可逆致盲性眼病，原发性开角型青光眼(primary open-angle glaucoma，POAG)是最常见的青光眼类型。近年来的研究发现HM与POAG的病理改变存在相似之处。由于HM眼底改变与早期POAG眼底改变容易混淆，HM患者早期发现POAG对延缓或阻止疾病进展很重要。HM患者长期随访不仅要观察黄斑病变，视神经形态与结构改变的观察也不容忽视。

As a special type of refractive eye disease, high myopia (HM) not only causes progressive and degenerative fundus changes, but also has a high prevalence of optic nerve damage. Glaucoma is the most common form of irreversible blinding eye diseases worldwide, among which, primary open-angle glaucoma (POAG) is the most common type. In recent studies, HM is found to have similarities on pathological changes as that of POAG. And HM fundus changes are easily confused with early stage POAG fundus changes; thus, the early detection of POAG on HM patients is highly important on disease deferment or prevention of disease progression. Macular degeneration as well as optic nerve morphology and structural changes are to be observed in the long-term follow-up for HM patients.

    随着近视患者人数的增多，高度近视( high myopia，HM)的患者数量也逐步增多。流行病学调查[1]显 示2050年全球将会有近47.58亿人口近视，其中H M有5.38亿。在多种族人群中，HM已被确定为原发性开角型青光眼(primary open-angle glaucoma，POAG)的危险因素，其原因可能与HM视乳头(optic nerve head，ONH)相关的结构变化有关[2-3]。研究[4]报道近视是POAG的一个重要危险因素，与非近视眼相比，中度至高度近视与POAG的患病率有更强的相关性。
    既往的研究中，HM患者视神经损伤的患病率异常高[5-6]，其中包括视神经、视盘、筛板(lamina cribrosa，LC)、视网膜神经纤维层(retinal nerve fibre layer，RNFL)等的改变。Jonas等[7]的研究认为与HM相关青光眼视神经病变(glaucoma-like optic neuropathy，GON)患病率增加的主要因素有L C的伸长和变薄导致板内结构变化和LC压力梯度变陡、巩膜缘拉伸变薄致使LC稳定性降低及视乳头周围巩膜突缘伸长致使Zin Haller视乳头周围动脉环到LC的距离增加。多项研究[5,8]显示，HMGON患病率急剧增加，HM患者GON改变与POAG也存在一定的相关性。以下将从HM视盘形态学改变、视盘旁萎缩、LC、RNFL变化对HM与青光眼之间的关系进行论述。

1 高度近视视盘形态学改变

    HM眼的视盘形态往往不规则，常出现视盘倾斜、扭转、萎缩、大视盘等改变。HM眼眼轴伸长导致视盘扩大，Nagaoka等[9]的研究发现眼轴长度与视盘面积相关，且视盘面积每增大1 mm，青光眼患病风险增加1.39倍。因此对于HM大视盘患者，应加强随访。在一项890例HM患者的横断面研究[10]中，HM视盘倾斜和视盘扭转发病率分别达到81.2%和48.3%；且在Chen等[11]的研究中，375例HM合并青光眼的患者视盘颞侧倾斜约占39%，说明视盘的倾斜和扭转在HM患者中普遍存在，且是青光眼的危险因素。此外，HM患者常出现RPE和光感受器的丢失，盘周萎缩是HM的常见体征，而其不同分区也与青光眼存在不同联系。HM视盘上述改变有可能会干扰标准青光眼测试的结果，因此从视盘形态学变化总结HM与青光眼之间的相关性对于HM合并青光眼患者早期发现、确诊以及干预治疗显得尤为重要。

1.1 高度近视视盘倾斜

    当视盘最长直径与最短直径比值>1.3时定义为视盘倾斜。既往的研究发现，HM视盘倾斜与青光眼视野缺损有关：Choi等[12]发现视盘倾斜方向与早期青光眼视野缺损的位置一致。Sawada等[13]和Lee等[14]发现更大的视盘倾斜比与更严重的青光眼视野缺损程度有关。然而有些报道也有相反结论：Hung等[15]的研究并没有发现视盘倾斜与青光眼视野缺损之间存在显著相关性。Lee等[16]也有同样的发现。究其不同结论原因，考虑可能为：1)许多研究都使用倾斜比来量化ONH变形量，而倾斜比为二维分析，无法真正反映ONH的三维结构，因此产生误差甚至相反结论[17]。2)选择的黄斑区视野缺损受试者百分比不同。早期视野缺损通常发生在周边，青光眼末期视野缺损往往发生在黄斑旁，黄斑旁视野缺损受试者百分比的不同可能会产生矛盾结果[18]。

