IMI – Report on Experimental Models of Emmetropization and Myopia
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RETINAL DISORDERS Eye63 (1)
RETINAL DISORDERS Eye63 (1) Retinal Disorders Last updated: May 9, 2019 CENTRAL RETINAL ARTERY OCCLUSION (CRAO) ............................................................................... 1 Pathophysiology & Ophthalmoscopy ............................................................................................... 1 Etiology ............................................................................................................................................ 2 Clinical Features ............................................................................................................................... 2 Diagnosis .......................................................................................................................................... 2 Treatment ......................................................................................................................................... 2 BRANCH RETINAL ARTERY OCCLUSION ................................................................................................ 3 CENTRAL RETINAL VEIN OCCLUSION (CRVO) ..................................................................................... 3 Pathophysiology & Etiology ............................................................................................................ 3 Clinical Features ............................................................................................................................... 3 Diagnosis ......................................................................................................................................... -
Theoretical Part Eye Examinations 1
Name and Surrname number Study group Theoretical part Eye examinations 1. Astigmatism Astigmatism is an optical defect in which vision is blurred due to the inability of the optics of the eye to focus a point object into a sharp focused image on the retina. Astigmatism can sometimes be asymptomatic, while higher degrees of astigmatism may cause symptoms such as blurry vision, squinting, eye strain, fatigue, or headaches. Types Regular astigmatism: Principal meridians are perpendicular. Simple astigmatism – the first focal line is on the retina, while the second is located behind the retina, or, the first focal line is in front of the retina, while the second is on the retina. Compound astigmatism – both focal lines are located behind or before the retina. Mixed astigmatism – focal lines are on both sides of the retina (straddling the retina). Irregular astigmatism: Principal meridians are not perpendicular. This type cannot be corrected by a lens. Tests Objective Refractometer, autorefractometer Placido keratoscope – A placido keratoscope consists of a handle and a circular part with a hole in the middle. The hole with a magnifying glass is viewed from a distance of 10–15 cm to the patients cornea. In the 200 mm wide circular portion there are concentric alternating black and white circles. They reflect the patient’s cornea. In the event of astigmatism, a deformation appears at the corresponding location. Sciascope Ophthalmometry Subjective Fuchs figure – This is a tool for evaluating astigmatism where examinee stands up against a pattern of circular shape (circular or striped rectangles) and fixes his/her gaze on the center of the pattern with one open eye. -
Comprehensive Pediatric Eye and Vision Examination
American Optometric Association – Peer/Public Review Document 1 2 3 EVIDENCE-BASED CLINICAL PRACTICE GUIDELINE 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Comprehensive 18 Pediatric Eye 19 and Vision 20 Examination 21 22 For Peer/Public Review May 16, 2016 23 American Optometric Association – Peer/Public Review Document 24 OPTOMETRY: THE PRIMARY EYE CARE PROFESSION 25 26 The American Optometric Association represents the thousands of doctors of optometry 27 throughout the United States who in a majority of communities are the only eye doctors. 28 Doctors of optometry provide primary eye care to tens of millions of Americans annually. 29 30 Doctors of optometry (O.D.s/optometrists) are the independent primary health care professionals for 31 the eye. Optometrists examine, diagnose, treat, and manage diseases, injuries, and disorders of the 32 visual system, the eye, and associated structures, as well as identify related systemic conditions 33 affecting the eye. Doctors of optometry prescribe medications, low vision rehabilitation, vision 34 therapy, spectacle lenses, contact lenses, and perform certain surgical procedures. 35 36 The mission of the profession of optometry is to fulfill the vision and eye care needs of the 37 public through clinical care, research, and education, all of which enhance quality of life. 38 39 40 Disclosure Statement 41 42 This Clinical Practice Guideline was funded by the American Optometric Association (AOA), 43 without financial support from any commercial sources. The Evidence-Based Optometry 44 Guideline Development Group and other guideline participants provided full written disclosure 45 of conflicts of interest prior to each meeting and prior to voting on the strength of evidence or 46 clinical recommendations contained within this guideline. -
