I was fascinated to consider the ramifications of the data brought forth by Drs Rocha and Krueger in August 2014’s American Journal of Ophthalmology . The idea of eyelid positioning exerting a not-insignificant force on the cornea’s topography cannot be overstated. That eyelid shape, rigidity, and course of action through the blink could contribute as a force of causation would be a novel way of considering the reason of why an individual’s cornea has its unique characteristics. The association of floppy eyelid syndrome and keratoconus has always been described in terms of coincidence, but what if that lack of rigidity in the diseased eyelid is what directly contributes to the protrusion of the cornea? Suppose that in the normal eye, the strength of the lid/tarsus gives an extra degree of support to the normal prolate arch. When the support is missing, the corneal shape cannot cope with normal stressors and becomes ectatic. Just as the small waves of the tides can completely reshape a coastline, could the constant effect of the blink influence refractive error?

While the authors are more interested in determining how to better predict the long-term course of refractive surgery, I would posit that their findings could eventually obviate (a corneal-based) refractive surgery altogether. If one could change the shape and rigidity of the tarsus, orthokeratology could be performed without the risks of overnight contact lens wear. Keratoconus’s progression might be halted without cross-linking. Although the means to this end would need to be discovered, I commend the authors for opening a door of knowledge that was heretofore not known to be closed.