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Boston, MA, United States

The New England College of Optometry in Boston, Massachusetts, is the oldest continually operating college of optometry in the United States. It was originally established as the Klein School of Optics in 1894 by Dr. August Andreas Klein, an ophthalmologist. The college moved to several locations around Boston, and was known as the Massachusetts School of Optometry and the Massachusetts College of Optometry until it came to reside in its current location in the Back Bay section of Boston. The College offers both Doctor of Optometry and Master of Science in Vision Science degrees. Special emphasis is placed on direct contact with patients, and to this end students make use of the College's affiliation with the New England Eye Institute network of eye care centers.The current president of the college is Dr. Clifford Scott.It has an enrollment of over 400 students. Wikipedia.

Nickla D.L.,The New England College of Optometry | Wallman J.,City College of New York
Progress in Retinal and Eye Research | Year: 2010

The choroid of the eye is primarily a vascular structure supplying the outer retina. It has several unusual features: It contains large membrane-lined lacunae, which, at least in birds, function as part of the lymphatic drainage of the eye and which can change their volume dramatically, thereby changing the thickness of the choroid as much as four-fold over a few days (much less in primates). It contains non-vascular smooth muscle cells, especially behind the fovea, the contraction of which may thin the choroid, thereby opposing the thickening caused by expansion of the lacunae. It has intrinsic choroidal neurons, also mostly behind the central retina, which may control these muscles and may modulate choroidal blood flow as well. These neurons receive sympathetic, parasympathetic and nitrergic innervation. The choroid has several functions: Its vasculature is the major supply for the outer retina; impairment of the flow of oxygen from choroid to retina may cause Age-Related Macular Degeneration. The choroidal blood flow, which is as great as in any other organ, may also cool and warm the retina. In addition to its vascular functions, the choroid contains secretory cells, probably involved in modulation of vascularization and in growth of the sclera. Finally, the dramatic changes in choroidal thickness move the retina forward and back, bringing the photoreceptors into the plane of focus, a function demonstrated by the thinning of the choroid that occurs when the focal plane is moved back by the wearing of negative lenses, and, conversely, by the thickening that occurs when positive lenses are worn. In addition to focusing the eye, more slowly than accommodation and more quickly than emmetropization, we argue that the choroidal thickness changes also are correlated with changes in the growth of the sclera, and hence of the eye. Because transient increases in choroidal thickness are followed by a prolonged decrease in synthesis of extracellular matrix molecules and a slowing of ocular elongation, and attempts to decouple the choroidal and scleral changes have largely failed, it seems that the thickening of the choroid may be mechanistically linked to the scleral synthesis of macromolecules, and thus may play an important role in the homeostatic control of eye growth, and, consequently, in the etiology of myopia and hyperopia. © 2009 Elsevier Ltd. All rights reserved. Source

Rucker F.J.,The New England College of Optometry
Ophthalmic and Physiological Optics | Year: 2013

Purpose: At birth most, but not all eyes, are hyperopic. Over the course of the first few years of life the refraction gradually becomes close to zero through a process called emmetropisation. This process is not thought to require accommodation, though a lag of accommodation has been implicated in myopia development, suggesting that the accuracy of accommodation is an important factor. This review will cover research on accommodation and emmetropisation that relates to the ability of the eye to use colour and luminance cues to guide the responses. Recent Findings: There are three ways in which changes in luminance and colour contrast could provide cues: (1) The eye could maximize luminance contrast. Monochromatic light experiments have shown that the human eye can accommodate and animal eyes can emmetropise using changes in luminance contrast alone. However, by reducing the effectiveness of luminance cues in monochromatic and white light by introducing astigmatism, or by reducing light intensity, investigators have revealed that the eye also uses colour cues in emmetropisation. (2) The eye could compare relative cone contrast to derive the sign of defocus information from colour cues. Experiments involving simulations of the retinal image with defocus have shown that relative cone contrast can provide colour cues for defocus in accommodation and emmetropisation. In the myopic simulation the contrast of the red component of a sinusoidal grating was higher than that of the green and blue component and this caused relaxation of accommodation and reduced eye growth. In the hyperopic simulation the contrast of the blue component was higher than that of the green and red components and this caused increased accommodation and increased eye growth. (3) The eye could compare the change in luminance and colour contrast as the eye changes focus. An experiment has shown that changes in colour or luminance contrast can provide cues for defocus in emmetropisation. When the eye is exposed to colour flicker the eye grows almost twice as much, and becomes more myopic, compared to when the eye is exposed to luminance flicker. Summary: Neural responses of the luminance and colour mechanisms direct accommodation and emmetropisation mechanisms to different focal planes. Therefore, it is likely that the set point of refraction and accommodation is dependent on the sensitivity of the eye to changes in spatial and temporal, colour and luminance contrast. © 2013 The College of Optometrists. Source

