Increase In Vitreous Chamber Depth Research Articles

Parasympathetic and sympathetic control of emmetropization in chick

Emmetropization can be altered by temporal visual stimulation and the spectral properties of the visual environment. The goal of the current experiment is to test the hypothesis that there is an interaction between these properties and autonomic innervation. For that purpose, selective lesions of the autonomic nervous system were performed in chickens followed by temporal stimulation. Parasympathetic lesioning involved transection of both the ciliary ganglion and the pterygopalatine ganglion (PPG_CGX; n = 38), while sympathetic lesioning involved transection of the superior cervical ganglion (SCGX; n = 49). After one week of recovery, chicks were then exposed to temporally modulated light (3 days, 2 Hz, Mean: 680 lux) that was either achromatic (with blue [RGB], or without blue [RG]), or chromatic (with blue [B/Y] or without blue [R/G]). Control birds with lesions, or unlesioned, were exposed to white [RGB] or yellow [RG] light. Ocular biometry and refraction (Lenstar and a Hartinger refractometer) was measured before and after exposure to light stimulation. Measurements were statistically analyzed for the effects of a lack of autonomic input and the type of temporal stimulation.In PPG_CGX lesioned eyes, there was no effect of the lesions one-week post-surgery. However, after exposure to achromatic modulation, the lens thickened (with blue) and the choroid thickened (without blue) but there was no effect on axial growth. Chromatic modulation thinned the choroid with R/G.In the SGX lesioned eye, there was no effect of the lesion 1-week post-surgery. However, after exposure to achromatic modulation (without blue), the lens thickened and there was a reduction in vitreous chamber depth and axial length. Chromatic modulation caused a small increase in vitreous chamber depth with R/G.Both autonomic lesion and visual stimulation were necessary to affect the growth of ocular components. The bidirectional responses observed in axial growth and in choroidal changes suggest that autonomic innervation combined with spectral cues from longitudinal chromatic aberration may provide a mechanism for homeostatic control of emmetropization.

Parasympathetic innervation of emmetropization

Emmetropization is affected by the temporal parameters of visual stimulation and the spectral composition of light, as well as by autonomic innervation. The goal of the current experiments is to test the hypothesis that different types of visual stimulation interact with ocular innervation in the process of emmetropization. For that, selective lesions of the autonomic nervous system were performed in chickens: involving transection of parasympathetic input to the eye from either the ciliary ganglion, innervating accommodation and pupil responses (CGX; n = 32), or pterygopalatine ganglion, innervating choroidal blood vessels and cornea (PPGX; n = 26). After 1 week of recovery, chicks were exposed to sinusoidally modulated light (3 days, 2 Hz, 680 lux) that was either achromatic (black to white [RGB], or black to yellow [RG]), or chromatic (blue to yellow [B/Y] or red to green [R/G]). Exposure to light stimulation was followed by ocular biometry (Lenstar and a Hartinger refractometer). Surgical conditions revealed a small reduction in anterior chamber depth with CGX but no other significant changes in ocular biometry/refraction under standard light conditions. With RGB achromatic stimulation, CGX eyes produced an effect on ocular components, with a further reduction in anterior chamber depth and an increase in vitreous chamber depth, while RG stimulation showed no effect. No effect was detected in PPGX under both achromatic protocols. With chromatic stimulation, CGX with R/G modulation increased eye length, while PPGX with B/Y modulation decreased eye length. We conclude that the two different types of parasympathetic innervations have antagonistic effects on eye growth and the anterior eye when challenged with the appropriate stimulus, with possible implications for the role of choroidal blood flow in emmetropization.

