Flashes and Floaters a Practical Approach to Assessment and Management Shyalle Kahawita Sumu Simon Jolly Gilhotra
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
GUIDE for the Evaluation of VISUAL Impairment
International Society for Low vision Research and Rehabilitation GUIDE for the Evaluation of VISUAL Impairment Published through the Pacific Vision Foundation, San Francisco for presentation at the International Low Vision Conference VISION-99. TABLE of CONTENTS INTRODUCTION 1 PART 1 – OVERVIEW 3 Aspects of Vision Loss 3 Visual Functions 4 Functional Vision 4 Use of Scales 5 Ability Profiles 5 PART 2 – ASSESSMENT OF VISUAL FUNCTIONS 6 Visual Acuity Assessment 6 In the Normal and Near-normal range 6 In the Low Vision range 8 Reading Acuity vs. Letter Chart Acuity 10 Visual Field Assessment 11 Monocular vs. Binocular Fields 12 PART 3 – ESTIMATING FUNCTIONAL VISION 13 A General Ability Scale 13 Visual Acuity Scores, Visual Field Scores 15 Calculation Rules 18 Functional Vision Score, Adjustments 20 Examples 22 PART 4 – DIRECT ASSESSMENT OF FUNCTIONAL VISION 24 Vision-related Activities 24 Creating an Activity Profile 25 Participation 27 PART 5 – DISCUSSION AND BACKGROUND 28 Comparison to AMA scales 28 Statistical Use of the Visual Acuity Score 30 Comparison to ICIDH-2 31 Bibliography 31 © Copyright 1999 by August Colenbrander, M.D. All rights reserved. GUIDE for the Evaluation of VISUAL Impairment Summer 1999 INTRODUCTION OBJECTIVE Measurement Guidelines for Collaborative Studies of the National Eye Institute (NEI), This GUIDE presents a coordinated system for the Bethesda, MD evaluation of the functional aspects of vision. It has been prepared on behalf of the International WORK GROUP Society for Low Vision Research and Rehabilitation (ISLRR) for presentation at The GUIDE was approved by a Work Group VISION-99, the fifth International Low Vision including the following members: conference. -
425-428 YOSHI:Shoja
European Journal of Ophthalmology / Vol. 19 no. 3, 2009 / pp. 425-428 Effects of astigmatism on the Humphrey Matrix perimeter TOSHIAKI YOSHII, TOYOAKI MATSUURA, EIICHI YUKAWA, YOSHIAKI HARA Department of Ophthalmology, Nara Medical University, Nara - Japan PURPOSE. To evaluate the influence of astigmatism in terms of its amount and direction on the results of Humphrey Matrix perimetry. METHODS. A total of 31 healthy volunteers from hospital staff were consecutively recruited to undergo repeat testing with Humphrey Matrix 24-2 full threshold program with various induced simple myopic astigmatism. All subjects had previous experience (at least twice) with Matrix testing. To produce simple myopic astigmatism, a 0 diopter (D), +1 D, or +2 D cylindrical lens was added and inserted in the 180° direction and in the 90° direction after complete correction of distance vision. The influences of astigmatism were evaluated in terms of the mean deviation (MD), pattern standard deviation (PSD), and test duration (TD). RESULTS. A significant difference was observed only in the MD from five sessions. The MD in cases of 2 D inverse astigmatism was significantly lower than that in the absence of astig- matism. CONCLUSIONS. In patients with inverse myopic astigmatism of ≥ 2 D, the influences of astig- matism on the visual field should be taken into consideration when the results of Humphrey Matrix perimetry are evaluated. (Eur J Ophthalmol 2009; 19: 425-8) KEY WORDS. Astigmatism, Frequency doubling technology, FDT Matrix, Perimetry Accepted: October 10, 2008 INTRODUCTION as an FDT perimeter and became commercially available. In this perimeter, the examination time was shortened due Refractive error is one of the factors affecting the results to changes in the algorithm, the target size was made of perimetry. -
Advice for Floaters and Flashing Lights for Primary Care
