FUCHS' UVEITIS SYNDROME: NO LONGER a SYNDROME? Elke

Total Page:16

File Type:pdf, Size:1020Kb

FUCHS' UVEITIS SYNDROME: NO LONGER a SYNDROME? Elke Academiejaar 2010 - 2011 FUCHS’ UVEITIS SYNDROME: NO LONGER A SYNDROME? Elke KREPS Promotor: Prof. Dr. Ph. Kestelyn Scriptie voorgedragen in de 2de Master in het kader van de opleiding tot MASTER IN DE GENEESKUNDE Acknowledgements I am very grateful to my supervisor, Professor Kestelyn, for his guidance and constructive criticism that enabled me to develop insight into the subject. I would also like to thank Dirk Desmet for his much appreciated linguistic assistance. Many thanks also go to Thierry Dervaux for his helpful comments on the first draft of this work and to Professor Van Maele for his statistical advice. Table of content ABSTRACT (ENGLISH) .................................................................................................................................................. 1 ABSTRACT (NEDERLANDS) .......................................................................................................................................... 2 1. INTRODUCTION ...................................................................................................................................................... 3 1.1 INTRODUCTION ............................................................................................................................................................. 3 1.2 MATERIALS AND METHODS .............................................................................................................................................. 4 2. CLINICAL FEATURES ................................................................................................................................................ 5 2.1 EPIDEMIOLOGY ............................................................................................................................................................. 5 2.2 TERMINOLOGY .............................................................................................................................................................. 5 2.3 CLINICAL SYMPTOMS AT PRESENTATION ............................................................................................................................. 6 2.4 CLINICAL SIGNS ............................................................................................................................................................. 6 2.4.1 Cornea ............................................................................................................................................................... 7 2.4.2 Anterior chamber .............................................................................................................................................. 7 2.4.3 Iris ...................................................................................................................................................................... 8 2.4.3.1 The normal iris ..............................................................................................................................................................8 2.4.3.2 Inflammation .................................................................................................................................................................8 2.4.3.3 Iris atrophy ....................................................................................................................................................................9 2.4.3.4 Heterochromia ..............................................................................................................................................................9 2.4.3.5 Bilateral cases..............................................................................................................................................................10 2.4.3.6 Iris nodules ..................................................................................................................................................................11 2.4.4 Anterior chamber angle .................................................................................................................................. 12 2.4.5 Lens ................................................................................................................................................................. 13 2.4.6 Vitreous cavity ................................................................................................................................................. 13 2.4.7 Fundus ............................................................................................................................................................. 14 2.5 DIAGNOSTIC CRITERIA ................................................................................................................................................... 14 3. COMPLICATIONS ....................................................................................................................................................16 3.1 CATARACT .................................................................................................................................................................. 16 3.1.1 Surgical procedure .......................................................................................................................................... 16 3.1.2 Postoperative complications ........................................................................................................................... 17 3.2 GLAUCOMA ................................................................................................................................................................ 19 3.2.1 Etiology of secondary glaucoma ..................................................................................................................... 19 3.2.2 Management................................................................................................................................................... 20 3.3 VITREOUS OPACITIES AND VITRECTOMY ............................................................................................................................ 21 4. TREATMENT AND PROGNOSIS ...............................................................................................................................21 5. IMMUNOLOGY AND PATHOGENESIS .....................................................................................................................22 5.1 ULTRASTRUCTURE OF THE IRIS ........................................................................................................................................ 22 5.2 CELLULAR COMPONENTS OF THE AQUEOUS ....................................................................................................................... 23 5.3 HUMORAL COMPONENTS OF THE AQUEOUS ...................................................................................................................... 23 5.4 CHARACTERISTICS OF INFLAMMATION .............................................................................................................................. 24 5.5 AUTO-IMMUNITY ......................................................................................................................................................... 24 6. ETIOLOGY ...............................................................................................................................................................25 6.1 FUCHS’ THEORY ........................................................................................................................................................... 25 6.2 THE ORTHOSYMPATHETIC THEORIES ................................................................................................................................. 25 6.2.1 Lesions of trophic fibers .................................................................................................................................. 25 6.2.2 Lesions of the orthosympathicus ..................................................................................................................... 26 6.2.3 Status dysraphicus ........................................................................................................................................... 27 6.2.4 Association with the syndrome of Parry-Romberg .......................................................................................... 27 6.3 INHERITANCE .............................................................................................................................................................. 28 6.4 VASCULAR THEORY ....................................................................................................................................................... 29 6.5 OCULAR TRAUMA ........................................................................................................................................................ 30 6.6 INFECTIOUS AGENTS ..................................................................................................................................................... 30 6.6.1 Toxoplasma gondii ........................................................................................................................................... 30 6.6.2 Herpes Simplex Virus (HSV) ............................................................................................................................. 33 6.6.3 Cytomegalovirus (CMV)..................................................................................................................................
