近距离工作引起的暂时性与永久性近视中的眼动参数（第二部分）
眼视光学杂志 1999年第2期第1卷 文献综述
作者：蒋百川
单位：蒋百川（美国休斯顿大学视光学院）
2 近距工作引起的永久性近视
人们已接受这样的结论：儿童的近视发展主要是由于眼轴的增长，该增长的速度无法被角膜和晶状体屈光力的下降所代偿[3，39，40，41]。直到最近，引起LOM的眼参数方面的机制才知晓，Kent[42]报道了对一病例纵向研究的资料，表明在青少年时期，角膜屈光力随近视发展而增大，Goss和Erickson[43]发现角膜曲率增加和近视进展之间的联系在两条主子午线都是很明显的，但是，他们没有检查随近视而变化的其他光学参数；Adams[44]报道他自己的角膜曲率保持不变，但近视在进展，由此下结论近视进展不是由于角膜变化而是由于眼轴变长；McBrien和Millodot[45]报道LOM比正视眼的玻璃体腔深，还发现LOM前房较深及晶状体较薄，但两者的角膜曲率无明显差别；Grosvenor和Scott[46]对三组年轻人随访三年：EOM（N＝29）、LOM（N＝26）、正视眼（N＝24）测量屈光状态和眼球参数的变化，他们发现与屈光变化有关的眼部成分只有玻璃体腔和眼轴长度，有趣的是，当将两近视组的度数进行匹配对照时，他们的眼部任何成分均无明显差异，他们从而得出结论，所有的近视都是轴性的。Jiang和Woessner[47]观察了一年轻人的屈光不正的进展，指出屈光不正变化是由于玻璃体腔的伸长。McBrien和Adams[11]在两年中从251名临床显微医师处收集了大量的屈光与生物统计学资料，也作出如下结论：玻璃体腔伸长是引起近视的发生和发展的主要因素。
我们相信最近动物模型的研究与人类眼动文献的结合，提供了强有力的依据，即眼动机制与眼轴增长有关。从对多种动物的研究表明，早期发育的异常视觉经历会干扰正常的眼各成分间的协调而出现屈光不正，目前的动物研究动向是鉴别影响正视化过程的环境因素和这些因素的作用机制.这类研究主要受Wiesel和Raviola[48]经典实验的影响，他们发现未成熟猴子眼缝合后会出现眼轴增长和近视现象（称为：剥夺性近视）。虽然眼睑缝合后有许多因素能改变视网膜的像[49，50]，与图形对比度减低有关的降低空间频率似乎最有可能使眼睑缝合后诱发剥夺性近视，但是，仅靠剥夺性近视的研究是不能说明视网膜图象如何“主动地”和“正常地”制约眼球根据环境来定焦生长（如，正常视觉经验在正视化中的作用）。虽然有多种方法可以改变视网膜像和可能改变眼球的生长，但是产生正视化的最可能的视觉反馈是光学离焦的信号和幅度。小鸡的研究表明视觉依赖（聚焦生长）的适应过程确实出现，配戴不同度数眼镜的小鸡眼睛能够生长以补偿诱发的离焦[51～57]，这种补偿主要是通过改变眼球的生长速率、特别是玻璃体腔的深度来达到的[57]，而且为造成屈光改变所需的离焦的幅度比原先想象的小，并不大于所估计的小鸡的焦深[58]。对灵长类动物的研究也表明视觉依赖性“为对焦而生长”机制，如Hung等[59]报告婴儿猴子表现出由于正或负镜诱发的光学离焦所引起的补偿性的眼轴生长。
形觉剥夺和光学离焦存在根本差别，光学离焦时，如果离焦量不是很大，眼睛能继续接受视觉反馈（即视网膜像质作为屈光状态的误差信号），当眼球朝合适的聚焦位置生长，像的质量得到了改善，但是，在形觉剥夺的情况下，视觉反馈毫无意义，因为无论眼球如何生长，视网膜像质无法有任何改进（即视觉反馈环是“开放”或固定在某一值），眼球增长的两种类型的明显区别是光学离焦类型要求大脑作为中介的机制而被牵涉进去，而剥夺性近视却没有这种要求，因为即使将视神经切断剥夺性近视也会出现[60]。在以人为受试者的研究方面，已有通过测量某些眼动及参数来确定光觉模糊机制在引起近视中的潜在作用，根据被测量参数差异，这些研究分为两类：一类测量调节刺激／反应函数，另一类测量分离性隐斜。
对不同的屈光组之间的调节刺激／反应函数进行比较，McBrien和Millodot[61]发现近距注视（4或5D）时，LOM的调节性反应比正视眼低。Rosenfield和Gilmartin[62]用3D近视标时证实上述结论。Bullimore等[63]证实LOM在被动注视条件下视近时调节反应低，但在主动注视条件下就不是这样。Gwiazda等[46]测量了正视与近视儿童的调节刺激／反应函数，发现近视儿童对三种视觉条件中的两种在视近时调节较差。Abbott等[64]用同样的方法对成人作了实验，他们发现进展性的近视对负镜片诱发的调节要求的反应较差，但是稳定的近视眼则和正视眼相同。Jiang[37]测量了双眼视、单眼视、用Badal光学系统的单眼视状态下的正视眼与LOM调节刺激／反应函数。在单眼视和Badal单眼视状态下，LOM的平均调节刺激／反应函数的坡度比正视眼低，但在双眼视状态下无明显差别。这些研究给出了初步证据：近视发生早期调节反应减少，但是，在模糊引起的调节与近视之间仍存在一个问题，就是是否其中之一可以诱发另一个，或有一共同因素诱发了两者[65]。把这些结论用到调节的控制理论上，仍不能清楚解释屈光组之间不同的调节反应或坡度是否由他们调节控制获得或调节死腔的不同决定，后者常被认为是眼的焦深。
