A Case of Artificially-Induced High Myopia and Implications for
the Mechanism of Accommodation
By Rich McCollim
Is it possible that the almost universally accepted theory of accommodation is
wrong? The following is an account of an experiment which produced a very
surprising and unexpected result which calls into question current theory.
The standard explanation of myopia is that in the myopic eye, the light rays
passing through the crystalline lens come to a focus in front of the retina,
and that this is usually caused by the eyeball being too long. The result is
blurred vision for objects at a distance. I decided to test this theory by
compress-ing the eyeball, with the idea that this would lengthen it
longitudinally (by compressing it approximately in the middle). In other
words, the object of the experiment was to deliberately produce myopia. My
method for compressing the eyeball is explained in Appendix A.
Since I could hardly ask someone to be the subject of an experiment designed
to worsen his vision, the subject of the experiment necessarily had to myself.
I reasoned that if I did succeed in lengthening the eyeball, then my vision
for distance would become blurred, i.e. I would become myopic. However,
because I was already myopic (O.D. -7.75-1.25; O.S. -5.50 -1.50), the object
of the experiment would be to increase the degree of myopia.
I began to wear the device, strapped to my head, for three to four hours per
day (used for distance vision only) and periodically checked my visual acuity
for any sign of increased blur. After several weeks of this regimen I noted
the first definite sign of change--but precisely the OPPOSITE of what I had
predicted: my visual acuity for distance had definitely increased! In fact,
with continual wearing of the device I eventually reached the point that my
visual acuity (which for many years had been myopic, with uncorrected acuity
at around 20/ ) was in the range of 20/30 - 20/40. To a lifelong myope this
seemed almost the equivalent of perfectly clear vision. At the time I was 35
years old and had been wearing corrective lenses, of gradually increased
power, since the age of six.
It seemed obvious that this remarkable change in acuity had been caused
by something to do with the experiment, but by what means? Another puzzling
factor, was that even with my near-sharp acuity, blur was still present. The
subjective experience of this effect was as if two photographic trans-
parencies, one blurred and one sharp, were superimposed one on the other.
It should be made clear that this was monocular, and approximately to the same
degree in each eye. The crucial question was, how had squeezing the eye
produced dual vision? There are a few reports in the literature on double
focal points resulting from cataracts, but this case was clearly different.
I hypothesized that the creation of dual vision was the result of contraction
of the superior oblique muscles which had exerted pressure on the globe, which
was transmitted through the sclera to the vitreous, forcing the vitreous
against the back of the lens and flattening its periphery. Rays passing
through this outer region of the lens came to a focus at a point very close to
the retina, which produced the secondary image (clear vision), while the rays
passing through the axial (central) region of the lens came to a focus in
front of the retina, which produced the primary image, which was severely
blurred. Moreover, this blur was of much greater degree than the blur of my
original myopia. In other words, I had increased the degree of my myopia by
some 5 diopters in less than two months! My original lenses had become totally
inadequate, and I required a new prescription: O.D. -11.75 -2.25; O.S. .9.00 -
2.00.
The Persistence of Accommodation and the Etiology of Myopia
The creation of a dual mode of vision was quite remarkable, but another
intriguing finding was that the dual vision persisted even after the
experiment was stopped. I reasoned that the lens had become permanently
distorted as a result of vitreous pressure. Further, despite the nearly sharp
acuity, this was present in only one of the two modes of vision, and that in
the other I had become much more myopic. (This, of course, quickly dampened my
initial enthusiasm that I had discovered a cure for myopia). The most
significant point, however, is that these changes in acuity came principally
not from elongation of the globe, but rather from changes in the shape of the
crystalline lens. So, the object of the experiment was achieved--increased
myopia; in fact my visual acuity with my original corrective lenses had
deteriorated drastically (around 5 diopters) in less than two months. I
eventually concluded that what I had was a case of spherical aberration
carried to an extreme degree. (See Spherical Aberration in Appendix B).
If it were true that the cause of my dual vision was spherical aberration
resulting from deformation of the lens, then the lens had become accommodated,
since accommodation is always accompanied by spherical aberration, and vice
versa. Therefore, the persistence of dual vision indicated that the
accommodation also persisted. In other words, I had increased my myopia
remarkably, but as a side effect had created a second mode of vision close to
emmetropic.
Implications
I concluded that the bizarre results of this experiment had major implications
for the conventional wisdom about eye mech-anisms in several areas. I could be
cautious here, but why be reticent? ii 1. The Helmholtz-Fincham theory of accommodation is wrong. Accommodation is actuated by contraction of the ciliary muscle, true, but probably not by relaxation of the zonule so much as pulling the vitreous against the posterior surface of the lens.
2. The principal cause of myopia resides in the lens, and to a lesser degree in axial length.
3. The argument that myopic lenses are not accommodated because they tend to be thin is wrong. This could be explained by long-term compression, which produces a permanently accommodated lens in which only the periphery is flattened.
4. The extraocular muscles can cause the lens to accommodate.
Obviously, these statements directly contradict much of the conventional knowledge about eye mechanisms, for which there is a mountain of evidence. Below I will attempt to answer.
