Amblyopia is a neurodevelopmental vision disorder resulting from abnormal visual input during the critical period of visual development, such as strabismus, uncorrected anisometropia, high refractive errors, and form deprivation. It is frequently associated with reduced visual acuity and deficits in binocular vision. Traditional occlusion therapy for amblyopia has typically been restricted to infants and young children during the critical period of visual development, as it is believed to be ineffective for older children and adults due to the decreased plasticity of the mature brain. Our research group has concentrated on pivotal scientific issues in amblyopia, including quantitative methods for detecting binocular vision, especially interocular visual suppression, the mechanisms underlying binocular vision impairment in amblyopia,treatment methods and their evaluations for amblyopia, and visual plasticity and its neural mechanismsin amblyopia. This paper summarizes the visual mechanisms and treatment modalitiesof amblyopia based on our research and both domestic and foreign sources, while also looking forward to the future development of this field in light of existing problems.

Amblyopia is a neurodevelopmental vision disorder resulting from abnormal visual input during the critical period of visual development, such as strabismus, uncorrected anisometropia, high refractive errors, and form deprivation. It is frequently associated with reduced visual acuity and deficits in binocular vision. Traditional occlusion therapy for amblyopia has typically been restricted to infants and young children during the critical period of visual development, as it is believed to be ineffective for older children and adults due to the decreased plasticity of the mature brain. Our research group has concentrated on pivotal scientific issues in amblyopia, including quantitative methods for detecting binocular vision, especially interocular visual suppression, the mechanisms underlying binocular vision impairment in amblyopia,treatment methods and their evaluations for amblyopia, and visual plasticity and its neural mechanismsin amblyopia. This paper summarizes the visual mechanisms and treatment modalitiesof amblyopia based on our research and both domestic and foreign sources, while also looking forward to the future development of this field in light of existing problems.

先天性白内障是严重影响婴幼儿视功能的疾病。随着白内障手术和人工晶状体植入手术技术的发展，先天性白内障患者术后多可获得高质量的视觉康复。然而，如何更好防治手术相关的不良事件和并发症、先天性白内障伴随的其他眼部发育不良疾病的治疗以及形觉剥夺性弱视的治疗，仍然是先天性白内障手术后需要重视的临床问题。

      封面展示的是双眼先天性白内障术后继发青光眼(左眼)与正常眼(右眼)的对比示意图。该并发症起病隐匿、难以预测，是先天性白内障术后二次致盲的首要原因。针对这一术后并发症，美国婴儿无晶状体眼治疗研究组 (infant aphakia treatment study, IATS)将儿童白内障术后青光眼相关不良事件(glaucoma-related adverse events,GRAEs，包括了青光眼和可疑青光眼)定义为：1)青光眼：眼压>21 mmHg(1 mmHg=0.133 kPa)，且有以下一种或以上的解剖学改变：(a)角膜直径增加；(b)双眼不对称进行性近视漂移伴角膜直径和(或)眼轴的增加；(c)视杯直径进行性增大，杯盘比增加≥0.2；(d)必须进行手术才能控制眼压。2)可疑青光眼：停用局部糖皮质激素(激素)后连续2次眼压>21 mmHg，或可通过抗青光眼药物控制眼压，但无上述任何青光眼的解剖改变。所以，如何更精准地预防该术后并发症，防止对患儿视功能造成进一步的损害，是目前关键的临床问题。

       因此，文章对先天性白内障摘除及人工晶状体植入术后继发性青光眼和可疑青光眼的发生、相关危险因素、治疗和预防的手段进行总结，以期进一步提高对先天性白内障术后高眼压和青光眼防治的认识，减少术后并发症对患儿视功能造成的进一步损害。

先天性白内障是严重影响婴幼儿视功能的疾病。随着白内障手术和人工晶状体植入手术技术的发展，先天性白内障患者术后多可获得高质量的视觉康复。然而，如何更好防治手术相关的不良事件和并发症、先天性白内障伴随的其他眼部发育不良疾病的治疗以及形觉剥夺性弱视的治疗，仍然是先天性白内障手术后需要重视的临床问题。