Recommended publications
  • 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).
    [Show full text]
  • Ophthalmic Pathologies in Female Subjects with Bilateral Congenital Sensorineural Hearing Loss
    Turkish Journal of Medical Sciences Turk J Med Sci (2016) 46: 139-144 http://journals.tubitak.gov.tr/medical/ © TÜBİTAK Research Article doi:10.3906/sag-1411-82 Ophthalmic pathologies in female subjects with bilateral congenital sensorineural hearing loss 1, 2 3 4 5 Mehmet Talay KÖYLÜ *, Gökçen GÖKÇE , Güngor SOBACI , Fahrettin Güven OYSUL , Dorukcan AKINCIOĞLU 1 Department of Ophthalmology, Tatvan Military Hospital, Bitlis, Turkey 2 Department of Ophthalmology, Kayseri Military Hospital, Kayseri, Turkey 3 Department of Ophthalmology, Faculty of Medicine, Hacettepe University, Ankara, Turkey 4 Department of Public Health, Gülhane Military Medical School, Ankara, Turkey 5 Department of Ophthalmology, Gülhane Military Medical School, Ankara, Turkey Received: 15.11.2014 Accepted/Published Online: 24.04.2015 Final Version: 05.01.2016 Background/aim: The high prevalence of ophthalmologic pathologies in hearing-disabled subjects necessitates early screening of other sensory deficits, especially visual function. The aim of this study is to determine the frequency and clinical characteristics of ophthalmic pathologies in patients with congenital bilateral sensorineural hearing loss (SNHL). Materials and methods: This descriptive study is a prospective analysis of 78 young female SNHL subjects who were examined at a tertiary care university hospital with a detailed ophthalmic examination, including electroretinography (ERG) and visual field tests as needed. Results: The mean age was 19.00 ± 1.69 years (range: 15 to 24 years). A total of 39 cases (50%) had at least one ocular pathology. Refractive errors were the leading problem, found in 35 patients (44.9%). Anterior segment examination revealed heterochromia iridis or Waardenburg syndrome in 2 cases (2.56%).