The Zonule Relaxation Theory of Accommodation
If the dual vision observed was caused by vitreous pressure, then the Helmholtz-Fincham theory of accommodation can not be correct. Briefly, the Helmholtz-Fincham theory states that the lens accommodates by means of relaxation of the zonular fibers. "Accommodation results from decreased tension: the driving
force--the motor--is the lens capsule. The decreased tension theory is attributed to Helmholtz. Considering the evidence, there is little reason to still call it a theory. Its only serious rival, proposed by Tscherning at the turn of the century, just survives by textbook repetition." (5, p. 87)
The hypothesis of vitreous pressure comes up against three exceptionally strong arguments. The conventional view is that:
1) The vitreous is unimportant in accommodation. This is proven by experiments in which accommodation occurs even without the presence of the vitreous in cases of vitrectomized eyes.
2) When the lens is freed from zonular tension, it assumes a more spherical shape, i.e. increases its power.
3) The zonular fibers relax during accommodation. When accommodation is observed in an eye in which the iris is absent, thereby exposing the zonules to view, they are clearly seen to relax their tension.
My answers to these objections are as follows:
1) That the vitreous is not required for the eye to accommodate. Almost all
eye researchers support this view. For example, Fisher states that "The
vitreous plays a negligible role during accommodation in modifying the
position or shape of the lens." Burian and Allen state that "...our
observations on the periphery of the vitreous surface strongly suggest that
the vitreous body, far from pressing on the periphery of the lens, was
actually under reduced tension during accommodation." (8)
However, a few researchers contradict this view. Araki reported that in
experiments on pig, dog and cat eyes, "...it is suggested that tension of the
ciliary muscle/zonules stretching from the posterior surface of the lens was
increased by forward movement of the ciliary body and consequently it resulted
in pressure to the posterior _peripheral_ (my emphasis) part of the lens...the
increase in pressure of the vitreous body due to contraction of the accom-
modative muscle is considered to be the most important factor for the
transformation of the lens." (10)
Suzuki performed an experiment in which he injected radiopaque material into
the vitreous of a cat's eye, which during accommodation moved in a direction
indicating that the vitreous was forced against the back of the lens and also
somewhat toward the posterior pole of the lens." (11)
An experiment by Koke produced a similar result. He injected cat eyes with
radiopaque material and took X-rays during miosis and mydriasis, which showed
that during accommodation the vitreous moved toward the lens and inward toward
the optic axis. (12)
The experiment that is most closely related to mine, because it involved
external pressure on the globe, is that of von Pflugk. He cut windows in the
equatorial region of bovine eyes and injected a drop of dye into the anterior
vitreous, midway between the ciliary body and the posterior pole of the lens.
Pressing against the ciliary body from the outside in a radial direction made
the dye move toward the lens capsule. (13)
2. The second objection to the vitreous/lens hypothesis is undoubtedly the
strongest of all: the demonstration that when freed from the tension of the
zonule, the lens assumes a more spherical form.
It is probable that the experiments of Fincham, more than any other factor,
tilted opinion away from Tscherning's theory and towards that of von
Helmholtz. In what is undoubtedly the demonstration that clinched the case for
zonular relaxation once and for all, he showed conclusively that without the
tension of the zonule, the lens becomes more spherical. An eye was made to
accommodate for distance viewing by the instillation of atropine and then
removed from the orbit and pointed upward after dissection of the cornea and
iris. The profile of the lens can then be photographed, and in this condition
it demonstrates the characteristics shape of the lens when the eye is looking
at a distance. However, when the fibers of the zonule are severed all around
by the sharp edge of a knife, the curvature of the anterior surface increases
markedly and "assumes the shape that it has under maximum accommodation," i.e.
the lens becomes thicker, as is clearly seen in the photographs taken by
Fincham.
This appears to be an unassailable argument. To recapitulate: when the
zonules that hold the lens in place are cut, the lens immediately becomes more
spherical, which obviously increases its power, a highly convincing
demonstration.
To counter this argument requires rejection, not of Fincham's observation (the
photographic evidence is too strong for that) but of his interpretation. When
the zonules were cut and the lens became more spherical, he ASSUMED that the
consequent change in the shape of the lens was the same as that which occurs
in accommodation. Could this be a non sequitur? I believe that it is at least
possible.
It is not inconceivable that the shape he observed was not the shape that
occurs in accommodation but merely looked like it. It is possible that the
lens could assume a more spherical shape under _two_ different conditions: 1)
When released from the tension of the zonule and 2) When molded by vitreous
pressure, with only the latter being true accommodation.
3. The third objection is based on the well-documented evidence that when the
lens accommodates, the zonular fibers relax their tension. The vitreous/lens
hypothesis, however, requires that there be some means to counteract the
vitreous pressure. If the lens is pushed forward by the vitreous, what could
hold the lens in its place? Obviously, the zonular fibers could not fulfill
this function if they are relaxed.
Although most of the standard textbooks on ophthalmology state simply that in
accommodation the zonular fibers relax their tension, this is not the whole
story. Several investigators have shown that there are TWO sets of fibers, and
that while the anterior fibers relax in accommodation, the posterior fibers
either remain tensed or increase their tension. I suspect that acceptance of
the relaxation theory was due in part to the fact that the anterior fibers,
being the most easily observed, were the first to be discovered and studied.
Evidence for the existence of two sets of zonular fibers has been reported by
several investigators. According to Suzuki, "during accommodation the
posterior valley became swollen toward the inner direction of the eyeball.
This could account for the relaxation of the zonules attached to the anterior
surface of the ciliary muscle.
