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Concerned About Unconventional Mental Health Interventions?

Concerned About Unconventional Mental Health Interventions?
Alternative Psychotherapies: Evaluating Unconventional Mental Health Treatments

Thursday, September 2, 2010

When a Scientist Doesn't Think Like a Scientist: Review of Susan Barry's "Fixing My Gaze"

Susan Barry’s recent book, Fixing my gaze (2009), is an engaging narrative of life with a
small but intrusive disability – strabismus, or “crossed eyes”, with its common effect, poor depth
perception. Barry recounts the events of her infancy, when her strabismus developed; the
surgeries that cosmetically corrected the condition without entirely dealing with problems of
vision; her awkward school days; difficulty with driving and other tasks requiring judgment of
depth; and so on until a behavioral treatment, she says, transformed her life. She describes
her early and recent experiences vividly, even poetically, and intersperses scientific discussions
with anecdotes that serve as the “spoonful of sugar that helps the medicine go down”. But she
seems to forget her training in neuroscience when she should be thinking critically about the
effectiveness of treatments. Regrettably, this rather charming and informative book serves as an
extended advertisement for “developmental optometry” or “orthoptics”, a program that claims to
correct some problems of vision by eye exercises that increase control of convergence and
divergence (co-ordinated eye movements that are needed for ideal visual ability). Barry notes
that she excludes from consideration self-help orthoptic methods like the Bates method, which
were critiqued by Worrall, Nevyas, and Barrett in 2009. However, the method she advocates, the
Brock method, appears to have as little plausibility and as weak an evidence basis as the others
do. In addition, Barry speaks of her improved visual functioning as due to “rewiring” of the
brain, and, like many others who resort to this inapt “wiring” metaphor, suggests that high levels
of juvenile brain plasticity persist throughout life. It’s possible that they do, but Barry’s examples
may be more parsimoniously explained by reference to the less dramatic brain changes we call
Barry’s experience of strabismus and its consequences was not unusual, but her book is
unique in providing an understanding of the subjective experience of a strabismic. She notes her
early problems with reading and later problems with looking into the distance and with driving
confidently-- these in spite of excellent acuity of vision in each eye tested separately.
Nevertheless, she did drive, used a stereomicroscope, played tennis, and did not have any sense
of missing the experience of depth. Indeed, because she could use monocular depth cues
(information that can come from one eye rather than needing both), she did have some ability to
judge depth. As far as is known, though, she could not experience the very clear and accurate
sense of distance that comes from using retinal disparity, or a comparison of images as they
occur simultaneously at the two eyes (the reason for this will be discussed a little later). In
middle age, she began to experience shifts or “jiggling” of vision to such an extent that she
consulted a number of specialists. Following treatment by a developmental optometrist, who
prescribed “orthoptic” or “vision therapy” eye exercises, she reports that she began to have vivid
experiences of depth and improved her confidence and skill in driving and other tasks needing
distance judgments. Barry attributes her improved visual skills to a type of vision therapy, a
treatment category that has been defined as “a proposed optometric treatment for developing
efficient visual skills and processing… as a treatment for accommodative disorders, amblyopia,
binocular disorders (strabismic and nonstrabismic), learning disabilities, and ocular motility
disorders” (CIGNA Medical Coverage Policy, 2008, p. 1).
Although there is much that is valuable in Barry’s description of her subjective visual
experience, it is notable that little in the way of objective measures can be retrieved from her
early life. She provides in endnotes some objective measures made at the beginning and at the
end of her treatment, a period of 7 years. These indicate improvements in co-ordinated control of
eye movements. However, at no time does there seem to have been measurement of actual
judgment of depth, using the simple Howard-Dohlman apparatus so familiar to past generations
of psychology students. This device allows an observer to look through a small window into an
illuminated box in which there are two vertical rods. A system of strings allows the observer to
pull each rod backward or forward until the two appear to be side-by-side, the same distance
away. Normally, people do this poorly when using one eye at a time, and very well when they
use both eyes, and the difference between the monocular and binocular conditions shows how
well the eyes are used in coordination and how well retinal disparity is taken into account.
To examine the claims Barry makes on behalf of developmental optometrists, we need to
consider the plausibility of the claimed “rewiring” mechanism, the possibility of alternative
mechanisms, and the empirical evidence that the treatment Barry received was an effective
treatment for strabismic problems.

Is It Plausible That Orthoptic Treatment Could Cause “Rewiring”?

Barry suggests that she had been unable to use retinal disparity to judge distance, that this
was impossible because of the absence of binocular cells in the visual cortex, and that orthoptic
exercises allowed her to develop binocular cells receiving information from both eyes at once.
To discuss these issues, we need first to consider the question of plasticity. This term refers to
the extent to which development is guided by environmental stimulation. If a characteristic is
pretty well determined by heredity no matter what stimulation occurs (e.g., eye color), plasticity
is low. If it were possible to “rewire” all sorts of brain structures, as Barry implies, very high
plasticity would be present. But some aspects of development show high plasticity only during a
certain period of life (experience-expectant plasticity), while others can be guided by the
environment throughout life (experience-dependent plasticity). Quick language learning in early
life is an example of experience-expectant plasticity, and our slow,plodding acquisition of
vocabulary words later on is an example of experience-dependent plasticity.
The use of retinal disparity is usually considered to be a matter of experience-expectant
plasticity. As Barry points out, babies in the first months do not use their eyes together, but
switch attention from one to the other. By about 6 months, they are moving the eyes together.
This causes the image of an object they are looking at to fall on matching areas (corresponding
points) on the left and on the right retina. Messages are sent to the visual cortex simultaneously
from the two stimulated areas, and they cause activity in a single neuron which “lights up” only
when it gets a message from both eyes. This binocular neuron’s activity indicates that the two
eyes are looking at the same object in the same place, rather than two different objects, one seen
by the right and one by the left eye.
Repeating this experience many times makes the binocular neuron more responsive and
strengthens the connection between retinal areas and their associated neurons. But covering one
of the baby’s eyes for as little as a week (perhaps because of an injury), or a big difference in
the clearness of the images at the two eyes, can prevent the development of the connection with
the binocular neuron, and can even reduce the number of neurons from a single eye to the brain
until that eye is functionally blind. Similarly, if the baby is cross-eyed, and if the eyes often do
not co-ordinate, binocular neurons would not be likely to make normal connections. Studies of
cats and monkeys, by Hubel and Wiesel (1965), showed that animals deprived of co-ordinated
visual experiences in early life would develop abnormal use of their eyes and poor depth
perception. Another relevant point is that human babies go through at about 8 months a period of
exuberant synaptogenesis-- they create many synaptic connections between neurons, and indeed
have more synapses than they will ever have again in their lives. But some months later they
begin a process called “pruning” in which unused synapses are destroyed, and neurons
themselves disappear through programmed cell death ( Blakemore, 1989).
All these points challenge the plausibility of a continuing plasticity of the visual cortex
that would allow for major changes during later adulthood. However, it would be not be wise to
assume that we can completely reject the existence of such plasticity. The animal work by Hubel
and Wiesel is the only experimental evidence we have to depend on, and there are two problems
about generalizing from it. One is that Hubel and Wiesel had to kill the animals in order to
examine most of the brain features that interested them, and this was done fairly soon, so there
was no opportunity to see whether functions would be recovered or whether neural connections
would shift back to what they had been. Generalizing from non-humans to humans does not
necessarily give accurate answers about humans, either; even very similar species may differ in
important respects. A critical period, or time when experience had to occur in order to have an
effect, may have been present for cats, even for monkeys, but may not be the case for human
beings.If human beings are different in this way, it might be plausible that later experience could
affect the use of retinal disparity, although the other points made earlier suggest it is not. The
available information about human beings comes from uncontrolled studies showing the loss of
acuity in an eye following strabismus or patching of an eye in infancy. Rare reports of humans
who have had life-long cataracts removed in adulthood indicate that these people have not
recovered normal vision in spite of therapeutic and educational efforts (Gregory, 1997), but it is
hard to know whether visual problems were caused by the strabismus or cataract experience, or by additional factors that caused the original problem.