Acquired Colour Vision Defects in Glaucoma—Their Detection and Clinical Significance
1396 Br J Ophthalmol 1999;83:1396–1402 Br J Ophthalmol: first published as 10.1136/bjo.83.12.1396 on 1 December 1999. Downloaded from PERSPECTIVE Acquired colour vision defects in glaucoma—their detection and clinical significance Mireia Pacheco-Cutillas, Arash Sahraie, David F Edgar Colour vision defects associated with ocular disease have The aims of this paper are: been reported since the 17th century. Köllner1 in 1912 + to provide a review of the modern literature on acquired wrote an acute description of the progressive nature of col- colour vision in POAG our vision loss secondary to ocular disease, dividing defects + to diVerentiate the characteristics of congenital and into “blue-yellow” and “progressive red-green blindness”.2 acquired defects, in order to understand the type of This classification has become known as Köllner’s rule, colour vision defect associated with glaucomatous although it is often imprecisely stated as “patients with damage retinal disease develop blue-yellow discrimination loss, + to compare classic clinical and modern methodologies whereas optic nerve disease causes red-green discrimina- (including modern computerised techniques) for tion loss”. Exceptions to Köllner’s rule34 include some assessing visual function mediated through chromatic optic nerve diseases, notably glaucoma, which are prima- mechanisms rily associated with blue-yellow defects, and also some reti- + to assess the eVects of acquired colour vision defects on nal disorders such as central cone degeneration which may quality of life in patients with POAG. result in red-green defects. Indeed, in some cases, there might be a non-specific chromatic loss. Comparing congenital and acquired colour vision Colour vision defects in glaucoma have been described defects since 18835 and although many early investigations Congenital colour vision deficiencies result from inherited indicated that red-green defects accompanied glaucoma- cone photopigment abnormalities. -
Colour Vision Deficiency
Eye (2010) 24, 747–755 & 2010 Macmillan Publishers Limited All rights reserved 0950-222X/10 $32.00 www.nature.com/eye Colour vision MP Simunovic REVIEW deficiency Abstract effective "treatment" of colour vision deficiency: whilst it has been suggested that tinted lenses Colour vision deficiency is one of the could offer a means of enabling those with commonest disorders of vision and can be colour vision deficiency to make spectral divided into congenital and acquired forms. discriminations that would normally elude Congenital colour vision deficiency affects as them, clinical trials of such lenses have been many as 8% of males and 0.5% of femalesFthe largely disappointing. Recent developments in difference in prevalence reflects the fact that molecular genetics have enabled us to not only the commonest forms of congenital colour understand more completely the genetic basis of vision deficiency are inherited in an X-linked colour vision deficiency, they have opened the recessive manner. Until relatively recently, our possibility of gene therapy. The application of understanding of the pathophysiological basis gene therapy to animal models of colour vision of colour vision deficiency largely rested on deficiency has shown dramatic results; behavioural data; however, modern molecular furthermore, it has provided interesting insights genetic techniques have helped to elucidate its into the plasticity of the visual system with mechanisms. respect to extracting information about the The current management of congenital spectral composition of the visual scene. colour vision deficiency lies chiefly in appropriate counselling (including career counselling). Although visual aids may Materials and methods be of benefit to those with colour vision deficiency when performing certain tasks, the This article was prepared by performing a evidence suggests that they do not enable primary search of Pubmed for articles on wearers to obtain normal colour ‘colo(u)r vision deficiency’ and ‘colo(u)r discrimination. -
Congenital Or Acquired Color Vision Defect – If Acquired What Caused It?