"During more advanced accommodation, the anterior valley sank toward the outer
direction of the eyeball. This could account for the *contraction* of the
zonules attached to the posterior surface of the lens (italics added). (11)
An experiment by Araki showed that "electric recordings of the changes in
tension of the ciliary zonules suggested relaxation of the zonules which was
(sic) stretched to the anterior surface of the lens and on the contrary,
increased tension of that stretching to the posterior surfa (cat and dog
eyes). (10)
The Iris
Although it is possible that tension of the posterior zonular fibers might be
sufficient to withstand the pressure of the vitreous against the lens, I find
this unconvincing.
What other mechanism could hold the lens in place? An obvious candidate would
be the iris, if it weren't for the fact that more than a hundred years ago von
Graefe showed that the lens can accommodate perfectly well even when the iris
is not present. The anterior surface of the lens is slightly conoidal, and
earlier investigators proposed that this was caused by constriction by the
iris, the lens being molded by being forced through the opening of the pupil.
Apparently, von Graefe's demonstration was all that was needed to disprove the
iris hypothesis, yet it would seem unwise to base such an important conclusion
on a single case. Further-more, as I suggested above, when the lens is
released from traction, the more spherical form that it assumes may not be
true accommodation. If this is correct, and if the full amplitude of
accommodation seen by von Graefe was not true accommodation, then his
conclusion that the iris is not required for accommodation may be wrong.
It is highly improbable that with the vast amount of research done on the
iris, such an important function as counterpressure on the lens could remain
undetected. Yet a number of reports do suggest an iris/lens connection. And it
is interesting that the researchers themselves seem to be surprised by their
findings. Lowe reported that "During examination of a large series of eyes
that had pupils dilated after peripheral iridectomy...I was struck by the
marked curvature of the anterior lens surface within the enlarged pupil. +The
lens frequently appeared as though it were herniating through the enlarged
pupil, with the pupillary margin of the iris seeming to grip the lens." (15)
Jampel and Mindel, in a report on stimulation of the oculomotor nucleus in
monkeys, observed changes "... characterized by a conspicuous forward bulging
of the pupillary or central portion of the iris which produced a marked
convexity of the iris diaphragm and a marked increase in the depth of the
anterior chamber...On observation of the eye from the side during iris-bulge,
the central portion of the lens appeared to become conoidal and to move
forward into the anterior chamber." (17)
Although it is generally believed that the changes in lens shape in
accommodation occur principally in the anterior surface of the lens, the
hypothesis proposed here suggests that the posterior surface might undergo
equal or greater changes due to its direct contact with the vitreous.
In the rhesus monkey there is a similar mechanism involving the iris and the
sphincter muscle, although it is not clear which of these is of greater
importance in molding the lens.
Burian and Allen reported that "The most remarkable change was seen in the
middle one-third of the body of the iris. This part of the iris bowed backward
during active accommodation, forming a deep hollow, and returned to its normal
position when the eye was relaxed."
And Suzuki states that "Concerning the iris, its silhouette was a slightly
curved line, being convex anteriorly in the form of a physiological 'iris
bombe'. On stimulation, the iris showed a peculiar change. That is, besides
the change of the contraction of he pupil, the iris was bent reversely to the
posterior chamber, so that the central half of the iris was held in contact
with the anterior surface of the lens and the iris-lens apposition became
tighter over a much larger area."
All four of these reports describe the iris as being pressed against the lens,
and two of them note that the conoid form of the lens appears to be the result
of bulging through the pupil. Could the iris play a major role in
accommodation after all? This may appear too speculative to be taken
seriously,, yet the iris/lens mechanism is a well-documented fact in certain
birds and mammals. According to Walls, "The avian iris is always of material
assistance during accommodation in holding back the lens against which it
presses, and in inhibiting the peripheral part of the anterior surface of the
lens from bulging, thus concentrating the change-of-curvature in the part of
the surface opposite the pupil." (18)
Posterior and interior lens changes
The conventional wisdom that the principal changes occur in the anterior lens
was challenged by Patnaik, who wrote that "...the often stated and commonly
accepted statement, that it is the anterior lens surface which moves forward
while the posterior surface remains stationary and that it is only the
anterior surface which changes its curvature during accommodation seems not to
be correct.
"Our observations strongly indicate that during accommodation the increase in
the thickness of the anterior cortex is minimal, and that the change in the
posterior cortex is greater, and that in the nuclear thickness change is
greatest." This last may be especially significant because is raises the
possibility that the principal source of increased lens power in myopes could
be the nucleus.
Young also commented on the importance of the posterior surface: "The pressure
changes in the vitreous chamber may also play a role in the process of
accommodation, since the back lens surface could be molded by the increase in
pressure more effectively than the front lens surface. Unpublished phakometric
studies now indicate that the back lens surface contributes almost twice as
much to the total vergence of light and is second only to the cornea in its
refractive power. The attachment of the hyaloid membrane to the back lens
surface may play a major role in the development of the greater lens power of
the back lens surface. There is some evidence from children (sic) phakometry
that the back lens may have several curvatures rather than the simple,
monotonic curve of the front lens surface."
The Lens Capsule
When Helmholtz first proposed his relaxation theory of accommodation, it was
criticized on the ground that relaxation of the zonule failed to explain how
the anterior central region of the lens assumes a conoidal shape. Tscherning
claimed that this could only be produced by pressure from the vitreous, which
he believed molded the softer cortex of the lens around the harder nucleus.
