A New (?) Concept for Preventive Visual Care
As a clinician trying to solve my patients’ visual problems and enhance their visual skills, I find myself frustrated at times. These are the times when it seems that I’m not understanding how the visual system is operating and why an optical system is now malfunctioning in acuity or performance, when the “design”, if you will, has stood the test of time.
Much of my curiosity and passion to be a healer, instead of just a caretaker, came from a 2 year-old girl who became 8.0 D. myopic in a three-week span. Thirteen years ago, in this very room, I reported on that case and some initial impressions of the impact of environmental, physiological and pathologically-induced stress. That report was published last month in final form in the JBO, although without her case story. Rachel had suffered from three severe viral infections within a 14-day period.. The changes she experienced were 80% permanent.
Diogenes searched the world over to find a honest man: I am continuing my quest for the answers to what I seek. To that end, I have some questions to ask of you all, which may help me think through and get past some potential road blocks. You see, I am considering some decidedly different possibilities about accommodation and convergence. I believe that if we can come to a better working understanding of the visual and visual-motor system, we will be better able to intervene and prevent the structural adaptations we call ametropias.
For me to ask the questions, I am going to have to give you some background, review some of the new data coming in, and ask you to speculate upon some things that may be nothing more than hunches. I think I can safely say that we will all take something out of here from all of this.
Rather than go into detail about that initial paper which was titled,Stress and Eye: New Speculations on Refractive Error, I am going to review just one aspect of it, because it is germane to the main question that I want your answers to when I am done. The question I put to you is this:
Why Can’t Accommodation and Convergence be a Unitary Process?
The concept we need to review from Stress and Eye was thought to be an original postulation that internal against-the-rule astigmatism is retinal in origin. I have since learned that it may not be fully original, and that doesn’t surprise me a whole lot. However, I believe that my reasoning is more detailed in the elaboration of the process: against-the-rule astigmatism probably stems from a horizontal torus created by the pull of the superior and inferior oblique muscles in the region of the macula.
Peter Greene, a mechanical engineer, wrote a brilliant piece in 1980 on the Mechanical Considerations of Myopia’ in the Academy Journal. He produced these next illustrations to demonstrate how the optic nerve and the insertions of the obliques form a three-point weakening of the posterior pole of the globe. Greene believed that this tensile weakening, plus the increase of IOP caused by the EOM’s — anywhere from 5 to 14 mm. of pressure increase during convergence — were the proximal causes of the myopic staphyloma formation seen in high myopia. When I showed this illustration at the symposium here in 1984, my observation was that the distention seen in the figure will actually form the plane of against-the-rule astigmatism, since relaxation of the distended fibers you can see between the two muscle insertions will, bunch outward horizontally when the intraocular pressure pushes outward after convergence has been relaxed, creating a horizontal torus.
Here we see the illustration of the distention of the posterior sclera into the myopic staphyloma, making the eye a distinct prolate spheroid, an exaggeration of the normal adult eye, which is only slightly prolate. At the bottom, you can see the artist’s view of the distention as viewed from an anterior perspective. Please note the horizontal torus being represented. The accuracy of this postulation should be able to be demonstrated easily with some of the new tools we have at our disposal.
The torus at the posterior pole helps us to understand the mildly perplexing shifts of myopia and against-the-rule astigmia in presbyopic patients if we realize that we may be just counter-balancing spherical equivalents as the aging lens loses index. (It is also possible that that phenomenon may be due to a change in length of the posterior chamber due to fibrosing of the sclera with normal aging processes and the calcium loss of maturity.)
People with high exophoria — almost always very intelligent persons — are more likely to have against-the-rule astigmia because of the extra demand on convergence. A Pitt math professor’s situation followed my theory: while I was explaining the how and why to him, he asked me why the muscles were pulling so hard?
This made me stop – why, indeed? What were the muscles pulling against? The globe of the eye weighs about 2 oz., so what was the big stress? Could it be, oh, say, ACCOMMODATION?
Here we have a picture of the globes in their orbits, and below, a single globe. We’ll look at them closer in a moment. But first…
Here are two ice cream cones. Take a good look – what do they remind us of anatomically speaking? (Keep it clean, guys, we are in mixed company.) The ocular orbits of the cranium have been described as being like two ice cream cones with their inner walls parallel, the way I am holding them. The axis of the orbits are at about a 45 degree angle or greater, and the lateral walls are almost 90 degrees from each other.
See how the muscle cones angle back in toward the optic foramen, where they arise from the Zonule of Zinn . If they contract simultaneously, the eyes are retracted not straight back, but at the angle of the orbital axis. Of course, they are prevented by the check ligaments, and’the oblique muscles! The next thing we need to do is to look at how the nerve supply is designed to control the muscles. We are considering the action of the muscles from a primary head orientation.
