We have read with interest the paper entitled ‘Changes in pupil size following panretinal retinal photocoagulation: conventional laser vs pattern scan laser (PASCAL)’ by Yilmaz et al1 This work reports… Click to show full abstract
We have read with interest the paper entitled ‘Changes in pupil size following panretinal retinal photocoagulation: conventional laser vs pattern scan laser (PASCAL)’ by Yilmaz et al1 This work reports an increase in pupil size under different illumination levels following conventional and PASCAL panretinal photocoagulation (PRP) in patients with proliferative diabetic retinopathy (PDR). The authors interpret these findings as a consequence of laser damage to the efferent pupillary pathway, notably the short posterior ciliary nerves. Although we agree with the authors’ interpretation, we bring forth the hypothesis that PRP may also affect pupil size via damage to the afferent retinal photoreception. Intrinsically photosensitive retinal ganglion cells (ipRGCs), located in the inner retina and expressing the photopigment melanopsin, are at the origin of the afferent pupillary pathway.2 These atypical ganglionic cells integrate their intrinsic photosensitivity with inputs from traditional outer-retina photoreceptors, before projecting to subcortical regions driving pupillary constriction. PRP for PDR purposefully destroys a considerable fraction of peripheral rods and cones, but also directly damages the inner retina.3 The extent of retinal damage generated by PRP is dependent upon the laser beam’s diameter, power, and duration.4 Even though the exact power of the used beams was not specified by the authors, it is conceivable that a light-intensity photocoagulation such as the one they have used, especially with conventional PRP, might have inflicted structural and functional damage not only to the photoreceptors, retinal pigment epithelium, and choroid, but also to the retinal nerve fiber layer and inner retina as well,4,5 possibly altering the photoreceptive and integrative capabilities of ipRGCs and increasing pupil size under various conditions of illumination. Furthermore, it would be of great benefit if the authors could clarify whether the non-studied/untreated eye was also exposed to light during the direct pupillometric measurement and whether anisocoria was observed. In conclusion, we suggest that damage sustained by the peripheral photoreceptors, especially in the inner retina, could partially account for changes in pupil size following PRP. Additional studies are required to establish whether inner-retina sparing, through adequate yet effective lasertreatment strategies, could reduce pupil dilation and consequently photophobia in PRP-treated patients.
               
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