UK Vision Strategy RCGP – Royal College of General Practitioners Advice for Floaters and Flashing Lights for primary care Key learning points • Floaters and flashing lights usually signify age-related liquefaction of the vitreous gel and its separation from the retina. • Although most people sometimes see floaters in their vision, abrupt onset of floaters and / or flashing lights usually indicates acute vitreous gel detachment from the posterior retina (PVD). • Posterior vitreous detachment is associated with retinal tear in a minority of cases. Untreated retinal tear may lead to retinal detachment (RD) which may result in permanent vision loss. • All sudden onset floaters and / or flashing lights should be referred for retinal examination. • The differential diagnosis of floaters and flashing lights includes vitreous haemorrhage, inflammatory eye disease and very rarely, malignancy. Vitreous anatomy, ageing and retinal tears • The vitreous is a water-based gel containing collagen that fills the space behind the crystalline lens. • Degeneration of the collagen gel scaffold occurs throughout life and attachment to the retina loosens. The collagen fibrils coalesce, the vitreous becomes increasingly liquefied and gel opacities and fluid vitreous pockets throw shadows on to the retina resulting in perception of floaters. • As the gel collapses and shrinks, it exerts traction on peripheral retina. This may cause flashing lights to be seen (‘photopsia’ is the sensation of light in the absence of an external light stimulus). • Eventually, the vitreous separates from the posterior retina. Supported by Why is this important? • Acute PVD may cause retinal tear in some patients because of traction on the retina especially at the equator of the eye where the retina is thinner. -
Bass – Glaucomatous-Type Field Loss Not Due to Glaucoma
Glaucoma on the Brain! Glaucomatous-Type Yes, we see lots of glaucoma Field Loss Not Due to Not every field that looks like glaucoma is due to glaucoma! Glaucoma If you misdiagnose glaucoma, you could miss other sight-threatening and life-threatening Sherry J. Bass, OD, FAAO disorders SUNY College of Optometry New York, NY Types of Glaucomatous Visual Field Defects Paracentral Defects Nasal Step Defects Arcuate and Bjerrum Defects Altitudinal Defects Peripheral Field Constriction to Tunnel Fields 1 Visual Field Defects in Very Early Glaucoma Paracentral loss Early superior/inferior temporal RNFL and rim loss: short axons Arcuate defects above or below the papillomacular bundle Arcuate field loss in the nasal field close to fixation Superotemporal notch Visual Field Defects in Early Glaucoma Nasal step More widespread RNFL loss and rim loss in the inferior or superior temporal rim tissue : longer axons Loss stops abruptly at the horizontal raphae “Step” pattern 2 Visual Field Defects in Moderate Glaucoma Arcuate scotoma- Bjerrum scotoma Focal notches in the inferior and/or superior rim tissue that reach the edge of the disc Denser field defects Follow an arcuate pattern connected to the blind spot 3 Visual Field Defects in Advanced Glaucoma End-Stage Glaucoma Dense Altitudinal Loss Progressive loss of superior or inferior rim tissue Non-Glaucomatous Etiology of End-Stage Glaucoma Paracentral Field Loss Peripheral constriction Hereditary macular Loss of temporal rim tissue diseases Temporal “islands” Stargardt’s macular due -
Visual Pathways
Visual Pathways Michael Davidson Professor, Ophthalmology Diplomate, American College of Veterinary Ophthalmologists Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh, North Carolina, USA <[email protected]> Vision in Animals Miller PE, Murphy CJ. Vision in Dogs. JAVMA. 1995; 207: 1623. Miller PE, Murphy CJ. Equine Vision. In Equine Ophthalmology ed. Gilger BC. 2nd ed. 2011: pp 398- 433. Ofri R. Optics and Physiology of Vision. In Veterinary Ophthalmology. ed. Gelatt KN 5th ed. 2013: 208-270, Visual Pathways, Responses and Reflexes: Relevant Structures Optic n (CN II) – somatic afferent Oculomotor n (CN III), Trochlear n (CN IV), Abducens n (CN VI) – somatic efferent to extraocular muscles Facial n (CN VII)– visceral efferent to eyelids Rostral colliculi – brainstem center that mediates somatic reflexes in response to visual stimuli Cerebellum Cerebro-cortex esp. occipital lobe www.studyblue.com Visual Pathway Visual Cortex Optic Radiation Lateral Geniculate Body www.studyblue.com Visual Field each cerebral hemisphere receives information from contralateral visual field (“the area that can be seen when the eye is directed forward”) visual field Visual Fiber (Retinotopic) Segregation nasal retinal fibers decussate at chiasm, temporal retinal fibers remain ipsilateral Nasal Temporal Retina Retina Fibers Fibers Decussate Remain Ipsilateral OD Visual Field OS Total visual field OD temporal nasal hemifield hemifield temporal nasal fibers fibers Nasal Temporal Retina = Retina = Temporal -
