Ophthalmic and Physiological Optics最新文献

Purpose: During refractive development, eye growth is controlled by a combination of genetically pre-programmed processes and retinal feedback to minimise the refractive error. This work presents a basic differential model of how this process may take place.

Methods: The description starts from two bi-exponential descriptions of the axial power P_ax (or dioptric distance) and total refractive power P_eye, the difference between which corresponds with the spherical refractive error S. This description is rewritten as an ordinary differential equation and supplemented by a retinal feedback function that combines retinal blur (closed loop) with a term describing excessive axial growth (open loop). This model is controlled by a total of 18 parameters that allow for a wide variety of developmental behaviours.

Results: The proposed model reproduces refractive development growth curves found in the literature for both healthy and myopic eyes. An early onset of myopisation, a large growth term and a high minimum for the crystalline lens power all lead to higher degrees of myopia. Assigning more importance to the feedback than to the pre-programmed growth makes the model more sensitive to myopogenic influences. Applying refractive corrections to the model, undercorrection is found to produce more myopia. The model compensates for a low-powered imposed lens and can return to (near) emmetropia if that imposed lens is removed quickly thereafter. Finally, simulating the effect of a diffuser leads to high myopia.

Conclusion: Using a series of basic assumptions, the proposed model recreates many well-known experimental and clinical results about refractive development from the literature while placing them in a standardised context. This contributes to a broader understanding of the origins of refractive errors, and future versions may help in the development of solutions for myopia control.

The cornea is one of the tissues responsible for covering and protecting the inner structures of the eye. Central corneal thickness (CCT) is defined as the distance between the anterior epithelial surface and the posterior surface of the endothelial layer. This parameter plays a very important role regarding intraocular pressure (IOP) measurement, evaluation of corneal uniformity, selection of a suitable technique for corneal refractive surgery and the planning of surgical procedures to overcome corneal disease. This comprehensive review elucidates the multifaceted factors influencing the central corneal thickness. Recognising the impact of these factors not only enhances our understanding of corneal dynamics but also contributes significantly to the refinement of diagnostic and therapeutic strategies in ophthalmology.

Individuals with Down syndrome are known to have a greater prevalence of ocular conditions such as strabismus, nystagmus, elevated refractive error, poor accommodative function, elevated higher-order optical aberrations and corneal abnormalities. Related to these conditions, individuals with Down syndrome commonly have reduced best-corrected visual acuity at both far and near viewing distances across their lifespan. This review summarises the various optical sources of visual acuity reduction in this population and describes clinical trials that have evaluated alternative spectacle prescribing strategies to minimise these optical deficits. Although refractive corrections may still have limitations in their ability to normalise visual acuity for individuals with Down syndrome, the current literature provides evidence for eye care practitioners to consider in their prescribing practices for this population to maximise visual acuity. These considerations include accounting for the presence of elevated higher-order aberrations when determining refractive corrections and considering bifocal lens prescriptions, even for young children with Down syndrome.

Purpose: To evaluate the 1-year effects of orthokeratology (OK) lenses and spectacle lenses with highly aspherical lenslets (HALs) on axial length (AL) elongation in children with unilateral myopic anisometropia.

Methods: This ambispective cohort study recruited 81 children aged 8-14 years with unilateral myopic anisometropia. Of these, 42 participants (mean age 11.07 ± 1.54 years; 23 males) were treated with monocular OK lenses (OK group), and 39 (mean age 10.64 ± 1.72 years; 22 males) with binocular HALs (HAL group). Changes in AL and spherical equivalent refraction (SER) from baseline at 3, 6 and 12 months were compared between eyes and groups. Kaplan-Meier estimation and Cox proportional hazard regression were performed to analyse the risk of myopia onset in the initially non-myopic eyes.

Results: Mean axial elongation in the myopic and non-myopic eyes at the 12-month follow-up visit were 0.17 ± 0.20 and 0.41 ± 0.26 mm in the OK group (p < 0.001) and 0.10 ± 0.15 and 0.12 ± 0.12 mm in the HAL group (p = 0.32), respectively. Compared with the OK group, the non-myopic eyes in the HAL group had less axial elongation, lower cumulative myopia incidence and percentage of participants with rapid myopic shift at the 6- and 12 month follow-up (all p < 0.05). Cox regression analysis showed that a higher initial SER decreased the risk of myopia onset significantly in the initially non-myopic eyes (B = -2.06; 95% CI, 0.03-0.49; p = 0.003).

