Category Archives: Cortical Organization

Myopia at a Mets Game

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When I was nine years old my father took me to my first New York Mets game at Shea Stadium and I was thrilled to watch my favorite baseball team play live. However, upon taking our seats way up in the stands during the first inning, I realized that there would be a major problem for the remainder of the game. As I looked hundreds of feet down to the field, everything was blurry- I couldn’t see David Wright’s number on his jersey; I couldn’t see the numbers on the scoreboard; I couldn’t even see where the ball was being thrown. This angered me because I could read the scorecard in front of my face just fine, but everything went from clear to blurry as the distance from myself increased.

Consequently, I took a trip to visit my eye doctor the following day. I informed Dr. Rubin of the difficulty I was faced with during the previous day’s activities and he asked me to sit in a chair so he can perform some tests. One specific evaluation that I remember was when Dr. Rubin placed a series of random letters in front of me that decreased in size with each progressive row. “Read aloud all the letters in row four,” he said. In response I called out, “E, H, F, B …” and so on. Next came row five and the same process was repeated. Finally when Dr. Rubin asked me to announce the letters in row six, it became obvious that my vision was blurry- I’m not sure if I was correct on even half of the letters that I shouted. At the end of my visit, Dr. Rubin said, “Okay Dylan, that’s all. It turns out that you have 20/30 vision and will need to wear glasses when looking at things far away because you’re near-sighted.” I had no clue what most of this meant at age nine, but I knew that I had dreaded the idea of having to use glasses in class, in the movies, and in any other public place.

What I didn’t realize at the time, was that those glasses that Dr. Rubin prescribed were very important for me to function properly. Apparently, I had vision that was considerably worse than the average person; the fact that my vision was 20/30 meant that I had to be at 20 feet to read the same letters that someone with normal vision could read at 30 feet. The test of decreasing letter sizes that Dr. Rubin used to determine this visual acuity, or the smallest spatial detail that I could resolve, happened to be the same that all eye doctors used. Additionally, the fact that I was considered “near-sighted” meant that I had myopia. To understand myopia, one must first know how light rays are focused in the eye.

First off, every person has a lens system that is responsible for refracting, or bending, light from many different angles onto the same point of the retina- the layer of neurons in the back of the eye. Although this system creates a bright image for a person to perceive things better, it can sometimes make that image appear out of focus. The cause of this problem is called accommodation, which is when the lens changes its original shape and thus alters its refractive power. The improper refracting from this accommodation in my particular lens system resulted in myopia. Since my eyeball was too long, the point of focus for that bending light fell in front of my retina, rather than on it. This is why Wright’s number appeared burry, while the scorecard appeared clear at the baseball game when I was nine years old. It’s a shame that the light that entered my eye couldn’t have been bended appropriately onto my retina, with no refractive error. Unfortunately, I was not lucky enough to have such emmetropia, as experts call it, and instead was stuck with myopia and those horrible glasses.

Despite my initial embarrassment about wearing glasses, in time I came to truly appreciate those helpful lenses because I was finally able to see things properly. Those negative lenses were able to diverge rays of light before they entered my eye and thus corrected my myopia issues. As a result, I was able to happily watch my favorite team play the next time I attended Shea Stadium for a Mets game and didn’t have to worry about anything being too blurry to see.

A Flash-Bang Phenomenon

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Waking up in the morning, for many, involves turning on a light after turning off an alarm.  Although some people learn to navigate their way to the shower in the dark, most of us have to deal with a dramatic change in luminance, opening our eyes and immediately being overwhelmed by light.  Whether this occurs because your parents are trying to get you up and moving, or because you want to see what you are doing in the bathroom, similar biological processes seem to be at work.  Throughout the night while we sleep, most of us with our eyelids sealed shut, we adapt to a world of darkness.  When experiencing such a sudden and drastic change in luminance – as when someone shines a flashlight in your eyes, you begin to see blobs of undefined figures circling around in your receptive field.  When this happens to me, I usually see what I would compare to a slightly transparent blue ameba – regardless my vision becomes impaired to the extent that it is much harder to make out what is directly in front of me.  I do not know exactly why this happens, but I believe it is primarily due to the bleaching of photopigments.

Retinal ganglion cells respond to changes in light, not the overall amount of light covering their receptive field – the change from dark to light is what causes visual impairment in the prior situations, not how bright either light source is.  Whenever someone shines a light in your eye, a lot of photopigments are used up because they are trying to adapt to the change in luminance. This leaves fewer pigments available to process whatever other information is in one’s environment.  Furthermore, I believe the more of one’s visual field encompassed by a sudden spurt of light, the more neurons fire, because light is coming at them from many more orientations/angles than if such a change occurred farther away.  The more cells that fire, the more information striate cortex neurons have to filter out.  Perhaps when there is too much information to process efficiently, this filtering sequence is slowed and disrupts the feed forward process.  If so, would one’s mind start to group objects/stimuli that it normally would not combine?  In essence, the more depleted photopigments, the more acuity is impaired, and the less detail an individual can make out.

Although cone photoreceptors regenerate more quickly than rods, they are also exhausted at a faster rate.  Since such an abundance of cones are used up when one perceives a drastic change in luminance, (I think) the whole visual processing system falls into a chain reaction of information overload.  The parvocellular pathway, dealing with details of stationary objects, simply tries to pass on too much information.  Because there are now less photopigments available to process the current environment, and the filtering process in the striate cortex is busy with information it has just received, middle vision processes start to receive jumbled information.  My guess is that this leads us to perceive similarities and differences from stimuli in our environment when such relationships do not exist.  Furthermore, the feed forward process allows our brain to draw conclusions about what it perceives without needing a later processing sequence to communicate with earlier processing events, which I believe can lead to uncontrollable perceptual errors. In other words, an error that causes us to see bright blue blobs where they don’t exist.  Perhaps law enforcement personnel use flash-bang grenades for the same reason; they have found a practical use for our visual system’s sensitivity to abrupt changes in luminance.