Color Atlas of Ophthalmology
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Fundus Signs in Temporal Arteritis
Br J Ophthalmol: first published as 10.1136/bjo.62.9.591 on 1 September 1978. Downloaded from British Journal of Ophthalmology, 1978, 62, 591-594 Fundus signs in temporal arteritis D. McLEOD, E. 0. OJI, E. M. KOHNER, AND J. MARSHALL From Moorfields Eye Hospital and Institute of Ophthalmology, London SUMMARY A patient with temporal arteritis developed a variety of ischaemic lesions in the eyes. Infarction of the inner retina and optic nerve head was delineated on presentation by white swelling in the retinal nerve fibre layer. The role of interrupted axoplasmic transport in the production of this sign is discussed. Outer retinal infarction was also noted on presentation and subsequently gave rise to striking pigmented scars. Temporal arteritis often presents with visual loss, the central venous tributaries were of normal and necropsy examination in such cases shows wide- calibre and colour. No abnormality of the inner spread disease of the ophthalmic artery and the retina was noted in the territory of supply of the extraocular course of its ciliary and retinal branches central retinal artery. (Henkind et al., 1970). The medial and lateral At first sight the left eye showed a similar ophthal- posterior ciliary arteries supply the optic nerve head, moscopic picture, with pale swelling of the nasal the outer retina, and, in 20 to 50% of individuals, part of the optic disc and a row of fluffy white by copyright. a variable area of inner retina contiguous with the cotton-wool spots crossing the papillomacular optic disc (Hayreh, 1969); the central retinal artery bundle (Fig. 2). -
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 ......................................................................................................................................... -
Outer Retina Changes on Optical Coherence Tomography in Vitamin a Defciency Meghan K
Berkenstock et al. Int J Retin Vitr (2020) 6:23 https://doi.org/10.1186/s40942-020-00224-1 International Journal of Retina and Vitreous CASE REPORT Open Access Outer retina changes on optical coherence tomography in vitamin A defciency Meghan K. Berkenstock, Charles J. Castoro and Andrew R. Carey* Abstract Background: Vitamin A defciency is rare in the United States and can be missed in patients with malabsorption syn- dromes without a high dose of suspicion. Ocular complications of hypovitaminosis A include xerosis and nyctalopia, and to a lesser extent reduction in visual acuity and color vision. Outer retinal changes, as seen on spectral domain optic coherence tomography (SD-OCT), in patients with vitamin A defciency have previously not been documented. Case presentation: We present two cases with symptoms of severe nyctalopia who were subsequently diagnosed with severe Vitamin A defciency and their unique fndings on SD-OCT of outer nuclear layer difuse thinning with irregular appearance of the interdigitating zone and the ellipsoid zone as well as normalization after vitamin A supplementation. Conclusions: Outer nuclear layer thinning and disruption of the outer retinal bands on SD-OCT are reversible with correction of vitamin A defciency. Improvement in visual acuity, color vision, and nyctalopia are possible with early diagnosis and appropriate treatment. Keywords: Vitamin A defciency, Optical coherence tomography, Nyctalopia Background reverse ocular complications prior to permanent vision Most commonly seen in regions with food insecurity, loss [16, 24, 25]. Only a few reports have described the nutritional defciencies, or restricted diets, vitamin A photoreceptor changes on spectral domain optical coher- defciency is rare in developed countries [1–9]. -
Genes in Eyecare Geneseyedoc 3 W.M
