Visual Acuity
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12 Retina Gabriele K
299 12 Retina Gabriele K. Lang and Gerhard K. Lang 12.1 Basic Knowledge The retina is the innermost of three successive layers of the globe. It comprises two parts: ❖ A photoreceptive part (pars optica retinae), comprising the first nine of the 10 layers listed below. ❖ A nonreceptive part (pars caeca retinae) forming the epithelium of the cil- iary body and iris. The pars optica retinae merges with the pars ceca retinae at the ora serrata. Embryology: The retina develops from a diverticulum of the forebrain (proen- cephalon). Optic vesicles develop which then invaginate to form a double- walled bowl, the optic cup. The outer wall becomes the pigment epithelium, and the inner wall later differentiates into the nine layers of the retina. The retina remains linked to the forebrain throughout life through a structure known as the retinohypothalamic tract. Thickness of the retina (Fig. 12.1) Layers of the retina: Moving inward along the path of incident light, the individual layers of the retina are as follows (Fig. 12.2): 1. Inner limiting membrane (glial cell fibers separating the retina from the vitreous body). 2. Layer of optic nerve fibers (axons of the third neuron). 3. Layer of ganglion cells (cell nuclei of the multipolar ganglion cells of the third neuron; “data acquisition system”). 4. Inner plexiform layer (synapses between the axons of the second neuron and dendrites of the third neuron). 5. Inner nuclear layer (cell nuclei of the bipolar nerve cells of the second neuron, horizontal cells, and amacrine cells). 6. Outer plexiform layer (synapses between the axons of the first neuron and dendrites of the second neuron). -
Move Your Wheelchair with Your Eyes
International Journal of Applied Mathematics, Advanced Technology and Science Electronics and Computers ISSN:2147-82282147-6799 www.atscience.org/IJAMEC Original Research Paper Move Your Wheelchair with Your Eyes Gökçen ÇETİNEL*1, Sevda GÜL2, Zafer TİRYAKİ3, Enes KUZU4, Meltem MİLLİGÜNEY5 Accepted : 12/05/2017 Published: 21/08/2017 DOI: 10.18100/ijamec.2017Special Issue30462 Abstract: In the proposed study, our goal is to move paralyzed people with their eyes. Otherwise, use this document as an instruction set. Paper titles should be written in uppercase and lowercase letters, not all uppercase. For this purpose, we use their Electrooculogram (EOG) signals obtained from EOG goggles completely designed by the authors. Through designed EOG goggles, vertical-horizontal eye movements and voluntary blink detection are verified by using 5 Ag-AgCl electrodes located around the eyes. EOG signals utilized to control wheelchair motion by applying signal processing techniques. The main steps of signal processing phase are pre-processing, maximum-minimum value detection and classification, respectively. At first, pre-processing step is used to amplify and smooth EOG signals. In maximum-minimum value detection we obtain maximum and minimum voltage levels of the eye movements. Furthermore, we determine the peak time of blink to distinguish voluntary blinks from involuntary blinks. Finally, at classification step k-Nearest Neighbouring (k-NN) technique is applied to separate eye movement signals from each other. Several computer simulations are performed to show the effectiveness of the proposed EOG based wheelchair control system. According to the results, proposed system can communicate paralyzed people with their wheelchair and by this way they will be able to move by their selves. -
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 ......................................................................................................................................... -
Neovascular Glaucoma: Etiology, Diagnosis and Prognosis
Seminars in Ophthalmology, 24, 113–121, 2009 Copyright C Informa Healthcare USA, Inc. ISSN: 0882-0538 print / 1744-5205 online DOI: 10.1080/08820530902800801 Neovascular Glaucoma: Etiology, Diagnosis and Prognosis Tarek A. Shazly Mark A. Latina Department of Ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear Massachusetts Eye and Ear Infirmary, Boston, MA, USA, and Infirmary, Boston, MA, USA and Department of Ophthalmology, Department of Ophthalmology, Tufts Assiut University Hospital, Assiut, University School of Medicine, Egypt Boston, MA, USA ABSTRACT Neovascular glaucoma (NVG) is a severe form of glaucoma with devastating visual outcome at- tributed to new blood vessels obstructing aqueous humor outflow, usually secondary to widespread posterior segment ischemia. Invasion of the anterior chamber by a fibrovascular membrane ini- tially obstructs aqueous outflow in an open-angle fashion and later contracts to produce secondary synechial angle-closure glaucoma. The full blown picture of NVG is characteristized by iris neovas- cularization, a closed anterior chamber angle, and extremely high intraocular pressure (IOP) with severe ocular pain and usually poor vision. Keywords: neovascular glaucoma; rubeotic glaucoma; neovascularization; retinal ischemia; vascular endothe- lial growth factor (VEGF); proliferative diabetic retinopathy; central retinal vein occlusion For personal use only. INTRODUCTION tive means of reversing well established NVG and pre- venting visual loss in the majority of cases; instead bet- The written -
