Microcoria Due to First Duplication of 13Q32.1 Including the GPR180
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Taking the Mystery out of Abnormal Pupils
Taking the mystery out of abnormal pupils No financial disclosures Course Title: Taking the mystery out [email protected] of abnormal pupils Lecturer: Brad Sutton, OD, FAAO Clinical Professor IU School of Optometry . •Review of Anatomy Iris anatomy Iris sphincter Iris dilator Parasympathetic pathway Sympathetic pathway Parasympathetic Pathway Parasympathetic Pathway Light stimulates the retina then impulse Four neuron arc travels with the ganglion cells through the Retina to the pretectal nucleus in the chiasm into the optic tracts. 80% go to the midbrain (1) LGN , 20% to the pretectal nuclei.They Pretectal nucleus to the EW nucleus (2) then hemidecussate and terminate at the EW nucleus EW nucleus to the ciliary ganglion (3) Ciliary ganglion to the iris sphincter with short ciliary nerves (4) 1 Points of Interest Sympathetic Pathway Within the second order neuron there are Three neuron arc 30 near response fibers for every light Posterior hypothalamus to ciliospinal response fiber. This allows for light - near center of Budge ( C8 - T2 ). (1) dissociation. Center of Budge to the superior cervical The third order neuron runs with cranial ganglion in the neck (2) nerve III from the brain stem to the ciliary Superior cervical ganglion to the dilator ganglion. Superficially located prior to the muscle (3) cavernous sinus. Points of Interest Second order neuron runs along the surface of the lung, can be affected by a Pancoast tumor Third order neuron runs with the carotid artery then with the ophthalmic division of cranial nerve V 2 APD Testing testing……………….AKA……… … APD / reverse APD Direct and consensual response Which is the abnormal pupil ? Very simple rule. -
Miotics in Closed-Angle Glaucoma
Brit. J. Ophthal. (I975) 59, 205 Br J Ophthalmol: first published as 10.1136/bjo.59.4.205 on 1 April 1975. Downloaded from Miotics in closed-angle glaucoma F. GANIAS AND R. MAPSTONE St. Paul's Eye Hospital, Liverpool The initial treatment of acute primary closed-angle Table i Dosage in Groups I, 2, and 3 glaucoma (CAG) is directed towards lowering intraocular pressure (IOP) to normal levels as Group Case no. Duration IOP Time rapidly as possible. To this end, aqueous inflow is (days) (mm. Hg) (hrs) reduced by a drug such as acetazolamide (Diamox), and aqueous outflow is increased via the trabecular I I 2 8 5 meshwork by opening the closed angle with miotics. 3 7 21 3 The use of miotics is of respectable lineage and hal- 5 '4 48 7 lowed by usage, but regimes vary from "intensive" 7 8 I4 5 9 I0 I8 6 (i.e. frequent) to "occasional" (i.e. infrequent) instilla- I I 2 12 6 tions. Finally, osmotic agents are used after a variable '3 5 20 6 interval of time if the IOP remains raised. Tlle pur- I5 '4 I8 6 pose of this paper is to investigate the value of '7 '4 i6 6 miotics in the initial treatment of CAG. I9 6 02 2 2 2 8 2I 5 Material and methods 4 20t 20 6 Twenty patients with acute primary closed-angle glau- 6 I i8 5 http://bjo.bmj.com/ coma were treated, alternately, in one of two ways 8 4 i8 5 detailed below: I0 6 I8 6 I2 I0 20 6 (I) Intravenous Diamox 500 mg. -
Drug Class Review Ophthalmic Cholinergic Agonists
Drug Class Review Ophthalmic Cholinergic Agonists 52:40.20 Miotics Acetylcholine (Miochol-E) Carbachol (Isopto Carbachol; Miostat) Pilocarpine (Isopto Carpine; Pilopine HS) Final Report November 2015 Review prepared by: Melissa Archer, PharmD, Clinical Pharmacist Carin Steinvoort, PharmD, Clinical Pharmacist Gary Oderda, PharmD, MPH, Professor University of Utah College of Pharmacy Copyright © 2015 by University of Utah College of Pharmacy Salt Lake City, Utah. All rights reserved. Table of Contents Executive Summary ......................................................................................................................... 3 Introduction .................................................................................................................................... 4 Table 1. Glaucoma Therapies ................................................................................................. 5 Table 2. Summary of Agents .................................................................................................. 6 Disease Overview ........................................................................................................................ 8 Table 3. Summary of Current Glaucoma Clinical Practice Guidelines ................................... 9 Pharmacology ............................................................................................................................... 10 Methods ....................................................................................................................................... -
