Wednesday 3 December 2008

Microtropia

"A misalignment of the eyes with an angular deviation so small (less than 5 degrees) that it would usually be controlled except on dissociation of the eyes, in which case it becomes a phoria."
  • Cosmetically fine and eyes work 'almost binocularly' (see later)
  • Often no movement seen on cover test
  • You could call it a strab that is 'perfectly adapted' - the EF and ARC are at the same point
Characteristic Features
  • Freq presents betw 2-3 yrs but may be found later in life when VA in one eye slightly low
  • Often made evident by crowding phenomenon
  • Presence of HARC in small angle strabismus is assoc w/EF and amblyopia
  • Normally ESO, EXO is rare
General Characteristics
  • Small angle (less that 6 prism dioptres)
  • Usually 1.50D anisotropia or more
  • Amblyopia but usually reduced VA to 6/9 or 6/12 only
  • EF always occurs. ANGLE OF ECCENTRICITY = ANGLE OF STRABISMUS thus no movement on cover test. The area on which the image falls in binocular conditions is the same as the eccentrically fixing area
  • Harmonious ARC - retinal area where img falls in px's habitual vision = anomalously corresponding area = area used for monocular fixation = "Microtropia w/identity"
  • Peripheral fusion which helps eyes to maintain their straight position
  • Monofixation Syndrome: in many cases the angle of deviation increases on alternating CT or if one eye is covered longer than usual giving an ESOP superimposed on the microtropia.
  • Stereopsis - low grade reported
Investigation & Diagnosis
  • VA: presence of amblyopia in one eye is usually the first clue. Crowding phenomena present and letters on chart might be missed due to the central scotoma.
  • FIXATION: EF (check using ophthalmoscope) present and may be assoc w/ ARC. Will be either (1) EF = angle of anomaly giving no shift on cover test or (2) EF doesn't equal angle of anomaly giving a shift w/CT
  • CVR TEST: May find esophoria but not usually a strabismic movement
  • 4D PRISM TEST placed before dominant eye - img moves across the retina and the eye moves to take up fixation. The non-dominant eye moves laterally (Hering's) in the same direction as it is not fixing so a VERSIONAL movement is seen and another recovery one when the prism is removed. If you put the same prism in front of the non-dom eye then there won't be any movement at all as the image has been moved across the retina and within the suppression area.
  • AMBLYOPIA + NO CT MOVEMENT + POSITIVE 4BASEOUT TEST = MICROTROPIA
  • BAGOLINI: Should get HARC - streak passes thru spot with or without a suppression gap.
  • AMSLER: Scotoma may be demonstrated due to the EF
Classification of Microtropia
  • Primary - remains constant throughout life and is rare
  • A primary microtropia which become decompensated particularly between 1-3 years as a result of an accommodative element or superimposed phoria
  • Secondary - optical or surgical correction of a concomitant strabismus
Lang's Classification of Microtropia
  • Central Fixation
  • Eccentric Fixation w/ARC where ang. of anomaly > degree of eccentricity
  • Eccentric Fixation w/ARC where angles are the same
First two will show up on cover test. Third one gives a sensory adaptation to the deviation.

Eccentric Fixation

A failure of the eye to take up fixation with the fovea and using some other point on the retina instead. In strabismic patients this is only seen when the better eye is covered (unless the patient has microtropia with identity).

Between the two eyes there is 'relative localisation' which is based on each receptor having its own 'local sign' which determines the direction of objects in visual space. It's localisation with reference to each eye separately. In eccentric fixation the relative localisation could be normal or abnormal at the eccentrically fixing point or normal/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 and this is known as eccentric viewing. This has a better prognosis for treatment that if the localisation is abnormal.

How EF is investigated

EF is nearly always present in strabismic amblyopia. The best way to investigate it in practice is with the ophthalmoscope w/the graticule on. If you get the patient to look straight into the light at the centre of the target the position of the fovea relative to that target can be noted. In esotropia the EF is usually slightly nasal. You can get a relative measurement by using the scale. NB graticule disc is 5x7 degrees. You induce accomodation using this method so cycloplegia/changing focus is useful.

