An examination of the relation between intraocular pressure, fundal stretching and myopic pathology

Abstract

Pathological myopia is one of the leading causes of visual impairment worldwide. Myopic development and progression is biomechanical and dominated by axial elongation. This clinical perspective examines some of the stretch-related fundal changes, which are associated with axial elongation and myopic pathology. The biomechanics of stretching of the fundus appears to depend on genetically and/or visual experience-based scleral changes, which reduce its thickness and elastic modulus so that it becomes more susceptible to the distending forces of intraocular pressure. These changes include reduced collagen synthesis, altered collagen fibres, tissue loss, altered proteoglycans and increased matrix metalloproteinase activity. Such changes are associated with reduced scleral rigidity and related increased potential to stretch in response to intraocular pressure. As axial elongation progresses, the sclera appears likely to continue to reduce in thickness and in its capacity to resist intraocular pressure, especially when pressure becomes elevated. Tessellation, lacquer cracks, myopic crescents, staphylomata, chorioretinal atrophy and retinal detachment are examined within a model for stretching of the fundus. Age, refractive error and axial length, for example, are associated with increased pathological progression. Myopic pathological progression can become dominated by vascular changes and include a greater risk of loss of acuity and blindness. Measures to control myopic pathology, which successfully slow or prevent stretching of the fundus, appear to be key factors in reducing or even avoiding permanent visual loss associated with this condition. For example, limiting axial elongation and related myopic fundus pathology by inhibiting changes which reduce the elastic modulus of scleral tissue is a desirable outcome from interventions to control myopia. Similarly, reducing exposure to the distending stress of elevated intraocular pressure appears to be a desirable form of intervention to control myopia, especially if myopic pathology can be reduced or prevented.

Scleral changes with accommodation

“…26 Thus, the myopic sclera reduces its rigidity. 27 All these biomechanical changes in sclera associated with myopia, might make it more susceptible to the distending forces caused by the ocular muscles that participate in the accommodation process. In our work, we found that scleral changes with accommodation are more noticeable in myopic subjects (for a 4.0 D stimulus, nasal part: 560 AE 350 lm) than emmetropic subjects (for a 4.0 D stimulus, nasal part: 220 AE 120 lm), despite myopes having accommodative response, on average, of less magnitude than that of the emmetropes.…”

Intraocular pressure and glaucoma: Is physical exercise beneficial or a risk?

“… 38 Increased IOP during weightlifting activities 20 , 35 suggests that any associated fundus stretching could contribute to reported adverse responses such as retinal detachment or haemorrhage. 39 Risk for ocular pathology may be a contraindication for weightlifting especially for patients with myopic fundus pathology. 39 and for keratoconus patients with increased susceptibility to cone formation or progression in a thin area of cornea, when IOP is elevated.…”

“… 39 Risk for ocular pathology may be a contraindication for weightlifting especially for patients with myopic fundus pathology. 39 and for keratoconus patients with increased susceptibility to cone formation or progression in a thin area of cornea, when IOP is elevated. 40 …”

Update on myopia

“…Corneal radius and corneal curvature change throughout life and also contributes to the feedback mechanisms affecting emmetropization and leads to axial elongation [21 & ]. Over time those increases can lead to pathologic changes such as lacquer cracks, myopic crescents, staphylomata, chorioretinal atrophy, retinal detachment, and possibly blindness [22].…”