Improved Preservation of Human Corneal Basement Membrane
BritishJournal ofOphthalmology 1994; 78: 863-870 863 Improved preservation ofhuman corneal basement membrane following freezing of donor tissue for Br J Ophthalmol: first published as 10.1136/bjo.78.11.863 on 1 November 1994. Downloaded from epikeratophakia Robert D Young, W John Armitage, Paul Bowerman, Stuart D Cook, David L Easty Abstract States, good results continue to be achieved by Current methods for the production of the small number ofBritish surgeons performing lenticules for epikeratophakia involve rapid the technique.4 However, no comprehensive freezing, cryolathing, and slow warming of the account of its long term outcome has yet been donor cornea. We have found that this pro- published. cedure causes structural damage to the Several complications resulting in the failure epithelial basement membrane in the donor of epikeratophakia have been reported, includ- cornea which may subsequently contribute to ing infection, graft dehiscence, persistent inter- poor postoperative re-epithelialisation of the face haze or opacity, ulceration, and imperfect implant, leading to graft failure. Endeavouring re-epithelialisation. Among these, the failure of to overcome these problems, the effects of host epithelial cells to migrate over and re- cryoprotection of donor cornea were investi- surface the anterior face of the grafted tissue gated, using dimethyl sulphoxide, in conjunc- continues to be the major reason for the removal tion with different cooling and warming rates ofepikeratophakia lenticules.'-'0 as part of the protocol for cryolathing. The Epithelial healing is itselfa complex phenome- structural integrity of the epithelial basement non involving mitosis of host cells at the graft membrane zone (BMZ) was then assessed by periphery, centripetal migration, and attach- electron microscopy and by immunofluores- ment. -
Electroretinography 1 Electroretinography
Electroretinography 1 Electroretinography Electroretinography measures the electrical responses of various cell types in the retina, including the photoreceptors (rods and cones), inner retinal cells (bipolar and amacrine cells), and the ganglion cells. Electrodes are usually placed on the cornea and the skin near the eye, although it is possible to record the ERG from skin electrodes. During a recording, the patient's eyes are exposed to standardized stimuli and the resulting signal is displayed showing the time course of the signal's Maximal response ERG waveform from a dark adapted eye. amplitude (voltage). Signals are very small, and typically are measured in microvolts or nanovolts. The ERG is composed of electrical potentials contributed by different cell types within the retina, and the stimulus conditions (flash or pattern stimulus, whether a background light is present, and the colors of the stimulus and background) can elicit stronger response from certain components. If a flash ERG is performed on a dark-adapted eye, the response is primarily from the rod system and flash ERGs performed on a light adapted eye will reflect the activity of the cone system. To sufficiently bright flashes, the ERG will contain an A patient undergoing an electroretinogram a-wave (initial negative deflection) followed by a b-wave (positive deflection). The leading edge of the a-wave is produced by the photoreceptors, while the remainder of the wave is produced by a mixture of cells including photoreceptors, bipolar, amacrine, and Muller cells or Muller glia.[1] The pattern ERG, evoked by an alternating checkerboard stimulus, primarily reflects activity of retinal ganglion cells. -
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. -
Photorefractive Keratectomy for Correction of Epikeratophakia