Fincham thought he found an answer in evidence that the thickness of the lens
capsule varies, and he believed that these minute differences in thickness
were sufficient to impose a conoidal shape on the anterior surface of the lens
(14).
Although it is conceivable that the capsule could mold the lens to a slight
degree in this manner, the evidence from my own experiment indicates that this
explanation is insufficient. Because the degree of spherical aberration was so
extreme, which indicated extreme flattening of the periphery of the lens, it
is difficult to believe that it could have been produced by such minute
differences in capsule thickness. In fact, the contrary could be argued just
as persuasively: that the differences in capsule thickness could be the RESULT
of pressure on the lens. The thin segment of the capsule in the anterior axial
area could be caused by stretching of the capsule, while the thin posterior
segment could be caused by the vitreous squeezing the capsule against the
lens.
The Extraocular Muscle Hypothesis
The hypothesis that the extraocular muscles play a role in the causation of
myopia is certainly not new. It has been suggested by numerous investigators
over the years. A major difference, however, is that in none of these
hypotheses has it been proposed that they have any effect on the lens. All are
limited to the concept of elongation of the globe, usually through elevation
of the intraocular pressure.
The case is similar with regard to the numerous hypotheses that propose
contraction of the ciliary muscle as a cause of myopia. They all postulate
that such contraction elongates the globe, and do not suggest any effect on
the lens.
The Persistence of Accommodation and the Etiology of Myopia
A significant feature of the experiment was the amount of time in which the
lens was subjected to pressure and, I believe, accommodation. An eye whose
lens remains accommodated will show blurred vision for distance gaze. But the
lens is not supposed to remain accommodated when the stimulus for
accommodation is removed. According to orthodox theory, accommodation is
maintained only as long as the gaze is directed at a near object. When the
gaze is shifted to a distant object, the lens reverts almost immediately to
the unaccommodated form required for distance vision. The consensus of opinion
is that these accommodative changes take about one second. I believe that this
view is too restrictive, probably a result of too much reliance on laboratory
studies that deal only with momentary accom-modation, and that there is a
crucial difference between momen-tary and repeated prolonged accommodation.
The persistence of dual vision in my own case, as well as the findings of a
number of investigators on the slowness of lens changes, leads to the
conclusion that the longer a lens is maintained in a particular form, the
longer it takes to return to its original form when released. Further, with
high degrees of deformation the lens does not return entirely to its original
form. In my case, the sharp image persisted for more than four years before it
gradually began to disappear. I assume that this was due to a gradual decrease
in the degree of flattening of the periphery when the pressure was removed.
Since the blurred component of the image remained largely unchanged,
apparently this was because the central region of the lens changed very
little.
On the question of the slowness of lens changes, I am not alone. Lancaster
states that "...if the accommodation is maintained a few minutes at the
maximum, the near point does get nearer and the eye may become accommodated
20% to 30% or more, nearer than at the first. If the near point at the start
was 6 D. it may become 7, 8, or 9 D. This...is due to the viscosity of the
lens substance. An immediate rapid (about one second) change takes place when
the lens adjusts itself for a near object, but if a maximum effort of
accommodation continues to be made, the lens slowly (5 to 10 minutes) goes on
changing its shape and becoming more strongly refractive.
"Commonly, when the eye, after such an intense effort of accommodation, is
shifted to a distant object, although the ciliary muscle may promptly relax,
it takes time (a few seconds to a few minutes depending on how long the near
effort was continued) for the lens to regain its normal shape adapted to a
distance. This is due to the viscosity which makes a change in the shape slow"
Other investigators have also demonstrated the slowness of lens changes.
According to Kikkawa and Sato, "Application of an external force to the lens
caused a rapid deformation followed by a second phase of slow deformation. On
removal of the force, a rapid partial reversal of the deformation occurred and
was followed by a gradual restoration; complete recovery was not achieved.
Kabe reported a similar result from his investigations. He showed that when
accommodation is increasing, the change in the apparent curvature of the
anterior surface of the lens is slow and continuous, but when accommodation is
decreasing, there is a prompt, followed by a slow phase (21).
The idea that myopia could be the result of increased lens power has always
been countered by a very strong argument. If in myopic eyes the lenses are
permanently accommodated, they would tend to be thicker than the lenses of
emmetropes. Not only is this not true, but in general, myopic eyes tend to
have even thinner lenses than emmetropes. As far as myopia is concerned, there
is a clear consensus of opinion as to the importance of the lens: It ranks
very low.
"Three variables, then, the axial length, the shape of the cornea, and the
power of the crystalline lens, exert the greatest effect upon refraction.
There is good agreement among authors as to the relative influence which each
of these exerts, the axial length being the greatest, followed by the cornea
and lens in that order. There are minor disagreements among investigators as
to the relative importance of the lest of these three elements, the
crystalline lens: Van Alphen's work suggests perhaps the lowest estimate of
the importance of the lens. However, all investigators arrive at the same
order of importance, and at relative values not too different from those
obtained by others".
Sorsby seemed to be puzzled by the existence of thin lenses in myopes and
tried to find a way out of the difficulty be speculating about the tension of
the zonule. He stated that, "Obviously, a large fairly spherical eye will have
not only a long anteropsterior axis but also a flatter cornea. Flattening of
the lens in a large eye is more difficult to understand, but a more marked
tension on the suspensory ligaments may be a possible factor."
