June-July 2020


Eyeworld Journal Club
Review of “Distinct differences in anterior chamber configuration and peripheral aberrations in negative dysphotopsia”

by Ravi Shah, MD, Brandon Wong, MD, Charles Flowers, MD

Residents of USC Roski Eye Institute


Why is temporal negative dysphotopsia so symptomatic in some patients, but not others? I invited the USC residents to review the findings from this interesting study published in the July issue of JCRS.

—David F. Chang, MD EyeWorld Journal
Club Editor

Negative dysphotopsias are now an increasingly well-established phenomenon in uncomplicated cataract surgery. Patients typically describe an arc or crescent-like shadow or dark region in the temporal visual field of the eye in question. While this occurs in up to 19% of patients following uncomplicated cataract surgery, many of these patients note spontaneous resolution by postoperative year 1. However, 3.2% of these patients have persistent complaints of this phenomenon after the first year.1 Given the aging population and expected increase in the number of cataract surgeries, the number of patients with negative dysphotopsias (NDs) can also be expected to increase. There have been several theories describing how this process occurs including increased (and decreased) axial distance between the iris and intraocular lens (IOL), corneal edema, IOL edge design, smaller pupil size, large positive angle kappa, and anterior capsule overlying the optic.1,2 These studies have limited clinical anatomical data supporting these theories. Additionally, there have been other studies analyzing surgical and medical management of this phenomenon with varying levels of success.3–5 Most notably, inducing reverse optic capture seems to relieve many of the symptoms described in patients with NDs.4 In this paper, the authors have performed novel analyses with both clinical imaging data and ray-tracing simulations to better pinpoint specific anatomical factors that could explain NDs in these patients.
The authors of this paper prospectively enrolled 30 pseudophakic controls and 27 pseudophakic patients with NDs (referred by outside ophthalmologists following uncomplicated cataract surgery). Initially, the diagnosis of NDs was confirmed, no evident explanation for this visual phenomenon was identified, and the IOL was found to be in normal position without significant anomalies. Imaging analysis of these patients and controls was performed with anterior segment tomography, using the Pentacam (Oculus), and biometry, using the LENSTAR LS900 (Haag-Streit). Anterior chamber depth, horizontal decentration of the pupil, and pupil diameter were obtained from tomography. Pupil decentration, pupil diameter, keratometry, and axial length were measured from biometry. Iris tilt was calculated by manipulating iris tomography data through a custom written program. Subsequently, peripheral and central ocular aberrations in the horizontal meridian were obtained using the VPR peripheral aberrometer (Voptica). Finally, the OpticStudio (Zemax) was used to create ray-tracing simulations detailing the spherical equivalent shifts seen in eccentric lateral gaze up to 30 degrees on modified and accepted ocular schematic models.
The authors found that corneal wavefront, anterior chamber depth, and central ocular aberrometry did not show statistical differences between the NDs group and pseudophakic controls. The NDs group had significantly more temporally tilted irides, temporally decentered pupils, smaller diameter pupils, and increased difference in relative spherical equivalent (SE) of nasal eccentricities compared with pseudophakic controls. Ray-tracing models showed more negative SEs 1) in nasal eccentricities of temporally decentered IOLs, 2) with temporal tilt of the iris and IOL, and 3) while inducing positive angle kappa. Additionally, increasing the axial distance between iris and IOL resulted in a 1 D increase in SE.
The novel use of anterior segment imaging targeting specific anatomical differences between patients with NDs and pseudophakic controls strengthens the conclusions in this paper. While the exact pathophysiology behind NDs is not yet definitive, Holladay and Simpson2 believe the phenomenon occurs due to the temporal retinal field angle gap in light rays that are refracted by the IOL and light rays missing the edge of the optic. However, this conclusion was based solely on ray-tracing simulations. Given the currently available evidence, the relative temporal scotoma in NDs likely occurs due to differences in reflected and refracted light rays at the IOL edge. Anatomical conditions that exploit those differences can characterize the types of patients most likely to experience NDs following uncomplicated cataract surgery. A temporally decentered pupil, a small pupil, a tilted iris/IOL complex, or a positive angle kappa all change the types of light ray interactions with the IOL at the nasal edge.2-4
There were several limitations to this study, some of which were addressed in the paper. First, a prospective cohort study with a more even IOL distribution would have been ideal. While all the IOLs seen in pseudophakic controls were also present in the NDs group, there was a wider variety of IOL types in the NDs group, and a more in-depth discussion on various IOL edge designs would be clinically useful. In fact, the initial reports of NDs began in the early 2000s when square-edge IOLs were taking off, as a means of reducing the incidence of posterior capsular opacification.6,7 The baseline characteristics between the two groups show almost twice the percentage of females and smaller axial lengths in the NDs group compared with pseudophakic controls, both statistically significant differences. These two specific factors may themselves be related and could help explain nasal light ray pathways in patients with persistent NDs. Much larger population studies are needed to make such a conclusion, however. Moreover, it is not entirely clear how decreased SEs in nasal eccentricities correlate to the symptoms of NDs including temporal shadows or dark spots. As seen in peripheral ocular aberrometry and ray-tracing simulations, there is a large myopic shift in nasal eccentricities. It may be that in eccentric gaze even beyond 30 degrees, the increasing myopic blur is perceived as a relative scotoma as light is split and bent away from this retinal field angle. Finally, the method of determining iris tilt using an individually coded program in Python has not yet been validated to the authors’ knowledge. While this method of analysis may provide accurate data, it has not yet been shown to effectively model the eye in the manner it was used in this study. The resulting data from this methodology, however, is quite promising and recapitulates some of the previous work on NDs.
In summary, this paper provides exciting clinical and anatomical support to previously posited theories on the etiology of negative dysphotopsias after uncomplicated cataract surgery. Small pupils, temporally decentered pupils, and positive angle kappa are anatomical factors that increase the risk of NDs. Screening patients preoperatively for these factors can better help us manage patient expectations and potentially elucidate definitive postoperative remedies. Horizontal and inferotemporal haptic orientation, reverse optic capture, capsular fibrosis over the IOL edge, IOL material, and IOL edge design are all considerations that have been previously explored with varying success.2–5 Newer work suggests a possible central nervous system etiology as symptoms were reduced on visual field perimetry with contralateral eye occlusion and a lack of reported symptoms in monocular patients.8 When in doubt, allowing time for spontaneous resolution can always buy some time before attempting other medical or surgical corrections.


