Corneal sensitivity is reduced and relates to the severity of neuropathy in patients with diabetes: response to Tavakoli et al.

The focus in relation to the consequences of nerve damage in diabetes has been the loss of sensation in the feet predisposing to the development of foot ulceration and lower extremity amputation (1). However, the cornea is 300– 600 times more sensitive than skin (2). In addition to serving a protective function, corneal nerves regulate corneal epithelial integrity, proliferation, and wound healing (3). In diabetic patients, corneal sensitivity is reduced (4), due to a loss of corneal nerve fibers (5), which leads to corneal keratopathy (6,7) and a susceptibility to injury, with recurrent erosions and ulcers (8). Thus, these changes are analogous to the diabetic foot, but because the cornea is not exposed to high pressures, ulceration infrequently occurs. Corneal sensation is mediated via myelinated Aand C-nerve fibers (9,10), which can be evaluated using the Cochet-Bonnet aesthesiometer (C-BA) (2) or the noncontact corneal aesthesiometer (NCCA) (11), respectively. In diabetic patients, the C-BA has been used to show a reduction in corneal sensitivity in some (12) but not other (13) studies. Furthermore, loss of corneal sensation has been related to the severity of retinopathy (12) and neuropathy (14). We have assessed corneal sensitivity in a large group of diabetic patients using both C-BA and NCCA to assess concordance between the two methods and also to define whether C-nerve fibers are the earliest to undergo damage (15). Using corneal confocal microscopy, we have previously shown that corneal nerve fiber damage is directly related to the severity of somatic neuropathy (16,17). Thus, detecting loss of corneal sensation may well be a logical screening tool for neuropathy, and hence we have assessed the relationship between loss of corneal sensitivity and the severity of diabetic neuropathy.