Visual Field Defects Essentials for Neurologists
J Neurol (2003) 250:407–411 DOI 10.1007/s00415-003-1069-1 REVIEW Ulrich Schiefer Visual field defects Essentials for neurologists Introduction I The visual pathway – a highly sensitive “functional trip-wire” The visual pathway achieves neuronal signal transduc- tion between retinal photoreceptors, visual cortex and higher order visual areas. Lesions affecting this “trip- wire” will result in visual impairment which should in- duce the affected person to contact a physician. Correct interpretation of such symptoms and choice of appro- priate psychophysical examination methods will usually provide the examiner with specific information on topography and eventual progression, if baseline results are available [3,6].These data are essential prerequisites for effective neuroimaging, as well as for an adequate follow-up. Fig. 1 Functional anatomy of the human visual pathways Functional anatomy of the human visual pathways About 7 million cones and approximately 120 million The different sections of the visual pathways differ rods are distributed on the human retinal surface (area markedly with respect to the number,density and extent ~ 12 cm2). Each retinal element is directly linked to a of “intermixture” of neuronal elements, which will specific location within the visual field. More than strongly influence local resolution power and diagnos- 10 million bipolar cells forward the visual information tic relevance (Fig. 1). onto only 1.2 million ganglion cells.These cells are wide- spread on the retinal surface, and converge to 300–500 fibre-bundles with a total surface area of less than Received: 18 January 2003 0.2 cm2. There is a maximum neuronal density in the re- Accepted: 30 January 2003 gion of the optic chiasm: the entire visual information is “packed” into this “visual bottleneck” of about 1 cm3! In Prof. -
Dominant Optic Atrophy
Lenaers et al. Orphanet Journal of Rare Diseases 2012, 7:46 http://www.ojrd.com/content/7/1/46 REVIEW Open Access Dominant optic atrophy Guy Lenaers1*, Christian Hamel1,2, Cécile Delettre1, Patrizia Amati-Bonneau3,4,5, Vincent Procaccio3,4,5, Dominique Bonneau3,4,5, Pascal Reynier3,4,5 and Dan Milea3,4,5,6 Abstract Definition of the disease: Dominant Optic Atrophy (DOA) is a neuro-ophthalmic condition characterized by a bilateral degeneration of the optic nerves, causing insidious visual loss, typically starting during the first decade of life. The disease affects primary the retinal ganglion cells (RGC) and their axons forming the optic nerve, which transfer the visual information from the photoreceptors to the lateral geniculus in the brain. Epidemiology: The prevalence of the disease varies from 1/10000 in Denmark due to a founder effect, to 1/30000 in the rest of the world. Clinical description: DOA patients usually suffer of moderate visual loss, associated with central or paracentral visual field deficits and color vision defects. The severity of the disease is highly variable, the visual acuity ranging from normal to legal blindness. The ophthalmic examination discloses on fundoscopy isolated optic disc pallor or atrophy, related to the RGC death. About 20% of DOA patients harbour extraocular multi-systemic features, including neurosensory hearing loss, or less commonly chronic progressive external ophthalmoplegia, myopathy, peripheral neuropathy, multiple sclerosis-like illness, spastic paraplegia or cataracts. Aetiology: Two genes (OPA1, OPA3) encoding inner mitochondrial membrane proteins and three loci (OPA4, OPA5, OPA8) are currently known for DOA. Additional loci and genes (OPA2, OPA6 and OPA7) are responsible for X-linked or recessive optic atrophy. -
Anatomy and Physiology of the Afferent Visual System
