The cornea is the most densely innervated tissue in the body, and this innervation provides
corneal sensitivity. Many diseases disrupt
corneal sensitivity, including ocular infections, herpetic eye disease, dry eye syndrome, and diabetes.
In this study, we found that
corneal sensitivity was significantly decreased in untreated diabetic rats, diabetic rats treated with salsalate alone, diabetic rats treated with 10% menhaden oil with or without salsalate, and diabetic rats treated with 25% menhaden oil compared to control rats (Table 2).
The patient did not experience any eye pain and
corneal sensitivity measured with Cochet-Bonnet esthesiometer was <10 mm in the right eye and 60 mm in the left, showing remarkable decline of
corneal sensitivity in the right.
Animal experimental studies revealed that topical application of NGF accelerated restoration of
corneal sensitivity and promoted cornea epithelial proliferation and nerve regeneration after laser in situ keratomileusis (LASIK) or photorefractive keratectomy (PRK) [85-87].
Corneal sensitivity in diabetic patients subjected to retinal laser photocoagulation.
The
corneal sensitivity, number of corneal nerve fibers, and contents of vascular endothelial growth factor (VEGF)-B and various neurotrophic factors such as nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) in corneal tissue of four groups were observed.
Multiple studies have revealed the influence of diclofenac and ketorolac in fading pain along with
corneal sensitivity consequent to corneal abrasion.4
Corneal sensitivity has alert function for possible injuries or diseases (BROOKS et al., 2000).
However, the microkeratome operated eyes showed significantly higher incidence of dry eyes than femto-LASIK operated eyes (p 0.05), but VisuMax offered faster recovery of
corneal sensitivity and tearfilm break-up time.26
Impairment of
corneal sensitivity results in diminished blink and lacrimal reflexes.
Chronic corneal ulceration, entropion, decreased
corneal sensitivity and some infectious agents like feline herpes virus-1 have been considered as triggering factors in formation of corneal sequestrum (Williams and Kim, 2009).
The effects of the topical administration of non-steroidal anti-inflammatory drugs on corneal epithelium and
corneal sensitivity in normal subjects.
