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Neurotrophic keratopathy (NK) is a devastating degenerative disease of the ocular surface, resulting in progressive corneal epithelial defects, ulceration, melting and in severe cases perforation.1 The disease results from dysfunction of trigeminal nerve afferents to the cornea; aetiologies include herpetic infection, ocular surgery, skull base tumours and surgery, brainstem cerebrovascular accidents, and congenital trigeminal nerve hypoplasia. The pathophysiology of NK encompasses loss of trophic support to the cornea, causing morphological and metabolic disturbances, and loss of sensory feedback, resulting in impaired blink and tearing reflexes.2 Though bandage contact lenses and topical medical therapies may halt disease progression and stimulate corneal healing,3 they do not address its underlying cause.
Terzis et al described reinnervation of the insensate cornea by direct surgical transfer of contralateral supraorbital and supratrochlear nerve branches to the perilimbal region as a means to reverse NK progression.4 Elbaz et al described a modification of this technique employing an interposition nerve autograft between the cornea and supratrochlear nerve to reduce procedural morbidity.5 6 The largest single-centre experience on the use of nerve autografts in corneal neurotisation for NK …
Contributors NJ and RP conceived of the presented work. NJ drafted and RP critically revised the manuscript. NJ and RP both approved the final version of the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.