We thank Drs. Afrooz and Gorantla for their interest in our recent article describing dry eye syndrome in patients who have undergone both blepharoplasty and laser in situ keratomileusis (LASIK).1 Under discussion is the possible mechanism for the exacerbation of dry eye symptoms in patients who had monocular LASIK and subsequent blepharoplasty. We hypothesized that the dry eye symptoms occurred in the LASIK-treated eye secondary to a blunted blink reflex. Afrooz and Gorantla raise the point that the efferent response of the corneal blink reflex is bilateral and not unilateral, and hence this cannot explain the dry eye symptoms in our study patients. We are reassured that we are all wholeheartedly in agreement with this well-established neuroanatomical pathway. However, what is lost in the understanding of this pathway is the source of the afferent input. Recall that in the case of the corneal blink reflex, afferent signals are carried by the nasociliary branch of the ophthalmic nerve (V1). The system requires only stimulation of either the right or left corneal nerves to generate a bilateral blink reflex. However, if there is now disruption of the afferent signal in one eye (i.e., by monocular LASIK), the blink reflex only responds to afferent stimuli from the nondisrupted cornea. Hence, in the monocular eye treated with LASIK, there is blunted corneal sensitivity, and hence the blink reflex is impaired when the LASIK eye is stimulated. The fellow eye, untreated by LASIK, still contains intact corneal fibers and can provide a bilateral blink reflex in response to noxious stimuli.
Afrooz and Gorantla state, “In the case of the two patients treated with LASIK in only one eye, the intact afferent arc in the opposite eye (with the blepharoplasty only) would preserve the blink response bilaterally, thus preventing a possible dry eye in the LASIK-treated eye.” The assumption that Afrooz and Gorantla make is that both corneas receive equal afferent input and that the non-LASIK eye will respond with the bilateral efferent response to protect the LASIK-treated eye. This is clearly not the case. First, the monocular eye treated with LASIK may have preexistent keratitis, which is not clinically manifest. However, after bilateral blepharoplasty and subsequent exposure keratopathy, the previously stable keratitis now worsens. But there is no significant afferent input to stimulate the blink reflex from the LASIK-treated eye. The fellow eye does not receive the same afferent signal from the LASIK-treated eye, and hence there is no added stimulus to blink from the LASIK-treated eye. In this manner, the fellow eye (untreated with LASIK) is in essence “blind” to afferent stimuli in the LASIK-treated eye. In addition, the LASIK-treated eye does not respond as well to inadvertent foreign body stimuli that may irritate the ocular surface, further worsening the keratopathy.
We appreciate the discussion and awareness raised by Afrooz and Gorantla of our article. Indeed, we agree that further studies are needed to explain this new syndrome.
Bobby S. Korn, M.D., Ph.D.
Don O. Kikkawa, M.D.
David J. Schanzlin, M.D.
Division of Ophthalmic Plastic and Reconstructive Surgery
Department of Ophthalmology
University of California, San Diego School of Medicine
La Jolla, Calif.
None of the authors has a financial interest in any of the drugs, devices or products mentioned in this communication.
1. Korn, B. S., Kikkawa, D. O., and Schanzlin, D. J. Blepharoplasty in the post-laser in situ keratomileusis patient: Preoperative considerations to avoid dry eye syndrome. Plast. Reconstr. Surg.
119: 2232, 2007.
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