12 Retina Gabriele K

Total Page:16

File Type:pdf, Size:1020Kb

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). 7. Outer nuclear layer (cell nuclei of the rods and cones = first neuron). 8. Outer limiting membrane (sieve-like plate of processes of glial cells through which rods and cones project). 300 12 Retina Thickness of the retina. Close to the ora At the equator: 0.18 mm serrata: 0.12 mm Around the fovea: 0.23 mm Fovea centralis: 0.10 mm At the optical disk: 0.56 mm Fig. 12.1 Retinal tears most often occur close to the ora serrata. 9. Layer of rods and cones (the actual photoreceptors). 10. Retinal pigment epithelium (a single cubic layer of heavily pigmented epithelial cells). 11. Bruch’s membrane (basal membrane of the choroid separating the retina from the choroid). Macula lutea: The macula lutea is a flattened oval area in the center of the retina approximately 3–4 mm (15 degrees)temporal to and slightly below the optic disk. Its diameter is roughly equal to that of the optic disk (1.7–2 mm). The macula appears yellow when examined under green light, hence the name macula lutea (yellow spot). Located in its center is the avascular fovea Fig. 12.2aLayers of the retina and examination methods used to diagnose abnormal ̈ processes in the respective layers (EOG = electro-oculogram; ERG = electroretinogram; VEP = visual evoked potential). b Histologic image of the 10 layers of the retina. 12.1 Basic Knowledge 301 Histology and function of the layers of the retina. Light 1. Inner limiting membrane 2. Layer of optic nerve fibers Optic nerve VEP 3. Layer of ganglion cells Pattern ERG 4. Inner plexiform layer Amacrine cells 5. Inner nuclear layer Bipolar cells 6. Outer plexiform layer Horizontal cells 7. Outer nuclear layer ERG Photoreceptors 8. Outer limiting membrane 9. Layer of rods and cones Supporting cells of Müller 10. Retinal pigment epithelium EOG 11. Bruch's membrane 1 2 3 4 5 6 7 8 9 10 Fig. 12.2 302 12 Retina centralis, the point at which visual perception is sharpest. The fovea centralis contains only cones (no rods)each with its own neural supply, which explains why this region has such distinct vision. Light stimuli in this region can directly act on the sensory cells (first neuron)because the bipolar cells (sec- ond neuron)and ganglion cells (third neuron)are displaced peripherally. Vascular supply to the retina: The inner layers of the retina (the inner lim- iting membrane through the inner nuclear layer)are supplied by the central artery of the retina. This originates at the ophthalmic artery, enters the eye with the optic nerve, and branches on the inner surface of the retina. The cen- tral artery is a genuine artery with a diameter of 0.1 mm. It is a terminal artery without anastomoses and divides into four main branches (see Fig. 12.8). Because the central artery is a terminal artery, occlusion will lead to reti- nal infarction. The outer layers (outer plexiform layer through the pigment epithelium)con- tain no capillaries. They are nourished by diffusion primarily from the richly supplied capillary layer of the choroid. The retinal arteries are normally bright red, have bright red reflex strips (see Fig. 12.8)that become paler with advancing age, and do not show a pulse. The retinal veins are dark red with a narrow reflex strip, and may show spontaneous pulsation on the optic disk. Pulsation in the retinal veins is normal; pulsation in the retinal arteries is abnormal. The walls of the vessels are transparent so that only the blood will be visible on ophthalmoscopy. In terms of their structure and size, the retinal vessels are arterioles and venules, although they are referred to as arteries and veins. Venous diameter is normally 1.5 times greater than arterial diameter. Capil- laries are not visible. Nerve supply to the retina: The neurosensory retina has no sensory supply. Disorders of the retina are painless because of the absence of sensory supply. Light path through the retinal layers: When electromagnetic radiation in the visible light