Is It Plausible That Other Mechanisms Could Be Affected by Eye Exercises?

Barry stresses the idea that the eye exercises she did might have altered the visual cortex
and other brain areas, perhaps through changes in long-term potentiation and consequent
improvement in the responsiveness of binocular neurons. However, there are other aspects of
vision that relate to retinal disparity; Barry mentions these, but returns to brain “rewiring” as her
preferred explanation. Given the arguments against persistence of early plasticity of the brain,
though, it is important to keep in mind that there are other plausible mechanisms by which
improved control over eye movements could cause better depth perception. These include the use
of the horopter for comparison of distances, constancy mechanisms, and visual adaptation.

Using the horopter.

How do people with a history of normal vision use retinal disparity?
The stimulation of a binocular neuron is not the only factor to be considered when we think
about judgment of depth using both eyes.
Older children or adults who have a normal visual history, and who have useful binocular
neurons, employ retinal disparity as their best way of judging distances. They can fixate (“fix”
the gaze) with both eyes on a single object, so the images at right and left eye fall on
corresponding points and activate the appropriate binocular neuron. This provides a single
“fused” image rather than separate images for each eye (double vision), and the fusion is
accompanied by a sense of depth. When this happens, however, the fixated object is not
necessarily the only one for which a single image is seen. Any object which is at any point on an
imaginary surface, all of whose points are at equal distances from the eyes, also has its images at
right and left eye fall on corresponding points, and is seen as a single object with fused images.
This imaginary surface, the horopter, shifts its position as the individual fixates objects at
different distances. Wherever the horopter may be, though, it determines which objects are seen
singly and which ones have double images. All objects that are off the horopter are experienced
as double images, but those that are very close to the horopter overlap so much that it is almost
as if they were fused. The farther the object from the horopter, the less the images overlap-- no
matter whether the object is on the same side of the horopter as the observer (near her) or on the
opposite side (far away). The overlapping or less-overlapping nature of the double images
provides information about depth.
Why don’t we consciously experience all these double images? We don’t pay attention to
them. We only pay attention to the object we are “looking at”. But we are able to pay attention
to double images by voluntary efforts. For example, when you are driving, you pay attention to
the road, or perhaps to your speedometer or other dashboard instrument. However, your hands on
the steering wheel are probably within your visual field. If you attend to them while still looking
ahead, you may notice that they look large; glance down at a hand, and it seems of normal size
again. Why? When the hand is not at the horopter, you see an overlapping doubled image--
larger than the single image by the amount that does not overlap. Fixating the hand gives you a
single image (assuming that you’re not strabismic) whose size is determined by the distance of
the hand from the eye, not by an extra image.
A person with a history of strabismus-- especially varying amounts of strabismus
produced by repeated surgical interventions-- may have learned that double images have no
reliable relation to the horopter, and learned to exclude them from consideration as depth
judgments are made. But it is not implausible that practice of eye movements, and increased
attentiveness to double images, could enable an adult to develop skill at comparing distances
with information about double or single images. Barry herself refers to a broadening of the part
of the visual field she actually pays attention too, an event that would help the observer pay
attention to images in the periphery.

Constancy and context.

Barry gives only slight attention to an essential aspect of
perception: the capacity for constancy. Constancy is the powerful tendency to experience objects
in the world as remaining the same, in spite of the continual changes in the ways they stimulate
our sense organs. Constancy is most obvious in visual perception. We see a square object as
retaining the same shape and size even though as we move relative to it its image becomes larger
or smaller and the image shape alters through a range of trapezoids. (Indeed, there are probably
few circumstances in which a square object creates a square image on the retina.)
Although the neural foundation of constancy is not well understood, it is clear that this
ability involves context. Shapes, sizes, and other aspects are judged in the context of a complex
surrounding visual field. Look at the square object through a tube that excludes the rest of the
field, and you see it as trapezoidal, not square. Similarly, a person who walks away from you
does not seem to shrink, but look through the tube and you will see that the image is much
smaller than before. Even when there is no movement of the object or the observer, constancy is
needed to overcome the effects of involuntary eye, head, and body movements, which make
images move across the retina.
Barry reports that her visual experience involved jiggling or shifting of the field, that she
had trouble recognizing where she was when driving, and that hawks went too fast for her to
count them on a bird-watching expedition. While other visual abilities are needed for keeping
the field still and so on, constancy also plays a role in these visual tasks. Constancy requires
some attention to the visual field surrounding the object being fixated. It is plausible that practice
and increased control over eye movements would enable an observer to improve constancy and
minimize some of the disturbing apparent movements or other problems with the fixated object. Barry calls attention to sudden changes in three-dimensional vision, as well as in other
aspects of visual experience, and attributes these to a “sudden and global change in brain state, a change in the activity of whole populations of neurons”(Barry, 2009, p. 236). Yet constancy
mechanisms are known for producing “flip-flops” of perceptual change in apparent distance,
size, brightness, and so on. Decades ago, the perception psychologist Adhemar Gelb
demonstrated abrupt changes in the perceived nature of a visual stimulus. He placed a piece of
coal so that it was illuminated by a spotlight that did not light any other part of the room.
Observers described the brightly-lit coal as appearing white. Gelb then introduced into the
spotlight beam a white piece of paper, holding it so that the observer saw coal and paper
simultaneously. Instantaneously, the coal “turned” black and the paper was seen as white.
Although one assumes that changes in neural activity underlie this effect of changed context, it
remains questionable whether there are “populations” involved, and if so, what the size of those
populations may be.


