Visual Electrophysiology Testing
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Optic Disc Drusen in Differential Diagnosis of Optic Neuritis Optik Nörit Ayrıcı Tanısında Optik Disk Druzeni
DO I:10.4274/tnd.56514 Images in Clinical Neurology Optic Disc Drusen in Differential Diagnosis of Optic Neuritis Optik Nörit Ayrıcı Tanısında Optik Disk Druzeni Erkingül Shugaiv1, Elif Aksoy Güzeller2, Sait Alim2 1Tokat State Hospital, Clinic of Neurology, Tokat, Turkey 2Tokat State Hospital, Clinic of Diases Eye, Tokat, Turkey Optic disc drusen is a condition where a hyaline-like calcific object is accumulated on the optical nerve ending, often bilaterally (1). Its prevalence in the general population is 0.34-3.7%. It can be confused with optic papillitis since it blurs the papillary border at the bottom of the eye. Drusens can be seen as opacity in B-scan ultrasonography and computerized tomography (2). Optic disc drusens present with slowly progressing visual field defects. The 21-year-old patient who complained of blurry vision on both eyes did not have a history of disease. Her vision was blurry for the past 10 days, especially on the left side. There was no history of eyeball pain, headache, infection or trauma. Her vision was 0.2 on the right and 0.1 on the left side. The papillary borders were undefined on both sides in the examination of the base of Figure 1. Optic disc drusen on both sides: Discs are protruded due the eyes (Figure 1). Due to the slow clinical decline over 10 days, to the drusen and their borders are not clearly defined. cranial and spinal magnetic resonance imaging was conducted in order to address any possible demyelinating disease but did not produce any remarkable findings. After this, cranial and orbital tomography was conducted with the pre-diagnosis of optic disc drusen. -
Bass – Glaucomatous-Type Field Loss Not Due to Glaucoma
Glaucoma on the Brain! Glaucomatous-Type Yes, we see lots of glaucoma Field Loss Not Due to Not every field that looks like glaucoma is due to glaucoma! Glaucoma If you misdiagnose glaucoma, you could miss other sight-threatening and life-threatening Sherry J. Bass, OD, FAAO disorders SUNY College of Optometry New York, NY Types of Glaucomatous Visual Field Defects Paracentral Defects Nasal Step Defects Arcuate and Bjerrum Defects Altitudinal Defects Peripheral Field Constriction to Tunnel Fields 1 Visual Field Defects in Very Early Glaucoma Paracentral loss Early superior/inferior temporal RNFL and rim loss: short axons Arcuate defects above or below the papillomacular bundle Arcuate field loss in the nasal field close to fixation Superotemporal notch Visual Field Defects in Early Glaucoma Nasal step More widespread RNFL loss and rim loss in the inferior or superior temporal rim tissue : longer axons Loss stops abruptly at the horizontal raphae “Step” pattern 2 Visual Field Defects in Moderate Glaucoma Arcuate scotoma- Bjerrum scotoma Focal notches in the inferior and/or superior rim tissue that reach the edge of the disc Denser field defects Follow an arcuate pattern connected to the blind spot 3 Visual Field Defects in Advanced Glaucoma End-Stage Glaucoma Dense Altitudinal Loss Progressive loss of superior or inferior rim tissue Non-Glaucomatous Etiology of End-Stage Glaucoma Paracentral Field Loss Peripheral constriction Hereditary macular Loss of temporal rim tissue diseases Temporal “islands” Stargardt’s macular due -
Optic Nerve Hypoplasia Plus: a New Way of Looking at Septo-Optic Dysplasia
Optic Nerve Hypoplasia Plus: A New Way of Looking at Septo-Optic Dysplasia Item Type text; Electronic Thesis Authors Mohan, Prithvi Mrinalini Publisher The University of Arizona. Rights Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. Download date 29/09/2021 22:50:06 Item License http://rightsstatements.org/vocab/InC/1.0/ Link to Item http://hdl.handle.net/10150/625105 OPTIC NERVE HYPOPLASIA PLUS: A NEW WAY OF LOOKING AT SEPTO-OPTIC DYSPLASIA By PRITHVI MRINALINI MOHAN ____________________ A Thesis Submitted to The Honors College In Partial Fulfillment of the Bachelors degree With Honors in Physiology THE UNIVERSITY OF ARIZONA M A Y 2 0 1 7 Approved by: ____________________________ Dr. Vinodh Narayanan Center for Rare Childhood Disorders Abstract Septo-optic dysplasia (SOD) is a rare congenital disorder that affects 1/10,000 live births. At its core, SOD is a disorder resulting from improper embryological development of mid-line brain structures. To date, there is no comprehensive understanding of the etiology of SOD. Currently, SOD is diagnosed based on the presence of at least two of the following three factors: (i) optic nerve hypoplasia (ii) improper pituitary gland development and endocrine dysfunction and (iii) mid-line brain defects, including agenesis of the septum pellucidum and/or corpus callosum. A literature review of existing research on the disorder was conducted. The medical history and genetic data of 6 patients diagnosed with SOD were reviewed to find damaging variants. -
Transient Monocular Visual Loss
Transient Monocular Visual Loss VALÉRIE BIOUSSE, MD AND JONATHAN D. TROBE, MD ● PURPOSE: To provide a practical update on the diagno- when most episodes of TMVL do not cause total loss of sis and management of transient monocular visual loss vision.2 (TMVL). The most important step in evaluating a patient with ● DESIGN: Perspective. visual loss is to establish whether the visual loss is ● METHODS: Review of the literature. monocular or binocular.2,5 Monocular visual loss always ● RESULTS: TMVL is an important clinical symptom. It results from lesions anterior to the chiasm (the eye or the has numerous causes but most often results from tran- optic nerve), whereas binocular visual loss results from sient retinal ischemia. It may herald permanent visual lesions of both eyes or optic nerves, or, more likely, of the loss or a devastating stroke, and patients with TMVL chiasm or retrochiasmal visual pathway. should be evaluated urgently. A practical approach to the Deciding whether an episode of abrupt visual loss evaluation of the patient with TMVL must be based on occurred in one eye or both is not always easy. Very few the patient’s age and the suspected underlying etiology. patients realize that binocular hemifield (homonymous) In the older patient, tests should be performed to inves- visual field loss affects the fields of both eyes. They will tigate giant cell arteritis, atherosclerotic large vessel usually localize it to the eye that lost its temporal field. The disease, and cardiac abnormalities. In the younger pa- best clues to the fact that visual loss was actually binocular tient, TMVL is usually benign and the evaluation should are reading impairment (monocular visual loss does not be tailored to the particular clinical setting. -
TUBB3 M323V Syndrome Presents with Infantile Nystagmus
G C A T T A C G G C A T genes Case Report TUBB3 M323V Syndrome Presents with Infantile Nystagmus Soohwa Jin 1, Sung-Eun Park 2, Dongju Won 3, Seung-Tae Lee 3, Sueng-Han Han 2 and Jinu Han 4,* 1 Department of Opthalmology, Yonsei University College of Medicine, Seoul 03722, Korea; [email protected] 2 Department of Ophthalmology, Institute of Vision Research, Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Korea; [email protected] (S.-E.P.); [email protected] (S.-H.H.) 3 Department of Laboratory Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Korea; [email protected] (D.W.); [email protected] (S.-T.L.) 4 Department of Ophthalmology, Institute of Vision Research, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06273, Korea * Correspondence: [email protected]; Tel.: +82-2-2019-3445 Abstract: Variants in the TUBB3 gene, one of the tubulin-encoding genes, are known to cause congenital fibrosis of the extraocular muscles type 3 and/or malformations of cortical development. Herein, we report a case of a 6-month-old infant with c.967A>G:p.(M323V) variant in the TUBB3 gene, who had only infantile nystagmus without other ophthalmological abnormalities. Subsequent brain magnetic resonance imaging (MRI) revealed cortical dysplasia. Neurological examinations did not reveal gross or fine motor delay, which are inconsistent with the clinical characteristics of patients with the M323V syndrome reported so far. A protein modeling showed that the M323V mutation in the TUBB3 gene interferes with αβ heterodimer formation with the TUBA1A gene. -
