Visual Field Defects After Stroke – a Practical Guide for Gps Been Reported in up to 50% of Patients, Usually Independently
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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. -
FUS-Mediated Functional Neuromodulation for Neurophysiologic Assessment in a Large Animal Model Wonhye Lee1*, Hyungmin Kim2, Stephanie D
Lee et al. Journal of Therapeutic Ultrasound 2015, 3(Suppl 1):O23 http://www.jtultrasound.com/content/3/S1/O23 ORALPRESENTATION Open Access FUS-mediated functional neuromodulation for neurophysiologic assessment in a large animal model Wonhye Lee1*, Hyungmin Kim2, Stephanie D. Lee1, Michael Y. Park1, Seung-Schik Yoo1 From Current and Future Applications of Focused Ultrasound 2014. 4th International Symposium Washington, D.C, USA. 12-16 October 2014 Background/introduction element FUS transducer with radius-of-curvature of Focused ultrasound (FUS) is gaining momentum as a 7 cm) was transcranially delivered to the unilateral sen- new modality of non-invasive neuromodulation of regio- sorimotor cortex, the optic radiation (WM tract) as well as nal brain activity, with both stimulatory and suppressive the visual cortex. An acoustic intensity of 1.4–15.5 W/cm2 potentials. The utilization of the method has largely Isppa, tone-burst-duration of 1 ms, pulse-repetition fre- been demonstrated in small animals. Considering the quency of 500 Hz (i.e. duty cycle of 50%), sonication dura- small size of the acoustic focus, having a diameter of tion of 300 ms, were used for the stimulation. A batch of only a few millimeters, FUS insonification to a larger continuous sonication ranging from 50 to 150 ms in dura- animal’s brain is conducive to examining the region- tion were also given. Evoked electromyogram responses specific neuromodulatory effects on discrete anatomical from the hind legs and electroencephalogram from the Fz areas, including the white matter (WM) tracts. The and Oz-equivalent sites were measured. The histology of study involving large animals would also establish preli- the extracted brain tissue (within one week and 2 months minary safety data prior to its translational research in post-sonication) was obtained. -
Customer Vision Report (MED 4)
MED 4 (11/25/2020) CUSTOMER VISION REPORT Purpose: Use this form to request vision examination information from your ophthalmologist or optometrist. Instructions: Complete the Customer Information section and have your Ophthalmologist/Optometrist complete the Vision Examination section. The vision examination must be conducted within 90 days prior to submission of the report to DMV. Mail the completed report to the address above. Questions can be referred to Medical Review Services, 804-367-6203. Acceptable standards of vision for safe driving are determined by the Code of Virginia and DMV under the guidance of the Medical Advisory Board. Note: Any charges incurred for the completion of this form are your responsibility. CSC STAFF Do NOT send MED 4 back with daily work unless there is an ocular condition or customer cannot be licensed due to a MED 6 calculation. CUSTOMER INFORMATION (To be completed by customer PRIOR to vision examination) If you change either your residence/home address or mailing address to a non-Virgina address, your driver license or photo identification (ID) card may be cancelled. NAME (last) (first) (mi) (suffix) CUSTOMER NUMBER (from your driver license) or SSN RESIDENCE/HOME ADDRESS BIRTHDATE (mm/dd/yyyy) CITY STATE ZIP CODE CITY OR COUNTY OF RESIDENCE MAILING ADDRESS (if different from above) CITY STATE ZIP CODE DAYTIME TELEPHONE NUMBER VISION EXAMINATION (to be completed by Ophthalmologist/Optometrist) FIRST EXAMINATION DATE MOST RECENT EXAMINATION DATE Does the patient have any visual/ocular condition(s) that could affect the ability to drive a motor vehicle? YES NO If YES, indicate condition below. -