Temporal color contrast guides emmetropization in chick

As a result of longitudinal chromatic aberration (LCA), longer wavelengths are blurred when shorter wavelengths are in focus, and vice versa. As a result, LCA affects the color and temporal aspects of the retinal image with hyperopic defocus. In this experiment, we investigated how the sensitivity to temporal color contrast affects emmetropization. Ten-day-old chicks were exposed for three days to sinusoidal color modulation. The modulation was either blue/yellow flicker (BY) (n = 57) or red/green flicker (RG) (n = 60) simulating hyperopic defocus with and without a blue light component. The color contrasts tested were 0.1, 0.2, 0.3, 0.4, 0.6, and 0.8 Michelson contrast. The mean illuminance of all stimuli was 680 lux. Temporal modulation was either of a high (10 Hz) or low (0.2 Hz) temporal frequency. To test the role of short- and double-cone stimulation, an additional condition silenced these cones in RG_0.4 (D-) and was compared with RG_0.4 (D+) (n = 14). Changes in ocular components and refractive error were measured using Lenstar and a photorefractometer. With high temporal frequency BY representing an in-focus condition for shorter-wavelengths, we found that high temporal frequency BY contrast was positively correlated with vitreous expansion (R2 = 0.87, p < 0.01), expanding the vitreous to compensate for hyperopic defocus. This expansion was offset by low temporal frequency RG, which represented blurred longer wavelengths. The reduction in vitreous expansion in RG_0.4, was enhanced in D+ compared to D- (p < 0.001), indicating a role for short- and/or double-cones. With high temporal frequency RG representing an in-focus condition for longer-wavelengths, we found that high temporal frequency RG contrast was also positively correlated with a linear increase in vitreous chamber depth (R2 = 0.84, p < 0.01) and eye length (R2 = 0.30, p ≤ 0.05), required to compensate for hyperopic defocus, but also with RG sensitive choroidal thickening (R2 = 0.18: p < 0.0001). These increases in the vitreous and eye length were enhanced with D+ compared to D- (p = 0.003) showing the role of short- and double-cones in finessing the vitreous response to hyperopic defocus. Overall, the increase in vitreous chamber depth in RG was offset by reduced expansion in BY, indicating sensitivity to the shorter focal length of blue light and wavelength defocus. Predictable changes in cone contrast and temporal frequency of the retinal image that occur with LCA and defocus result in homeostatic control of emmetropization.

Temporal whole field sawtooth flicker without a spatial component elicits a myopic shift following optical defocus irrespective of waveform direction in chicks

PurposeMyopia (short-sightedness) is the commonest visual disorder and greatest risk factor for sight threatening secondary pathologies. Myopia and hyperopia can be induced in animal models by rearing with optical lens defocus of opposite sign. The degree of refractive compensation to lens-induced defocus in chicks has been shown to be modified by directionally drifting sawtooth spatio-temporal luminance diamond plaids, with Fast-ON sawtooth spatio-temporal luminance profiles inhibiting the myopic shift in response to negative lenses, and Fast-OFF profiles inhibiting the hyperopic shift in response to positive lenses. What is unknown is whether similar sign-of-defocus dependent results produced by spatio-temporal modulation of sawtooth patterns could be achieved by rearing chicks under whole field low temporal frequency sawtooth luminance profiles at 1 or 4 Hz without a spatial component, or whether such stimuli would indiscriminately elicit a myopic shift such as that previously shown with symmetrical (or near-symmetrical) low frequency flicker across a range of species.MethodsHatchling chicks (n = 166) were reared from days five to nine under one of three defocus conditions (No Lens, +10D lens, or −10D lens) and five light conditions (No Flicker, 1 Hz Fast-ON/Slow-OFF sawtooth flicker, 4 Hz Fast-ON/Slow-OFF sawtooth flicker, 1 Hz Fast-OFF/Slow-ON sawtooth flicker, or 4Hz Fast-OFF/Slow-ON sawtooth flicker). The sawtooth flicker was produced by light emitting diodes (white LEDs, 1.2 –183 Lux), and had no measurable dark phase. Biometrics (refraction and ocular axial dimensions) were measured on day nine.ResultsBoth 1 Hz and 4 Hz Fast-ON and Fast-OFF sawtooth flicker induced an increase in vitreous chamber depth that was greater in the presence of negative compared to positive lens defocus. Both sawtooth profiles at both temporal frequencies inhibited the hyperopic shift in response to +10D lenses, whilst full myopic compensation (or over-compensation) in response to −10D lenses was observed.ConclusionsWhole field low temporal frequency Fast-ON and Fast-OFF sawtooth flicker induces a generalized myopic shift, similar to that previously shown for symmetrical sine-wave and square-wave flicker. Our findings highlight that temporal modulation of retinal ON/OFF pathways per se (without a spatial component) is insufficient to produce strong sign-of-defocus dependent effect.

