Neurology of Vision 1. Lens Develops from A. Neural Ectoderm B. Surface
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Pupillary Disorders LAURA J
13 Pupillary Disorders LAURA J. BALCER Pupillary disorders usually fall into one of three major cat- cortex generally do not affect pupillary size or reactivity. egories: (1) abnormally shaped pupils, (2) abnormal pupillary Efferent parasympathetic fibers, arising from the Edinger– reaction to light, or (3) unequally sized pupils (anisocoria). Westphal nucleus, exit the midbrain within the third nerve Occasionally pupillary abnormalities are isolated findings, (efferent arc). Within the subarachnoid portion of the third but in many cases they are manifestations of more serious nerve, pupillary fibers tend to run on the external surface, intracranial pathology. making them more vulnerable to compression or infiltration The pupillary examination is discussed in detail in and less susceptible to vascular insult. Within the anterior Chapter 2. Pupillary neuroanatomy and physiology are cavernous sinus, the third nerve divides into two portions. reviewed here, and then the various pupillary disorders, The pupillary fibers follow the inferior division into the orbit, grouped roughly into one of the three listed categories, are where they then synapse at the ciliary ganglion, which lies discussed. in the posterior part of the orbit between the optic nerve and lateral rectus muscle (Fig. 13.3). The ciliary ganglion issues postganglionic cholinergic short ciliary nerves, which Neuroanatomy and Physiology initially travel to the globe with the nerve to the inferior oblique muscle, then between the sclera and choroid, to The major functions of the pupil are to vary the quantity of innervate the ciliary body and iris sphincter muscle. Fibers light reaching the retina, to minimize the spherical aberra- to the ciliary body outnumber those to the iris sphincter tions of the peripheral cornea and lens, and to increase the muscle by 30 : 1. -
May Clinical-Sharma (Pdf 143KB)
CLINICAL New-onset ptosis initially diagnosed as conjunctivitis Neil Sharma, Ju-Lee Ooi, Rebecca Davie, Palvi Bhardwaj Case Question 2 divides into superior and inferior branches, Joe, 66 years of age, was referred with What are the causes of an isolated which enter the orbit through the superior a 2-week history of a right upper eyelid oculomotor nerve palsy? orbital fissure. abnormality. He complained of associated The superior division innervates diplopia initially, but this subjectively Question 3 the levator palpebrae superioris and improved after a few days as the eye What clinical features raise the index of superior rectus, while the inferior division became more difficult to open. He had a suspicion of a compressive lesion? mild, intermittent headache for 4 weeks, relieved with oral paracetamol. There Question 4 were no other neurological symptoms. What investigation does this patient He had no other symptoms of giant cell urgently require? arteritis. His past medical history included hypercholesterolaemia for which he was Case continued taking regular statin therapy. He was an Joe was referred for an urgent CT ex-smoker with a 40 pack-year history. angiogram. This showed a large Initially, Joe’s general practitioner (GP) unruptured posterior communicating diagnosed conjunctivitis and prescribed artery aneurysm (Figure 1). He was chloramphenicol drops four times daily. admitted under the neurosurgical team. One week later the symptoms had not improved and Joe was referred to the eye Question 5 Figure 1. 3-dimensional reconstruction image clinic complaining of increasing right What are the surgical options for dealing of the CT-angiogram showing an unruptured periocular pain. -
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. -
Commentary on the Masquerades of A
perim Ex en l & ta a l ic O p in l h t C h f Journal of Clinical & Experimental a o l m l a o n l r o Chua, J Clin Exp Ophthalmol 2016, 7:2 g u y o J Ophthalmology 10.4172/2155-9570.1000543 ISSN: 2155-9570 DOI: Commentary Open Access Commentary on the Masquerades of a Childhood Ciliary Body Medulloepithelioma: A Case of Chronic Uveitis, Cataract, and Secondary Glaucoma Jocelyn Chua* Eye Specialist Clinic, 290 Orchard Road, Singapore *Corresponding author: Dr Jocelyn Chua, Eye Specialist Clinic, 290 Orchard Road, #06-01 to 05, 238859, Singapore; Tel: +65 96897919; Email: [email protected], [email protected] Received date: February 09, 2016; Accepted date: April 20, 2016; Published date: April 25, 2016 Copyright: © 2016 Chua J. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Commentary Ciliary body medulloepithelioma is the commonest ciliary body tumor in childhood. The term “medulloepithelioma”, coined by "The masquerades of a childhood ciliary body medulloepithelioma: Grinker in 1931, best describes the origin of the tumor from the A case of chronic uveitis, cataract and secondary glaucoma" by Chua et primitive medullary epithelium located along the inner layer of the al. [1] is a case report of a healthy two year old boy who presented with optic cup. This undifferentiated medullary epithelium forms the non- a unilateral cataract, anterior uveitis and glaucoma after an innocuous pigmented ciliary body epithelium in the later years of development. -
