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