The barrier to a resolution of this contradiction seems to be the belief that
a thin lens can not be an accommodated lens. But if the slowness of lens
changes is correct, and there seems to be no dispute about this, then in
myopes the lens must be accommodated. Consider the case of a myope with a
history of nearwork, e.g. with hour after hour of reading over months and
years. It could very well be that with repeated periods of prolonged
accommodation the lens, with its slow reaction time, would never return
completely to the unaccommodated state.
The conventional wisdom is that the lenses of myopes are not only not of the
same power as emmetropes, but are of even lower power. How can this be? It
would appear that eye research is so compartmentalized that two such
contradictory facts--thin lenses in myopes and the slowness of lens changes--
can go unnoticed and unresolved.
The possibility that a lens subjected to frequent prolonged accommodation for
months and years may not have the same shape as a lens that is ad for months
and years may not have the same shape as a lens that is accommodated
momentarily has apparently not been considered.
The hypothesis of vitreous pressure suggests that such prolonged pressure
might produce a lens with a flattened periphery but with a high degree of
curvature in the axial region, i.e. a lens that is thin yet accommodated. I
have found only one reference in the literature that even indirectly supports
this hypothesis. In a study of accommodation, Otsuka stated that "the thicker
the lens became during accommodation, the thinner the lens became annually."
This is intriguing, but unfortunately he did not elaborate.
It may be that a single factor, external pressure on the globe, produces two
separate effects, in opposite directions: anteriorly it accommodates the lens,
and posteriorly it elongates the globe. I believe that one consequence of this
dual effect is that axial elongation has masked the role of the lens. With
such a logical and easily demonstrated explanation available, there has been
little incentive to look for an additional factor, and thus the lens has been
practically ignored.
The indications that external pressure had produced accommodation by forcing
the vitreous against the lens suggests the possibility that the vitreous plays
a part in normal accommodation, i.e. that the experiment mimicked what happens
in normal accommodation. It is possible that in normal accommodation,
contraction of the ciliary muscle pulls the vitreous forward against the lens
(as suggested by Cramer in 1851, and later by Tscherning), whereas in this
experiment the vitreous was _pushed_forward by external pressure exerted on
the globe.
Theory versus Observation
Curiously, there is a case of photographic evidence that the lens becomes
thinner with accommodation, even momentary accommodation. This appears in a
paper by Burian and Allen which shows photographs of the lens during three
stages: 1) Relaxation of accommodation; 2) Active accommodation; and 3) Active
accommodation (apparently further). However, instead of showing that the lens
thickens with accommodation, it shows precisely the opposite. In each
photograph it can be clearly seen that the lens becomes progressively thinner,
at least in the peripheral area.
These photographs are reproduced in Duke-Elder's System of Ophthalmology (25,
p. 163--possibly different pages in other editions) and in a more recent work
by the late David Michaels, Visual Optics and Refraction. Nevertheless, except
for noting the flatness of the posterior surface of the lens, none of these
authors comment on the striking fact that the lens clearly becomes thinner as
it accommodates. In fact, in the text preceding the photographs, Duke-Elder
states: "All are agreed that the lens increases in thickness during
accommodation" (!!). It seems that theory is more potent than direct
observation.
An additional note on this photograph: Burian and Allen state that "our
observations on the periphery of the vitreous surface strongly suggested that
the vitreous body, far from pressing upon the periphery of the lens, was
actually under reduced tension during accommodation." They believe that the
evidence for this is the bowing back of the vitreous, which they believe
creates "an optically empty space in front of the vitreous." They fail to
explain how this "optically empty space" could occur. A possible explanation
is that this space, apparently the canal of Petit (the space between the
zonule and the vitreous) has expanded from an inflow of aqueous under
pressure. Johnson demonstrated such an inflow by the use of dyes, and he
believed that accommodation was actuated by hydraulic pressure exerted around
the periphery of the lens (9). Duke-Elder dismissed this as a "bizarre
hydraulic theory," but the opening and closing of the trabecular meshwork by
the action of the ciliary muscle does suggest a hydraulic component of
accommodation.
Lens Changes Hidden
If significant lens changes do occur in the posterior surface of the lens,
this would be one more example of how the clues to lens involvement in myopia
are hidden.
Consider the case of a myope who undergoes a routine eye examination. If he
has a moderate degree of myopia, the posterior surface of the lens could be
flattened just enough to have created a second focal point. However, the
examiner would never discover this for two reasons: He will probably not look
for something whose existence he is unaware of; and because the second focal
point would not reach all the way to the retina, no clear secondary image is
formed. Only with a particular lens power which would push the secondary focal
point to the retina would a clear secondary image be formed.
Additional Secondary Images
In order to simplify this discussion, I have limited it to the primary and
secondary focal points and their images. Actually, however, testing of myopes
with different lens powers reveals that there are often other images, fainter
and more difficult to detect, which indicate the presence of other focal
points situated between the primary and secondary focal points. The origin of
these could be the various isoindicial surfaces within the lens. Some high
myopes, when tested with various lens powers, describe not a smooth, diffuse
blur, but rather several superimposed blurred images.
Although I didn't appreciate it at the time, it was fortunate that the first
subject for the experiment was myself. What if I had found a willing
emmetrope, or a subject with only a small degree of myopia? The outcome would
probably been very different. The experiment would probably produced a small
degree of myopia, partly from axial elongation and partly from lens changes
(just as I believe occurs in normal myopia).
