An examination of the baropathic nature of axial myopia


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Abstract

An examination of how intraocular pressure distending forces on the posterior sclera are an important mechanism in the development and progression of axial myopia has been made. Papers were selected from the results of PubMed (143) and Science Direct (1,398) searches using the key word combinations of ‘axial myopia’ and ‘intraocular pressure’. The main points include that the sclera is exposed to distending forces at all levels of physiological and pathological intraocular pressure. Reversible axial elongation is a common physiological response to elevated intraocular pressure in healthy eyes but more so in myopic eyes. Key variables, which appear to determine pathological (non-reversible) axial elongation include the thickness, rigidity and viscoelasticity of the posterior sclera and the associated increased susceptibility of it to distending forces. Intraocular pressure appears likely to have a greater role when it is above normal. Intraocular pressure elevations, which are not detected by clinical or experimental tonometry, may be significant contributors to axial elongation. Axial elongation can be pathological in myopic or myopically predisposed eyes, when elongation is not reversible. Axial elongation has also been associated with retinal defocus in both animals and humans, when thinning due to loss of scleral collagen and/or ground substance, which is driven by the retina, appears likely to be associated with increased scleral susceptibility to intraocular pressure. As myopia progresses, signs of retinal and choroidal stretching are an increasingly apparent consequence of the balloon-like expansion of the posterior sclera in response to intraocular pressure. Avoidance or moderation of activities which are known to elevate intraocular pressure may improve the prognosis for patients with genetic and/or environmental predisposition to myopic progression and may be an important consideration, even when other myopic control measures are being used.

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