DOCSLIB.ORG

Central Serous Choroidopathy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Central Serous Choroidopathy Br J Ophthalmol: first published as 10.1136/bjo.66.4.240 on 1 April 1982. Downloaded from British Journal ofOphthalmology, 1982, 66, 240-241 Visual disturbances during pregnancy caused by central serous choroidopathy J. R. M. CRUYSBERG AND A. F. DEUTMAN From the Institute of Ophthalmology, University of Nijmegen, Nijmegen, The Netherlands SUMMARY Three patients had during pregnancy visual disturbances caused by central serous choroidopathy. One of them had a central scotoma in her first and second pregnancy. The 2 other patients had a central scotoma in their first pregnancy. Symptoms disappeared spontaneously after delivery. Except for the ocular abnormalities the pregnancies were without complications. The complaints can be misinterpreted as pregnancy-related optic neuritis or compressive optic neuropathy, but careful biomicroscopy of the ocular fundus should avoid superfluous diagnostic and therapeutic measures. Central serous choroidopathy (previously called lamp biomicroscopy of the fundus with a Goldmann central serous retinopathy) is a spontaneous serous contact lens showed a serous detachment of the detachment of the sensory retina due to focal leakage neurosensory retina in the macular region of the from the choriocapillaris, causing serous fluid affected left eye. Fluorescein angiography was not accumulation between the retina and pigment performed because of pregnancy. In her first epithelium. This benign disorder occurs in healthy pregnancy the patient had consulted an ophthal- adults between 20 and 45 years of age, who present mologist on 13 June 1977 for exactly the same with symptoms of diminished visual acuity, relative symptoms, which had disappeared spontaneously http://bjo.bmj.com/ central scotoma, metamorphopsia, and micropsia. after delivery. Except during pregnancy the patient Males are affected more commonly than females by at never had visual complaints. least 10 to one.' Most eyes have a complete visual Delivery was 5 days later. Without treatment the recovery over a variable period of time. The cause of central scotoma and serous detachment disappeared the condition is unknown. within 2 weeks. Both pregnancies had been normal Although this disease usually affects males, we from the obstetrical point of view. have observed central serous choroidopathy in on October 2, 2021 by guest. Protected copyright. pregnant females. The course of symptoms in these CASE 2 patients made a causal relationship with pregnancy A 27-year-old woman (gravida 1) noted a relative probable. central scotoma in her right eye when she was 20 weeks pregnant. Ophthalmological examination on Case reports 18 July 1980 disclosed a serous detachment of the sensory retina in the macular region of the right eye. CASE 1 The macular lesion was evident by the slit-lamp A 34-year-old woman (gravida 2) noted visual microscope and Goldmann contact lens, so blurring and a relative central scotoma in the left eye fluorescein angiography was not performed in when she was 28 weeks pregnant. Ophthalmological pregnancy. The visual acuity was 6/30 in the right eye examination was performed 10 weeks later, on 17 after correction (S+2-0) of hypermetropia and 6/6 in March 1981. Visual acuity was 6/5 in the right eye and the emmetropic left eye. Without treatment the 6/6 in the left eye. Indirect ophthalmoscopy and slit- serous detachment persisted during pregnancy. After delivery the first ocular examination was Correspondence to J. R. M. Cruvsherg. MD. University of performed on 6 March 1981. The visual complaints Nijmegen, Institute of Ophthalmology. Philips van Levdenlaan 15. had disappeared, and visual acuity had returned to Nijmegen, The Netherlands. 