The significant point, however, is that I would never have suspected the lens,
but would have attributed the myopia to axial elongation alone. Because I was
a myope of fairly high degree, I believe that flattening of the periphery of
the lens was fairly well advanced, so that the secondary focal point was
already located very close to the retina. It then required very little
additional flattening to push all the way, or very close to, the retina, at
which time I became aware of the secondary image.
A laymen who reads textbooks on ophthalmology can easily get the impression of
a solid edifice of knowledge built on firm foundations. Yet at least one
researcher, Ludlam, suggests that some of the most basic facts about the eye
are based on faulty data and should be re-evaluated. These include invalid
mathematical assumptions, mixed sampling, inadequate experimental technique,
and oversimplified models of the refractive system, some of these dating from
the nineteenth century.
"Nevertheless, the analyses and conclusions drawn from such studies can be no
better than either the methods of acquisition of the basic data or the
validity of the assumptions underlying the mathematical formulation of the
ocular model.
"It is well to note that in all of these studies the model of the ocular
system utilized has consisted of:
1. Spherical refracting surfaces, causing a systematic under-estimation of the
paraxial refracting power of each surface. 5. A homogeneous monoindicial lens.
This places a high order of importance on the accuracy and precision of the
measures of curvature of both the anterior and posterior surfaces of the lens
and concomitantly increases the potential effects of spherical assumption.
" In addition, in none of these studies have all the refractive components of
any given eye been measured. There has always been _at least one_ component
whose value was calculated from the other measured elements, so that the
measurement errors would all tend to accumulate in the non-measured element.
Since the measurement errors have not always been stated with sufficient
clarity to enable the effects of these errors to be asses, the probability
exists that measurement errors have contributed substantially to spurious
correlations of measured and calculated elements, as for example between the
lens and axial length." (29)
To say that long-standing theories are not easily overturned is to state the
obvious. As Kuhn put it, "...few scientists will easily be persuaded to adopt
a viewpoint that again opens to question many problems that had previously
been solved" (30, p. 169). Ophthalmology is no exception, and scattered
reports in the literature that cast doubt on the conventional wisdom, for just
one example, a case described by Luedde (31), are simply ignored.
How Not to Cure Myopia
The lens/vitreous hypothesis provides an explanation for the failure of two
therapeutic measures aimed at preventing or slowing the progress of myopia:
the use of cycloplegics, and base-in prisms. In the case of cycloplegics, they
relax the ciliary muscle for only a few hours at a time, while the lens
requires many months for a significant reduction in the degree of
accommodation. More importantly, in all these regimens the subjects are
permitted to continue doing nearwork, so that accommodation could still have
been maintained largely by vitreous pressure alone.
The use of base-in prisms to prevent convergence, and consequently
accommodation has, I believe, failed for an unsuspected reason: the optical
distortion inherent in such prisms. I used base-in prisms extensively in
various experiments aimed at reducing accommodation and was surprised to find
that in some cases the degree of myopia _increase_. Strong base-in prisms
produce considerable distortion, and a possible explanation is that in trying
to fuse the distorted images, the eyes were forced to incyclorotate in
antagonism to each other, and this in turn required the superior oblique
muscles to maintain contraction as long as the image was fused, thereby
exerting pressure on the globe and maintaining accommodation.
Scientific Error
It is highly unlikely that such well-established concepts as the theory of
accommodation and the role of the crystalline lens could be wrong. The
relaxation theory is extremely well documented and for more than forty years
has been considered the only acceptable explanation of how the eye
accommodates for near vision. The possibility that many researchers in many
different countries could be wrong about such a basic theory will not be taken
seriously.
Nevertheless, there have been a few cases of major reversals of scientific
opinion. The case of nervous system plasticity provides a good example. For
more than fifty years it was universally believed, and confirmed by hundreds
of experiments by reputable scientists, the plasticity of the central nervous
system allowed any muscle nerve to reconnected to any other muscle and, with
training, achieve full restoration of function. it is now known that this is
not true.
According to R.W. Sperry, "During the past 15 years, however, scientific and
medical opinion has undergone a major shift, amounting to an almost complete
about-face ... The evidence for this view, which comes from new experiments
and exacting clinical observations, is so persuasive that it is difficult to
understand how the opposite view could have prevailed for so long. It appears
that most of the earlier reports of the high functional plasticity of the
nervous system will go down in the record as unfortunate examples of how an
erroneous medical or scientific opinion, once implanted can snowball until it
biases experimental observations and curshes dissenting opinions...Hundreds
of experiments seemed to support the now-discounted opinion..." (28).
CONCLUSION
1. An experiment in long-term compression of the globe of the eye created
monocular diplopia, seen as two separate images superimposed, one on the
other.
2. It is hypothesized that the cause of this effect was the spherical
aberration of the crystalline lens resulting from pressure of the superior
oblique muscles transmitted through the sclera, which forced the vitreous
forward, pressing it against the posterior surface of the lens.
3. This suggests a role of the vitreous in normal accommodation, i.e. that
ciliary contraction pulls the vitreous forward to mold the lens.
4. This vitreous-mediated accommodation may be enhanced by additional
compression from the vitreous from an external source, the action of the
extraocular muscles.
5. The extremely slow changes in lens shape strongly implicate nearwork in the
etiology of myopia. Because of the slowness of recovery from accommodation,
long periods of accommodation with insufficient intervals of rest result in a
lens that becomes permanently accommodated. The accommodated state of the lens may be additionally enhanced by the action of the extraocular muscles in
nearwork, particularly reading.