    [Show full text]
  • Differentiate Red Eye Disorders
    Introduction DIFFERENTIATE RED EYE DISORDERS • Needs immediate treatment • Needs treatment within a few days • Does not require treatment Introduction SUBJECTIVE EYE COMPLAINTS • Decreased vision • Pain • Redness Characterize the complaint through history and exam. Introduction TYPES OF RED EYE DISORDERS • Mechanical trauma • Chemical trauma • Inflammation/infection Introduction ETIOLOGIES OF RED EYE 1. Chemical injury 2. Angle-closure glaucoma 3. Ocular foreign body 4. Corneal abrasion 5. Uveitis 6. Conjunctivitis 7. Ocular surface disease 8. Subconjunctival hemorrhage Evaluation RED EYE: POSSIBLE CAUSES • Trauma • Chemicals • Infection • Allergy • Systemic conditions Evaluation RED EYE: CAUSE AND EFFECT Symptom Cause Itching Allergy Burning Lid disorders, dry eye Foreign body sensation Foreign body, corneal abrasion Localized lid tenderness Hordeolum, chalazion Evaluation RED EYE: CAUSE AND EFFECT (Continued) Symptom Cause Deep, intense pain Corneal abrasions, scleritis, iritis, acute glaucoma, sinusitis, etc. Photophobia Corneal abrasions, iritis, acute glaucoma Halo vision Corneal edema (acute glaucoma, uveitis) Evaluation Equipment needed to evaluate red eye Evaluation Refer red eye with vision loss to ophthalmologist for evaluation Evaluation RED EYE DISORDERS: AN ANATOMIC APPROACH • Face • Adnexa – Orbital area – Lids – Ocular movements • Globe – Conjunctiva, sclera – Anterior chamber (using slit lamp if possible) – Intraocular pressure Disorders of the Ocular Adnexa Disorders of the Ocular Adnexa Hordeolum Disorders of the Ocular
    [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]
  • 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]
  • A Description of the Clinical Features of Brimonidine- Associated Uveitis Alyssa Louie Primary Care Resident, San Francisco VA
    Drug-induced intraocular inflammation: A description of the clinical features of brimonidine- associated uveitis Alyssa Louie Primary Care Resident, San Francisco VA Abstract: A description of the clinical features, diagnostic work-up, and management of acute anterior uveitis caused by brimonidine, a widely used glaucoma medication. I. Case History a. Patient demographics: 74 year-old white male b. Chief complaint: eye pain, redness, irritation for last 2 weeks c. Ocular and medical history: i. Ocular history 1. Primary open angle glaucoma OU, diagnosed 8 years ago 2. Senile cataracts OU, not visually significant 3. Type 2 Diabetes without retinopathy OU 4. No prior history of uveitis ii. Medical history: Diabetes Mellitus Type 2 iii. No known drug allergies d. Medications i. Ocular: dorzolamide BID OU (1.5 years), brimonidine BID OU (11 months), travatan QHS OU (5.5 years) ii. Medical: metformin 500mg tab BID PO II. Pertinent Findings a. Clinical exam i. Visual acuities: OD 20/20-, OS 20/20- ii. Goldmann applanation tonometry: 13 mm Hg OD, 13 mm Hg OS iii. Anterior segment 1. OU: 3+ diffuse conjunctival injection 2. OU: central and inferior granulomatous keratic precipitates 3. OU: Grade 1+ cell, 1+ flare 4. OU: No synechiae or iris changes were present iv. Posterior segment 1. Optic Nerve a. OD: Cup-to-disc ratio 0.70H/V, distinct margins b. OS: Cup-to-disc ratio 0.75H/V, distinct margins 2. Posterior pole, periphery, vitreous: unremarkable OU b. Laboratory Studies i. ACE, Lysozyme, FTA-ABS, VDRL, HLA-B27, Rheumatoid Factor, ANA, PPD, Chest X- ray: all negative/unreactive III.
    [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]
  • Anterior Segment Ischemia with Rubeosis Iridis After A
    ANTERIOR SEGMENT ISCHEMIA WITH RUBEOSIS IRIDIS AFTER A CIRCULAR BUCKLING OPERATION TREATED SUCCESSFULLY WITH AN INTRAVITREAL BEVACIZUMAB INJECTION: A CASE REPORT AND REVIEW OF THE LITERATURE JANSSENS K, ZEYEN T, VAN CALSTER J ABSTRACT ly detection of rubeosis iridis. This report demon- strates the rapid resolution of rubeosis iridis on iris Purpose: To report a case of anterior segment ischemia fluorescein angiography after a second intravitreal in- (ASI) with rubeosis iridis after circular buckling sur- jection of bevacizumab. How long this regression will gery in a highly-myopic patient which was success- persist is unknown and repeated injections of fully treated with a second intravitreal bevacizumab bevacizumab may be necessary if rubeosis re- injection. appears. Methods: Case report and review of the literature. KEYWORDS Discussion: ASI is a rare but potentially serious com- plication of posterior segment surgery. Finally it leads Anterior segment ischemia (ASI); rubeosis iridis; to neovascular glaucoma as a result of rubeosis iri- neovascular glaucoma (NVG); circular buckling dis. An encircling band can compromise anterior seg- surgery; intravitreal bevacizumab (IVB); iris ment circulation in different ways: by manipulation fluorescein angiography. or disinsertion of the recti muscles, by occlusion of the vortex veins through compression or by changes in the blood supply of iris and ciliary body. This pa- tient developed rubeosis iridis secondary to ASI. There was a remarkable regression of rubeosis iridis one month after a second intravitreal bevacizumab in- jection. Other case reports of bevacizumab use in neovascular glaucoma have shown clinical improve- ments of these patients, with intraocular pressure control and reduction of the neovascularization process.