6/6 without correction. There was no evidence of 240 Br J Ophthalmol: first published as 10.1136/bjo.66.4.240 on 1 April 1982. Downloaded from Visual disturbances during pregnancy caused by central serous choroidopathy 241 serous detachment of the sensory retina. The macula pregnancy from the obstetrical point of view, without of the right eye showed a slight granularity of the signs of toxaemia. pigment epithelium. The pregnancy had been It is of the utmost importance to distinguish the uneventful from the obstetrical point of view. correct causes of visual disturbances and field defects during pregnancy. In all cases a careful examination CASE 3 of the ocular fundus is necessary to exclude a retinal A 32-year-old woman (gravida 1) noted blurred cause. The central scotoma can be misinterpreted as a vision and central scotoma in her right eye when result of optic neuritis. The association of optic she was 32 weeks pregnant. Ophthalmological neuritis and pregnancv has previously been examination on 14 August 1980, one week after the suggested.47 Visual disturbances during pregnancy initial symptoms. disclosed a serous detachment of have been reported as a result of the expansion of the sensory retina in the macular region of her right intracranial tumours (meningiomas, pituitary eve. Visual acuity was 6/30 in the right eye and 6/6 in adenomas, and craniopharyngiomas) owing to the left eve. hormonal changes.5 8-11 As in our patients with After deliverv on 29 September visual complaints central serous choroidopathy the spontaneous disappeared spontaneously. On 27 November 1980 recovery of visual functions after delivery has been ophthalmological examination disclosed visual acuitv described in patients with intracranial tumrours.9'2 6/6 in the right eye. There was still some If central serous choroidopathv is the cause of metamorphopsia (Amsler grid). but the serous visual disturbances during pregnancv. its correct detachment had disappeared. The pregnancy had diagnosis mav avert superfluous diagnostic and been normal from the obstetrical point of view. therapeutic measures. Discussion References The occurrence of central serous choroidopathy in 4 I Gass JDM. Stereoscopic Atlas of Macular Diseases: A pregnancies of these 3 patients, and the spontaneous finduscopic and Angiographic Presentation. St Louis: Mosby. recovery after delivery, suggested a causal relation- 1977:28. 2 RN. serous retinopathv and pregnancy. and Chumblev LC. Frank Central ship of the disorder and Chumbley pregnancv. Am J Ophthalrnol 1974: 77: 158-60. Frank2 reported central serous retinopathy in a 34- 3 Fastenberg DM. Fetkenhour CL. Choromokos E. Shoch DE. vear-old woman during 4 consecutive pregnancies, Choroidal vascular changes in toxemia of pregnancv. Am J with remission after delivery or spontaneous Ophthalmol 1980:89: 362-8. 4 Kogan JA. Retrobulbar neuritis during pregnancv. Sov'et Vestn abortion. The authors suggest that a hormonal agent, Oftalmol 1934; 5: 503-5. http://bjo.bmj.com/ which increases in concentration during pregnancy, is 5 Hagedoorn A. The chiasmal svndrome and retrobulhar neuritis one possible causative factor in this disease. in pregnancv. Am J Ophthalmol 1937; 20: 690-9. However, since the disorder is more common in men, 6 Caderas de Kerleau J. Cazahan R. Etude clinique des atteintes du nerf optique au cours de la grossesse. Presse Mid 1952; 60:943-4. and usually unilateral, other svstemic and ocular 7 Caderas de Kerleau J. Durand G. Cazahan R. Nevrite retro- factors must play a role. hulbaire gravidique aggrav6e apres l'accouchement. Apparition One of the changes in a normal pregnancv is an de lesions chorior6tiniennes deux mois apres. Blull Soc Ophtalmol France 1952: 52: 319-21. increase of plasma volume and total blood volume. on October 2, 2021 by guest. Protected copyright. 8 Enoksson P. Lundberg N, Sjdstedt S, Skanse B. Influence of Probably circulatory changes in the choriocapillaris pregnancv on visual fields in suprasellar tumours. Acta Psvchiatr can provoke central serous choroidopathv in pre- Nelurol Scand 1961; 36: 524-38. disposed eyes. The importance of the ocular factor is 9 Swver GIM, Little V. Harries BJ. Visual disturhance in suggested by the fact that in consecutive pregnancies pregnancv after induction of ovulation. Br Med J 1971: iv: 9(- 1. I0 Corbev RS, Cruvsberg JRM, Rolland R. Visual ahnormalities in the relapse of central serous choroidopathv occurred a pregnancv following hromocriptin medication. Obstet Givnecol in the same eye. 1977: 50: 69s-71 s. Fastenberg et al.3 found predominantly abnormal 11 Lamberts SWJ. Seldenrath HJ. Kwa HG. Birkenh5ger JC. choroidal vascular patterns in toxaemia of pregnancy, Transient bitemporal hemianopsia during pregnancv after treatment of galactorrhea-amenorrhea svndrome with implicating choroidal vascular insufficiencv as the bromocriptine. J Clin Endocrinol Metah 1977;:44: 190-4. basis for secondary retinal detachments seen in this 12 Husami N. Jewelewicz R. Vande Wiele RL. Pregnancv in complication. However, our patients had a normal patients with pituitarv tumors. Fertil Steril 1977; 28: 920-5..