Mydriasis Associated with Local Dysfunction of Parasympathetic Nerves in Two Dogs
NOTE Internal Medicine Mydriasis Associated with Local Dysfunction of Parasympathetic Nerves in Two Dogs Teppei KANDA1), Kazuhiro TSUJI1), Keiko HIYAMA2), Takeshi TSUKA1), Saburo MINAMI1), Yoshiaki HIKASA1), Toshinori FURUKAWA3) and Yoshiharu OKAMOTO1)* 1)Department of Veterinary Medicine, Faculty of Agriculture, Tottori University, 4–101, Koyama-minami, Tottori 680–8553, 2)Takamori Animal Hospital, 3706–2, Agarimichi, Sakaiminato, Tottori 684–0033 and 3)Department of Comparative Animal Science, College of Life Science, Kurashiki University of Science and the Arts, 2640, Tsurajima-nishinoura, Kurashiki, Okayama 712–8505, Japan. (Received 13 August 2009/Accepted 16 November 2009/Published online in J-STAGE 9 December 2009) ABSTRACT. In clinical practice, photophobia resulting from persistent mydriasis may be associated with dysfunction of ocular parasympa- thetic nerves or primary iris lesions. We encountered a 5-year-old Miniature Dachshund and a 7-year-old Shih Tzu with mydriasis, abnormal pupillary light reflexes, and photophobia. Except for sustained mydriasis and photophobia, no abnormalities were detected on general physical examination or ocular examination of either dog. We performed pharmacological examinations using 0.1% and 2% pilo- carpine to evaluate and diagnose parasympathetic denervation of the affected pupillary sphincter muscles. On the basis of the results, we diagnosed a pupillary abnormality due to parasympathetic dysfunction and not to overt primary iris lesions. The test revealed that neuroanatomic localization of the lesion was postciliary ganglionic in the first dog. KEY WORDS: autonomic nervous system, canine, mydriasis, ophthalmology, tonic pupil. J. Vet. Med. Sci. 72(3): 387–389, 2010 Mydriasis and miosis are normal physiological reactions and we report herein the clinical features, diagnosis, and that allow the eye to adjust to the level of incoming light. -
COMPLEMENTARY THERAPY ASSESSMENT VISUAL TRAINING for REFRACTIVE ERRORS August 2013
COMPLEMENTARY THERAPY ASSESSMENT VISUAL TRAINING FOR REFRACTIVE ERRORS August 2013 SUMMARY DESCRIPTION OF VISUAL TRAINING Vision training consists of a variety of programs designed to enhance visual efficiency and processing. Vision training, or orthoptics, typically addresses how well both eyes work together. Eye exercises may include, muscle relaxation techniques, biofeedback, eye patches, eye massages, the use of under-corrected prescription lenses, and/or nutritional supplements. Training is most often provided by an optometrist. BENEFITS One randomized controlled trial (RCT) of biofeedback training for control of accommodation for myopia reported no statistically significant benefits from training (Level I evidence). Another RCT (2013), which investigated vision training modalities to evaluate changes in peripheral refraction profiles in myopes, also found no evidence of benefits (Level 1 evidence). In other studies undertaken over the last 60 years, an improvement in subjective visual acuity (VA) in myopes with no corresponding improvement in objective VA has been reported (Level II/III evidence). RISKS The only risk attributable to visual training is financial. Most health insurers do not cover visual training programs. At the start of treatment, the optometrist should provide a reasonable estimate of what improvement to expect and how long it will take. CONCLUSIONS There is Level I evidence that visual training for control of accommodation has no effect on myopia. In other studies (Level II/III evidence), an improvement in subjective VA for patients with myopia that have undertaken visual training has been shown, but no corresponding physiological cause for the improvement has been demonstrated. It is postulated that the improvements in myopic patients noted in these studies were due to improvements in interpreting blurred images, changes in mood or motivation, creation of an artificial contact lens by tear film changes, or a pinhole effect from miosis of the pupil. -
