Visual Impairment Age-Related Macular

Total Page:16

File Type:pdf, Size:1020Kb

Visual Impairment Age-Related Macular VISUAL IMPAIRMENT AGE-RELATED MACULAR DEGENERATION Macular degeneration is a medical condition predominantly found in young children in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thickening, atrophy, and in some cases, watering. This can result in loss of side vision, which entails inability to see coarse details, to read, or to recognize faces. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for those under the age of twenty years. Although some macular dystrophies that affect younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration (AMD or ARMD). Age-related macular degeneration begins with characteristic yellow deposits in the macula (central area of the retina which provides detailed central vision, called fovea) called drusen between the retinal pigment epithelium and the underlying choroid. Most people with these early changes (referred to as age-related maculopathy) have good vision. People with drusen can go on to develop advanced AMD. The risk is considerably higher when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula. Recent research suggests that large and soft drusen are related to elevated cholesterol deposits and may respond to cholesterol lowering agents or the Rheo Procedure. Advanced AMD, which is responsible for profound vision loss, has two forms: dry and wet. Central geographic atrophy, the dry form of advanced AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. While no treatment is available for this condition, vitamin supplements with high doses of antioxidants, lutein and zeaxanthin, have been demonstrated by the National Eye Institute and others to slow the progression of dry macular degeneration and in some patients, improve visual acuity. Neovascular or exudative AMD, the wet form of advanced AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, through Bruch's membrane, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated. Until recently, no effective treatments were known for wet macular degeneration. However, new drugs, called anti-angiogenics or anti-VEGF (anti-Vascular Endothelial Growth Factor) agents, when injected directly into the vitreous humor of the eye using a small, painless needle, can cause regression of the abnormal blood vessels and improvement of vision. The injections frequently have to be repeated on a monthly or bi-monthly basis. Examples of these agents include Lucentis, Avastin and Macugen. Only Lucentis and Macugen are FDA approved as of April 2007. Macugen has been found to have only minimal benefits in neovascular AMD and is no longer used. Worldwide, Avastin has been used extensively despite its "off label" status. The cost of Lucentis is approximately $2000 US per treatment while the cost of Avastin is approximately $150 per treatment. Lucentis is a close chemical relative of Avastin. Both drugs are made by Genentech. Risk factors • Ageing: Approximately 10% of patients 66 to 74 years of age will have findings of macular degeneration. The prevalence increases to 30% in patients 75 to 85 years of age • Family history: The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration vs. 12% for people who do not have relatives with macular degeneration, i.e. a fourfold higher risk. • Macular degeneration gene: The genes for the complement system proteins factor H (CFH) and factor B (CFB) have been determined to be strongly associated with a person's risk for developing macular degeneration. CFH is involved in inhibiting the inflammatory response mediated via C3b (and the Alternative Pathway of complement) both by acting as a cofactor for cleavage of C3b to its inactive form, C3bi, and by weakening the active complex that forms between C3b and factor B. C- reactive protein and polyanionic surface markers such as glycosaminoglycans normally enhance the ability of factor H to inhibit complement . But the mutation in CFH(Tyr402His) reduces the affinity of CFH for CRP and probably also alters the ability of factor H to recognise specific glycosaminoglycans. This change results in reduced ability of CFH to regulate complement on critical surfaces such as the specialised membrane at the back of the eye and leads to increased inflammatory response within the macula. In two 2006 studies at Yale Department of Epidemiology and Public Health and the Department of Ophthalmology and Visual Sciences, Moran Eye Center at the University of Utah School of Medicine, another gene that has implications for the disease, called HTRA1 (encoding a secreted serine protease), was identified. • Arg80Gly variant of the complement protein C3 A genetic study published in the New England Journal of Medicine in 2007 showed that a certain, common mutation in the C3 gene which is a central protein of the complement system is strongly associated with the occurrence of Age-related Macular Degeneration. The authors consider their study to underscore the influence of the complement pathway in the pathogenesis of this disease. • Hypertension : Also known as high blood pressure. • Cardiovascular status — high cholesterol, obesity. • High fat intake is associated with an increased risk of macular degeneration in both women and men. Fat provides about 42% of the food energy in the average American diet. A diet that derives closer to 20-25% of total food energy from fat is probably healthier. Reducing fat intake to this level means cutting down greatly on consumption of red meats and high-fat dairy products such as whole