At this very moment, the sophisticated design of your eyes makes it possible for you to read these words. It is the geometry of each part of your eye and the correct arrangement of cells that make the miracle of sight possible.

Neuroscientist Alan Springer, a Ph.D. at the New York Medical College in Valhalla, N.Y., is studying how the shape of important eye tissues and the arrangement of light-sensing cells develop. Greater understanding of eye development may lead to major advances in the treatment of eye diseases and abnormalities.

As part of his research, Springer has created virtual biomechanical models that simulate the development of the eye and provide insight into the formation of an organic structure that is a key to good vision.

According to Springer, behavior of the computer model so far supports his hypothesis that, as the eye grows, the retina stretches. This mechanical process of deformation causes cells to assume the shape and distribution needed for sharp eyesight.

Retinal development: About three months before birth (A), the retina thickens near its center. For the next five to eight years (B), cells in the retina's inner layer move away from the center, leaving the cone-shaped fovea, and (C) cone photoreceptors move toward the foveaÕs center from behind.

As light enters your eye, a lens directs it onto the retina, the interior back surface of the eye, where the photoreceptors are. In an adult's eye, the light-sensing photoreceptors tend to cluster in their highest concentration in a small region called the fovea, in the center of the retina.

The arrangement provides high visual acuity, but it is something people are not born with. A newborn's retina contains a much more even distribution of photoreceptors.

Springer's research is attempting to discover how the retina takes its final shape and how photoreceptors become concentrated in the fovea. Springer's models simulate foveal development, and his tests support his hypothesis that eye growth causes the retina to stretch and the resulting stresses rearrange cells to develop the human fovea.

Scientists believe that two vision disorders may be related to improper eye growth. A recent study of induced myopia by David Troilo, a colleague of Springer's, concluded that myopic eyes are larger than normal eyes and have a higher density of photoreceptors in the fovea.

Strabismus, a disorder in which both eyes cannot fix on the same point at the same time, may be caused by uneven rates of eye growth. The link between eye growth and strabismus is supported by experiments in animals in which one eye is enlarged. Not only does strabismus result in some of these experiments, but researchers also find that the fovea is located differently in each eye.

Medical researchers have observed the changes that take place in the retina during eye development. The retina consists of an outer layer of photoreceptors and an inner layer made up of nerve cells (ganglion and inner nuclear cells). The photoreceptor layer is initially one cell thick.

At the beginning of an unborn child's third trimester, the inner retinal layer in the area that will become the fovea is thicker than the surrounding retina. From that time until the child is five to eight years old, retinal cells in the inner layer move away from the center of the fovea, resulting in a cone-shaped pit. The pit starts as a mere shallow notch and grows larger over time. This movement removes cells that presumably obstruct light from reaching the underlying photoreceptors.

At the same time, photoreceptors behind the retina move toward the center of the fovea, where eventually they are gathered in a multilayered mass. In addition to observing changes in cell distribution, scientists have noticed that photoreceptors in the foveal region are thinner and longer than those in the peripheral retina.

Although medical researchers and doctors have observed the changes that have taken place, they have not come to a consensus on how or why those changes come about.

Springer believes that the retina stretches like an inflating balloon as the eye grows. The formation of the fovea results from eye growth and the stretching of the retina. According to Springer, the stretching may also account for the difference in shape of photoreceptors in the fovea and in the peripheral retina.

Springer wanted to see how the shape of the fovea changes over time, but because the organic process takes as long as eight years, direct observation in real time was impractical. That's where a computer came in handy.

A hemisphere (shown in cross-section) demonstrates displacement patterns that are similar to those of the two-dimensional models.

Using Accupak/VE mechanical event simulation software from Algor Inc. of Pittsburgh, Springer developed his model to recreate, at a much faster rate, the forming of the adult eye. The software is designed to simulate motion in mechanical events and to show resulting stresses on the computer model at each instant in time. To keep a check on the accuracy of the simulation, Springer compared stages of the model with researchers' real-world observations at corresponding stages of eye development.

Springer found that for the purposes of learning about the changes in foveal shape, nonlinear and Mooney-Rivlin material models could supply meaningful results. He used published values for the collective material properties of eye tissues. Springer began with a two-dimensional model and used tangential forces, rather than a radial force such as pressure, to simulate stretching. The model represented the inner retinal layers with a small notch. The model was fixed on one end and displaced in the X direction with a force applied to the other end.

"As I expected, the notch grew larger during the virtual event," Springer said. But he was surprised to see the retina behind the foveal pit deflect inward. So he notched a sheet of rubber, stretched it by hand, and got a similar result. This movement behind the fovea may explain the migration of photoreceptors toward the retina's center.

Springer next created a curved, two-dimensional model of the retina. He used Mooney-Rivlin material properties to simulate the elastic nature of the tissue. Boundary conditions fixed the model at both ends, and pressure applied to the inner surface caused displacement. The results were similar to those obtained using a tangential stretching force. Increasing pressure wid-ened the notch and the material behind it was displaced less than material farther from the notch.

A model of an elastic hemisphere starting with a notch in its inner surface added more confirmation. Springer said the 3-D model had more value because it was very useful for presentations. "When non-engineers can see the displacement in three dimensions," he said, "it is easier for them to understand." Pressure increased as the hemisphere inflated; the notch in the inner surface wid-ened, and the outer surface over the notch pressed inward.

The next step was to examine the mechanical interaction between the retinal and photoreceptor layers. Springer adapted the first model by adding a second layer representing the photoreceptors. Beam elements connected the two layers and communicated stresses between them.

As in the first model, the layered model simulated force in one direction; that is, one end was fixed and force was applied to the other. To simulate the contour found in a normal retina, Springer constrained the nodes on the outer surface of the photoreceptor layer in the X, but not the Y, plane. As the combined model was stretched, the back of the retina deflected inward and pulled photoreceptors toward the center.

These stresses also deformed the photoreceptor material under the notch in the Y plane, suggesting that the same force could account for the elongated shape of the photoreceptors as well as the accumulation in the fovea.

Springer's research to date supports the hypothesis that the fovea's development from a notch to a pit is biomechanical. He plans to study how the notch forms initially.

In connection with his hypothesis, Springer is initiating clinical research into strabismus. Currently, doctors use surgery to treat eyes that cannot both fix on the same point at the same time, but the treatment leaves some residual problems with vision.

Working with the idea that strabismus is caused by uneven eye growth, Springer says corrective lenses may help dur-ing the critical period when the brain learns about eye fixation. The uneven growth may make it difficult for the brain to learn how to coordinate the sight of both eyes. Lenses might be able to train eyes to fixate until the slower- growing eye catches up to its partner.

"More understanding of eye development could lead to better treatment of poor vision due to improper eye growth," Springer said. "Or we may be able to treat retinal or other eye diseases. The outcome of our research is impossible to predict."

This article was prepared by staff writers in collaboration with outside contributors.

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