Handbook of Clinical Neurology, Vol. 102 (3rd series) Neuro-ophthalmology C. Kennard and R.J. Leigh, Editors # 2011 Elsevier B.V. All rights reserved Chapter 1 Anatomy and physiology of the afferent visual system SASHANK PRASAD 1* AND STEVEN L. GALETTA 2 1Division of Neuro-ophthalmology, Department of Neurology, Brigham and Womens Hospital, Harvard Medical School, Boston, MA, USA 2Neuro-ophthalmology Division, Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, PA, USA INTRODUCTION light without distortion (Maurice, 1970). The tear–air interface and cornea contribute more to the focusing Visual processing poses an enormous computational of light than the lens does; unlike the lens, however, the challenge for the brain, which has evolved highly focusing power of the cornea is fixed. The ciliary mus- organized and efficient neural systems to meet these cles dynamically adjust the shape of the lens in order demands. In primates, approximately 55% of the cortex to focus light optimally from varying distances upon is specialized for visual processing (compared to 3% for the retina (accommodation). The total amount of light auditory processing and 11% for somatosensory pro- reaching the retina is controlled by regulation of the cessing) (Felleman and Van Essen, 1991). Over the past pupil aperture. Ultimately, the visual image becomes several decades there has been an explosion in scientific projected upside-down and backwards on to the retina understanding of these complex pathways and net- (Fishman, 1973). works. Detailed knowledge of the anatomy of the visual The majority of the blood supply to structures of the system, in combination with skilled examination, allows eye arrives via the ophthalmic artery, which is the first precise localization of neuropathological processes. -
Clinical Findings and Management of Posterior Vitreous Detachment
American Academy of Optometry: Case Report 5 Clinical Findings and Management of Posterior Vitreous Detachment Candidate’s Name, O.D. Candidate’s Address Candidate’s Phone number Candidate’s email Abstract: A posterior vitreous detachment is a degenerative process associated with aging that affects the vitreous when the posterior vitreous cortex separates from the internal limiting membrane of the retina. The composition of the vitreous gel can degenerate two collective ways, including synchysis or liquefaction, and syneresis or shrinking. Commonly, this process of separation occurs with the posterior hyaloid resulting in a Weiss ring overlying the optic nerve. Complications of a posterior vitreous detachment may include retinal breaks or detachments, retinal or vitreous hemorrhages, or vitreomacular traction. This case presentation summarizes the etiology of this ocular condition as well as treatment and management approaches. Key Words: Posterior Vitreous Detachment, Weiss Ring, Vitreous Degeneration, Scleral Depression, Nd:YAG Laser 1 Introduction The vitreous humor encompasses the posterior segment of the eye and fills approximately three quarters of the ocular space.1 The vitreous is a transparent, hydrophilic, “gel-like” substance that is described as a dilute solution of collagen, and hyaluronic acid.2,3,4 It is composed of 98% to 99.7% water.4 As the eye matures, changes may occur regarding the structure and composition of the vitreous. The vitreous functions to provide support to the retina against the choroid, to store nutrients and metabolites for the retina and lens, to protect the retinal tissue by acting as a “shock absorber,” to transmit and refract light, and to help regulate eye growth during fetal development.3,4 Case Report Initial Visit (03/23/2018) A 59-year-old Asian female presented as a new patient for examination with a complaint of a new onset of floaters and flashes of light in her right eye. -
Floaters-Survey-Ophthalmol-2016.Pdf
survey of ophthalmology 61 (2016) 211e227 Available online at www.sciencedirect.com ScienceDirect journal homepage: www.elsevier.com/locate/survophthal Major review Vitreous floaters: Etiology, diagnostics, and management Rebecca Milston, MOptoma, Michele C. Madigan, PhDb,c, J. Sebag, MD, FACS, FRCOphth, FARVOd,* a Centre for Eye Health, University of New South Wales, Sydney, New South Wales, Australia b School of Optometry and Vision Science, University of New South Wales, Sydney, New South Wales, Australia c Save Sight Institute and Discipline of Clinical Ophthalmology, Sydney Medical School, University of Sydney, New South Wales, Australia d VMR Institute for Vitreous Macula Retina, Huntington Beach, California, USA article info abstract Article history: Vitreous is a hydrated extracellular matrix comprised primarily of water, collagens, and Received 3 July 2015 hyaluronan organized into a homogeneously transparent