ETIOLOGIES REVISITED

 

So what causes ametropia?

 

Well, myopia is just what we were told in grade school - the eye is too long.  Almost all of that extra length is in the posterior chamber.

 

And astigmias are toroidal surfaces of the cornea and posterior pole of the eye.23

 

Hyperopia is still a puzzle, in the main.  It is not an optically weak crystalline lens because Gawron,36 some Russians,40 and others have noted that myopes actually have the weakest lenses.  Axial length doesn’t correlate well with hyperopia, but I have not seen any statistics for any relationship between the amount of hyperopia and axial length. I suspect that there probably is.  The index of the lens is the most underappreciated component in the possible production of farsightedness -- even sudden farsightedness.  The culprits are probably hypercalcemia and sugar alcohols.  Stop and think:  at least once or twice a year, we all get  patients  whose myopia has suddenly gone from -6.00 or -3.00 to a -3.75 or a -1.00 in a matter of a week or two.

 

You have seen them, too.  What is the problem with them?  Hyperglycemia.  Sudden onset of diabetes, which is documented to result in hyperopia, not myopia.  (Slow onset diabetes results in myopia.)41

 

So, while I am not saying that hyperopes are diabetics - I am saying that there are physiological processes in the body which are quite capable of producing hyperopia above 1.00 D, which Rosner has shown is associated with reduced academic skills.42

 

ACCOMMOVERGENCE

 

In my paper on Stress and Eye I outline a mechanism by which hypercalcemia may produce geometric changes and probably indiceal changes in the crystalline lens structure.  In that paper, I also describe how against-the-rule astigmia is probably best described as the horizontal torus formed by the pull of the superior oblique and inferior oblique muscles across the posterior pole.23  In a paper I presented at the 1997 Kraskin-Skeffington, I began the detailing of a model of accommodation and convergence as unified, rather than merely synkinetic, processes. I called it "Accommovergence".  That work is still progressing, and it is gaining new weight with just about all the literature I have found.43

 

Some understanding of that model is necessary for the rest of this discussion.  As this theory is worked out, it’s more and more apparent that the driver and power behind ametropic changes is the ongoing battle among the sympathetic and parasympathetic branches of the autonomic nervous system, and their fight with the voluntary nervous system.  The interference patterns that are set up can be studied and interrupted by the clinician - that means that prevention is and always has been possible

 

OEP THEORY & TRANSIENT/SUSTAINED ACCOMMODATION

 

The preliminary indications are that Skeffington and Alexander and all the other functional fathers that we owe allegiance to were right.  For as far as they went, they were right - and decades ahead of their peers. The "check, chaining and typing" appear to be solidly based in the neurodevelopmental principals of vision, cognition and personality.

 

The evidence suggests, theoretically, that the ciliary muscle and lens system functions primarily as an oscillating analyser with a dual-phase mechanism.  This phenomenon of oscillation is known, consisting of a fast and slow phase.  The fast phase is controlled by pulse rate.  The oscillation of the image may help to find the retina and the direction of blur.  It performs the function of a transient accommodative system.  Peering postures - including the "myopic slouch" - appear then to help the EOM’s to compress the globe, squeezing it like an egg in a fist, nestled inside the constricting muscles, with the recti pulling back and the obliques pulling forward. The globe can be either lengthened or shortened, depending upon which muscles have been primarily stimulated.  Lengthening of the eye under accommodation has been reported by at least one set of researchers.44

 

With-the-rule astigmatism appears to be formed when the superior and inferior recti are stimulated, stretching the cornea vertically as the individual peers at far.  The cornea has been measured to horizontally flatten with convergence by Lopping and Weale.45  If the ciliary mechanism is being functionally blocked from higher centers, the EOM’s will be called on for longer, more sustained accommodation. Anatomically and functionally, the EOM’s appear to be functioning as a long-term accommodative system.  They are hereby postulated to perform the function of the sustained accommodative system.