milk, cheese, and butter. Eating more cold-water fish (at least twice weekly), rather than red meats, and eating any type of nuts may help macular degeneration patients. • Oxidative stress: It has been proposed that age related accumulation of low molecular weight, phototoxic, pro-oxidant melanin oligomers within lysosomes in the retinal pigment epithelium may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with lipofuscin formation - a classic sign associated with macular degeneration • Fibulin-5 mutation Rare forms of the disease are caused by geneic defects in fibulin- 5, in an autosomal dominant manner. In 2004 Stone et al performed a screen on 402 AMD patients and revealed a statistically significant correlation between mutations in Fibulin-5 and incidence of the disease. Furthermore the point mutants were found in the Calcium binding sites of the cbEGF domains of the protein. there is no structural basis for the effects of the mutations. • Race Macular degeneration is more likely to be found in whites than in blacks. • Exposure to sunlight especially blue light. There is conflicting evidence as to whether exposure to sunlight contributes to the development of macular degeneration. A recent study in the British Journal of Ophthalmology on 446 subjects found that it does not. High-energy visible light (HEV) has been implicated as a cause of age- related macular degeneration. Signs • Drusen • Pigmentary alterations • Exudative changes: hemorrhages in the eye, hard exudates, subretinal/sub- RPE/intraretinal fluid • Atrophy: incipient and geographic • Visual acuity drastically decreasing (two levels or more) ex: 20/20 to 20/80. Symptoms • Blurred vision: Those with nonexudative macular degeneration may by asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss. • Central scotomas (shadows or missing areas of vision) • Distorted vision (i.e. metamorphopsia ) - A grid of straight lines appears wavy and parts of the grid may appear blank. Patients often first notice this when looking at mini-blinds in their home. • Trouble discerning colors; specifically dark ones from dark ones and light ones from light ones. • Slow recovery of visual function after exposure to bright light The Amsler Grid Test is one of the simplest and most effective methods for patients to monitor the health of the macula. The Amsler Grid is essentially a pattern of intersecting lines (identical to graph paper) with a black dot in the middle. The central black dot is used for fixation (a place for the eye to stare at). With normal vision, all lines surrounding the black dot will look straight and evenly spaced with no missing or odd looking areas when fixating on the grid's central black dot. When there is disease affecting the macula, as in macular degeneration, the lines can look bent, distorted and/or missing. Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains. Other complicating conditions may possibly lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.), but few macular degeneration patients experience total visual loss. The area of the macula comprises about 5% of the retina and is responsible for about 35% of the visual field. The remaining 65% (the peripheral field) remains unaffected by the disease. The loss of central vision profoundly affects visual functioning. It is not possible, for example, to read without central vision. Pictures which attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters 6 inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side.
Recommended publications
  • Screening Guide for Usher Syndrome
    Screening Guide for Usher Syndrome Florida Outreach Project for Children and Young Adults Who Are Deaf-Blind Bureau of Exceptional Education and Student Services Florida Department of Education 2012 This publication was produced through the Bureau of Exceptional Education and Student Services (BEESS) Resource and Information Center, Division of Public Schools, Florida Department of Education, and is available online at http://www.fldoe.org/ese/pub-home.asp. For information on available resources, contact the BEESS Resource and Information Center (BRIC). BRIC website: http://www.fldoe.org/ese/clerhome.asp Bureau website: http://fldoe.org/ese/ Email: [email protected] Telephone: (850) 245-0475 Fax: (850) 245-0987 This document was developed by the Florida Instructional Materials Center for the Visually Impaired, Outreach Services for the Blind/Visually Impaired and Deaf/Hard-of-Hearing, and the Resource Materials and Technology Center for the Deaf/Hard-of-Hearing, special projects funded by the Florida Department of Education, Division of Public Schools, BEESS, through federal assistance under the Individuals with Disabilities Education Act (IDEA), Part B, in conjunction with the Florida Outreach Project for Children and Young Adults Who Are Deaf- Blind, H326C990032, which is funded by the Office of Special Education Programs, U.S. Department of Education. Information contained within this publication does not necessarily reflect the views of the U.S. Department of Education. Edited by: Susan Lascek, Helen Keller National Center Emily Taylor-Snell, Florida Project for Children and Young Adults Who Are Deaf-Blind Dawn Saunders, Florida Department of Education Leanne Grillot, Florida Department of Education Adapted with permission from the Nebraska Usher Syndrome Screening Project (2002) Copyright State of Florida Department of State 2012 Authorization for reproduction is hereby granted to the state system of public education consistent with section 1006.03(2), Florida Statutes.
