Central Serous Papillopathy by Optic Nerve Head Drusen
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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 -
Meeting Materials
BUSINESS, CONSUMER SERVICES, AND HOUSING AGENCY EDMUND G. BROWN JR., GOVERNOR STATE BOARD OF OPTOMETRY 2450 DEL PASO ROAD, SUITE 105, SACRAMENTO, CA 95834 0 P (916) 575-7170 F (916) 575-7292 www.optometry .ca.gov OPToMi fikY Continuing Education Course Approval Checklist Title: Provider Name: ☐Completed Application Open to all Optometrists? ☐ Yes ☐No Maintain Record Agreement? ☐ Yes ☐No ☐Correct Application Fee ☐Detailed Course Summary ☐Detailed Course Outline ☐PowerPoint and/or other Presentation Materials ☐Advertising (optional) ☐CV for EACH Course Instructor ☐License Verification for Each Course Instructor Disciplinary History? ☐Yes ☐No BUSINESS, CONSUMER SERVICES, AND HOUSING AGENCY GOVERNOR EDMUND G. BROWN JR. ~~ TATE BOARD OF OPTOMETRY }I /~E{:fLi\1 ~1' DELWSO ROAD, SUITE 105, SACRAMENTO, CA 95834 op'i,otii~l~ 1~0-A~ifiF' t\,rffi-7170 F (916) 575-7292 www.optometry.ca.gov EDUCATION COU Rw1t;--ftf""~'-!-J/-i~--,--__:___::...:..::....::~-~ $50 Mandatory Fee APPLICATION ,-~Jg l Pursuant to California Code of Regulations (CCR) § 1536, the Board will app~romv~e~c~ott=nfli1~nuFTT1t;tngn'zeWl:uc~rRif'tf-:~MT~~=ilt,;;,,_J receiving the applicable fee, the requested information below and it has been determined that the course meets criteria specified in CCR § 1536(g). In addition to the information requested below, please attach a copy of the course schedule, a detailed course outline and presentation materials (e.g., PowerPoint presentation). Applications must be submitted 45 days prior to the course presentation date. Please type or print -
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. -
National Eye Institute Visual Function Questionnaire (NEI- VFQ25) in Subjects with IIH and Normal Controls
Title: Correlation of Visual Function and National Eye Institute Visual Function Questionnaire (NEI- VFQ25) in subjects with IIH and normal controls. Melanie Truong, DO OD Introduction and Purpose Aims of the study: 1. To assess contrast sensitivity acuity and rapid eye movements (saccades) as a measure of visual function in Idiopathic Intracranial Hypertension (IIH) patients compared to normal patients using the King-Devick Variable Contrast Acuity Chart and the K-D rapid eye movement. 2. To assess subjects quality of visual function using the National Eye Institute Visual Function Questionnaire (NEI-VFQ25) questionnaire and Supplement as a comparison between IIH subjects and normal controls. 3. To study the correlation between visual function and quality of visual function questionnaire in subjects with IIH compared to normal controls. Contrast sensitivity is a measure of afferent visual system. Contrast sensitivity deficit with preservation of normal Snellen acuity has also been reported in glaucoma, compressive disorders of the anterior visual pathways, retinal diseases, and with cerebral lesions.1 This test is significantly more sensitive than Snellen acuity .1 It is also superior for serial testing in patients as there was significant improvement in contrast scores and papilledema grade but no significant change in Snellen acuity.1 Visual manifestation of IIH can also include parafoveal deficits. This can lead to deficits in spatial frequency contrast sensitivity.1 Contrast sensitivity is abnormal initially and improved with regression of papilledema.2 Since decisions on therapy in IIH are based on the presence and change in visual function, assessing visual acuities is not the most accurate measure of visual status in IIH. -
Idiopathic Intracranial Hypertension
