• Users Online: 589
  • Print this page
  • Email this page

 Table of Contents  
Year : 2023  |  Volume : 3  |  Issue : 2  |  Page : 349-353

Could this be a lead for a solution to negative dysphotopsia?

Consultant Neurologist, Department of Neurology, Sathbhavana Brain Clinic, Secunderabad, Hyderabad, Telangana, India

Date of Submission23-Jun-2022
Date of Acceptance24-Nov-2022
Date of Web Publication28-Apr-2023

Correspondence Address:
Nagabhushana R Potharaju
H.No. 10-3-185, St. John's Road, Secunderabad, Hyderabad - 500 025, Telangana
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_1497_22

Rights and Permissions

Negative dysphotopsia (ND) was diagnosed when the mydriatic effect waned off by 4 h after intraocular lens implantation providing time for the institution of immediate rectification measures. ND was a peripheral temporal visual field defect (VFD) and manifested as a 100% black shadow having an inner arc with a sharp, smooth, and concave edge and outer border extending to the temporal periphery. ND disappeared when two fingers were kept blocking the ND over the affected side within ≤1” of the temple. The extent of VFD varied with eye movement. Clinically, intraocular lens is the cause of ND and not neuroadaptation.

Keywords: Cataract surgery, corneal incisional edema, intraocular lens implantation, neuroadaptation, optic neuritis, road traffic accident, visual field defect

How to cite this article:
Potharaju NR. Could this be a lead for a solution to negative dysphotopsia?. Indian J Ophthalmol Case Rep 2023;3:349-53

How to cite this URL:
Potharaju NR. Could this be a lead for a solution to negative dysphotopsia?. Indian J Ophthalmol Case Rep [serial online] 2023 [cited 2023 Jun 10];3:349-53. Available from: https://www.ijoreports.in/text.asp?2023/3/2/349/374899

This case report highlights some hitherto unreported early clinical findings, which seem to be pathognomonic of negative dysphotopsia (ND) caused by the intraocular lens (IOL). They appear before the development of neuroadaptation.

ND occurs in up to 26% after uncomplicated surgery for cataract phacoemulsification with in-the-bag IOL implantation. The ND shadows are due to the limitation of the extent of the focused image because the implanted intraocular lens is smaller than the natural crystalline lens.[1] ND is a dark peripheral temporal arc-shaped shadow or line.[2],[3] It mimics a retinal detachment or vascular insult. The cause is uncertain.[3] Until now, no definitive criteria have been published for a proper diagnosis of ND. No pathology of the eye can be found to explain ND.[4] Progress in understanding ND is hindered by the lack of sufficient objective data on the precise visual angle at which the patient sees the shadow and whether, in patients reporting an arc-like shadow, there is an inner arc with everything within it darker or a dark crescent that has an outer arc also.[3],[5]

Many observations that were made (after neuroadaptation occurred) in the past 3 decades suggested the role of the Central Nervous System (CNS) in causing ND. ND scotoma is significantly larger with both eyes open suggesting a CNS factor to ND.[2],[6],[7] ND is stimulated by contralateral light input[7] and improves if the temporal light source is blocked.[2] ND symptoms were noticeably reduced with contralateral opaque contact lenses.[7] The contralateral monocular occlusion reduces symptoms and VFD of ND in the ipsilateral eye by a mean of 65% in approximately 80% of cases.[7] Blocking temporal light in the contralateral eye with a peripherally opaque contact lens was effective in reducing the ND symptoms of the ipsilateral eye.[7] They concluded that the CNS plays a role in the etiopathogenesis of ND.[7] ND is more of a CNS adaptation and might denote the central manifestation of a local ocular disorder.[8],[9] ND symptoms are reduced with pupil dilation and are worsened with pupil constriction.[5]

No specific objective tests exist to examine the presence of either positive dysphotopsia (PD) or ND. Therefore, clinicians rely primarily on patient-reported clinical findings and outcomes. Resolving the VFD of ND will reduce the risk of bumping into objects on the side of surgery, road traffic accidents that occur while driving a vehicle or a pedestrian crossing a road and improve patient satisfaction.