Conclusions: Monocular OK lenses suppressed axial elongation in the myopic eye and minimised anisometropia; however, the non-treated contralateral eye may experience faster myopia onset and myopic shift. Binocular HALs can effectively reduce axial elongation in both eyes of children with unilateral myopic anisometropia.

Purpose: To quantify the magnitude and recovery of central and limbal corneal oedema induced by short-term unilateral eyelid closure without contact lens wear.

Methods: The left eye of 10 adults with healthy corneas was patched using a folded eye pad for 30 min. High-resolution optical coherence tomography images (which captured the limbal and central corneal regions simultaneously) were obtained before patching, immediately after eye opening and again at 1, 2, 5, 6, 9, 10, 14 and 15 mins after eyelid opening. Oedema was measured from the limbus (scleral spur) to the central cornea (thinnest corneal location) along the horizontal meridian.

Results: A greater amount of limbal oedema was noted (mean [SD] 3.84 [1.79] %) compared to the central cornea (2.48 [0.61] %; p = 0.04) after 30 mins of unilateral eyelid closure. Both central and limbal corneal oedema recovered rapidly following eyelid opening, with no significant differences in the rate of corneal recovery between corneal locations (p = 0.90).

Conclusions: Short-term unilateral eyelid closure resulted in ~55% more relative oedema in the limbal region compared to the central cornea. Rapid recovery of oedema and corneal overshoot (thinning beyond the baseline corneal thickness) was observed within 1-2 min of eyelid opening for both central and peripheral regions.

Objective: To investigate the effect of spectacle correction on refractive progression in children with unilateral myopic anisometropia (UMA).

Methods: In this retrospective study, 153 children with UMA (aged 8-12 years) were recruited and classified into an uncorrected (UC) group (n = 47) and a spectacle (SP) group (n = 106). The spherical equivalent refraction (SER) of the myopic eyes ranged from -0.75 to -4.00 D; the SER of the emmetropic eyes ranged from +1.00 to -0.25 D; anisometropia was ≥1.00 D and the follow-up duration was 1 year. Nineteen subjects from the SP group with follow-up records spanning at least 6 months before and after wearing spectacles were selected as a subgroup. Changes in the SER and axial length (AL), the degree of anisometropia and interocular AL differences of the two groups and the subgroup were analysed.

Results: During the 1-year follow-up period, AL and SER changes in myopic eyes were significantly greater than those in emmetropic eyes in the UC group (p < 0.001). For the UC group, the degree of anisometropia and AL change increased (all p < 0.001). For the SP group, there were no significant differences in the degree of anisometropia or AL change (all p > 0.05). When comparing the groups, AL elongation of the myopic eyes in the UC group occurred significantly faster than in the SP group (p = 0.02), and AL elongation for the emmetropic eyes in the UC group occurred significantly slower than in the SP group (p = 0.04). For the subgroup, the AL and SER changes in the myopic eyes 6 months before wearing spectacles occurred significantly faster than those after correction (p < 0.001).

Conclusions: Spectacle correction could prevent increased anisometropia in uncorrected children with UMA by slowing myopia progression in the myopic eyes and accelerating the myopic shift in the contralateral eye.

Purpose: To quantify the impact of varying central fluid reservoir depth, lens thickness/mass and the addition of a peripheral fenestration upon scleral lens centration.

Methods: Ten young, healthy adults participated in a series of repeated-measures experiments involving short-term (90 min) open eye scleral lens wear. Scleral lens parameters (material, back optic zone radius, diameter, back vertex power and landing zone) were controlled across all experiments, and the central fluid reservoir depth (ranging from 144 to 726 μm), lens thickness (ranging from 150 to 1200 μm), lens mass (101-241 mg) and lens design (with or without a single 0.3 mm peripheral fenestration) were altered systematically. Scleral lens decentration was quantified using over-topography maps.

Results: On average, scleral lens centration varied by <0.10 mm over 90 min of wear. Medium and high initial fluid reservoir conditions resulted in 0.17 mm more temporal and 0.55 mm more inferior lens decentration, compared to the low fluid reservoir depth (p < 0.001). Changes in lens thickness or the addition of a peripheral fenestration did not cause clinically significant changes in centration (<0.10 mm on average) when controlling for fluid reservoir depth. Central fluid reservoir depth was the best predictor of horizontal and vertical lens decentration, explaining 62-73% of the observed variation, compared to 40-44% for lens thickness and mass.