    [Show full text]
  • Reiter's Syndrome
    iMedPub JOURNALS ARCHIVES OF MEDICINE | 2009 | Vol. 1 | No. 1:1 | doi: 10.3823/032 Review Reiter's Syndrome Digna Llorente Molina, Susandra Cedeño Facultad de Ciencias Médicas 10 de Octubre. Ciudad Habana, Cuba. E-mail: [email protected] Reiter’s syndrome is a systemic disorder characterized by ocular conjunctivitis or uveitis, reactive arthritis, and urethritis manifestations. The exact cause of reactive arthritis is unknown. It occurs most commonly in men before the age of 40. It may follow an infection with Chlamydia, Campylobacter, Salmonella or Yersinia. Certain genes may make you more prone to the syndrome. The diagnosis is based on symptoms. The goal of treatment is to relieve symptoms and treat any underlying infection. Reactive arthritis may go away in 3 - 4 months, but symptoms may return over a period of several years in up to a half of those affected. The condition may become chronic. Preventing sexually transmitted diseases and gastrointestinal infection may help prevent this disease. Wash your hands and surface areas thoroughly before and after preparing food. © Archives of Medicine: Accepted after external review ■ The first description of Reiter’s syndrome was attributed in occasionally, cutaneous-mucosal lesions such as keratodermia 1916 to the re-known German physician Hans Reiter, linked to blennorrhagica and balanitis circinata; yellow papule lesions Nazi powers, and to his experiments in the concentration on the soles, palms and with less frequency on the nails, camps. In 1918, Junghanns described the first case in a young scrotum, scalp and trunk, amongst others (3), (4), (5).. The patient (1), (2). earliest manifestation of joint disorder is entesitis, normally in the Achilles tendon and in the plantar fascia of the calcaneus, Due to the syndrome’s abnormal immunological reactivity to causing shortening or lengthening of fingers and toes certain pathogens as a result of the interaction between resembling "sausage fingers and toes".
    [Show full text]
  • The Uveo-Meningeal Syndromes
    ORIGINAL ARTICLE The Uveo-Meningeal Syndromes Paul W. Brazis, MD,* Michael Stewart, MD,* and Andrew G. Lee, MD† main clinical features being a meningitis or meningoenceph- Background: The uveo-meningeal syndromes are a group of disorders that share involvement of the uvea, retina, and meninges. alitis associated with uveitis. The meningeal involvement is Review Summary: We review the clinical manifestations of uveitis often chronic and may cause cranial neuropathies, polyra- and describe the infectious, inflammatory, and neoplastic conditions diculopathies, and hydrocephalus. In this review we define associated with the uveo-meningeal syndrome. and describe the clinical manifestations of different types of Conclusions: Inflammatory or autoimmune diseases are probably uveitis and discuss the individual entities most often associ- the most common clinically recognized causes of true uveo-menin- ated with the uveo-meningeal syndrome. We review the geal syndromes. These entities often cause inflammation of various distinctive signs in specific causes for uveo-meningeal dis- tissues in the body, including ocular structures and the meninges (eg, ease and discuss our evaluation of these patients. Wegener granulomatosis, sarcoidosis, Behc¸et disease, Vogt-Koy- anagi-Harada syndrome, and acute posterior multifocal placoid pig- ment epitheliopathy). The association of an infectious uveitis with an acute or chronic meningoencephalitis is unusual but occasionally the eye examination may suggest an infectious etiology or even a The uveo-meningeal syndromes are a specific organism responsible for a meningeal syndrome. One should consider the diagnosis of primary ocular-CNS lymphoma in heterogeneous group of disorders that share patients 40 years of age or older with bilateral uveitis, especially involvement of the uvea, retina, and meninges.
