EYE ADVICE: Professional Papers

C. Theory of Initiation of MA

From a theoretical point of view, it seems necessary that the visual system be able to distinguish between blur that is caused by spherical ametropia and blur that is due to astigmatic ametropia. If PSA and PMA both responded to any given blur stimulus, both types of accommodation would be stimulated without necessity. This is simply not practical as it would pose a greater delay in focusing.

A much more effective focusing would be achieved if the visual cortex and related structures of the brain had the ability to detect meridional blur. An MA response could then be initiated in the direction required, so as to overcome any WTR corneal astigmatism which may be causing the meridional blur.

Evidence in support of the existence of a mechanism to detect meridional blur can be found in the study of contrast sensitivity, in cases of nystagmus. Loshin and Browning (1982) point out that these cases are associated with a loss of contrast sensitivity in the horizontal meridian, which is attributed to the horizontal nystagmoid eye movements. They found that a similar loss of contrast sensitivity was found in cases of albinism which they attributed to the associated nystagmus.

Of relevance is the study of Nathan et al (1985), who looked at data of 256 children attending a low vision clinic. They found distinctly higher levels of astigmatism in those children with albinism, retinitis pigmentosa and idiopathic nystagmus. They stated that the differences in the amount of astigmatism between the 14 disease groups did not seem to be associated with depth of visual loss.

My belief is that detection of meridional blur is the essential factor in eliciting a purposeful PMA response to counteract corneal astigmatism. If, as in cases of idiopathic nystagmus, or secondary nystagmus in albinism, this sensitivity to blur is diminished, so will the ability of the visual system to elicit a PMA response. The findings that RP children also had significant levels of astigmatism, and that depth of visual loss did not seem to be a crucial factor, suggest that information from the whole retina is used in assessing the meridional blur stimulus for PMA.

The means by which meridional blur detection is carried out is somewhat speculative. It would seem that basic information about orientation, edge detection and contrast sensitivity, would be essential in order to achieve this. This information is available in simple cortical cells, and it could be further processed to enable detection of the orientation of ever-small increments of meridional blur. This higher level of information could be passed on to a specific subnucleus, which would be closely related to the sub-nucleus for PSA, via such intermediary nuclei as the pulvinar and superior colliculus. Innervation from the IIIrd nerve nucleus to the temporal ciliary muscle could be relayed via the ciliary ganglion as for PSA. The temporal long ciliary nerve is best positioned anatomically to innervate the PMA muscle fibres. SMA could be relayed through the cervical ganglion and the long ciliary nerve. (Morgan 1944).

It is worth noting the experiments performed on chicks by Irving et al (1995). These experiments demonstrate the remarkable ability of the chick's visual system to adapt to induced astigmatic ametropia by appropriate meridional changes in power, primarily of the lens and to a slightly lesser extent, the cornea. Whilst the 9D cylindrical lenses which were applied did not induce the exact power change in the eyes, the axis was always accurate.

Part II: CLINICAL IMPLICATIONS OF MERIDIONAL ACCOMMODATION was available at the 11th APOC conference as a handout accompanying the Proceedings Manual.

I wish to thank Dr. B Pierscionek for her advice and comments. I also wish to thank Lorraine Lipson for her library assistance in the Victorian College of Optometry, Melbourne Australia.

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