Visual adaptation—learning by experience to interpret visual stimulation in
different ways-- is a capacity well-documented through experimental work, but also personally
familiar to wearers of corrective lenses. A new lens prescription for eyeglasses usually takes
several days before vision seems completely normal, and the experience can be accompanied by
“swinging of the scene” as movements of images seen through the lens and at the periphery are
compared. Adaptation may be related to cues such as the feeling of the eyeglass frame pressing
on the nose. (After cataract surgery, I wear glasses when driving, to correct the myopia of my
unoperated eye. Initially I saw double when I looked into the side mirror. Now my experience is
normal as long as I sit in the car-- but if I get out while still wearing the glasses, I lose my
Experimentally, adaptation can take place in a few hours for subjects wearing prism
lenses that shift all images to one side or make all images tilt by 10 or 15 degrees. Not only do
these prism-wearers report that their visual world recovers its normal appearance, but they show this in objectively measurable ways. Asked to position a dim light straight in front of them, or to
set an illuminated rod to the vertical position, they initially respond in ways that compensate for
the prism displacement, but after a few hours of activity while wearing the prisms, they make
more accurate placements. Taking off the prism lenses, they show temporary after-effects in
which they set straight-ahead or vertical as if objects appear to them to be displaced in the
opposite way from the original prism displacement.
Because visual adaptation occurs quite quickly, and because it can easily be reversed, it
seems to be a matter of ordinary learning, rather than the brain “rewiring” suggested by Barry.
Adaptation may be a plausible alternative explanation for Barry’s much-increased ability to use
information from retinal disparity. Such an explanation might be supported by her anecdotal
reports of people whose new abilities diminished when they stopped doing the exercises, but
recovered when they began again.

Is There Non-Anecdotal Evidence for the Effect of Eye Exercises?

Whether or not there are plausible ways in which eye exercises that improve control of
co-ordinated eye movements might help depth perception and other visual abilities, the most
important way to evaluate “orthoptics” is through systematic tests of perceptual changes
following treatments by developmental optometrists. Barry’s book emphasizes individual
experiences to the almost complete exclusion of the kind of systematic investigation we normally
call “science”. The book’s index does not include the words “research”, “evidence”, or

CIGNA HealthCare has declined to cover vision therapy treatments on the grounds that
they are considered “experimental, investigational, or unproven for the management of visual
disorders and learning disabilities” (CIGNA Medical Coverage Policy, 2008, p. 1). The company
states that “insufficient evidence exists in the published, peer-reviewed literature to conclude that vision therapy is effective for the treatment of any of the strabismic disorders except preoperative prism adaptation for acquired esotropia” (CIGNA, 2008, p. 3). In its policy, Aetna provides coverage for some uses of vision therapy (Aetna Clinical Policy Bulletins, 2009) but considers it experimental and investigational for anomalous retinal correspondence, one of Susan Barry’s problems.

Most serious research on aspects of vision therapy has concentrated on its role in
treatment of amblyopia (lazy eye). A Cochrane review (Shotton & Elliott, 2008) reported three
randomized controlled trial studies on this subject, but said they showed no clear evidence of an
effect of near visual activity of the kind used in vision therapy protocols. One study which used
retrospective comparisons to case records reported that eye exercises did not appear to reduce
symptoms in patients with esophoria, a mild version of the “in-turned” eye position Susan Barry
had to cope with (Aziz, Cleary, Stewart, & Weir, 2006). A randomized controlled study using
several placebo and other treatments reported significant improvement using specific vision
therapy methods, but had excluded from the study strabismics and patients with a history of
strabismus surgery-- the category into which Susan Barry would fall (Convergence Insufficiency
Treatment Trial (CITT) Study Group, 2008). None of these high-quality investigations appear to have used the Brock protocol which Barry advocates.

In Conclusion

The idea that many aspects of vision can be corrected by training goes back a long way.
Erasmus Darwin, grandfather of Charles, described in the Transactions of the Royal Society a 5-
year-old who used one eye only, turning his head so that images fell on the blind spot of the
other eye. Darwin proposed that the child wear a large false nose that would force use of the
problem eye by occluding the view of the good eye (King-Hele, 1999). As I noted earlier, there
are a number of plausible mechanisms for improvement of visual skills under this type of
regimen. However, Darwin found that the visual ability of his patient got worse in spite of his
efforts, and modern vision therapists have failed to present evidence that their more complicated
methods are any more effective.
One cannot argue with Barry’s subjective experiences and her sense that improved eye
co-ordination opened a new world of visual excitement as well as improved visually-related
skills. Whether others can benefit equally from vision therapy remains questionable, however,
and it is regrettable that Barry’s book, while stressing scientific facts, nevertheless fails to model
scientific thought for its readers. As has occurred before (Linus Pauling and Niko Tinbergen are
unfortunate examples), expertise in one area of science does not seem to guarantee critical
thinking on other topics. However, the general public, and even many more sophisticated
readers, are likely to accept questionable conclusions like Barry’s on the basis of her training in
biology combined with her personal experience. Indeed, Barry’s book was selected as a Library
Journal Best Sci-Tech Book of 2009. Certainly, it is in many ways a “good” book, vividly
written, with a suitable balance between subjective and objective material, and with an
informative discussion of neuroscience issues. But Barry has not shown her readers how to take
an investigative sip at the developmental optometry Koolaid. Instead, she drains the pitcher and offers packets for others to mix up.