Genes in Eyecare geneseyedoc 3 W.M. Lyle and T.D. Williams 15 Mar 04 This information has been gathered from several sources; however, the principal source is V. A. McKusick’s Mendelian Inheritance in Man on CD-ROM. Baltimore, Johns Hopkins University Press, 1998. Other sources include McKusick’s, Mendelian Inheritance in Man. Catalogs of Human Genes and Genetic Disorders. Baltimore. Johns Hopkins University Press 1998 (12th edition). http://www.ncbi.nlm.nih.gov/Omim See also S.P.Daiger, L.S. Sullivan, and B.J.F. Rossiter Ret Net http://www.sph.uth.tmc.edu/Retnet disease.htm/. Also E.I. Traboulsi’s, Genetic Diseases of the Eye, New York, Oxford University Press, 1998. And Genetics in Primary Eyecare and Clinical Medicine by M.R. Seashore and R.S.Wappner, Appleton and Lange 1996. M. Ridley’s book Genome published in 2000 by Perennial provides additional information. Ridley estimates that we have 60,000 to 80,000 genes. See also R.M. Henig’s book The Monk in the Garden: The Lost and Found Genius of Gregor Mendel, published by Houghton Mifflin in 2001 which tells about the Father of Genetics. The 3rd edition of F. H. Roy’s book Ocular Syndromes and Systemic Diseases published by Lippincott Williams & Wilkins in 2002 facilitates differential diagnosis. Additional information is provided in D. Pavan-Langston’s Manual of Ocular Diagnosis and Therapy (5th edition) published by Lippincott Williams & Wilkins in 2002. M.A. Foote wrote Basic Human Genetics for Medical Writers in the AMWA Journal 2002;17:7-17. A compilation such as this might suggest that one gene = one disease. -
Supranuclear and Internuclear Ocular Motility Disorders
CHAPTER 19 Supranuclear and Internuclear Ocular Motility Disorders David S. Zee and David Newman-Toker OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN OCULAR MOTOR SYNDROMES CAUSED BY LESIONS OF THE MEDULLA THE SUPERIOR COLLICULUS Wallenberg’s Syndrome (Lateral Medullary Infarction) OCULAR MOTOR SYNDROMES CAUSED BY LESIONS OF Syndrome of the Anterior Inferior Cerebellar Artery THE THALAMUS Skew Deviation and the Ocular Tilt Reaction OCULAR MOTOR ABNORMALITIES AND DISEASES OF THE OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN BASAL GANGLIA THE CEREBELLUM Parkinson’s Disease Location of Lesions and Their Manifestations Huntington’s Disease Etiologies Other Diseases of Basal Ganglia OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN THE PONS THE CEREBRAL HEMISPHERES Lesions of the Internuclear System: Internuclear Acute Lesions Ophthalmoplegia Persistent Deficits Caused by Large Unilateral Lesions Lesions of the Abducens Nucleus Focal Lesions Lesions of the Paramedian Pontine Reticular Formation Ocular Motor Apraxia Combined Unilateral Conjugate Gaze Palsy and Internuclear Abnormal Eye Movements and Dementia Ophthalmoplegia (One-and-a-Half Syndrome) Ocular Motor Manifestations of Seizures Slow Saccades from Pontine Lesions Eye Movements in Stupor and Coma Saccadic Oscillations from Pontine Lesions OCULAR MOTOR DYSFUNCTION AND MULTIPLE OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN SCLEROSIS THE MESENCEPHALON OCULAR MOTOR MANIFESTATIONS OF SOME METABOLIC Sites and Manifestations of Lesions DISORDERS Neurologic Disorders that Primarily Affect the Mesencephalon EFFECTS OF DRUGS ON EYE MOVEMENTS In this chapter, we survey clinicopathologic correlations proach, although we also discuss certain metabolic, infec- for supranuclear ocular motor disorders. The presentation tious, degenerative, and inflammatory diseases in which su- follows the schema of the 1999 text by Leigh and Zee (1), pranuclear and internuclear disorders of eye movements are and the material in this chapter is intended to complement prominent. -
Retina and Neuro Ophthalmology
