My Eye - memoirs
In the summer of 1957 (at the age of 10), I had an accident in my left eye
that resulted in a unilateral traumatic cataract. There was a doctor in
St. Clair hospital (Dr. Black?) who thought that my eye might have to be
removed or I might go blind in the other eye. I presume, from what I learned
later, that the reason was autoimmunity to S (soluble) antigen (48 k protein,
arrestin). Fortunately, Dr. Davies took over and decided that was not needed.
My eye doctor, Dr. Davies partner, John Kenneth Hootman (1923-2001) attempted
an operation in 1958, but it failed. He referred me to a specialist who,
in the summer of 1959, did an operation that cut a window in that cataract.
The operation was sloppy by today's standards. My pupil is off center and
misshapen, resulting in loss of peripheral vision (tunnel vision), especially
at photopic light levels (when that pupil is constricted). Also, my eye
doctors have complained that they cannot see into that eye. For instance,
when I went to an eye doctor at Saint Louis University about 10 years ago,
he decided to order an ultrasound because of the importance of information
on retinal imaging. Finally, I noticed a shadow if I was laying on my back
and rolled my head. One time, about 35 years ago, an eye doctor said he
saw a chunk in my eye and tilted me back and forth in his chair, very amused.
Eventually I saw it, about the size of the tip of a mechanical pencil, getting
stuck in the aqueous at various locations between the iris and the cornea.
I have not noticed it (the shadow or the visible chunk) for about a decade.
I was very photophobic in that eye after the operation and have squinted
ever since giving me the scowl wrinkle in my brow. It was not until college,
the days of day-glow posters and "black" lights, that I realized
that I saw UV with that eye.
Human UV visual sensitivity was the entry point to this diary page about
my eye, and this topic has been adequately covered for years on my
web page dedicated to this topic. Out of the score of research topics
on the starklab home page, this page has generated the most interest and
correspondence. Also, I summarized many of my convergent interests in UV
vision in this seminar.
Typically this starts at age 10. The conventional wisdom decades ago had
been that genetics, not "environment" (visual experience) determined
myopia. That was in contrast with my intuition as the myopia in my right
eye worsened (and also in contrast with this
[anti-ophthalmologist] web site). (That correction is now -6.25, not quite
as strong as it was a few years ago.) I was interested as research demonstrated
environmental contributions to myopia. One pioneer, Josh Wallman at CCNY
fit chickens with goggles to distort their vision and found that their eyes
changed in compensation; they need to see up close to peck seeds. Interestingly,
I was one of the referees for Wallman's promotion to tenure (why? - maybe
a senior faculty colleague at CCNY knew me?). I wondered, "was my aphakic
eye excused from progressive myopia?" Susan Yang, MD, my ophthalmologist,
recently determined that the correction is +11.5 (+11.75 if the eye was
dilated). To answer my question, all I needed to know was the power of the
human lens, but that information was impossible to find, perhaps because
it is different for each person. So I found the glasses I had at that early
age in my souvenir box, and Dr. Yang determined that the correction was
+12.25. On the basis of the similarities of the corrections across a 48
year period, I conclude that my right eye, but not my left eye (the aphakic
one), had undergone progressive myopia. This is important information substantiating
experiential causes of myopia.
It about the age of 49, I began to experience floaters in my myopic eye.
I did not know about floaters and was worried until after a description
of what they were at my next eye doctor visit. I was surprised that the
text I used in my neuroscience course (Purves et al., Neuroscience, Sinauer)
touched on the topic: "The housekeeping abilities of the vitreous humor
are limited, however, as a large number of middle-aged and elderly individuals
with vitreous 'floaters' will attest. Floaters are collections of debris
too large for phagocytic consumption that therefore remain to cast annoying
shadows on the retina; they typically arise when the aging vitreous membrane
pulls away from the overly long eyeballs of myopic individuals." (fourth
edition, 2008, p. 254). I do not have floaters in my aphakic eye. You'll
have to take my word for that observation because it is so difficult for
an eye care professional to see into that eye. But I trust my introspection,
even though (maybe especially because) I do not correct the vision in that
eye: floaters are less noticeable in a contrast-rich scene. I wanted to
track down the conventional wisdom about the relationship of floaters with
myopia and recently found this interesting piece in Wikipedia: "People
with high myopia are more likely to experience floaters, shadow-like shapes
which appear singly or in clusters in the field of vision ."
Here is a
picture a friend (Lynette Feeney-Burns) gave me before she retired (in about
1990). It is labeled "normal macular pigment - chow diet," and
it demonstrates the density of yellow pigment around the fovea in (presumably)
monkeys fed a diet adequate in carotenoids. A similar picture is in your
book (Fig. 10-28 b), but the darkened area is called the "fovea."
Currently, it is known that the carotenoids lutein and zeaxanthin are in
nerve layers in the light path to the receptors of the fovea (cones). We
get these yellow-appearing caroteinois in our diet (e.g. from spinach and
corn). It is thought that they help to protect cones from damage that may
be induced by blue light. It was found that the concentration is increased
with dietary increases, and now lutein is included in multi-vitamins.
I have this optical
set up. I've set the wavelength at about 460 nm (blue), near the peak absorbance
of the macular pigments. I've glued a polarizing filter to a motor that
rotates at about 1 rotation per second. The reason to rotate this filter
is that your ability to see the pattern of polarized light is so subtle
that you will only notice it if it is continuously changing. Using this
apparatus, I can see Haidinger's brushes clearly with both eyes. Nice, but
this is only a qualitative demonstration.
Has a half century of retinal exposure to UV light damaged my macular pigments?
For 10 years, I have been going to this
dinner at the ARVO (Association for Research in Vision and Ophthalmology).
As you see, it is called the "Macula and nutrition group," but
my first invitation referred to "investigators and students interested
in the role of carotenoids in the eye." You'll be happy to note that
there are many carotenoids
in the food served. There is a huge amount of interest in macular pigments
and their possible role in protecting against age-related macular degeneration
(ARM). Here is Dennis Gierhart
(left), Chairman and Chief Scientific Officer of ZeaVision.
I've only known him for a few years, amazingly, since his company is here
in St. Louis. I have several common interests with his St. Louis corporation,
ZeaVision. They are working toward
regular clinical measuremtnts of macular pigment optical density as part
of a visit to your eye professional. Here is "quantifeye,"
a clinical psychophysical apparatus marketed for ophthalmologists and optometrists
to quantify patient's macular pigments. They get a reading of 0.43 (optical
density) for my right eye, much lower for my left eye.
I have noticed for years that, if I come in from bright light, and my
right eye is hugely too light adapted to see well in dim light, my left
eye is much better. The most likely explanation is trivial. As mentioned
above, I squint that eye. Also, again mentioned above, a "deformed"
pupil may cut light abnormally in bright light. Despite these uninteresting
possibilities, I wanted to mention how this eye is preadapted to a move
to dimmer light; if the explanation is physiological, it could be very interesting.
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this web page was posted 8/13/08