Two previous reports have disclosed that Goldmann perimetry can define a scotoma induced by negative dysphotopsia (ND).1,2 The findings of the two studies are somewhat similar; however, we used the Haag-Streit model 900 perimeter, whereas Makhotkina et al2 used a traditional Goldmann perimeter.1 We also reported that contralateral monocular occlusion reduces symptoms and visual field (VF) defects associated with ND in the fellow eye by a mean of 65% in approximately 80% of cases.1 Furthermore, we noted that blocking temporal light in the contralateral eye with a peripherally opaque contact lens was also effective in reducing the ND symptoms of the fellow eye.1 This led us to conclude that the central nervous system (CNS) plays a role in ND, irrespective of the causal intraocular mechanism, the latter remaining unclear. The CNS findings were novel and remain unexplained. Among other aspects of our prior Correspondence,1 unlike patients with VF defects due to glaucoma, retinal, or neurologic disease, the patient with ND tends to be significantly more symptomatic. However, we were unable to achieve a long-term therapeutic effect with contralateral occlusion by either a patch or a peripherally opaque contact lens, in part due to poor treatment tolerance. This differs from a case report in which a recent post-operative patient with ND required eyelid surgery after injury and noted improved ND after ipsilateral ocular occlusion during healing.3
Using a contact lens with an opaque periphery for partial contralateral occlusion (Figure 1), we expanded our previous study to investigate the VF of patients with ND under binocular conditions. To our knowledge, this is the first report concerning binocular Goldmann VF testing of ND. In the present pilot investigation, patients with either monocular or binocular chronic ND (symptoms persistent beyond 3 months) were queried as before regarding improvement in ND with contralateral occlusion under ambient lighting conditions (543 lux).1 All reported improvement of ND with occlusion and all eyes were physically normal (except for uncomplicated pseudophakia), and no patient had any condition that could induce a VF defect other than ND.
Subsequently, patients had binocular Goldmann VF testing using the V4e target. To plot a scotoma, they were asked to identify when the target, moving from the periphery centrad, was first noted, when/if it became obscured or abnormal, and then when it normalized again as the target moved centrad. Next, a soft contact lens with a 7 mm central clear zone (Kontour) was applied to the fellow eye and the VF study repeated in the same fashion. The pupil size was measured before and after instillation of the contact lens using the Colvard pupillometer.
As can be observed in Figure 2, the ND scotoma is far greater in extent when both eyes are fully open than when a peripherally occluding contact lens is 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. 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). All previous reported VF studies of ND have been under monocular conditions.1–3 We have observed this VF phenomenon in 3 of 4 tested patients. The one negative test occurred in a patient with vastly improved ND over time. For this case, we could not discern a scotoma.
From the present investigation and from our previously reported study, it would appear that ND has CNS manifestations that are, as of yet, poorly understood.1 Why should blockage of temporal light in the fellow eye (contralateral) improve ND symptoms? One potential explanation could be alteration in the pupil size. However, we found no consistent change in the pupil aperture after the application of the specialized contact lens. In some eyes, there was no change, in others it was larger by 0.5 mm, whereas it was smaller by 0.5 mm in others. Therefore, we doubt that the change in the pupil size could account for our observations. Future investigations regarding functional magnetic resonance imaging studies are planned, and we anticipate that other centers will investigate binocular Goldmann VFs to corroborate and help explain our findings.
1. Masket S, Rupnik Z, Fram NR. Neuroadaptive changes in negative dysphotopsia during contralateral eye occlusion. J Cataract Refract Surg 2019;45:242–243
2. Makhotkina NY, Berendschot TT, Nuijts RM. Objective evaluation of negative dysphotopsia with Goldmann kinetic perimetry. J Cataract Refract Surg 2016;42:1626–1633
3. Wenzel M, Langenbucher A, Eppig T. Causes, diagnosis and therapy of negative dysphotopsia [in German]. Klin Monbl Augenheilkd 2019;236:767