The relationship between anisometropia and amblyopia.
The relationship between anisometropia and amblyopia.
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DOI：
10.1016/j.preteyeres.2013.05.001
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发表时间：
2013-09
影响因子：
17.8
通讯作者：
Candy TR
中科院分区：
文献类型：
--
作者：
Barrett BT;Bradley A;Candy TR
本综述旨在理清屈光参差和弱视之间关系的因果关系。具体来说，我们检查文献中的证据来支持不同的可能的发展顺序，这些顺序可能最终导致这两种情况的出现。当眼间等效球镜屈光度差为0.5D或以上时，屈光参差的患病率约为20%；当眼间差为3D或以上时，屈光参差的患病率降至2-3%。屈光参差患病率在出生后几周、近视发病的青少年时期相对较高，尤其是在老花眼发病后开始的老年人中。它的患病率约为同等程度的双边屈光不正的三分之一。重要的是，屈光参差的患病率在高度屈光参差人群中较高，这表明屈光参差和屈光参差潜在的正视失败可能是相似的。 1-3% 的人类患有弱视，大约二分之一到三分之二的弱视患者单独患有屈光参差或同时患有斜视。在儿童的第一次临床检查中，弱视和屈光参差经常同时存在，这促使人们相信屈光参差导致了弱视，正如该病的动物模型所证明的那样。然而，在回顾人类和猴子文献时，很明显，除了这个经典假设之外，还有其他途径可以导致屈光参差和弱视同时出现。例如，继发于剥夺或斜视的弱视出现后，往往会出现屈光参差。在没有明显剥夺或斜视的屈光参差病例中，常规消除婴儿屈光参差的正视眼矫正机制的失败仍然存在疑问。此外，在“纯”屈光参差性弱视病例中，弱视发展的时间顺序记录很少。尽管是间接的，但屈光矫正对屈光参差性弱视的治疗作用为屈光参差引起弱视的假设提供了强有力的支持。屈光参差性弱视病因学的直接证据需要对高危婴儿进行纵向追踪，这带来了许多方法学挑战。然而，如果我们要预防这种情况，我们必须了解导致其发生的因素。
This review aims to disentangle cause and effect in the relationship between anisometropia and amblyopia. Specifically, we examine the literature for evidence to support different possible developmental sequences that could ultimately lead to the presentation of both conditions. The prevalence of anisometropia is around 20% for an inter-ocular difference of 0.5D or greater in spherical equivalent refraction, falling to 2-3%, for an inter-ocular difference of 3D or above. Anisometropia prevalence is relatively high in the weeks following birth, in the teenage years coinciding with the onset of myopia and, most notably, in older adults starting after the onset of presbyopia. It has about one-third the prevalence of bilateral refractive errors of the same magnitude. Importantly, the prevalence of anisometropia is higher in highly ametropic groups, suggesting that emmetropization failures underlying ametropia and anisometropia may be similar. Amblyopia is present in 1-3% of humans and around one-half to two-thirds of amblyopes have anisometropia either alone or in combination with strabismus. The frequent co-existence of amblyopia and anisometropia at a child’s first clinical examination promotes the belief that the anisometropia has caused the amblyopia, as has been demonstrated in animal models of the condition. In reviewing the human and monkey literature however it is clear that there are additional paths beyond this classic hypothesis to the co-occurrence of anisometropia and amblyopia. For example, after amblyopia secondary to either deprivation or strabismus has emerged, anisometropia often follows. In cases of anisometropia with no apparent deprivation or strabismus, questions remain about the failure of the emmetropization mechanism that routinely eliminates infantile anisometropia. Also, the chronology of amblyopia development is poorly documented in cases of ‘pure’ anisometropic amblyopia. Although indirect, the therapeutic impact of refractive correction on anisometropic amblyopia provides strong support for the hypothesis that the anisometropia caused the amblyopia. Direct evidence for the aetiology of anisometropic amblyopia will require longitudinal tracking of at-risk infants, which poses numerous methodological challenges. However, if we are to prevent this condition, we must understand the factors that cause it to develop.
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影响因子：
0.9
作者：
Astle AT;McGraw PV;Webb BS
通讯作者：
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通讯作者：
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