Posterior Uveitis Signs
Uveitis unplugged: sorting out infectious uveitis Hobart 2017 Peter McCluskey Save Sight Institute Sydney Eye Hospital Sydney Medical School University of Sydney Sydney Australia No financial or proprietary interest in any material discussed Immunosuppression for IED The fundamental principle for managing uveitis: Is the disease: infective inflammatory neoplastic What is the worst, most acute threat to vision this could be? Immunosuppression for IED The fundamental principle for managing uveitis: Is the disease: infective inflammatory neoplastic What is the worst, most acute threat to vision this could be? usually infection! Common Causes of Uveitis in Sydney 2015 Idiopathic 505 (50%) • idiopathic 424 Infective 203 (20%) • Fuchs 26 • Herpetic 105 • WDS 55 - anterior 83 - posterior 22 Inflammatory 358 (35%) • HLA B27 188 TB 40 (+systemic B27) 46 • • Toxoplasmosis 38 • sarcoid 56 • syphilis 10 (25) • Behcets 18 4 Assessing the patient with uveitis How do I sort this out??? • clinical assessment + carefully selected tests • clinical assessment is the key investigation • critical to take as comprehensive a history and review of systems as possible plus • thorough careful complete examination of each eye Sorting out Uveitis: anterior uveitis signs Anterior Uveitis Signs: • comprehensive a history and systems review • there are some unofficial “rules” can’t diagnose anterior uveitis without a normal fundus on dilated exam • anterior uveitis: mostly non specific signs • KPs, iris and pupil: useful clues Sorting out Uveitis: posterior uveitis -
Multiple Ocular Developmental Defects in Four Closely Related Alpacas
Veterinary Ophthalmology (2018) 1–8 DOI:10.1111/vop.12540 CASE REPORT Multiple ocular developmental defects in four closely related alpacas Kelly E. Knickelbein,* David J. Maggs,§ Christopher M. Reilly,†,1 Kathryn L. Good*,2 and Juliet R. Gionfriddo‡,3 *The Veterinary Medical Teaching Hospital, University of California, Davis, CA 95616, USA; §Department of Surgical and Radiological Sciences, University of California, Davis, CA 95616 USA; †Department of Pathology Microbiology, and Immunology, University of California, Davis, CA 95616, USA; and ‡The College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80528, USA Address communications to: Abstract D. J. Maggs Objective To describe the clinical, gross pathologic, and histopathologic findings for a Tel.: (530) 752-3937 visually impaired 5.8-year-old female alpaca with multiple ocular abnormalities, as well Fax: (530) 752-6042 as the clinical findings for three closely related alpacas. e-mail: [email protected] Animals studied Four alpacas. Present addresses: 1Insight Procedures Ophthalmic examination was performed on a 16-month-old female alpaca Veterinary Specialty Pathology, following observation of visual impairment while hospitalized for an unrelated illness. Austin, TX 78752, USA Following acute systemic decline and death 4.5 years later, the alpaca’s brain, optic 2Department of Surgical and Radiological Sciences, nerves, and eyes were examined grossly and histologically. Ophthalmic examination of University of California, Davis, three closely related alpacas was subsequently performed. CA 95616, USA Results The 16-month-old female alpaca (Alpaca 1) had ophthalmoscopic findings sug- 3 Red Feather Lakes, CO 80545, gestive of a coloboma or hypoplasia of the retinal pigment epithelium (RPE) and chor- USA oid, and suspected optic nerve hypoplasia OU. -
Eleventh Edition