Conclusion: Scleral lens decentration remained relatively stable over 90 min of lens wear. A greater initial central fluid reservoir depth resulted in significantly more lens decentration, particularly inferiorly. Large variations in lens thickness, mass or the addition of a single peripheral fenestration did not substantially affect lens centration.

Purpose: To introduce a method to calculate retinal irradiance caused by ophthalmoscopy. This may be used to verify the compliance of an instrument with the radiation limits set by light hazard standards. The proposed method is simpler to use and less prone to error than the methods currently found in the light hazard standards.

Methods: The optical properties of the standardised human eye, specified by current light hazard standards, are used to calculate the magnification of an aerial image of the retinal surface by the combination of the optics of eye and the auxiliary lens used for ophthalmoscopy. The magnification of the aerial image is used to transform the spectral irradiance of the instrument illumination source to retinal irradiation values. The spectral irradiance of the instrument illumination source can be measured directly as the aerial image is located in the focal plane of the viewing optics of the ophthalmoscope. These spectral irradiation values are then processed using weightings specified by current light hazard standards to give a weighted irradiance which is converted directly to a retinal irradiance value.

Results: A single formula is provided to calculate the retinal irradiance using the processed, measured spectral irradiance values of the illumination source.

Conclusion: The new method introduced here is simpler to use, requires fewer physical measurements and is less likely to introduce measurement error than that currently found in light hazard standards. The only physical measurement that needs to be taken is the illumination source spectral irradiance measured in the viewing focal plane of the instrument. These values are weighted using given in the light hazard standards. The combined irradiance value is then converted to retinal irradiance using the formula given in this paper.

Purpose: Simulation techniques are used in healthcare education to support the development of clinical skills. The aim of this study was to investigate the perceived value of a tonometry model eye (TME) when used in teaching and learning the clinical skill of Goldmann applanation tonometry (GAT) in optometric education in the UK.

Methods: A retrospective two-armed cross-sectional study was conducted to investigate the perceived value of using a model eye for teaching and learning GAT in optometric education. Focus group discussion (FGD) was employed to explore the views of academic experts experienced in teaching GAT using a TME. Semi-structured surveys were conducted to elicit the opinions of optometry students following GAT simulation training. Qualitative thematic analysis of the FGD and open-ended survey questions was undertaken. Quantitative data based on rated student responses was assessed using Chi-square analysis to examine differences between year-group responses.

Results: The TME was reported to be a useful experiential tool, facilitating a safe learning environment for students to develop the technical skills required to perform GAT before moving on to real-eye experiences. Whilst limitations of the model eye were noted, these did not diminish the value of the model eye as an instructional tool. Students reported improved confidence (86%) and would highly recommend (82%) the TME to other students.

Conclusion: The model eye for tonometry was perceived by academic tutors and optometry students to be a valuable instruction tool as part of a scaffolded process for learning GAT. Irrespective of their learning stage, students reported a range of benefits from the model eye, such as being able to make mistakes, taking repeat measurements and getting used to the equipment, all whilst not having to worry about patient safety.

Purpose: To estimate the astigmatic power of the crystalline lens and the whole eye without phakometry using a set of linear equations and to provide estimates for the astigmatic powers of the crystalline lens surfaces.

Methods: Linear optics expresses astigmatic powers in the form of matrices and uses paraxial optics and a 4 × 4 ray transfer matrix to generalise Bennett's method comprehensively to include astigmatic elements. Once this is established, the method is expanded to estimate the contributions of the front and back lens surfaces. The method is illustrated using two examples. The first example is of an astigmatic model eye and compares the calculated results to the original powers. In the second example, the method is applied to the biometry of a real eye with large lenticular astigmatism.

Results: When the calculated powers for the astigmatic model eye were compared to the actual powers, the difference in the power of the eye was ${\left(0.030.130.04\right)}^{T}D$ (where T represents the matrix transpose) and for the crystalline lens, the difference was ${\left(0.080.290.08\right)}^{T}D$ (power vector format). A second example applies the method to a real eye, obtaining lenticular astigmatism of -5.84 × 175.

Conclusions: The method provides an easy-to-code way of estimating the astigmatic powers of the crystalline lens and the eye.