M to L cone ratios determine eye sizes and baseline refractions in chickens

Following a hypothesis raised by M. and J. Neitz, Seattle, we have tested whether the abundance and the ratio of Long wavelength-sensitive (L) to Middle wavelength-sensitive (M) cones may affect eye size and development of myopia in the chicken. Fourteen chickens were treated with frosted plastic diffusers in front of one eye on day 10 post-hatching for a period of 7 days to induce deprivation myopia. Ocular dimensions were measured by A-scan ultrasonography at the beginning and at the end of the treatment and development of refractive state was tracked using infrared photorefraction. At the end of the treatment period, L and M cone densities and ratios were analyzed in retinal flat mounts of both myopic and control eyes, using the red and yellow oil droplets as markers. Because large numbers of cones were counted (>10000), software was written in Visual C++ for automated cone detection and density analysis. (1) On average, 9.7 ± 1.7D of deprivation myopia was induced in 7 days (range from 6.8D to 13.7D) with an average increase in axial length by 0.65 ± 0.20 mm (range 0.42 mm–1.00 mm), (2) the increase in vitreous chamber depth was correlated with the increase in myopic refractive error, (3) average central M cone densities were 10,498 cells/mm2, and L cone densities 9574 cells/mm2. In the periphery, M cone densities were 6343 cells/mm2 and L cones 5735 cells/mm2 (4) M to L cone ratios were highly correlated in both eyes of each animal (p < 0.01 in all cases), (5) the most striking finding was that ratios of M to L cones were significantly correlated with vitreous chamber depths and refractive states in the control eyes with normal vision, both in the central and peripheral retinas (p < 0.05 to p < 0.01), (6) M to L cone ratios did however not predict the amount of deprivation myopia that could be induced. M and L cone ratios are most likely genetically determined in each animal. The more L cones, the deeper the vitreous chambers and the more myopic were the refractions in eyes. M to L cone ratios may determine the set point of emmetropization and thereby ultimately the probability of becoming myopic. Deprivation myopia was not determined by M to L cone ratios.

Influence of Ametropia and Its Correction on Measurement of Accommodation

Amplitude of accommodation (AA) is reportedly greater for myopic eyes than for hyperopic eyes. We investigated potential explanations for this difference. Analytical analysis and computer ray tracing were performed on two schematic eye models of axial ametropia. Using paraxial and nonparaxial approaches, AA was specified for the naked and the corrected eye using the anterior corneal surface as the reference plane. Assuming that axial myopia is due entirely to an increase in vitreous chamber depth, AA increases with the amount of myopia for two reasons that have not always been taken into account. First is the choice of reference location for specifying refractive error and AA in diopters. When specified relative to the cornea, AA increases with the degree of myopia more than when specified relative to the eye's first Gaussian principal plane. The second factor is movement of the eye's second Gaussian principal plane toward the retina during accommodation, which has a larger dioptric effect in shorter eyes. Using the corneal plane (placed at the corneal vertex) as the reference plane for specifying accommodation, AA depends slightly on the axial length of the eye's vitreous chamber. This dependency can be reduced significantly by using a reference plane located 4 mm posterior to the corneal plane. A simple formula is provided to help clinicians and researchers obtain a value of AA that closely reflects power changes of the crystalline lens, independent of axial ametropia and its correction with lenses.

Both the central and peripheral retina contribute to myopia development in chicks.

This study examined the contribution of the central and peripheral retina to the development of form deprivation myopia in chicks. Chicks were treated for 7 days either with centrally form-deprived (CFD) lenses of 2/4/6/8 mm diameter central diffuse zone, or a full size diffuser lens on their right eyes. The left eyes wore a full field plano lens. Axial dimensions and refractions were measured before and after 4 and 7 days of lens wear. All eyes that had worn CFD lenses of 2/4/6/8 mm had significant changes in refractive errors (from -2.69 ± 0.40 D to -6.13 ± 0.76 D, p < 0.05), vitreous chamber depth (from 0.19 ± 0.04 mm to 0.56 ± 0.04 mm, p < 0.05) and axial length (from 0.42 ± 0.03 mm to 0.96 ± 0.04 mm, p < 0.05) during the experiment, except for the changes in refractive error (-2.81 ± 0.33 D, p = 0.053) and axial length (0.77 ± 0.04 mm, p = 0.050) in the 2 mm lens group after 7 days of lens wear. The myopic shift in the CFD lens wearing eyes was due primarily to an increase in vitreous chamber depth. Linear regression analysis showed that the changes of refractive error, vitreous chamber depth and axial length were positively correlated with the size of central form-deprived retina. Form depriving the central retina produced axial myopia even in the presence of clear peripheral vision. The current study showed that both the central and peripheral retina contributes to myopia development in chicks. The amount of myopia induced increased linearly with the area of retina being form-deprived. It suggests that in terms of decoding optical input for growth, the area of retina being exposed to optical signals may be critical in determining eye growth.