Name : …………………………………………………………… Roll No. : ………………………………………………………… Invigilator's Signature : ……………………………………….. CS/B.OPTM/SEM-5/BO-504/2010-11 2010-11 OCULAR DISEASE - II POSTERIOR SEGMENT ( RETINA & NEURO-OPHTHALMOLOGY ) Time Allotted : 3 Hours Full Marks : 70 The figures in the margin indicate full marks. Candidates are required to give their answers in their own words as far as practicable. GROUP – A ( Multiple Choice Type Questions ) 1. Choose the correct alternatives for any ten of the following : 10 × 1 = 10 i) Which is not an important diagnostic criterion of giant cell arteritis ? http://www.makaut.com/ a) ESR > 70 mm/hour b) C-reactive protein > 2·45 mg/dl c) Jaw caludication d) Neck pain. ii) Unilateral blindness in a male child with massive exudation under the retina is most likely a case of a) Coat's disease b) Retinoblastoma c) Sturge-Weber syndrome d) Louis-Bar's syndrome. 5323 [ Turn over http://www.makaut.com/ CS/B.OPTM/SEM-5/BO-504/2010-11 iii) A retinal detachment patient mostly complains of a) pain b) good vision c) flashes and floaters d) diplopia. iv) In myasthenia gravis, during a diagnostic test, we use a drug called a) Piperazine citrate b) Azathioprim c) Edrophonium d) Carbamazepine. v) Sillicone oil is a/an a) aqueous substitute b) lens substitute c) vitreous substitute d) artificial lens. vi) In retinoblastoma, if the microscopical examination shows Flexner-Wintersteiner rosettes, it is considered to be a) highly malignant b) less malignant c) not malignant d) none of these. vii) Dyschromatopsia is the term for defective a) day vision b) night vision http://www.makaut.com/ c) colour vision d) light brightness sensitivity. -
A Case of Multiple Sclerosis Presenting As Eight and Half Syndrome
Online Journal of Health and Allied Sciences Peer Reviewed, Open Access, Free Online Journal Published Quarterly : Mangalore, South India : ISSN 0972-5997 This work is licensed under a Volume 11, Issue 4; Oct-Dec 2012 Creative Commons Attribution- No Derivative Works 2.5 India License Case Report: A Case of Multiple Sclerosis Presenting as Eight and Half Syndrome. Authors Rajiv Raina, Professor, Madan Kaushik, Assistant Professor, Sanjay K Mahajan, Assistant Professor, Sushil Raghav, Senior Resident, Sharathbabu NM, Junior Resident, Dept. of Medicine, Indira Gandhi Medical College, Shimla. Address for Correspondence Dr. Sharathbabu NM, Junior Resident, Dept. of Medicine, Indira Gandhi Medical College, Shimla, India. E-mail: [email protected] Citation Raina R, Kaushik M, Mahajan SK, Raghav S, Sharathbabu NM. A Case of Multiple Sclerosis Presenting as Eight and Half Syndrome. Online J Health Allied Scs. 2012;11(4):15. Available at URL: http://www.ojhas.org/issue44/2012-4-15.html Open Access Archives http://cogprints.org/view/subjects/OJHAS.html http://openmed.nic.in/view/subjects/ojhas.html Submitted: Dec 5, 2012; Accepted: Jan 7, 2013; Published: Jan 25, 2013 Abstract: Multiple sclerosis (MS) is a chronic disease spinal cord. MRI showed hyperintensities on T2 weighted characterized by inflammation, demyelination, gliosis images oriented perpendicular to the ventricular surface, (scarring), and neuronal loss; the course can be relapsing- corresponding to the pathologic pattern of perivenous remitting or progressive. Manifestations of MS vary from a demyelination (Dawson's fingers) and hyperintensities in the benign illness to a rapidly evolving and incapacitating dorsal tegmentum of caudal pons(Fig. 3a & 3b). Patient was disease requiring profound lifestyle adjustments. -
Retinitis Pigmentosa and Allied Disorders Yog Raj Sharma, P
JK SCIENCE REVIEW ARTICLE Retinitis Pigmentosa and Allied Disorders Yog Raj Sharma, P. Raja Rami Reddy, Deependra V. Singh Retinitis pigmentosa (RP) is a generic term for a group Visual field loss is insidious, progressive, peripheral of disorders characterized by hereditary diffuse usually and symmetric between two eyes (except x-linked RP bilaterally symmetrical progressive dysfunction, cell loss which can have bizarre and asymmetric patterns). In the and eventual atrophy of retina. Initially photoreceptors majority of patients the earliest defects are relative are involved and subsequently inner retina is damaged. scotomas in the periphery between 30 and 50 degrees Although both rods and cones are involved, damage to from fixation, which enlarge, deepen