Recovery of corneal sensation after myopic correction by laser in situ keratomileusis with a nasal or superior hinge.

PURPOSE: To measure corneal sensitivity after laser in situ keratomileusis (LASIK) to determine the time required for recovery of this parameter. SETTING: Ohshima Hospital of Ophthalmology, Fukuoka, Japan. METHODS: Corneal sensation was measured with a Cochet-Bonnet-type esthesiometer in 75 patients before and 1, 3, 6, and 12 months after correction of myopia by photorefractive keratectomy (n = 21) or LASIK (n = 54). RESULTS: Photorefractive keratectomy did not affect corneal sensation. In the LASIK group, a large and significant decrease in corneal sensitivity was apparent at 1 month (P<.05). Although corneal sensitivity appeared to have recovered slightly at 3 months, it remained significantly decreased (P<.05). By 6 or 12 months, the corneal sensitivity in LASIK patients was not statistically different from the preoperative values in the study patients. A significantly greater decrease in corneal sensitivity was apparent in the LASIK patients with a nasal hinge than in those with a superior hinge (F = 7.54, P<.01). Corneal sensitivity was in the normal range in 31.5% of LASIK patients at 3 months and in 57.4% and 82.1% at 6 and 12 months, respectively. CONCLUSION: Recovery of corneal sensation had begun 3 months after LASIK and appeared complete after 12 months.

An analysis of BIGH3 mutations in patients with corneal dystrophies in the Kyushu district of Japan.

PURPOSE: To assess the involvement of BIGH3 in corneal dystrophies (CD) with an autosomal dominant trait, in patients referred to a hospital in the Kyushu district of Japan. METHODS: Forty-five CD patients from 44 families were studied. Genomic DNA was extracted from peripheral blood, and exons 4 and 12 of the BIGH3 gene were amplified by polymerase chain reaction followed by direct sequencing. RESULTS: In exon 4, an R124H mutation associated with Avellino corneal dystrophy (ACD) was found in 39/44 families (86.4%) and an R124C mutation associated with lattice corneal dystrophy type 1 (LCD1) was detected in 2/44 families (4.5%). In exon 12, an R555W mutation associated with granular corneal dystrophy (GCD) was detected in 4/44 families (9.1%). CONCLUSIONS: Codons R124 and R555 of the BIGH3 gene represent mutational hotspots in the genomes of Japanese patients with autosomal-dominant CD.