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early entry myopia versus pseudomyopia - how to test?
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peter...@gmail.com
Nov 16, 2012, 10:46:52 PM11/16/12
to
Hi Eye Care Professionals,
I see some of my sincere questions get lost in the continuing flame wars.
I was hoping to have some clarification on whether an optometrist or opthamologist tests for early stage myopia to ensure it is not pseudomyopia.
More clearly, I am wondering if it is necessary for the eye care professional or the patient to know if it is early stage myopia. Would the treatment be the same regardless, i.e. regular distance vision correction?
As I tried to state in the other thread, my first cycloplegic refraction was at age 39. I never received cycloplegic drops on any exam or for any purposes prior to that. I had my first optometrist visit at age 13 when I got my first set of glasses.
I am trying to understand why the optometrist, especially at my first visit did not consider it necessary to do a cycloplegic refraction? Would he have been able to figure it out another way? The first 10 years of my optometric visits were done at an optometry school btw. What I think I was told is that children tend to have very strong accomodation power, and so to be certain if it is early myopia a rather strong cycloplegic refraction would be necessary, one that may not wear off in several days. Not sure if that idea was correctly explained either.
The reason I am asking is I am trying to understand my unique situation to the best of my ability, and understand why things happened to me as they did.
Peter
I see some of my sincere questions get lost in the continuing flame wars.
I was hoping to have some clarification on whether an optometrist or opthamologist tests for early stage myopia to ensure it is not pseudomyopia.
More clearly, I am wondering if it is necessary for the eye care professional or the patient to know if it is early stage myopia. Would the treatment be the same regardless, i.e. regular distance vision correction?
As I tried to state in the other thread, my first cycloplegic refraction was at age 39. I never received cycloplegic drops on any exam or for any purposes prior to that. I had my first optometrist visit at age 13 when I got my first set of glasses.
I am trying to understand why the optometrist, especially at my first visit did not consider it necessary to do a cycloplegic refraction? Would he have been able to figure it out another way? The first 10 years of my optometric visits were done at an optometry school btw. What I think I was told is that children tend to have very strong accomodation power, and so to be certain if it is early myopia a rather strong cycloplegic refraction would be necessary, one that may not wear off in several days. Not sure if that idea was correctly explained either.
The reason I am asking is I am trying to understand my unique situation to the best of my ability, and understand why things happened to me as they did.
Peter
Mike Tyner
Nov 17, 2012, 12:35:55 AM11/17/12
to
The standard test for pseudomyopia is cycloplegic refraction. But
significant pseudomyopia also causes symptoms like headache and double
vision, and it's usually accompanied by pronounced esophoria (the eyes tend
to turn in because you're accommodating extra hard.)
But (write this down) pseudomyopia does no harm. Pseudomyopia does not
progress to anatomical myopia. Pseudomyopia disappears as you get older. If
you have early myopia with no symptoms of strain, no double vision and no
esophoria, why would you want to blur a child's vision for three days just
to answer an academic question?
30-40% of kids in the US will develop real myopia between ages 8-15. There
is nothing to be gained by hard-cyclopleging every one of them unless there
are symptoms or findings that suggest pseudomyopia.
ALL kids have some degree of accommodative tonus. Farsighted kids have TONS
of "pseudomyopia" and it doesn't make them nearsighted. We wish it would,
but it doesn't.
<peter...@gmail.com> wrote in message
news:73da8fda-967b-4190...@googlegroups.com...
significant pseudomyopia also causes symptoms like headache and double
vision, and it's usually accompanied by pronounced esophoria (the eyes tend
to turn in because you're accommodating extra hard.)
But (write this down) pseudomyopia does no harm. Pseudomyopia does not
progress to anatomical myopia. Pseudomyopia disappears as you get older. If
you have early myopia with no symptoms of strain, no double vision and no
esophoria, why would you want to blur a child's vision for three days just
to answer an academic question?
30-40% of kids in the US will develop real myopia between ages 8-15. There
is nothing to be gained by hard-cyclopleging every one of them unless there
are symptoms or findings that suggest pseudomyopia.
ALL kids have some degree of accommodative tonus. Farsighted kids have TONS
of "pseudomyopia" and it doesn't make them nearsighted. We wish it would,
but it doesn't.