IDIOPATHIC INTRACRANIAL HYPERTENSION William L Hills, MD Neuro-ophthalmology Oregon Neurology Associates Affiliated Assistant Professor Ophthalmology and Neurology Casey Eye Institute, OHSU No disclosures CASE - 19 YO WOMAN WITH HEADACHES X 3 MONTHS Headaches frontal PMHx: obesity Worse lying down Meds: takes ibuprofen for headaches Wake from sleep Pulsatile tinnitus x 1 month. Vision blacks out transiently when she bends over or sits down EXAMINATION Vision: 20/20 R eye, 20/25 L eye. Neuro: PERRL, no APD, EOMI, VF full to confrontation. Dilated fundoscopic exam: 360 degree blurring of disc margins in both eyes, absent SVP. Formal visual field testing: Enlargement of the blind spot, generalized constriction both eyes. MRI brain: Lumbar puncture: Posterior flattening of Opening pressure 39 the globes cm H20 Empty sella Normal CSF studies otherwise normal Headache improved after LP IDIOPATHIC INTRACRANIAL HYPERTENSION SYNDROME: Increased intracranial pressure without ventriculomegaly or mass lesion Normal CSF composition NOMENCLATURE Idiopathic intracranial hypertension (IIH) Benign intracranial hypertension Pseudotumor cerebri Intracranial hypertension secondary to… DIAGNOSTIC CRITERIA Original criteria have been updated to reflect new imaging modalities: 1492 Friedman and Jacobsen. Neurology 2002; 59: Symptoms and signs reflect only those of - increased ICP or papilledema 1495 Documented increased ICP during LP in lateral decubitus position Normal CSF composition No evidence of mass, hydrocephalus, structural -
Amaurosis Fugax (Transient Monocular Or Binocular Vision Loss)
Amaurosis fugax (transient monocular or binocular vision loss) Syndee Givre, MD, PhD Gregory P Van Stavern, MD The next version of UpToDate (15.3) will be released in October 2007. INTRODUCTION AND DEFINITIONS — Amaurosis fugax (from the Greek "amaurosis," meaning dark, and the Latin "fugax," meaning fleeting) refers to a transient loss of vision in one or both eyes. Varied use of common terminology may cause some confusion when reading the literature. Some suggest that "amaurosis fugax" implies a vascular cause for the visual loss, but the term continues to be used when describing visual loss from any origin and involving one or both eyes. The term "transient monocular blindness" is also often used but is not ideal, since most patients do not experience complete loss of vision with the episode. "Transient monocular visual loss" (TMVL) and "transient binocular visual loss" (TBVL) are preferred to describe abrupt and temporary loss of vision in one or both eyes, since they carry no connotation regarding etiology. Transient visual loss, either monocular or binocular, reflects a heterogeneous group of disorders, some relatively benign and others with grave neurologic or ophthalmologic implications. The task of the clinician is to use the history and examination to localize the problem to a region in the visual pathways, identify potential etiologies, and, when indicated, perform a focused battery of laboratory tests to confirm or exclude certain causes. Therapeutic interventions and prognostic implications are specific to the underlying cause. This topic discusses transient visual loss. Other ocular and cerebral ischemic syndromes are discussed separately. APPROACH TO TRANSIENT VISUAL LOSS — By definition, patients with transient visual loss almost always present after the episode has resolved; hence, the neurologic and ophthalmologic examination is usually normal. -
Neuroradiology for Ophthalmologists
Eye (2020) 34:1027–1038 https://doi.org/10.1038/s41433-019-0753-z REVIEW ARTICLE Neuroradiology for ophthalmologists 1 2 1 1,3,4,5,6,7 Bayan Al Othman ● Jared Raabe ● Ashwini Kini ● Andrew G. Lee Received: 3 June 2019 / Revised: 29 October 2019 / Accepted: 24 November 2019 / Published online: 2 January 2020 © The Author(s), under exclusive licence to The Royal College of Ophthalmologists 2020 Abstract This article will review the best approaches to neuroimaging for specific ophthalmologic conditions and discuss characteristic radiographic findings. A review of the current literature was performed to find recommendations for the best approaches and characteristic radiographic findings for various ophthalmologic conditions. Options for imaging continue to grow with modern advances in technology, and ophthalmologists should stay current on the various radiographic techniques available to them, focusing on their strengths and weaknesses for different clinical scenarios. Introduction Computed tomography (CT) 1234567890();,: 1234567890();,: Modern imaging technology continues to advance the CT imaging reconstructs a three-dimensional image made boundaries and increase the options available to physicians of many conventional x-ray images. The conventional x-ray with respect to neuroradiology. In ophthalmology, the most images