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Visual Optics 2007/2008

Visual Optics 2007/2008. Chapter 4 Emmetropia and Ametropia. For 5% bonus points in Visual Optics II, I would prefer:. Clicker question format as in Visual Optics I Pop quizzes ~ once per week Clicker questions and Pop quizzes

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Visual Optics 2007/2008

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  1. Visual Optics 2007/2008 Chapter 4 Emmetropia and Ametropia

  2. For 5% bonus points in Visual Optics II, I would prefer: • Clicker question format as in Visual Optics I • Pop quizzes ~ once per week • Clicker questions and Pop quizzes • not to be tested at all and I’m happy to forego the bonus points

  3. For the clicker questions, I would prefer the option: • of discussing the question with the person sitting next to me and being able to refer to my notes • of being able to refer to my notes, but NO discussion allowed • of “test” conditions with NO reference to notes and NO discussion

  4. Number of Visual Optics II tests. I want: • Two. (1) midterm and (2) final • Three. (1) ~end of week 4; (2) ~end of week 8; (3) finals week

  5. Visual Optics 2007/2008 Chapter 4 Emmetropia and Ametropia

  6. Most newborn babies are: • Emmetropic • Hyperopic • Myopic • Presbyopic

  7. Cook et al, 1951

  8. Emmetropization: Two Processes Page 4.9 • Passive • ocular scaling: shorter eyes have steeper (higher power) cornea and crystalline lens • Active • Form Deprivation (no “signal”) → axial myopia • Optical Defocus – eye “grows toward” focused image

  9. How does the Retina Interpret Optical Defocus? Page 4.10 • Animal Models: optical defocus-sensing mechanism must differentiate hyperopic from myopic defocus. Possible candidates: • Chromatic aberration? – asymmetric wavelength spread could be interpreted by R, G, B retinal cones

  10. Paraxial Focus LCA Chromatic Aberration n = 1 n' > 1 400 nm 700 nm

  11. How does the Retina Interpret Optical Defocus? Page 4.10 • Optical Defocus sensing mechanism must differentiate hyperopic from myopic defocus. Possible candidates: • Chromatic aberration? – asymmetric wavelength spread could be interpreted by R, G, B retinal cones • Off-axis astigmatism? – focal line and COLC distribution

  12. Focal Lines in Off-axis Astigmatism Figure 3.52 – Oblique (radial) astigmatism. A point object (B) below the optic axis (A) creates an image spread along the optic axis direction from the tangential to sagittal focus.

  13. How does the Retina Interpret Optical Defocus? Page 4.10 • Optical Defocus sensing mechanism must differentiate hyperopic from myopic defocus. Possible candidates: • Chromatic aberration? – asymmetric wavelength spread could be interpreted by R, G, B retinal cones • Off-axis astigmatism? – focal line and COLC distribution • Other monochromatic aberrations? – e.g. SA: image asymmetric either side of the WOLA

  14. Paraxial Focus Marginal Focus WOLA Spherical Aberration

  15. How does the Retina Interpret Optical Defocus? Page 4.10 • Optical Defocus sensing mechanism must differentiate hyperopic from myopic defocus. Possible candidates: • Chromatic aberration? – asymmetric wavelength spread could be interpreted by R, G, B retinal cones • Off-axis astigmatism? – focal line and COLC distribution • Other monochromatic aberrations? – e.g. SA, image asymmetric either side of the WOLA Nature of the defocus-sensing mechanism is not known. May be some combination of the above factors No proof in humans that the visual system can differentiate hyperopic from myopic defocus

  16. Emmetropization and Development of Ametropia Page 4.11 • Emmetropization: close to complete by age 5, but does not produce the ideal outcome in ALL cases • Successful emmetropization does not guarantee that the eye will remain emmetropic throughout life • Low Ametropia: most cases result from imperfect emmetropization. Ametropia is not clearly axial or refractive; simply a mismatch between Fe and ax. “Correlation” ametropia • Higher Ametropia: usually axial in origin. Most evident cause-and-effect relationship in higher myopia (axial). “Component” ametropia

  17. Ametropia: Age-related Patterns Page 4.11 • Hyperopia • emerges post-“emmetropization;” relatively stable through life • higher hyperopia often associated with higher astigmatism.Suggestsnormal emmetropization was blocked (newborns are usually astigmatic). • emmetropization appears to arrive at the wrong “balance point” between axial length and refractive power • High hyperopia tends to be axial, but rarely exceeds 8 D (high myopia can exceed 25 D)