The Nepal Longitudinal Study: Biometric Characteristics of Developing Eyes

To identify differences in potential biometric markers for predicting refractive error in school children. Biometric data on 895 Tibetan children, aged 6 to 18 years, residing in Katmandu, Nepal, were collected biennially from 1992 to 2000. Measurements included cycloplegic autorefraction, A-scan ultrasonography, and video phakometry. Only those children who had been studied at least once at age 12 years or more were included in the analysis. Subjects were divided into two groups: a myopia group if the refractive error was myopic by more than -0.50 D and a nonmyopia group if the refractive error was maximally myopic by -0.50 D, expressed as a spherical equivalent error in the left eye. Biometric measures that differed significantly with increasing age between the two refractive groups included: anterior chamber depth + 0.012 mm/year (p = 0.014), anterior lens radius of curvature + 0.073 mm/year (p = 0.001), lens power -0.059 D/year (p = 0.082), lens thickness -0.005 mm/year (p = 0.02), and vitreous chamber depth + 0.084 mm/year (p < 0.001). Corneal radii of curvature of the myopic group were steeper at all ages by 0.09 mm (p < 0.001), but the rate of change with age was equivalent across the refractive groups. Compared with those who remained nonmyopic, children who developed myopia had a crystalline lens that was initially thicker and steeper, and a vitreous chamber that was initially shorter. With age, children who became myopic developed greater lens thinning, greater flattening of the anterior lens surface radius, and a greater increase in vitreous chamber depth than their nonmyopic counterparts.

The response to visual form deprivation differs with age in marmosets.

To characterize the effects of visual form deprivation by diffuser in marmoset monkey eyes across a range of ages. Twenty-four common marmosets were grouped by onset of deprivation (group 1: 0-39 days, n = 6; group 2: 40-99 days, n = 10; and group 3: 100-200 days, n = 8). Monocular form deprivation was induced with a white translucent diffuser worn for 28 to 88 days (mean durations: group 1, 32 days; group 2, 56 days; and group 3, 51 days). Refractive state, corneal curvature, and vitreous chamber depth were measured after cycloplegia. Both experimental and control eyes were measured multiple times before, during, and after the visual deprivation period. Marmosets in all age groups tested were susceptible to visual form deprivation myopia; however, the response to form deprivation was variable and included a majority with axial myopia (n = 15), several nonresponders (n = 4), a single late responder (axial myopia after the end of deprivation period), and several axial hyperopes (n = 4). For all animals that responded with axial myopia, the increase in vitreous chamber depth and myopia was inversely proportional to the age of onset of deprivation (ANOVA, P < 0.05). After the end of the period of deprivation, recovery from myopia by reduction of the axial growth rate was observed in three animals from group 1 and three animals from group 2. Form deprivation by diffusers disrupted emmetropization in marmosets over a range of ages. The responses varied among individuals and with age, suggesting that the maturity of the eye may influence the response to visual signals responsible for form deprivation myopia and perhaps emmetropization. Recovery from diffuser-induced form deprivation myopia was apparent in some animals, in contrast to that reported for visual deprivation by lid-suturing, and appears more prevalent in the younger animals.

The Nepal longitudinal study: predicting myopia from the rate of increase in vitreous chamber depth.

Biometric data on 897 Tibetan children living in Kathmandu, Nepal were collected over the period 1992 to 2000 with regular visits every 2 years. Measurements included cycloplegic autorefraction, A-scan ultrasonography, and video phakometry. Children who had not been studied at least once at age 12 years or older were not included in these analyses. The other subjects were divided into two groups; myopic if the refractive error was ever <-0.50 D, and emmetropic/hyperopic if the refractive error was never <-0.50 D, the nonmyopic group. Using all children who had been examined with four or five observations over time, the change of vitreous chamber depth with age by group was determined using a mixed-model regression method. The increase in vitreous length was 0.070 mm/year for the emmetropic group and 0.165 mm/year for the myopic group, with the differences apparent before the onset of myopia. An independent group of 59 children in whom there were two vitreous chamber depth measures before the age of 12 years and one measure taken after 12 years of age were used to assess the rate of increase in vitreous chamber depth as a predictor of myopia. Two other methods were examined using the independent group; the ratio of axial length to corneal radius of curvature and refractive error at age 10 years. Predictors based on rate of increase in vitreous chamber depth and axial length/corneal radius of curvature had sensitivities of 75% and 45%, respectively, and refractive error at age 10 years as a predictor for those who will not become myopic had a sensitivity of 88%.

Continuous ambient lighting and eye growth in primates.

