Post-LASIK regression can occur via several possible mechanisms.
Firstly, corneal epithelial remodelling. The surface layer of cells on the cornea, called the epithelium, can undergo remodelling after LASIK. This may increase the corneal curvature at the peripheral edge of the optical zone as well as more centrally and can cause refractive shifts especially if the treated optical zone was small.
Secondly, changes in corneal stromal shape. There may be changes in the corneal stromal shape (not amounting to progressive ectasia). Although direct evidence for this is difficult to come by, 2 observations support this.
- Simultaneous crosslinking with LASIK seems to provide better refractive stability (Kanellopoulos et al. Clin Ophthalmol. 2014; 8: 2373–2381). Crosslinking stiffens the corneal stroma, making it less likely to deform.
- Treating with Timolol (which lowers intraocular pressure) can reduce myopic regression to some extent (Shojaei et al Am J Ophthalmol. 2012 Nov;154(5):790-798). Lowering eye pressure reduces the outward force on the cornea, thereby allowing the stroma to assume a flatter shape.
Lastly, continued changes in the length of the eyeball. There may be late progressive increase in the axial length of the eyeball. This may happen in people with a very high axial length, in a condition some call pathological myopia.
The greater the ablation and change in corneal shape, the higher the risk of regression. It follows that the risk of regression for low myopic corrections (-1 to -2D) is close to zero, while it is higher for very high myopes of -9 or higher both due to the biomechanical factors described as well as the higher incidence of pathological myopia for those with higher degrees of myopia.
While the mechanism with which corneal cross-linking works is uncertain, it is possible that the collagen stiffening caused by corneal cross-linking helps to prevent post-operative changes in corneal stromal shape.