1.2 高度近视视盘扭转

    与青光眼相关的另一个重要的HM眼ONH变形的因素是视盘扭转。视盘扭转是指视盘扭转与垂直子午线的偏差角度。HM视盘倾斜往往伴随着视盘扭转。目前关于视盘的扭转与视野缺损之间的关系，报道不一。一些研究显示两者具有明显相关性。例如Park等[19]回顾性分组对照分析韩国225例正常眼压性青光眼患者，发现视盘扭转的方向可以预测视野损伤的位置。在正常眼压性青光眼受试者中，下视盘旋转预测上视野缺损，上视盘旋转预测下视野缺损。他们认为视盘的上旋转可对上神经轴突施加压力，导致上区RNFL受损，而下旋转视盘可诱导下区域RNFL损伤。Choi等[12]发现在HM合并POAG的患者中，上视盘旋转预测了上方RNFL缺损和下方视野损伤。Hung等[15]也认为，只有较大程度的视盘旋转与视野缺损的存在相关性。

1.3 高度近视大视盘改变

    在HM患者中(等效球镜<-8 D或眼轴≥26.5 mm)，当视盘面积超过3.8 mm2 ，青光眼患病率随着视盘面积的增大而增加。相比于正常大小或者小视盘的患者，有大视盘改变的HM患者发生GON的风险高3.2倍[9]。HM患者眼轴伸长导致视乳头解剖结构发生明显变化。许多HM眼患者会出现继发性大视盘的改变，继而出现LC的伸长和变薄，从而造成LC的压力梯度变陡，这可能是HM青光眼易感性增加的因素。

2 筛板

    LC是视网膜神经节细胞轴索损伤的一个主要部位[20]。解剖上，视神经管可分为3层，Bruch膜开口为内层，脉络膜开口为中层，视盘旁巩膜开口为外层，外层被LC覆盖。与POAG相关的HM眼LC改变有：1)LC变薄。L C的扩大会导致L C的伸长和变薄以及LC内结构的改变，从而导致其对压力的耐受性降低。H M眼青光眼易感性增加的原因与LC变薄减小了眼内隔室和球后隔室之间的距离，LC压力梯度变陡有关[21]。2)LC及视神经血流。LC由Zinn Haller的毛细血管周围动脉环的分支滋养，该动脉环大致位于视神经硬脑膜与后巩膜在毛细血管周围巩膜凸缘外端的汇合线处[22]。动脉环和LC之间的距离扩大可能是HM患者青光眼易感性增加的另一个解剖因素。其次，除了机械因素外，LC的轴向伸长、纵向压缩及相关形态学改变可能诱发层前或层内毛细血管塌陷，导致ONH缺血[23]。3)局灶性筛板缺损(focal lamina cribrosa defect，FLCD)。FLCD与青光眼视野缺损密切相关，相对于没有FLCD的青光眼患者，患有FLCD的青光眼患者视野缺损更严重[24]。Suh等[25]利用光学相干断层扫描血管成像(optical coherence tomography angiography，OCTA)测量POAG患者的血流密度，发现在患有FLCD的POAG患者中，从RNFL提取的视乳头周围血管密度显著低于没有FLCD的POAG患者。此外，血管密度的降低与FLCD的位置在空间上相关，表明FLCD和眼部血流动力学受损可能与病因有关，青光眼视神经损伤的机制和血管机制密不可分。总之，FLCD可被认为是青光眼中LC和ONH受压损伤的临床体征[26]。光学相干断层扫描(optical coherence tomography，OCT)的最新进展显示，一些HM患者存在FLCD，可能与视野缺损密切相关[27-28]。Kimura等[29]证明HM的人比没有近视的人有更高的FLCD发生率。这些发现表明HM和FLCD存在重要关系，提示FLCD参加了HM患者视野异常的发病机制。这也提示针对LC形态学、视野、视盘周围微结构和微血管系统进行基于人群的流行病学调查和纵向研究，可能有助于探索HM青光眼的发病机制。

