Eccentric Fixation A failure of an eye in monocular vision to take up fixation with the fovea, but with some other point. This hardly occurs except in clinical conditions as the patient is generally not fixing with that eye anyway. It is only shown when the better eye is covered (Exception = microtropia with identity)
Four Theories as to the cause of Eccentric Fixation
Suppression Theory (Worth, 1906, Bangerter,1953)
Anomalous correspondence theory (Chavasse, 1939, Cuppers, 1956)
a change in the central area of localisation resulting from a central scotoma in the amblyopic eye
EF secondary to the development of ARC
Major problem with this theory is that the angle of anomaly is usually much greater than angle of EF
Schor (1978) :
failure of the EOM to relax from the deviation (in strabismus) = MUSCLE POTENTIATION. This is a likely cause as habitual strabismic deviation causes an adaptive after-effect which modifies the subsequent monocular localisation
Pickwell (1981) :
a sequel to an enlargement of Panums fusional area following decompensated heterophoria at an early age – eventually leads to microtropia – a loss of accurate correspondence
Also a sensorimotor theory by Cuiffreda, Levi and Selenow (1991) NB One or more of these theories may apply to any one patient
Based on each retinal receptor having its own “local sign”, which determines the direction of objects in visual space.
Refers to localisation with reference to each eye separately.
In EF the relative localisation may be as follows: - Normal or abnormal at eccentrically fixing retinal point - Normal or abnormal at the fovea of the same eye
Usually if the eccentric point continues to be localised eccentrically and the fovea centrally then patients describe objects as being slightly to one side = ECCENTRIC VIEWING.
This has a better prognosis for treatment than if localisation is abnormal.
Investigation of EF
is best to use two methods.
EF is nearly always present in strabismic amblyopia
A target is projected and focussed onto the retina and is seen by both the Px and the practitioner.
Px is asked to look at the centre of the target and the position of the fovea is noted.
Position is then recorded in diagram – also record if steady/unsteady - usually EF is slightly nasal in SOT - can calibrate using the size of the optic disc in the graticule Disc = 5 deg x 7 deg NB accommodation is usually induced using this method – change focus or cycloplegia
In amblyopia –
reduced VA by one Snellen line per 0.5 degree of eccentricity (very rough guide)
Past Pointing Test
related to localisation
carry out test initially with good eye (checks normal ability and increases confidence)
occlude amblyopic eye, hold pen 25cm in front and ask patient to touch pen with the tip of their finger
repeat with the non-amblyopic eye occluded.
If finger goes a few cm to the side then past pointing has been demonstrated (do not repeat too many times as PX adapt)
this result indicates that fixation does not coincide with the centre of localisation
Corneal Reflex Test
compare reflex position in each eye in turn (other eye occluded). The relative displacement of the reflex by 1mm = approx. 11degrees or 20 PD
eccentricity is not usually this great however making EF difficult to detect by this method.
Bjerrum Screen Method
In normal subjects the blind spot is the same angular distance from fixation in both eyes.
Plot the blind spot carefully in both eyes and compare positions
Degree of eccentricity can be measured by the difference in angular distance of blind spot from fixation in each eye
Requires good co-operation
5mm square in a 10 cm square, printed in white or red and black
amblyopes often have small foveal scotoma which shows up as a disturbance on Amsler
occurs centrally if central localisation
eccentrically if EF
this is not a very convincing test
After-image Transfer Test
After images are transferred to normally corresponding points in the other eye.
photography flashgun that is masked to provide a very bright strip of light
occlude amblyopic eye and PX fixates the centre of the strip
flash then produces a central after-image
occluder is then changed to the good eye and PX looks at a small fixation target (eg Snellen letter)
the after image then appears after a few seconds (transferred at cortical level)
Px is then asked to locate position of after-image in relation to the fixation point.
If it appears at one side of the letter = EF
an entoptic phenomenon due to characteristics of the central fovea area
seen with a brightly illuminated blue polarised field when the direction of the polarisation is rotated
looks like two darkened and opposing sections rotating in the central field
in EF they are not seen at the point of fixation but somewhere to the side or not at all if VA < 6/30
also Maxwell’s spot
Crowding phenomena : difference of 1 line can be normal but more indicates amblyopia, especially with EF
Neutral density Filters
If a ND filter is added and no reduction in VA occurs then EF is likely to be present
Speed of Accommodation
Much slower in EF (?also in other amblyopes)
Assessment of Fixation
Centricity of Fixation (central vs eccentric)
Quality of fixation (steady vs unsteady)
Pattern of fixation (drifts, saccades, nystagmus)
Percent foveation (30second visuoscopy)
Directional bias (nasal, temporal etc)
Subjective localisation of primary visual direction
Zero retinomotor point
Treatment of EF
As in amblyopia, have to encourage foveal fixation
Direct Occlusion alone may improve fixation but often a slight eccentricity remains
Pleoptic Treatment – desensitises eccentrically fixing area
After image transfer – use to locate foveal fixation
NB Established EF is hard to remove. Remember in amblyopia treatment VA will not improve beyond that expected for eccentrically fixating point
Treatment of EF
Cuiffreda, Levi and Selenow (1991)
2 types of treatment strategy
Patient A - direct patching - break down inhibition of dominant eye
Patient B - break down the EF - fine fixation tasks under controlled conditions
brain to look to side to make centre at fixation point
Not usually very successful and can not be done at home.
