Exp Eye Res. 2004 Mar;78(3):513-25.
Neural basis of sensation in intact and injured corneas.
Belmonte C, Acosta MC, Gallar J.
Instituto de Neurociencias de Alicante, Universidad Miguel Hern?ndez-CSIC, Apdo correos 18, 03550 San Juan de Alicante, Spain.
carlos.belmonte@umh.es
Excerpts:
In humans, the magnitude of stromal nerve injury and the temporal pattern of regeneration consecutive to the various refractive surgery procedures (radial keratotomy, photorefractive keratectomy, laser-assisted in situ keratomileusis) seem also to be variable. Nonetheless, in all circumstances in which stromal and epithelial nerves were destroyed, the injured area in the cornea was first entered by sprouts of intact neurons, some of them that had their receptive field limited originally to the conjunctiva (de Felipe and Belmonte, 1999), followed in the next weeks by the advance of regenerating axons of the severed nerves. Only a proportion of regenerated axons succeed in penetrating the denervated, injured corneal tissue. Microneuromas and nerves presenting a random and disorderly distribution pattern, with hyperregeneration and abnormal shapes, were often observed in the scar region and in the reinnervated territory long time after the lesion (Wolter, 1966; Chan et al., 1990; Trabucchi et al., 1994).
The differences in sensitivity disturbances as well as the variability found among individuals in the degree and time course of sensibility recovery after PRK or LASIK are not surprising considering the variability among studies in the type of lesion, excision depth, extension of nerve damage, etc. The reduced discrimination capacity of the Cochet? Bonnet esthesiometer is also a limiting factor.When the more sensitive gas esthesiometer (Belmonte et al., 1999) was employed and corneal mechanical and chemical sensitivity was measured at variable times after LASIK surgery (Gallar et al., 2003b) corneal sensitivity to mechanical and chemical stimulation was noted to be seriously reduced in the first week after surgery, appeared enhanced around the flap and in the hinge area 2 weeks later, and then dropped remarkably and remained significantly below control levels, 3 and 6 months post-LASIK. Sensitivity to both types of stimuli was close to normal only 2 years post-surgically (Fig. 5).
It is worth noting that the incidence of long-lasting discomfort symptoms attributable to nerve damage that was reported by patients subjected to this type of surgery is surprisingly high. A study with 231 PRK patients and 550 LASIK patients performed by Hovanesian et al. (2001) revealed an incidence of dryness symptoms in 43 and 48%, respectively. Soreness of the eye to touch was reported by 26.8% and 6.7%, respectively (P <.0001). Sharp pains occurred in 20.4% of PRK patients and 8.0% of LASIK patients (P =.0001). Complaints of the eyelid sticking to the eyeball occurred in 14.7% and 5.6%, respectively (P =.0001).
In LASIK surgery, the lamellar incision made with the microkeratome to create the flap, cuts the nerve fibre bundles of the superficial stroma and the subbasal nerve plexus at the flap. Nerve fibre bundles in the corneal bed located in the middle-third of the stroma are spared but suffer a variable degree of injury during photoablation.
Link to the full text:
http://www.lasikfraud.com/articles/neur ... sation.pdf