    [Show full text]
  • Management of Chronic Anterior Uveitis Relapses: Efficacy of Oral Phospholipidic Curcumin Treatment. Long-Term Follow-Up
    Clinical Ophthalmology Dovepress open access to scientific and medical research Open Access Full Text Article ORIGINAL RESEARCH Management of chronic anterior uveitis relapses: efficacy of oral phospholipidic curcumin treatment. Long-term follow-up Pia Allegri1 Abstract: Curcumin has been successfully applied to treat inflammatory conditions in Antonio Mastromarino1 experimental research and in clinical trials. The purpose of our study is to evaluate the efficacy Piergiorgio Neri2 of an adjunctive-to-traditional treatment with Norflo tablets (curcumin-phosphatidylcholine complex; Meriva) administered twice a day in recurrent anterior uveitis of different etiologies. The 1Uveitis Center, Ophthalmological Department of Lavagna Hospital, study group consisted of 106 patients who completed a 12-month follow-up therapeutic period. Genova, Italy; 2Uveitis Unit, The We divided the patients into three main groups of different uveitis origin: group 1 (autoimmune Eye Clinic, Azienda Ospedaliero- uveitis), group 2 (herpetic uveitis), and group 3 (different etiologies of uveitis). The primary Universitaria, Ospedali Riuniti di Ancona, Ancona, Italy end point of our work was the evaluation of relapse frequency in all treated patients, before and after Norflo treatment, followed by the number of relapses in the three etiological groups. Wilcoxon signed-rank test showed a P , 0.001 in all groups. The secondary end points were the evaluation of relapse severity and of the overall quality of life. The results showed that Norflo was well tolerated and could reduce eye discomfort symptoms and signs after a few weeks of treatment in more than 80% of patients. In conclusion, our study is the first to report the potential therapeutic role of curcumin and its efficacy in eye relapsing diseases, such as anterior uveitis, and points out other promising curcumin-related benefits in eye inflammatory and degenerative conditions, such as dry eye, maculopathy, glaucoma, and diabetic retinopathy.
    [Show full text]
  • Causes of Heterochromia Iridis with Special Reference to Paralysis Of
    CAUSES OF HETEROCHROMIA IRIDIS WITH SPECIAL REFER- ENCE TO PARALYSIS OF THE CERVICAL SYMPATHETIC. F. PHINIZY CALHOUN, M. D. ATLANTA, GA. This abstract of a candidate's thesis presented for membership in the American Ophthal- mological Society, includes the reports of cases, a general review of the literature of the sub- ject, the results of experiments, and histologic observations on the effect of extirpation of the cervical sympathetic in the rab'bit, the conclusions reached from the investigation, and a bib- liography. That curious condition which con- thinks that the word hetcrochromia sists in a difference in the pigmentation should apply to those cases in which of the two eyes, is regarded by the parts of the same iris have different casual observer as a play or caprice of colors. In those cases where a cycli- nature. This phenomenon has for cen- tis accompanies the iris decoloration, turies been noted, and was called hcte- Butler8 uses the term "heterochromic roglaucus by Aristotle1. One who cyclitis," but the "Chronic Cyclitis seriously studies the subject, is at once with Decoloration of the Iris" as de- impressed with the complexity of the scribed by Fuchs" undoubtedly gives a situation, and soon learns that nature more accurate description of the dis- plays a comparatively small part in its ease, notwithstanding its long title. causation. It is however only within The commonly accepted and most uni- a comparatively recent time that the versally used term Hetcrochromia Iri- pathologic aspect has been considered, dis exactly expresses and implies the and in this discussion I especially wish picture from its derivation (irtpoa to draw attention to that part played other, xpw/xa) color.
    [Show full text]