Microtropia (Microsquint, microstrabismus)
a misalignment of the eyes with an angle deviation so small (less than 5 degrees) that it would usually be controlled except on dissociation of the eyes in which case in becomes a phoria.
Certain characteristic features
Frequently presents between ages 2-3 years but may be overlooked until later life where it is found on routine check as VA is slightly low.
Often made evident by the crowding phenomenon.
Amsler charts are useful for demonstrating the abnormal fixation pattern
Presence of HARC in small angle squint is associated with eccentric fixation and amblyopia
Is invariably eso, exo is rare
Very subtle tests are required to discover microtropia
Small angle (<6∆)
usually 1.50D or more. Occassionally the patient has equal refractive errors.
usually VA is reduced by 1 or 2 lines only (6/9 – 6/12)
always occurs in microtropia.
ANGLE OF ECCENTRICITY = ANGLE OF SQUINT -
no movement is detected on the CT (the area of the retina where the image falls in binocular conditions is the same as the eccentrically fixing area)
Occasionally the degree of EF < angle of squint and a very small CT movement can be seen (small relative or absolute scotoma at the fovea)
the retinal area where the image falls in Pxs habitual vision = anomalously corresponding area = area used for monocular fixation = MICROTROPIA WITH IDENTITY
Most microtropia’s are of this type.
this is a fully adapted strabismus in terms of both motor and sensory aspects.
peripheral vision provides fusional impulses that help maintain the eyes in their straight position.
Can be measured like prism vergences.
in many cases the angle of deviation increases on alternating CT or if one eye is covered longer than usual.
An SOP is seen superimposed on the microtropia.
This is also called a monofixational heterophoria (due to the eye moving from its adapted position to the full angle of squint under the cover)
a low grade stereopsis has been reported.
Investigation and Diagnosis
the presence of amblyopia in one eye is usually the first clue that microtropia may be found.
Crowding phenomenon present and letters may be missed due to the central scotoma.
The presence of eccentric fixation should be checked for using an ophthalmoscope, visuscope.
The EF may be associated with ARC in the microtropia.
Eccentric fixation = angle of anomaly (no shift on CT)
Eccentric fixation does not equal the angle of anomaly (shift on CT).
Not usually a strabismic movement but may find esophoria in monofixational syndrome.
This could result in microstrabismus being missed.
4-Dioptre Prism Test
4 base out prism is placed before the dominant eye
the image moves across the retina and the eye moves to take up fixation.
The non-dominant eye moves laterally in the same direction (Herings Law of equal innervation) as it is not fixing – VERSIONAL movement is seen.
The prism is then removed and a recovery versional movement is seen.
The prism is then place before the amblyopic eye.
This time the image is moved across the retina within the suppression area: no movement of either eye. AMBLYOPIA + NO CT MOVEMENT + POSITIVE 4∆ TEST = MICROTROPIA
Bagolini Lens Test
Should get HARC – streak passes through the spot, with or without a suppression gap.
Scotoma may be demonstrated due to the eccentric fixation.
Classification of Microtropia
Primary – remains constant throughout life and is rare.
A primary microtropia which becomes decompensated particularly between 1 –3 years as a result of an accommodative element or superimposed phoria
Secondary – follows optical or surgical correction of a concomitant squint
Lang – 3 types of microtropia (reference to fixation)
Eccentric Fixation with ARC, where the angle of anomaly is greater than the degree of eccentricity
Eccentric Fixation with ARC where these angles are the same On CT 1 and 2 will give positive results whilst 3 gives a negative CT Also 3 gives a sensory adaptation to the deviation envisaged by Cuppers in his correspondence theory for the development of eccentric fixation
The mechanism is not fully understood.
It is likely that the condition arises as a response to a scotoma that occurs in the foveal area of one eye, usually due to a blurred retinal image caused by uncorrected anisometropia.
Fixation is therefore established at the edge of the scotoma in an area of the retina that is not suppressed.
This implies that it develops on the basis of eccentric viewing.
It is natural that the onset of EF should be followed by the development of HARC.
SOP causes an expansion of Panums areas with an alteration of visual direction
this results in ARC that in turn causes the development of eccentric fixation because of deep suppression at the fovea.
Problems with this theory
Difficult to explain why this does not happen in all patients with esophoria (unless some additional abnormality is present)
Does not explain microtropia in the absence of SOP.
Familial Studies – Lang claims ARC is inherited as primary congenital defect
Refractive Error Correction, especially in high anisometropia.
Aniseikonia is often a problem.
Contact lenses correction may help.
Treat underlying amblyopia by occlusion of non-squinting eye (if patient <6 years old).
Full time occlusion of the fixing eye will occasionally produce a complete cure of the esotropia with restoration of normal visual and stereo acuity.
Regular review – improvement must be seen within 4 months or discontinue.
Orthoptics are not appropriate.
In patients >6 years – correct refractive error, otherwise do not treat the microtropia.
In most cases correction of the refractive error, if necessary, is the only profitable action.