gel. Gel liquefaction results from Received in revised form 25 molecular alterations with dissociation of collagen from hyaluronan and aggregation of November 2015 collagen fibrils forming fibers that cause light scattering and hence symptomatic floaters, Accepted 25 November 2015 especially in myopia. With aging, gel liquefaction and weakened vitreoretinal adhesion Available online 8 December 2015 result in posterior vitreous detachment, the most common cause of primary symptomatic floaters arising from the dense collagen matrix of the posterior vitreous cortex. Recent Keywords: studies indicate that symptomatic floaters are not only more prevalent, but also have a vitreous negative impact on the quality of life that is greater than previously appreciated. We review collagen the literature concerning management of symptomatic vitreous floaters, currently either myopia with observation, vitrectomy, or Nd:YAG laser. -
NEUROLOGY in TABLE.Pdf
ZAPORIZHZHIA STATE MEDICAL UNIVERSITY DEPARTMENT OF NEUROLOGY DISEASES NEUROLOGY IN TABLE (General neurology) for practical employments to the students of the IV course of medical faculty Zaporizhzhia, 2015 2 It is approved on meeting of the Central methodical advice Zaporozhye state medical university (the protocol № 6, 20.05.2015) and is recommended for use in scholastic process. Authors: doctor of the medical sciences, professor Kozyolkin O.A. candidate of the medical sciences, assistant professor Vizir I.V. candidate of the medical sciences, assistant professor Sikorskaya M.V. Kozyolkin O. A. Neurology in table (General neurology) : for practical employments to the students of the IV course of medical faculty / O. A. Kozyolkin, I. V. Vizir, M. V. Sikorskaya. – Zaporizhzhia : [ZSMU], 2015. – 94 p. 3 CONTENTS 1. Sensitive function …………………………………………………………………….4 2. Reflex-motor function of the nervous system. Syndromes of movement disorders ……………………………………………………………………………….10 3. The extrapyramidal system and syndromes of its lesion …………………………...21 4. The cerebellum and it’s pathology ………………………………………………….27 5. Pathology of vegetative nervous system ……………………………………………34 6. Cranial nerves and syndromes of its lesion …………………………………………44 7. The brain cortex. Disturbances of higher cerebral function ………………………..65 8. Disturbances of consciousness ……………………………………………………...71 9. Cerebrospinal fluid. Meningealand hypertensive syndromes ………………………75 10. Additional methods in neurology ………………………………………………….82 STUDY DESING PATIENT BY A PHYSICIAN NEUROLOGIST -
Acute Visual Loss 5 Cédric Lamirel , Nancy J
Acute Visual Loss 5 Cédric Lamirel , Nancy J. Newman , and Valérie Biousse Abstract Visual loss is a common symptom in neurologic emergencies. Although ocular causes of visual loss are usually identifi ed by eye care specialists, many patients appear in an emergency department or a neurologist’s offi ce when the ocular examination is normal or when it suggests a neurologic disorder. Indeed, many causes of monocular or binocular acute visual loss may reveal or precede a neurologic process. In this situation, a quick and simple clinical examination done at bedside in the emergency department allows the neurologist to localize the lesion and determine whether an urgent neurologic workup or further ophthalmologic consultation is necessary. Keywords Central retinal artery occlusion • Funduscopic examination • Optic neuropathy • Retinal emboli • Visual fi eld • Visual loss Acute vision changes typically precipitate emer- gency consultation. Although ocular causes are usually identifi ed by eye care specialists, many patients appear in an emergency department or a C. Lamirel , MD neurologist’s offi ce when the ocular examination Service d’ophtalmologie , Fondation Ophtalmologique is normal or when it suggests a neurologic disor- Adolphe Rothschild , Paris , France der. Indeed, many causes of monocular or binoc- e-mail: [email protected] ular acute visual loss may reveal or precede a N. J. Newman , MD • V. Biousse, MD () neurologic process. In this situation, a quick and Neuro-Ophthalmology Unit , simple clinical examination done at bedside in Emory University School of Medicine , Atlanta , GA , USA the emergency department allows the neurologist e-mail: [email protected]; [email protected] to localize the lesion and determine whether an K.L.