Glaucoma Medical Treatment: Philosophy, Principles and Practice
Glaucoma medical CLIVE MIGDAL treatment: philosophy, principles and practice Abstract assessment of these parameters. Indeed There have been numerous recent advances in compounds are under evaluation that affect the the management of glaucoma, not least the function of the optic nerve (via improved blood development of new drugs to help manage supply or improved neuronal cell physiology) raised intraocular pressure. In addition, the but may or may not lower lOP. It may even be concepts of improving blood flow to the optic possible in the future to therapeutically alter the nerve head and neuroprotection are currently human genome, genetically deliver provoking considerable interest. This article neuroprotective substances or aid regeneration considers the aims and philosophy of of the optic nerve axons. glaucoma drug therapy, summarises some of The main aim of glaucoma therapy must still the basic facts and principles of modem be the preservation of visual function. At the glaucoma medications, and suggests a same time, the therapy should not have adverse practical approach to the choice of therapy. side effects and should not affect the quality of life of the patient (by causing either side effects Key words Blood flow, Intraocular pressure, or inconvenience and disruption of daily Neuroprotection, Primary open angle glaucoma, Topical medications lifestyle). The cost of the therapy, both direct and indirect, must also be taken into consideration.s Currently, typical glaucoma management Philosophy consists of lowering the lOP to a satisfactory Primary open-angle glaucoma is a complex and safe target leve1.6 To determine the success disease for which a number of risk factors have of this treatment, the patient must be followed been identified, including intraocular pressure, long-term with routine assessment of lOP, discs age, race and family history.l,2 Due to our and fields to exclude progressive damage. -
Miotic Adie's Pupils
Journal of Cll/lical Neuro-ophtllJllmology 9(1): 43-45, 1989. RilVen Press, Ltd., New York Miotic Adie's Pupils Michael L. Rosenberg, M.D. Two young adults, aged 24 and 31, had a long history of Adie's syndrome or, pupillotonia, is typically small, poorly reactive pupilS. There was no history of characterized by either unilaterally or bilaterally large pupils, and a review of old photographs confirmed enlarged pupils that are unresponsive to light (1). 10 and 5 years, respectively, of miosis. Both were found to have bilateral tonic pupils that were supersensitive to The diagnosis is made clinically by watching for a diluted pilocarpine. Although it is possible that they had tonic constriction to near stimulation followed by a an unusually early onset of bilateral Adie's syndrome tonic redilatation. with dilated pupils that was not noticed, it is suggested Two young adults are described who were noted that some patients might have primary miotic Adie's during routine examinations to have bilaterally mi pupils without ever passing through a mydriatic phase. Key Words: Adie's syndrome-Argyll Robertson pu otic pupils that were thought to be fixed to light. pils-Miosis. They were both referred for the evaluation of Ar gyll Robertson pupils. Evaluation revealed bilat eral tonic reactions to near stimulation in both pa tients, typical of Adie's tonic pupilS. The diagnosis of parasympathetic denervation was confirmed in both patients as their pupils constricted with di luted pilocarpine. The cases reinforce the principle that any pupil regardless of size should be evalu ated for the possibility of pupillotonia. -
Anisocoria Greater in the Dark: It’S Not Just All About Horner Pupil