Congenital or Acquired Color Vision Defect – If Acquired What Caused it? Terrace L. Waggoner O.D. 3730 Tiger Point Blvd. Gulf Breeze, FL 32563 [email protected] Course Handout AOA 2017 Conference: I. Different types of congenital colorblindness. A. Approximately 8% of the population has a congenital color vision deficiency. B. Dichromate 1. Protanopia is a severe type of color vision deficiency caused by the complete absence of red retinal photoreceptors (L cone absent). 2. Deuteranopia is a type of color vision deficiency where the green photoreceptors are absent (M cone absent). 3. Tritanopia is a very rare color vision disturbance in which there are only two cone pigments present and a total absence of blue retinal receptors (S cone absent). It is related to chromosome 7. C. Anomalous Trichromate 1. Protanomaly is a mild color vision defect in which an altered spectral sensitivity of red retinal receptors (closer to green receptor response) results in poor red–green hue discrimination. 2. Deuteranomaly, caused by a similar shift in the green retinal receptors, is by far the most common type of color vision deficiency, mildly affecting red–green hue discrimination in 5% males. 3. Tritanomaly is a rare, hereditary color vision deficiency affecting blue–green and yellow–red/pink hue discrimination. D. Rates of color blindness 1. Dichromacy Males 2.4% Females .03% a. Protanopia (red deficient: L cone absent) Males 1.3% Females 0.02% b. Deuteranopia (green deficient: M cone absent) Males 1.2% Females 0.01 c. Tritanopia (blue deficient: S cone absent) Males 0.001% Females 0.03% 2. -
Intraocular Pressure During Phacoemulsification
J CATARACT REFRACT SURG - VOL 32, FEBRUARY 2006 Intraocular pressure during phacoemulsification Christopher Khng, MD, Mark Packer, MD, I. Howard Fine, MD, Richard S. Hoffman, MD, Fernando B. Moreira, MD PURPOSE: To assess changes in intraocular pressure (IOP) during standard coaxial or bimanual micro- incision phacoemulsification. SETTING: Oregon Eye Center, Eugene, Oregon, USA. METHODS: Bimanual microincision phacoemulsification (microphaco) was performed in 3 cadaver eyes, and standard coaxial phacoemulsification was performed in 1 cadaver eye. A pressure transducer placed in the vitreous cavity recorded IOP at 100 readings per second. The phacoemulsification pro- cedure was broken down into 8 stages, and mean IOP was calculated across each stage. Intraocular pressure was measured during bimanual microphaco through 2 different incision sizes and with and without the Cruise Control (Staar Surgical) connected to the aspiration line. RESULTS: Intraocular pressure exceeded 60 mm Hg (retinal perfusion pressure) during both standard coaxial and bimanual microphaco procedures. The highest IOP occurred during hydrodissection, oph- thalmic viscosurgical device injection, and intraocular lens insertion. For the 8 stages of the phaco- emulsification procedure delineated in this study, IOP was lower for at least 1 of the bimanual microphaco eyes compared with the standard coaxial phaco eye in 4 of the stages (hydro steps, nu- clear disassembly, irritation/aspiration, anterior chamber reformation). CONCLUSION: There was no consistent difference in IOP between the bimanual microphaco eyes and the eye that had standard coaxial phacoemulsification. Bimanual microincision phacoemul- sification appears to be as safe as standard small incision phacoemulsification with regard to IOP. J Cataract Refract Surg 2006; 32:301–308 Q 2006 ASCRS and ESCRS Bimanual microincision phacoemulsification, defined as capable of insertion through these microincisions become cataract extraction through 2 incisions of less than 1.5 mm more widely available. -
PEDIATRIC EYE and VISION EXAMINATION Reference Guide for Clinicians