Aetna Clinical Policy Bulletins: Vision Therapy. (2009). Retrieved on Aug. 31, 2009 from
Aziz, S., Cleary,M., Stewart, H.K., & Weir, C.R. (2006). Are orthoptic exercises an effective treatment for convergence and fusional deficiencies? Strabismus, 14(4), 183-189.
Barry, S. (2009). Fixing my gaze. New York: Basic.
Blakemore, C. (1989). Principles of development in the nervous system. In C. von Euler, H.Forssberg, & H. Lagerkrantz (Eds.), Neurology of early infant behavior (pp. 7-18). New York: Stockton Press.
CIGNA Medical Coverage Policy (2008). Retrieved on Aug. 30, 2020 from
Convergency Insufficiency Treatment Trial (CITT) Study Group. (2008). The Convergence Insufficiency Treatment Trial: Design,methods, and baseline data. Ophthalmic Epidemiology, 15, 24-36.
Gregory, R.L. (1997). Eye and brain. Princeton: Princeton University Press.
Hubel, D., & Wiesel, T. (1965). Binocular interaction in striate cortex of kittens reared with artificial squint. Journal of Neurophysiology, 28, 1041-1059.
King-Hele, D.(1999). Erasmus Darwin. London: Giles de la Mare.
Shotton, K., & Elliott, S. (2008, Issue 2). Intervention for strabismic amblyopia. Cochrane Database of Systematic Reviews. Art. No.: CD006461. DOI: 10.1002/14651858.CD006461.pub2.
Worrall, R.S., Nevyas, J., & Barrett, S. (2009). Eye-related quackery. Retrieved Aug. 26, 2009, from


  1. With all due respect, Jean, I find it curiuos that you can't discern the science in Susan Barry's book, when two Nobel Laureates in Physiology/Medicine found her book illuminating. No less than David Hubel, among the pre-eminent researchers in strabismus of the past century,stated: "And as a neurbiologist she is able to discuss the science as an expert."

    Perhaps the reason that you take issue with the science in this book is that you approached the subject with an agenda. Much as you read the book as an advertisement for developmental optometry, your "Childmyth" piece is the typical pablum offered by those who take pot shots at our field without doing their homework.

    Not a single reference offered in your critique is from the field of developmental optometry. Dr. Barry, on the other hand, did quite a bit of homework and offers abundant references and notes in her book.

    Citing insurance company databases used as a smokescreen for rejecting claims is like reading Cliff's notes back in high school. Aside from actually reading some of Dr. Barry's references, you would do well to look at the website of the American Optometric Association to understand standards of care in areas of clinical practice pertinent to the book such as strabismus, vergence, and learning-related vision problems. See:

    Your hyperbole about the Howard Dolman apparatus is lovely for Psychology 101, but does not play out in the real world of clinical practice, where measures of stereopsis and 3-D are more sophisticated. The rest of your review is simply rife with speculation, an odd tact for a scientist to take in criticizing someone for an alleged lack of science. Then again, lumping the fine work of Susan Barry in with a refernce to "quackwatch" makes you agenda abundantly clear.

  2. Dear "pressvision":

    Let me repeat some points.
    1. There is a lot of information to suggest that "rewiring" after a certain age is not likely. David Hubel, whom you cite, has provided a lot of this.
    2. There are alternative plausible explanations of Dr. Barry's experiences, and they are actually less speculative than the explanation she suggests.
    3. However, plausible explanations are not the last word in these matters.Systematic evidence of efficacy is needed, and the research I mentioned does not provide these.

    If you can cite studies that do provide such evidence, we'd all like to hear about them. I wasn't able to find any and the Cochrane reviews have not suggested that any exist.

    By the way,it's important for patients who might seek vision therapy to know beforehand that their insurance companies may not reimburse for this poorly-supported intervention. As for your concern about "Quackwatch", whom the shoe fits, let him wear it.

  3. Dear Jean,
    I cite several references demonstrating the effectiveness of vision training for strabismus including the following:
    Etting GL. Strabismus therapy in private practice: Cure rates after
    three months of therapy. Journal of the American Optometric Association
    49 (1978): 1367–73.

    Flax N, Duckman RH. Orthoptic treatment of strabismus. Journal of
    the American Optometric Association 49 (1978): 1353–61.

    Ludlam WM. Orthoptic treatment of strabismus: A study of one hundred
    forty nine non-operated, unselected, concomitant strabismus patients
    completing orthoptic training at the Optometric Center of New
    York. American Journal of Optometry and Archives of the American Academy
    of Optometry 38 (1961): 369–88.

    Ludlam WM, Kleinman BI. The long range results of orthoptic treatment
    of strabismus. American Journal of Optometry and Archives of the
    American Academy of Optometry 42 (1965): 647–84.

    As for amblyopia, there are increasing reports that the disorder is treatable well beyond age 8 such as
    Wick B, Wingard M, Cotter S, Scheiman M. Anisometropic amblyopia:
    Is the patient ever too old to treat? Optometry and Vision Science 69 (1992): 866–78.

    In addition perceptual learning studies are increasingly supporting the concept of adult plasticity and the possibilities for treatment of amblyopia beyond early childhood. One nice summary is included below:
    Levi DM. Perceptual learning in adults with amblyopia: A reevaluation
    of critical periods in human vision. Developmental Psychobiology 46
    (2005): 222–32.

    Finally, insurance companies support strabismic surgery even though the chances that the surgery will improve vision after the age of 1 is only 20%. Clearly, more effective forms of treatment are needed for this common disorder. Scientists, doctors, and others need to move beyond knee-jerk reactions against vision therapy and look more carefully at the consequences of strabismus for the individual patient and the sensible and sound rationale behind the vision therapy procedures.

  4. Dear Jean,
    Thank you for your review of my book. You seem skeptical about the use of the term "rewriring." Please take a look at chapter 6 in which I suggest one way that this rewiring could have happened. This involves changing the relative weight of synapses onto visual cortical cells. This sort of rewiring through long-term potentiation has been observed and documented in the visual cortex and seems entirely plausible. Moreover, this sort of rewiring, a shift in synaptic weights, can occur following vision therapy procedures which teach the patient to simultaneously point the two eyes at the same spatial location, thus allowing the eyes to deliver correlated input to visual cortical neurons.

    The CITT study you mentioned concerning convergence insufficiency did indeed use vision therapy techniques that involved the "Brock method" (as you call it.) One of the mainstays of the therapy used was the Brock string.

    You claim that my book does not model scientific thought yet you don't question scientific dogma itself. For example, all the studies done on binocular neurons in the visual cortex have been done on neurons whose receptive fields are within 5 to 8 degrees of the fovea. The properties of these neurons has then been generalized to the entire cortex without any discussion as to whether this generalization was valid. Many good scientists then will tell you that a person with strabismus has no binocular cells, yet, if you ask or test most strabismics, you will find that they retain some latent binocularity ie they appreciate some stereo depth for large moving objects in their peripheral fields. This ability would never be discerned from the results of the scientific experiments.