SUPPLEMENT TO April 15, 2009 A JOBSON PUBLICATION www.revoptom.com Eleventh Edition Joseph W. Sowka, O.D., FAAO, Dipl. Andrew S. Gurwood, O.D., FAAO, Dipl. Alan G. Kabat, O.D., FAAO Supported by an unrestricted grant from Alcon, Inc. 001_ro0409_handbook 4/2/09 9:42 AM Page 4 TABLE OF CONTENTS Eyelids & Adnexa Conjunctiva & Sclera Cornea Uvea & Glaucoma Viitreous & Retiina Neuro-Ophthalmic Disease Oculosystemic Disease EYELIDS & ADNEXA VITREOUS & RETINA Blow-Out Fracture................................................ 6 Asteroid Hyalosis ................................................33 Acquired Ptosis ................................................... 7 Retinal Arterial Macroaneurysm............................34 Acquired Entropion ............................................. 9 Retinal Emboli.....................................................36 Verruca & Papilloma............................................11 Hypertensive Retinopathy.....................................37 Idiopathic Juxtafoveal Retinal Telangiectasia...........39 CONJUNCTIVA & SCLERA Ocular Ischemic Syndrome...................................40 Scleral Melt ........................................................13 Retinal Artery Occlusion ......................................42 Giant Papillary Conjunctivitis................................14 Conjunctival Lymphoma .......................................15 NEURO-OPHTHALMIC DISEASE Blue Sclera .........................................................17 Dorsal Midbrain Syndrome ..................................45 -
A Case of Cerebral Granuloma and Optic Papillitis Due to Brucella Sp
Hindawi Case Reports in Infectious Diseases Volume 2020, Article ID 5216249, 3 pages https://doi.org/10.1155/2020/5216249 Case Report A Case of Cerebral Granuloma and Optic Papillitis due to Brucella sp. A. Chiappe-Gonzalez 1,2 and A Solano-Loza2 1Hospital Nacional Dos de Mayo, Lima, Peru 2Cl´ınica Angloamericana, San Isidro, Peru Correspondence should be addressed to A. Chiappe-Gonzalez; [email protected] Received 21 December 2019; Revised 18 April 2020; Accepted 29 June 2020; Published 18 July 2020 Academic Editor: Larry M. Bush Copyright © 2020 A. Chiappe-Gonzalez and A Solano-Loza. ,is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We document a case of a 24-year-old woman who presented with cerebral granuloma and optic papillitis associated to Brucella sp. infection, whose diagnosis was made with a brain biopsy and serology tests, with clinical improvement following specific antibiotic therapy. ,e patient was followed up for over a year without evidence of relapse. 1. Introduction Seven months prior to presentation, she had been eval- uated for this complaint; a head computed tomography (CT) Brucellosis is a common zoonotic infection in many angiography was performed which showed a hypodense, right countries, including Mediterranean and Middle Eastern occipital lesion with ill-defined borders and peripheral con- countries. In Peru, the prevalence of brucellosis has been trast enhancement (Figure 1); the study was followed by a poorly documented, with higher frequency in the cities of brain magnetic resonance imaging (MRI), which confirmed Lima, Callao, and Ica probably due to the informal goat the presence of a solid cortical formation of about 0.7 cen- farming in these regions. -
Internuclear Ophthalmoplegia and Horner's Syndrome Due To
362 Journal of the Royal Society of Medicine Volume 86 June 1993 Internuclear ophthalmoplegia and Her erythrocyte sedimentation rate (ESR) was 105 in the Horner's syndrome due to presumed first hour, the white blood cell count was 11.1 x109/l, giant cell arteritis platelets 475x 109/1, the blood film showed some target cells and ++ rouleaux. Her alkaline phosphatase was 226 and her 7y-glutamine transferase 102. A computerized tomography scan reported atrophic changes in the cerebral hemispheres, and an old infarct was noted in the left temporal lobe. Within Ayman Askari MRCP1 0 M P Jolobe FRCP2 6 days of starting treatment the headache improved remarkably, and in the following 2 months the patient D I Shepherd FRCP2 'Princess Royal Hospital; maintained her progress with no change in the neurological Telford, Shropshire and 2Tameside General Hospital signs. The ESR was 47 within 8 days of admission and 3 by Ashton-under-Lyne, Lancashire day 38 of starting treatment. Keywords: giant cell arteritis; ophthalmoplegia; Horner's syndrome; Discussion ataxic nystagmus Our aim is to draw attention to the association between neuro-ophthalmic signs and presumed GCA. Leukocytosis, abnormal latex fixation test and fever are in keeping with cell arteritis is an inflammatory, the diagnosis. It is likely that many patients with GCA have Giant (GCA) occlusive ophthalmoplegia in the course of their illness and failure arteriopathy of unknown aetiology. It is common in the to detect it may be due to the transient nature of this elderly, with an incidence of 17.4 per 100 000 ofthe popula- manifestation3. -