      封面展示的是双眼先天性白内障术后继发青光眼(左眼)与正常眼(右眼)的对比示意图。该并发症起病隐匿、难以预测，是先天性白内障术后二次致盲的首要原因。针对这一术后并发症，美国婴儿无晶状体眼治疗研究组 (infant aphakia treatment study, IATS)将儿童白内障术后青光眼相关不良事件(glaucoma-related adverse events,GRAEs，包括了青光眼和可疑青光眼)定义为：1)青光眼：眼压>21 mmHg(1 mmHg=0.133 kPa)，且有以下一种或以上的解剖学改变：(a)角膜直径增加；(b)双眼不对称进行性近视漂移伴角膜直径和(或)眼轴的增加；(c)视杯直径进行性增大，杯盘比增加≥0.2；(d)必须进行手术才能控制眼压。2)可疑青光眼：停用局部糖皮质激素(激素)后连续2次眼压>21 mmHg，或可通过抗青光眼药物控制眼压，但无上述任何青光眼的解剖改变。所以，如何更精准地预防该术后并发症，防止对患儿视功能造成进一步的损害，是目前关键的临床问题。

       因此，文章对先天性白内障摘除及人工晶状体植入术后继发性青光眼和可疑青光眼的发生、相关危险因素、治疗和预防的手段进行总结，以期进一步提高对先天性白内障术后高眼压和青光眼防治的认识，减少术后并发症对患儿视功能造成的进一步损害。

目的：比较单眼发作的原发性急性房角关闭(acute primary angle closure，APAC)患者发作眼与未发作眼眼部生物学参数的差异，分析急性房角关闭发作的可能危险因素。方法：回顾性分析2008年1月至2020年3月中山眼科中心青光眼科222例45岁以上单眼发作的APAC病例。排除双眼发作、另眼有发作史及晶状体源性、外伤性等继发因素。A超测量晶状体厚度、眼轴长度，超生生物显微镜测前房深度。对单眼发作APAC患者的发作眼与未发作眼眼轴长度、前房深度、晶状体厚度、晶状体相对位置等进行统计学分析。结果：患者发作年龄为(62.57±9.14)岁。发作眼与未发作眼前房深度分别为(1.75±0.27) mm和(1.88±0.31) mm，眼轴长度分别为(22.34±0.80) mm和(22.35±0.83) mm，晶状体厚度分别为(5.14±0.38) mm和(5.17±0.42) mm，晶状体相对位置分别为0.195和0.198。发作眼前房深度较浅，晶状体相对位置较靠前，差异有统计学意义(均P<0.001)，发作眼的眼轴长度、晶状体厚度较未发作眼差异无统计学意义(P>0.05)。APAC发作年龄较小(45~59岁)的患者双眼眼轴均短于发作年龄较大(60~69、70岁以上)的患者；发作年龄70岁以上患者双眼前房深度均较浅，双眼晶状体相对位置均较靠前，差异均有统计学意义(P<0.05)。相关性分析表明APAC发作年龄较小的患者双眼眼轴均较短(P<0.001)。结论：APAC发作眼的前房较浅、晶状体相对位置靠前。短眼轴、女性与不同个体的APAC发作相关。浅前房、晶状体厚、晶状体相对位置靠前可能是高龄人群APAC发作的危险因素。

Objective: To compare the ocular biometric parameters between the acute primary angle closure (APAC) eyes and the fellow eyes as well as the risk factors associated with APAC. Methods: From January 2008 to March 2020,222 monocular APAC patients over 45 years old from the Glaucoma Department of Zhongshan Ophthalmic Center, Sun Yat-sen University were retrospectively studied. Patients with binocular attack, previous attack in the fellow eyes, and secondary factors such as lens-induced and traumatic glaucoma were excluded. Ocular biometric parameters including axial length (AL) and lens thickness (LT) were measured with A-scan ultrasound, while the anterior chamber depth (ACD) was measured by ultrasonic biological microscope. AL, ACD, LT and relative lens position (RLP) were compared between the APAC and the fellows eyes. Results: The average age of onset was (62.57±9.14) years. The ACD was (1.75±0.27) and (1.88±0.31) mm, AL was (22.34±0.80) and (22.35±0.83) mm,LT was (5.14±0.38) and (5.17±0.42) mm, and the RLP was 0.195 and 0.198 for the APAC and the fellow eyes,respectively. Compared with the fellow eyes, the ACD of the APAC eyes was shallower, and the RLP was more anterior (both P<0.001), while the differences of AL and LT were not statistically significant (both P>0.05).Furthermore, AL of patients with a younger age of onset (aged 45 to 59 years) was shorter than that of those with an older age of onset (aged 60 to 69 or over 70 years); patients with an onset age of over 70 years have shallower ACD and more anterior RLP, all statistically significant (P<0.05). In addition, correlation analysis indicated that younger onset age was significantly correlated to shorter axial length of APAC eyes (P<0.001). Conclusion:APAC eyes had shallower ACD and more anterior RLP. Shorter AL and female were associated with APAC attack between individuals. Shallower ACD, thicker lens and more anterior RLP are potential risk factors for APAC among aged population.

