=====Neurotrophic keratitis===== Neurotrophic keratitis (NK) is a rare degenerative corneal disease caused by impairment of trigeminal innervation leading to corneal epithelial breakdown, impairment of healing, and development of corneal ulceration, melting, and perforation. The hallmark of NK is a decrease or absence of corneal sensation. NK was initially described as “neuroparalytic keratitis” and experimentally demonstrated by Magendie, who hypothesized the presence of trophic nerve fibers in the trigeminal nerve regulating tissue metabolism. It is now demonstrated that the trigeminal nerve provides corneal sensation and also supplies trophic factors to the cornea, playing a key role in maintaining the anatomical integrity and function of the ocular surface. The ocular surface epithelium, tear gland, and sensory and autonomic nerve fibers exert a mutual influence of their structures and functions by the release of cytokines, neuropeptides, and neuromediators.1,4 Impairment of corneal trigeminal innervation causes morphological and metabolic epithelial disturbances and leads to development of recurrent or persistent epithelial defects. Ocular and systemic conditions associated with damage at any level of the fifth cranial nerve, from the trigeminal nucleus to the corneal nerve endings, may cause the development of NK. The most common causes of impairment of corneal sensation are herpetic keratitis, intracranial space-occupying lesions, and/or neurosurgical procedures that damage the trigeminal ophthalmic branch. Other ocular causes of impairment of corneal sensitivity include chemical burns, physical injuries, corneal dystrophy, chronic use of topical medications, and anterior segment surgery involving nerve transection. Many systemic conditions are also associated with the development of corneal anesthesia, including diabetes, multiple sclerosis, congenital syndromes, and leprosy ((Sacchetti M, Lambiase A. Diagnosis and management of neurotrophic keratitis. Clin Ophthalmol. 2014 Mar 19;8:571-9. doi: 10.2147/OPTH.S45921. eCollection 2014. Review. PubMed PMID: 24672223; PubMed Central PMCID: PMC3964170.)).