  Case Report Top

The patient was a 73-year-old male neurologist with 43 years of clinical experience. He underwent left eye age related cataract extraction with a IOL implantation. He noticed an ND 4 h after surgery. His observations are tabulated [Table 1].
Table 1: Characteristic clinical findings of ND observed 4 hours after cataract extraction and IOL implantation in the left eye

Click here to view

He also observed PD mimicking an abnormally bright picture lasting a fraction of a second in the mid-periphery of the retina at the 8 O'clock position a few times a day measuring about 1/16 in the visual field. It was mostly precipitated by a voluntary saccade while trying to read the beginning of the next line in a document file while working on a 31.5” computer 1080 pixels monitor and while watching TV on a 32” Full HD TV. PD was not precipitated by a voluntary saccade if the affected eye was closed. Rarely was reflexive saccade also associated with PD. Whenever PD occurred, it could not be reproduced by voluntarily repeating the same movement.

There was no difference in ND for 43 weeks. PD disappeared at 8 weeks.

  Discussion Top

PD: Disappearance of PD at 8 weeks is due to neuroadaptation.

ND: Clinical findings alone were diagnostic of ND. Characteristics b, c, d, e, and g in [Table 1] seem to be pathognomonic of ND and exclude nonorganic causes, and lesions of the retina and CNS. In addition, the absence of an increase in the visual field area with increasing distance from the patient suggests nonorganic visual field constriction.

Anatomic localization of peripheral temporal VFD could theoretically be in A. The optic nerve, B. Retina, C. IOL, or D. Cornea [Figure 2].
Figure 1: Variation of visual field defect of negative dysphotopsia with ocular movements of the left eye (cataract extracted and IOL implanted). Please note the disappearance of negative dysphotopsia on looking to the temporal side and down (g). This does not happen with lesions in the Central Nervous System. (a). Left temporal and up. (b). Up. (c). Nasal and up. (d). Left temporal. (e). Straight. (f) Nasal. (g). Left temporal and down. (h). Down. (i). Nasal and down. Please note that the visual field defect changes on looking to the left temporal side (a, d, g). The defect is same on looking straight and to nasal side (b & c are same, e & f are same, and h & i are also same). Arrows: Visual field defect of negative dysphotopsia

Click here to view
Figure 2: Anatomical localization of a peripheral temporal visual field defect in the left eye. There are only four possible anatomical sites. (A). Optic nerve, (B). Retina, (C). IOL-intraocular lens, and (D). Cornea

Click here to view

A. Optic nerve. [Figure 2]: A surrounding pial plexus (not end arteries) formed by small branches of the ophthalmic artery supplies the posterior portion of the optic nerve and a plexus formed by small branches of the posterior ciliary arteries supplies the anterior portion. Because of this rich circulation, ischemia of the medial peripheral (carrying temporal field fibers) optic nerve does not occur and consequently, a peripheral temporal VFD does not result from ischemia.

Acute demyelinating optic neuritis is a very rare possibility. Differentiating it from ND is presented in [Table 2]. Multiple sclerosis may present with optic neuritis as the initial manifestation in 25% of cases.
Table 2: Differences between negative dysphotopsia and optic neuritis VFD

Click here to view

B. Retina [Figure 2]: Retinal detachment, retinal vascular, giant cell arteritis, anterior ischemic optic neuropathy, etc.

C. IOL [Figure 2]: ND.

D. Cornea [Figure 2]: Corneal edema at the incision location causes temporary temporal cloudiness appearing after 5 h[10] that disappears in a few weeks. It can be differentiated from ND by the symptoms [Table 3].
Table 3: Differentiation of ND from corneal incisional edema VFD

Click here to view

Role of IOL: “Illumination gap” of the nasal retina, causes ND.[2] Nasal anterior capsule override, large-angle κ value, haptic orientation, and high hyperopia are known risk factors for ND.[2]

Severe ND symptoms consistently occur in the setting of technically excellent cataract surgery, including perfect centration and uniform anterior capsule overlap of the optic.[2]