The past pointing test involves touching the px's finger to the tip of a pen 25cm away, first with the good eye to increase confidence, then with the good eye occluded. If the patient's finger goes slightly to one side of the pen this indicates fixation doesn't coincide with the centre of localisation. The corneal reflexes can also be assessed by occluding one eye in turn. Relative displacement of the reflex in the bad eye by 1mm = about 11 degrees or 20PD. This is a gross test as eccentricity isn't usual that great. Other tests include the Bjerrum screen, Amsler chart, after image transfer test, Haidinger's brushes, acuity measurement and ND filters. The speed of accommodation is much slower in EF but also slower in other amblyopes.

Treatment of EF

As w/amblyopia treatment you have to encourage foveal fixation. Treatment of EF isn't done often and is far too time consuming for a mild effect.
  • Direct occlusion alone may improve fixation but often a slight eccentricity remains
  • Pleoptic treatment desensitises the eccentrically fixing area
  • After-image transfer is used to locate foveal fixation
NB Established EF is real hard to remove. In amblyopia treatment VA won't improve beyond that expected for an eccentrically fixing point.

Tuesday 2 December 2008

Critical Period In Humans

Von Noorden (him again) demonstrated that human amblyopia was accompanied by structural changes in the visual pathway. The LGN of a human amblyope was examined and cells in the parvocellular layers innervated by the amblyopic eye were about 18% smaller than the equiv from the other eye. The decrease in size was more pronounced in the layers receiving crossed fibres (1,4 and 6)

Preferential looking techniques have been used in thee past to monitor VA and stereo in both human and monkey infants w/convergent strabismus. Recent studies suggest VA is originally equal and coarse stereopsis is present. If strabismic infants below 2 are tested wearing prisms to correct the deviation then coarse stereopsis can be demonstrated but it can't without the treatment. The deviating eye doesn't actually develop amblyopia until after 6 months of age. Esotropia can be detected early w/a cover test.

Few deficits lead to amblyopia before six months of age. Emmetropisation sorts out refractive errors as long as they are modest within 6-12mths. An Rx needs to be persistent for two years or more from an early age before a permanent VA deficit occurs.

Cataract and other forms of stimulus deprivation (ptosis?) have a much more severe effect than anisometropia/astigmatism over a shorter period. If your baby has a congenital cataract then it needs to be removed pronto and the removal needs to be followed by a period of vigorous therapy. Weeks of deprivation can have a substantial effect between 6-18 months and months of dep can have an effect until 8 years of age.

In strabismic patients amblyopia and binocular function (w/stereopsis) must be considered. Amblyopia doesn't seem to develop in congen. esot until close to 1yr of age. Acuity differences didn't exceed normal limits until 9-11 months. The period of peak sensitivity lies between nine months and two years and then sensitivity declines until around the age of 8. Stereopsis in untreated esotropes is crude at best. If it's at worst alignment before 1.5 years can get it up to the dizzy heights of 'very crude'. Alignment after 1.5 years of age won't provide stereoscopic vision.

Occlusion therapy is the most common therapy in the treatment of amblyopia but its efficacy is unknown. Not good really. Retrospective studies have shown that 50% of patients show a marked improvement in VA following occlusion. These outcomes were independent of age. Occlusion must be administered with care to avoid the dreaded 'reverse amblyopia'. If the good eye is patched 50-70% of the time and both eyes open the rest of the time it can be avoided. The critical period for the cure of amblyopia seems to be longer than the critical period for its creation.

Summary

3 periods of development in the visual system
  • Prestereoscopic (0-4 months) - acuity develops and direction and orientation specificity are refined
  • Onset of Stereopsis (4-6 months) - stereopsis goes from zero to adult-like levels within a month at the same time as ocular dominance columns segregate
  • Poststereoscopic (6-24 months) - acuity continues to develop
Restoration of BV may only be possible in the first 18 months of life although less dramatic improvement may be seen in px up to 3.

