In all his years as a cataract and refractive surgeon, Samuel Masket, MD, of Advanced Vision Care, and clinical professor at the Stein Eye Institute, UCLA, is still perplexed by dysphotopsias. “They’re fascinating and there’s no simple theory to explain them,” he says. “That’s why I continue to study them. I like to solve the unsolvable.”

Puzzling as they may be, good research exists that dysphotopsias can be managed by surgeons who take time to address their patients’ concerns. We spoke with several physicians who offered their experiences in mitigating these disturbances.


Describing Dysphotopsias

Dysphotopsias have become a recognized phenomenon that occurs following an otherwise uncomplicated cataract surgery and implantation of monofocal IOLs. “They’re a common cause of patient dissatisfaction,” says Linda Tsai, MD, FACS, a professor in the department of ophthalmology and visual sciences at Washington University in St. Louis. “It can be very frustrating and anxiety-provoking for the patients when, after surgery, they notice new visual disturbances. These dysphotopsias have two types. Positive dysphotopsias are usually bright, flickering lights off to the side of their vision. Sometimes if they put their hand up, it doesn’t seem to be there as much. Patients can describe this as ‘something always flashing on the side part of my vision.’ ”

Dysphotopsias often resolve on their own over time, but some conservative management strategies can help patients find relief initially. If the symptoms persist, surgeons can turn to surgical interventions as a last resort.

The second type is negative dysphotopsias. “These are very commonly described as a dark, crescent-shaped shadow on the temporal side of their vision,” Dr. Tsai continues. “These can be very bothersome and disturbing to patients. Positive dysphotopsias have been reported in over 60 percent of patients in a previous study, but they often go away and are less likely to necessitate a surgical intervention. Negative dysphotopsias are reported to be less common (less than 30 percent), but these are more commonly the ones that might need surgical intervention later on if patients don’t neuroadapt.”

Positive dysphotopsias were first described in 1993 by Dr. Masket and co-authors.1 Their research determined that the undesired optical images were produced by the shape of the ovoid IOLs used at that time. Negative dysphotopsias were described in 2000 by James A. Davidson, MD.2 These have been linked to the squared edge of IOLs, which were popularized for their reduced risk of posterior capsule opacification. More recently, ray-tracing optical modeling described the cause of negative dysphotopsias as an “illumination gap” between rays refracted by the IOL and those that refract directly to the retina.3 

“When I first started performing cataract surgery, we were implanting PMMA lenses, and dysphotopsias didn’t seem to be an issue,” recalls Dr. Tsai. “Then, as we got to the hydrophobic acrylic implants with the square edge to prevent the posterior capsule opacification, there was an increase of dysphotopsias. There’s some thought that negative dysphotopsias have to do with the square edge and how it reflects light, creating an illumination gap. I think manufacturers are starting to round the edges more or use different materials with different refractive indexes to try to decrease this kind of illumination gap.”

Dr. Masket says there’s no doubt that PD are related to the IOL. “Not one IOL is manufactured in the United States today without some form of a square edge, and the square edge is hard to get rid of because it delays and inhibits PCO so people don’t want to get rid of the square edge,” he says. “It’s also related to the index of refraction of the IOL. The higher the index of refraction, the greater the surface reflectability and the greater the units of PD. If you take a lens with a higher index of refraction and exchange it for one with a lower index, you’ll cure between 85 and 90 percent of those patients with PD.”

However, Dr. Masket believes negative dysphotopsias are related to the IOL’s position in the eye. ND hasn’t been reported with ciliary sulcus-, anterior chamber-, or scleral suture-fixated IOLs.4 “It’s not the material,” he says. “It’s not the edge design. It’s not the size. It’s really the position in the eye. There’s a carload of evidence that if you take the very same lens that’s sitting in the capsule bag and inducing ND and you bring the optic out of the bag and move it forward (reverse optic capture) then we’re going to cure the patient. Alternatively, if we put the lens in the sulcus, if it’s a three-piece lens, symptoms will go away.”

Unfortunately, dysphotopsias can happen to anyone, making it impossible to predict who will fall victim. However, suggestions within the literature have identified some patients who may be more prone to experiencing them.

“Looking at the literature, it’s been suggested that some patients with larger eyes or more shallow anterior chambers might be more likely to notice dysphotopsias,” says Dr. Tsai. One study found that ND scotoma was associated more commonly with short axial length and high IOL power and another study found correlation with high angle kappa, commonly observed in hyperopic eyes.5, 6

“There’s a greater incidence of dysphotopsias in people with migraine,” adds Dr. Masket. “We also know that the incidence of ND is higher in females than males. There isn’t evidence that shows race, geographic location or age differences, however, we also think that perhaps patients who have a more sensitive central nervous system and are more perceptive are more likely to have dysphotopsias. But the one chief problem is that we haven’t developed an ability to tell preoperatively who’s likely to suffer postoperatively.”