  18. Ametropia: Age-related Patterns Page 4.11 • Myopia • Much more complex and variable than hyperopia; often progressive; suggests multiple etiological factors • Higher myopia: typically develops and progresses after the emmetropization phase (but, can begin during emmetropization) • Age of Onset: Caucasians 10-16; Asians 10 years of age • Asian children typically less hyperopic at birth than Caucasians

  19. Ametropia: Nature (Heredity) vs. Nurture (Environment) Page 4.11-12 E Higher prevalence of myopia in Taiwanese cities vs. villages __ Children with one or two myopic parents 4 more likely to be myopic __ Higher rate of myopia in mono- than di-zygotic twins __ Number of daily “book hours” definitely a factor in myopia __ Myopia genes recently identified __ Recent studies indicate that hereditary factors are likely to drive both susceptibility and resistance to environmentally-induced myopia (only susceptible patients will develop myopia if exposed to environmental “risk factors”) __ Increased prevalence of myopia in Asian communities has occurred more rapidly than can be accounted for by Asian gene pool turnover __ H H E H &E H E

  20. Classification of Myopia (U.S. Figures) Page 4.12 • Early Onset/School/Juvenile Myopia (9-11 years) • Majority of myopes in U.S. (60%) • Progresses through early teenage years (“lag” of accommodation?) • Stabilizes at around 3 - 4 D in early adulthood • High Myopia (> 6 D) • 1% of Caucasian adolescents; 15% of Asian adolescents • Late Onset Myopia (15 – 18 years; sometimes later) • 8-15% of myopes; probably a delayed version of school myopia • Slower progression than school myopia; rarely > 2 D • Sustained and/or “high cognitive demand” near work appear causal • Other types: congenital, disease-related and lenticular

  21. Myopia Statistical Facts (Zadnik) Myopes (ages 8-13) have a deficient accommodative response to a near target relative to emmetropes, on the order of 0.20 D difference for a 4 D stimulus Best single predictor of myopia is spherical refraction at age 8-9 years (threshold > or < +0.75 D hyperopia) Sporting activities in youth appear to protect against myopic progression (equal “book” hours to non-participants)

  22. Myopia “Treatments” (Zadnik) • Progressive Addition Lenses (PALs): limited success (COMET Study) • Rigid Gas Permeable (RGP) Contact Lenses (Singapore Study): limited success. Is the “cure” worse than the “disease”? • Pharmacological Treatment of Myopia (pirenzepine) • progression in 1 year with pirenzepine (US) in 174 children 8-12 years old vs. placebo: • 0.26 D compared to 0.53 D • >1.00 D of progression: 2% compared to 20%

  23. Hyperopia (Zadnik) • 1. Why doesn’t anybody care about hyperopia? • Less prevalent than myopia • Often asymptomatic in childhood • Onset and progression poorly understood • Vision scientists are myopes

  24. Ametropia: Summary • The human eye “tries” to develop emmetropia • Most cases of low ametropia didn’t quite get it right (Correlation Ametropia) • Component Ametropia • Hyperopia: breakdown in emmetropization (wrong endpoint)? • Myopia: multifactorial • Prevalence increasing worldwide, especially in Asian countries • Both hereditary and environmental factors involved • Etiology of both hyperopia and myopia poorly understood • Key question: what drives susceptibility?

  25. Examples of Axial & Refractive Ametropia Page 4.13 • High myopia is nearly always axial in origin • Aphakia (e.g. cataract extraction without IOL implant) is refractive. The previously emmetropic patient becomes ~20 D hyperopic in the crystalline lens plane and ~17 D hyperopic at the cornea

  26. Simplified Schematic Eye - Removing Cr. Lens +43.08 D ~ +20 D Feff (CrLens)~ +17 D

  27. Simplified Schematic Eye - Removing Cr. Lens APHAKIA +43.08 D

  28. Examples of Axial & Refractive Ametropia Page 4.13 • High myopia is nearly always axial in origin • Aphakia (e.g. cataract extraction without IOL implant) is refractive. The previously emmetropic patient becomes ~20 D hyperopic in the crystalline lens plane and ~17 D hyperopic at the cornea • Cataract often leads to increased crystalline lens index and therefore a myopic shift. This would also be refractive in origin • Astigmatism is always refractive in origin. Because the two ocular principal meridians have different powers, at least one meridian must have refractive ametropia. Astigmatism can be combined with axial ametropia.