and coalesce to the rods is predominant. RP may be seen in isolation form a ring of visual field loss. As ring scotomas enlarge (Typical RP) or in association with systemic diseases. toward the far periphery, islands of relatively normal The reported prevalence of typical RP is approximately vision remain usually temporal but occasionally 1: 50000 worldwide. Most commonly 46% of the cases inferiorly. In typical RP the progression of visual loss is are sporadic with only one affected member in a given slow and relentless. Berson et al found that overall about family. X- linked recessive inheritance is least common, 4.6% of remaining visual field was lost per year (3). amounting to 8%. Autosomal dominant inheritance is Central visual loss found in 19% and recessive in 19%. The age of onset This can occur early in typical RP while significant and the natural history of the disease depend on the peripheral field remains cystoid macular edema, macular inheritance. -
Eye Disease 1 Eye Disease
Eye disease 1 Eye disease Eye disease Classification and external resources [1] MeSH D005128 This is a partial list of human eye diseases and disorders. The World Health Organisation publishes a classification of known diseases and injuries called the International Statistical Classification of Diseases and Related Health Problems or ICD-10. This list uses that classification. H00-H59 Diseases of the eye and adnexa H00-H06 Disorders of eyelid, lacrimal system and orbit • (H00.0) Hordeolum ("stye" or "sty") — a bacterial infection of sebaceous glands of eyelashes • (H00.1) Chalazion — a cyst in the eyelid (usually upper eyelid) • (H01.0) Blepharitis — inflammation of eyelids and eyelashes; characterized by white flaky skin near the eyelashes • (H02.0) Entropion and trichiasis • (H02.1) Ectropion • (H02.2) Lagophthalmos • (H02.3) Blepharochalasis • (H02.4) Ptosis • (H02.6) Xanthelasma of eyelid • (H03.0*) Parasitic infestation of eyelid in diseases classified elsewhere • Dermatitis of eyelid due to Demodex species ( B88.0+ ) • Parasitic infestation of eyelid in: • leishmaniasis ( B55.-+ ) • loiasis ( B74.3+ ) • onchocerciasis ( B73+ ) • phthiriasis ( B85.3+ ) • (H03.1*) Involvement of eyelid in other infectious diseases classified elsewhere • Involvement of eyelid in: • herpesviral (herpes simplex) infection ( B00.5+ ) • leprosy ( A30.-+ ) • molluscum contagiosum ( B08.1+ ) • tuberculosis ( A18.4+ ) • yaws ( A66.-+ ) • zoster ( B02.3+ ) • (H03.8*) Involvement of eyelid in other diseases classified elsewhere • Involvement of eyelid in impetigo -
A Rare Cause of Bilateral Corneal Ulcers: Vitamin a Deficiency in the Setting of Chronic Alcoholism
Open Access Case Report DOI: 10.7759/cureus.7991 A Rare Cause of Bilateral Corneal Ulcers: Vitamin A Deficiency in the Setting of Chronic Alcoholism Raman J. Sohal 1 , Thu Thu Aung 1 , Sandeep Sohal 2 , Abha Harish 1 1. Internal Medicine, State University of New York (SUNY) Upstate Medical University, Syracuse, USA 2. Internal Medicine, The Brooklyn Hospital Center, Brooklyn, USA Corresponding author: Raman J. Sohal, [email protected] Abstract Vitamin A deficiency is rarely encountered in the western world. When encountered, vitamin A deficiency is seen as a component of the malabsorption spectrum of disease. Given the infrequency of nutritional deficits in the developed world, vitamin A-associated ophthalmologic disease is rarely encountered. We report a case of a 56-year-old male with severe vitamin A deficiency in the setting of alcoholic liver cirrhosis. This case emphasizes two important points. First, it considers vitamin A deficiency as a cause of corneal ulceration in patients with chronic alcoholism. Second, it raises awareness of hepatotoxicity that can result after the supplementation of vitamin A in patients with chronic alcoholism. Although an uncommon diagnosis, it should be considered when other causes, such as infectious and autoimmune conditions, are ruled out. Categories: Internal Medicine, Ophthalmology Keywords: bilateral corneal ulcers, vitamin a deficiency, alcoholism, liver cirrhosis, nutritional deficiency Introduction Vitamin deficiency is not a commonly encountered cause of non-healing corneal ulcers. However, in cirrhotic patients when other differentials, such as infectious and autoimmune etiologies, have been excluded, vitamin A deficiency should be considered. In patients with liver cirrhosis, the deficiency stems from both decreased gastrointestinal absorption as well as decreased oral intake. -