spectrum (wavelengths of 380–760 nm)strikes the retina, it is absorbed by the photopigments of the outer layer. Electric signals are created in a multi-step photochemical reaction. They reach the photoreceptor synapses as action potentials where they are relayed to the second neuron. The signals are relayed to the third and fourth neurons and finally reach the visual cortex. Light must pass through three layers of cell nuclei before it reaches the photosensitive rods and cones. This inverted position of the photore- ceptors is due to the manner in which the retina develops from a diver- ticulum of the forebrain. 12.1 Basic Knowledge 303 Sensitivity of the retina to light intensity: The retina has two types of pho- toreceptors, the rods and the cones. The 110–125 million rods permit mesopic and scotopic vision (twilight and night vision). They are about 500 times more photosensitive than the cones and contain the photopigment rhodopsin. Twilight vision decreases after the age of 50, particularly in patients with additional age-related miosis, cataract, and decreased visual acu- ity. Therefore, glaucoma patients undergoing treatment with miotic agents should be advised of the danger of operating motor vehicles in twilight or at night. The six to seven million cones in the macula are responsible for photopic vision (daytime vision), resolution, and color perception. There are three types of cones: ❖ blue cones, ❖ green cones, ❖ red cones. Their photopigments contain the same retinal but different opsins. Beyond a certain visual field luminance, a transition from dark adaptation to light adaptation occurs. Luminance refers to the luminous flux per unit solid angle per unit projected area, measured in candelas per square meter (cd/m2). The cones are responsible for vision up to a luminance of 10 cd/m2, the rods up to 0.01 cd/m2 (twilight vision is 0.01–10 cd/m2; night vision is less than 0.01 cd/m2). Adaptation is the adjustment of the sensitivity of the retina to varying degrees of light intensity. This is done by dilation or contraction of the pupil and shifting between cone and rod vision. In this manner, the human eye is able to see in daylight and at night. In light adaptation, the rhodopsin is bleached out so that rod vision is impaired in favor of cone vision. Light adap- tation occurs far more quickly than dark adaptation. In dark adaptation, the rhodopsin quickly regenerates within five minutes (immediate adaptation), and within 30 minutes to an hour there is a further improvement in night vision (long-term adaptation). An adaptometer may be used to determine the light intensity threshold. First the patient is adapted to bright light for 10 minutes. Then the examining room is darkened and the light intensity threshold is measured with light test markers. These measurements can be used to obtain an adaptation curve (Fig. 12.3). Sensitivity to glare: Glare refers to disturbing brightness within the visual field sufficiently greater than the luminance to which the eyes are adapted such as the headlights of oncoming traffic or intense reflected sunlight. Because the retina is adapted to a lesser luminance, vision is impaired in these cases. Often the glare will cause blinking or elicit an eye closing reflex. Sensitivity to glare can be measured with a special device. Patients are shown a series of visual symbols in rapid succession that they must recognize despite intense glare. 304 12 Retina Normal and abnormal dark adaptation curves. cd/m2 3,2 .10–7 3,2 .10–5 3,2 .10–3 3,2 0 10 20 30 40 50 min Fig. 12.3 X axis: adaptation time in minutes. Y axis: luminance of the respective test marker in candelas per square meter. The blue curve shows normal progression with Kohlrausch’s typical discontinuity indicating the transition from cone to rod vi- sion. The red curve in retinitis pigmentosa is considerably less steep. The sensitivity to glare or the speed of adaptation and readaptation of the eye is important in determining whether the patient is fit to operate a motor vehicle.