<peter...@gmail.com> wrote in message
news:73da8fda-967b-4190...@googlegroups.com...
Mike Tyner
Nov 17, 2012, 12:52:05 AM11/17/12
to
Oh and there's little need to do a cycloplegic refraction at age 39 because
nature has pretty well eliminated all pseudomyopia by then. I don't know why
they would do a cycloplegic refraction at age 39. You might mean that you
didn't have a dilated fundus examination until 39.
For a dilated fundus examination, similar drops are used but not for their
effect on accommodation. Rather we use drops to dilate the pupil to see more
of the retina. There was a time when optometrists were not permitted to use
eye drops for dilating or for cycloplegia, but most states have allowed it
for the past 40 years.
Even so, I usually dilate young emerging myopes but I always refract before
dilating and I don't recheck refraction after dilating, unless by history or
phoria testing I have a suspicion they have accommodative spasm
(pseudomyopia.)
You must understand that "pseudomyopia" is just a term for "excessive
accommodation" and that EVERY kid accommodates excessively, as soon as they
wake up. We arbitrarily say 0.50D is "normal" but accommodative tonus varies
with fatigue, anxiety, and other factors and it doesn't go away when you
take glasses off or put them on.
I test refraction in the natural state because that's how people wear their
glasses. I remove "minus" until the subject says a distant target just
starts to blur, then add back enough to clear the blur. That's how
refraction is tested and "overcorrection" is avoided.
nature has pretty well eliminated all pseudomyopia by then. I don't know why
they would do a cycloplegic refraction at age 39. You might mean that you
didn't have a dilated fundus examination until 39.
For a dilated fundus examination, similar drops are used but not for their
effect on accommodation. Rather we use drops to dilate the pupil to see more
of the retina. There was a time when optometrists were not permitted to use
eye drops for dilating or for cycloplegia, but most states have allowed it
for the past 40 years.
Even so, I usually dilate young emerging myopes but I always refract before
dilating and I don't recheck refraction after dilating, unless by history or
phoria testing I have a suspicion they have accommodative spasm
(pseudomyopia.)
You must understand that "pseudomyopia" is just a term for "excessive
accommodation" and that EVERY kid accommodates excessively, as soon as they
wake up. We arbitrarily say 0.50D is "normal" but accommodative tonus varies
with fatigue, anxiety, and other factors and it doesn't go away when you
take glasses off or put them on.
I test refraction in the natural state because that's how people wear their
glasses. I remove "minus" until the subject says a distant target just
starts to blur, then add back enough to clear the blur. That's how
refraction is tested and "overcorrection" is avoided.
peter...@gmail.com
Nov 17, 2012, 11:31:29 PM11/17/12
to
Mike,
Thanks very much for taking the time to respond. It was very helpful. And also going forward I can slowly digest your message. Very much appreciated.
The explanation for pseudomyopia was very helpful as well as the statement it does not lead to axial myopia. Is that statement proven because the farsighted do not develop axial myopia no matter what level of pseudomyopia they have?
When you state that people get better (or worse if farsighted) after 30, can I conclude that a large majority of them improve (or worsen if farsighted) because of falling levels of pseudomyopia or would there be other more likely explanations that are more frequently the cause, i.e. thickening of the lens, curvature, etc? Or do we just not know?
Regarding the drops, you are also likely correct. At 39 I did not get a cycloplegic refraction, but probably it was only the retinal examination. I did get the records of that exam released to me last year. The optometrist took a photo of my retina once I was dilated. And she told me I was starting to lose my reading vision, and she demonstrated that by having me try to read through my glasses after I had gotten the drops.
May I ask you another related question for your opinion. With respect to the growing rates of myopia, in the US or abroad, do you think it is a case of more people with the genetic pre-disposition in the current generation? Or do you think it is the same (relative) levels of genetic pre-disposition but that the gene is just being activated more frequently due to some still unknown cause? Some of the things that point to the latter being more likely are studies that show time spent outdoors improves outcomes statistically, as well as your point that while you would never recommend them, using atropine drops for 25 years will retard myopia development. The March OD I saw believes that while they haven't found the myopia gene, if you are destined genetically to be a -6 myope, you will become a -6 myope and environmentally there is nothing you can do to affect the outcome.
