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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. -
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. -
RETINAL DISORDERS Eye63 (1)
RETINAL DISORDERS Eye63 (1) Retinal Disorders Last updated: May 9, 2019 CENTRAL RETINAL ARTERY OCCLUSION (CRAO) ............................................................................... 1 Pathophysiology & Ophthalmoscopy ............................................................................................... 1 Etiology ............................................................................................................................................ 2 Clinical Features ............................................................................................................................... 2 Diagnosis .......................................................................................................................................... 2 Treatment ......................................................................................................................................... 2 BRANCH RETINAL ARTERY OCCLUSION ................................................................................................ 3 CENTRAL RETINAL VEIN OCCLUSION (CRVO) ..................................................................................... 3 Pathophysiology & Etiology ............................................................................................................ 3 Clinical Features ............................................................................................................................... 3 Diagnosis ......................................................................................................................................... -
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 -
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. -
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 -
Intracranial Mass Lesion in a Patient Being Followed up for Amblyopia
DOI: 10.4274/tjo.galenos.2020.36360 Turk J Ophthalmol 2020;50:317-320 Case Report Intracranial Mass Lesion in a Patient Being Followed up for Amblyopia Ali Mert Koçer, Bayazıt İlhan, Anıl Güngör Ulucanlar Ophthalmology Trainig and Research Hospital, Clinic of Ophthalmology, Ankara, Turkey Abstract A 12-year-old boy being followed up for amblyopia presented to our hospital with visual disturbance in the left eye. The patient’s best corrected visual acuity on Snellen chart was 1.0 in the right eye and 0.3 in the left eye. Increased horizontal cup-to-disc ratio was detected on dilated fundus examination. Retinal nerve fiber layer measurement showed diffuse nerve fiber loss and visual field test showed bitemporal hemianopsia. Magnetic resonance imaging revealed a lesion that filled and widened the sella and suprasellar cistern and compressed the optic chiasm. The patient was operated with transcranial approach. The pathologic examination revealed craniopharyngioma. Keywords: Amblyopia, craniopharyngioma, hemianopsia Introduction cylindrical refractive errors of 1.5-2 diopters (D) or more and is more common in hyperopic eyes than in myopia.2 Amblyopia is poor best corrected visual acuity (BCVA) in one Craniopharyngioma is a benign tumor that develops from or both eyes due to low vision or abnormal binocular interaction the remnant of Rathke’s pouch and is located in the sellar/ without any detectable structural defect in the eye or visual parasellar region.3 It shows a bimodal age distribution, with pathways. Amblyopic vision loss can be corrected if treated at patients usually diagnosed between the ages of 5 and 14 or after an early age. -
VISUAL FIELD Pathway Extends from the „Front‟ to the „Back‟ of the RETINA Brain
NOTE: To change the image on this slide, select the picture and delete it. Then click the Pictures icon in the placeholde r to insert your own image. Visual Pathway Disorders Amr Hassan, MD, FEBN Associate professor of Neurology - Cairo University Optic nerve • Anatomy of visual pathway • How to examine • Visual pathway disorders • Quiz 2 Optic nerve • Anatomy of visual pathway • How to examine • Visual pathway disorders • Quiz 3 Optic nerve The Visual Pathway VISUAL FIELD Pathway extends from the „front‟ to the „back‟ of the RETINA brain. ON OC OT LGN OPTIC RADIATIONS ON = Optic Nerve OC = Optic Chiasm OT = Optic Tract LGN = Lateral Geniculate Nucleus of Thalamus VISUAL CORTEX 5 The Visual Pathway Eyes & Retina Light >> lens >> retina (inverted and reversed image). Eyes & Retina Eyes & Retina • Macula: oval region approximately 3-5 mm that surrounds the fovea, also has high visual acuity. • Fovea: central fixation point of each eye// region of the retina with highest visual acuity. Eyes & Retina • Optic disc: region where axons leaving the retina gather to form the Optic nerve. Eyes & Retina • Blind spot located 15° lateral and inferior to central fixation point of each eye. Object to be seen Peripheral Retina Central Retina (fovea in the macula lutea) 12 Photoreceptors © Stephen E. Palmer, 2002 Photoreceptors Cones • Cone-shaped • Less sensitive • Operate in high light • Color vision • Less numerous • Highly represented in the fovea >> have high spatial & temporal resolution >> they detect colors. © Stephen E. Palmer, 2002 Photoreceptors Rods • Rod-shaped • Highly sensitive • Operate at night • Gray-scale vision • More numerous than cons- 20:1, have poor spatial & temporal resolution of visual stimuli, do not detect colors >> vision in low level lighting conditions © Stephen E. -
Erounds on Wednesday Mornings, the West LA VA Optometry Residents & Student Participate in Erounds
