Transcript Dragged Fovea Diplopia Syndrome

‘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, p1455-1462
De 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.
 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, Harvard
Neurology. 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.
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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.
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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
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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
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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
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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
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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
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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:
Metamorphopsia
Aniseikonia
…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 imbalance
Need 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