CN Palsy Update for the Primary Care OD 2018
CN Palsy Update for the Primary Care OD 2018 Christopher Wolfe, OD, FAAO, Dipl. ABO Oculomotor Nerve Palsy (CN 3) Signs and Symptoms The primary symptom is diplopia caused by misalignment of the visual axes, the pattern of image separation (horizontal, vertical, oblique) is the key to diagnosing which particular ocular motor cranial nerve (and extraocular muscle) is involved. With a complete unilateral third cranial nerve palsy, the involved eye is deviated "down and out" with partial or complete ptosis. • Pupillary dilatation (involvement) can cause: • Anisocoria (greater in the light) • Symptomatic glare in bright light • Blurred vision for near objects – due to accommodation deficit A painful pupil-involved oculomotor nerve palsy may result from a life-threatening intracranial aneurysm. Prompt diagnosis of an oculomotor nerve palsy is critical to ensure appropriate evaluation and management. Pathophysiology The clinical features of a CN 3 palsy are due to the anatomical relationship of the various branches of the oculomotor nerve and the location of the problem causing the palsy. These anatomical sites can be broken down into: • Nuclear portion: The axons start on each side of the midbrain. Each of the axon origination within the midbrain that travel to a specific extraocular and intraocular muscle can be further classified into a subnucleus. • Fascicular intraparenchymal midbrain portion: This portion of the oculomotor nerve travels courses ventrally (forward) from the nucleus, through the red nucleus, and emerges medially from the cerebral peduncle. • Subarachnoid portion: The nerve then travels in the subarachnoid space anterior to the midbrain and near the posterior communicating artery. An aneurysm at the INTRAOCULAR junction between the posterior communicating artery and INNERVATION the internal carotid artery is one of the critical reasons to differentiate a pupil involved CN 3 palsy. -
Congenital Oculomotor Palsy: Associated Neurological and Ophthalmological Findings
CONGENITAL OCULOMOTOR PALSY: ASSOCIATED NEUROLOGICAL AND OPHTHALMOLOGICAL FINDINGS M. D. TSALOUMAS1 and H. E. WILLSHA W2 Birmingham SUMMARY In our group of patients we found a high incidence Congenital fourth and sixth nerve palsies are rarely of neurological abnormalities, in some cases asso associated with other evidence of neurological ahnor ciated with abnormal findings on CT scanning. mality, but there have been conflicting reports in the Aberrant regeneration, preferential fixation with literature on the associations of congenital third nerve the paretic eye, amblyopia of the non-involved eye palsy. In order to clarify the situation we report a series and asymmetric nystagmus have all been reported as 1 3 7 of 14 consecutive cases presenting to a paediatric associated ophthalmic findings. - , -9 However, we tertiary referral service over the last 12 years. In this describe for the first time a phenomenon of digital lid series of children, 5 had associated neurological elevation to allow fixation with the affected eye. Two abnormalities, lending support to the view that con children demonstrated this phenomenon and in each genital third nerve palsy is commonly a manifestation of case the accompanying neurological defect was widespread neurological damage. We also describe for profound. the first time a phenomenon of digital lid elevation to allow fixation with the affected eye. Two children demonstrated this phenomenon and in each case the PATIENTS AND METHODS accompanying neurological defect was profound. The Fourteen children (8 boys, 6 girls) with a diagnosis of frequency and severity of associated deficits is analysed, congenital oculomotor palsy presented to our paed and the mechanism of fixation with the affected eye is iatric tertiary referral centre over the 12 years from discussed. -
Multiple Sclerosis Presenting As Isolated Oculomotor Nerve Palsy Ryan J
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES Multiple Sclerosis Presenting as Isolated Oculomotor Nerve Palsy Ryan J. Uitti and A.H. Rajput ABSTRACT: A 23-year old woman came to the emergency room with an isolated oculomotor nerve palsy (including pupillary dilatation) of rapid onset. Investigations and history revealed no cause. The subsequent course of events indicated a diagnosis of multiple sclerosis. While the third nerve has been shown to be involved during the course of multiple sclerosis, this is the first report of a case presenting as an isolated oculomotor nerve paralysis. RESUME: La paralysie isolee du nerf moteur oculaire commun commc manifestation initiale de la sclerose en plaques. Une femme agee de 23 ans se presente a la salle d'urgence avec une