3 视盘旁萎缩

    视盘旁萎缩(parapapillary atrophy，PPA)与近视有关，又称近视弧，是视盘旁视网膜和脉络膜的萎缩，初始分为α区(α-parapapillary atrophy，α-PPA)和β区(β-parapapillary atrophy，β-PPA；图1)。α区位于周边，为不规则色素沉着，β区位于中间，紧邻视盘，此区域视网膜色素上皮层缺失，可以见到裸露的巩膜和脉络膜血管。β-PPA被认为与青光眼有关[30]。Jonas等[8]证实与杯盘比相比，β-PPA的存在对GON的检测更敏感。到目前为止，多项研究[31-32]已描述了β-PPA在POAG中的临床意义，但发病机制尚不明确。HM患者常常伴有视盘周围萎缩病变。Asai等[33]发现HM眼视盘越倾斜，其脉络膜越薄，PPA面积越大。在近视眼中，β-PPA与青光眼风险和轴向长度有关，在患有β-PPA的HM患者中，青光眼发病率为50%。HM眼的PPA面积明显大于中度、轻度近视眼及正常眼[34]。此外，Kim等[35]认为较大的PPA面积的患者视野损伤更重；Teng等[32]发现在表现出β-PPA和视野缺损进展的POAG患者中，β-PPA与未来视野缺损进展的位置在空间上相关。近年来有研究根据Bruchs膜是否存在，将原始的β-PPA分为存在Bruchs膜(Bruch’s membrane，BM)的β-PPA+BM和不存在Bruchs膜的β-PPA△BM，其中β-PPA△BM又常被称为γ区[36](图2)。已知β-PPA+BM可能是由于RPE层的年龄相关性萎缩，并与青光眼的发展密切相关。β-PPA△BM常被认为是眼轴伸长致使视乳头周围巩膜和边界组织机械拉伸的结果，一些报道认为眼轴和PPA之间存在显著关联[36-37]，并且可能与眼轴伸长有关[31,38]。
20230206101533_6480.png
图1 中度近视眼视盘旁α区(白点)，β区(黄点)
Figure 1 Fundus photographs showing parapapillary alpha zone (white dots), beta zone (yellow dots) in a moderately-myopic eye
20230206101749_1854.png
图2 高度近视眼视盘旁γ区(黑点)
Figure 2 Parapapillary gamma zone (black dots) in a highly-myopic eye
    为探讨β-PPA与青光眼进展的关系，Yamada等[39]进行了一项随访期≥2年回顾性队列研究，发现与没有β-PPA+BM的患者相比，β-PPA+BM较大的患者视野缺损进展更快。关于β区与视野缺损的相关性，考虑其可能原因与此区域视网膜色素上皮层缺失、光感受器和RPE细胞的丢失有关，这也提示β区PPA与青光眼有明显相关性，且β区面积的增加可能是青光眼进展的一个指标。Park等[40]发现β-PPA内的脉络膜微血管网缺损易出现在合并HM的POAG患者中，且视野缺损程度更大，提示β-PPA对青光眼损伤的影响可能与视盘形态和血流动力学的改变有关。在HM视盘形态学改变的过程中，其视乳头周围的血管可能受到额外的压力，从而引起视网膜深层微血管的损害。视网膜深层的微血管系统和视盘周围的脉络膜具有特别的临床意义，因为这些血管区域都位于短的后睫状动脉的下游、灌注层前组织和LC[7]。

4 视网膜神经纤维层厚度

    RNFL厚度发生变化是HM与青光眼共同的特征。研究[41]发现，RNFL厚度与近视程度呈负相关。在近视的发展过程中，整个视盘旁RNFL下降并逐渐转移到颞侧象限，导致视盘颞侧RNFL增加，上方、下方和鼻侧RNFL减少[42-44]。在儿童H M眼患者中，盘周RNFL厚度较低度近视眼更薄，其中上、下及鼻侧象限明显，而颞侧无明显改变[45]。Hwang等[46]在一项前瞻性研究中也有类似发现，且还发现视盘向颞侧倾斜角越大，颞侧周围RNFL越厚。H M眼RNFL发生这种变化的原因可能是：1 )随着HM眼眼轴的增长，巩膜和视网膜进一步拉伸变薄，使神经纤维扩散到更大的表面积上，可能导致RNFL变薄[47]。2)颞侧RNFL较厚的原因是眼轴伸长导致视网膜向颞侧拖曳，视盘的倾斜、扭转导致RNFL再分布[46]。临床上在通过RNFL鉴 别H M与青光眼时，可考虑通过不同方位视盘旁RNFL厚度的不同作为鉴别方向。

5 小结

    综上，HM与POAG存在密切的联系。HM患者视盘倾斜与扭转，盘周萎缩大小，LC形态改变，RNFL厚度及血流改变，视野变化及眼压波动情况等亦可为POAG的筛查提供参考。探索HM与POAG之间的联系与区别，早期发现并对H M中具有青光眼趋势的患者进行干预治疗尤其重要。未来的研究可能会涉及到临床研究中改进OCT的检测技术，提高诊断精度，检测H M视神经损伤甚至对其进行分期。视盘旁萎缩弧不同位置(特别是β区)的病因以及其与青光眼视神经改变的关系也有可能成为新的研究热点。POAG诊断与鉴别应考虑以下几点：1 )临床上在通过RNFL鉴别H M与青光眼时，可考虑通过不同方位视盘旁RNFL厚度的不同作为鉴别方向，尤其注意视盘颞侧的RNFL。2 )在临床鉴别HM与POAG时，应综合考虑眼轴、眼压波动情况、视野、视盘形态、视网膜神经纤。HM和青光眼都可导致ONH内结缔组织重塑和微血管异常[20]，HM患者长期随访不仅要观察黄斑病变，视神经形态与结构改变的观察也尤为重要。

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1、李炳宏. 体检人群青光眼患病情况及与外周血生物标志物的相关性研究[D].电子科技大学,2023.
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