THE ETIOLOGY OF PRESBYOPIA - A SUMMARY OF THE ROLE OF LENTICULAR AND EXTRALENTICULAR STRUCTURES

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. The stimulus for innovation in the correction and remediation of presbyopia is strong as at least 98% of individuals from the industrialised nations will survive until 45 years-of-age; it is salutary to note that the survival rate 100 years ago was only 60%.