Chronic dry eye symptoms after LASIK: parallels and lessons to be learned from other persistent post-operative pain disorders

Alexandra E Levitt, Anat Galor, Jayne S Weiss, Elizabeth R Felix, Eden R Martin, Dennis J Patin, Konstantinos D Sarantopoulos, Roy C Levitt, Alexandra E Levitt, Anat Galor, Jayne S Weiss, Elizabeth R Felix, Eden R Martin, Dennis J Patin, Konstantinos D Sarantopoulos, Roy C Levitt

Abstract

Laser in-situ keratomileusis (LASIK) is a commonly performed surgical procedure used to correct refractive error. LASIK surgery involves cutting a corneal flap and ablating the stroma underneath, with known damage to corneal nerves. Despite this, the epidemiology of persistent pain and other long-term outcomes after LASIK surgery are not well understood. Available data suggest that approximately 20-55% of patients report persistent eye symptoms (generally regarded as at least 6 months post-operation) after LASIK surgery. While it was initially believed that these symptoms were caused by ocular surface dryness, and referred to as "dry eye," it is now increasingly understood that corneal nerve damage produced by LASIK surgery resembles the pathologic neuroplasticity associated with other forms of persistent post-operative pain. In susceptible patients, these neuropathological changes, including peripheral sensitization, central sensitization, and altered descending modulation, may underlie certain persistent dry eye symptoms after LASIK surgery. This review will focus on the known epidemiology of symptoms after LASIK and discuss mechanisms of persistent post-op pain due to nerve injury that may be relevant to these patients. Potential preventative and treatment options based on approaches used for other forms of persistent post-op pain and their application to LASIK patients are also discussed. Finally, the concept of genetic susceptibility to post-LASIK ocular surface pain is presented.

Figures

Figure 1
Figure 1
A simplified version of the ocular sensory apparatus. First order neuron (red solid line) with nerve ending in the cornea, cell body in the trigeminal ganglion, and synapse in the subnucleus caudalis. In actuality, however, there are multiple synapses for each nociceptor in the trigeminal subnucleus interpolaris/subnucleus caudalis (Vi/Vc) transition zone, and in the subnucleus caudalis/upper cervical transition zone (Vc/C1–2). Second order neurons (red dashed line) decussate and join the contralateral spinothalamic pathways and synapse in the thalamus. Third-order neurons (red dashed line) then relay information to the supra-spinal centers, including the somatosensory cortex. Reproduced with permission from Ocul Surf. 2012 Jan;10(1):2–14.

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