1. Osher RH. Negative dysphotopsia: Long-term study and possible explanation for transient symptoms. J Cataract Refract Surg. 2008;34:10:1699–1707.
2. Holladay JT, Simpson MJ. Negative dysphotopsia: Causes and rationale for prevention and treatment. J Cataract Refract Surg. 2017;43:2:263–275.
3. Masket S, Fram NR. Pseudophakic negative dysphotopsia: Surgical management and new theory of etiology. J Cataract Refract Surg. 2011;37:1199–1207.
4. Masket S, et al. Surgical management of negative dysphotopsia. J Cataract Refract Surg. 2018;44:6–16.
5. Henderson BA, et al. New preventative approach for negative dysphotopsia. J Cataract Refract Surg. 2016;42:1449–1455.
6. Davison JA. Positive and negative dysphotopsia in patients with acrylic intraocular lenses. J Cataract Refract Surg. 2000;26:1346–1355.
7. Holladay JT, et al. Negative dysphotopsia: The enigmatic penumbra. J Cataract Refract Surg. 2012;38:1251–1265.
8. Masket S, et al. Neuroadaptive changes in negative dysphotopsia during contralateral eye occlusion. J Cataract Refract Surg. 2019;45:242–243.


Flowers: Charles.Flowers@med.usc.edu
Wong: Brandon.Wong@med.usc.edu

Review of “Distinct differences in anterior chamber configuration and peripheral aberrations in negative dysphotopsia” Review of “Distinct differences in anterior chamber configuration and peripheral aberrations in negative
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