Jiang[66，67]提出了一个改进的静态调节模型。在该模型中加入了系统增益作为对于系统的感觉及系统的一种线型模拟（ASG）。模型得出的结论表明：感觉部分不仅影响调节反应函数的坡度，而且会改变系统对离焦信号有效阈值（ET）。为检验该理论结果，Jiang比较了13名正视眼与10名LOM的ET值，差异是显著的。但是没有发现两组在暗焦点或调节刺激／反应坡度上的明显差异。分析坡度和ET资料后，他推测在LOM人员中，对离焦感觉的敏感性不如正视眼那么高。结合前面讲到的，这突出了光学离焦在引起屈光不正病因中的重要作用。
临床研究也为眼动参数随近视发展而变化的理论提供了让人感兴趣的初步证据。Birnbaom[68]观察了近视发展中调节与辐辏的临床测量值变化，他提出：早期近视可能与低的正相关调节和调节幅度以及视近内隐斜增大或视近外隐斜减少有关。Drobe和de Saint－Andre[69]比较了法国视光学医生测定的保持正视的和后来发展为近视的一批儿童和青年的近距隐斜数据，发现两组的差距有2.9棱镜度（P＝0.008）而原近视组内隐斜更明显。Gosss和Jackson[70]也发现发展为近视组视近时的内隐斜更明显。这组的儿童中，近视开始前与近视后，视近时常常表现为内隐斜，这结果与成人中的发现类似，即发展成LOM的人在近视前与近视后表现出较高的反应性AC／A值[32]。而且，高AC／A值与高分离性近距隐斜有关[71]。这一发现揭示了调节与辐辏相互作用在近视发展中的重要作用。同样的辐辏反应，高AC／A值者视近的调节量比正常或低AC／A者有较大的滞后。而且，调节滞后可能在视网膜上产生模糊像质，这可以成为误差信号引起眼的补偿性生长，而导致近视的发展。
3 讨论
关于近视的病因学说有很多，但还没有一个被广泛接受。但是有一点很明确，就是近距工作是近视发生相关的环境因素之一。在这篇综述中，我集中阐述了近距工作后眼动参数改变，以及这种变化在近视与正视者之间的差别。眼动参数中，暗焦点被认为是调节的基态，持续近距工作后，暗焦点近移，被称为调节适应或近距工作后效应。我讨论了四种状态下的调节参数：即静态开环，静态闭环，动态开环，动态闭环。由于调节系统可被认为是一个负反馈环，在静态闭环状态下，如果系统增益很高，暗焦点移动对调节反应影响很少。但在静态和动态开环状态甚至于动态闭环状态，调节反应表现为调节紧张现象。这与调节或睫状肌痉挛有关。临床上，睫状肌痉挛被认为是睫状肌过度的不必要的及不适当的收缩[20]。这种近距工作引起的异常调节痉挛，如果持久，就是假性近视。另一方面，持久性近视主要表现为眼轴的伸长，动物模型及以人为对象的研究都支持这假设，即：视网膜成像的精确性或视网膜像质对眼后段的发育起反馈作用。上面讲到的对近刺激调节反应的减少，高AC／A值，近距内隐斜视，高离焦阈等导致像在视网膜离焦，都支持了这个假设。
很多研究工作已经做过，但仍未揭开近视发展的病因之谜。我们仍不知道为什么不是所有的近距工作者都会变成近视眼。最近的研究让我们进一步倾向近视发展的眼动力理论的假设。“在敏感个体，发生屈光不正前，近距工作已引起了眼动参数的改变，这一系列改变显然可能导致光学离焦从而成为诱发近视的补偿性变化的潜在因素”[70]。如何将近距工作与近视发展相联系仍有许多不足之处，以至我们无法完全把这理论肯定下来。虽然暂时性近视不是每个屈光不正者所必经历的，但可以肯定，暂时性近视有可能发展为永久性近视。因此，现在的主要问题是弄清这个转化过程是如何发生，这种转变是否与眼动参数有关。这方面的进一步研究显得非常重要及必要。
感谢：Dr.Harold and Dr Stephen Morse对形成本文初稿的讨论和建议。
作者单位：蒋百川（美国休斯顿大学视光学院）
Oculomotor function in nearwork-induced transiant and permanent myopia（Part Ⅱ）
Bai-chuanJiang
2 Nearwork－induced permanent myopia
