CHAPTER E11 Video Library of Neuro-Ophthalmology
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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. -
Transient Monocular Visual Loss
Transient Monocular Visual Loss VALÉRIE BIOUSSE, MD AND JONATHAN D. TROBE, MD ● PURPOSE: To provide a practical update on the diagno- when most episodes of TMVL do not cause total loss of sis and management of transient monocular visual loss vision.2 (TMVL). The most important step in evaluating a patient with ● DESIGN: Perspective. visual loss is to establish whether the visual loss is ● METHODS: Review of the literature. monocular or binocular.2,5 Monocular visual loss always ● RESULTS: TMVL is an important clinical symptom. It results from lesions anterior to the chiasm (the eye or the has numerous causes but most often results from tran- optic nerve), whereas binocular visual loss results from sient retinal ischemia. It may herald permanent visual lesions of both eyes or optic nerves, or, more likely, of the loss or a devastating stroke, and patients with TMVL chiasm or retrochiasmal visual pathway. should be evaluated urgently. A practical approach to the Deciding whether an episode of abrupt visual loss evaluation of the patient with TMVL must be based on occurred in one eye or both is not always easy. Very few the patient’s age and the suspected underlying etiology. patients realize that binocular hemifield (homonymous) In the older patient, tests should be performed to inves- visual field loss affects the fields of both eyes. They will tigate giant cell arteritis, atherosclerotic large vessel usually localize it to the eye that lost its temporal field. The disease, and cardiac abnormalities. In the younger pa- best clues to the fact that visual loss was actually binocular tient, TMVL is usually benign and the evaluation should are reading impairment (monocular visual loss does not be tailored to the particular clinical setting. -
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. -
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 -
Internuclear Ophthalmoplegia and Horner's Syndrome Due To
362 Journal of the Royal Society of Medicine Volume 86 June 1993 Internuclear ophthalmoplegia and Her erythrocyte sedimentation rate (ESR) was 105 in the Horner's syndrome due to presumed first hour, the white blood cell count was 11.1 x109/l, giant cell arteritis platelets 475x 109/1, the blood film showed some target cells and ++ rouleaux. Her alkaline phosphatase was 226 and her 7y-glutamine transferase 102. A computerized tomography scan reported atrophic changes in the cerebral hemispheres, and an old infarct was noted in the left temporal lobe. Within Ayman Askari MRCP1 0 M P Jolobe FRCP2 6 days of starting treatment the headache improved remarkably, and in the following 2 months the patient D I Shepherd FRCP2 'Princess Royal Hospital; maintained her progress with no change in the neurological Telford, Shropshire and 2Tameside General Hospital signs. The ESR was 47 within 8 days of admission and 3 by Ashton-under-Lyne, Lancashire day 38 of starting treatment. Keywords: giant cell arteritis; ophthalmoplegia; Horner's syndrome; Discussion ataxic nystagmus Our aim is to draw attention to the association between neuro-ophthalmic signs and presumed GCA. Leukocytosis, abnormal latex fixation test and fever are in keeping with cell arteritis is an inflammatory, the diagnosis. It is likely that many patients with GCA have Giant (GCA) occlusive ophthalmoplegia in the course of their illness and failure arteriopathy of unknown aetiology. It is common in the to detect it may be due to the transient nature of this elderly, with an incidence of 17.4 per 100 000 ofthe popula- manifestation3. -
Cranial Nerve Palsies in Spontaneous Carotid Artery Dissection
J7ournal ofNeurology, Neurosurgery, and Psychiatry 1993;56:1191-1199 1 191 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1191 on 1 November 1993. Downloaded from Cranial nerve palsies in spontaneous carotid artery dissection Matthias Sturzenegger, P Huber Abstract the reported "idiopathic" jugular foramen Two patients had isolated unilateral cra- (Vernet) and similar syndromes (Villaret, nial nerve palsies due to spontaneous Collet Siccard) in the older literature might internal carotid artery (ICA) dissection well have been caused by spontaneous- carotid without ischaemic cerebral involvement. dissection.5 In those times ICA dissection as a One had acute glossopharyngeal and cause of cranial nerve palsy was poorly vagal, the other isolated hypoglossal known, angiography quite risky, and ultra- nerve palsy. Reviewing all reported cases sound and MRI not available. Out of 31 con- of angiographically confirmed ICA dis- secutive patients with ICA dissection section in the literature, 36 additional diagnosed at our department within four cases with unequivocal ipsilateral cranial years, two presented with cranial nerve palsies nerve palsies were analysed. While an without cerebral involvement. isolated palsy ofthe IXth and Xth has not been reported previously, palsies of the XIIth nerve or the IXth to XIIth nerves Case reports were most frequently found. In these PATEENT 1 patients, lower cranial nerve palsies are A 42-year-old man had been in excellent probably the result of compression by an health. He had no vascular risk factors. After enlarging ICA due to mural haematoma. strenuous activity (cutting wood) in military Symptoms and signs indicative of carotid service he suddenly felt pain in the right dissection were concurrently present upper jaw which later extended to the ear and only in some reported cases. -