Load more

Recommended publications
  • GUIDE for the Evaluation of VISUAL Impairment
    International Society for Low vision Research and Rehabilitation GUIDE for the Evaluation of VISUAL Impairment Published through the Pacific Vision Foundation, San Francisco for presentation at the International Low Vision Conference VISION-99. TABLE of CONTENTS INTRODUCTION 1 PART 1 – OVERVIEW 3 Aspects of Vision Loss 3 Visual Functions 4 Functional Vision 4 Use of Scales 5 Ability Profiles 5 PART 2 – ASSESSMENT OF VISUAL FUNCTIONS 6 Visual Acuity Assessment 6 In the Normal and Near-normal range 6 In the Low Vision range 8 Reading Acuity vs. Letter Chart Acuity 10 Visual Field Assessment 11 Monocular vs. Binocular Fields 12 PART 3 – ESTIMATING FUNCTIONAL VISION 13 A General Ability Scale 13 Visual Acuity Scores, Visual Field Scores 15 Calculation Rules 18 Functional Vision Score, Adjustments 20 Examples 22 PART 4 – DIRECT ASSESSMENT OF FUNCTIONAL VISION 24 Vision-related Activities 24 Creating an Activity Profile 25 Participation 27 PART 5 – DISCUSSION AND BACKGROUND 28 Comparison to AMA scales 28 Statistical Use of the Visual Acuity Score 30 Comparison to ICIDH-2 31 Bibliography 31 © Copyright 1999 by August Colenbrander, M.D. All rights reserved. GUIDE for the Evaluation of VISUAL Impairment Summer 1999 INTRODUCTION OBJECTIVE Measurement Guidelines for Collaborative Studies of the National Eye Institute (NEI), This GUIDE presents a coordinated system for the Bethesda, MD evaluation of the functional aspects of vision. It has been prepared on behalf of the International WORK GROUP Society for Low Vision Research and Rehabilitation (ISLRR) for presentation at The GUIDE was approved by a Work Group VISION-99, the fifth International Low Vision including the following members: conference.
    [Show full text]
  • Vision Rehabi I Itation for Patients with Age Related Macular Degeneration
    Vision rehabi I itation for GARY S. RUBIN patients with age­ related macular degeneration Epidemiology of low vision The over-representation of macular degeneration patients in the low-vision clinic is The epidemiology of vision impairment is dealt reflected in the chief complaints of those with in detail elsewhere.1 However, there is one referred for rehabilitation. A study of 1000 particularly salient factor that bears emphasis. consecutive patients seen at the Wilmer Low The prevalence of vision impairment increases Vision clinic indicated that 64% listed 'reading' dramatically with advancing age. Statistics as their chief complaint, while other activities compiled in the UK by the Royal National were identified by fewer than 8% of patients. Institute for the Blind2 indicate that there were Undoubtedly the bias towards reading approximately 1.1 million blind or partially problems results partly from the nature of the sighted persons in 1996, of whom 82% were 65 low-vision services offered. Those served by a years of age or older. Thus it is not surprising to community-based programme that includes learn that the major causes of vision impairment home visits might be more likely to report are age-related eye diseases. Fig. 1 illustrates the problems with activities of daily living, while a distribution of causes of vision impairment blind rehabilitation centre would be more likely 5 from three recent studies?- Approximately to address mobility issues. Nevertheless, most equal percentages are attributed to macular macular degeneration patients are referred to degeneration and cataract, with smaller hospital or optometry clinic services, and as percentages for glaucoma, diabetic retinopathy their overwhelming concern is with reading, and optic neuropathies.
    [Show full text]
  • URGENT/EMERGENT When to Refer Financial Disclosure
    URGENT/EMERGENT When to Refer Financial Disclosure Speaker, Amy Eston, M.D. has a financial interest/agreement or affiliation with Lansing Ophthalmology, where she is employed as a ophthalmologist. 58 yr old WF with 6 month history of decreased vision left eye. Ache behind the left eye for 2-3 months. Using husband’s contact lens solution made it feel better. Seen by two eye care professionals. Given glasses & told eye exam was normal. No past ocular history Medical history of depression Takes only aspirin and vitamins 20/20 OD 20/30 OS Eye Pressure 15 OD 16 OS – normal Dilated fundus exam & slit lamp were normal Pupillary exam was normal Extraocular movements were full Confrontation visual fields were full No red desaturation Color vision was slightly decreased but the same in both eyes Amsler grid testing was normal OCT disc – OD normal OS slight decreased RNFL OCT of the macula was normal Most common diagnoses: Dry Eye Optic Neuritis Treatment - copious amount of artificial tears. Return to recheck refraction Visual field testing Visual Field testing - Small defect in the right eye Large nasal defect in the left eye Visual Field - Right Hemianopsia. MRI which showed a subacute parietal and occipital lobe infarct. ANISOCORIA Size of the Pupil Constrictor muscles innervated by the Parasympathetic system & Dilating muscles innervated by the Sympathetic system The Sympathetic System Begins in the hypothalamus, travels through the brainstem. Then through the upper chest, up through the neck and to the eye. The Sympathetic System innervates Mueller’s muscle which helps to elevate the upper eyelid.
