Clinical Policy: Fundus Photography Reference Number: CP.VP.29 Coding Implications Last Review Date: 05/2020 Revision Log
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An Unusual Presentation of Subfrontal Meningioma: a Case Report and Literature Review for Foster Kennedy Syndrome
Intern Emerg Med (2011) 6:267–269 DOI 10.1007/s11739-010-0437-y CE - MEDICAL ILLUSTRATION An unusual presentation of subfrontal meningioma: a case report and literature review for Foster Kennedy syndrome Shahram Lotfipour • Kris Chiles • J. Akiva Kahn • Tareg Bey • Scott Rudkin Received: 17 December 2009 / Accepted: 13 July 2010 / Published online: 26 August 2010 Ó SIMI 2010 Introduction head trauma. She admitted to abusing crack cocaine for 13 years with her last use 4 months ago. She denied any Foster Kennedy syndrome, named after neurologist Robert trouble with ambulation, dizziness, and changes in hearing or Foster Kennedy (1884–1952), describes unilateral ipsilat- other alterations in sensation. She denied any suicidal or eral optic atrophy and contralateral papilledema from an homicidal ideation. The patient denied any auditory halluci- intracranial mass. This syndrome is unreliably associated nations, but did report that she had been experiencing with anosmia and ipsilateral proptosis [1]. It originates visual hallucinations and visual disturbances for at least from variety of intracranial pathologies, but most often a 6–8 months. She reported complete blindness in the left eye, subfrontal mass. We present a case of Foster Kennedy and shadow perception in her right for an unknown length of syndrome and review its etiology, pathology and incidence time. Her past medical history was notable for major in intracranial tumors. depression. The patient did not have a previous history of hallucinations or psychosis, and had never been hospitalized for psychiatric reasons. The patient was not on any medica- Case report tions, and was allergic to penicillin and codeine. -
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. -
The Acute and Long-Term Ocular Effects of Accelerated Hypertension: a Clinical and Electrophysiological Study
THE ACUTE AND LONG-TERM OCULAR EFFECTS OF ACCELERATED HYPERTENSION: A CLINICAL AND ELECTROPHYSIOLOGICAL STUDY 1 2 2 3 3 L2 S. J. TALKS , , P. GOOD , C. G. CLOUGH , D. G. BEEVERS and P. M. DODSON Birmingham SUMMARY the invention of the ophthalmoscope in 1851 the Thirty-four patients with accelerated hypertension were causes of this disturbance could be described? clinically examined. The visual evoked potential (VEP) Leibreich,4 in 1859, was the first to describe and electroretinogram (ERG) were recorded: acutely 'albuminuric retinitis' in Bright's disease. However, in 12 patients, being repeated in 7 patients up to 6 it was not until 1914, after the invention of the Riva months later. In the remaining 22 patients these tests Rocci sphygmomanometer at the end of the nine were performed 2-4 years after presentation. Visual teenth century, that Volhard and Fahr6 related the acuity was 5.6/12 in 22 of 68 (32 %) eyes at presentation retinopathy to arterial hypertension. and 5.6/12 in 10 of 58 (19%) eyes at follow-up. The It was then realised that the fundal appearance cause of severest loss of vision appeared to be anterior was associated with the severity of the hypertension ischaemic optic neuropathy, found in 3 cases. During and with the prognosis of the patient. In 1939 Keith the acute stage 11 patients (92%) had abnormal VEPs et aC drew up a four-group grading system. Grade 3 and all had abnormal ERGs. The group mean PI00 (more recently called accelerated hypertensionS) latency, of the 7 patients (14 eyes) seen acutely and consisted of 'angiospastic retinitis', 'characterised followed up at 6 months, was 123.8 ms with significant especially by oedema, cotton wool patches, and recovery of latency (p<0.005) to 110.9 ms. -
MOC PORT/DOCK Practice Core Modules Content Outline
MOC PORT/DOCK Practice Core Modules Content Outline 1 Cataract and Anterior Segment (10%) 1.1 Basic Anatomical and Scientific Aspects 1.1.1 The Normal Lens 1.1.1.1 Anatomy 1.2 Assessment Techniques 1.2.1 History-Taking and Preoperative Examination of Ocular Structures 1.2.1.1 Take patient history 1.2.1.2 Examine ocular structures 1.2.1.3 Signs and symptoms 1.2.1.4 Indications for surgery 1.2.1.6 External examination 1.2.1.7 Slit-lamp examination 1.2.1.8 Fundus evaluation 1.2.1.9 Impact on visual functioning and quality of life 1.2.2 Measurement of Visual and Macular Function 1.2.2.1 Visual acuity testing 1.2.2.2 Test visual acuity 1.2.2.5 Visual field testing 1.2.2.6 Test visual field 1.2.2.7 Cataract's effect on visual acuity 1.2.2.8 Estimate cataract's effect on visual acuity 1.2.2.10 Measure visual (and macular) function 1.2.4.3 Evaluate glare disability: subjective and objective 1.3 Clinical Disease Conditions and Manifestations 1.3.1 Types of Cataract 1.3.1.1 Identify types of cataracts 1.3.2 Anterior Segment Disorders 1.3.2.1 Diagnose anterior segment disorders 1.3.2.2 Cataract associated with uveitis 1.3.2.3 Diabetes mellitus and cataract formation 1.3.2.4 Lens-induced glaucoma 1.3.2.4.1 Lens particle 1.3.2.4.2 Phacolytic 1.3.2.4.3 Phacomorphic Copyright and Use Policy for ABO Content Outlines © 2017 – American Board of Ophthalmology. -
Ophthalmology July 10-11, 2018 Bangkok, Thailand