Restoration of VA depends on who you ask; Von Noorden thinks it's only really successful up to 5 years and Birbaum thinks 16! Experience suggests <6>10 little success.

Animal Studies of Abnormal BV Development

Studies have been limited. Well, not that limited but you can't just patch a babies eye, ruin its BV and then kill it to assess how the visual cortex has developed. It's not allowed. You can do it on cats and macaque monkeys though! That's probably still against many people's wishes but ho hum. Hubel and Wiesel did the most famous early work. Here's what they found w/cats
  • VC of neonatal kitten possesses at least the skeleton of organisation present in adults. Orientation columns are present even before the eyes are opened but they subsequently become modified by experience.
  • Disruption of binocular input via unilateral eye closure, alternating eye occlusion or artificial strabismus completely disrupts cortical binocular interaction
  • Complete binocular deprivation actually has less effect than two monocular ones. It doesn't abolish visual responsiveness with the finality that monocular dep does.
  • The physiological effects of abnormal visual experience are mostly confined to the cortex and aren't expressed to any great degree in the LGN. Changes in the LGN are probably due to suppression of the bad eye which in turn alters the neural connections between cortex and LGN.
  • The effects of abnormal vis.exp. are only obtained during the moggy's critical period early in its life
  • Short periods of occlusion produce severe changes, longer irreversible. When the cat reaches visual maturity, boom! Permanent changes!
The visual system is more plastic and stays more plastic at higher levels of processing. The retina is pretty much hard-wired but the output layers of the primary visual cortex are relatively very plastic indeed! Hubel and Wiesel also saw (when they used monkeys) that the critical period in the visual cortex for the magnocellular system ends earlier than that of the parvocellular system. When reverse suture was done at 3 weeks of age the open eye can reverse the effects of the initial deprivation for the parvocellular system but not the magnocellular system.

Critical period for monocular deprivation in cats starts at 3 weeks, monkeys soon after birth, peaks at one month and ends in one year. It's 0-3 years in humans. The critical period for ocular dominance changes starts soon after the eyes open and continues until some time near puberty.

The peak of the critical period for ocular dominance occurs when ocular dominance columns in V4 (which receives equal input from the right and left eye) are segregating and cells sensitive to disparity are being formed. These crucial peaks:

  • Cats 4-6 weeks
  • Monkey one month
  • Humans 3-5 months
As you may have guessed functions requiring higher levels of processing have later sensitive periods. Interestingly some functions remain plastic until a far later stage in life. If some random human loses its good eye the amblyopic eye can show a marked improvement in VA.

Summary
  • Mammals compensate for optical deficits occuring at a young age by anatomical and physiological changes @ the visual cortex. There's very little compensation at the retina and LGN.
  • Animal studies have shown the plasticity of the immature visual system and the importance of a sharply focussed image in both eyes to normal binocular visual development.
  • Early diagnosis/treatment of infants at risk of amblyopia is important!

Review of Pathway Underlying Vision

  1. Partial decussation allows binoc interaction @ VC
  2. Visual Cortex = first level of convergence of signals from the two eyes
  3. Retina & LGN cells have circular receptive fields but cortex has rectangular visual fields which respond best to line stimuli at a particular meridian
  4. Cells in the cortex are orientated in a columnar manner
  5. Majority of cortical cells are binocularly driven but not equally influenced by each eye
  6. Groups one and seven are monocular
  7. Group four is equally responsive
  8. When identical stimuli are presented to both eyes the firing rates of most cortical binocular cells exceed the sum of the individual firing rates for each eye. These cells may provide the basis for fusion.
  9. There are binocular disparity cells. The optimal stimuli for a few of the binocular cells are not located at corresponding regions of the visual field of the two eyes - they are shifted horizontally. These cells may provide the basis for stereopsis.