    [Show full text]
  • Blue Cone Monochromacy: Visual Function and Efficacy Outcome Measures for Clinical Trials
    RESEARCH ARTICLE Blue Cone Monochromacy: Visual Function and Efficacy Outcome Measures for Clinical Trials Xunda Luo1☯‡, Artur V. Cideciyan1☯‡*, Alessandro Iannaccone2, Alejandro J. Roman1, Lauren C. Ditta2, Barbara J. Jennings2, Svetlana A. Yatsenko3, Rebecca Sheplock1, Alexander Sumaroka1, Malgorzata Swider1, Sharon B. Schwartz1, Bernd Wissinger4, Susanne Kohl4, Samuel G. Jacobson1* 1 Scheie Eye Institute, Department of Ophthalmology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America, 2 Hamilton Eye Institute, Department of Ophthalmology, University of Tennessee Health Science Center, Memphis, Tennessee, United States of America, 3 Pittsburgh Cytogenetics Laboratory, Center for Medical Genetics and Genomics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America, 4 Molecular Genetics Laboratory, Institute for Ophthalmic Research, Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany ☯ These authors contributed equally to this work. ‡ OPEN ACCESS These authors are joint first authors on this work. * [email protected] (SGJ); [email protected] (AVC) Citation: Luo X, Cideciyan AV, Iannaccone A, Roman AJ, Ditta LC, Jennings BJ, et al. (2015) Blue Cone Monochromacy: Visual Function and Efficacy Abstract Outcome Measures for Clinical Trials. PLoS ONE 10(4): e0125700. doi:10.1371/journal.pone.0125700 Academic Editor: Dror Sharon, Hadassah-Hebrew University Medical Center, ISRAEL Background Blue Cone Monochromacy (BCM) is an X-linked retinopathy caused by mutations in the Received: December 29, 2014 OPN1LW / OPN1MW gene cluster, encoding long (L)- and middle (M)-wavelength sensitive Accepted: March 21, 2015 cone opsins. Recent evidence shows sufficient structural integrity of cone photoreceptors in Published: April 24, 2015 BCM to warrant consideration of a gene therapy approach to the disease.
    [Show full text]
  • Hereditary Reversion Pigmentation of the Eyelids with Heterochromia of the Iris
    874 LEE MASTEN FRANCIS enucleated. The following report on the Other cells were round with hyper- specimen was submitted from the New chromatic nuclei; while scattered thruout York State Institute for the Study of the tumor were large deeply staining Malignant Diseases: cells with one or two nuclei but free from The gross appearance of a cross sec- pigment. There were apparently two tion of the eye shows a tumor lying in types of pigmented cells, the one a large the lower temporal quadrant of the eye, irregular cell with long protoplasmic evidently springing from the choroid processes densely filled with fine yellow- near the margin of the optic disc. This ish granules, evidently chromatophores. tumor measured 15x10 mm. and was The other type of pigmented cell was a slightly nodular irregular ovoid tumor. evidently a tumor cell of the type men- The surface appeared smooth, was dark tioned above but containing fewer gran- gray in color and was of a soft consist- ules than the chromatophores. Thruout ency. The retina was markedly detached the tumor were small areas of hemor- and contained a clear serous fluid. Cross rhage and between the cells could be section of the tumor mass showed a demonstrated here and there, free pig- deeply pigmented homogeneous surface. ment granules. Microscopically, the tumor varied as From this picture, we would make a to the cellular constituents. There were diagnosis of malignant melanoma, fre- areas showing many pigment cells and quently called melanosarcoma, but by other areas almost free from the same. some authorities considered as melanotic The tumor was very vascular showing many fine capillaries around which in carcinoma.
