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.

AMBLYOPIA #2: Investigating it

• Accurate H&S

Age of onset of strab, previous treatment (rx, occlusion, other - when given, for how long, successful? Why stopped?)

• Acuity assessment

Crowding: first thought to be specific to amblyopia. People demonstrate better acuity for widely spaced targets and when letters are brought closer together giving contour interaction acuity is reduced. VA must be measured w/optimum Rx. Try and measure line and single letter acuity under standard illumination etc

• Neutral Density Filters - Functional Vs Organic Amblyopia
  

VA is similar in each eye under mesopic vision but is reduced @ photopic levels. Von Noorden and Buren (1959) found that as luminance levels decreased the difference in VA decreased and at the lowest luminance levels the VAs were similar. Px w/functional amblyopia didn't see an improvement in the VA of the amblyopic eye from light to dark, but the VA simply decreased less than that of the normal eye. Px w/organic amb. --> VA decreased in similar manner both eyes.

The ND filter can also help differentiate between eccentric fixation and macular function type people.

• Dark adaptation

Wald & Burian found that dark adaptation is normal in amblyopes but there is a slight elevation in central threshold.

• Evaluation & Prognosis

If you're going to suggest treatment first think

1. Am I going to cause intractable diplopia?
2. Type of amblyopia - the relative importance of rx correction/strab correction
3. Age of px - younger is better, must be under 10, co-operation - understanding of exercises, ease of patching?
4. Duration of amblyopia - shorter = better
5. Acuity - poor acuity = worse prognosis

Treatment tomorrow.

AMBLYOPIA #1

Amblyopia is yet another sensory adaptation that may be present in strabismus. It's some kind of monocular adaptation occuring in the strabismic eye in cases of unilateral strabismus. The adaptation remains when the good eye is covered. Features:

• Reduced VA
• Normal fundus & good optics
• Strabismus, anisometropia or form deprivation in early life

You can divide the causes up into passive and active factors, both of which are involved in unilateral amblyopias.

• W/passive factors good VA never develops. It results from deprivation of form vision due to dense congenital cataract (complete deprivation) or a defocussed image (partial deprivation).

• W/active factors VA is actively suppressed. This is the result of abnormal binocular interaction or competition ie confusion caused by strabismus or incompatible images in anisometropia.

During development, neurones from both eyes compete for control over cortical connections. The neurones from the better eye succeed at the expense of the crap eye and the unwanted image is suppressed and amblyopia occurs. Amblyopia only develops in the critical/plastic periods. The neural plasticity makes the entire system vulnerable to any sort of abnormal experience. The most damaging period is between 0 and 18 months - if VA doesn't develop then it may never do so. The depth of amblyopia depends more on the length of time the px has a strabismus rather than the age of onset.

The retina has been found to be basically uninvolved in amblyopia. Cortical mechanisms involved in form and shape perception are thought to be involved.

Strabismic and anisometropic amblyopia seem to have different characteristics which could mean that they have a different physiological basis. To this very day the mechanism causing amblyopia is still unknown. Anisometroptic amblyopia usually occurs in the eye with the highest refractive error.

If anisometropia is responsible for amblyopia then the cause could be a combination of monocular contrast reduction and image size differences.

In the optic tract there are sustained/X cells and transient/Y cells. The X cells give a continuous response to a grating stimulus and the transient Y cells give an initial response but then return to their unstimulated state. The receptive field capacity of sustained cells is best for fine spatial discrimination so provide a basis for visual acuity. They respond poorly to large low contrast stimuli. Transient cells have large receptive field centres and weak surrounds and are poor spatial discriminators but are very sensitive to large objects w/high contrast fluctuations in time. They are more commonly found in the peripheral retina whereas the X cells are in or around the area centralis. Hawerth and Levi (1978) showed that amblyopic eyes had normal activity in the transient detection channels but reduced activity in the sustained detection channels.

Measuring contrast sensitivity at various spatial frequencies may also indicate the presence of amblyopia. Hess and Howell (1977) suggested a two type classification

• Amblyope w/only a high spatial freq. abnormality
• w/ significantly depressed CSF for all frequencies but a more severe reduction @ high

SUMMARY:

The visual deficits in amblyopia

• Reduced VA
• Reduced contrast sensitivity
• Reduced positional acuity

Spatial misperception has been measured using gratings and after-images.
Cortical undersampling of amblyopic eye: "the eye is partially disconnected from the cortical machinery required for the normal processing and interpreting of visual information" (Horton & Stryker 1993)

There hasn't been an awful lot of amblyopia testing on humans brain-wise: w/animals we can induce amblyopia and then kill em an analyse the brain! Meanness in the name of science. Monocular deprevation studies have been done on monkeys and cats. The majority of cells respond to the non-deprived eye but there was a change in the relative widths of ocular dominance columns - Shrinkage in the ODC of the deprived eye. There was also a shift in cortical dominance away from the deprived eye in severely affected animals. Hubel & Wiesel were the pioneers of that sort of stuff.

The human tests are less in-depth. Through analysis of CSF Bradley, Levi & Hess found that low spatial frequencies were spared but high spatial frequencies were affected w/accompanying loss of VA. I've already typed that above.

The cortical undersampling in humans gave misperception of vertical gratings. Patients were asked to draw what they saw. It's been argued (Barret et al 2003) that the ODC shrinkage would selectively distort the the orientation representation and lead to the patients' perceptual errors. Bedell and Flom (1983) found that strabismic amblyopes report distortion of visual space when viewing with their amblyopic eye but anisometropic patients do not but more recent research has suggested that amblyopia really varies more in severity than in kind. As you can read this is all very confusing/conflicted and more research will probably make better sense of the condition in the future.

CONCLUSIONS

• The old view that strabismus/anisometropia was the cause of amblyopia is too simplistic
• Amblyopia might actually be the cause of anisometropia rather than the other way around
• Evidence is building that residual binocular interactions are omnipresent in the amblyopic cortex
• Form deprivation and strabismus have different effects on the development of cortical binocular connections