RESIDENT & FELLOW SECTION Pearls & Oy-sters: Anisocoria Greater in the Dark: It’s Not Just All About Horner Pupil Emily Witsberger, MD, Sasha A. Mansukhani, MBBS, John J. Chen, MD, PhD, and M. Tariq Bhatti, MD Correspondence Dr. Bhatti Neurology 2021;96:719-722. doi:10.1212/WNL.0000000000011221 ® Bhatti.Muhammad@ mayo.edu Pearls MORE ONLINE c An initial step in the evaluation of anisocoria is assessing the pupillary light reflex. If a pupil Video is not responsive to light, then the near pupillary reflex needs to be evaluated. Unilateral light-near pupil dissociation occurs due to a lesion of the ciliary ganglion, postganglionic parasympathetic pathway, retina, or optic nerve. Oy-sters c In addition to a Horner pupil, anisocoria can be more pronounced in the dark with physiologic anisocoria, miosis due to posterior iris synechiae, pharmacologic miosis due to a parasympathomimetic agent (i.e., pilocarpine), traumatic miosis, iris ischemia, and a chronic Adie tonic pupil. c Adie tonic pupil most frequently presents with a mydriatic pupil, light-near dissociation, vermiform iris sphincter muscle movement, and anisocoria greater in the light. However, a chronic Adie tonic pupil may be characterized by a miotic pupil, light-near dissociation, and anisocoria that is greater in the dark. An asymptomatic 65-year-old patient with no prior ocular surgery but a history of hypertension, hyperlipidemia, and hypothyroidism was noted to have a left miotic pupil during a routine ophthalmic examination. The anisocoria was noted to be greater in the dark and was interpreted as a left Horner pupil. No pharmacologic testing was performed. -
Congenital Horner Syndrome with Heterochromia Iridis Associated with Ipsilateral Internal Carotid Artery Hypoplasia
CASE REPORT Print ISSN 1738-6586 / On-line ISSN 2005-5013 J Clin Neurol 2014 Open Access Congenital Horner Syndrome with Heterochromia Iridis Associated with Ipsilateral Internal Carotid Artery Hypoplasia Fabrice C. Deprez,a Julie Coulier,b Denis Rommel,a Antonella Boschib aDepartments of Radiology and bOphthalmology, Cliniques Universitaires Saint-Luc, UCL, Brussels, Belgium BackgroundzzHorner syndrome (HS), also known as Claude-Bernard-Horner syndrome or Received August 5, 2013 oculosympathetic palsy, comprises ipsilateral ptosis, miosis, and facial anhidrosis. Revised April 15, 2014 Accepted April 21, 2014 Case ReportzzWe report herein the case of a 67-year-old man who presented with congenital HS associated with ipsilateral hypoplasia of the internal carotid artery (ICA), as revealed by Correspondence heterochromia iridis and confirmed by computed tomography (CT). Fabrice C. Deprez, MD Department of Radiology, ConclusionszzCT evaluation of the skull base is essential to establish this diagnosis and dis- Cliniques Universitaires Saint-Luc, tinguish aplasia from agenesis/hypoplasia (by the absence or hypoplasia of the carotid canal) or UCL, Avenue Hippocrate 10, from acquired ICA obstruction as demonstrated by angiographic CT. 1200 Woluwe-Saint-Lambert, J Clin Neurol 2014 Belgium Tel +32.472.93.34.80 Key Wordszzcongenital horner syndrome, internal carotid artery agenesis, Fax +32.81.42.35.05 heterochromia iridis, computed tomography. E-mail [email protected] Introduction spindly left ICA, which was misinterpreted as ICA thrombosis (Fig. 1). The left anterior cerebral artery and MCA were sup- Horner syndrome (HS), also known as Claude-Bernard-Horn- plied by a large posterior communicating artery from the bas- er syndrome or oculosympathetic palsy, comprises ipsilateral ilar artery. -
Ophthalmology
LECTURE NOTES For Health Science Students Ophthalmology Dereje Negussie, Yared Assefa, Atotibebu Kassa, Azanaw Melese University of Gondar In collaboration with the Ethiopia Public Health Training Initiative, The Carter Center, the Ethiopia Ministry of Health, and the Ethiopia Ministry of Education 2004 Funded under USAID Cooperative Agreement No. 663-A-00-00-0358-00. Produced in collaboration with the Ethiopia Public Health Training Initiative, The Carter Center, the Ethiopia Ministry of Health, and the Ethiopia Ministry of Education. Important Guidelines for Printing and Photocopying Limited permission is granted free of charge to print or photocopy all pages of this publication for educational, not-for-profit use by health care workers, students or faculty. All copies must retain all author credits and copyright notices included in the original document. Under no circumstances is it permissible to sell or distribute on a commercial basis, or to claim authorship of, copies of material reproduced from this publication. ©2004 by Dereje Negussie, Yared Assefa, Atotibebu Kassa, Azanaw Melese All rights reserved. Except as expressly provided above, no part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without written permission of the author or authors. This material is intended for educational use only by practicing health care workers or students and faculty in a health care field. PREFACE This lecture note will serve as a practical guideline for the hard-pressed mid-level health workers. We hope that it will be a good introduction to eye diseases for health science students working in Ethiopia. -