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. -
GAZE and AUTONOMIC INNERVATION DISORDERS Eye64 (1)
GAZE AND AUTONOMIC INNERVATION DISORDERS Eye64 (1) Gaze and Autonomic Innervation Disorders Last updated: May 9, 2019 PUPILLARY SYNDROMES ......................................................................................................................... 1 ANISOCORIA .......................................................................................................................................... 1 Benign / Non-neurologic Anisocoria ............................................................................................... 1 Ocular Parasympathetic Syndrome, Preganglionic .......................................................................... 1 Ocular Parasympathetic Syndrome, Postganglionic ........................................................................ 2 Horner Syndrome ............................................................................................................................. 2 Etiology of Horner syndrome ................................................................................................ 2 Localizing Tests .................................................................................................................... 2 Diagnosis ............................................................................................................................... 3 Flow diagram for workup of anisocoria ........................................................................................... 3 LIGHT-NEAR DISSOCIATION ................................................................................................................. -
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. -
Conjoint Ophthalmology Scientific Conference (COSC 2017)
Artwork for the 7th Conjoint Ophthalmology Scientific Conference (COSC 2017) Logo COSC 2017 (designed by Dr Aliff Irwan Cheong) The logo symbolizes: 1. “C” represents as the whole eye, and its fluidic and wave like angle shape, exhibit the conference main theme “Angles and Curves”. The inferior tail of the “C” crosses and twist towards the word 2017 represents the conference aim in achieving advancement in Ophthalmology especially in Malaysia. 2. “O” represents the cornea and pupil – exhibit the specialty of interest : Glaucoma & Cornea. 3. “7” signify in RED is a hallmark of conference by COSC 2017. 4. BLUE – Theme color for conference and shown with the year its being held 5. BLACK – Second theme color for conference and shown in the other structure of interest Front Cover Artwork (designed by Dr Tan Li Mun) 1. Image of Cornea and Kuala Lumpur City Centre (KLCC) - Signifies the theme of our conjoint "Angles and Curves" and the location of our event held in Kuala Lumpur 2. Image of Pupil and Iris on the background - Signifies the other parts of anterior segment of the eye. ii Foreword The 7th Conjoint Ophthalmology Scientific Conference (COSC 2017) was held on 15-17 September 2017 at the Pullman Kuala Lumpur Bangsar, Kuala Lumpur. These Scientific Conferences have been held by the Malaysian Universities Conjoint Committee of Ophthalmology every year since 2011, and the theme for this year‟s meeting was „Angles and Curves - New Perspectives on Glaucoma and Cornea Management‟. The programme consisted of workshops, lectures and case discussions conducted by expert international and local speakers, and updated participants on latest developments in the two exciting fields. -
Juxtaposition of One and a Half Syndrome with Pseudo One and a Half Syndrome
Case Report Annals of Clinical Case Reports Published: 11 Dec, 2018 Juxtaposition of One and a Half Syndrome with Pseudo One and a Half Syndrome Edward Chai, Sirac Cardoza*, Ivan Rosado, Prabjhot Manes, Haidy Rivero and Adam Bernstein Department of Neurology, The Brooklyn Hospital Center, USA Abstract Conjugate gaze palsy with contralateral internuclear ophthalmoplegia or One and a Half Syndrome, is a rare neurological condition that was originally described in 1967. The authors present two patients, one with true one and a half syndrome caused by a CVA and another with pseudo one and a half syndrome caused by myasthenia gravis. Clinical presentation of these syndromes can be similar with minute differences appreciated on physical exam; however, the clinical relevance is quite large as the management is entirely different. Abbreviations INO: Internuclear Ophthalmoplegia; MLF: Medial Longitudinal Fasciculus; PPRF: Para Median Pontine Reticular Formation; CT: Computed Tomography; MRI: Magnetic Resonance Imaging Introduction “One and a half syndrome” was originally described in 1967 as conjugate gaze palsy with a contralateral Internuclear Ophthalmoplegia (INO) [1]. The syndrome is typically due to a single unilateral lesion of the Paramedian Pontine Reticular Formation (PPRF) or the abducens nucleus, and the adjacent Medial Longitudinal Fasciculus (MLF) [2,3]. Damage to the former manifests as the ipsilateral conjugate gaze palsy. Damage to the latter interrupts the internuclear fibers crossing midline to the contralateral medial rectus resulting in contralateral adduction failure on opposite gaze [2]. The side of the INO refers to the direction in which the previous adductor palsy manifests and is contralateral to the gaze palsy.