    [Show full text]
  • Oct Institute
    Low Vision, Visual Dysfunction and TBI – Treatment, Considerations, Adaptations Andrea Hubbard, OTD, OTR/L, LDE Objectives • In this course, participants will: 1. Learn about interventions involving specialized equipment to adapt an environment for clients with low vision. 2. Learn about the most typical low vision presentations/conditions. 3. Gain increased knowledge of eye anatomy and the visual pathway. Overview of TBI Reference: Centers for Disease Control and Prevention Overview of TBI Risk Factors for TBI Among non-fatal TBI-related injuries for 2006–2010: • Men had higher rates of TBI hospitalizations and ED visits than women. • Hospitalization rates were highest among persons aged 65 years and older. • Rates of ED visits were highest for children aged 0-4 years. • Falls were the leading cause of TBI-related ED visits for all but one age group. – Assaults were the leading cause of TBI-related ED visits for persons 15 to 24 years of age. • The leading cause of TBI-related hospitalizations varied by age: – Falls were the leading cause among children ages 0-14 and adults 45 years and older. – Motor vehicle crashes were the leading cause of hospitalizations for adolescents and persons ages 15-44 years. Reference: Centers for Disease Control and Prevention Overview of TBI Risk Factors for TBI Among TBI-related deaths in 2006–2010: • Men were nearly three times as likely to die as women. • Rates were highest for persons 65 years and older. • The leading cause of TBI-related death varied by age. – Falls were the leading cause of death for persons 65 years or older.
    [Show full text]
  • Neuroanatomy Crash Course
    Neuroanatomy Crash Course Jens Vikse ∙ Bendik Myhre ∙ Danielle Mellis Nilsson ∙ Karoline Hanevik Illustrated by: Peder Olai Skjeflo Holman ​ Second edition October 2015 The autonomic nervous system ● Division of the autonomic nervous system …………....……………………………..………….…………... 2 ● Effects of parasympathetic and sympathetic stimulation…………………………...……...……………….. 2 ● Parasympathetic ganglia ……………………………………………………………...…………....………….. 4 Cranial nerves ● Cranial nerve reflexes ………………………………………………………………….…………..…………... 7 ● Olfactory nerve (CN I) ………………………………………………………………….…………..…………... 7 ● Optic nerve (CN II) ……………………………………………………………………..…………...………….. 7 ● Pupillary light reflex …………………………………………………………………….…………...………….. 7 ● Visual field defects ……………………………………………...................................…………..………….. 8 ● Eye dynamics …………………………………………………………………………...…………...………….. 8 ● Oculomotor nerve (CN III) ……………………………………………………………...…………..………….. 9 ● Trochlear nerve (CN IV) ………………………………………………………………..…………..………….. 9 ● Trigeminal nerve (CN V) ……………………………………………………................…………..………….. 9 ● Abducens nerve (CN VI) ………………………………………………………………..…………..………….. 9 ● Facial nerve (CN VII) …………………………………………………………………...…………..………….. 10 ● Vestibulocochlear nerve (CN VIII) …………………………………………………….…………...…………. 10 ● Glossopharyngeal nerve (CN IX) …………………………………………….……….…………...………….. 10 ● Vagus nerve (CN X) …………………………………………………………..………..…………...………….. 10 ● Accessory nerve (CN XI) ……………………………………………………...………..…………..………….. 11 ● Hypoglossal nerve (CN XII) …………………………………………………..………..…………...………….