Recommended publications
  • Morphological Aspect of Tapetum Lucidum at Some Domestic Animals
    Bulletin UASVM, Veterinary Medicine 65(2)/2008 pISSN 1843-5270; eISSN 1843-5378 MORPHOLOGICAL ASPECT OF TAPETUM LUCIDUM AT SOME DOMESTIC ANIMALS Donis ă Alina, A. Muste, F.Beteg, Roxana Briciu University of Angronomical Sciences and Veterinary Medicine Calea M ănăş tur 3-5 Cluj-Napoca [email protected] Keywords: animal ophthalmology, eye fundus, tapetum lucidum. Abstract: The ocular microanatomy of a nocturnal and a diurnal eye are very different, with compromises needed in the arrhythmic eye. Anatomic differences in light gathering are found in the organization of the retina and the optical system. The presence of a tapetum lucidum influences the light. The tapetum lucidum represents a remarkable example of neural cell and tissue specialization as an adaptation to a dim light environment and, despite these differences, all tapetal variants act to increase retinal sensitivity by reflecting light back through the photoreceptor layer. This study propose an eye fundus examination, in animals of different species: cattles, sheep, pigs, dogs cats and rabbits, to determine the presence or absence of tapetum lucidum, and his characteristics by species to species, age and even breed. Our observation were made between 2005 - 2007 at the surgery pathology clinic from FMV Cluj, on 31 subjects from different species like horses, dogs and cats (25 animals). MATERIAL AND METHOD Our observation were made between 2005 - 2007 at the surgery pathology clinic from FMV Cluj, on 30 subjects from different species like cattles, sheep, pigs, dogs cats and rabbits.The animals were halt and the examination was made with minimal tranquilization. For the purpose we used indirect ophthalmoscopy method with indirect ophthalmoscope Heine Omega 2C.
    [Show full text]
  • Current Trends in Ophthalmology Autonomic Regulation of The
    Review Article Current Trends in Ophthalmology Autonomic Regulation of the Function of the Vitreous Body and Retina Lychkova AE1*, Severin AE2, Torshin VI2, Starshinov YP2, Sdobnikova SV3, Ashrafov RA4, Ashrafova SR4, Golubev YY5 Golubeva GY6 and Puzikov AM1 1Department of Health, Moscow’s Clinical Research Center, Moscow, Russia 2Russian People’s Friendship University, Moscow, Russia 3Research Institute of Eye Diseases, Moscow, Russia 4Center for Laser Surgery, Moscow, Russia 5Russian National Research Medical University, Moscow, Russia 6City Clinical Hospital, Moscow, Russia *Correspondence: Lychkova Alla Edward, Department Head of the Moscow’s Clinical Research Center, DZM, Shosse Enthusiasts 86, 111123, 11-1-53, Amundsen 129343, Moscow, Russia, Tel: (+7) 962-965-4923; E-mail: [email protected] Received: May 08, 2018; Accepted: June 25, 2018; Published: June 29, 2018 Abstract The data of the literature on the structure and physiology of the vitreous body and the retina in normal and pathological conditions are presented. The mechanism of vitreous detachment and its role in the development of vitreoretinal proliferation are described. Described adren-choline-peptide and NO-ergic mechanisms in signal transduction of the vitreous body and retina. Pharmacological and surgical methods of treatment of vitreoretinal proliferation are briefly described. Keywords: Vitreous body; Retina; Detachment; Vitreoretinal proliferation Introduction density of collagen fibers and a greater concentration of hyaluronic acid as compared to the central part. Cortical Vitreous Body (VB) is a transparent, colourless, gel- gel is comparatively more stable and more resistant to like mass containing water with an admixture of salts, age-related changes [1]. The VB contains two channels sugars, hyaluronic acid, a network of collagen fibers II, IX, (optociliary and lenticular) and three rows of cisterns, a XI types and few cells (mainly phagocytes, contributing to bursa premacularis and a precapillary space [1,3-5].