The VI n. controls the lateral recti. Ever think of comparing the construction of the body and eye in terms of design and engineering? It is as though some engineer seems to have said “Let’s do this right, we can’t have the eyes wandering all over the place!” So He laid down the Abducent nerve to keep the eye in check from overconvergence. (Bear with me — it may seem that I am oversimplifying things, but my studies have revealed an enormous complexity to everything I have been researching and am sharing, and much to my wife’s dismay, it will possibly take a book to detail what I am dealing with this simplistic level I am sharing today.)
Back to my hypothetical engineer. He realized that convergence is important, and we mere humans have to have a fine trim mechanism for looking down and reading. So, the Trochlear nerve got laid in for the superior oblique.
All of a sudden, the quartermaster came running in, shouting, “We’re running low on nerve supplies!” So, the Big Boss decides they’ll just lay in the pupil;, the ciliary body, the superior rectus, the inferior rectus, the medial rectus, and the inferior oblique all on the same nerve. As Groucho would say, “Now, that’s a lot of nerve!”
Getting serious now, has it ever troubled any of you that one nerve, with several nuclei, apparently controls all those multiple functions and two other muscles have their own individual supply? I never really lost sleep over it — well, not until I started to put it all together for today — but it troubled me for years. Somewhere along the way, I realized that it makes sense that the intent of the III n. “the Oculomotor Triad” is a singular function: accommovergence.
Professor Puzzle’s question (that is the math professor’s nickname), “Why are the muscles pulling so hard?” generated an epiphany (well, okay, more of a V-8 moment) — the obliques — particularly the superior oblique — were perhaps working to drive some accommodation. What were the evidences of that?
Well, I am in the winding down stages of a literature review. I would be here another couple of hours to adequately share all the support for this concept, but my wife suggested otherwise. That’s why she’s back in Oakmont.
So, before we get to the point where you give me your feedback on the question I asked earlier, let me briefly cover a number of the supports I have found, talk about the clinical significance in prophyllaxis that it will mean if these are true and are significant, and then I’d like to listen to you for a while.
First of all, this idea is not new. Thorington, Duane, and Bates have all suggested a role for the extraocular muscles in accommodation. What I am uncovering is the very real likelihood that like myopia, emmetropization and presbyopia, accommodation is a multifactoral process involving the total eye and is inseparable from convergence. Young, in 1801, proposed four possible locations for accommodation.
…and he ruled out all but the last. Actually, Young missed one other site that had been considered earlier — the iris — or pupil; and its depth of field focus effect. At any rate, the three that he discounted have all since been shown to actually be viable mechanisms.
Looking at the eye from front to back, there is good clinical and research evidence for all that I am summarizing for you.
The Cornea – in preliminary studies, the cornea shows signs of curvature changes in the periphery upon accommodative effort. This was reported to me privately by Dr. James Begin. He has done a topographical study of the cornea under accommodation and found steepening of the topography, creeping up from the inferior region, much in the shape of an Ultex A bifocal segment. He’s continuing to study this and is writing a paper which should include this information. Sam Horner and Gerry Getman both felt that With-the-Rule (WITH-THE-RULE) astigmatism was associated with accommodative difficulty and Begin’s observation may be a tantalizing clue as to how it may happen.
The Anterior Chamber – becomes shallower as the iris and ciliary body pull forward upon accommodation. This pulls in the punctum remotum and punctum proximum, aiding the accommodative effort.
The Iris – surgically aniridic monkeys had 40 percent less accommodation in the operated eye than the fellow control eye. Weale believed that the pupil contributed up to 25 percent of accommodative effect.
The Lens – Schachar has proposed that ciliary constriction creates tension on the lens occurs and reports restoration of six and more diopters of accommodation by a surgical artifice. It is amazing that in his first four articles in the Annals of Ophthalmology, he had yet to explain how ciliary constriction can increase tension. Later papers finally proposed a purported mechanism, but his rationale requires that a very tiny area of the ciliary muscle “curl” inward and that the proper zonules attach at precisely that point. This is not impossible, but it tends to run counter to the design wisdom of the body that a specific muscle or organ does a specific job: a flexor flexes, an extensor extends, and a sphincter “sphincts”. Alpha scans have affirmed the change of shape of the lens. But we also know that the lens oscillates under two control mechanisms, to function like an analyzer system to perhaps drive a more sustained response by a mechanism with intermediate and long-term focus and adaptation capabilities. One of those control mechanisms is almost certainly regulated by the pulse rate of the heart.
Fincham’s theory involving the lens action is most acceptable, but the ignorance of how the ciliary muscle is organized and operates and how the ciliary processes attach to the lens is monumental, almost a free-for-all.
The Vitreous Moves – Coleman’s theory that the vitreous forces the lens into accommodation has come under attack, the way that he detailed it, but the movement almost certainly occurs, supported by van Alphens’ experiments of the ’50’s and ’60’s. The most proximal effect is to support the lens as it is propelled into or towards, the anterior chamber.
The Axial Length – increases in length, found on alpha scans. The methodology is lacking somewhat, but the length did increase, though the amount is arguable.