OPTOMETRIC CLINICAL PRACTICE GUIDELINE OPTOMETRY: THE PRIMARY EYE CARE PROFESSION Doctors of optometry are independent primary health care providers who examine, diagnose, treat, and manage diseases and disorders of the visual system, the eye, and associated structures as well as diagnose related systemic conditions. Optometrists provide more than two-thirds of the primary eye care services in the United States. They are more widely distributed geographically than other eye care providers and are readily accessible for the delivery of eye and vision care services. There are approximately 32,000 full-time equivalent doctors of optometry currently in practice in Pediatric Eye the United States. Optometrists practice in more than 7,000 communities across the United States, serving as the sole primary eye care provider in more than 4,300 communities. And Vision The mission of the profession of optometry is to fulfill the vision and eye care needs of the public through clinical care, research, and education, all Examination of which enhance the quality of life. OPTOMETRIC CLINICAL PRACTICE GUIDELINE PEDIATRIC EYE AND VISION EXAMINATION Reference Guide for Clinicians First Edition Originally Prepared by (and Second Edition Reviewed by) the American Optometric Association Consensus Panel on Pediatric Eye and Vision Examination: Mitchell M. Scheiman, O.D., M.S., Principal Author Catherine S. Amos, O.D. Elise B. Ciner, O.D. Wendy Marsh-Tootle, O.D. Bruce D. Moore, O.D. Michael W. Rouse, O.D., M.S. Reviewed by the AOA Clinical Guidelines Coordinating Committee: John C. Townsend, O.D., Chair (2nd Edition) John F. Amos, O.D., M.S. -
Intermixing the OPN1LW and OPN1MW Genes Disrupts the Exonic Splicing Code Causing an Array of Vision Disorders
G C A T T A C G G C A T genes Review Intermixing the OPN1LW and OPN1MW Genes Disrupts the Exonic Splicing Code Causing an Array of Vision Disorders Maureen Neitz * and Jay Neitz Department of Ophthalmology and Vision Science Center, University of Washington, Seattle, WA 98109, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-206-543-7998 Abstract: Light absorption by photopigment molecules expressed in the photoreceptors in the retina is the first step in seeing. Two types of photoreceptors in the human retina are responsible for image formation: rods, and cones. Except at very low light levels when rods are active, all vision is based on cones. Cones mediate high acuity vision and color vision. Furthermore, they are critically important in the visual feedback mechanism that regulates refractive development of the eye during childhood. The human retina contains a mosaic of three cone types, short-wavelength (S), long-wavelength (L), and middle-wavelength (M) sensitive; however, the vast majority (~94%) are L and M cones. The OPN1LW and OPN1MW genes, located on the X-chromosome at Xq28, encode the protein component of the light-sensitive photopigments expressed in the L and M cones. Diverse haplotypes of exon 3 of the OPN1LW and OPN1MW genes arose thru unequal recombination mechanisms that have intermixed the genes. A subset of the haplotypes causes exon 3- skipping during pre-messenger RNA splicing and are associated with vision disorders. Here, we review the mechanism by which splicing defects in these genes cause vision disorders. Citation: Neitz, M.; Neitz, J. -
17-2021 CAMI Pilot Vision Brochure
Visual Scanning with regular eye examinations and post surgically with phoria results. A pilot who has such a condition could progress considered for medical certification through special issuance with Some images used from The Federal Aviation Administration. monofocal lenses when they meet vision standards without to seeing double (tropia) should they be exposed to hypoxia or a satisfactory adaption period, complete evaluation by an eye Helicopter Flying Handbook. Oklahoma City, Ok: US Department The probability of spotting a potential collision threat complications. Multifocal lenses require a brief waiting certain medications. specialist, satisfactory visual acuity corrected to 20/20 or better by of Transportation; 2012; 13-1. Publication FAA-H-8083. Available increases with the time spent looking outside, but certain period. The visual effects of cataracts can be successfully lenses of no greater power than ±3.5 diopters spherical equivalent, at: https://www.faa.gov/regulations_policies/handbooks_manuals/ techniques may be used to increase the effectiveness of treated with a 90% improvement in visual function for most One prism diopter of hyperphoria, six prism diopters of and by passing an FAA medical flight test (MFT). aviation/helicopter_flying_handbook/. Accessed September 28, 2017. the scan time. Effective scanning is accomplished with a patients. Regardless of vision correction to 20/20, cataracts esophoria, and six prism diopters of exophoria represent series of short, regularly-spaced eye movements that bring pose a significant risk to flight safety. FAA phoria (deviation of the eye) standards that may not be A Word about Contact Lenses successive areas of the sky into the central visual field. Each exceeded. -