Boosting Learning Efficacy with Non-Invasive Brain Stimulation in Intact and Brain-Damaged Humans
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. Research Articles: Behavioral/Cognitive Boosting learning efficacy with non-invasive brain stimulation in intact and brain-damaged humans F. Herpich1,2,3, F. Melnick, M.D.4 , S. Agosta1 , K.R. Huxlin4 , D. Tadin4 and L Battelli1,5,6 1Center for Neuroscience and Cognitive Systems@UniTn, Istituto Italiano di Tecnologia, Corso Bettini 31, 38068 Rovereto (TN), Italy 2Center for Mind/Brain Sciences, University of Trento, 38068 Rovereto, Italy 3kbo Klinikum-Inn-Salzach, Gabersee 7, 83512, Wasserburg am Inn, Germany 4Department of Brain and Cognitive Sciences, Flaum Eye Institute and Center for Visual Science, University of Rochester, Rochester, NY, USA 5Berenson-Allen Center for Noninvasive Brain Stimulation and Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, 02215 Massachusetts, USA 6Cognitive Neuropsychology Laboratory, Harvard University, Cambridge, MA, USA https://doi.org/10.1523/JNEUROSCI.3248-18.2019 Received: 28 December 2018 Revised: 10 April 2019 Accepted: 8 May 2019 Published: 27 May 2019 Author contributions: F.H., M.D.M., K.H., D.T., and L.B. designed research; F.H., M.D.M., and S.A. performed research; F.H., M.D.M., and D.T. analyzed data; F.H., M.D.M., and L.B. wrote the first draft of the paper; M.D.M., S.A., K.H., D.T., and L.B. edited the paper; K.H., D.T., and L.B. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. The present study was funded by the Autonomous Province of Trento, Call “Grandi Progetti 2012”, project “Characterizing and improving brain mechanisms of attention — ATTEND (FH, SA, LB), “Fondazione Caritro — Bando Ricerca e Sviluppo Economico” (FH), NIH (DT, MM and KRH: R01 grants EY027314 and EY021209, CVS training grant T32 EY007125), and by an unrestricted grant from the Research to Prevent Blindness (RPB) Foundation to the Flaum Eye Institute. -
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REVIEW OF OPTOMETRY EARN 2 CE CREDITS: Positive Visual Phenomena—Etiologies Beyond the Eye, PAGE 58 ■ VOL. 155 NO. 1 January 15, 2018 www.reviewofoptometry.comwww.reviewofoptometry.com ■ ANNUAL CORNEA REPORT JANUARY 15, 2018 ■ CXL ■ EPITHELIAL DEFECTS How to Heal Persistent Epithelial Defects PAGE 38 ■ TRANSPLANTS Corneal Transplants: The OD’s Role PAGE 44 ■ INFILTRATES Diagnosing Corneal Infiltrative Disease PAGE 50 ■ POSITIVE VISUAL PHENOMENA CXL: Your Top 12 Questions —Answered! PAGE 30 001_ro0118_fc.indd 1 1/5/18 4:34 PM ĊčĞĉėĆęĊĉĆĒēĎĔęĎĈĒĊĒćėĆēĊċĔėĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊĘ ĊđĎĊċĎēĘĎČčę ċċĊĈęĎěĊ Ȉ 1 Ȉ 1 ĊđđǦęĔđĊėĆęĊĉ Ȉ Ȉ ĎĒĕđĊĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊ Ȉ Ȉ ĔēěĊēĎĊēę Ȉ͝ Ȉ Ȉ Ƭ 1 ǡ ǡǡǤ͚͙͘͜Ǥ Ȁ Ǥ ͚͙͘͜ǣ͘͘ǣ͘͘͘Ǧ͘͘͘ ĕĕđĎĈĆęĎĔēĘ Ȉ Ȉ Ȉ Ȉ Ȉ čĊĚėĎĔē̾ėĔĈĊĘĘ Ȉ Ȉ Katena — Your completecomplete resource forfor amniotic membrane pprocedurerocedure pproducts:roducts: Single use speculums Single use spears ͙͘͘ǡ͘͘͘ήĊĞĊĘęėĊĆęĊĉ Forceps ® ,#"EWB3FW XXXLBUFOBDPNr RO0118_Katena.indd 1 1/2/18 10:34 AM News Review VOL. 155 NO. 1 ■ JANUARY 15, 2018 IN THE NEWS Accelerated CXL Shows The FDA recently approved Luxturna (voretigene neparvovec-rzyl, Spark Promise—and Caution Therapeutics), a directly administered gene therapy that targets biallelic This new technology is already advancing, but not without RPE65 mutation-associated retinal dystrophy. The therapy is designed to some bumps in the road. deliver a normal copy of the gene to By Rebecca Hepp, Managing Editor retinal cells to restore vision loss. While the approval provides hope for patients, wo new studies highlight the resulted in infection—while tradi- the $425,000 per eye price tag stands as pros and cons of accelerated tional C-CXL has a reported inci- a signifi cant hurdle. -
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 -