are ordered in tomographic slices that have been common studies employed are computed tomography (CT) computerized so a viewer can scroll through the images, and magnetic resonance imaging (MRI). There are several analyzing sequential cross-sections [1]. Density is the pri- different types of protocols that provide unique advantages mary characteristic that determines image appearance on a and disadvantages depending on the clinical scenario. This CT scan. As with traditional x-rays, tissues appear on a grey article endeavours to review those options and discuss how scale ranging from white (i.e., hyperdense tissues such as they are best employed to evaluate a variety of specific bone) to black (i.e., hypodense materials such as air). -
Polycythemia Vera Presenting with Bilateral Papilledema Retinitis
July - August 2009 Lett ers to the Editor 325 Amjad Salman, Pragya Parmar, vary signiÞ cantly. With the increasing use of MRI in all cases Vanila G Coimbatore, Rajmohan Meenakshisunderam, suspected to be a brain syndrome, CVT has been increasing Nelson Jesudasan A Christdas diagnosed. MRI is now the gold standard in the diagnosis of CVT as rightly done in this case. Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli - 620 001, India Visual loss in CVT maybe due to thrombotic ischemia of any structure of the visual pathway or due to pressure on the optic Correspondence to Dr. Salman Amjad, Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli - 620 001, India. nerve due to the transmitt ed raised intracranial pressure (ICP). E-mail: [email protected] All cases of CVT with visual loss require visual Þ eld analysis and measurement of optic nerve sheath diameter using B-scan References ultrasonography (USG). Visual loss in patients with CVT due to transmitt ed raised ICP (indicated by increased optic nerve sheath 1. Gillies MC, Simpson JM, Billson FA, Luo W, Penfold P, Chua W, et al. diameter on USG) not amenable to medical management is an Safety of an intravitreal injection of triamcinolone: Results from a indication for optic nerve sheath decompression (ONSD). ONSD randomized clinical trial. Arch Ophthalmol 2004;122:336-40. as a treatment option for the visual loss in the left eye should have 2. Thompson JT. Cataract formation and other complications of intravitreal triamcinolone acetonide for macular edema. Am J been off ered to the patient in this case, as it has been shown to [4,5] Ophthalmol 2006;141:629-37. -
Progressive Visual Failure in an Eye with Optic Disc Drusen and an Orbital Mass
PHOTO ESSAY Progressive Visual Failure in an Eye with Optic Disc Drusen and an Orbital Mass Nancy M. Younan MB, BS, MPH, and Ian C. Francis, FASOPRS FIG. 1. Axial computed tomography demonstrating high attenuation in the right optic nerve head consistent with drusen, and a lobular mixed attenuation mass in the right orbital apex consistent with dermoid. Abstract: A 44-year-old woman with progressive monoc 44-year-old woman with long-standing subnormal vi ular visual loss was found to have ipsilateral optic disc A sual acuity in the OD attributed to amblyopia presented drusen and an ipsilateral orbital apex mass compressing the with a 1-month history of further decline in OD vision. The optic nerve. The mass, not the drusen, was considered re patient stated that visual acuity in that eye had been mea sponsible for the worsening vision. Visual loss should not sured at 20/120 3 years earlier. There was no other signifi be glibly attributed to drusen, particularly if the visual loss cant medical history. Examination revealed visual acuities is rapidly progressive. Retrobulbar imaging should be con of count fingers OD and 20/15 OS. There was a marked sidered in such cases. right relative afferent pupillary defect. Funduscopy of the OD demonstrated optic nerve pallor with gross optic nerve (JNeuro-Ophthalmol 2003;23: 31-33) drusen and a thin nerve fiber layer. In the OS, funduscopy revealed a normal left optic nerve head. Ocular rotations and alignment were normal and there was no proptosis. Au The Ocular Plastics Unit, The Prince of Wales Hospital, Randwick, tomated static perimetry demonstrated patchy right central Sydney, Australia, and the University of NSW, Sydney, Australia. -
Optic Disc Drusen, Glaucoma, Or Could It Be Both?