    [Show full text]
  • Genetic Defects of CHM and Visual Acuity Outcome in 24 Choroideremia
    www.nature.com/scientificreports OPEN Genetic defects of CHM and visual acuity outcome in 24 choroideremia patients from 16 Japanese families Takaaki Hayashi1,2*, Shuhei Kameya3, Kei Mizobuchi2, Daiki Kubota3, Sachiko Kikuchi3, Kazutoshi Yoshitake4, Atsushi Mizota5, Akira Murakami6, Takeshi Iwata4 & Tadashi Nakano2 Choroideremia (CHM) is an incurable progressive chorioretinal dystrophy. Little is known about the natural disease course of visual acuity in the Japanese population. We aimed to investigate the genetic spectrum of the CHM gene and visual acuity outcomes in 24 CHM patients from 16 Japanese families. We measured decimal best-corrected visual acuity (BCVA) at presentation and follow-up, converted to logMAR units for statistical analysis. Sanger and/or whole-exome sequencing were performed to identify pathogenic CHM variants/deletions. The median age at presentation was 37.0 years (range, 5–76 years). The mean follow-up interval was 8.2 years. BCVA of the better-seeing eye at presentation was signifcantly worsened with increasing age (r = 0.515, p < 0.01), with a high rate of BCVA decline in patients > 40 years old. A Kaplan–Meier survival curve suggested that a BCVA of Snellen equivalent 20/40 at follow-up remains until the ffties. Fourteen pathogenic variants, 6 of which were novel [c.49 + 5G > A, c.116 + 5G > A, p.(Gly176Glu, Glu177Ter), p.Tyr531Ter, an exon 2 deletion, and a 5.0-Mb deletion], were identifed in 15 families. No variant was found in one family only. Our BCVA outcome data are useful for predicting visual prognosis and determining the timing of intervention in Japanese patients with CHM variants.
    [Show full text]
  • Neuroophthalmology
    Neuroophthalmology MAREK MICHALEC, MD PHD Clinic of Ophthalmology Faculty Hospital Brno and Masaryk University Version 12/2019 Content • Visual pathway affection • Diseases and affections of optic nerve • Optic chiasm pathology • Pathology of retrochiasmic part • Eye movement disorders • Binocular diplopia • Pupillary reaction abnormalities • Anisocoria • Combined disorders Examination - part I • Medical history • subjective (visual loss, diplopia) • When it started/ how long lasts it? • Does it change in time/ during the day? • Any progression? • What about the fellow eye? • Other signs? • Personal medical history? • Pharmacological history? • objective (pupillary dysfunction, eye movement disorders, ptosis of upper eyelid, red eye) Examination - part II • Visual acuity • Without and with correction • Monocular vision / binocular vision • Basic ophthalmological examination • Anterior segment (by slit lamp) • Posterior segment - arteficial mydriasis is essential (indirect ophthalmoscopy) • Visual field examination (static / kinetic perimetry) Examination - part III • Basic examination (GP) • Neurological examination • Intracranial conditions (including MRI) • neurological signs • Endocrinology • Thyroid associated orbitopathy / ophthalmopathy • Pituitary dysfunction Examination - part IV • Imaging techniques • Ultrasonography (eye bulb, orbit) • X-ray of skull (orbit, paranasal cavities) • Computerised Tomography of head (brain, skull bones, orbital bones) • MRI of head (brain, orbital structures) Optic nerve disorders Clinical signs •
    [Show full text]
  • Color Blindness LEVELED BOOK • W a Reading A–Z Level W Leveled Book Word Count: 1,349 Color Blindness Connections Writing Choose Two Forms of Color Blindness
    Color Blindness LEVELED BOOK • W A Reading A–Z Level W Leveled Book Word Count: 1,349 Color Blindness Connections Writing Choose two forms of color blindness. Write a report that compares the two conditions and their effects on a person’s life. Math Research the statistics about the number of people with the various forms of color blindness in your country. Organize your results in a pie chart. • W Q •T Written by Cheryl Reifsnyder Visit www.readinga-z.com for thousands of books and materials. www.readinga-z.com Words to Know Color ancestry molecules complementary photopigments cone cells prism Blindness defects retina genetic disorder rod cells hereditary wavelengths Photo Credits: Front cover, Back cover: © pretoperola/123RF; title page (Both): © shironosov/ iStock/Thinkstock; page 3: © Véronique Burger/Science Source; page 4 (Both): © Michael Shake/Dreamstime.com; page 5: © Designua/Dreamstime.com; page 6 (top): © Gunilla Elam/Science Source; page 6 (Bottom): © Steve Gschmeissner/Science Source; page 7 (Both): © Ted Kinsman/ Science Source; page 8 (left, Both): © anatchant/iStock/Thinkstock; page 8 (center, Both): © Nadezhda Bolotina/Hemera/Thinkstock; page 8 (right, Both): © iremphotography/iStock/Thinkstock; page 9 (all): © Popartic/iStock Editorial/Thinkstock; page 10: © RVN/Alamy Stock Photo; page 12: © Alexander Kaludov/123RF; page 13: © EnChroma; page 14: © Neitz LaBoratory; page 15: © Phanie/Alamy Stock Photo Written by Cheryl Reifsnyder www.readinga-z.com Focus Question Color Blindness Level W Leveled Book Correlation © Learning A–Z LEVEL W Written By Cheryl Reifsnyder What causes color blindness, and how Fountas & Pinnell S can it affect a person’s life? All rights reserved.