Mechanisms Compensating for Visual Field Restriction in Adolescents With
Eye (2012) 26, 1437–1445 & 2012 Macmillan Publishers Limited All rights reserved 0950-222X/12 www.nature.com/eye 1;2 3;4 1 Mechanisms L Jacobson , F Lennartsson , T Pansell ,GO¨ qvist CLINICAL STUDY Seimyr2 and L Martin2;5 compensating for visual field restriction in adolescents with damage to the retro-geniculate visual system 1Eye Unit, Department of Neuropaediatrics, Astrid Lindgren Children’s Hospital, Karolinska University Abstract Hospital, Stockholm, Background To describe visual field (VF) Conclusion Congenital and later-acquired Sweden outcome in three adolescents with damage to homonymous VF defects may, at least in 2 the optic radiation and to focus on young subjects, be compensated for by Department of Clinical Neuroscience, mechanisms that may compensate the scanning. Exotropia may compensate VF Ophthalmology and Vision, practical functional limitations of VF defects. defects and, therefore, the VF should be Karolinska Institutet, Design Descriptive, prospective multi-case tested before strabismus surgery. Stockholm, Sweden study in a hospital setting. Eye (2012) 26, 1437–1445; doi:10.1038/eye.2012.190; Participants Three teenagers with cerebral published online 21 September 2012 3Department of Medical visual dysfunction because of damage to the Physics, Karolinska University Hospital, retro-geniculate visual pathways. Keywords: VF defects; retro-geniculate visual Stockholm, Sweden Methods Best-corrected visual acuity and system; compensating mechanisms; eye alignment were assessed. Visual field adolescents 4Department of function was tested with Goldmann Neuroradiology, Karolinska perimetry, and with Rarebit, Humphrey University Hospital, Introduction Visual Field Analyzer and Esterman Stockholm, Sweden computerized techniques. Fixation was Brain damage has become the most common 5School of Health and registered with video oculography during cause of visual impairment in children in Welfare, Ma¨ lardalen 1–3 Rarebit examination. -
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. -
Case Report: Superior Homonymous Quadrantanopia in a Patient with an Infective Endocarditis
Case Report: Superior homonymous quadrantanopia in a patient with an infective endocarditis Jennifer Nim, O.D. Long Island, New York, [email protected] An infective endocarditis, specifically bacterial endocarditis, is usually caused by bacteria carried in the blood that may originate from an infection in other parts of the body besides the heart.1 Injuries, surgeries or preexisting heart conditions make the body vulnerable to infections. Emboli may arise during this type of infection that may lead to visual field defects. Case Report A 62-year-old white male from New York presented with the primary complaint of a recent loss of his left peripheral vision in his left eye and moving white and red flashes in both eyes. The patient had a history of floaters which have subsided in the past years. In addition, the patient reported an acute loss of hearing. The patient denies any head trauma, slurred speech or paralysis in the limbs. Medical history revealed hypercholesteremia and hypertension, for which he takes vytorin and lotrel, respectively. The patient’s best-corrected visual acuities were 20/20 in the right eye (OD) and in the left eye (OS). Pupil and extraocular motility testings were normal. Slit lamp evaluation revealed trace arcus and cortical cataracts in both eyes (OU). Intraocular pressures were within normal ranges in OU. The dilation fundus examination revealed posterior vitreal detachments in OU and a flat, choroidal nevus in the OD. The posterior pole (see Figures 1) and peripheral retina were flat and intact in OU. An automated threshold visual field revealed left superior homonymous quandrantanopia that respected the vertical line but not the horizontal line (see Figures 2).