When Samuel Masket, MD, and colleagues conducted visual field testing on patients with negative dysphotopsias, they found the scotoma to be far greater in extent when both eyes were fully open (B) than when a peripherally occluding contact lens (A) was applied to the fellow eye (C).7 This suggests the involvement of the central nervous system, according to Dr. Masket.


Initial Management Strategies

There’s no way to accurately prevent dysphotopsia but there are various ways to manage the symptoms, from reassuring patients to surgical intervention. 

• Listen to patients. Management strategies differ for both PD and ND, but the first step for both is to acknowledge your patient’s concerns, say surgeons.

“I think it’s very important how we approach these patients because the dysphotopsias occur when everything else is perfect,” Dr. Masket says. “So the patient complains of seeing disturbances, and yet the surgeon looks at his or her work and this eye looks perfect, and many surgeons have kind of poo-pooed the patient’s complaints, sending them to neurologists and psychiatrists with no resolution. And that’s a very unfortunate thing because the symptoms are real and the patient deserves the opportunity to have the condition discussed.

“It’s very important that they’re made to understand that there isn’t anything wrong with them,” he continues, “and that the surgery was perfect but these are optical phenomena we haven’t completely figured out as of yet, but that we do have ways that can help them.”

Dr. Tsai makes sure to counsel patients that neuroadaptation can take up to a year in some cases. “I use a lot of reassurance to the patients and continue to follow them until their symptoms improve,” she says. “Patients need to understand this is a fairly common phenomenon that often improves. They need to know their surgeon is supportive. Reassuring them that this is normal and the rest of their eye is fine is important. I try to encourage them to focus on how improved their vision is.”

• Conduct diagnostic exams. “When a patient complains of dysphotopsias after cataract surgery, you have to start by making sure to rule out any ocular pathology that may be causing the symptoms, especially retina problems,” advises Dr. Tsai. “We check their vision and dilate them to evaluate the posterior pole. Underlying refractive error and tear film abnormalities can also be contributing to visual complaints. I try to maximize their vision by working on their tear film and making sure they have no underlying refractive error.”

If pathology is excluded, ND can be measured with visual field testing, says Dr. Masket. Some have studied the incidence of ND with a Goldmann perimeter, he says, while he has personally used a Haag-Streit Octopus 900 perimeter which has a Goldmann module. Dr. Masket and colleagues published on this topic in 2019, plotting the ND scotoma on visual fields.7 They found the ND scotoma to be far greater in extent when both eyes are fully open than when a peripherally occluding contact lens was applied to the fellow eye. “This phenomenon offers an understanding of why patients with ND may be more symptomatic than can be explained by the ND scotoma under monocular vision testing with full occlusion of the contralateral eye,” they wrote. “However, under binocular VF testing, one can easily note that the scotoma is large enough to interfere with visual function in the temporal field of the involved eye(s).”

“One of the first things I do when I see the patient initially with these complaints is to ask them to cover their fellow eye with their hand, and very often the symptoms improve,” Dr. Masket says. “Patching takes the symptoms away, but when the patch comes off, their symptoms return. I’ve also tried a peripherally opaque contact lens on the fellow eye and patients have improved, but most patients don’t like how it blocks their vision, even though it works.”

• Dilation drops. How the patient responds to dilation can also confirm the dysphotopsia diagnosis.

“One of the things that’s interesting about ND is that the patient’s symptoms almost invariably will be improved when we dilate the pupil,” says Dr. Masket. “If your patient has been referred for symptoms of ND you can dilate the pupil and re-question the patient on whether the symptoms seem better or worse. With ND the symptoms will improve with dilation and worsen with constriction, which is the opposite of PD. PD can be helped by making the pupil smaller and worsened by making the pupil larger. Sometimes the ND and PD symptoms can overlap, so by dilating the pupil it helps us discern if their symptoms are more negative or positive.

“We can put them on dilute topical pilocarpine or brimonidine and either of those agents make the pupil smaller and to a great extent help the patient,” continues Dr. Masket. “In my experience, the PD patient tends to be more tolerant of the problem than the ND patient because the ND patient loses a piece of their visual field and that seems to be really disconcerting, whereas the PD symptoms aren’t constant—it varies with the lighting conditions so they may not be as bothered.”


Surgical Interventions

Often, just knowing that nothing is wrong and they’re likely to get better is enough for the great majority of patients and no further action is needed, say surgeons.

“I’ll offer, ‘Well, if it’s really a bother, down the road (after a year or so) there’s always the option of doing a surgical intervention like an IOL exchange, although I can’t promise it will completely resolve your symptoms,’ ” says Dr. Tsai. “However, patients often say, ‘No, it’s not that bad, it’s getting better,’ and they’re very happy to wait. They just want to be reassured that there’s no other ocular pathology they need to be concerned with. They often just notice the dysphotopsias but aren’t so severely affected by the symptoms that they would choose a surgical intervention.”

Dr. Tsai only recalls two patients in 20 years who needed a surgical intervention. In one case she implanted a silicone piggyback IOL, and in the other she exchanged the original acrylic IOL for a silicone IOL. “Both procedures were successful, but I really try to avoid rushing into additional procedures if possible in the hopes that the patients will neuroadapt to the dysphotopsias,” she says.