    [Show full text]
  • Localisation of Visual Hallucinations
    BRITISH MEDICAL JOURNAL 16 JULY 1977 147 of hypothermia; the duration of cardiac arrest; and the disturbances of sleep or consciousness.4 Hallucinations may be promptness and correctness of treatment. Peterson's pessi- evoked by sensory deprivation, but other factors are usually mistic report from California,8 in which all 15 near-drowned present; thus the "black-patch" delirium that may follow children who had fits, fixed dilated pupils, flaccidity, and loss cataract extraction in the elderly probably results from sensory Br Med J: first published as 10.1136/bmj.2.6080.147 on 16 July 1977. Downloaded from of pain sensation suffered severe anoxic encephalopathy, deprivation and mild senile brain changes and is more frequent may be explained by the high water temperatures there. In when hearing is also impaired.5 warm water the protective effect of hypothermia against brain Hallucinations may be due to focal lesions. Past experiences, damage would be missing. In contrast was the case described the quality of eidetic imagery, and psychodynamic "actors in Trondheim, Norway,9 in which a 5-year-old fell through influence the content of organic hallucinosis,6 and it would be ice in fresh water with an outside temperature of 10° below unwise to lean too heavily on the occurrence and nature of zero centigrade. He was in the water for 22 minutes and was hallucinosis in localising intracranial lesions. Visual hallucina- brought out apparently dead, with widely dilated pupils and tions are a relatively infrequent accompaniment oflesions ofthe bluish white skin. He was warmed up (the method was not calcarine cortex (Brodmann's area 17), which has few thalamo- described) and-despite the risks noted above-was given cortical connections; yet they may occur as a false-localising external cardiac massage without suffering ventricular symptom of frontal or subtentorial lesions.
    [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]
  • Characteristics of Structures and Lesions of the Eye in Laboratory Animals Used in Toxicity Studies
    J Toxicol Pathol 2015; 28: 181–188 Concise Review Characteristics of structures and lesions of the eye in laboratory animals used in toxicity studies Kazumoto Shibuya1*, Masayuki Tomohiro2, Shoji Sasaki3, and Seiji Otake4 1 Testing Department, Nippon Institute for Biological Science, 9-2221-1 Shin-machi, Ome, Tokyo 198-0024, Japan 2 Clinical & Regulatory Affairs, Alcon Japan Ltd., Toranomon Hills Mori Tower, 1-23-1 Toranomon, Minato-ku, Tokyo 105-6333, Japan 3 Japan Development, AbbVie GK, 3-5-27 Mita, Minato-ku, Tokyo 108-6302, Japan 4 Safety Assessment Department, LSI Medience Corporation, 14-1 Sunayama, Kamisu-shi, Ibaraki 314-0255, Japan Abstract: Histopathology of the eye is an essential part of ocular toxicity evaluation. There are structural variations of the eye among several laboratory animals commonly used in toxicity studies, and many cases of ocular lesions in these animals are related to anatomi- cal and physiological characteristics of the eye. Since albino rats have no melanin in the eye, findings of the fundus can be observed clearly by ophthalmoscopy. Retinal atrophy is observed as a hyper-reflective lesion in the fundus and is usually observed as degenera- tion of the retina in histopathology. Albino rats are sensitive to light, and light-induced retinal degeneration is commonly observed because there is no melanin in the eye. Therefore, it is important to differentiate the causes of retinal degeneration because the lesion occurs spontaneously and is induced by several drugs or by lighting. In dogs, the tapetum lucidum, a multilayered reflective tissue of the choroid, is one of unique structures of the eye.