    [Show full text]
  • An Update on Progress and the Changing Epidemiology of Causes of Childhood Blindness Worldwide
    Major Articles An update on progress and the changing epidemiology of causes of childhood blindness worldwide Lingkun Kong, MD, PhD,a Melinda Fry, MPH,b Mohannad Al-Samarraie, MD,a Clare Gilbert, MD, FRCOphth,c and Paul G. Steinkuller, MDa PURPOSE To summarize the available data on pediatric blinding disease worldwide and to present current information on childhood blindness in the United States. METHODS A systematic search of world literature published since 1999 was conducted. Data also were solicited from each state school for the blind in the United States. RESULTS In developing countries, 7% to 31% of childhood blindness and visual impairment is avoidable, 10% to 58% is treatable, and 3% to 28% is preventable. Corneal opacification is the leading cause of blindness in Africa, but the rate has decreased significantly from 56% in 1999 to 28% in 2012. There is no national registry of the blind in the United States, and most schools for the blind do not maintain data regarding the cause of blindness in their students. From those schools that do have such information, the top three causes are cortical visual impairment, optic nerve hypoplasia, and retinopathy of prematurity, which have not changed in past 10 years. CONCLUSIONS There are marked regional differences in the causes of blindness in children, apparently based on socioeconomic factors that limit prevention and treatment schemes. In the United States, the 3 leading causes of childhood blindness appear to be cortical visual impairment, optic nerve hypoplasia, and retinopathy of prematurity; a national registry of the blind would allow accumulation of more complete and reliable data for accurate determination of the prevalence of each.
    [Show full text]
  • Ocular Surface Changes Associated with Ophthalmic Surgery
    Journal of Clinical Medicine Review Ocular Surface Changes Associated with Ophthalmic Surgery Lina Mikalauskiene 1, Andrzej Grzybowski 2,3 and Reda Zemaitiene 1,* 1 Department of Ophthalmology, Medical Academy, Lithuanian University of Health Sciences, 44037 Kaunas, Lithuania; [email protected] 2 Department of Ophthalmology, University of Warmia and Mazury, 10719 Olsztyn, Poland; [email protected] 3 Institute for Research in Ophthalmology, Foundation for Ophthalmology Development, 61553 Poznan, Poland * Correspondence: [email protected] Abstract: Dry eye disease causes ocular discomfort and visual disturbances. Older adults are at a higher risk of developing dry eye disease as well as needing for ophthalmic surgery. Anterior segment surgery may induce or worsen existing dry eye symptoms usually for a short-term period. Despite good visual outcomes, ocular surface dysfunction can significantly affect quality of life and, therefore, lower a patient’s satisfaction with ophthalmic surgery. Preoperative dry eye disease, factors during surgery and postoperative treatment may all contribute to ocular surface dysfunction and its severity. We reviewed relevant articles from 2010 through to 2021 using keywords “cataract surgery”, ”phacoemulsification”, ”refractive surgery”, ”trabeculectomy”, ”vitrectomy” in combina- tion with ”ocular surface dysfunction”, “dry eye disease”, and analyzed studies on dry eye disease pathophysiology and the impact of anterior segment surgery on the ocular surface. Keywords: dry eye disease; ocular surface dysfunction; cataract surgery; phacoemulsification; refractive surgery; trabeculectomy; vitrectomy Citation: Mikalauskiene, L.; Grzybowski, A.; Zemaitiene, R. Ocular Surface Changes Associated with Ophthalmic Surgery. J. Clin. 1. Introduction Med. 2021, 10, 1642. https://doi.org/ 10.3390/jcm10081642 Dry eye disease (DED) is a common condition, which usually causes discomfort, but it can also be an origin of ocular pain and visual disturbances.