J Clin Exp Ophthalmol 2018, Volume 9 conferenceseries.com DOI: 10.4172/2155-9570-C4-088 3rd International Conference on Ophthalmology July 10-11, 2018 Bangkok, Thailand Stage of Hypertensive Retinopathy among Patients who undergone Cataract Surgery in Zamboanga City Medical Center Jerne Kaz Niels B. Paber Dr.evangelista st, sta. Catalina Background: Individuals who are not known hypertensive are noted to have blurring of vision as an initial presentation. Preventable co- morbidity such as hypertension is essential in saving sight in patients with cataract. Objective: To determine the prevalence of hypertension and stage of hypertensive retinopathy among individuals who undergone cataract surgery and to identify the association between the stage of hypertension and the risk factors for hypertension and the stage of hypertensive retinopathy. Methods: This prospective study included 203 individuals. All of the participants were noted to have mature cataract surgery done and was noted to have followed up at Tzu Chi Eye center from July 1 2017 to March 30, 2018. The nature, significance and procedure of the study were explained to every identified respondent. There was only one ophthalmologist who saw the participants who enrolled in the study. Once they understood the study, a written informed consent was taken. They were asked to answer questions provided by the researcher and their laboratory results were recorded. A follow up after 2 weeks was done in order to determine the stage of retinopathy of the patients. Demographic variables, hypertensive retinopathy, history of hypertension, medication usage, compliance, ECG changes, proteinuria, creatinine, and cardiomegaly on chest x-ray, radiographic identification of Atheromatous aorta and fundoscopic examination were analyzed. -
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. -
Bilateral Acquired Progressive Retinal Nerve Fiber Layer Myelination
Bilateral Acquired Progressive Retinal Nerve Fiber Layer Myelination Abstract We present the multimodal imaging findings of an unusual case of bilateral acquired progressive myelination of the optic disc over a 10-year follow up period, in a hyperopic adolescent patient in the absence of an underlying ocular or systemic abnormality. Myelination of the left optic disc was noted at age 7 and of the right optic disc at age 13 but no other ocular or systemic abnormalities were identified. Cross sectional OCT and en face OCT angiography confirmed the presence of myelination of the retinal nerve fiber layer and excluded other etiologic possibilities including an astrocytic hamartoma. Keywords: Optic Nerve; Optic Fiber Myelination, Acquired, Hyperopia INTRODUCTION Myelination of the retinal nerve fiber layer occurs in 1% of the population and is most frequently congenital and non-progressive. (1) Congenital cases are typically isolated but may be rarely associated with the syndrome of ipsilateral high myopia, strabismus and amblyopia (2,3), although cases have been reported in hyperopic eyes. Reports of acquired and progressive myelination associated with congenital optic nerve disorders such as Arnold-Chiari malformation, hydrocephalus, optic disc drusen, and iatrogenic causes such as optic nerve sheath fenestration, are relatively rare.(4–8) PLEASE ADJUST THE REFERENCE CITATIONS While affected patients are typically asymptomatic, retinal nerve fiber layer myelination can be rarely associated with visual loss. Even more unusual are reports of acquired and progressive myelination of the nerve fiber layer. We present the multimodal imaging findings of such a case in a healthy young patient with a 10-year follow up. -
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 -
Annual Report Research Activity 2019
Annual Report Research Activity 2019 Division of Clinical Neuroscience University of Oslo and Oslo University Hospital 0 Contents Oslo University Hospital and the University of Oslo .................................................................................... 4 From Division Director Eva Bjørstad ........................................................................................................... 4 Division of Clinical Neuroscience (NVR) Organizational Chart ..................................................................... 5 Department of Physical Medicine and Rehabilitation Rehabilitation after trauma....................................................................................................................... 6 Group Leader: Nada Andelic Painful musculoskeletal disorders .............................................................................................................. 9 Group Leader: Cecilie Røe Department of Refractory Epilepsy - National Centre for Epilepsy Complex epilepsy .................................................................................................................................... 11 Group Leader: Morten Lossius Department of Neurosurgery Neurovascular-Hydrocephalus Research Group ..................................................................................... 16 Group Leader: Per Kristian Eide Oslo Neurosurgical Outcome Study Group (ONOSG) ................................................................................. 19 Group Leaders: Eirik Helseth and Torstein -
Ocular Co-Morbidity in Patients with Refractive Errors in Nigeria
N igerian Journal of Ophthalmology 2011; 19(1): 19-24 Ocular Co-morbidity in Patients with Refractive Errors in Nigeria BO Adegbehingbe FWA CS, O Adeoye FWA CS, BA Adewara M BBS Ophthalmology Unit, Faculty of Clinical Sciences, Obafemi Awolowo University, Ile-Ife 1-4 ABSTRACT a high proportion of patients attend ing ophthalm ic clinics. Refractive errors can be easily d iagnosed , m easured and Purpose: To d eterm ine the pattern and prevalence of other corrected w ith spectacles or other refractive corrections to ocular problem s seen in patients w ith refractive errors attain normal vision. H ow ever, non correction or inad equate in a N igerian teaching hospital. correction of refractive errors becom es a m ajor cause of low Methods: A retrospective hospital-based review of all vision and even blind ness. Globally, there are 8 m illion consecutive patients w ho presented w ith signs and people w ho are blind and 153 m illion w ith visual sym ptom s of refractive errors at the Obafem i Aw olow o im pairm ent (presenting visual acuity <6/ 18 in the better University Teaching H ospitals Com plex betw een 1st eye) d ue to uncorrected refractive errors; this exclud es January 2007 and 31st August 2007. Patients w ho had a presbyopia.5 Poor visual outcom e in patients w ith refractive d iagnosis of refractive error and su bsequently had errors could be in part d ue to other associated ocular d etailed eye exam ination w ere includ ed in this stud y.