    [Show full text]
  • Visual Dysfunction in Optic Chiasm Syndrome an Atomy
    1 4/12/2019 Optic chiasm, most important Arrangement of visual fibers Characteristic of visual field VISUAL DYSFUNCTION Bitemporal defects: IN OPTIC CHIASM SYNDROME Superior Inferior Complete Peripheral, central M.HIDAYAT FACULTY OF MEDICINE, A N DALAS UNIVERSITY /M .DJAMIL HOSPITAL PADANG AN ATOMY OF CHIASM OPTIC CHIASM Width : 12 mm 53% fiber from nasal retina crossed to opposite — Length : 8 mmfantero posterior) contra lateral. ■ Inclined : 45 0 Inferior nasal fibers cross anterior loop in to contra lateral (Willbrand's knee) Location : anterior hypothalamus & anterior third Macular fiber cross posterosuperior ventricle 10 mm above sella Vascular supply: Anterior communicating artery Anterior cerebri artery Circle of Willis ANTERIOR ANGLE OF CHIASM Compression to anterior angle of chiasm Small lesion damages the crossing fibers of ipsilaferal eye -> field defect: monocular and temporal Damage of macular crossed fibers: monocular, temporal defects and parasentral scotoma Damage fiber from nasal contralateral, anterior extension : central ipsilateral scotoma and contralateral upper temporal quadrant {"Willbrand’s Knee") 1 4/12/2019 Chiasmal compression from below defects stereotyped pattern : bitemporal defect Example: pituitary adenoma Peripheral fiber damage, defects begin from superior quadrants of both eyes Can be not similar Similar defects causes from tubercullum sellae, meningioma, craniopharyngiomas, aneurysm t Sella or supra sella lesion : damage superior fiber defect bitemporal inferior Bitemporal Hemianopsia Example: angioma
    [Show full text]
  • IMI Pathologic Myopia
    Special Issue IMI Pathologic Myopia Kyoko Ohno-Matsui,1 Pei-Chang Wu,2 Kenji Yamashiro,3,4 Kritchai Vutipongsatorn,5 Yuxin Fang,1 Chui Ming Gemmy Cheung,6 Timothy Y. Y. Lai,7 Yasushi Ikuno,8–10 Salomon Yves Cohen,11,12 Alain Gaudric,11,13 and Jost B. Jonas14 1Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Tokyo, Japan 2Department of Ophthalmology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan 3Department of Ophthalmology and Visual Sciences, University Graduate School of Medicine, Kyoto, Japan 4Department of Ophthalmology, Otsu Red-Cross Hospital, Otsu, Japan 5School of Medicine, Imperial College London, London, United Kingdom 6Singapore Eye Research Institute, Singapore National Eye Center, Singapore 7Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong Eye Hospital, Hong Kong 8Ikuno Eye Center, 2-9-10-3F Juso-Higashi, Yodogawa-Ku, Osaka 532-0023, Japan 9Department of Ophthalmology, Osaka University Graduate School of Medicine, Osaka, Japan 10Department of Ophthalmology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan 11Centre Ophtalmologique d’Imagerie et de Laser, Paris, France 12Department of Ophthalmology and University Paris Est, Creteil, France 13Department of Ophthalmology, APHP, Hôpital Lariboisière and Université de Paris, Paris, France 14Department of Ophthalmology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany Correspondence: Kyoko Pathologic myopia is a major cause of visual impairment worldwide. Pathologic myopia is Ohno-Matsui, Department of distinctly different from high myopia. High myopia is a high degree of myopic refractive Ophthalmology and Visual Science, error, whereas pathologic myopia is defined by a presence of typical complications in Tokyo Medical and Dental the fundus (posterior staphyloma or myopic maculopathy equal to or more serious than University, Tokyo, Japan; diffuse choroidal atrophy).