    [Show full text]
  • Onchocerciasis
    11 ONCHOCERCIASIS ADRIAN HOPKINS AND BOAKYE A. BOATIN 11.1 INTRODUCTION the infection is actually much reduced and elimination of transmission in some areas has been achieved. Differences Onchocerciasis (or river blindness) is a parasitic disease in the vectors in different regions of Africa, and differences in cause by the filarial worm, Onchocerca volvulus. Man is the the parasite between its savannah and forest forms led to only known animal reservoir. The vector is a small black fly different presentations of the disease in different areas. of the Simulium species. The black fly breeds in well- It is probable that the disease in the Americas was brought oxygenated water and is therefore mostly associated with across from Africa by infected people during the slave trade rivers where there is fast-flowing water, broken up by catar- and found different Simulium flies, but ones still able to acts or vegetation. All populations are exposed if they live transmit the disease (3). Around 500,000 people were at risk near the breeding sites and the clinical signs of the disease in the Americas in 13 different foci, although the disease has are related to the amount of exposure and the length of time recently been eliminated from some of these foci, and there is the population is exposed. In areas of high prevalence first an ambitious target of eliminating the transmission of the signs are in the skin, with chronic itching leading to infection disease in the Americas by 2012. and chronic skin changes. Blindness begins slowly with Host factors may also play a major role in the severe skin increasingly impaired vision often leading to total loss of form of the disease called Sowda, which is found mostly in vision in young adults, in their early thirties, when they northern Sudan and in Yemen.
    [Show full text]
  • 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
    [Show full text]
  • Visual Perception in Migraine: a Narrative Review
    vision Review Visual Perception in Migraine: A Narrative Review Nouchine Hadjikhani 1,2,* and Maurice Vincent 3 1 Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA 2 Gillberg Neuropsychiatry Centre, Sahlgrenska Academy, University of Gothenburg, 41119 Gothenburg, Sweden 3 Eli Lilly and Company, Indianapolis, IN 46285, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-617-724-5625 Abstract: Migraine, the most frequent neurological ailment, affects visual processing during and between attacks. Most visual disturbances associated with migraine can be explained by increased neural hyperexcitability, as suggested by clinical, physiological and neuroimaging evidence. Here, we review how simple (e.g., patterns, color) visual functions can be affected in patients with migraine, describe the different complex manifestations of the so-called Alice in Wonderland Syndrome, and discuss how visual stimuli can trigger migraine attacks. We also reinforce the importance of a thorough, proactive examination of visual function in people with migraine. Keywords: migraine aura; vision; Alice in Wonderland Syndrome 1. Introduction Vision consumes a substantial portion of brain processing in humans. Migraine, the most frequent neurological ailment, affects vision more than any other cerebral function, both during and between attacks. Visual experiences in patients with migraine vary vastly in nature, extent and intensity, suggesting that migraine affects the central nervous system (CNS) anatomically and functionally in many different ways, thereby disrupting Citation: Hadjikhani, N.; Vincent, M. several components of visual processing. Migraine visual symptoms are simple (positive or Visual Perception in Migraine: A Narrative Review. Vision 2021, 5, 20. negative), or complex, which involve larger and more elaborate vision disturbances, such https://doi.org/10.3390/vision5020020 as the perception of fortification spectra and other illusions [1].
    [Show full text]
  • Vitreous and Developmental Vitreoretinopathies Kevin R
    CHAPTER 3 Vitreous and Developmental Vitreoretinopathies Kevin R. Tozer, Kenneth M. P. Yee, and J. Sebag Invisible (Fig. 3.1) by design, vitreous was long unseen the central vitreous and adjacent to the anterior cortical as important in the physiology and pathology of the eye. gel. HA molecules have a different distribution from col- Recent studies have determined that vitreous plays a sig- lagen, being most abundant in the posterior cortical gel nificant role in ocular health (1) and disease (1,2), includ- with a gradient of decreasing concentration centrally ing a number of important vitreoretinal disorders that and anteriorly (6,7). arise from abnormal embryogenesis and development. Both collagen and HA are synthesized during child- Vitreous embryology is presented in detail in Chapter 1. hood. Total collagen content in the vitreous gel remains Notable is that primary vitreous is filled with blood ves- at about 0.05 mg until the third decade (8). As collagen sels during the first trimester (Fig. 3.2). During the second does not appreciably increase during this time but the trimester, these vessels begin to disappear as the second- size of the vitreous does increase with growth, the den- ary vitreous is formed, ultimately resulting in an exqui- sity of collagen fibrils effectively decreases. This could sitely clear gel (Fig. 3.1). The following will review vitreous potentially weaken the collagen network and destabilize development and the congenital disorders that arise from the gel. However, since there is active synthesis of HA abnormalities in hyaloid vessel formation and regression during this time, the dramatic increase in HA concentra- during the primary vitreous stage and biochemical abnor- tion may stabilize the thinning collagen network (9).