Physical Assessment of the Newborn: Part 3
Physical Assessment of the Newborn: Part 3 ® Evaluate facial symmetry and features Glabella Nasal bridge Inner canthus Outer canthus Nasal alae (or Nare) Columella Philtrum Vermillion border of lip © K. Karlsen 2013 © K. Karlsen 2013 Forceps Marks Assess for symmetry when crying . Asymmetry cranial nerve injury Extent of injury . Eye involvement ophthalmology evaluation © David A. ClarkMD © David A. ClarkMD © K. Karlsen 2013 © K. Karlsen 2013 The S.T.A.B.L.E® Program © 2013. Handout may be reproduced for educational purposes. 1 Physical Assessment of the Newborn: Part 3 Bruising Moebius Syndrome Congenital facial paralysis 7th cranial nerve (facial) commonly Face presentation involved delivery . Affects facial expression, sense of taste, salivary and lacrimal gland innervation Other cranial nerves may also be © David A. ClarkMD involved © David A. ClarkMD . 5th (trigeminal – muscles of mastication) . 6th (eye movement) . 8th (balance, movement, hearing) © K. Karlsen 2013 © K. Karlsen 2013 Position, Size, Distance Outer canthal distance Position, Size, Distance Outer canthal distance Normal eye spacing Normal eye spacing inner canthal distance = inner canthal distance = palpebral fissure length Inner canthal distance palpebral fissure length Inner canthal distance Interpupillary distance (midpoints of pupils) distance of eyes from each other Interpupillary distance Palpebral fissure length (size of eye) Palpebral fissure length (size of eye) © K. Karlsen 2013 © K. Karlsen 2013 Position, Size, Distance Outer canthal distance -
Eyes and Stroke: the Visual Aspects of Cerebrovascular Disease
Open Access Review Stroke Vasc Neurol: first published as 10.1136/svn-2017-000079 on 6 July 2017. Downloaded from Eyes and stroke: the visual aspects of cerebrovascular disease John H Pula,1 Carlen A Yuen2 To cite: Pula JH, Yuen CA. Eyes ABSTRACT to the LGBs,1 5 6 the terminal anastomosis is and stroke: the visual aspects of A large portion of the central nervous system is dedicated vulnerable to ischaemia.7 Optic radiations cerebrovascular disease. Stroke to vision and therefore strokes have a high likelihood 2017; : originate from the lateral geniculate nucleus and Vascular Neurology 2 of involving vision in some way. Vision loss can be the e000079. doi:10.1136/svn- (LGN) and are divided into superior, inferior, 2017-000079 most disabling residual effect after a cerebral infarction. and central nerve fibres. The optic radiations Transient vision problems can likewise be a harbinger of are predominantly supplied by the posterior stroke and prompt evaluation after recognition of visual and middle cerebral arteries1 and the AChA.6 Received 12 March 2017 symptoms can prevent future vascular injury. In this review, Inferior fibres, known as Meyer’s Loop,6 travel Revised 30 May 2017 we discuss the visual aspects of stroke. First, anatomy and Accepted 2 June 2017 the vascular supply of the visual system are considered. to the temporal lobe, while the superior and Published Online First Then, the different stroke syndromes which involve vision central nerve fibre bundles travel to the pari- 6 July 2017 1 are discussed. Finally, topics involving the assessment, etal lobes. The termination of optic radia- prognosis, treatment and therapeutic intervention of vision- tions is located in the visual striate cortex (V1) specific stroke topics are reviewed.