The authors sought to determine the effect of continuous light exposure on ocular growth and emmetropization in infant monkeys. Nine infant rhesus monkeys were reared with the normal vivarium lights on continuously. The 24-hour light cycle was initiated between 1 and 4 weeks of age and maintained for 6 months. The ocular effects of continuous light were assessed by cycloplegic retinoscopy, keratometry, and A-scan ultrasonography. Longitudinal control data were obtained from 23 normal infants that were reared with an illumination cycle that included defined light and dark phases (either 12-hour light: 12-hour dark or 8.5-hour light: 15.5 hour dark). In contrast to previous studies involving light-reared chickens, no monkeys exhibited exaggerated ocular growth. There were no significant differences between treated and control monkeys in corneal radius, overall eye size, or the axial dimensions of individual ocular components. At the end of the treatment period, eight of the nine experimental monkeys also exhibited the moderate hyperopic errors (range, +1.5 to +3.4 D) that are typically found in normal animals. Aspects of emmetropization were, however, unusual for three monkeys. One monkey manifested a −0.50 D myopic error that was associated with an abnormally steep cornea but had normal axial lengths. Two additional monkeys developed persistent axial anisometropias. The authors conclude that in infant primates constant light exposure does not promote the constellation of ocular changes (in particular corneal flattening, a decrease in anterior chamber depth, and an increase in vitreous chamber depth) that has been observed in light-reared chickens. The slight variations from the expected developmental sequence observed in three infants may reflect individual differences. It is also possible, however, that aspects of the emmetropization process may not operate as effectively under constant light as they do under an ordinary light/dark cycle.—Thomas J. Liesegang

Refractive component changes in adult‐onset myopia: evidence from five studies

Because the growth of the eys is considered to be complex by the age of 13 of 14 years, many vision scientists and practitioners have believed that myopia having its onset in the lated teen or early adult years is due to refractive component changes other than axial elongation. During the past several years, five studies of the refrative components in early adult-onset myopia, as compared to those in emmetropia and youth-onset myopia, have been reported. Three of these studies include only cross-sectional data, whereas two have provided longitudinal data. The results of these studies, taken together, leave no doubt that early adult-onset mypoia occurs, as does youth-onset myopia, as a result of an uncompensated increase in vitreous chamber depth. Many studies, including two to the five studies reviewed here, have provided evidence that corneal steepening occurs prior to or consequent with the development of mypoia. The role of corneal steeping is particularly well illustrated by evidence that an increase in the ration between axial length and corneal radius (the axial length/corneal radius ration) appears to be a risk factor for the developement of myopia. None of the studies cited here supplies evidence for a form of myopia that is caused by an increase in corneal power or lens power in the absence of vitreous chameber elongation.

Early signs of myopia in Chinese schoolchildren.

We looked for the earliest signs of the onset of myopia in 194 emmetropic (-0.25 to +0.75 D) eyes by following them for 1 to more than 2 years. Visual acuity examination, cycloplegic retinoscopy, and A-scan ultrasonography were performed at intervals of 6 to 12 months. Of the 194 eyes 64 became myopic during the observation time. Our results show that during the progression from emmetropia to myopia the change in visual acuity is not a good indicator of the onset of myopia. When visual acuity decreased to below 6/6 (20/20) cycloplegic retinoscopy showed that most of the 64 eyes had become truly myopic and A-scan ultrasonography revealed a significant increase in vitreous chamber depth and axial length as compared to the non-myopic eyes. In the early stage of myopia development the anteroposterior diameter of the eye elongates. However, changes in anterior chamber depth and lens thickness did not differ between the myopic and non-myopic group. Our results suggest that routine ocular refraction should be conducted in addition to the school vision screening. For those who have visual acuity 6/6 (20/20) and ametropia of -0.25 D or more minus we would like to be able to prevent or at least retard the development of myopia.

The development of experimental myopia and ocular component dimensions in monocularly lid-sutured tree shrews ( Tupaia belangeri)

Tree shrews were monocularly deprived (MD) from the day of eye opening for periods of 15, 30, 45, 60 and 75 days. The initial structural change after 15 days of MD was a flattening of the corneal curvature in the deprived eye causing a hyperopic increase in refraction, relative to the fellow control eye. A relative myopia was first observed after 30 days of deprivation and increased as the length of MD increased. Animals monocularly deprived for 75 days consistently showed high degrees of myopia (greater -10 D). An increase in vitreous chamber depth was found after 30 days of deprivation and continued to increase, relative to the control eye, throughout the developmental period under investigation. There was a strong correlation (r = 0.84) between increase in vitreous chamber depth and the amount of experimentally-induced myopia. Anterior chamber depth was shallower in the deprived eyes of all animals. The crystalline lens was also consistently thinner in the deprived eye. Based on optical modeling, the observed myopia was consistent with the changes in ocular component dimensions. The susceptible period for experimental myopia begins about 15 days after eye opening.