  29. Astigmatism - Refractive Ametropia Page 4.13, 14 Fig. 4.4 - Reduced eye representation of an astigmatic eye (relaxed) showing focal lines formed by parallel incident light (distant point object).

  30. Determining the Nature of Ametropia Page 4.14 • When are we interested in determining the nature of ametropia? • Certainly not for the routine patient with low to moderate refractive errors and isometropia (unless history suggests risk factors  set baseline) • We become interested when: • The patient has high ametropia • The patient is anisometropic; especially higher levels • The patient has only moderate ametropia, or slight anisometropia, but is symptomatic

  31. Determining the Nature of Ametropia Page 4.10 • Important signs during routine examination: • Clinical refraction will identify candidates – e.g. high ametropia or anisometropia. Routine refraction gives no information about origin • Ophthalmoscopy – myopic conus (crescent) seen in patients with axial myopia. Caused by stretching of the globe

  32. Myopic crescent Temporal Nasal

  33. Myopic crescent T N

  34. Determining the Nature of Ametropia p 4.15 • Important signs during routine examination: • Clinical refraction will identify candidates – e.g. high ametropia or anisometropia. Routine refraction gives no information about origin • Ophthalmoscopy – myopic conus (crescent) seen in patients with axial myopia. Caused by stretching of the globe • Retinoscopy or biomicroscopy (slit-lamp) – cataract often produces a myopic shift. In particular, anisometropia in a previously emmetropic, older patient may be due to different stages of cataract development between eyes

  35. More advanced nuclear cataract in left eye O.D. O.S. http://www.cvr.org.au/pages/common-eye-diseases/cataract-risk-factors.htm

  36. Cortical Cataract (“spoke” opacities) http://www.cvr.org.au/pages/common-eye-diseases/cataract-risk-factors.htm

  37. Posterior Subcapsular Cataract Why would this type of cataract be associated with significant loss of visual function? http://www.cvr.org.au/pages/common-eye-diseases/cataract-risk-factors.htm

  38. Clinical Methods to Determine the Nature of Ametropia Page 4.15 • A-Scan Ultrasonography – measures axial length • Same principle as sonar; echoes occur when sound waves strike interface between “refractive” media • A –scan detector measures return time for each echo • Transducer aligned with patient’s visual axis, and 10-20 MHz sound waves directed at fovea • Sound wave velocity varies between “refractive” media. Usually set device to a weighted average velocity for given patient, e.g. normal, cataract, aphake, etc. • Theoretical accuracy ±0.02 mm; practical accuracy ±0.1 – 0.2 mm • Practical accuracy consistent with dioptric tolerance ± 0.25 – 0.50 D

  39. Single corneal peak Measuring Axial Length – A-Scan Biometry (Applanation Method) Page 4.15 Fig. 4.6 - A-Scan (time-amplitude) ultrasonograph. Time intervals between peaks (in sec) are multiplied by sound velocity in each medium to compute axial length).

  40. Applanation A-Scan Biometry Page 4.15 • “Probe” applied directly to patient’s cornea (with gel) • Pressing on cornea “compresses” axial length • Result: variable underestimation

  41. Immersion A-Scan Biometry Page 4.15 • Fluid-filled immersion cup applied to suppine patient’s cornea • Probe does not contact cornea • More accurate axial length measurement • Down-side: more time-consuming

  42. Measuring Axial Length – Immersion A-Scan Biometry Page 4.11 Immersion A-Scan biometry. Note two corneal peaks (C1 and C2)

  43. Optical Coherence Tomography • Broad bandwidth polychromatic source • Light split into two beams: one enters eye and reflects back from retina; other reflects from movable reference mirror • Beams recombine at detector. Only produce constructive interference when pathlengths almost identical • Reference mirror movement produces clear image at corneal surfaces, cr. lens surfaces, and retina  precise axl value Page 4.17

  44. Optical Coherence Tomography Page 4.17 • Precision of OCT to within lens “tolerance” (0.25 D) • Method of choice for post-cataract IOL design (main design parameters are axial length, “total” corneal power, and anterior chamber depth)

  45. Clinical Methods to Determine the Nature of Ametropia Page 4.16 • A-Scan Ultrasonography – measures axial length • Keratometry – measures anterior corneal radius. Provides reasonable estimate of total corneal power

  46. Keratometer (B & L Clone)

  47. Keratometer (B & L Clone)

  48. Keratometer (B & L Clone)

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