Assessing Binocular Function in Children

Stereopsis

At birth the mechanism req. for binocular interaction is not present. At 3-4mths the binoc. cells in the cortex receive input from both the right and left eyes and gross stereo is present. This reaches adult levels at 6mths according to computerised preferential looking, w/a slower improvement in clinical tests. Sensitivity to pictorial depth info doesn't develop until after 6 months. Stereopsis is an important screening technique - loss of stereopsis can often mean development of strab/amb or blur from uncorrected refractive error. Gross stereo doesn't necessarily rule out the possibility of milder levels of amb/aniso/strab eg microtropia.

Accommodation

Newborn infants are capable of accommodation but aren't too accurate. They are fairly accurate by 3-4mths. Younger kids are fairly insensitive to blur compared w/older kids and adults.

Convergence

Appropriate vergence eye movements are found in infants below 2mths of age. The ability to maintain constant fixn (eg w/moving objects) and alter convergence over large ranges improves w/age. The response is well developed by 6mths but acc and conv systems aren't correlated until at least two months of age

Assessment of Infants

  • Neonate is visually responsive
  • Need to differentiate between normal and abnormal visual development
  • Max info in the shortest time
  • First do VA, Cover test, motility, stereo. If kid has good VA and stereo Rx not likely to be a problem
  • Use appropriate tests and make it fun
INFANTS
  • Simple obs. look for saccades etc
  • Behavioural tests - alternate occlusion, visual cliff - stereopsis
  • VA: <6mths>6mths pref looking @40cm, tracking (OKN), VEPs.
  • Hirschberg - central + symmetrical. 1mm diff = 20D squint
  • BV - 20D base out - eg base OUT in front of RE: eyes turn to left then LE converges - fusional movement
  • Cvr test w/interesting targets and hand as occluder
  • Stereopsis - LANG or Frisby if >7mths
  • Ret - gross differences between eyes or large Rx, near ret, cyclo
1-2 YEARS OLD
  • Cover test, motil, ret, ophthalmoscopy
  • VA w/Cardiff cards prefer pref looking w/picture, vertical so better for px w/nystagmus
  • Kay's Pics 18mths-3yrs
>3 YEARS OLD
  • H+S, VA, motility, stereo, TNO, Frisby, Titmus
  • Cyclo ret, ophthalmoscopy
  • VA w/Sheridan Gardner - child points to letter, cambridge crowding cards, LogMAR crowded

More on Development

The visual system develops at all levels of the visual pathway after birth. From cortex to retina.

Retina
  • At birth perip retina well developed (temporal bit more than nasal)
  • Postnatally most important change is @ macula. Recent studies show development of fovea lasts beyond 3rd postnatal yr, when foveal width + cone diameter have reached adult levels.
  • Much of the postnatal development of VA results from foveal cone maturation.

Myelination in visual pathways
  • Incomplete at birth. Midbrain fully myelinated @ 3 months, Optic nerve/tract @ 2 yrs, extrastriate areas/intracortical neurones @ mid childhood

Cells
  • Number of cells is complete @ birth but they grow in size/synapse numbers/interconnectivity especially during first 6 mths. Max density occurs @ 8mths-2yrs then declines to adult levels (60% of max) by age 11
How we objectively assess visual function
  • Preferential looking - can do VA, stereo acuity, vernier acuity, colour vision, dark adaptation
  • VEPs - w/flash & patterned stimuli, applicable to any age, VEP disappears when pattern can no longer be resolved
  • OKN - repetitive eye movements induced by moving visual field VA = finest pattern that induces the movement
VEP data shows better visual performance in general as you aren't relying on the child to do something, merely recording the amount of activity in their cortex. VEP acuity levels are adult like at 6-8mths (PL @ 3.5yrs - correlates well w/data on cone density).

