Diclofenac sodium attenuates neural activity after photorefractive keratectomy in rabbits

Photorefractive keratectomy for treating myopia has been associated with severe postoperative pain. The purpose of the present study was to investigate, in a rabbit model, the early effects of laser ablation on the physiology of the sensory nerves of the cornea.

Neurophysiologic monitoring of the corneal nerves was carried out 4 to 6 hours after 5-mm diameter, circular PRK ablations with a central depth of 85 microns. The effect of topical 0.1%, 0.25%, and 0.5% diclofenac sodium on the physiologic response to chemical and mechanical stimulation was evaluated. Corneas were prepared for anatomic studies of corneal innervation.

Heightened neural activity was observed in the corneal nerves after ablation, and exaggerated responses to sensory stimulation with hypertonic sodium chloride solutions were recorded. Diclofenac sodium at 0.1% decreased the response to 0.5 M NaCl and 0.7 M NaCl to 67 +/- 9% and 68 +/- 7% (mean +/- standard error) of the control response. Mechanically sensitive nerves were more resistant to diclofenac; 0.1% diclofenac had no effect, but 0.25% diclofenac reduced the response significantly (P < 0.05). Anatomic observations showed that the ablation extended through the neural plexus. By 72 hours, long neurites tipped with growth cones had advanced into the injured region, indicating the initiation of neural regeneration.

Diclofenac sodium was effective in attenuating neural activity in the cornea after excimer laser ablation. The action of this agent was shown to be different from that of a topical anesthetic, which rapidly and totally inhibited the response to all forms of stimulation.