Cranial Nerve Palsies in Spontaneous Carotid Artery Dissection
J7ournal ofNeurology, Neurosurgery, and Psychiatry 1993;56:1191-1199 1 191 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1191 on 1 November 1993. Downloaded from Cranial nerve palsies in spontaneous carotid artery dissection Matthias Sturzenegger, P Huber Abstract the reported "idiopathic" jugular foramen Two patients had isolated unilateral cra- (Vernet) and similar syndromes (Villaret, nial nerve palsies due to spontaneous Collet Siccard) in the older literature might internal carotid artery (ICA) dissection well have been caused by spontaneous- carotid without ischaemic cerebral involvement. dissection.5 In those times ICA dissection as a One had acute glossopharyngeal and cause of cranial nerve palsy was poorly vagal, the other isolated hypoglossal known, angiography quite risky, and ultra- nerve palsy. Reviewing all reported cases sound and MRI not available. Out of 31 con- of angiographically confirmed ICA dis- secutive patients with ICA dissection section in the literature, 36 additional diagnosed at our department within four cases with unequivocal ipsilateral cranial years, two presented with cranial nerve palsies nerve palsies were analysed. While an without cerebral involvement. isolated palsy ofthe IXth and Xth has not been reported previously, palsies of the XIIth nerve or the IXth to XIIth nerves Case reports were most frequently found. In these PATEENT 1 patients, lower cranial nerve palsies are A 42-year-old man had been in excellent probably the result of compression by an health. He had no vascular risk factors. After enlarging ICA due to mural haematoma. strenuous activity (cutting wood) in military Symptoms and signs indicative of carotid service he suddenly felt pain in the right dissection were concurrently present upper jaw which later extended to the ear and only in some reported cases. -
Myelin Oligodendrocyte Glycoprotein-Igg-Positive Recurrent Bilateral Optic Papillitis with Serous Retinal Detachment: a Case Report
doi: 10.2169/internalmedicine.9840-17 Intern Med Advance Publication http://internmed.jp 【 CASE REPORT 】 Myelin Oligodendrocyte Glycoprotein-IgG-positive Recurrent Bilateral Optic Papillitis with Serous Retinal Detachment: A Case Report Tomoya Kon 1, Hiroki Hikichi 1, Tatsuya Ueno 1, Chieko Suzuki 1, Jinichi Nunomura 1, Kimihiko Kaneko 2, Toshiyuki Takahashi 2,3, Ichiro Nakashima 2 and Masahiko Tomiyama 1 Abstract: Autoantibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been detected in inflamma- tory demyelinating central nervous system diseases. A 30-year-old woman had blurred vision, marked optic nerve disc swelling, serous retinal detachment at the macular on optic coherence tomography, and MOG-IgG seropositivity. The patient was thought to have optic papillitis associated with MOG-IgG. Her symptoms rap- idly improved after high-dose methylprednisolone therapy. We hypothesize that serous retinal detachment was secondary, arising from optic papillitis. This is the first report of the concurrence of optic papillitis with MOG-IgG and serous retinal detachment. MOG-IgG should be tested in patients with marked optic disc swelling. Key words: IgA nephropathy, MOG, myelin oligodendrocyte glycoprotein, optic neuritis, optic papillitis, serous retinal detachment (Intern Med Advance Publication) (DOI: 10.2169/internalmedicine.9840-17) inflammatory diseases, such as Vogt-Koyanagi-Harada dis- Introduction ease, sarcoidosis, and Behçet’s disease, disrupt the blood- retinal barrier, resulting in the development of serous retinal Autoantibodies against myelin oligodendrocyte glycopro- detachment (4, 5). However, to our knowledge, serous reti- tein (MOG-IgG) have been detected in patients with central nal detachment in a patient with MOG-IgG-positive optic nervous system demyelinating diseases, including acute dis- neuritis has not been reported to date.