West Los Angeles VA Health Care Center, Los Angeles, CA eRounds On Wednesday mornings, the West LA VA Optometry residents & student participate in eRounds. An eRounds typically includes presentation of one or more illustrative cases of the condition under consideration. During the case presentations, trainees are asked to identify normal and abnormal findings, list ocular differential diagnoses, list systemic differential diagnoses when applicable, and state options for ocular (and systemic) management. This is usually followed by a presentation of information on the topic, which may include epidemiology, presenting signs and symptoms of the condition, clinical diagnostic testing, ancillary testing, ocular and systemic management, etc. Topics include: Acne rosacea Conjunctival actinic keratosis Conjunctivochalasis Entropion and ectropion Floppy eyelid syndrome Fat prolapse Herpetic eye disease Hyphema Neovascular glaucoma Corneal degenerations Squamous cell carcinoma of the eyelid Basal cell carcinoma of the eyelid Sebaceous carcinoma Pemphigoid Phthisis bulbi Ocular manifestations of Valsalva maneuver Xanthelasma Branch retinal artery occlusion Central retinal artery occlusion Giant cell arteritis Fibrinoplatelet retinal embolus Ophthalmic artery occlusion Multiple Hollenhorst plaques Solitary Hollenhorst plaque Best dystrophy Retinitis pigmentosa Cone-rod dystrophies Optic disc drusen Tilted disc syndrome Stargardt’s disease Diabetic retinopathy Diabetes mellitus and ocular media disorders Diabetes mellitus and neuro-ophthalmic disease -
PG Series Ophthalmology Buster
PG Series Ophthalmology Buster PG Series Ophthalmology Buster E Ahmed Formerly Head, Department of Ophthalmology Calcutta National Medical College Consultant, Eye Care and Research Centre Kolkata JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3, EMCA House, 23/23B Ansari Road, Daryaganj New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672, Rel: 32558559 Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected] Visit our website: www.jaypeebrothers.com Branches • 2/B, Akruti Society, Jodhpur Gam Road Satellite, Ahmedabad 380 015 Phones: +91-079-26926233, Rel: +91-079-32988717, Fax: +91-079-26927094 e-mail: [email protected] • 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East, Bangalore 560 001 Phones: +91-80-22285971, +91-80-22382956, Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected] • 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road, Chennai 600 008 Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089 Fax: +91-44-28193231 e-mail: [email protected] • 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road, Hyderabad 500 095 Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: [email protected] • No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road, Kochi 682 018, Kerala Phones: +91-0484-4036109, +91-0484-2395739, +91-0484-2395740 e-mail: [email protected] • 1-A Indian Mirror Street, Wellington Square, Kolkata 700 013 Phones: +91-33-22451926, +91-33-22276404, +91-33-22276415, Rel: +91-33-32901926 Fax: +91-33-22456075, e-mail: [email protected] • 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel, Mumbai 400 012 Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896 Fax: +91-22-24160828, e-mail: [email protected] • “KAMALPUSHPA” 38, Reshimbag, Opp. -
Visual Field Defects and Aphasia Testing : a Proposed Adaptation of the Boston Diagnostic Aphasia Examination
University of Montana ScholarWorks at University of Montana Graduate Student Theses, Dissertations, & Professional Papers Graduate School 1985 Visual field defects and aphasia testing : a proposed adaptation of the Boston diagnostic aphasia examination. Laura L. Smith The University of Montana Follow this and additional works at: https://scholarworks.umt.edu/etd Let us know how access to this document benefits ou.y Recommended Citation Smith, Laura L., "Visual field defects and aphasia testing : a proposed adaptation of the Boston diagnostic aphasia examination." (1985). Graduate Student Theses, Dissertations, & Professional Papers. 7199. https://scholarworks.umt.edu/etd/7199 This Thesis is brought to you for free and open access by the Graduate School at ScholarWorks at University of Montana. It has been accepted for inclusion in Graduate Student Theses, Dissertations, & Professional Papers by an authorized administrator of ScholarWorks at University of Montana. For more information, please contact [email protected]. COPYRIGHT ACT OF 1976 This is an unpublished m a n u s c r i p t in w h i c h copyright s u b s i s t s . Any further rep r i n t i n g of its contents must be a p p r o v e d BY THE AUTHOR. Ma n s f i e l d Library Uni v e r s i t y of Montana Date : 1 S o o ______ Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Visual Field Defects and Aphasia Testing: A Proposed Adaptation of the Boston Diagnostic Aphasia Examination by Laura L. -
Permanent Central Scotoma Caused by Looking at the Sun During an Eclipse, and Complicated by Uniocular, Transi- Ent, Revolving Hemianopsia
PERMANENT CENTRAL SCOTOMA CAUSED BY LOOKING AT THE SUN DURING AN ECLIPSE, AND COMPLICATED BY UNIOCULAR, TRANSI- ENT, REVOLVING HEMIANOPSIA. From Dr. Knapp’s Practice, Reported by Dr. A. DUANE, New York. Reprinted from the Archives of Ophthalmology, Vol. xxiv., No. i, 1895 PERMANENT CENTRAL SCOTOMA CAUSED BY LOOKING AT THE SUN DURING AN ECLIPSE, AND COMPLICATED BY UNIOCULAR, TRANSI- ENT, REVOLVING HEMIANOPSIA. From Dr. Knapp’s Practice, Reported by Dr. A. DUANE, New York, instances of central scotoma after expos- ALTHOUGHure to sunlight are by no means rare, the subjoined case seems worthy ofrecord, because of the persistence of the scotoma twelve years afterwards, and because of the pres- ence of a peculiar hemiopic and scotoma scintil- lans, which apparently was likewise the result of the action of the sun’s rays. The patient, P. W., a man twenty-four years of age, consulted Dr. Knapp on Feb. 5, 1895, and gave the following history: Twelve years previous he had, on the occasion of the transit of Venus, 1 looked directly at the sun through the tube formed by the nearly closed fist. Soon after, he found that when both eyes were open, but not when the left was closed, a greenish cloud hid com- pletely the centre of every object looked at. This had exactly the shape of the illuminated portion of the sun at the time of the transit, i. e., was a circle with a crescentic defect at the upper part corresponding to the spot occupied by the planet at the time. It was then of considerable size, covering an area 5 inches in width when projected upon a surface 15 or 20 inches off.