    [Show full text]
  • 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 .........................................................................................................................................
    [Show full text]
  • Ministry of Public Health of Ukraine Ukrainian Medical Stomatological Academy
    Ministry of Public Health of Ukraine Ukrainian Medical Stomatological Academy Approved At the meeting of the department of neurological diseases with neurosurgery and medical genetic "__"__ ____________20___ Protocol №________ Head of department _______________ prof. Delva M.Yu. METHODICAL INSTRUCTIONS FOR THE INDEPENDENT WORK OF STUDENTS FOR PREPARATION TO PRACTICAL CLASSES AND DURING PRACTICAL CLASSES Academic subject Neurology The module № 1 General neurology Topic Syndromes of defeat oculomotor nerves. Pathology of olfactory and visual analyzers. Year of study IV Faculty Foreign Students Training (Medicine) Poltava 20___ 1.Relevance of the topic: the olfactory and visual analyzers play a role in receptor function of the nervous system. With the functions of these disorders analyzers, as well as with oculomotor disturbances faced by doctors of different specialties - neurologists, ophthalmologists, neurosurgeons, pediatricians, phthisiatricians, endocrinologists, internists. Violations of the functions of these analyzers is observed in a variety of inflammatory, demyelinating processes, tumors, trauma, endocrine disorders. The correct methodological approach to the study of functions, pathological changes of the olfactory and visual analyzers, oculomotor nerves makes it possible to deliver topical and clinical diagnosis and treatment in a timely manner. 2. Specific Objectives: To investigate the function of I, II, III, IV, VI pairs of cranial nerves, identify signs of a lesion of the nerve disorder Examine the identification functions
    [Show full text]
  • 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.
    [Show full text]
  • BOSTON TERRIER EYE DISEASE Corneal Ulcers and Prevention
    BOSTON TERRIER EYE DISEASE Corneal Ulcers and Prevention Corneal Ulcers are the single largest eye problem in Boston Terriers. Perhaps 1 dog in 10 will experience a corneal ulcer sometime during its life based on the l903 dogs surveyed in the 2000 Boston Terrier Health Survey. The Boston Terrier Standard for the Breed calls for eyes to be “wide apart, large and round and dark in color. The eyes are set square in the skull and the outside corners are on a line with the cheeks as viewed from the front". The ideal Boston Terrier eye does not protrude but is "set square in the skull". Unfortunately the Boston eye is fairly prone to eye injury because of its large size and prominence. Corneal ulcers are caused initially by injury to the eyes. The common practice of removing Boston Terrier whiskers may be a reason that eyes become injured due to lack of sensory feelers. Some breeders do not trim whiskers once a dog's show career is finished because they know that whiskers can prevent injury to the eye. There are a number of external reasons why an injured eye doesn't heal. These may include irritation from eyelashes or from facial hairs, infection, and lack of moisture in the eye. Some of these reasons are hereditary. Internal reasons for an eye not healing include glaucoma and infection. Corneal ulcers can be difficult and expensive to treat and often result in the loss of the eye. This is a case where an "ounce of prevention is worth a pound of cure".
    [Show full text]