paralysie isolee du nerf moteur oculaire commun (incluant une dilatation pupillaire) a debut brusque. L'investigation et l'histoire sont non contributives. L'eVolution subsequente de la maladie r6vele un diagnostic de sclerose en plaques. Meme s'il a ete demontre que le troisieme nerf cranien peut etre atteint a un moment ou l'autre de revolution de la sclerose en plaques, nous rapportons pour la premiere fois un cas dont la manifestation initiale de la maladie est une paralysie isolee du nerf moteur oculaire commun. Can. J. Neurol. Sci. 1986; 13:270-272 The onset of multiple sclerosis (MS) is monosymptomatic in gaze was possible. The right pupil was dilated and nonreactive to light approximately 45% of cases.1 When the disease presents as an and accomodation. Optic fundi were normal. A provisional diagnosis of posterior communicating aneurysm was made. -
Pia, Ptosis, and Other Defects of Ocular Movement. Paradoxical
748 CLINICAL NEURO-OPHTHALMOLOGY gia, paralysis of vertical gaze, loss of convergence, exotro- EFFERENT ABNORMALITIES: ANISOCORIA pia, ptosis, and other defects of ocular movement. The presence of anisocoria usually indicates a structural defect of one or both irides or a neural defect of the efferent Paradoxical Reaction of the Pupils to Light and pupillomotor pathways innervating the iris muscles in one Darkness or both eyes. A careful slit-lamp examination to assess the health and integrity of the iris stroma and muscles is an Barricks et al. described three unrelated boys, 2, 6, and important step in the evaluation of anisocoria. If the irides 10 years of age, with congenital stationary night blindness, are intact, then an innervation problem is suspected. As most myopia, and abnormal electroretinograms, who showed a efferent disturbances causing anisocoria are unilateral, two ‘‘paradoxical’’ pupillary constriction in darkness (108). In simple maneuvers are helpful in determining whether it is a lighted room, all three patients had moderately dilated pu- the sympathetic or parasympathetic innervation to the eye pils; however, when the room lights were extinguished, the that is dysfunctional: (1) checking the pupillary light reflex patients’ pupils briskly constricted and then slowly redilated. and (2) measuring the anisocoria in darkness and in bright Subsequent investigators confirmed this observation and re- light. ported similar paradoxical pupillary responses in children When the larger pupil has an obviously impaired reaction and adults with congenital achromatopsia, blue-cone mono- to light stimulation, it is likely the cause of the anisocoria. chromatism, and Leber congenital amaurosis (109,110). In One can presume the problem lies somewhere along the addition, such responses occasionally occur in patients with parasympathetic pathway to the sphincter muscle. -
(Diktyoma) Presenting As a Perforated, Infected Eye
Br J Ophthalmol: first published as 10.1136/bjo.61.3.229 on 1 March 1977. Downloaded from British Journal of Ophthalmology, 1977, 61, 229-232 Medulloepithelioma (diktyoma) presenting as a perforated, infected eye MOHAMED A. VIRJI Central Pathology Laboratory, Ministry of Health, Dar-es-Salaam, Tanzania SUMMARY A case of embryonal medulloepithelioma (diktyoma) presenting with perforated infected eye in a 13-year-old Black African girl is described. The tumour mass occupied most of the deformed eye, and invasion of the sclera anteriorly was seen. There was no evidence of orbital or distant tumour involvement. It is suggested that with increasing age these tumours are more likely to show frankly malignant features. Medulloepithelioma (diktyoma) is a rare neoplasm anteriorly perforated left eye, with loss of cornea, of the eye which is characterised by slow growth and purulent discharge, and a fragmenting mass of local invasion and is composed of glandular, irregular brownish-grey tissue attached mainly to neural, and mesenchymal elements (Andersen, the superior and temporal portion of the eye and 1962). It presents even rarely as an infected perfor- extending into the posterior chamber. The infection ated eye with a fungating mass replacing the ocular was controlled with systemic antibiotics and the left copyright. contents. Soudakoff (1936) reported the case of a eye was enucleated. Radiological examination of 28-year-old Chinese who had a perforated eye with the skull showed no orbital involvement, and chest tumour mass completely filling it. This paper x-rays were normal. Postoperative recovery was reports the case of a young black African girl who uneventful. -
Retinoblastoma Simulators