    The situation with amblyopia is even worse. Most of the treatments on amblyopia are based on studies involving animals in which one eye was deprived of all form vision from very early in life. This does not mirror the human situation in the vast majority of amblyopes. In this regard, by generalizing from these animals experiments, scientists have not used the scientific thinking you

  5. Dear "Stereo Sue":

    If you are actually the author, Susan Barry, I'd appreciate your identifying yourself as such. As you know, it's quite easy for people to impersonate others when commenting.

    If you'll read my review carefully, you'll see that I also noted the real difficulties of conclusions about human brain plasticity, and pointed out that generalization between species is awkward at best. I agree that continuing neural plasticity is a possibility, but I offered as even more plausible alternatives some perceptual phenomena that were not mentioned in "Fixing my gaze". To say that the proposed mechanism is not the only plausible one, when there is evidence that can be interpreted as rejecting that mechanism, is very appropriate and is the basis of the experimentum crucis, which unfortunately cannot be done in this case.

    In any case, those points are not the most important, nor are they why I characterized the thinking in "Fixing my gaze" as "unscientific". My concern is with the book's apparent declaration that describing a plausible mechanism is the same thing as providing evidence of efficacy. On the contrary, before it can be claimed that vision therapy is a good way to treat problems of visual attention and depth judgment for specific kinds of patients, there needs to be research that meets the standards of evidence-based practice, and the work needs to be done on patients whose characteristics are similar to the people to whom generalization is desired. As you know, these studies also need to be randomized controlled trials comparing to usual treatment, there need to be guarantees of intervention fidelity, there should be analysis on intention-to-treat, and so on.

    To question an intervention that lacks a clear evidence basis is not a knee-jerk reaction, but an appropriate step in scientific thinking.


  6. The comment purporting to be from "Stereo Sue" has come in several times, and is being counted as spam. However, reading it again reminded me of something I thought about while reading "Fixing my gaze". Is there any evidence that the superior colliculus can take over any of the functions usually performed by the visual cortex, as it does in "blindsight"? If "Stereo Sue" is actually Susan Barry, I'd like very much to hear her comments on that possibility. J.M.

  7. Dear Jean,
    I am indeed the author of Fixing My Gaze. Sorry if this was not clear.

    As I indicated in an earlier comment, there are studies indicating the efficacy of vision therapy for strabismus. See the above comments and please read the papers.

    I agree that more controlled studies need to be done regarding the efficacy of vision therapy, but this does not mean that vision therapy procedures are quackery. When one reviews the rationale behind the procedures, they make a great deal of scientific sense. In contrast, conclusions about the lack of plasticity for adult strabismics and amblyopes that are drawn from scientific experiments do not hold up because the experiments do not closely mirror the human situation. Moreover, surgery for strabismus clearly has very limited effectiveness for promoting binocular vision after the first year of life.

    I don't think the superior colliculus can take over the perceptual function of stereopsis. The SC receives enormous input from the visual cortex so my guess would be that the cortex has to set the stage for binocularity.

  8. Dear "Stereo Sue":

    You still haven't signed yourself Susan Barry, you know. Sorry, but I'm unfortunately all too used to internet masquerades. But it doesn't matter, really.

    I've read the papers, of course. They all have various difficulties for the present purpose. The older ones aren't RCTs, and the newer ones exclude certain kinds of subjects, etc., as I said in the review.

    I expected your book to discuss some of the issues of establishing an evidence basis for this type of intervention, but you didn't do so, even though you apparently thought your readers would be able to get through Hubel and Wiesel and the rest of the background. It seems to have been your choice to go anecdotal, and that's why I'm questioning your conclusions.

    On a less important level, if you revise the book, it would be a good idea to give more thought to descriptions of experiences of visual cues. For example, you say that when a person moves along,the visual field appears to move backward. Of course this does not happen-- that's what constancy is all about. The retinal images move as if the objects were moving backward, but the person sees them as staying in the same place as he or she passes. There are a number of other problems of this kind, like saying that an object approaching you "looks bigger" when its images fills more of the field.

    You might want to think over the collicular contribution and "blindsight" more carefully. Many cues work together in depth perception, and it seems unlikely that there's just a single area of the brain that does the work.


  9. Thank you for your reply, Jean, though you're skirting the issue. I've given you references - they're contained in the Clinical Practice Guidelines on Esotropia and Exotropia (forms fo Strabismus) from the AOA with the website link I indicated. I see that you've been supplied with other references as well from Sue Barry.

    Relying on self-serving insurance company summaries of these studies doesn't make your argument more "scientific" than the evidence we're furnishing. Unless you have your mind made up, read the evidence and let me know if it's any less "scientific" than the evidence that supports insurance reimbursement for eye muscle surgery. After all, if you don't question strabismus surgery studies as non-scientific regarding binocular outcomes because they haven't undergone RCTs, why would you question the efficacy of optometric vision therapy?

    Why you accuse Dr. Barry of misleading the public, you have done a far better job of that than she.

  10. What? I wasn't talking about strabismus surgery, or effects of vaccination, or chiropractic treatment, or anything else. I was talking about vision therapy. And what I said was that before anyone claims that vision therapy causes improvement in strabismics' depth perception, that person needs to provide evidence that meets certain criteria. I would have said the same about strabismus surgery if I had been talking about that.

    Once again, of course it's plausible that it could work the way you say. Erasmus Darwin thought so too! But plausibility isn't the end of the line. Systematic evidence meeting certain standards is what's required.

    By the way, "pressvision", it would be a step toward transparency if you would identify yourself. You know who I am and can see my CV on this blog, but all I know about you is that you have something to do with Point Pleasant and DJs.

  11. Thanks for your comments on perception. Constancy is an important issue especially for people with binocular, vestibular, vestibulo-ocular, and oculomotor problems since they may have difficulty perceiving a stable world. In my book, I described the role of the vestibulo-ocular reflex and smooth pursuit in our ability to maintain a stable image while walking (pp. 76-8); I discussed size constancy on pages 118 and 119, and the role of optic flow and peripheral vision in perceiving a stable world on pages 84 and 85.

    I wrote my book to help others with their vision and I found that developmental optometry had a lot to offer in this regard. But before I wrote my book, I did what any good scientist would do. I investigated. I traveled the country to visit developmental optometrists at their practices, talked with their patients (and not just patients the optometrists suggested), attended their meetings, and read their journals (Journal of Behavioral Optometry; Optometry and Vision Development.) What I discovered was a group of intelligent, thoughtful, and resourceful clinicians.
    Susan Barry

  12. I'm sure you immersed yourself in vision therapy,practice,lore, and publications before writing the book, and I know you sincerely believe that the tretament helped you. I can't and don't say that it didn't; I only ask for the kind of evidence that supports claims that an intervention will help people in general.

