Abstract
We examined the effect of anterior ischemic optic neuropathy (AION) on the activity of intrinsically photosensitive retinal ganglion cells (ipRGCs) using the pupil as proxy. Eighteen patients with AION (10 unilateral, 8 bilateral) and 29 age-matched control subjects underwent chromatic pupillometry. Red and blue light stimuli increasing in 0.5 log steps were presented to each eye independently under conditions of dark and light adaptation. The recorded pupil contraction was plotted against stimulus intensity to generate scotopic and photopic response curves for assessment of synaptically-mediated ipRGC activity. Bright blue light stimuli presented monocularly and binocularly were used for melanopsin activation. The post-stimulus pupil size (PSPS) at the 6th second following stimulus offset was the marker of intrinsic ipRGC activity. Finally, questionnaires were administered to assess the influence of ipRGCs on sleep. The pupil response and PSPS to all monocularly-presented light stimuli were impaired in AION eyes, indicating ipRGC dysfunction. To binocular light stimulation, the PSPS of AION patients was similar to that of controls. There was no difference in the sleep habits of the two groups. Thus after ischemic injury to one or both optic nerves, the summated intrinsic ipRGC activity is preserved when both eyes receive adequate light exposure.
Highlights
The intrinsically photosensitive retinal ganglion cells express the photopigment melanopsin which confers the capacity of intrinsic phototransduction[1,2]
The relative afferent pupillary defect (RAPD) was significantly correlated with the interocular difference in mean deviation (MD) of the visual field defect but not with visual acuity, color vision or retinal nerve fiber layer (RNFL)
All anterior ischemic optic neuropathy (AION) eyes demonstrated loss of visual field and reduction of the peripapillary RNFL compared to control eyes, and there were no significant differences in the visual function or RNFL between non-arteritic AION eyes and eyes with drusen-associated AION
Summary
The intrinsically photosensitive retinal ganglion cells (ipRGCs) express the photopigment melanopsin which confers the capacity of intrinsic phototransduction[1,2]. The rapid kinetics of rod and cone activation are primarily reflected in the immediate pupil response to light onset and offset whereas the slow kinetics of the melanopsin photoresponse are better discerned in the post-stimulus pupillary behavior. There is a growing body of evidence that ipRGCs display greater resistance to certain models of ganglion cell injury and death[13,14,15,16,17,18,19] This robustness of ipRGCs is the basis for the visual-pupillary dissociation that is observed in patients with isolated hereditary mitochondrial optic neuropathy. Glaucoma patients show a reduction in the light-induced suppression of nocturnal melatonin secretion and have disturbances in sleep quality Taken together, these findings implicate involvement of ipRGCs in glaucomatous optic neuropathy[24,25]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