    [Show full text]
  • 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
    [Show full text]
  • Dominant Optic Atrophy
    Lenaers et al. Orphanet Journal of Rare Diseases 2012, 7:46 http://www.ojrd.com/content/7/1/46 REVIEW Open Access Dominant optic atrophy Guy Lenaers1*, Christian Hamel1,2, Cécile Delettre1, Patrizia Amati-Bonneau3,4,5, Vincent Procaccio3,4,5, Dominique Bonneau3,4,5, Pascal Reynier3,4,5 and Dan Milea3,4,5,6 Abstract Definition of the disease: Dominant Optic Atrophy (DOA) is a neuro-ophthalmic condition characterized by a bilateral degeneration of the optic nerves, causing insidious visual loss, typically starting during the first decade of life. The disease affects primary the retinal ganglion cells (RGC) and their axons forming the optic nerve, which transfer the visual information from the photoreceptors to the lateral geniculus in the brain. Epidemiology: The prevalence of the disease varies from 1/10000 in Denmark due to a founder effect, to 1/30000 in the rest of the world. Clinical description: DOA patients usually suffer of moderate visual loss, associated with central or paracentral visual field deficits and color vision defects. The severity of the disease is highly variable, the visual acuity ranging from normal to legal blindness. The ophthalmic examination discloses on fundoscopy isolated optic disc pallor or atrophy, related to the RGC death. About 20% of DOA patients harbour extraocular multi-systemic features, including neurosensory hearing loss, or less commonly chronic progressive external ophthalmoplegia, myopathy, peripheral neuropathy, multiple sclerosis-like illness, spastic paraplegia or cataracts. Aetiology: Two genes (OPA1, OPA3) encoding inner mitochondrial membrane proteins and three loci (OPA4, OPA5, OPA8) are currently known for DOA. Additional loci and genes (OPA2, OPA6 and OPA7) are responsible for X-linked or recessive optic atrophy.
    [Show full text]
  • Neuroimaging in Ophthalmology
    Saudi Journal of Ophthalmology (2012) 26, 401–407 Oculoplastic Imaging Update Neuroimaging in ophthalmology ⇑ James D. Kim, MD, MS b; Nafiseh Hashemi, MD a; Rachel Gelman, BA c; Andrew G. Lee, MD a,b,c,d,e, Abstract In the past three decades, there have been countless advances in imaging modalities that have revolutionized evaluation, manage- ment, and treatment of neuro-ophthalmic disorders. Non-invasive approaches for early detection and monitoring of treatments have decreased morbidity and mortality. Understanding of basic methods of imaging techniques and choice of imaging modalities in cases encountered in neuro-ophthalmology clinic is critical for proper evaluation of patients. Two main imaging modalities that are often used are computed tomography (CT) and magnetic resonance imaging (MRI). However, variations of these modalities and appropriate location of imaging must be considered in each clinical scenario. In this article, we review and summarize the best neuroimaging studies for specific neuro-ophthalmic indications and the diagnostic radiographic findings for important clinical entities. Keywords: Neuroophthalmology, Imaging, Magnetic resonance imaging, Computed tomography Ó 2012 Saudi Ophthalmological Society, King Saud University. All rights reserved. http://dx.doi.org/10.1016/j.sjopt.2012.07.001 Introduction Computed tomography Advances in neuroimaging have revolutionized the evalua- The computed tomography (CT) scan obtains image by tion, management, and treatment of neuro-ophthalmic disor- conventional X-ray technology. The CT X-ray source moves ders. Despite the ever-increasing resolution ability of modern around the patient and the X-ray detectors located on the neuroimaging technology, it remains critical that both the opposite side of the X-ray source measure the amount of ordering eye physician and the interpreting radiologist com- attenuation.
    [Show full text]
  • Optic Neuritis – More Than a Loss of Vision
    CLINICAL PRACTICE Edward R Chu Celia S Chen MBBS, is resident medical officer, MBBS, MPHC, FRANZCO, is a consultant ophthalmologist Department of Ophthalmology, Flinders and Senior Lecturer, Department of Ophthalmology, Flinders Medical Centre and Flinders University, Medical Centre and Flinders University, South Australia. South Australia. [email protected] Optic neuritis More than a loss of vision Optic neuritis (ON) is the presence of an acute Background inflammation of the optic nerve that results in painful loss of Optic neuritis is an acute inflammation of the optic nerve that vision. It is the most commonly encountered optic neuropathy results in painful loss of vision. Patients often present to a general in general practice,1–4 and is often associated with multiple practitioner, and early recognition is important as treatment may 3,4 improve the speed of vision recovery. sclerosis (MS). Studies show that in about 15–20% of MS cases, ON was the presenting symptom and more than half of Objective people with MS experience at least one episode of ON during This article provides information on the signs and symptoms of optic their disease.5,6 The risk of developing MS can be stratified by neuritis and discusses appropriate referral, investigations appropriate imaging investigations at the diagnosis of ON. and management. Therefore, early recognition is important to ensure timely Discussion referral, investigation and treatment; prompt treatment can Optic neuritis is the presenting symptom in up to one-fifth of people hasten visual recovery. with multiple sclerosis. Diagnosis of optic neuritis is based on history and examination, therefore obtaining pertinent information Epidemiology and performing proper ophthalmic examination is essential.
    [Show full text]
  • 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
    [Show full text]