Jack Holladay, MD, MSEE was instrumental in describing the causes of negative dysphotopsias with his enigmatic penumbra explanation. Sam Masket MD also has been a pioneer in this topic with his explanation of the causes and the surgical management. And now there is an excellent study by Bonnie An Henderson MD and colleagues which proposes an orientation for single-piece acrylic IOLs which may produce less negative dysphotopsia by using the haptic-optic junction to block certain rays of light. Let’s review that study (and I encourage you to read the entire paper).
The study showed that on post-op day #1, patients with the proposed inferotemporal positioning of the haptic-optic junction had a lower rate of negative dysphotopsias when compared to patients who had the haptic-optic junction positioned vertically at the 6 to 12 o’clock meridian. Patients with silicone IOLs performed better than both groups of acrylic IOL patients with regards to negative dysphotopsias.
By post-op day #28, or about 1 month after surgery, there was no statistical difference between the rate of negative dysphotopsias between the two groups of acrylic IOL patients, meaning that orientation of the IOL was not critical at this time. This is a welcome finding for astigmatic patients because if we are using single-piece acrylic toric IOLs then their orientation is dependent on the axis of astigmatism and they cannot all be placed in the proposed inferotemporal position. It also gives us assurance that over the first month of healing, the negative dysphotopsias settle down to a very low rate.
Dr. Henderson’s findings make sense because on the first post-operative day, there is virtually no contraction or opacification of the anterior lens capsule. The haptic-optic junction at the inferotemporal position may block the penumbra effect explained so eloquently by Dr. Holladay. Then once a month has passed, the capsular bag has contracted and the anterior capsule leaflet has become more opaque, both of which may serve to decrease the penumbra effect.
Unfortunately this is dead wrong.
come on Steven — give us more detail than that! We would love to hear alternate opinions. We are all here to learn.
[from Facebook}
Brent Bellotte: Super interesting. Thank you.
Abdul Hamid Awan: Thanks for sharing
Steven Safran: Uday…this paper is dead wrong. If you look at the paper it shows a GREATER incidence of ND at 28 days in the treatment group than the control group. I wrote a letter to the editor about this that was published in JCRS.
Uday Devgan: Steven Safran Yes — I show the same graph if you click on the link above. Good points.
Steven Safran: Uday…..the whole article is dead wrong. ND is not caused by light hitting the infero temporal optic it’s caused by light hitting the nasal optic and the shadow that is created. The infero temporal haptic has absolutely NOTHING to do with ND in any…
Steven Safran: Also….Jack Holladay threw out his 2012 explanation of the “type 3 shadow” caused by the posterior edge of the lens in his “Enigmatic penumbra article ” in 2017 in an article he asked me to review prior to publication. In his new article he embrace…See More
Uday Devgan: good stuff. Please do note that in the title of my post, I ask a question. We are all here to learn!
Steven Safran: We are but I’m trying to keep people from treating ND by rotating IOLs because that is a total waste of time. You can orient the IOL however you like but it does not inhibit persistant ND. In fact it may increase the incidence of it for reasons beyond Facebook. Could explain over a beer.
Uday Devgan: Steven Safran ok, deal. Next time, I owe you at least 2 beers — because I want the full explanation along with figures on the back of napkins!
Steven Safran: No problem. I can also explain to you why ND occurs much more frequently in left eyes than right eyes. This is true in EVERY article that has ever been published on ND and nobody has been able to explain why but I can. Guaranteed that you will agree. Even Sam reluctantly agreed with my explanation (earlier tonight by chance as I sent him some slides on this this afternoon as we were discussing a case I did and I wanted his thoughts on it….will be using it for TLIS )
Arup Chakrabarti: Steven Safran what’s TLIS? 🙂
Steven Safran: Telling it like it is…..Osher’s meeting.
Steven Safran: Arup, I wrote my talk for our course today by the way….it’s all done. Also took care of the other stuff for AA0 so we should be good to go. Very pleased with my productivity this weekend!
Vikram Bhagat: Negative Dysphtopsia is a diagnosis of exclusion. First one should rule out any peripheral Retinal Degeneration & Dystrophy ,Retinal Detachment ,Optic nerve problem etc………
Steven Safran: The characterisitcs of ND are verry easy to discern in most patients. Geometric arc in temporal peripheral vision ….usually of left eye, Can be recreated easily at the slit lamp with a small slit beam from the side and goes away when you dilate the pupil. Not a difficult diagnosis to make but more challenging to treat.
Alan N. Carlson: To eliminate this problem, the Staar Nanoflex IOL has a lower refractive index = greater transmission and less internal reflection. YAG laser capsulotomy sooner 4-6 months – yes – but worth it.
Steven Safran: I had one patient with a Staar lens referred to me for ND. It’s good but not perfect. Reverse optic capture with a low index of refraction IOL is the best approach that we have. The lowest index of refraction IOL currently on the U.S. market is the B&L Softport A0….slightly lower index of refraction than the Staar. The Staar also has polyimide haptics which will degrade over time and can spontaneously shatter. Good lens otherwise though.
Larry Patterson: I agree about the B+L Sofport AO lens. I was using it and its predecessors for years when I first heard or read about negative dysphotopsia. I had never had a patient have such symptoms that I was aware of. Even now, years later, it’s extremely rare with the AO lens.
Richard Hakalmazian: A topic many of the surgeons I see discuss and struggle with telling me why their patient’s experience negative dysphotopsia. Great article and comments. Always learning, thank you
Steve Hantman: So when a patient with a single piece acrylic 1+ year out vehemently complains of ND do you, 1.exchange it for a 3 pc silicone or nanoflex in bag or sulcus; 2. Reverse optic capture the current IOL-and pray it stays there 3. Piggyback a 0 diopter sulcus lens ?? 4. Do nothing but empathize and tell them they’ll get used to it and hope brain adapts ?
Obviously simply rotating current lens doesn’t seem worth it?
Jay McDonald: The issue of negative dysphotopsias has been acknowledged for years. A series of speculations and explanations have ensued. I experienced my patients complaints and stopped the use of acrylic lenses when my acrylic lens patients complained and my silicone patients did not. For many years on the ASCRS internet discussion group The etiology was debated with each new idea. The cause is still being debated. My decision years ago-was to only use acrylic when there was a future likelihood of retinal issues or diabetics with retinopathy. The fact that there is still causal debate should not preclude choosing a a visual outcome for our patients that limited the chance for negative dysphotopsia. I chose silicone for myself and all family members who have had cataract surgery.
Milton Yogi: Lukan Mishev
Steven Safran: The cause of negative dysphotopsia is understood. It is a shadow created by the most peripheral light ray that passes through the outermost edge of the lens and the least peripheral light ray that is able to get around the lens. Between those 2 rays there is a scotoma that the patient will see IF the scotoma lands on viable retina that the patient is aware of. There will be much greater ND with higher refractive index lenses, smaller pupils, greater angle kappa, increased SA correcting lenses, and a sweet spot in terms of distance from the iris that maximizes it. Can explain more but have to get to O.R. and do an IOL exchange (for ND) as it so happens.