The Choroid Thickens – Wallman has done several experiments showing that chick choroid changes in response to deprivation of form focus. The effect is actually regional, that is, local areas of the uvea will thicken and thin, when deprived of form focus, able to do so because the choroid is an erectile tissue under autonomic control — and this capability has implications in uncorrected astigmatism, if the mechanism exists in human eyes. The effect occurs without visual cortex communication and probably involves retinal edge analyzer capabilities along with dopamine or enzyme release.
Are you getting a feel for the complexity so far? The whole eye is capable of functioning in the accommodative process, so why not the extraocular muscles (EOM’s) as well? Bates shortsightedly believed that only the EOM’s were involved in accommodation. He felt that the superior oblique and inferior oblique were the primary muscles. Indeed, Takeda and a crew of others measured an accommodative effect occurring upon downward gaze at far, suggesting a role of the superior oblique and inferior rectus. This may be the source of the changes that Begun has measured with his corneal topographs. Owens and Tyrrell found that lateral phorias were dependent upon accommodative activity – accommodative divergence accounted for the difference between dark vergence values and the lateral phoria at far.
Further implication of the EOM’s is possibly seen in the fact that binocular accommodative values are higher than monocular values.
The scleral role in refractive changes may be supported by the fact that CA/C ratios decline faster in aging than AC/A ratios do; atropine control of myopia is being postulated to work through non-ciliary mechanisms and frequently results in the uncovering of latent hyperopia in hyperopes but only rarely does in myopes, according to Van Alphen; and dilute atropine has more effect upon older eyes than younger eyes — it sounds like the sclera may be shrinking under the effect of atropine and this, by reverse logic, would implicate the sclera in the accommodative process.
Looking at the globe in the orbit, if we were to draw the eye back in EOM-driven accommodation, we would see shaping of the globes into prolate spheroids purely by the action of the orbital cones. Would the globe retract? Probably some, but not necessarily. An individual who reads, however, would be more likely to be exophoric because of the physical relation of the orbits and the need for an increase of tonus in the lateral rectus to help compensate for sustained convergence and accommodation.
The nervous supply to the ciliary muscle is not as simple as many of us were once taught, I’m sure many of you all realize. Since dark vergence and dark focus tonic values pull the eyes well inside optical infinity, then divergence and sympathetic stimulation are needed to restore focus to optical infinity. Exophoria may be the inadvertent result of these processes, since lateral phoria and accommodative divergence are related, as cited above.
At any rate, the globe drawn back by the frontal EOM’s and forward by the posterior EOM’s (the obliques) would be “squozen” like a fat lady in a girdle, or a ball in a fist, further enhancing the shaping of the eye into the prolate spheroid of adulthood or of progressive myopia.
Can we blend the historically described processes of accommodation and “convergence synkinetic processes” into a unikinetic process of Accommovergence? There appears to be a great deal of circumstantial evidence that they are. I’m asking testable questions, I believe.
Accommodation and convergence have transient and sustained components as they react across time. Ultimately, they force adaptation to reduce the alarm phase of systemic distress. The element I found missing in most studies on vergence and focus is TIME. The Timecourse of the reading process has been greatly ignored in the literature critical of behavioral rationales.
The clinical implications are significant. As Peter Greene said, the use of low power plus with prism to reduce the nearpoint distress may not be the perfect answer, but it almost certainly will do no harm and may do a lot of good. If these preliminary ideas are on the right track, then the value of low power prisms may be in the alteration of the CA/C demand. This gives structural as well as neurological support to their use. And, NO, in 5 or 6 years of use, I have yet to find patients who absorb the prism and gallop away down the prism trail. It gives us a theoretical basis for another valuable tool in dealing with the unacceptable task of reading this time in a bottom up fashion, as long as the AC/A ratio is not too low, it would seem. Tod Davis, in his brief chapter in the OEP book on prisms, nicely describes the subjective benefits of mini- and microprisms.
If myopia, astigmatism, progressive hyperopia, suppressions and asthenopia are symptoms of the avoidance response of the central nervous system, then it makes sense to make a preemptory strike against them by providing relief with prism as well as plus. This can’t be done willy-nilly, however, because of the variance in the AC/A and the CA/C. Thereare important individual variables in the central nervous system. The preventive value of prisms and plus lenses may be in moving the patient’s working distance out nearer to the dark vergence and dark focus values of about 1.00 – 2.00D., so that the optical system is at perhaps a homeostatic balance point. It is up to the diagnostician to uncover, as best he can, the position of that balance point. That may, indeed, be the value of the OEP formulations.
So I raise the questions…
- Why can’t we consider accommodation and convergence as a unikinetic system?
- What are the prescriptive implications?
- Do any of you routinely measure CA/C and what is your method?
Is WITH-THE-RULE astigmatism merely the geometric counterpart to AGAINST-THE-RULE astigmatism as I proposed it? Why, or why not?