Contrast Sensitivity
  • Newborn - 1 month don't show low freq attenuation. Sensitivity greatly reduced
  • At 2-3 mths shape of function similar to adult one but is shifted to lower spat.freq. and lower sensitivities
  • CSF nearly adult-like at seven months (VEP) or 3-5 yrs (behavioural data)
Refractive error

  • Newborn around +2.00 with SD of +2.75
  • 6-8 yr old +0.25 SD +1.00
  • Passive emmetropisation occurs w/normal eye growth. Optical bits decrease in power to comp for eye growth, reducing Rx
  • Active emmetropisation is less understood but it's the role of visual feedback in controlling eye growth. Visual system seems to recognise the value/direction of refractive error and guides the growth accordingly. Can be disrupted by congen.cat, ptosis etc
  • 80% of full term kids hyperopic. Range of refractive errors tends to decrease during first year of life. Hyperopia declines in the first year onset 3-8 months. In 82% of children emmetrop. complete within 12 months
  • Astig common during first 18 months. Most of it is corneal
  • If emmet. fails and rx is +3.50 or more/+0.75 astig into the second year then incidence of amblyopia/strab is greatly increased.
  • Anisometropia not the norm in kids older than 2-3months of age.
  • Significant Rx after one year of age = +3.50 hyperopia, +1.00D astig, +1.00D anisometropia.
  • Best to correct any myopia if significant in the second year. Premature babies tend to be more myopic

Causes of Dissociation of Ocular Motility (of)

1. DEVELOPMENTAL
  • Failure of orientation fixn (anomalies in central vision, fov nervous system, occlusion, v blurred image, strabismus) - CONGENITAL NYSTAGMUS innate attempts to fixate
  • Failure of conjgate fixn - COMITANT STRAB
  • Failure of disjuntive reflex - ANOM OF CONVERGENCE/NEAR STRAB
  • Stress of corrective fusion reflex - HETEROPHORIA
  • Failure of conj. eye movements - CONGEN/INFANTILE INCOMITANT STRAB
2. ACQUIRED
  • Pathological accident in neuro-muscular mechanism - NON COMITANT STRAB
  • Path. accident in central mechanism - CONJUGATE DEVIATION (eg gaze palsy)
  • Disruption of fixn/a postural mechanism - ACQUIRED NYSTAGMUS

Development of BV

Although all the visual apparatus is intact soon after birth BV is not inborn but must be acquired gradually during the first few years of life. Several factors affect the development of BV

Motor Mechanisms favouring development of BV are concerned w/maintenance of the two eyes in the correct position at rest and during movement

Anatomical factors: structure of bony orbit & contents, structure of eye and posn in orbit (eyes should be visually aligned correctly at rest - slightly divergent. This is only apparent when px is dead)

Physiological factors
  • Postural reflexes - these show how the head and eyes work together, independent of visual stimuli. The eyes are maintained in their correct relative posn in the orbit so that the visual axes are correctly aligned despite changes in the head rel. to the body etc. Dolls head phenom. UNCONDITIONED REFLEXES THAT DEVELOP @ BIRTH
  • Fixational reflexes - maintenance of two eyes in the correct posn in the orbit. Vis axes aligned as a result of visual stimuli reaching visual cortex. GRADUALLY DEVELOP OVER FIRST FEW YRS OF LIFE
Those fixational reflexes in mo' detail

