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Corneal hypoesthesia with normal sub‐basal nerve density following surgery for trigeminal neuralgia
Author(s) -
Dhillon Virinder K.,
Elalfy Mohamed S.,
AlAqaba Mouhamed,
Gupta Ankur,
Basu Surajit,
Dua Harminder S.
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/aos.12697
Subject(s) - hypoesthesia , medicine , trigeminal nerve , trigeminal neuralgia , ophthalmology , basal (medicine) , cornea , surgery , anatomy , insulin
Purpose To evaluate the corneal sub‐basal nerve plexus in patients presenting with hypoesthesia following surgery for trigeminal neuralgia. Methods Twenty‐one patients who had unilateral medically uncontrolled trigeminal neuralgia and underwent ipsilateral surgery from 2006 to 2012 were included. Of these, 10 had microvascular decompression ( MVD group) and 11 had balloon compression of the trigeminal ganglion ( BC group). Slit lamp examination, Cochet–Bonnet aesthesiometery and in vivo confocal microscopy were carried out on both eyes of each patient. Nerve density data were statistically analysed. Results Corneal sensations and sub‐basal nerve densities in MVD group were normal and equal in both the operated and unoperated sides, indicating that there was no intra‐operative damage of the ophthalmic division of the trigeminal nerve (V1). However, those in BC group, despite having significantly reduced corneal sensations on the operated side (p = 0.007), did not demonstrate any significant difference in their sub‐basal nerve densities (p = 0.477). No patient had any ocular symptoms. Conclusions This study supports the hypothesis that complete ganglionic damage and/or postganglionic damage of V1 results in corneal hypoesthesia and neurotrophic keratitis, but partial ganglionic or preganglionic damage would preserve trophic function despite hypoesthesia and not result in clinically significant symptoms or signs of neurotrophic keratitis. The trophic and sensory functions of V1 are therefore independent and can be dissociated by disease or injury.