Swanson William H, Cohen Jay M
Glaucoma Institute, State College of Optometry, State University of New York, New York, NY 10036, USA.
Ophthalmol Clin North Am. 2003 Jun;16(2):179-203. doi: 10.1016/s0896-1549(03)00004-x.
Many visual disorders produce acquired color vision defects. Color vision theory emphasizes several stages of visual processing: prereceptoral filters (lens, macular pigment, pupil), cone photopigments (L-, M-, and S-cones), and postreceptoral processes (red-green, S-cone, and luminance channels). Congenital color defects, which affect 8% to 10% of males and 0.4% to 0.5% of females, result from alterations in the photopigment absorption spectra or the absence of one or more photopigments. The most common defects are color vision deficiencies (protan and deutan defects), which are milder than the rarer achromatopsias (complete loss of color vision). Acquired color vision defects can be attributed to a number of different causes: alteration of prereceptoral filters, reduced cone photopigment optical density, greater loss of one cone type than the others, and disruption of postreceptoral processes. Acquired color vision defects have been divided into three classes: type 1, red-green defect with scotopization; type 2, red-green defect without scotopization; and type 3, blue defects (with or without pseudoprotanomaly). Blue defects are usually type 3 acquired defects because congenital tritan defects have an incidence of one in several tens of thousands. Red-green defects can be acquired or congenital, and ruling out acquired defects can require a battery of tests (plates and arrangement tests, anomaloscopy, perhaps genetic analysis). Color vision tests must be administered carefully (with a standard illuminant and protocol), and pupillary miosis or high lens density should be noted and their possible effects considered when interpreting test results. Plate tests provide a simple screening method but do not provide a diagnosis. Arrangement tests and anomaloscope testing take more time and make greater demands on the tester, but they provide a more thorough evaluation. When standard protocols are followed and results are interpreted in terms of prereceptoral filters, photopigment optical density, cone loss, and disruption of postreceptoral processes, a battery of color vision tests can be useful in the differential diagnosis, after progression of the disease, and for evaluating the effectiveness of treatment.
许多视觉障碍会导致后天性色觉缺陷。色觉理论强调视觉处理的几个阶段:感受器前滤光器(晶状体、黄斑色素、瞳孔)、视锥细胞光色素(L-、M-和S-视锥细胞)以及感受器后过程(红绿色、S-视锥细胞和亮度通道)。先天性色觉缺陷影响8%至10%的男性和0.4%至0.5%的女性,是由光色素吸收光谱的改变或一种或多种光色素的缺失引起的。最常见的缺陷是色觉不足(红色盲和绿色盲缺陷),比罕见的全色盲(色觉完全丧失)症状较轻。后天性色觉缺陷可归因于多种不同原因:感受器前滤光器的改变、视锥细胞光色素光密度降低、一种视锥细胞类型比其他类型损失更多以及感受器后过程中断。后天性色觉缺陷已分为三类:1型,伴有暗点形成的红绿色缺陷;2型,无暗点形成的红绿色缺陷;3型,蓝色缺陷(有或无假性红色盲)。蓝色缺陷通常是3型后天性缺陷,因为先天性蓝色盲的发病率为万分之几。红绿色缺陷可以是后天性的或先天性的,排除后天性缺陷可能需要一系列测试(图片和排列测试、色觉异常检查,可能还需要基因分析)。色觉测试必须仔细进行(使用标准光源和方案),在解释测试结果时应注意瞳孔缩小或晶状体密度高的情况,并考虑其可能的影响。图片测试提供了一种简单的筛查方法,但不能提供诊断。排列测试和色觉异常检查需要更多时间,对测试者要求更高,但它们能提供更全面的评估。当遵循标准方案并根据感受器前滤光器、光色素光密度、视锥细胞损失和感受器后过程中断来解释结果时,一系列色觉测试在疾病进展后进行鉴别诊断以及评估治疗效果方面可能会很有用。