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老视的病因学:晶状体及晶状体外结构作用的综述

The aetiology of presbyopia: a summary of the role of lenticular and extralenticular structures.

作者信息

Gilmartin B

机构信息

Department of Vision Sciences, Aston University, Birmingham, UK.

出版信息

Ophthalmic Physiol Opt. 1995 Sep;15(5):431-7.

PMID:8524570
Abstract

Presbyopia is a condition of age rather than ageing and, as such, is devolved from the lamentable situation where the normal age-related reduction in amplitude of accommodation reaches a point when the clarity of vision at near cannot be sustained for long enough to satisfy an individual's requirements. Most of our facility to accommodate has been lost by 55 years-of-age and subsequent deterioration in visual performance at near is attributable to characteristics of senescent vision familiar to the optometrist. Our understanding of the cause of presbyopia has then to be derived principally from our understanding of the mechanism of accommodation in young eyes. Hermann von Helmholtz did much to clarify these mechanisms, but despite much research in the 100 years since his death, there is still no consensus on their precise nature. This paper presents a summary of issues, past and present, which have figured in the literature on the physiology of accommodation and presbyopia, and confirms that the pathophysiology of presbyopia is likely to result from deterioration in structure and function of a number of inter-related tissues. Changes in crystalline lens dimensions with age, the associated change in geometry of zonular attachments, and changes in viscoelastic properties of the lens capsule and lens matrix would, however, appear to be the principal correlates for the onset of presbyopia. Recent models of the biomechanics of accommodation have drawn attention to the feasibility of extralenticular contributions to presbyopia and have examined properties of the elasticity and leverage provided by posterior, anterior and tensile fibre systems.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

老花眼是一种与年龄相关而非衰老过程导致的状况,它源于这样一种令人遗憾的情况:随着年龄增长,正常的调节幅度下降到一定程度,使得近视力的清晰度无法维持足够长的时间来满足个人需求。到55岁时,我们大部分的调节能力已经丧失,随后近视力表现的恶化可归因于验光师所熟知的衰老视力特征。因此,我们对老花眼成因的理解主要源于我们对年轻人眼睛调节机制的理解。赫尔曼·冯·亥姆霍兹在阐明这些机制方面做出了很大贡献,但自他去世后的100年里,尽管进行了大量研究,对于这些机制的确切性质仍未达成共识。本文总结了过去和现在在调节生理和老花眼文献中出现的问题,并确认老花眼的病理生理学可能是由一些相互关联组织的结构和功能恶化导致的。然而,晶状体尺寸随年龄的变化、悬韧带几何形状的相关变化以及晶状体囊膜和晶状体基质粘弹性特性的变化,似乎是老花眼发病的主要相关因素。最近的调节生物力学模型已经关注到晶状体外部因素导致老花眼的可能性,并研究了后纤维系统、前纤维系统和张力纤维系统提供的弹性和杠杆作用特性。(摘要截选至250词)

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