The observation that pseudophakic negative dysphotopsia may be reduced to 50% by a maneuver of rotating the intraocular lens to orientate the optic-haptic junctions at 180° thus interrupting the IOL edge in the critical nasal region of the capsular bag,[11] indicates that ND is due to the IOL. Additional proofs that confirm IOL to be the cause of ND are: reverse (anterior) optic capture, piggyback IOLs, sulcus IOL placement, neodymium: yttrium-aluminum-garnet nasal capsulectomy,[2] targeted lens pitting with Nd: YAG laser.[12] IOL exchange,[13] and supplementary implantation of Sulcoflex IOL.[14]

[Table 1] illustrates that IOL is responsible for ND and a clinical diagnosis of ND can be made inexpensively and immediately as soon as the mydriatic effect wanes off after surgery.

Whether the higher frequency of ND in the left eye[9] is related to the surgeon's right-handedness needs to be investigated.

Role of Neuroadaptation: ND is thought to be caused by a central nervous system factor for a long time.[6],[7],[8],[9],[15]

Characteristics mentioned in [Table 1] (points b to h) prove that ND is caused by the IOL itself and the CNS has no role in its etiopathogenesis. When we update our glasses, it usually takes a few days to adjust to the new glasses. When we learned about bicycling, we were able to balance in a few days. These facts mean that neuroadaptation requires a few days. Since neuroadaptation cannot occur in 4 h, it cannot be the cause of ND appearing 4 h after IOL implantation. Our clinical findings were recorded before neuroadaptation started and all earlier publications were recorded after neuroadaptation set in. Persistence of ND after 43 weeks in our case shows that neuroadaptation has not reduced it.

Hypothesis: Clinical diagnosis of VFD of ND can be made, with the pathognomonic symptoms, as early as 4 h after IOL implant as the mydriatic effect wanes off [Table 1] and exclude other possibilities with a worse prognosis.

The ability to diagnose ND at 4 h after IOL implantation opens up the consideration for many rectification treatment options at that point in time for the patient. The first is inexpensive where the maneuver of rotating the intraocular lens to orientate the optic-haptic junctions at 180° may be tried. The second option is expensive and involves the consideration of replacing the IOL with a different model. The third option is replacing the natural crystalline lens with an equal-sized IOL. Other options like optic out of capsular bag, piggyback IOL, and anti-dysphotopic IOL may also be considered. This avoids a second operation later. Since the left eye is more susceptible to ND, if there is a choice, it may be preferable to implant in the left eye first so that the same IOL and procedure may be used in the right eye also.

The clinical details presented here may help define the pathogenesis and plan appropriate treatment more effectively for ND. Because ND is more frequent in the left eye and varies with ocular movement, designing different lenses for the left and right eyes must be investigated to check if it solves the problem.

Planning for the future: Localization of ND to the IOL gives a direction to the research on the pathogenesis of ND. Research in a restricted field like IOL will save funds and it is easier to find a solution within a few years for the enigma, which is challenging ophthalmologists for the past 3 decades. Research must focus on increasing IOL's size, its orientation, placement, shape, or composition in that order singly or in combination. Trying to find a solution to the ND problem in the brain (presuming it to be responsible) will waste both money and time. Neural plasticity and neuroadaptation are highly complex phenomena and occur throughout the nervous system. Neuroadaptation is not the cause of ND. It only attempts to resolve ND after it develops. Hoping for neuroadaptation to resolve ND, weeks after it develops, is not a wise decision because adaptative plasticity can be misdirected or unadapted, and become counterproductive and harmful.[16] Whether any such complications developed in cases of ND have to be investigated by a follow-up observational study.

A pilot study of ND in senior neurologists and ophthalmologists undergoing surgery for age-related cataracts can assess the reliability of our case report, and the options for treatment of ND at 4 h after implantation.

A randomized case-control study can then assess various lens designs/surgical procedures and draw evidence-based conclusions.

Development of shorter-acting mydriatics (mydriasis lasting 1-2 hours) will enable the diagnosis of ND within 1-2 hours of surgery.

Our patient is willing to cooperate/participate in all future ND research both as a patient and a neurophysician.