 

Do the EOM’s really control accommodation?  We will try to demonstrate this now.  This won’t work well enough for everyone, but those of you who are myopes and low hyperopes should see the phenomenon I want to demonstrate.  Astigmats will get an extra run for their money. In your program is printed a Reduced Snellen chart and an astigmatic dial.  If you will remove your glasses - you hyperopes can attempt this with the distance portion of your Rx., if you are presbyopic, otherwise,  leave your glasses on.  Hold the chart at arm’s length and bring it in slowly, until you find your punctum remotum, or the best focus you can attain - WITHOUT STRAIN, please.  Consciously avoid accommodating, if possible.  You hyperopes will probably be at full arms’ extension.  This should still work.  Keep the chart straight ahead of your eyes, in primary gaze position. Now, tip your head down while still looking at the chart, so that you are peering up under your eyebrows.  Don’t move your arms yet.  Some of you will notice that the target blurs, some will see it get clearer.  Those of you who see it blur, slowly move the chart in and you should find it refocuses - perhaps clearer than ever - at about 1" closer.  Those of you with AGAINST-THE-RULE cylinder will note that the smear is reduced or gone.  Now, if you repeat it, but drop your eyes, to look down your cheeks, you will find it gets even closer -- about 1-1/12".

 

Your EOM’s are helping your eye to accommodate.  Blumenthal theorized this and Takeda and his colleagues tried to demonstrate this experimentally but found it only worked for them at far.  They suspected that the equipment - a modified Badal stimulator - limited their results at near. Well, you don’t need an instrument.  A chart -  or want ad section - will suffice.  Those of you with cylinder of over 1.00 D will note on the astigmatic dial that the axis rotates about 15 degrees.

 

So what is the point?  The point is that striated muscle - the EOM’s are probably an important part of the accommodative mechanism.  They have collateral and simultaneous function with the smooth muscle of the ciliary focusing system.  Vergence during all of this is kept in fine tune by the Trochlear and Abducent nerves so that diplopia will not occur.

 

DUCTIONS

 

We probe these complex relationships with duction and blur findings.  We study what the patient wants (that’s the blurs) and his range of freedom (that’s the breaks and recoveries) as he or she inhibits the pattern of blur.  As Skeff told us 50 years ago, we are not looking at muscle strengths, we are looking at and should be studying the relationship existing between (at least) two patterns - neural patterns - learned neural patterns.47

 

At the same time, Skeff told us that any rational program of lens application must be based upon a study of ductions. This dual effector model of accommodation, with transient and sustained components that intimately integrate with the vergence system, furthers our understanding of why ametropia develops by helping us to put structural legs under a theoretical platform.

 

Stop and think: we can’t - shouldn’t - go fitting glasses and contacts onto living, thinking persons like their eyeballs were mounted on an optical bench, yet that is what is done in 90% of the offices in the world.

 

If we do not intervene in the individual’s visual problem, then the ametropia and suppression patterns and deviations that can occur, which we consider clinically "wrong", are actually  the visual system’s best solution to its problems.

 

The stressors that provoke the psycho-physiological changes are complex.  Much of what stresses humans varies considerably from one person to another, based on three unique factors.

 

[OVERHEAD #8 -- 3 variables]

 

1) Heredity: we can’t choose our parents. (Nature)

2) Experiences: unique to each individual. (Nurture)

3) Apperception: how we respond emotionally to an experience (Beliefs)

 

One, our heredity, because we can’t choose our parents (Nature).  Two, our experiences, unique to each individual - that is the nurture; and Three, our Apperception - that’s how we respond emotionally to an experience (or stimuli) - and that is based in our beliefs, built on prior experiences.

 

SCHOOL WORK

 

Let’s consider what a child is subjected to in a classroom:

 

 Schoolrooms present a contained environment to a child comparable to a caged animal’s. He or she is constrained to a seat and nearwork environment for four to six hours a day - and the mental processing adds further stress. 

 

Containment of an animal is one of eight factors that raises ACTH levels,47 which then increases cortisol levels (hydrocortisone) and cortisol does not-so-nice things to collegen, the main protein of the eye.  Only one report that I found has attempted to study cortisol in myopia, and the model was fatally flawed.  Angi and Rupola, et al,37 had sampled Cortisol once a day, yet since its production varies widely throughout the day, it needs to be studied on a diurnal basis - 24 hour urine samples need to be brought to each of our offices for study - can’t you just see it?