  1. Orientational fixn reflex - ability of each eye INDEPENDENTLY to fix a definite object. Depends on each retinal receptor having visual spatial sense (in turn need functioning retina & adequate FOV). NO BINOCULARITY INVOLVED. Is present @ birth feebly DEVELOPS AS MYELINATION OF NF DEVELOPS & IS COMPLETED W/IN 2-3 WKS. NB Vision at birth is less than 6/60 - the fovea is not developed @ birth - fixation reflexes are present but the VA is too poor for them to be brought into use.
  2. Re-fixation reflex (saccades and pursuits) - develops shortly after fixn reflex - the ability of the eye to retain fixn of a moving object (passive) or change fixn from one object to the other (active). STILL NO BINOCULARITY. CAN DO THIS BY 10-12 WKS AT MOST
  3. Conjugate fixn reflex - fixn reflex applied to both eyes at the same time - both eyes retain fixn during versional movement. USUALLY PRESENT WITHIN 5-6WKS OF BIRTH AND WELL ESTABLISHED BY 6 MONTHS. Should be able to do motility test then
  4. Disjunctive fixn reflex - both eyes retaining fixn at same turn during vergence movement. Develops later than (3), WELL ESTAB BY 6 MTHS.
  5. Corrective fusion reflex - elaboration of (3) & (4) - permits eyes to function binocularly even under conditions of stress. FUNCTIONS @ 1YR BUT ONLY FULLY AT 5 YRS. Should be able to do 20 base out prism test & see the fusional movement.
***Critical period for establishing cent. fixn = first 3 mths of life. Can easily be lost during this time. Plastic period is up to about 5 yrs.
***Critical period for BV is the first year, but can still go wrong in plastic period

Sensory Mechanisms (visual apparatus, extrinsic oc. muscles)
  1. VA - adequate degree of central vision dependent on reasonable integrity of fovea & macular elements, refracting media of the eye, degree of refractive compatibility between the two eyes & adequate perip. vision
  2. NORMAL CORRESPONDENCE betw retinal recep of the two eyes - stimulus of corresponding visual points despite existence of 2 separate patterns of stimulation
  3. HEMI-DECUSSATION OF ON FIBRES @ CHIASMA enables nerve fibres from corres. areas of the two eyes to become associated with one another ultimately in visual area of occipital cortex. Become closely assoc in optic radiations & near termination of fibres in the visual cortex
  4. PROPRIOCEPTIVE IMPULSES OF THE EXTRINSIC OC. MUSC. This provides brain w/sensory info. Not known if plays role in BV development
Central Mechanisms - act of fusion & cortical control of sensory movement

  1. Fusion - single picture of obj built up by activity of the striate areas on both sides of the vis.cort. and the final analysis is implemented by the higher visual centres - the relatively crude visual image of the striate area is given meaning & is integrated w/other sensory inputs/past experience. ANATOMICAL/PHYSIOLOGICAL POTENTIAL PRESENT @ BIRTH, ESTAB. GRADUALLY DURING FIRST YEARS OF LIFE. All the different fixation reflexes need to be working properly for it to be maintained.
  2. Cortical Motor Control - the integrity of parts of the cerebral hemisphere controlling cranial nuclei concerned in final efferent impulses to extrinsic ocular nuclei
Summary

All of the the above mechanisms develop side by side and each require the others to be functioning correctly - one visual system. They are all conditioned reflexes w/the exception of the postural reflex and depend on visual stimuli. If px has congenital cataracts you have to get rid of em fast!

Critical period(s)
  • 2-3 months for fixation
  • 2-3 yrs for VA
VA won't develop if the above factors aren't favourable and during the plastic period (up to about 5 yrs) any disturbance may break it down. After the age of 5 the reflexes start to acquire the fixity comparable to an unconditioned reflex. They will be maintained throughout life unless there's some serious kind of pathology

If BV isn't allowed to develop the neurons and cortical cells develop differently and the system is abnormally conditioned ie ARC & SUPPRESSION. These will become fixed at around 5 yrs also. EARLY DETECTION IS IMPORTANT FOR TREAMENT WHICH MUST AT LEAST TAKE PLACE DURING THE PLASTIC PERIOD TO BE SUCCESSFUL.

Monday 1 December 2008

AMBLYOPIA #3: Management

When treating amblyopia you may have to use more than one method or change methods depending on how well they're working. The patient has to be told that he isn't likely to get full binocular function and may at best just get a good 'spare eye'.

Amblyopia can be prevented if detected at an early age - screening, identifying the risk factors (family history), correction of refractive errors esp. if px has full accommodative strabismus, anisometropia, high astigmatism. If px is less than 10 years old with VA of 6/24 or better the spec correction may improve the VA on its own. You would get the px to wear the new rx and reassess in 6-8 weeks.

