Binocular Vision, Amblyopia, and Refractive Development in Esotropia

描述（由申请人提供）：美国2 - 3%的儿童患有婴儿期和矫正性内斜视（ET）。婴儿期和矫正性ET会在生命的最初几年内破坏双眼视觉体验，并可能导致弱视和严重的永久性立体视损伤。弱视是可以治疗的，但由于残余弱视的复发和持续，它仍然是年轻人中最常见的单眼视觉障碍形式。我们的合作研究小组现在准备解决三个关键问题。目标1：目前对婴儿和预防性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觉。然而，我们最近的工作挑战了公认的范式，并导致我们假设，在视差敏感性的先天性缺陷是存在于中央视野。我们建议使用立体VEP，视差聚散度，和重复视差聚散度来检查第一次的替代假设-有一个先天性缺陷的视差敏感性在中央4 <$i婴儿与婴儿ET和在一个大的子集的儿童重复ET。这些研究将使我们对婴儿和辅助性ET的双眼缺陷有一个新的、广泛的理解，并对非常复杂干预的风险/获益的临床评价产生直接的翻译影响。目的2：目前尚不清楚为什么有些ET儿童交替注视并避免弱视，而另一些儿童则偏爱单眼弱视。基于弱视的灵长类动物模型的数据和弱视婴儿和成人的视觉诱发电位数据的抑制，我们的假设是，抑制性双眼皮层相互作用的不对称性可能使一些内斜视的婴儿和儿童发展为弱视。此外，我们假设，持续残留弱视，尽管长期或反复治疗是由于存在强烈的不对称性抑制双眼的相互作用，未能减少与闭塞治疗。我们建议使用一种新的方法，使我们能够量化抑制的相互作用，以确定是否不对称的抑制弱视之前，这些不对称性是否解决时，治疗是有效的，以及持续性和复发性弱视是否持续不对称抑制的结果。目标3：在确定引导正视化的视觉信号的独特方法中，我们将利用与正常婴儿的初始屈光不正分布相同但在生命的第一年内未能经历正视化的婴儿队列;即，患有婴儿内斜视的婴儿这 方法将被用来识别丢失的视觉引导机制，通常刺激轴向生长，以减少婴儿远视。在一项对学龄前/学龄期婴儿ET队列的前瞻性评价中，我们将首次研究腋镜和周边屈光不正、调节和眼形对正视化先前受到抑制的学龄儿童近视轴向生长的发生和进展的影响。

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.