    Let's hope that by the time you have a second edition, such evidence will be available.

    Best regards,
    Jean Mercer

  13. I read the above discourse with great interest. One wonders why, Dr. Mercer, you are so suspicious of modern scientific methods used to measure stereopsis. Rather than supporting the almost universal scientific use of random dot stereograms, you prefer to revert back to such antiquated methods as the Howard-Dollman apparatus. Why is this?

    Furthermore, while you explore the "plausibility" of learned factors that might account for Dr. Sue Barry's improved perception of depth, you state: "A person with a history of strabismus-- especially varying amounts of strabismus produced by repeated surgical interventions-- may have learned that double images have no reliable relation to the horopter, and learned to exclude them from consideration as depth judgments are made. But it is not implausible that practice of eye movements, and increased attentiveness to double images, could enable an adult to develop skill at comparing distances with information about double or single images."

    This argument begs the question, what kind of horopter does a person with strabismus have? By definition, the horopter is a binocular phonemenon that emerges from images falling on corresponding points. All images seen by a strabismics, however, fall on non-corresponding points. Thus, initially at least, strabismics will see double. Then, they may either suppress the image from one eye or the other or develop some form of anomalous correspondence in order to deal with diplopia and confusion. Only the person who develops anomalous correspondence has any appreciable "fusion" of non-corresponding points that can be said to have an horopter anything like a person with normal binocularity. Nevertheless, as Dr. Barry states, peripheral fusion, and stereopsis can be maintained even in persons with strabismus. These persons may, theoretically at least, retain some kind of a peripheral horopter where fusion and diplopia awareness is maintained. In Sue Barry's case, however, it is clear that she had an alternating esotropia and was also an alternating central suppressor. She likely had normal retinal correspondence. So any discussion of a non-amblyopic, alternating strabismic, with alternating central suppression and normal retinal correspondence who is nevertheless able to increase their attentiveness to double images off the horoptor when not alternately suppressing must begin by explaining how Dr. Barry achieved the bifixation and the elimination of suppression so as to establish a "normal" horopter in the first place.

    It should also be noted that the horopter represents two types of binocular fusion: second degree/Grade II fusion (flat fusion), in the case of images projected onto corresponding points to the left or to the right of fixation (contralateral hemispheric representation of sensory inputs) via the optic chiasm; and third degree/Grade III fusion (stereopsis), where disparate images in front or behind fixation stimulate disparate retinal points which then stimulate cells on both hemispheres, communicating via the corpus calossum. If one is not comfortable with modern stereometric techniques used to prove the existence of true cross-talk across the hemispheres as the reason for Dr. Barry's perceptual stereoscopic changes, one can measure stereopsis electrophysiologically, rather than speculate on spurious alternative "plausibilities" for Dr. Barry's enhanced sense of depth. Maybe for sake of poor scientific thinkers, she will!

  14. The reason I suggested the old Howard-Dohlman approach is that it provides a measure of the actual real-world use of depth information. As for suggesting other plausible explanations of Susan Barry's experiences, my goal was to try to bring more systematic thinking to this issue, and to counter the claim that because binocular neurons are established in the course of normal development, any changes in visual experience must mean that something has happened with respect to binocular neurons.

    But there is no point in arguing about how something works without having demonstrated that it does work. The real concern, which neither you, David, nor other commenters have addressed, is that there is no foundation of evidence for the effectiveness of vision therapy for the problems Susan Barry reported. No amount of Hubel-ing and Wiesel-ing, or of telling personal stories, can replace this. Why not get to work and do the research that is needed? I would be very pleased to hear that such evidence had been provided. In the meantime, we seem to have, at the best, material for the Scotch verdict, "not proven".

  15. Point taken, Dr. Mercer. We could all use more research. But until that happens, we have this curious phenomenon of Stereo Sues who, after being told by the medical establishment that stereopsis for longstanding strabismus is impossible, show up in certain optometric offices only to leave those same offices sometime later with a newly recovered visual function. With such evidence, it seems to me that the onus is now on the skeptical scientist to somehow, with the same solid research they demand of others, disprove the theory of activation of binocular neurons for strabismics who have later achieved stereopsis from vision therapy, rather than throwing out Occam's Razor altogether.

  16. I'm not at all sure the point actually was taken. There's a particular kind of research that's needed to support your claim that vision therapy is an effective treatment for strabismics of Susan Barry's type. After that, it would be possible to explore a mechanism for the treatment. I suggested some alternatives for the mechanism, none of which are less parsimonious than creating or restoring the function of binocular neurons and which in fact are much easier to test in human beings-- but there's not much point wrangling about them when it's not even clear that there's a replicable phenomenon..

    Please understand that I don't deny the possibility of bringing in some new binocular neuron function. I'm very wary of generalizing between species on issues like critical periods.

    What I do deny is that the available information supports the claim that vision therapy effectively treats this problem. There appears to be one Stereo Sue (not several Sues)for whom a set of data have been reported. You must be aware that this won't do as an evidence basis... and I'm pretty sure you are aware of that, or you wouldn't be concentrating on the red herring of whether binocular neurons are or are not at work. Nor would you be throwing in the old CAM bromide that if I can't prove something's not true, that's evidence that it is true.

    Also, perhaps you'd care to identify yourself and disclose your professional or financial interest in this matter? That might be meaningful information for readers who are trying to sort this out.

    One more point, and I would genuinely like to know what you and/or Sue think of this. Sue began her treatment at a point in her life where natural changes in accommodation are likely to become noticeable, and as I recall she was in treatment for long enough for considerable change to occur. Are there any ways in which this confounding variable could have influenced her visual experience? Has anyone ever done a longitudinal study of spontaneous changes in strabismics' vision?