CASE REPORTS AND SMALL CASE SERIES high myopia resulting from poste- results might be related to the pre- Photorefractive Keratectomy rior lenticonus. Postsurgical refrac- existing corneal stromal abnormali- for Correction of tion was stable for 8 years, then a ties in their patients, which were not Epikeratophakia Regression rapid myopic regression of the epi- observed in our group. Thus, PRK keratophakic lenses was observed can effectively be used to treat epi- Excimer laser photorefractive kera- the following year (Table). In- keratophakic regressed lenses in a se- tectomy (PRK) is widely used for the stead of removing the failed epikera- lected group of patients in whom correction of myopia, astigmatism, tophakic lenses, we performed PRK both the epikeratograft and the sur- and hyperopia.1,2 It has also been on the eyes. rounding cornea are clear. This used for correction of astigmatism method eliminates the need for re- after penetrating keratoplasty.3 Results. Two and a half years after moval of the epikeratograft and ex- Epikeratophakia has been used PRK, the refraction in all 4 eyes is posing the patient to the risks of suc- in the treatment of nontolerant con- stable and the epigrafts are clear. The cessive penetrating keratoplasty. tact lens keratoconous patients.4,5 Table presents the refraction and vi- The epigrafts were made from ma- sual acuity results for the eyes be- Hirsh Ami, MD chined corneal tissue that was found fore PRK and at 3 months, 1 year, Solberg Yoram, MD, PhD unsuitable for penetrating kerato- and 21⁄2 years after PRK. No haze has Cahana Michael, MD plasty. -
Genes in Eyecare Geneseyedoc 3 W.M
Genes in Eyecare geneseyedoc 3 W.M. Lyle and T.D. Williams 15 Mar 04 This information has been gathered from several sources; however, the principal source is V. A. McKusick’s Mendelian Inheritance in Man on CD-ROM. Baltimore, Johns Hopkins University Press, 1998. Other sources include McKusick’s, Mendelian Inheritance in Man. Catalogs of Human Genes and Genetic Disorders. Baltimore. Johns Hopkins University Press 1998 (12th edition). http://www.ncbi.nlm.nih.gov/Omim See also S.P.Daiger, L.S. Sullivan, and B.J.F. Rossiter Ret Net http://www.sph.uth.tmc.edu/Retnet disease.htm/. Also E.I. Traboulsi’s, Genetic Diseases of the Eye, New York, Oxford University Press, 1998. And Genetics in Primary Eyecare and Clinical Medicine by M.R. Seashore and R.S.Wappner, Appleton and Lange 1996. M. Ridley’s book Genome published in 2000 by Perennial provides additional information. Ridley estimates that we have 60,000 to 80,000 genes. See also R.M. Henig’s book The Monk in the Garden: The Lost and Found Genius of Gregor Mendel, published by Houghton Mifflin in 2001 which tells about the Father of Genetics. The 3rd edition of F. H. Roy’s book Ocular Syndromes and Systemic Diseases published by Lippincott Williams & Wilkins in 2002 facilitates differential diagnosis. Additional information is provided in D. Pavan-Langston’s Manual of Ocular Diagnosis and Therapy (5th edition) published by Lippincott Williams & Wilkins in 2002. M.A. Foote wrote Basic Human Genetics for Medical Writers in the AMWA Journal 2002;17:7-17. A compilation such as this might suggest that one gene = one disease. -
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. -
Assessment and Management of Infantile Nystagmus Syndrome
perim Ex en l & ta a l ic O p in l h t C h f Journal of Clinical & Experimental a o l m l a o n l r o Atilla, J Clin Exp Ophthalmol 2016, 7:2 g u y o J Ophthalmology 10.4172/2155-9570.1000550 ISSN: 2155-9570 DOI: Review Article Open Access Assessment and Management of Infantile Nystagmus Syndrome Huban Atilla* Department of Ophthalmology, Faculty of Medicine, Ankara University, Turkey *Corresponding author: Huban Atilla, Department of Ophthalmology, Faculty of Medicine, Ankara University, Turkey, Tel: +90 312 4462345; E-mail: [email protected] Received date: March 08, 2016; Accepted date: April 26, 2016; Published date: April 29, 2016 Copyright: © 2016 Atilla H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract This article is a review of infantile nystagmus syndrome, presenting with an overview of the physiological nystagmus and the etiology, symptoms, clinical evaluation and treatment options. Keywords: Nystagmus syndrome; Physiologic nystagmus phases; active following of the stimulus results in poor correspondence between eye position and stimulus position. At higher velocity targets Introduction (greater than 100 deg/sec) optokinetic nystagmus can no longer be evoked. Unlike simple foveal smooth pursuit, OKN appears to have Nystagmus is a rhythmic, involuntary oscillation of one or both both foveal and peripheral retinal components [3]. Slow phase of the eyes. There are various classifications of nystagmus according to the nystagmus is for following the target and the fast phase is for re- age of onset, etiology, waveform and other characteristics.