PT  - JOURNAL ARTICLE
AU  - Tessa Fayers
AU  - Stephanie R Shaw
AU  - Scott C Hau
AU  - Daniel G Ezra
TI  - Changes in corneal aesthesiometry and the sub-basal nerve plexus in benign essential blepharospasm
AID  - 10.1136/bjophthalmol-2014-306426
DP  - 2015 Nov 01
TA  - British Journal of Ophthalmology
PG  - 1509--1513
VI  - 99
IP  - 11
4099  - http://bjo.bmj.com/content/99/11/1509.short
4100  - http://bjo.bmj.com/content/99/11/1509.full
SO  - Br J Ophthalmol2015 Nov 01; 99
AB  - Background The aetiology of blepharospasm remains unclear. There is evidence that the afferent pathway is important, but this area remains under-researched.Aim To explore the hypothesis that the afferent arm of the blink reflex is abnormal in blepharospasm by assessing a range of measures of corneal sensory function.Methods In this prospective case–control study, 21 patients with blepharospasm and 21 age-matched and gender-matched controls completed the Ocular Surface Disease Index questionnaire and underwent the following assessments: tear osmolarity, Shirmer test, tear-film break up time, corneal and conjunctival vital staining, meibomian gland dysfunction, corneal aesthesiometry and confocal microscopy.Results Corneal sensitivity was significantly lower in patients with blepharospasm than in controls (right eyes p=0.009; left eyes p=0.009, paired t test). The median number of main nerve trunks was lower for patients with blepharospasm than for controls, and this was statistically significant at the 5% level (p=0.04, paired t test). Mean nerve density, median number of nerve branches and median total number of nerves were lower for blepharospasm cases than controls, but this did not reach statistical significance. Tortuosity was greater for blepharospasm cases than controls, but this was not statistically significant.Conclusions Blepharospasm is associated with reduced corneal aesthesiometry and a tendency towards a reduced number of nerves in the sub-basal plexus, implying an impairment in corticosensory processing, possibly a defect of the sensorimotor gating mechanism resulting in a loss of inhibition of the blink reflex.