Etiology of negative dysphotopsia

Meaningful contributions to the study of negative dysphotopsia are welcome additions to the literature, as undesired optical phenomena represent a significant and largely unresolved problem. This has been clearly documented by Olson in his eloquent American Society of Cataract and Refractive Surgery 2012 Binkhorst Medal Lecture.A In fact, the dysphotopsias, positive and negative, represent a failure of current-day cataract surgery and need to be addressed by alterations of surgical methods, intraocular lens (IOL) designs, or both. The article by Holladay et al.1 uses ray tracing to establish a theoretical basis for dysphotopsias. The authors propose that 3 types of shadows (penumbrae) are induced by the interaction of the IOL and its edge with respect to reflected, refracted, and other light rays that pass peripheral to the IOL. They suggest that negative dysphotopsia, a type 3 shadow in their treatise, is largely caused by light images associated with posterior square-edged acrylic IOL design. While we appreciate their contribution and suggestions, we believe that there are meaningful flaws in their manuscript that contradict our previous findings and clinical observations.2 The chief concern with their investigation is the absence of any clinical correlation with their theories. Alternatively, we addressed negative dysphotopsia by correlating clinical findings, ultrasound biomicroscopy (UBM), and, in a subsequent separate publication, ray-tracing analysis.3 Based on our observations, we stipulated 10 clinical concepts that continue to be accurate in our experience. In their article, Holladay et al. report that their hypothesis is in keeping with our observations. However, this is not necessarily the case, as described below. Questionable is Holladay et al.'s comment that negative dysphotopsia is more common with acrylic than silicone optic material IOLs. The authors offer no data or references for this statement. While it may turn out to be correct, there are no large-scale meaningful epidemiologic studies of negative dysphotopsia that compare IOL material, shape, or edge design. Given that acrylic IOLs account for the majority of IOLs implanted, it should come as no surprise that they would be associated with a higher incidence of negative dysphotopsia. As we reported, negative dysphotopsia has been seen with all current IOLs implanted in the United States, and while our reported case preponderance was with square-edged high-index of refraction acrylic IOLs, the one common factor in all cases of negative dysphotopsia, irrespective of IOL material or design, was capsular bag implantation with the IOL underlying the anterior capsulorhexis. Moreover, when the offending IOL is transferred to the ciliary sulcus or exchanged for a sulcus-fixated IOL, the negative dysphotopsia symptoms are alleviated or improved. The latter observation confirmed the report by Vámosi et al.4 In their study, as in ours, negative dysphotopsia symptoms persisted if the exchanged IOL was placed in the capsular bag regardless of IOL material or edge design. Regarding the postulates from our publication, the Holladay et al. theory would not explain the fact that negative dysphotopsia has never been reported with anterior chamber IOLs or sulcus-placed IOLs. Additionally, the contribution of the corneal temporal incision, even though suggested as transient and associated with incision edema early after surgery by Osher,5 is difficult to appreciate given that negative dysphotopsia has also been reported with superiorly placed incisions and has not been reported with any other form of corneal incisions (astigmatic or radial keratotomy, penetrating or lamellar keratoplasty, laser in situ keratomileusis flaps, penetrating or perforating wounds). Additionally, the major contribution of UBM to our understanding of negative dysphotopsia and the findings in our report were misinterpreted or ignored in the Holladay et al. article. In our Figure 1, one can note a marked reduction in posterior chamber depth following iris suture fixation of the capsular bag–IOL complex. In fact, this patient had an in-the-bag round-edged silicone IOL (Staar AQ2010V). It is evident that the IOL has been anteriorly placed, whereas Holladay et al. interpret the findings to suggest that the iris has been retro-displaced. They also overlook UBM examples of patients with negative dysphotopsia symptoms and extremely shallow posterior chambers with silicone or acrylic IOLs.Figure 1: Preoperative (top) and postoperative (bottom) UBM demonstrating reduced posterior chamber depth after capsular bag–IOL complex iris suture fixation.Both investigations support bag diffusiveness as a possible mitigating factor in improvement of transient negative dysphotopsia. However, we have observed cases of recalcitrant negative dysphotopsia despite anterior capsule opacification. Bag diffusiveness alone does not explain why these cases of negative dysphotopsia respond to reverse optic capture. We believe that the majority of early negative dysphotopsia symptoms abate by neuroadaptation. The discrepancies between our ray-tracing analyses and those by Holladay et al. will be the subject of a separate and subsequent communication. While we appreciate the contributions of Holladay et al. regarding negative dysphotopsia, the absence of clinical correlation undermines the accuracy of their findings, particularly in light of our previously established and ongoing clinical observations. The cause of negative dysphotopsia likely remains multifactorial and variation in patient anatomy with regard to the peripheral retina is a consideration, as may be IOL material, index of refraction, and surface reflectivity. Our studies, however, do not support the concept that negative dysphotopsia is a product of IOL edge design.