Retinoblastoma: Atypical Presentation & Simulators Dr. Njambi Ombaba; Paediatric Ophthalmologist, University of Nairobi Objectives • To review of typical presentation of retinoblastoma • To understand the atypical presentation • To understand the Rb simulators Presentation of retinoblastoma Growth patterns Endophytic: Inner retina, vitreous mass, no overlying vessels, pseudohypopyon Exophytic: Outer retina, SR space mass, overlying vessels, RD Diffuse: No mass, signs of inflammation/ endophthalmitis Echogenic soft tissue mass Variable shadowing – calcification Persistent on reduced gain Heterogeneous – necrosis/ haemorrhage Floating debris- vitreous seeds, increased globulin MRI- • Pre-treatment staging T1- Hyper intense to vitreous T2-Hypo intense to vitreous T1:C+Gd- homo/ heterogeneous Enhancement: Choroid & AC ON involvement Hypo intense sclera- Normal Trilateral retinoblastoma CT SCAN Typically a mass of high density Usually calcified and moderately enhancing on iodinated contrast CT has a sensitivity of 81–96%, and a higher specificity for calcification detection However, delineation of intraocular soft-tissue detail is limited. Low sensitivity for ON invasion Atypical presentation Non calcified Retinoblastoma Calcification is key to diagnosis retinoblastoma US detects calcifications in 92–95% of positive cases Non-calcified retinoblastomas: 1. Tumefaction with irregular internal structure 2. Medium reflectivity 3. Typical signs of vascularity 4. Retinal detachment with part of the retinal surface destroyed. Rare, 2% of all -
Prevalence of Amblyopia in Congenital Blepharoptosis: a Systematic Review and Meta-Analysis
Int J Ophthalmol, Vol. 12, No. 7, Jul.18, 2019 www.ijo.cn Tel: 8629-82245172 8629-82210956 Email: [email protected] ·Meta-Analysis· Prevalence of amblyopia in congenital blepharoptosis: a systematic review and Meta-analysis Jia-Ying Zhang1,2, Xiao-Wei Zhu1,2, Xia Ding1,2, Ming Lin1,2, Jin Li1,2 1Department of Ophthalmology, Shanghai Ninth People’s and management of amblyopia should be integral to the Hospital, Shanghai Jiao Tong University School of Medicine, treatment of congenital ptosis. Shanghai 200011, China ● KEYWORDS: amblyopia; congenital ptosis; blepharophimosis; 2Shanghai Key Laboratory of Orbital Diseases and Ocular systematic review Oncology, Shanghai 200011, China DOI:10.18240/ijo.2019.07.21 Correspondence to: Jin Li. Department of Ophthalmology, Shanghai Ninth Peolple’s Hospital, Shanghai Jiao Tong Citation: Zhang JY, Zhu XW, Ding X, Lin M, Li J. Prevalence of University School of Medicine, No.639, Zhizaoju Road, amblyopia in congenital blepharoptosis: a systematic review and Shanghai 200011, China. [email protected] Meta-analysis. Int J Ophthalmol 2019;12(7):1187-1193 Received: 2018-09-25 Accepted: 2019-03-05 INTRODUCTION Abstract ongenital blepharoptosis is an eyelid disorder that ● AIM: To conduct a systematic review and Meta-analysis of C is characterized by an involuntary drooping of the the published literature to evaluate the pooled prevalence upper eyelid since birth. Etiologically, myogenic factors are rate of amblyopia in patients with congenital ptosis. most common, referring to dysgenesis or weakness of the ● METHODS: We searched the PubMed, Embase, the levator muscle and sometimes the superior rectus muscle. Cochrane Central Register of Controlled Trials, China The etiological subtypes of congenital ptosis include simple National Knowledge Infrastructure, Wanfang Data, and congenital ptosis, blepharophimosis-ptosis-epicanthus inversus Chongqing VIP databases for studies reporting the syndrome (BPES), Marcus Gunn jaw-winking syndrome prevalence of amblyopia in patients with congenital ptosis. -
PG Series Ophthalmology Buster
PG Series Ophthalmology Buster PG Series Ophthalmology Buster E Ahmed Formerly Head, Department of Ophthalmology Calcutta National Medical College Consultant, Eye Care and Research Centre Kolkata JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3, EMCA House, 23/23B Ansari Road, Daryaganj New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672, Rel: 32558559 Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected] Visit our website: www.jaypeebrothers.com Branches • 2/B, Akruti Society, Jodhpur Gam Road Satellite, Ahmedabad 380 015 Phones: +91-079-26926233, Rel: +91-079-32988717, Fax: +91-079-26927094 e-mail: [email protected] • 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East, Bangalore 560 001 Phones: +91-80-22285971, +91-80-22382956, Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected] • 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road, Chennai 600 008 Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089 Fax: +91-44-28193231 e-mail: [email protected] • 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road, Hyderabad 500 095 Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: [email protected] • No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road, Kochi 682 018, Kerala Phones: +91-0484-4036109, +91-0484-2395739, +91-0484-2395740 e-mail: [email protected] • 1-A Indian Mirror Street, Wellington Square, Kolkata 700 013 Phones: +91-33-22451926, +91-33-22276404, +91-33-22276415, Rel: +91-33-32901926 Fax: +91-33-22456075, e-mail: [email protected] • 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel, Mumbai 400 012 Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896 Fax: +91-22-24160828, e-mail: [email protected] • “KAMALPUSHPA” 38, Reshimbag, Opp.