Generally，it is accepted that childhood myopia progression is due to axial elongation，which is not compensated by reductions in corneal and crystalline lens powers[3，39，40，41]. Until recently，the component mechanisms that produce LOM become clear. Kent[70]reported longitudinal data，for one subject，showing that corneal power increased as myopia progressed during the early adult years. Goss and Erickson[43] found that correlations between corneal steepening and myopia progression were significant in both principal meridians. However，they did not check whether other optical components changed with the progress of myopia. Adams[44] reported that his own keratometer findings remained stable as his myopia progressed during the adult years，and concluded that the progression was not due to corneal steepening but due to axial elongation. McBrien and Millodot[45] reported that LOMs had deeper vitreous chambers than emmetropes. Their LOM subjects were also found to have deeper anterior chambers and thinner crystalline lenses，but no differences were found in corneal curvature. Grosvenor and Scott[46] measured the changes in refraction and ocular components over 3 years for three groups of young adults：EOM（n＝29），LOM（n＝26），and emmetropes（n＝24）. They found that the only ocular components that significantly correlated with changes in refraction were vitreous chamber depth and axial length. Interestingly，when subjects from the two groups of myopes were matched for the amount of myopia，there were no significant differences in any of the ocular components，and they concluded that all myopia is axial in origin. Jiang and Woessner[47]observed a young adult's refractive error development and suggested that her vitreous chamber elongation was responsible for the refractive error change. McBrien and Adams[11] collected refractive and biometric data from 251 clinical microscopists during a 2－year period and concluded that the vitreous chamber elongation caused the onset and／or progress of myopia.