Rucker F.J.,The New England College of Optometry
Journal of vision | Year: 2012

As the eye changes focus, the resulting changes in cone contrast are associated with changes in color and luminance. Color fluctuations should simulate the eye being hyperopic and make the eye grow in the myopic direction, while luminance fluctuations should simulate myopia and make the eye grow in the hyperopic direction. Chicks without lenses were exposed daily (9 a.m. to 5 p.m.) for three days on two consecutive weeks to 2 Hz sinusoidally modulated illumination (mean illuminance of 680 lux) to one of the following: in-phase modulated luminance flicker (LUM), counterphase-modulated red/green (R/G Color) or blue/yellow flicker (B/Y Color), combined color and luminance flicker (Color + LUM), reduced amplitude luminance flicker (Low LUM), or no flicker. After the three-day exposure to flicker, chicks were kept in a brooder under normal diurnal lighting for four days. Changes in the ocular components were measured with ultrasound and with a Hartinger Coincidence Refractometer (aus Jena, Jena, East Germany. After the first three-day exposure, luminance flicker produced more hyperopic refractions (LUM: 2.27 D) than did color flicker (R/G Color: 0.09 D; B/Y Color: -0.25 D). Changes in refraction were mainly due to changes in eye length, with color flicker producing much greater changes in eye length than luminance flicker (R/G Color: 102 μm; B/Y Color: 98 μm; LUM: 66 μm). Our results support the hypothesis that the eye can differentiate between hyperopic and myopic defocus on the basis of the effects of change in luminance or color contrast. Source

He J.C.,The New England College of Optometry
Ophthalmic and Physiological Optics | Year: 2014

Purpose: The purpose of this study was to theoretically model the contributions of corneal asphericity (Q) and anterior chamber depth to peripheral wavefront aberrations. Methods: Ray-tracing was performed on a model eye using a customised MatLab program to calculate Zernike aberrations up to the 5th order across ±60° of the horizontal visual field. The corneal Q was varied from -0.5 to 0.8, and the anterior chamber depth was changed from 2.05 to 4.05 mm while axial length was held constant. Spherical equivalent refractive error derived from Zernike defocus was used to estimate peripheral refraction. Results: Relative to axial Zernike aberrations, both defocus and astigmatism in the peripheral field increased with the corneal Q value, but the increases in relative peripheral astigmatism were much smaller in amplitude than relative peripheral defocus. Anterior chamber depth shortening caused the relative peripheral defocus and astigmatism to increase toward more positive values, although the changes in relative peripheral astigmatism with anterior chamber depth were small. Combination of the variations in both corneal Q and anterior chamber depth does not produce linear sum of the changes in relative peripheral defocus. The relative peripheral refractive error was more myopic when either the corneal Q was increased or the anterior chamber depth was shortened. The changes in relative peripheral x-axis coma, trefoil and spherical aberration with corneal Q value were complex but were barely changed with anterior chamber depth within the central 60° visual field. Conclusions: Both corneal asphericity and anterior chamber depth play important roles in determining peripheral wavefront aberrations. The two factors nonlinearly interact to affect peripheral aberrations. Higher corneal Q and/or shorter anterior chamber depth tend to produce relatively more myopic peripheral refraction. Increasing the Q value of the anterior surface of a contact lens might provide an interesting intervention to slow myopia progression. © 2014 The College of Optometrists. Source

Nickla D.L.,The New England College of Optometry
Experimental Eye Research | Year: 2013

Many ocular processes show diurnal oscillations that optimize retinal function under the different conditions of ambient illumination encountered over the course of the 24h light/dark cycle. Abolishing the diurnal cues by the use of constant darkness or constant light results in excessive ocular elongation, corneal flattening, and attendant refractive errors. A prevailing hypothesis is that the absence of the Zeitgeber of light and dark alters ocular circadian rhythms in some manner, and results in an inability of the eye to regulate its growth in order to achieve emmetropia, the matching of the front optics to eye length. Another visual manipulation that results in the eye growth system going into a "default" mode of excessive growth is form deprivation, in which a translucent diffuser deprives the eye of visual transients (spatial or temporal) while not significantly reducing light levels; these eyes rapidly elongate and become myopic. It has been hypothesized that form deprivation might constitute a type of "constant condition" whereby the absence of visual transients drives the eye into a similar default mode as that in response to constant light or dark. Interest in the potential influence of light cycles and ambient lighting in human myopia development has been spurred by a recent study showing a positive association between the amount of time that children spent outdoors and a reduced prevalence of myopia. The growing eyes of chickens and monkeys show a diurnal rhythm in axial length: Eyes elongate more during the day than during the night. There is also a rhythm in choroidal thickness that is in approximate anti-phase to the rhythm in eye length. The phases are altered in eyes growing too fast, in response to form deprivation or negative lenses, or too slowly, in response to myopic defocus, suggesting an influence of phase on the emmetropization system. Other potential rhythmic influences include dopamine and melatonin, which form a reciprocal feedback loop, and signal "day" and "night" respectively. Retinal dopamine is reduced during the day in form deprived myopic eyes, and dopamine D2 agonists inhibit ocular growth in animal models. Rhythms in intraocular pressure as well, may influence eye growth, perhaps as a mechanical stimulus triggering changes in scleral extracellular matrix synthesis. Finally, evidence shows varying influences of environmental lighting parameters on the emmetropization system, such as high intensity light being protective against myopia in chickens. This review will cover the evidence for the possible influence of these various factors on ocular growth. The recognition that ocular rhythms may play a role in emmetropization is a first step toward understanding how they may be manipulated in treatment therapies to prevent myopia in humans. © 2013 Elsevier Ltd. Source

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