Thanks very much for taking the time to respond. It was very helpful. And also going forward I can slowly digest your message. Very much appreciated.
The explanation for pseudomyopia was very helpful as well as the statement it does not lead to axial myopia. Is that statement proven because the farsighted do not develop axial myopia no matter what level of pseudomyopia they have?
When you state that people get better (or worse if farsighted) after 30, can I conclude that a large majority of them improve (or worsen if farsighted) because of falling levels of pseudomyopia or would there be other more likely explanations that are more frequently the cause, i.e. thickening of the lens, curvature, etc? Or do we just not know?
Regarding the drops, you are also likely correct. At 39 I did not get a cycloplegic refraction, but probably it was only the retinal examination. I did get the records of that exam released to me last year. The optometrist took a photo of my retina once I was dilated. And she told me I was starting to lose my reading vision, and she demonstrated that by having me try to read through my glasses after I had gotten the drops.
May I ask you another related question for your opinion. With respect to the growing rates of myopia, in the US or abroad, do you think it is a case of more people with the genetic pre-disposition in the current generation? Or do you think it is the same (relative) levels of genetic pre-disposition but that the gene is just being activated more frequently due to some still unknown cause? Some of the things that point to the latter being more likely are studies that show time spent outdoors improves outcomes statistically, as well as your point that while you would never recommend them, using atropine drops for 25 years will retard myopia development. The March OD I saw believes that while they haven't found the myopia gene, if you are destined genetically to be a -6 myope, you will become a -6 myope and environmentally there is nothing you can do to affect the outcome.
Mike Tyner
Nov 18, 2012, 2:20:47 AM11/18/12
to
<peter...@gmail.com> wrote
> Is that statement proven because the farsighted do not develop
> axial myopia no matter what level of pseudomyopia they have?
nearsighted. I remember a paper titled "tonic accommodation is not
correlated with myopia" and the conclusion was based on measuring tonic
accommodation and comparing with refractive state.
> When you state that people get better (or worse if farsighted) after 30,
> can I conclude that a large majority of them improve (or worsen if
> farsighted) because of falling levels of pseudomyopia or would there
> be other more likely explanations that are more frequently the cause,
> i.e. thickening of the lens, curvature, etc? Or do we just not know?
accommodation. It doesn't reduce accommodative effort - that may continue or
even increase. It reduces the effective convergent power of the crystalline
lens to the point where cycloplegics do not alter the measurement of
refraction except by altering pupil size.
Secondly, ultrasound shows that the lens continues to grow in diameter
(therefore decrease in curvature).
Both of these processes contribute to the shift away from myopia.
> May I ask you another related question for your opinion. With respect to
> the growing rates of myopia, in the US or abroad, do you think it is a
> case
> of more people with the genetic pre-disposition in the current generation?
that more myopia is expressed epigenetically because of lifestyle changes.
I believe in evolution. Evolution is change in the gene pool due to
environmental factors. If a population of animals shifts its food-hunting
and gathering behavior from far to near there will be a corresponding shift
in the average visual metrics for that population over time. And if you find
a shift in the average refraction of a population, you might expect to find
a change in feeding and gathering behavior. Why is this difficult?
peter...@gmail.com
Nov 18, 2012, 8:58:19 PM11/18/12
to
On Sunday, November 18, 2012 2:20:48 AM UTC-5, Mike Tyner wrote:
> <peterg> wrote
My wife is a cancer researcher, and one thing she mentions often to me (relating to cancer) is how people carry certain genes which can lead to a certain cancer but they are inactive. They can get activated when they bind to a certain protein. There are also other proteins that act to maintain certain genes in an inactive state. So, if it were scientifically known that excess accomodation leads to myopia for those people carrying the myopia gene, it may be that with hyperopes either don't carry the same gene, or they don't carry the gene that activates it, or they carry the protein that prevents its activation.
If you understand the principal of how genes get activated, then it doesn't seem unreasonable that a hyperope accomodates mightily yet never gets myopic, yet a non-hyperope does (assuming it was proven that mighty accomodation causes myopia).
> I remember a paper titled "tonic accommodation is not
> correlated with myopia" and the conclusion was based on measuring tonic
> accommodation and comparing with refractive state.
I will try to find it and look at it.