6. The argument that myopic lenses are not accommodated because they tend to
be thin could be explained by long-term compression. This could produce an
accommodated lens with either a flattened periphery and convex axial region,
or a thin lens with accommodative changes in the nucleus.
It would be curious if, after the tremendous amount of work and speculation on
the causes of myopia, the answer turned out to a simple one, the kind of
answer that might be given by a layman applying superficial logic. Assume that
this hypothetical layman hears a brief explanation of the mechanism of
accommodation: that when looking at distant objects the lens becomes somewhat
flat, but that in order to see near objects clearly, it becomes more
spherical; and if it were able to retain its spherical form while looking at
distant objects, they would be seen as blurred since the eye is adjusted for
near vision. Then he is given a brief description of myopia, that the myope
sees near objects clearly, but distant objects are seen as blurred. He is
further told that the longer the eye is focused on a near object, the longer
it takes to change its shape. It would be not at all surprising if he made the
logical connection and said, "I get it. The eye adjusted for near vision and
then sort of got stuck so it can't re-adjust for distant vision."
Although the lens/vitreous hypotheses doesn't resolve all problems, I believe
it resolves some, and anyway, as Kuhn Points out, "no paradigm ever solves all
the problems it defines and since no two paradigms leave all the same problems
unsolved, paradigm debates always involve the question: Which problems is it
more significant to have solved?" (30, p. 110).
It is interesting to consider the extent to which a mistaken theory is a
barrier to solution of a problem, and how a new point of view can open up
previously unconsidered possibilities. These possibilities could include not
only finally determining the etiology of myopia, but could include prevention,
or even cure.
The pessimistic view was expressed by Donders over a hundred years ago: "The
more our knowledge of the basis of this anomaly has been established, the more
certainly does any expectation (of a cure) appear to be destroyed, even with
respect to the future" (32, p. 415). Today, probably most eye researchers
would share this view.
If the hypothesis of oblique muscle/vitreous/lens connection is confirmed, it
could open the way to new techniques to prevent or slow the progression of
m/lens connection is confirmed, it could open the way to new techniques to
prevent or slow the progression of myopia. Further, it is not impossible that
a cure for myopia could be devised, e.g. invasive techniques to reshape the
curvature of the lens.
Appendix A.
As far as I know, the debate on the etiology of myopia between those who claim
a hereditary basis and those who point to environmental causes still favors
the former. Nevertheless, the reports of a relationship between nearwork and
myopia should not be ignored. No one would dispute that the most common form
of nearwork and the most "unnatural" use of the eyes is reading. Because the
continuous horizontal scanning movements of the eyes in reading with downward
gaze require alternate contraction and relaxation of the oblique muscles, I
decided to simulate this condition in an enhanced form to determine if such
contraction could produce elongation of the globe. (Actually, the axial
elongation theory is an oversimplification, in that it fails to explain, for
example, normal vision in elongated eyes and myopia in relatively short eyes.
The investigations of Steiger (2) and others produced a shift in emphasis to
the question of the variability of the different ocular components and how
they interact with each other to produce emmetropia (absence of a refractive
error) or ametropia (presence of a refractive error).
Because the eye muscles are not subject to individual voluntary control, it
was necessary to devise some means to force the superior obliques to contract
while maintaining relative relaxation of the other extraocular muscles. I
thought that the natural tendency of the eyes to fuse to disparate images
could be utilized for this purpose. I constructed a viewing device which
contained two identical photographic transparencies depicting a visually rich
pattern. When the subject looked through the device, each eye viewed one of
the transparencies; the visual cortex then fuses the two images to form a
single scene. The transparencies were then incyclorotated, i.e. as seen by the
subject, the right-side image was rotated counterclockwise and the left-side
image was rotated clockwise. In order to maintain fusion of the two images,
each eye must then rotate in the same direction as the image it is viewing,
i.e. the upper end of the vertical meridian of each eye leans nasalwards.
The movement of incyclorotation is effected principally by the superior
oblique muscles, but there is a limit as to how far the globe can rotate,
since this is opposed by the check ligaments and other fascial structures of
the orbit. If an effort is made to maintain fusion, the traction of the
superior obliques, which wrap part way around the globe, will exert pressure
in the general area of the equatorial meridian.
The device was later modified for portable use to facilitate long-term
viewing. Instead of viewing transparencies, the subject looked through a
system of mirrors that tilted in like manner any scene viewed. The amount of
tilt (incyclorotation) varied between 6 and 12 degrees. This is not to say
that if the images are rotated, say, 8 degrees, each eye will also rotate
exactly 8 degrees; eye rotation can be as much as 2 degrees less. This is
because of Panum's fusional area, which in stereopsis allows the image to be
pulled apart by some 2 degrees before being broken up into two separate
images. The images are actually pulled apart on the retina, but a supra-
retinal function maintains perception of a single image (33). In order to
eliminate any stimulus to accommodation, distance fixation of at least six
meters was maintained.
Because I was unable to make axial length measurements, I had to rely on
changes in the visual acuity to determine if there had been any changes in
axial length. Thus, if my visual acuity began to deteriorate in the course of
the experiment, this could be an indication that the globe had elongated,
presumably due to compression of the globe by the superior obliques.
Appendix B.