  Conclusion Top

This case report presents significant clinical evidence to prove that ND is caused by IOL. Neuroadaptation, which is being blamed for decades, is not responsible. This gives a direction to future research in finding a solution to this enigma. VFD caused by ND can be diagnosed as soon as the mydriasis wanes off (within four hours), after intraocular lens implantation, using inexpensive and simple but pathognomonic clinical findings. It may be possible to resolve the issue immediately, thereby avoiding a second surgery. Resolving the VFD caused by ND will not only reduce the resultant risk of bumping into objects, road traffic accidents that occur while driving a vehicle or a pedestrian crossing a road but also improve patient satisfaction. This case report illustrates how a personal tragedy of a doctor can lead to the description of new clinical findings.

Declaration of patient consent

The author certifies that he has obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.


The help of Dr. Kamala Devi, Dr. Anil Kumar, Dr. Kai Rou Tey, Dr. Rahul, Sinduja, and Dr. Vishnu is acknowledged.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Simpson MJ. Simulated images of intraocular lens negative dysphotopsia and visual phenomena. J Opt Soc Am A 2019;36:B44-51.  Back to cited text no. 1
Masket S, Fram NR. Pseudophakic dysphotopsia: Review of incidence, cause, and treatment of positive and negative dysphotopsia. Ophthalmology 2021;128:e195-205.  Back to cited text no. 2
Adre E, Tonk R. Positive and negative dysphotopsias: Causes, prevention, and best strategies for treatment. Curr Ophthalmol Rep 2021;9:1-10.  Back to cited text no. 3
Wenzel M, Langenbucher A, Eppig T. [Causes, diagnosis and therapy of negative dysphotopsia]. Klin Monbl Augenheilkd 2019;236:767-76.  Back to cited text no. 4
Henderson BA, Geneva II. Negative dysphotopsia: A perfect storm. J Cataract Refract Surg 2015;41:2291-312.  Back to cited text no. 5
Masket S, Magdolna Rupnik Z, Fram NR, Vikesland RJ. Binocular Goldmann visual field testing of negative dysphotopsia. J Cataract Refract Surg 2020;46:147-8.  Back to cited text no. 6
Masket S, Rupnik Z, Fram NR. Neuroadaptive changes in negative dysphotopsia during contralateral eye occlusion. J Cataract Refract Surg 2019;45:242-3.  Back to cited text no. 7
Holladay JT, Simpson MJ. Negative dysphotopsia: Causes and rationale for prevention and treatment. J Cataract Refract Surg 2017;43:263-75.  Back to cited text no. 8
Masket S, Fram NR, Cho A, Park I, Pham D. Surgical management of negative dysphotopsia. J Cataract Refract Surg 2018;44:6-16.  Back to cited text no. 9
Agrawal V, Tsai R. Corneal epithelial wound healing. Indian J Ophthalmol 2003;51:5-15.  Back to cited text no. 10
[PUBMED]  [Full text]  
Manasseh GSL, Pritchard EWJ, Rothwell AEJ, Luck J. Pseudophakic negative dysphotopsia and intraocular lens orientation: A prospective double-masked randomized controlled trial. Acta Ophthalmol 2020;98:e743-6.  Back to cited text no. 11
Feng Y, Weinlander E, Shah M. Targeted lens pitting to treat negative dysphotopsia. J Refract Surg 2021;37:212-4.  Back to cited text no. 12
Weinstein A. July consultation #4. J Cataract Refract Surg 2013;39:1125.  Back to cited text no. 13
Makhotkina NY, Berendschot TT, Beckers HJ, Nuijts RM. Treatment of negative dysphotopsia with supplementary implantation of a sulcus-fixated intraocular lens. Graefes Arch Clin Exp Ophthalmol 2015;253:973-7.  Back to cited text no. 14
Osher RH. Negative dysphotopsia: Long-term study and possible explanation for transient symptoms. J Cataract Refract Surg 2008;34:1699-707.  Back to cited text no. 15
Potharaju NR. Excessive crying in children with cerebral palsy and communication deficits. Glob J Res Anal 2022;11:25-44.  Back to cited text no. 16


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Case Report
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded425    
    Comments [Add]    

Recommend this journal