Binocular Vision, Amblyopia, and Refractive Development in Esotropia

描述(由申请人提供)：婴儿和调节性内斜视(ET)影响美国2-3%的儿童。婴儿和调节性内斜视会在出生后的第一年扰乱双眼视觉体验，并可能导致弱视和严重和永久性的立体视障碍。弱视是可以治疗的，但由于残留弱视的复发和持续性，它仍然是年轻人最常见的单眼视力损害形式。我们的合作研究小组现在准备解决三个关键问题。目的1：目前关于婴儿型和调节性ET的共识是，早期发现和及时干预以重新调整视轴可以保持正常的立体视敏度。然而，我们最近的工作挑战了公认的范式，并导致我们假设中央视野存在先天的视差敏感度缺陷。我们建议首次使用立体视觉诱发电位、视差聚焦和调节性视差聚焦来检验另一种假说，即在患有婴儿ET的中央4éi婴儿和患有调节性ET的儿童中，存在视差敏感度的先天性缺陷。这些研究将使我们对婴儿和调节性ET的双眼缺陷有一个新的、广泛的理解，并对早期干预的风险/益处的临床评估产生直接的翻译影响。目的2：不清楚为什么一些ET儿童交替注视并避免弱视，而另一些儿童则偏爱一只眼和弱视。根据灵长类弱视模型的数据和弱视婴儿和成人的视觉诱发电位数据，我们的假设是，抑制性双眼皮质相互作用的不对称性可能会使一些内斜视的婴儿和儿童发展为弱视。此外，我们假设，尽管长期或重复治疗，持续性残余弱视是由于抑制性双眼相互作用存在强烈的不对称性，这种不对称性未能通过遮盖治疗而减少。我们建议使用一种新的方法来量化抑制相互作用，以确定抑制中的不对称是否先于弱视，这些不对称是否在治疗有效时消失，以及持续性和复发性弱视是否源于持续性的不对称抑制。目的3：以一种独特的方法来确定引导正视的视觉信号，我们将利用一组婴儿队列，这些婴儿与正常婴儿的初始屈光不正的分布相同，但在出生第一年未能进行正视，即婴儿内斜视。这 方法将被用来确定缺失的视觉引导机制，该机制通常刺激轴向生长以减少婴儿远视。在一项对学龄前/学龄儿童ET队列的前瞻性评估中，我们将首次研究腋窝和周边屈光不正、调节和眼睛形状对正视化被抑制的学龄儿童近视轴向生长的发生和发展的影响。

DESCRIPTION (provided by applicant): Infantile and accommodative esotropia (ET) affect 2-3% of children in the U.S. Infantile and accommodative ET disrupt binocular visual experience during the first years of life and may cause amblyopia and severe and permanent impairment of stereoacuity. Amblyopia can be treated but, due to recurrence and persistence of residual amblyopia, it remains the most common form of monocular visual impairment in young adults. Our collaborative research group is now poised to address three critical issues. Aim 1: Current consensus on infantile and accommodative ET is that that early detection and prompt intervention to realign the visual axes can preserve normal stereoacuity. However, our recent work challenges the accepted paradigm and has led us to hypothesize that a congenital deficit in disparity sensitivity is present in the central visual field. We propose to use stereo VEPs, disparity vergence, and accommodative disparity vergence to examine an alternative hypothesis for the first time - that there is a congenital defect in disparity sensitivity in the central 4¿ i infants with infantile ET and in a large subset of children with accommodative ET. These studies will give us a new, broad understanding of binocular deficits infantile and accommodative ET and have a direct translational impact on the clinical evaluation of the risk/benefits of very earl intervention. Aim 2: It is unknown why some children with ET alternate fixation and avoid amblyopia while others develop a preference for one eye and amblyopia. Based on data from primate models of amblyopia and visual evoked potential data on suppression in amblyopic infants and adults, our hypothesis is that asymmetry in suppressive binocular cortical interactions may predispose some esotropic infants and children to develop amblyopia. In addition, we hypothesize that persistent residual amblyopia despite prolonged or repeated treatment is due to the presence of strong asymmetry in suppressive binocular interactions that fails to diminish with occlusion therapy. We propose to use a novel method that allows us to quantify suppressive interactions to determine whether asymmetries in suppression precede amblyopia, whether these asymmetries resolve when treatment is effective, and whether persistent and recurrent amblyopia result from persistent asymmetric suppression. Aim 3: In a unique approach to determining the visual signal that guides emmetropization, we will utilize an infant cohort that shares the distribution of initial refractive errors of normal infants but failsto undergo emmetropization during the first year of life; i.e., infants with infantile esotropia. This approach will be used to identify the missing visually guided mechanism that normally stimulates axial growth to reduce infantile hyperopia. In a prospective evaluation of a preschool/school-age infantile ET cohort, we will, for the first time, examine the influence of axil and peripheral refractive error, accommodation, and ocular shape on the onset and progression of myopic axial growth in school-age children whose emmetropization had previously been inhibited.