  17. I honestly don't know of any longitudinal study that has looked at "spontaneous" recovery of binocularity in strabismics, if that is what you are asking. . .by the way, I'm just a lowly optometrist. . .and not in any way financially connected to Dr. Barry or the proceeds from her book sales! But I do provide vision therapy in my practice (gasp!). Be that as it may. . .I, like you, share a passionate search for that particular type of study that actually supports claims of an effective treatment for strabismics. Believe it or not, I think I found another such pseudo-scientific claim! It seems some eye doctors in India (right there, I'm suspicious) published an article entitled: Beyond Cosmesis: Recovery of fusion and stereopsis in adults with longstanding strabismus. . .K.S. Santhan Gopol, Indian Journal of Ophthalmology, 2009, Mar-Apr; 57(2):141-3. They claim that out of 15 chronically strabismic, non-fusing adults, 13 were able to achieve near stereopsis and fusion after their treatment. Although the authors did not speculate in the article whether or not their treatment "re-wired" any binocular cells, my guess that such was the presupposed thinking! We can only hope that this extended advertisement for the author's claims, masquerading as science, does not reach the ears of the unsuspecting public. And thankfully, at least for us in the U.S., it is unlikely that any of the adults who were treated for strabismus by these authors will be publishing a book about their experiences any time soon! As you so skillfully point out in your blog, Dr. Mercer, people should read claims like this with a scientific mind that explores all plausible alternative mechanisms for the supposed effectiveness of their strabismus "treatment". Oh, pardon me. . . .I failed to mention that the eye doctors in India who wrote the journal article were ophthalmologists. And, their "treatment" was surgical realignment. Oh, no! GIGNA better watch out. . .or they might be coerced into adopting surgical benefits for strabismic patients over the age of 5 someday!

  18. I can't put my hands on that journal. Can you tell me the design? Was there a comparison group of any kind? There's so much information about how vision can get worse spontaneously, but little about natural variations in either direction, or even about the effects of repeated testing on skills.

    I don't know why you make such a point of whether there were binocular cells at work. At this juncture, isn't the important question whether or not the treatment was effective?

  19. Do we really care, Dr. Mercer, how rigorous the study is or whether or not the treatment is effective? We've already determined its Koolaid. . .now we just pick the flavor!

  20. I'm not sure who "we" is. I myself would like to know the evidence behind the claim of effectiveness for the surgical treatment,just as I'd like to know it for vision therapy. I think it would be great if either or both of them were effective treatments, but it's important to examine the procedures behind any such claims before assuming that they're correct. When I referred to Koolaid-drinking I wasn't discriminating among flavors.

    I must say I don't see where you're going with your comments-- do you imagine that I'll turn out to be an ophthalmologist in disguise? And , by the way, wouldn't you take a different tone if you knew you could be identified?

  21. Dr. Mercer, I mean no disrespect. But you have characterized "Fixing my Gaze" as unscientific, you've excoriated the author for not bowing to your methods of scientific inquiry, you've questioned her motives, you've suggested that somehow a "learned" method of seeing depth is a more plausible explanation for Dr. Barry seeing in actual 3-D than are clinical methods of testing stereopsis (even though none of the examples you gave would enable a strabismic person to pass a random dot stereo test), you've set up your own arbitrary (Howard Dollman ?) criteria for what constitutes the definitive existence of true stereopsis (even though monocular cues to depth are not altogether eliminated with this apparatus) and when challenged with the literature presented on this blog by two outstanding scientists, you have, without reading them, implied that all of these studies, like the book, must be anecdotal and must be simply dismissed (ignored) out of hand.

    So, forgive me for being just a little bit cynical when you claim that you are truly interested in knowing whether or not vision therapy or surgery or both are truly effective in treating strabismus.

    The short answer to your question is no, the authors of the Indian study did not set up "randomized controlled trials comparing the usual treatment, [with] guarantees of intervention fidelity, [and] analysis on intention-to-treat, and so on." So for you, at least, like the studies supporting vision therapy for treatment of strabismus, this study cannot be worth the paper it is printed on.

    So forgive me, Dr. Mercer, but I think that perhaps, as has occurred before (Linus Pauling and Niko Tinbergen are unfortunate examples), your expertise in one area of science does not guarantee critical thinking on other topics!

  22. So what do you think? That I'm committed to a strict critical period view? As I've said,that isn't true.

    Or is it that you think I swear by the rules about evidence-based practice and am trying to force them on people who have their own, possibly much better, way of doing things? Well, yes,I am committed to them, and I would like it if other people also took them seriously. If that commitment is a sign of an absence of critical thinking as you define it, so be it. Meanwhile, you must know that someone has to show that there is evidence of a high standard (as defined in conventional circles) for these various claims, or many people will continue to doubt you and use that nasty Q-word. You can't just turn up with testimonials or before-and-after studies.

    If you'd like to have a serious discussion of this matter, that's fine-- but I'm not going to spend much more time being grouched at, you know.

  23. Dr. Mercer, I admire your defense and commitment to evidence-based practice. Believe it or not, most optometrists are committed to that too! But, unless one has unlimited resources, and time, one must deal with the literature that is available, even though it does not meet the standards we all would like to have. Actually, much of medicine has never operated in this fashion (pardon the pun). Take, for instance, the practice of another accepted treatment method used for strabismus: botulinum toxin. Do you think the ophthalmologists who first used this treatment went about setting up double-blind controls, injecting saline into one group of age-matched patients' muscles, while the other group got botox, and then each group was evaluated by masked clinicians to assess the efficacy of the treatment, not knowing which one was sham? Heck no! Yet it is an accepted practice of treatment, nonetheless. Do you think the surgeons who first developed the extra-ocular surgical techniques that Dr. Barry had performed on her eyes years ago went about carefully matching their groups in a similar fashion, faking muscle recessions on one group, performing actually recessions on another so that the efficacy of their techniques could not be challenged? Heck no! So why is it when another approach is used by a profession which uses the same outcome evidence, stereopsis via random dot stereograms. . .which cannot be faked. . .that that evidence and profession suddenly come under extra-ordinary scrutiny and suspicion? When the demands on one profession to give proof beyond "before and after" studies outweighs the demands on another profession, it doesn't take a rocket scientist to see the bias!

    Take it from someone who deals with strabismics day in and day out, Dr. Mercer. Random dot stereo testing is strong evidence. Oliver Sacks, Dr. Barry and a whole lot of vision specialists know it too! Would that the public understood it as well.

    Sorry if I grouched at you!

  24. Times have changed, and the levels of evidence that used to be acceptable for any kind of intervention are no longer accepted. It's not that optometrists today are treated differently from surgeons today or psychologists today-- it's that everybody today is asked to do a better job of producing evidence than was the case even 20 years ago. Lots of people don't like this, and some even go on trying to claim they have a high level of evidence when it's obvious they don't. In my own field, there are people who really resent the idea that the intervention they use may be harmful, and others who try to weaken the idea of evidence-based practice by adding "practice wisdom" and "family values" to the research component. Nevertheless, here we are in 2010, and people who make claims of intervention effectiveness are all going to be asked for systematic evidence to support the claims. That goes for the Indian surgeons you mentioned, too.