Final Version (2017-06-28) of the Vision Camp
Young Researcher VisionCamp An international Career building Symposium 2017 Castle Wildenstein Leibertingen Germany www.vision-camp.eu Contact: Jugendherberge Burg Wildenstein 88637 Leibertingen-Wildenstein Tel: +49 7466-411 Fax: +49 7466-417 E-Mail: [email protected] www.leibertingen-wildenstein.jugendherberge-bw.de Preamble Dear Colleagues, Dear Participants of the Young Researcher Vision Camp 2017, The aim of this camp is to give young investigators (MSc and PhD students, young MDs and post-docs) an opportunity to present themselves and their work to fellow researchers, to allow them to build and strengthen personal networks in an international environment. Take the time for professional and social networking Take the time for new views on career paths to shape your future Take the time to bridge the gap between basic and clinical research Take the time to revive a medieval castle ENJOY THE YOUNG RESEARCHER VISION CAMP Thomas Wheeler-Schilling on behalf of the organising committee (in alphabetical order) Michaela Bitzer Sigrid Diether Philipp Hunger Norbert Kinkl Arne Ohlendorf Francois Paquet-Durand Vera Schmid Timm Schubert 3 Agenda FRIDAY, JUNE 30th, 2017 until 16:00 Arrival (for details see ‘How to get there’) 16:25 - 16:30 Welcome 16:30 - 17:00 Keynote Lecture I ‘Primary Cilia in the Visual System’ Helen May-Simera 17:00 - 18:00 Scientific Session I: ‘Retinal development and homeo- stasis’ Chair: Jérôme Roger • Elena Braginskaja: “Glycogen Synthase Kinases 3 are Critical for Retinal Develop- ment and Homeostasis” -
New Developments in Glaucoma Therapy
New Developments in Glaucoma Therapy 100 - Oral Author: Ganesh Prasanna Presenter: Ganesh Prasanna Institution: Alcon Research Ltd Department: Glaucoma Research Ganesh Prasanna, Ph.D. Ocular Biology, Pfizer Global R&D, San Diego, CA 92121 Current affiliation: Alcon Research Ltd., Fort Worth, TX 76134 EFFECT OF PF-04217329 A PRO-DRUG OF A SELECTIVE PROSTAGLANDIN EP2 AGONIST ON INTRAOCULAR PRESSURE IN PRECLINICAL MODELS OF GLAUCOMA Purpose: While prostaglandin FP analogs are leading the therapeutic intervention for glaucoma, new target classes also are being identified with new lead compounds being developed for IOP reduction. One target class currently being investigated includes the prostaglandin EP receptor agonists. Recently PF-04217329 (Taprenepag isopropyl), a prodrug of CP-544326 (active acid metabolite), a potent and selective EP2 receptor agonist, was successfully evaluated for its ocular hypotensive activity in a clinical study involving patients with primary open angle glaucoma. The preclinical attributes of CP-544326 and PF-0421329 will be presented. Methods: PF-04217329 and active acid metabolite, CP-544326 were evaluated in cell based assays for receptor binding and EP2 receptor functional activity were used. Rabbits were used for assessing corneal permeability, ocular pharmacokinetic studies, EP2 receptor activation and IOP, whereas normal dogs and lasered ocular hypertensive cynomolgus monkeys were also used for IOP studies. Results: CP-544326 was found to be a potent and selective EP2 agonist (receptor binding IC50 = 10 nM; functional activity EC50 = 0.25 nM) whose corneal permeability and ocular bioavailability were significantly increased when the compound was dosed as the isopropyl ester prodrug, PF-04217329. Topical ocular dosing of PF-04217329 was well tolerated in preclinical species and caused an elevation of cAMP in aqueous humor/iris-ciliary body indicative of in-vivo EP2 target receptor activation.