Recent findings from the animal modeling literature can be integrated with the oculomotor literature in human studies resulting in strong evidence that oculomotor mechanisms are involved in inducing axial－length elongation in certain individuals. In a wide variety of animal species，abnormal visual experience during early development interferes with the normally coordinated growth of ocular components and produces anomalous refractive status. Research on animals is currently directed toward identifying the environmental factors that influence the emmetropization process and the mechanisms by which these factors affect the eye's refractive status. Animal studies on myopia were influenced mainly by the classical experiment of Wiesel and Raviola[48] who found that lid suture in the immature monkey results in an increase in axial length and a myopic eye（called‘deprivation myopia’or'form－deprivation myopia'）. Although，many factors could alter the retinal image of the lid sutured eye[49，50]，degraded spatial vision associated with reduced image contrast appears to be the most likely aspect of lid closure that triggers the onset of lid－sutured myopia. However，studies of form deprivation alone do not reveal how，or if，the quality of the retinal image‘actively' and ‘normally' regulates the eye to grow to‘be in focus'for its environment（i.e.，the role of normal visual experience in emmetropization）. Although there are several ways to change the retinal image and possibly alter the eye's growth，the most plausible visual feedback that can be used by the eye to perform emmetropization is the sign and magnitude of optical defocus. Studies in chicken have shown that a vision－dependent，“grow－to－be－in－focus”，adaptive process is indeed present. Chicken eyes that are fitted with different powered spectacle lenses，can grow to compensate for the induced defocus[51～56]. This compensationis mainly achieved by changing the eye's axial growth rate，especially vitreous chamber depth[57]. Furthermore，the magnitude of the defocus that will result in refractive change is smaller than previously believed，i.e.，not much greater than the estimated depth of focus of the chick eye[58]. Studies in primates have also demonstrated a vision－dependent“grow-to-be-in-focus”mechanism，e.g.，Hung et al.[59] reported that infant monkeys exhibit compensating ocular growth for optical defocus induced by positive or negative lenses.
There is a fundamental difference between form deprivation and optical defocus. With optical defocus，if the amount of defocus is not very large，the eye can continuously receive visual feedback（i.e.，the quality of the retinal image serves as an error signal for the refractive status）. When the eye grows toward the appropriate focus position the quality of the image improves. However，in form deprivation rearing strategies，visual feedback is meaningless because no matter how the eye grows，the retinal image quality is not improved（i.e.，the visual feedback loop is ‘opened'or‘fixed at a constant value'）. The striking difference between the two types of axial elongation is that the optical defocus type requires the involvement of abrain-mediated mechanism and the other type（deprivation myopia）does not because it still occurs if the optic nerve is cut[60].
There have been some human studies that looked at the potential role of the optical blur mechanism in producing myopia by examining a specific oculomotor parameter. According to the parameter being measured，these studies can be divided into two categories. In one，the accommodative stimulus／response function was measured and in the other，the dissociated near phoria was measured.
The accommodative stimulus／response function has been compared in different refractive groups. McBrien and Millodot[61] found that the accommodative response for near targets（4 and 5 D）is lower in LOM versus in emmetropes. With a 3 D target，Rosenfield and Gilmartin[62] confirmed the above findings. Bullimore et al.[63] confirmed that LOMs have a lower response for near targets under a passive viewing condition，but not under an active condition. Gwiazda et al.[46] measured accommodative stimulus／response functions for emmetropic and myopic children and found that myopic children accommodated less to high accommodative demands in their two of three viewing conditions. Abbott et al[64]. applied the same method on young adults. They found that progressing myopes had reduced accommodative response to negative lens－induced accommodative demands，but the accommodative responses in stable myopes were same as in emmetropes. Jiang[37] measured the accommodative stimulus／response functions of emmetropes and LOMs under binocular，monocular，and monocular with a Badal optical system viewing conditions. The mean slope of the function of the LOMs was lower than the mean slope of the emmetropes in the monocular and the Badal conditions，but there was no difference in the binocular condition. These studies provided preliminary evidence that reduced accommodative responses occurred during the onset of myopia. However，a remaining question regarding the correlation between blur－driven accommodation and myopia is whether one could cause the other，or whether a common factor influences both[65]. Applying these results to the control theory model of accommodation，it is still not very clear whether the difference in accommodative responses and／or slope between refractive groups is caused by the difference in their accommodative controller's gain or in the accommodative dead－space，the latter usually being thought of as the depth－of－focus of the eye.
Jiang[66，67] suggested a modified model of static accommodation，in which an accommodative sensory gain（ASG）was added as a linear operator to simulate the sensory part of the system. Results derived from the model showed that the sensory part not only affected the slope of the accommodative response function but also increased the system's effective threshold（ET）to the defocus signal. To test the theoretical result，Jiang compared calculated values of ET between 13 emmetropic and 10 LOMs. This difference in ET between the two groups was significant. However，no significant difference was found in the dark－focus or the accommodative stimulus／response slopes between the groups. From analyzing the data of the slope and ET，he speculated that the sensory system in LOM subjects might be less sensitive to defocus than that of emmetropic subjects. This，combined with the information provided by the studies described above，emphasizes the role of optical defocus in inducing refractive error change.
[1] [2] 下一页 |