Spherical aberration
Spherical aberration is that condition in which the rays passing through a
convex lens do not all come to a focus on a single point. Ivanoff (4) and
others have shown that spherical aberration is normal in the human eye. When
the eye is ate rest the spherical aberration is positive, which means that the
rays passing through the periphery of the lens come to a focus in front of
rays passing through the axial region of the lens. As the lens accommodates to
view a near object and begins to change its shape, the spherical aberration
decrease, and at around 3 diopters there is almost no aberration at all, i.e.
all the rays come to a focus at the same point. If the eye accommodates
further, the aberration begins to reverse, in which case the peripheral rays
come to a focus at a point behind the axial rays.
REFERENCES
1. Curtin B. The Myopias. Philadelphia: Harper and Row, 1985. 2. Steiger A.
Die Entstehung del Spharischen Refraktionen des menschlichen Auges. Berlin:
S. Karger, 1913.
3. Deller J, O'Connor A, and Sorsby A. X-ray measurements of the
diameter of the living eye. Proc. R. Soc. (Biol.), Lond. 134: 456-462, 1947.
4. Ivanoff A. Au Sujet de l'Aberration spherique de l'oeil. Optica Acta 3: 47-
48, 1956.
5. Michaels D. Visual Optics and Refraction. Third edition. St.
Louis: C.V. Mosby, 1985.
6. Fisher R. The vitreous and lens in accommodation.
Trans Opthalmol. Soc. UK. 102: 318-322, 1982.
7. Fisher R. Br. J. Ophthalmol.
67: 206, 1983.
8. Buran H. and Allen L. Mechanical changes during
accommodation observed by gonioscopy. Arch. Ophthalmol. 54: 66-72, 1955.
9.Johnson L. A new theory of accommodation. Arch Ophthalmol. 53: 426-430, 1924.
10. Araki M. Changes of the ciliary region and the ciliary zonule in
accommodation. Jpn. J. Ophthalmol. 9: 50-58, 1965.
11. Suzuki H. Observations on the intraocular changes associated with
accommodation. Jpn. J. Ophthalmol. 15: 47-58, 1971.
12. Koke M. Mechanism of accommodation. Arch. Ophthalmol. 27: 950-968, 1942.
13. Von Pflugk A. New ways in the study of accommodation V. The vitreous in
the accommodating eye. Graefes Arch. Clin. Exp. Ophthalmol. 133: 545-558,
1935.
14. Fincham E F. The Mechanism of Accommodation. Br. J. Ophthalmol 8
(Supple.) 1937.
15. Lowe R F. Anteiror lens curvature. Comparison between
normal eyes and those with primary angle-closure glaucoma. Br. J. Ophthalmol.
56: 409-413, 1972.
16 Suzuki H. Observations on the intraocular changes asociated with
accommodation: an experimental study using radiographic technique. Exp. Eye
Res. 17: 119-128, 1973.
17. Jampel R S. and Mindel J. The nucleus for accommodation in the midbrain of
the macaque. Invest. Ophthalmol. Vis. Sci. 6: 40-50, 1967.
18. Walls G. The Vertebrate Eye and its Adaptive Radiation. New York: Hafner,
1967. 19. Lancaster W. Refraction and Motility. Springfield: Charles C.
Thomas, 1952.
20. Kikkawa Y. and Sato T. Elastic properties of the lens. Exp Eye REs. 2:
210-215, 1963.
21. Kabe S. Dynamic aspects of accommodation. Photographic records of the 3rd
Purkinje-image showing changes in size associated with accommodation. Rincho
Ganka (Jpn J. Clin Ophthalmol.) 21: 341-352, 1967.
22. Hirsch M. In Refractive Anomalies of the Eye. Public Health Service
Publication No. 1687, National Institute of Neuroological Diseases and
Blindness, Monograph No. 5, U.S. Department of Health, Education and Wlefare,
1967. Hirsch, M.
23. Sorsby A. Modern Ophthalmology, 2nd Ed. Vol. 3. London: Butterworth, 1972.
24. Otsuka J, Hirano S, Suzuki K, and Imagawa N. A New Approach to the Theory
of Accommodation. Excerpta Medica INternational Congress Series No. 222: 983-
990, 1970.
25. Duke-Elder S. System of Ophthalmology Vol. V. London: Henry Kimpton, 1970.
26. Patknaik B. A photographic study of accommodative mechanisms: Changes in
the lens nucleus during accommodation. Invest. Ophthalmol. Vis. Sci. 6: 601-
611, 1967.
27. Young F. Documenta Ophthalmologica Proceedings Series, Volume
28 (Third International Conference on Myopia, Copenhagen, 1980).
28. Sperry R. W. The Growth of Nerve Circuits. Sci Am. 68-75, Nov. 1959.
29. Ludlam W. In Refractive Anomalies of the Eye. Public Health Service
Publication No. 1687, National Institute of Neurological Diseases and
Blindness, Monograph No. 5, U.S. Department of Health, Education and Wlefare,
1967.
30. Kuhn T S. The Structure of Scientific Revolutions. Chicago: University of
Chicago Press, 1970.
31 Luedde H. What subluxated lenses reveal about the mechanism of
accommodation. Am J. Ophthalmol. 24: 40-45, 1941.
32. Donders F.C. On the Anomalies of Accommodation and Refraction of the Eye.
London: The Sydenham Society, 1864.
33. Fender D. Extension of Panum's fusional area in binocularly stabilized
vision. J. Opt. Soc. Am. 57: 819-830, 1967.