目的：探究短期周边遮盖对成年视皮层双眼优势平衡的作用。方法：对12名正常成年人的各眼 (24只眼)分别进行单眼短期周边遮盖。遮盖方式为单眼佩戴90 min的环形、半透明的塑料遮盖板，遮盖板仅能透光，中央留有1 0°~15°视野范围的圆孔，从而实现周边遮盖。受试者在周边遮盖前、遮盖后的0~3、3~6、6~9、9~12、12~15、30、60和90 min均完成双眼竞争任务 (binocular rivalry task)。记录并分析各时间段中各眼的占优时间、双眼竞争在眼别间切换周期数和各眼占优概率随时间改变的特点等。每位受试者左右眼测试间隔1周进行。结果：在遮盖前，12名正常成年受试者被遮盖眼的占优时间与非遮盖眼的差异无统计学意义(92.78±6.33 s vs 87.22±6.23 s，P>0.05)，提示眼优势平衡。遮盖去除后的0~3 min，被遮盖眼占优比例显著增加至 0.721±0.11(P<0.001)，该效应在遮盖去除后的3~30 min均存在(P<0.05)，直至60 min(P=0.445)双眼基本恢复优势平衡。双眼优势转换周期在周边遮盖前后差异无统计学意义(P=0.064)。主导眼在去除周边遮盖后的0~3 min遮盖眼占优时间比例相对基线的改变幅度与遮盖非主导眼的差异无统 计学意义(P=0.835)。结论：短期的周边遮盖可改变成年双眼优势平衡，有望应用于视觉关键期后的弱视治疗中。视觉关键期后双眼视功能仍保留有一定的可塑性。

Objective: To study the effect of short-term peripheral patching on binocular dominance in adult visual cortex. Methods: Monocular short-term peripheral patching was performed on each eye (24 eyes) of 12 normal adults. The patching was achieved by monocularly wearing a ring-shaped, translucent and plastic patch for 90 minutes. The patch could only transmit light, but not pattern, and there was a circular hole with a visual field of 10°–15°, so as to achieve peripheral patching. Participants completed the binocular rivalry task at baseline and 0–3, 3–6, 6–9, 9–12, 12–15, 30, 60 and 90 min after peripheral patching. The dominance duration of each eye and the number of dominance switches between eyes were recorded. The probability of perceiving stimulus of each eye was calculated in each time period. Each participant’s both left and right eyes performed peripheral patching one week apart. Results: Before patching, the dominance duration of the patched eye was not significantly different from the non-patched eye (92.78±6.33 s vs 87.22±6.23 s, P>0.05), which suggests that the eye dominance was balanced. At 0–3 min after the removal of the patch, the dominance duration of the patched eye was increased significantly (P<0.001), and this effect existed until 30 min after the removal of the patch (P<0.05). The dominance duration of the patched eye at post-60 min was not significantly different from the baseline (P=0.445). There was no significant difference in the dominance switches among baseline and each period after patching (P=0.064). After the removal of patch on the dominant eye, the amplitude of change in the dominance duration of the patched eye at 0–3 min was not significantly different from that after the removal of patch on the non-dominant eyes (P=0.835). Conclusion: Short-term peripheral patching can also change the binocular dominance in adults, and it has the potential to be applied in treatment of adult amblyopia. After the critical period for visual development, binocular vision function still retains plasticity.