‘RETINAL DIPLOPIA’

Inspired by Sue Strachan and Mr GA

From Sue:

Dragged Fovea Diplopia ‘Syndrome’

The Dragged Fovea Diplopia Syndrome consists of central diplopia in the presence of peripheral fusion, secondary to dragging of the fovea in one or both eyes by retinal disease. The central diplopia cannot be eliminated by prism therapy or eye muscle surgery. The “lights on-off test” [on: central diplopia; off: peripheral fusion, no central diplopia] has proved pathognomonic for this syndrome. Many patients benefit from partial monocular occlusion with Scotch Satin Tape.

REF: Ophthalmology Vol 112, Issue 8, 8/ 2005, p1455-1462De Pool, Campbell, Broome and Guyton

LK comment

This is a diagnostic test, not a ‘syndrome’. Not enough effort was made to fix or compensate or exploit every barrier to sensory and motor fusion e.g. inadequate effort to compensate for aniseikonia, to operate for torsion alone, to seek a suppression area with prisms,….

Patient GA aged 43 y interested in laser refractive surgery Dec 1998

RGP lens wearer for many years

Rx R -9.00/-0.25x125 L -9.00/-1.50x5. 6/6 R&L

A few fine drusen at right macula, mild pigmentary disturbance at left macula.

Advised against LASIK by surgeon due to border flat K readings and risk of poor quality vision post-surgery.

Proceeded with intra-ocular contact lens surgery:

R 26/05/99 L 13/07/99

VA 6/6++ both eyes post operatively with low minus refraction. Very happy!

Returned 09/05/01 reporting reduced quality vision.

Early lens opacities noted both eyes.

Resumed contact lens wear (soft torics) as myopia increased with lookovers for near

cataract surgery and removal of ICLs in early 2005.

Right IOL angled forward in immediate post-operative period and so one month later the IOL was repositioned. Left surgery was uneventful.

Visual acuities returned to 6/6 R&L but 6 months later the right VA had dropped to 6/12 due to posterior capsule opacification.

YAG laser returned the right VA to 6/6.

Wore multifocal glasses for driving and near happily but returned reporting trouble with night driving and small print in February 2007.

VA still 6/6+ R&L but thickening of the capsulotomy edge was noted.

3 months later the thickening was markedly more pronounced within the pupil zone and the R VA was down to 6/15+.

YAG laser was repeated but the VA did not improve and so GA was referred for a retinal investigation.

Thickening of the right macula and epiretinal membrane was diagnosed with a coincidental peripheral retinal detachment being found.

vitrectomy, membrane peel intraocular gas and cryo were performed on 31/05/07.

Retinal surgeon was happy post-operatively but GA returned for refraction reporting symptoms of right micropsia as well as some vertical double vision, relieved by occluding one eye.

Refraction showed a 3∆ right hyperphoria and so a new right spectacle lens was prescribed incorporating 3 ∆ BD RE.

The double vision was not alleviated by the prism and so GA was referred back to his retinal surgeon with suspicions of “Dragged Fovea Diplopia Syndrome”.

Retinal surgeon refers GA to Dr Lionel Kowal – appointment scheduled 24/09/07.

"Retinal diplopia" associated with macular wrinkling. Barton JJ.Department of Neurology, HarvardNeurology. 2004 Sep 14;63(5):925-7

3 pts with chronic binocular vertical diplopia and small comitant hypotropic deviations due to macular displacement (heterotopia) associated with monocular retinal wrinkling are described… idiopathic in 2 and secondary to treated retinal detachment in the third.

Diplopia secondary to aniseikonia associated with macular disease.

We identified 7 patients who had binocular diplopia concurrent with epiretinal membranes or vitreomacular traction.

In addition to complete ophthalmologic and orthoptic examinations, evaluation of aniseikonia using the Awaya New Aniseikonia Tests (Handaya Co Ltd, Tokyo, Japan) was performed on all patients.

6 of the patients had epiretinal membranes and 1 had vitreomacular traction.

Diplopia secondary to aniseikonia associated with macular disease.

All 7 patients had aniseikonia, ranging from 5 - 18%. In 5 pts the image in the involved eye was larger, and in the other 2 patients it was smaller than in the fellow eye.

All patients had concomitant small-angle strabismus and at least initially did not fuse when the deviation was offset with a prism. Response to optical management and retinal surgery was variable.

Diplopia secondary to aniseikonia associated with macular disease.

CONCLUSIONS: Aniseikonia caused by separation

or compression of photoreceptors can be a contributing factor to diplopia and the inability to fuse in patients with macular disease. Concomitant small-angle strabismus and the inability to fuse with prisms may lead the clinician to the incorrect diagnosis of central disruption of fusion. Surgical intervention does not necessarily improve the aniseikonia.