Uveitis Is Most Likely Because of an Immune Complex Hypersensitivity
Isolated conjunctival neurofibromas S Fenton and MPh Mourits 665 uveitis is most likely because of an immune complex Sir, hypersensitivity reaction, and not because of any specific Isolated conjunctival neurofibromas at the puncta, 3 toxicity to the eye. It could possibly be related to the an unusual cause of epiphora individual’s previous exposure to streptococcal antigens. Eye (2003) 17, 665–666. doi:10.1038/sj.eye.6700429 Streptokinase may also be associated with other 4 immunological reactions such as serum sickness and We report an unusual case of epiphora caused by 5 Guillain–Barre syndrome. mechanical obstruction of the puncta by isolated Apart from streptokinase, this gentleman also had neurofibromas. diamorphine and cyclizine as part of his immediate medical treatment. Ocular side effects of these drugs include miosis for diamorphine and nonspecific Case report blurred vision for cyclizine. However, anterior uveitis is not a recognised or reported side effect of either A 45-year-old lady, originally from Surinam, presented of these drugs. Hence, streptokinase was thought to be with a 3 year history of epiphora and irritation of both the most likely culprit in this case. Other causes of eyes. There was no other relevant past medical or family acute bilateral hypopyon include Behcet’s disease, history. Visual acuity was normal. External examination HLA B-27 positive status and endogenous revealed ‘hypertrophy’ of the upper and lower puncta endophthalmitis. (Figure 1) of both eyes. Peripheral vascularization of the The widespread use of streptokinase as a thrombolytic cornea and hyperaemia of the conjunctiva were also agent could lead to an increased incidence of this noted. -
Genetics of the Corneal Dystrophies What We Have Learned in the Past Twenty-Five Years
Cornea 19(5): 699–711, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Genetics of the Corneal Dystrophies What We Have Learned in the Past Twenty-five Years Anthony J. Bron, F.R.C.S. Purpose. To indicate important changes in our understanding of The term corneal dystrophy will be used here to define primary, the corneal dystrophies. Methods. A review of the literature of the inherited, bilateral disorders of the cornea affecting transparency last quarter of a century. Results. The earliest clinical classifica- or refraction. Such disorders may or may not disturb vision. At tions of the corneal dystrophies were based on the application of various times in the past they have been said to be of early onset, clinical, biological, histochemical, and ultrastructural methods. axially symmetrical, slowly progressive, or stationary. Earlier defi- Since then, the first great impetus to our understanding has come nitions also required that the affected corneas be free from vascu- from the application of techniques to map disorders to specific chromosome loci, using polymorphic markers. More recently, us- larization and not associated with systemic disease. These are rea- ing candidate gene and related approaches, it has been possible to sonable guidelines, which draw attention to the possibility of a identify genes causing several of the corneal dystrophies and the corneal dystrophy in a given clinical situation. But there are ex- mutations responsible for their phenotypic variation. A notable ceptions to each of these characteristics in conditions generally success has been to show that several important “stromal” dystro- accepted to be corneal dystrophies. Thus, asymmetrical or even phies result from mutations in the gene ig-h3, which encodes for unilateral Meesmann’s and lattice dystrophy are reported, and vas- the protein keratoepithelin (ig-h3).