 

Retinal defocus while reading probably occurs due to centralizing of attention.  Josh Wallman has proposed that the large areas of peripheral image degradation is a form of form deprivation.48  research seems to point to a retinal growth factor, probably involving dopamine and a collagen synthesis factor.49  One researcher (Angrist), in particular, noted that scleral tissue is normally a wondrously complex structure and questioned why it should give way and stretch as it does in myopia - this is an enigma, he said.50  Part of the answer may be that there are time-dependent ocular rigidity actions in the sclera that allows a vicso-elastic property to do a slow stretch after an initial resistance.51

 

Time alone may be a significant factor when the myopic candidate’s eye has been subjected to EOM tension, increased intraocular pressure, and the retinal factors released by form deprivation like Wallman talks about in myopes, plus the possibility of some unknown chemical release over time with ciliary muscle tension on the retina, as Van Alphen demonstrated. Van Alphen was just one of the researchers who suspected that since the stretching of the sclera occurs at relatively low IOP’s, it must be affected by some other mechanism.34

 

The local and general adaptation syndrome, as put forth by Hans Selye,52 would seem to offer a productive area for research.  You will have to read Stress and Eye for a better discussion than this right now.

 

Weisel & Raviola53 concluded that myopia was caused neurally by alteration of the visual perception, not by the local effect on the eye. Van Alphen believed that the competitive environment of the classroom was an element that should not be underestimated, because learning has a much more complex psycho-visual mechanism than mere closework does.34  If we can take any lead from these researchers’ conclusions, it appears that the brain must be "in gear" for myopia to gain a foothold.

 

In 1987, Bullimore & Gilmartin found that tasks with high cognitive demand cause the dark focus point to pull in, independent of the optical stimulus of focus.54  So we could conclude that the classroom is an ergonomic and psychogenic breeding ground for ametropias.

 

THE EXTRAOCULAR MUSCLES [EOM’s]

 

The EOM’s have been noted in the literature since 1794 as suspects in changing the size of the eye.55  Prentice in 1895 appears to have been on a solid track when he noted that the muscles acted upon a disturbance in the sclerotic coat.56  He felt the disturbance was nutritional.  Bates, back in 1912, felt that the EOM’s were responsible for accommodation - unfortunately, he discounted the ciliary mechanism.57  He observed myopic astigmatism produced by children straining to see.  Scientists have tended to discount all that he did because of some significant errors in his premise.

 

However, we have difficulties explaining some phenomenon if we discount the EOM’s.  Against-the-rule astigmia has had any number of proposed etiologies and the EOM’s fit in well with some, make others unnecessary. With-the-rule astigmia is associated with accommodative deficiency,58 but no mechanism has been widely promoted.  The role of the EOM’s in accommodation would answer this nicely - the horizontal torus generated by the recti seems to fit the puzzle pretty well, for now.

 

And there’s another major problem that the role of the EOM’s in accommodation and hyperopization might readily explain, in part or in whole: the trouble with sympathetic inhibition.  Oh, you didn’t know it was in trouble?  Well, it appears that it is.  Here is why:

 

1)  If dark focus (DF) and dark vergence (DV) are both intermediate values59   - and they are); and,

 

 

2) We also know how DF and DV pull in - it’s the EOM’s and ciliary mechanisms.

 

We have a problem with:

 

 3)  How do DF and DV get restored (or reach out) to optical infinity?

 

You see, we have been told all along that sympathetic stimulation focused the eye to 20 feet. But  HOW?  What’s the mechanism?

 

I asked several colleagues if they were taught anything other than the radial fibers of the ciliary muscles.  None were.  Anatomists tell us, though, that the radial fibers are few in number, weak, and may not even exist, that they are just transitional fibers from the sphincter to the longitudinal fibers.

 

However, if the EOM’s were involved, then sympathetic stimulation would excite contraction, and the correct combination of EOM’s would result in a fore-and-aft compression of the globe, resulting in a "hyperopization" of the entire optical system via axial foreshortening.

 

We know that it is sympathetic stimulation that puts focus out to optical infinity,59 but I have not found anyone who has suggested a practical way from known anatomical features for that to happen.  This model of the EOM’s as primary activators in the accommodative and emmetropization processes starts to open new concepts for examination, literally and figuratively.

 

The somewhat mysterious intricacies of the empirical OEP formulas are perhaps scientifically unraveled a bit if we can accept the theory that accommodation is biphasic - transient and sustained components requiring voluntary and involuntary kinesis in not a synkinetic manner, but unikinetic. Secondly, distance acuity is maintained by the action of the EOM’s in global compression. 

 

Prisms in our prescription formulas have been meted out judiciously in the past.  However, if low power (mini-) prisms help to center the patient’s visual range or help him to learn a new neural pattern of operation, we may be gifting that patient with instant changes, like I will play for you in a reading demonstration.

 

CONCLUSION:

 

A little girl had just finished reciting her times tables to her grandfather. He then asked her what 2x13 was.  "Oh, Grandpa," she said. "Everyone knows there’s no such thing as a 13’s tables." - The moral is that just because you don’t know the answer to a question doesn’t meant that there isn’t one - that includes ametropia. 