Nonsurgical management of binocular diplopia induced by macular pathology. Silverberg M, Schuler E, Veronneau-Troutman S, Wald K, Schlossman A, Medow N Arch Ophthalmol. 1999 Jul;117(7):900-3

7 pts had constant vertical diplopia caused by various maculopathies, including subretinal neovascularization, epiretinal membrane, and CSR.

VA 20/20 to 20/30 in the affected eye. 6 had a small-angle, comitant hyperdeviation

with no muscle paresis. Sensory evaluation demonstrated peripheral fusion and reduced stereoacuity. Neither prism correction nor manipulation of the refractive errors corrected the diplopia.

Nonsurgical management of binocular diplopia induced by macular pathology.

A partially occlusive foil (Bangerter) of density ranging from 0.4 to 1.0 was placed in front of the affected eye to restore stable, single vision.

Bangerter foil eliminated diplopia in all pts. 2 pts elected not to wear the foil - 1 pt was afraid of becoming dependent, the other was bothered by the visual blur.

VA in the affected eye was reduced on average by 3 lines. All patients maintained similar sensory fusion, 2 having reduced stereoacuity. Symptoms returned when the foil was removed or its density was reduced.

[Disturbances of binocular vision in macular heterotopia]

Schroeder B, Krzizok T, Kaufmann H, Kroll P. Tractive translocation of the macula (secondary

macular heterotopia) may result in disturbance of binocular vision.

40 yo male who had decreased acuity and loss of binocular vision for several years due to episodes of uveitis with intravitreous hemorrhage and cataract formation. After bilateral vitrectomy and cataract extraction good VA was restored in both eyes.

[Disturbances of binocular vision in macular heterotopia]

Schroeder B, Krzizok T, Kaufmann H, Kroll P. Postoperatively, the patient monocularly

complained about disturbed egocentric localization (tilting of the visual environment, "past-pointing") and metamorphopsia.

Binocularly he was confused by double vision with tilted images.

Both maculae showed a tractive translocation of 15 degrees downward.

Measurements of binocular alignment with the tangent screen showed excyclotropia of 8˚ and exotropia of 7˚

[Disturbances of binocular vision in macular heterotopia]

Schroeder B, Krzizok T, Kaufmann H, Kroll P. Haploscopic examination with fusion images

suggested that sensorial fusion was not possible even with perfect ocular alignment due to disturbed relative retinal localization (obligate fixation disparity).

THERAPY AND OUTCOME: Initially, full time occlusion of the left eye was required. After improvement of symptoms occlusion therapy was slowly tapered. Within one year the patient had learned to suppress the image of his left eye and reported only minor residual visual disturbances even without occlusion of his left eye.

[Disturbances of binocular vision in macular heterotopia]

Schroeder B, Krzizok T, Kaufmann H, Kroll P.

CONCLUSIONS: Secondary translocation of the macula monocularly results in a disturbance of egocentric localization and in metamorphopsia. Binocularly doubled vision with tilted images and a loss of sensorial fusion are seen. With monocular vision, perceptual adapting to the aberration in egocentric localisation is possible within weeks by reallocation of the retinal meridians in the central nervous system. Binocular improvement of symptoms is limited to the learning of suppression. Improvement of binocular symptoms by adaptation of retinal correspondence does not occur

[Acquired vertical diplopia in macular dystrophy as a model for obligate fixation disparity]Steffen H, …. Ophthalmologe. 1996 Aug;93(4):383-6

In patients with obligate fixation disparity central objects may be perceived as double when peripheral fusion is achieved. The diplopia cannot be resolved with prisms because the fusional power of the periphery is stronger than the central power. A different cortical integration of the peripheral and central parts of the retina is thought to be the underlying cause.

[Acquired vertical diplopia in macular dystrophy as a model for obligate fixation disparity]

We report on the clinical findings in a 45-year-old man with macular dystrophy who complained of binocular vertical diplopia of up to 1 degree. Investigation with the phase-difference haploscope revealed inhomogeneous retinal correspondence in the vertical plane, with a displacement of the visual field center relative to the periphery by 0.6 ˚. We suggest that paracentral scarring had caused displacement of receptors such that the center and the periphery could not be fused simultaneously. The case represents a model for a retinal origin of fixation disparity.

LK: Things to look for…Sensory Barriers to fusion:MetamorphopsiaAniseikonia…can ‘allow’ a small [objectively trivial] phoria to become a

symptomatic tropia

Motor Barriers to fusion:Diplopia may be due to macular displacement or to muscle

imbalanceNeed both Subjective and objective measurements of diplopia

[4∆ superimposes images, but cover test is 0 or 6∆]Torsion often missed : surgery requ’d to fix this