Title: Where are the defects coming from…Optic Disc Drusen, Glaucoma, or could it be both? Authors: Rachel Goretsky OD, Biana Gekht OD Abstract: Optic disc drusen and glaucoma cause similar retinal nerve fiber layer(RNFL) as well as visual field defects. This paper describes a patient who has both conditions and the management involved. I. Case History: 66 year old African-American male presents for dilation and imaging. Patient has a history of Glaucoma for several years; he is taking Brimonidine bid OU and Latanoprost qhs OU with reported good compliance. Medical & Ocular History: • Hypertension, gout, cholesterol and stents placed in leg and chest. Glaucoma OU. History of peripheral iridotomy OU one year ago. Medications:Amplodipine, clopidogrel, allopurinol II. Pertinent findings: • Maximum pressure history is 17 OD, 19 OS, current visit 16 OD, 19 OS • Anterior chamber : Grade 2 Van Herick Angles OU • Iris: Peripheral Iridotomy, patent at 12 o’clock OD,OS • Optic disc: 0.3r OD, OS small nerves, mild blurry margins indicative of disc drusen • Macula: diffuse epiretinal membrane OU • Pachymetry : 556 OD/ 566 OS • Gonioscopy: open to trabecular meshwork (TM) superiorly, otherwise no structures visible OD, open to TM inferiorly, otherwise no structures visible OS • Spectralis Optical Coherence Tomography(OCT): optic disc drusen with small cups and disc area OU • Visual field exhibited no defects OD, inferior nasal defects OS. III. Differential Diagnosis: • Papilledema, tilted discs, pseudotumor cerebri, myelinated nerve fiber layer IV. Diagnosis and Discussion Optic nerve head drusen are hyaline deposits made of calcium phosphate as well as amino acids, among other materials. -
Papilledema": Neuroradiologic Evaluation of Optic Disk Protrusion with Dynamic Orbital CT
681 "Papilledema": Neuroradiologic Evaluation of Optic Disk Protrusion with Dynamic Orbital CT John R. Jinkins 1 Current-generation CT scc·lners enable the visualization in vivo of structures and substructures that were previously unobservable. Certainly the orbit and optic nerve/ sheath complex have demonstrated a great number of pathologic and normal anatomic variations. It has been found in patients with elevated intracranial pressure that what was previously thought to be simple papilledema in fact masks a surprisingly large component of optic papilla protru<;ion, There may be a variable amount of increased intercellular/axonal fluid within tt.. - optic disk in patients with increased intracranial pressure; however, a significant factor in the " swollen disk" is the simple transmission of pressure along the optic nerve sheath to the papilla, causing it to bulge. Further investigations with dynamic CT reveal that there is decreased perfusion of the optic disk in the active phase of severe increased intracranial pressure in patients with papilledema and/or protrusion as compared with normal control subjects. This de pressed flow pattern seems to originate subacutely and appears to resolve in certain patients after normalization of the elevated pressure. These findings apparently indicate that clinical intervention in cases of intracranial hypertension to restore the hemodynamic status of the optic disk would be timely, and thereby avert irreversible damage. This suggests and supports the theory that increased intracranial pressure may lead to rapid vision loss by the mechanical mechanism of pressure projected directly to the junction of the optic nerve and optic nerve head, leading to decreased perfusion, ischemia, axonal flow stasis, and resultant optic nerve atrophy. -
Pseudotumor Cerebri and Papilledema an OVERVIEW of THIS PERPLEXING SYNDROME and ITS HALLMARK PRESENTATION
Pseudotumor Cerebri and Papilledema AN OVERVIEW OF THIS PERPLEXING SYNDROME AND ITS HALLMARK PRESENTATION. BY RUI WANG; ASHWINI KINI, MD; BAYAN AL OTHMAN, MD; AND ANDREW G. LEE, MD seudotumor cerebri, also IIH and secondary intracranial hyper- specific, headaches associated with IIH known as idiopathic intra- tension due to cerebral venous throm- are often daily and are retroocular.9 Pcranial hypertension (IIH), bosis and other causes of obstructed The headaches may resemble migraine describes the perplexing syndrome of venous outflow. headaches with associated symptoms increased intracranial pressure (ICP) Additionally, several systemic dis- of nausea, vomiting, and photophobia. in the absence of a space-occupying eases, drugs, and vitamin deficiencies In fact, many patients with IIH have lesion on neuroimaging or other or excesses have been reported to be coexisting migraine headaches, mak- etiology. Although the disease can associated with IIH. Of medications ing the diagnosis difficult.10 be observed in patients of any age, associated with IIH, growth hormones, Transient visual obscurations IIH classically presents among obese tetracyclines, and retinoids have been (TVOs) have been found to occur (body mass index >30) women of the most often reported.3-5 Other in about two-thirds of patients with childbearing age. Due to the increased systemic illnesses associated with papilledema. TVOs typically last only prevalence of obesity in recent years, pseudotumor cerebri include Addison seconds at a time and may be bilater- a significant