> > When you state that people get better (or worse if farsighted) after 30,
> > can I conclude that a large majority of them improve (or worsen if
> > farsighted) because of falling levels of pseudomyopia or would there
> > be other more likely explanations that are more frequently the cause,
> > i.e. thickening of the lens, curvature, etc? Or do we just not know?
>
> There's no question that the lens stiffens and that this impacts tonic
> accommodation. It doesn't reduce accommodative effort - that may continue or
> even increase. It reduces the effective convergent power of the crystalline
> lens to the point where cycloplegics do not alter the measurement of
> refraction except by altering pupil size.
>
> Secondly, ultrasound shows that the lens continues to grow in diameter
> (therefore decrease in curvature).
>
> Both of these processes contribute to the shift away from myopia.
I think you might remember that I shifted my optometrist measured perscription by .75D (slightly more in the right eye) in about 6-8 weeks doing naked eye print pushing as well as distance gazing breaks. The 6-8 weeks is my estimate, as the next OD refraction (pre and post drops) was 3 months after the first exam. This happened about 10 months ago, and try as I might I have not been able to notice or state that there have been further changes. The OD I spoke with indicated that such a large change in such a short period of time is not normal (over his 30 years experience). Given that I am in the midst of developing presbyopia, and given that reduced myopia improvement timeline, do you think removal of excess accomodation (or pseudomyopia) is the most plausible explanation? Or do you see an equal possibility of the lens stiffening or curvature changes in that short period of time being the answer? The OD in March seemed to imply pseudomyopia as he claimed if the Dec. OD did a cycloplegic refraction pre and post drops, he would have noticed a discrepancy.
> > May I ask you another related question for your opinion. With respect to
> > the growing rates of myopia, in the US or abroad, do you think it is a
> > case
> > of more people with the genetic pre-disposition in the current generation?
>
> If the rate is increasing, I can only speculate on the mechanism. It may be
> that more myopia is expressed epigenetically because of lifestyle changes.
Yes, I understand we are discussing ideas here and not something that is scientifically proven. Identifying the myopia gene in lower order animals, and then finding what activates the gene would be the big breakthrough that is needed. Can I say that as a layman, your statement means "it may be myopia is expressed because of lifestyle (or environmental) changes".
> I believe in evolution. Evolution is change in the gene pool due to
> environmental factors. If a population of animals shifts its food-hunting
> and gathering behavior from far to near there will be a corresponding shift
> in the average visual metrics for that population over time. And if you find
> a shift in the average refraction of a population, you might expect to find
> a change in feeding and gathering behavior. Why is this difficult?
This is why evolutionary biology is such a difficult suggestion. I find it difficult to find other examples (both animals or humans) where such a rapid change has been noted. The theory is changes occur over millenia, natural selection assisting in the process whereby those with the weaker genes are eliminated. I don't know of any ideas expressed within evolutionary biology that suggest such rapid change over 3 or 4 decades or just a few generations. This is why claiming evolution is a very difficult suggestion to make with respect to myopia, and can seem unreasonable based on the timeline. Do you square that circle by believing the gene is already there from long ago, but the changes in lifestyle (environment) are what cause the activation to just be happening now?
This also goes back to your proof that over-accomodation does not lead to myopia. Cearly from an evolutionary perspective, they would not be carrying the gene even though the engage in similar lifestyles as the myope.
Peter
> <peterg> wrote
>
> > Is that statement proven because the farsighted do not develop
> > axial myopia no matter what level of pseudomyopia they have?
>
> Seems like good evidence for me. The people who accommodate most are least
> nearsighted.
The reason why I find that one ton jackhammer statement not completely reasonable is that the scientific community considers myopia to be a genetic trait. Similarly I have to believe that hyperope must be genetic trait as well. Perhaps some people carry both genes. Or maybe the same gene affects hyperopia and myopia and all people have it, but it depends on whether it is activated.
> > Is that statement proven because the farsighted do not develop
> > axial myopia no matter what level of pseudomyopia they have?
>
> Seems like good evidence for me. The people who accommodate most are least
> nearsighted.
My wife is a cancer researcher, and one thing she mentions often to me (relating to cancer) is how people carry certain genes which can lead to a certain cancer but they are inactive. They can get activated when they bind to a certain protein. There are also other proteins that act to maintain certain genes in an inactive state. So, if it were scientifically known that excess accomodation leads to myopia for those people carrying the myopia gene, it may be that with hyperopes either don't carry the same gene, or they don't carry the gene that activates it, or they carry the protein that prevents its activation.