Occlusion

  • Total occlusion - excluding all light and form (patch, spec occluder, opaque contact lens)
  • Total occlusion excluding form only - frosted glass
  • Partial occlusion - allows form appreciation but diminishes acuity (clear nail varnish, ND filters, also near occlusion only)
Occlusion can be direct or indirect - occluding the amblyopic or non-amblyopic eye
  • Bagerter and Cuppers thought indirect was best for amblyopia associated with eccentric fixation in an attempy to weaken the EF through disuse.
  • Von Noorden found no evidence that direct occlusion reinforces eccentric fixation and found it superior to direct occlusion in children under 4.
  • Schapero found that direct occlusion does not intensify EF. It's a simpler approach and should be the initial approach for all age groups
  • Indirect occlusion could be of value to the px who doesn't respond well to direct occlusion or has steady EF prior to direct patching
Occlusion can be full time or part time
  • The most common method of occlusion is direct & total excluding light but when binocularity is present as in small angle SOT, intermittent strab & anisometropia w/out strab partial patching is preferable
  • For px under 4 part time occlusion for several hours a day is better and prevents deprivation amblyopia. It should be assessed every week at first
  • For strabismic amblyopes over 4 years full time occlusion is best. It gets quicker results, is less disturbing to the Px and prevents ARC. Anisometropic Px can be patched full or part time.
  • It's important to obtain maximum VA before the child goes to school.
Occlusion Amblyopia
  • If there's no improvement after two weeks discontinue & check fields and VA with a view to determining an organic cause.
  • When VA has stabilised remove occlusion gradually to prevent the amblyopia returning
  • When doing direct occlusion it's best to give the Px a visual task like crossing out letter Es in newsprint or something like that.
Optical Penalisation/Fogging Method

This involves fogging the non-amblyopic eye for distance by sticking an additional +3.00 in front of it, sorta like a reading add. The amblyopic eye is then used for distance and the good eye for near. It can be worn either full time or in the evenings for tv. It's more acceptable cosmetically but not as effective as occlusion.

Drug Penalisation/Cycloplegia

This is achieved by using 1% atropine ointment on the non-amblyopic eye. This is the reverse of optical penalisation in that the Px uses the amblyopic eye for near and the non-amblyopic eye for distance. This treatment is good for supplementing or replacing occlusion but is rarely the first thing tried. It's good when co-operation is poor. Unfortunately it's only useful in mild/moderate amblyopia - if the amblyopia is too deep then the non-amblyopic eye will still be used. The lack of involvement of patching or glasses means it's good when cosmesis is a problem (ie in older kids).

If the patient has nystagmus with a latent component this method is also very good. If you patch the good eye and the other eye starts doing a nystagmus movement then it's obvious that you aren't going to get good 6/5 vision in that eye.

CAM Visual Stimulator

Px exposed to intense visual stimulation for short periods of time w/good eye occluded. Rotating grating of different contrast & spatial frequencies to stimulate large number of cells at one time. Method is better in anisometropic amblyopia rather than strabismic but the results are dubious.

Pleoptic Treatment

After-images - useful when EF is present. A large bright after image is produced in the amblyopic eye - a ring centred on and also sparing the fovea. It desensitises the EF point - Px then looks at a near fixation target with true foveal fixation. It requires a mydriatic and daily treatment is required. Very time consuming, not easy or popular.

After Image Transfer Method

This was first used for eccentric fixation but has been shown useful in amblyopia too. A central AI is created in the dominant eye and then transferred to the amblyopic eye. Px is then asked to locate AI at the point of fixation and to see the smaller fixation letters. This must be repeated as the AI fades. Best if VA is 6/24 or better esp when VA has deteriorated again following success with other orthoptic procedures.

Anti-Suppression

Useful in older Px w/good chance of binocularity

Mallett Intermittent Photic Stimulator Unit

Red light stimulation at 4Hz with an interesting detailed visual task for 20-30 minutes. One or two times a week. Results dubious again.