 

To conclude, refractive error is a psychophysiological adaptive disease that originates in the neural substrates of the brain, thoroughly mixed in with nature and nurture, nutrition and personality. Learning and anxiety - including performance anxiety, especially - seem to be direct triggers for expression of ametropias, primarily in a nearpoint environment.

 

We probe these relationships through our case history, and, with blur and duction findings.  When we compare distance and near values, the "low" break and recovery shows the direction of interference, Skeff always said.44

 

We can expect the individual to operate freely within his ranges of freedom. Glenn Fry said that it is only when the direction of interference gets to the point where accommodation changes will there be a perceptual blurring.60  When the blur occurs, then accommodation must be changed.  I believe that my very liberal use of base in prism - just like the German ophthalmologists of 150 years ago61 - is operating successfully in changing performance and preventing refractive changes just because of  this.

 

Remember how Skeff always said, 

 

[OVERHEAD - Skeff quote]

 

"The value of a lens is neural, not optical."44

 

To demonstrate this, let me play two short recordings for you.  They are short, but loaded.  These recordings are both 10-year old girls.  The first is in academic trouble of long-standing, the second recently dropped in math from her normal A’s and B’s and complained of distance blur - not near blur - she is a 1.00 D hyperope.  The narration should be self-evident as to what is going on.

 

[TAPES]

 

[Audio available on tape from OEP -- see above.]

 

The differences you have heard were neural, not optical.  The first girl’s mother asked a good question - she said, "Yes, but is she comprehending?"  I replayed her the tape and I pointed out where she enumerates the items of the cat in the mirror.  The brain changes, with the lenses and prisms. Comprehension changes.

 

I had a narcoleptic, who fell asleep every time he read - he went out three times on me during the duction tests. He had attended two years of college: "How," I said, suspecting that he was malingering, "can you read for college without falling asleep?" He explained he only fell asleep if he paid attention, so he was able to read all his books into a tape recorder, and then listen to the tape.  Reading, it would seem from this illustration, probably occurs at two different levels, neurally.

 

[OVERHEAD - qEEG’s]

 

Here is a rare case from my files.  This 30-year old college student had been referred by a psychologist.  His electrical activity in his brain has apparently changed after just eight weeks of visual therapy.  In the first set of maps, we have a brain that is low power and not unusual specifically but generalized in dysfunction consistent with the man’s history of  mild cerebral palsy, was the interpretation of the neurologist who read these.

 

[OVERHEAD qEEG #2]

 

Here, twelve weeks after the 1st qEEG, his beta waves - associated with cognition and alertness - have increased by more than 2 S.D.’s.  The overall power had increased as well. The neurologist was at a loss and said it gave the appearance of someone on benzodiazepines.  (He wasn’t.) His whole visual and cognitive performances had changed due to proper lenses, prisms, and eight weeks of visual and perceptual therapy.

 

Is there any great doubt that the brain is changed by the environment impinging upon it?  Optometrists change the brain when we impose lenses and prisms and thus change the visual environment.  [But we must be judicious - many of the failures in bifocal control of myopia experiments either used reading adds substantially higher than most clinicians would use, or did not specify the height of the segment (it needs to be mid-pupil or a bit below).]  Prism powers in the <4P.D. range have the greatest effect.

 

Can we control the ametropias?  YES.

 

Are we helpless victims of our genetics?  Not necessarily.

 

As a final point of illustration, let me show an example of myopia control in one family - my family.  This is their refractive family tree. One advantage of this illustration, as small a sample as it is, is that the refractions are known for the entire group.

 

[OVERHEAD #11 - FAMILY TREE (See attachment)]

 

Note that the grandparents’ average  refractive error is a +2.00 D.  The parents’ of the cousins and my wife and myself is -4.75 D.  the refractive error among the eight cousins is -4.12 D., pretty consistent with the parents, aunts and uncles.  The refractive error among our own children is significantly different - and that is probably statistically significant, as well.  The average is -0.40 D.  What made the difference?  It’s that I have intervened with lenses, prisms, nutrition, and visual therapy variously on all five of our children. Our daughter who is -4.00 D. had a debilitating illness, but was significantly myopic even before her sickness.

 

[HANDOUT - The Myopia About Nearsightedness]

 

Can we control refractive error? Yes. Is it perfect?  No.