If you understand the principal of how genes get activated, then it doesn't seem unreasonable that a hyperope accomodates mightily yet never gets myopic, yet a non-hyperope does (assuming it was proven that mighty accomodation causes myopia).
> I remember a paper titled "tonic accommodation is not
> correlated with myopia" and the conclusion was based on measuring tonic
> accommodation and comparing with refractive state.
> > When you state that people get better (or worse if farsighted) after 30,
> > can I conclude that a large majority of them improve (or worsen if
> > farsighted) because of falling levels of pseudomyopia or would there
> > be other more likely explanations that are more frequently the cause,
> > i.e. thickening of the lens, curvature, etc? Or do we just not know?
>
> There's no question that the lens stiffens and that this impacts tonic
> accommodation. It doesn't reduce accommodative effort - that may continue or
> even increase. It reduces the effective convergent power of the crystalline
> lens to the point where cycloplegics do not alter the measurement of
> refraction except by altering pupil size.
>
> Secondly, ultrasound shows that the lens continues to grow in diameter
> (therefore decrease in curvature).
>
> Both of these processes contribute to the shift away from myopia.
> > May I ask you another related question for your opinion. With respect to
> > the growing rates of myopia, in the US or abroad, do you think it is a
> > case
> > of more people with the genetic pre-disposition in the current generation?
>
> If the rate is increasing, I can only speculate on the mechanism. It may be
> that more myopia is expressed epigenetically because of lifestyle changes.
> I believe in evolution. Evolution is change in the gene pool due to
> environmental factors. If a population of animals shifts its food-hunting
> and gathering behavior from far to near there will be a corresponding shift
> in the average visual metrics for that population over time. And if you find
> a shift in the average refraction of a population, you might expect to find
> a change in feeding and gathering behavior. Why is this difficult?
This also goes back to your proof that over-accomodation does not lead to myopia. Cearly from an evolutionary perspective, they would not be carrying the gene even though the engage in similar lifestyles as the myope.
Peter
Mike Tyner
Nov 18, 2012, 10:03:43 PM11/18/12
to
<peter...@gmail.com> wrote
>> The people who accommodate most are least nearsighted.
> The reason why I find that one ton jackhammer statement not completely
> reasonable is that the scientific community considers myopia to be a
> genetic trait.
The nutjob fringe are those who insist beyound all
fostered by Otis and his minions is whether excess accommodation causes
myopia.
Mike Tyner
Nov 18, 2012, 10:06:25 PM11/18/12
to
Sorry I pulled the trigger on this reply too soon. It's too late for me to
reply to every point and it seems a little like arguing angels on a pin
anyway.
I may look at it later when I'm not so exhausted and short-tempered.
-MT
"Mike Tyner" <mty...@mindspring.com> wrote in message
news:Otqdncoed_kSPDTN...@giganews.com...
reply to every point and it seems a little like arguing angels on a pin
anyway.
I may look at it later when I'm not so exhausted and short-tempered.
-MT
"Mike Tyner" <mty...@mindspring.com> wrote in message
news:Otqdncoed_kSPDTN...@giganews.com...
peter...@gmail.com
Nov 18, 2012, 11:43:43 PM11/18/12
to
On Sunday, November 18, 2012 10:06:26 PM UTC-5, Mike Tyner wrote:
> Sorry I pulled the trigger on this reply too soon. It's too late for me to
> reply to every point and it seems a little like arguing angels on a pin
> anyway.
>
> I may look at it later when I'm not so exhausted and short-tempered.
>
> -MT
Thanks Mike, I understand. Appreciate your willingness to engage in a discussion to this point. My intent was not to argue, but a desire to engage a reasonably qualified expert in the field to help me understand some of the more succint points that I may be missing or have questions about. I apologize if my ignorance or error in logic are exhausting. If you do reply further, please know that I will greatly appreciate it.
> Sorry I pulled the trigger on this reply too soon. It's too late for me to
> reply to every point and it seems a little like arguing angels on a pin
> anyway.
>
> I may look at it later when I'm not so exhausted and short-tempered.
>
> -MT
Peter
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