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EYE ADVICE: Professional Papers

 

B. Reflex or 2° PMA and Induced ATR Astigmatic changes

Throughout my practicing career, I have observed ATR lenticular changes preceding ATR corneal changes in under or uncorrected presbyopes. I have also observed similar ATR lenticular and corneal changes in some younger people who actively accommodate. An example of this latter finding is reported by Weisz (1978).

I initially considered these astigmatic changes to be due to incidental spread of firing to the PMA subnucleus from the anatomically adjacent PSA nucleus. After becoming familiar with the phenomenon of primary accommodative astigmatism (PAA) as discussed above, it soon dawned on me that reflex PMA is an integral component of the normal visual system. It appears that increasing accommodation proportionately decreases the leverage of tonic PMA in compensating for WTR corneal astigmatism. Reflex PMA aims to supply the additional PMA that is required to overcome the adverse effects of PSA and thus prevent manifesting of astigmatism (PAA).

One may refer to reflex PMA as 2° PMA to distinguish it from 1° PMA that is initiated by a purposeful response to meridional blur. As 2° PMA is stimulated reflexly in response to PSA, it also forms part of the ocular motor near reflex, serving to counteract PAA. The amount of 2° PMA stimulated is proportional to the amount of PSA innervation. Thus one can talk of a 2° PMA/PSA ratio in the way that one talks of an AC/A ratio. There is thus a tetrad, not a triad of motor functions involved in the ocular motor near reflex.

Those with low 2° PMA/PSA are prone to PAA, while those with normal 2° PMA/PSA are not, despite the magnitude of the L.A. On the other hand, a relatively high 2° PMA/PSA ratio accounts for the induced ATR ocular astigmatism that is sometimes noted in younger people (non-presbyopes) who actively accommodate.

In order to prove that any observed ATR ocular astigmatism in non-presbyopes is related to active accommodation and consequent induced ATR lenticular and corneal changes due to a high 2° PMA/PSA ratio, one must be able to demonstrate an increase in ATR ocular astigmatism with increasing accommodation. A documented increase in ATR ocular astigmatism associated with active accommodating in non-presbyopes strongly suggests a relatively high PMA/PSA ratio. Pro-active prescribing is then necessary for those who actively engage in much close work to alleviate the associated eyestrain and permanent ATR ocular astigmatic changes that can increasingly impair distance vision. The most effective intervention is the use of spherical plus lenses in a form that does not blur distance vision. This will reduce the effects of 2° PMA. Any ATR changes that are permanent will still remain after several months of wearing these glasses, at which time an astigmatic component may be incorporated in the lenses.

The ATR corneal toricity and ocular astigmatism changes in presbyopes are widely known. Their cause has not previously been well understood. ATR changes do not affect all presbyopes to the same extent. If it were possible to have presbyopes continuously wearing their full correction so that there are no periods of time where they are slightly under-corrected (e.g. prior to changing their lenses), these presbyopes would not normally undergo any ATR astigmatic changes.

These changes mainly occur in under-corrected or uncorrected presbyopes. In these cases of insufficient lenticular accommodation, the striving for clear vision would necessitate near-maximal activity of the sub-nucleus responsible for PSA. This reflexly stimulates the sub-nucleus for PMA producing 2° PMA and consequent ATR astigmatic changes. Most insufficiently corrected presbyopes are prone to these changes as even those who have normal 2° PMA/PSA ratios will have relatively high amounts of reflex PMA innervation due to the high demand on PSA.

Over longer periods of time, 2° PMA causes an apparent spasm or over-action of PMA which shows up as ATR astigmatism on distance refraction. In time, ATR corneal changes are induced through attachments of the PMA muscle fibres to the temporal corneo-scleral junction. This applies to both to the insufficiently corrected presbyopes as well as the younger people with high 2° PMA/PSA ratios.

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Paper 1 - Meridional (Astigmatic) Accommodation  Abstract

PART I
Physiology of Meridional Accommodation (A) Ciliary Muscle Action and Innervations
(B) Corneal Changes due to Ciliary Muscle Action
(C) Theory of Initiation of Meridional Accommodation
References

PART II
Clinical Implications of Meridional Accommodation

Introduction

(A) Astigmatic Changes Related to WTR Corneal Toricity (i) Latent Astigmatism
(ii) Primary Accommodative Astigmatism (PAA)       (B) Reflex or 2°PMA and Induced ATR Astigmatic Changes
(C) Eye Preference and Meridional Accommodation (i) 1° PMA and Eye Preference
(ii) 2° PMA and Eye Preference (D) Proactive Prescribing for Presbyopia (i) Phakic Presbyopes
(ii) Pseudophakes and ATR Corneal Changes (E) Refractive Techniques and MA (i) Balancing Meridional Accommodation
(ii) Binocular Test of Cylinder Power (F) Further Clinical Subject Areas and Meridional Accommodation (i) Preventing Induced Oblique Astigmatism in Children
(ii) Low Vision
(iii) Keratoconus
(iv) Hard Contact Lenses
(v) PRK and PARK (Photorefractive Astigmatic Keratectomy)

CONCLUSION

References

Paper 2 - Common Chronic (Infective) Conjunctivitis and Nasal Rinsing

Paper 3 - Primary Open-Angle Glaucoma

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