    [Show full text]
  • MOC PORT/DOCK Practice Core Modules Content Outline
    MOC PORT/DOCK Practice Core Modules Content Outline 1 Cataract and Anterior Segment (10%) 1.1 Basic Anatomical and Scientific Aspects 1.1.1 The Normal Lens 1.1.1.1 Anatomy 1.2 Assessment Techniques 1.2.1 History-Taking and Preoperative Examination of Ocular Structures 1.2.1.1 Take patient history 1.2.1.2 Examine ocular structures 1.2.1.3 Signs and symptoms 1.2.1.4 Indications for surgery 1.2.1.6 External examination 1.2.1.7 Slit-lamp examination 1.2.1.8 Fundus evaluation 1.2.1.9 Impact on visual functioning and quality of life 1.2.2 Measurement of Visual and Macular Function 1.2.2.1 Visual acuity testing 1.2.2.2 Test visual acuity 1.2.2.5 Visual field testing 1.2.2.6 Test visual field 1.2.2.7 Cataract's effect on visual acuity 1.2.2.8 Estimate cataract's effect on visual acuity 1.2.2.10 Measure visual (and macular) function 1.2.4.3 Evaluate glare disability: subjective and objective 1.3 Clinical Disease Conditions and Manifestations 1.3.1 Types of Cataract 1.3.1.1 Identify types of cataracts 1.3.2 Anterior Segment Disorders 1.3.2.1 Diagnose anterior segment disorders 1.3.2.2 Cataract associated with uveitis 1.3.2.3 Diabetes mellitus and cataract formation 1.3.2.4 Lens-induced glaucoma 1.3.2.4.1 Lens particle 1.3.2.4.2 Phacolytic 1.3.2.4.3 Phacomorphic Copyright and Use Policy for ABO Content Outlines © 2017 – American Board of Ophthalmology.
    [Show full text]
  • 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.
    [Show full text]
  • Passport to Success
    The following terms and other boldface terms in the chapter are defined in the Glossary accommodation choroid After careful study of this chapter, you should be able to: cochlea conjunctiva 1. Describe the function of the sensory system convergence 2. Differentiate between the special and general senses and give examples of each cornea 3. Describe the structure of the eye gustation 4. List and describe the structures that protect the eye lacrimal apparatus 5. Define refraction and list the refractive parts of the eye lens (crystalline lens) 6. Differentiate between the rods and the cones of the eye olfaction 7. Compare the functions of the extrinsic and intrinsic muscles of organ of Corti the eye ossicle 8. Describe the nerve supply to the eye proprioceptor 9. Describe the three divisions of the ear refraction 10. Describe the receptor for hearing and explain how it functions retina 11. Compare static and dynamic equilibrium and describe the sclera location and function of these receptors semicircular canal 12. Explain the function of proprioceptors sensory adaptation 13. List several methods for treatment of pain sensory receptor 14. Describe sensory adaptation and explain its value tympanic membrane 15. Show how word parts are used to build words related to the vestibule sensory system (see Word Anatomy at the end of the chapter) vitreous body PASSport to Success Visit thePoint or see the Student Resource CD in the back of this book for definitions and pronun- ciations of key terms as well as a pretest for this chapter. ® Paul’s Second Case: Seeing More of the Sun’s Effects aul glanced once again at the postcard condition, and it does have a hereditary fac- sitting on his entranceway table as he ar- tor.” The doctor dilated Paul’s eyes with drops Prived home in the evening.
    [Show full text]