Pathophysiology of neurotrophic keratopathy

Leigh Spielberg

Posted: Friday, October 6, 2017



Professor Harminder Dua

Professor Harminder Dua, Queen’s Medical Centre, Nottingham, UK, addressed delegates at the 8th EuCornea Congress in Lisbon on the topic of “Pathophysiology of neurotrophic keratoplasty” (NK).

“As we all know, the cornea is the most richly innervated structure in the human body, and these nerves have not only sensory functions, but also crucial trophic functions,” said Dr Dua.

These trophic functions stimulate the release of neuromediators that provide trophic support to corneal epithelial cells and keratocytes, providing a range of biologically active neurochemicals, such as nerve growth factor (NGF), that contribute to the maintenance of a healthy ocular surface. They are, in turn, supported by trophic substances produced by epithelial cells and keratocytes.

“Loss of corneal sensory innervation leads to decreased corneal epithelial renewal rate, reduced tear formation and blinking and ultimately development of NK,” he said. The neurological dysfunction not only lies at the aetiology of the disease, but can also influence the presentation and progression of diseases such as infectious keratitis, with a far less pronounced inflammatory and vascular reaction.

This is relevant not only for corneal specialists in tertiary referral centres, but also for general ophthalmologists who perform refractive surgery.

Dr Dua noted that: “Even years after LASIK, corneal innervation can remain structurally abnormal. Whether that is functionally important, we don’t yet know, but the ‘pain without stain’ phenomenon might be due to hyper-regeneration of nerves, leading to hyperesthesia and patient complaints.”