“If I were to do a surgical intervention (for ND), I would consider a reverse optic capture of the IOL,” she says. “There’s a thought that if the lens is moved more anteriorly in the eye, then that could help decrease their symptoms. In a reverse optic capture, you would lift the optic above the capsulorhexis, but you leave the IOL haptics in the capsular bag. That might cause a refractive change, however, and make the patient more myopic.”

In reverse optic capture, the optic of the IOL is lifted above the capsulorhexis, while the haptics remain in the bag. Studies have shown that when an IOL is moved anteriorly in the chamber, the symptoms of negative dysphotopsias subside. 

Dr. Masket also agrees he would consider reverse optic capture, but says there are downsides. “If a patient was highly symptomatic for ND in their first eye, I would do a primary reverse optic capture in their second eye—implanting the lens in the bag but at the end of the surgery I pop the optic in front of the capsule,” he says. “That worked 100 percent of the time for me in patients who are highly symptomatic in the first eye, but there’s a downside to it.

“The downside is that it changes the optical power a little bit, which isn’t a total disaster,” he continues, “but with the optic out of the bag, there’s a very rapid onset of fibrotic PCO.”

For those who fail to adapt to PD and don’t respond to conservative treatments, IOL exchange to PMMA, silicone or copolymer IOLs in the capsular bag or ciliary sulcus have been reported to be successful overall.8 In that study, Dr. Masket and his co-authors reported their outcomes with IOL exchange for chronic PD between 76 and 88 percent with both silicone and co-polymer IOLs when exchanged for hydrophobic acrylic IOLs as the inciting device. When square-edged acrylic IOLs were the inciting PCIOL, then the success rate from acrylic to silicone was 87 percent and from acrylic to co-polymer was 88 percent.

Dr. Masket says reinvented IOLs with capsulotomy fixation may ultimately provide the resolution needed for ND symptoms. He notes three IOLs currently in use in Europe: the Tassignon (Morcher) and Femtis (Oculentis) and one of his own design, the Masket 90S IOL (Morcher). 

“Obviously physicians would like an IOL that doesn’t produce dysphotopsias, as would the patient,” Dr. Masket says. “The problem is that our present style of surgery to place a lens inside the capsular bag is what is associated with ND and it’s only when we bring the optic anterior to the level of the capsule that the patient won’t have any symptoms. So ideally there needs to be a groove on the anterior optic edge to capture the anterior capsulotomy and the IOL has to have a low index of refraction, which would reduce the incidence of either PD or ND. The downside (of the lens I’ve designed) is that it requires a perfectly sized and positioned anterior capsulotomy, so you’d need an automated capsulotomy whether by laser or other device in order to get that lens perfectly centered.”


More Work to be Done

Much has been learned about dysphotopsias since they first became prevalent, but for Dr. Masket, it’s ND that still has so many unanswered questions. “We know that ND is multifactorial and could benefit from IOL design, but there are so many more factors about ND that are poorly understood,” he says. “Why does it occur in more left eyes than right? Why is it greater in women? There’s a central nervous system connection not explained by any simple theory and we’d like to conduct functional MRI studies to determine what’s going on in the brain when a patient sees negative dysphotopsias.”

Dr. Masket is the designer of the Masket 90S IOL from Morcher and receives royalties from Haag-Streit. He is also a consultant for Ocular Therapeutix and CAPSULaser. Dr. Tsai has no disclosures.


1. Masket S, et al. Undesired light images associated with ovoid intraocular lenses. J Cataract Refract Surg 1993;19:690-694.

2. Davison JA. Positive and negative dysphotopsias in patients with acrylic intraocular lenses. J Cataract Refract Surg 2000;26:9:1346-1355.

3. Holladay JT, Zhao H, Reisin CR. Negative dysphotopsia: The enigmatic penumbra. J Cataract Refract Surg 2012;38:7:1251-65.

4. Masket S, Fram N. Pseudophakic negative dysphotopsia: Surgical management and new theory of etiology. J Cataract Refract Surg 2011;37:1199-1207.

5. Makhotkina NY, Dugrain V, Purchase D, et al. Effect of supplementary implantation of a sulcus-fixated intraocular lens in patients with negative dysphotopsia. J Cataract Refract Surg 2018;44:209-218.

6. Van Vught L, Luyten G, Beenakker JWM. Distinct differences in anterior chamber configuration and peripheral aberrations in negative dysphotopsia. J Cataract Refract Surg 2020;46:7:1007-1015.

7. Masket S, Magdolna Rupnik Z, Fram NR, Vikesland RJ. Binocular Goldmann visual field testing of negative dysphotopsia. J Cataract Refract Surg 2020;46:1:147-148.

8. Masket S, Rupnick Z, Fram NR, et al. Surgical Management of positive dysphotopsia: US perspective. J Cataract Refract Surg 2020;46:11:1474-1479.