    As for the random dot stereogram, that's not the point, or dot. I would have liked to see additional measures that were more obviously related to real-world use of depth perception, but the real issue is that so far there has been no randomized controlled study of the effect of visual therapy on stereopsis. I keep saying this, and you keep changing the subject.

    You know, what I'd really like to hear from you is how optometrists handle some of the problems that perception psychologists are concerned with-- variations in thresholds, effects of expectation, starting position effects. Do you use any of the technology that resembles the Bekesy audiometer? All those things would be essential for pulling the signal you're looking for out of a lot of noise.

    Also, don't turn up your nose or roll your eyes about longitudinal studies. Hubel thought they'd be of interest.

  25. The reason your real-world use of "depth perception" measures cannot be a substitute for tests of "stereopsis" in determining whether or not a treatment has truly made a strabismic binocular is because of the confounding variables that are monocular cues to depth. Relative size, overlap, linear perspective, light and shade, motion parallax. . .these are all real world cues for depth that can also be seen with a single eye. What is needed is a test exclusive to two-eyed vision in order to be sure that stereopsis has really, truly been established. With a random dot stereogram, there is no extraneous monocular noise! Now, we could also use an fMRI to actually observe the real-time differences in brain activity before and after therapy for strabismus to make sure it is actually "stereopsis" that is being perceived by the treated patient. If you have one, send it my way and we'll do a study next week. But even that won't satisfy you, cause you demand randomized controlled studies as evidence.

    Did you know that the last randomized controlled, multi-center study that was conducted by the NEI regarding vision therapy took 16 years to implement and complete? And, it cost over 7 million dollars. Yep. Check it out. It is called the Convergence Insufficiency Treatment Trial (CITT). Now, did the profession of optometry sit around for 16 years waiting for the study to be completed because it felt its current clinical methods weren't scientific enough or that it might be unethical to treat kids with headaches, eyestrain, and double vision, knowing those outside of the profession, like yourself, might demand a higher level of evidence for vision therapy's efficacy before these kids had their headaches and diplopia treated? Thankfully, no. What the CITT study discovered, beyond the shadow of a doubt, was that the only effective treatment for convergence insufficiency is. . .vision therapy. And yet, when the study results were released in 2008, what did the editor of a leading ophthalmological journal have say about it? After conducting an informal poll among his ophthalmology colleagues, their consensus was that a minimalist approach to convergence insufficiency, contrary to the study's results, was just as effective. That's right! The editor of a leading scientific journal felt this anecdotal "practice wisdom" trumped the 7 million dollar randomized control double-blind gold standard study! What irony! After demands that vision therapy needed a double blind study to be clinically valid, pseudoscience carried the day. . .Care to retract your comment about optometrists and surgeons not treated differently? And since the study was released, have the eye care professions changed their practices to conform to the new study's results? Are ophthalmologist and optometrists now referring all their patients with convergence insufficiency to practices specializing in vision therapy? Dream on.

    Believe me, Dr. Mercer, I'm all for randomized controlled longitudinal studies. But even though we are living in 2010, you'd be rather naive to believe that the levels of evidence that used to be acceptable in medicine are no longer accepted today. In fact, according to the journal Academic Pediatrics (2009; 9:81-88/Bazzano, et al) 62% of all outpatient pediatric visits include off-label prescribing. Is this common practice of off-label prescribing based on the kind of scientific evidence you feel is keeping with the times? Hardly!

    So, before you look at optometric vision therapy with a jaundiced eye (pardon the pun), either hold every profession to the same exact standard of evidence you demand, or stand back and let those clinicians who are skilled and knowledgeable in the diagnosis and treatment of binocular vision disorders use their tools to treat patients, like Dr. Barry, who seek their care.

  26. David: I'm sorry, but your last comment disappeared when I tried to publish it. If you want to re-send, I'll put it up.

    N.B. though-- there's no such thing as a randomized controlled longitudinal study. Longitudinal studies by definition compare data from one part of a person's life to data from another part, and there's no way that can be randomized.

  27. "there's no such thing as a randomly controlled, longitudinal study". . .Excuse me? And I thought you knew something about research. Wasn't it you who wondered about the longterm visual changes of strabismics? Does that curiousity suddenly end once a treatment trial for strabismus is over? If you're not interested in finding out the results of a proposed treatment years after a proposed treatment supposedly "fixed" a problem, how will you be able to truly judge its efficacy? And after all that bluster about outcome research, Hubel, etc. . . .

  28. The independent variable in a longitudinal study is age. You can't randomly assign people to be different ages. All studies that examine age effects are quasi-experimental (but not vice-versa), and by definition subjects are not assigned to groups.

    These are things developmental psychologists have thought a lot about, and optometrists will need to do that too if they want to do longitudinal studies.

  29. Wait a minute, I think I see the problem here.

    There are two different research designs. One, an experimental study using randomized controlled trials, has the purpose of investigating the outcome of a treatment. It could be done with repeated measures if you wanted to see what happens over time, but for each comparison, the intervention group would be compared to the usual-treatment or whatever group.

    A longitudinal study investigates the spontaneous changes that form a normal developmental trajectory. Measurements taken from each individual at any given point are compared to measurements from the same person at other points. This is done for each individual in a group, and the changes are also combined to see how much variation there is.

    I had suggested that it would be interesting to do a longitudinal study of strabismics as they aged, to see what spontaneous changes might occur, especially at points like age 50 when loss of accommodation is apparent.

    Both of these are useful approaches, but they answer different questions. So let's hear less about the bluster, hmmm?

  30. I think, Dr. Mercer, that a longitudinal study of strabismics as they age, looking for spontaneous vision changes is, from a clinical perspective, uninspiring. There is really no reason to expect, hope or imagine that during the years when presbyopia sets in that the eyes of a strabismic will magically align themselves, or that stereopsis will somehow suddenly emerge. The problem of non-bifixation still remains. And until that problem is solved, either with surgery, with prisms, with therapy, or a combination of the above, it is safe to say that spontaneous recovery of fusion is most unlikely.

  31. The reason you think that is thatyou assume there's a single possible mechanism for the recovery of function you believe can follow vision therapy. If there's more than one factor at work-- a combination of cues, as in the likelihood principle-- it would be useful to know how various functions other than stereopsis alter in the natural course of events. But as long as you consider stereograms as the most important measure of vidual change, you'll be missing other changes that may be occurring.

    I'm not talking about a magical spontaneous remission-- I'm talking about developmental changes in a variety of aspects of vision, which all together may normally be the foundation of well-functioning depth perception.

    But honestly, I give up too. We speak different languages.