Some Neuro-Ophthalmological Observations'
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Stroke and Transient Ischaemic Attacks
53454ournal ofNeurology, Neurosurgery, and Psychiatry 1994;57:534-543 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.57.5.534 on 1 May 1994. Downloaded from NEUROLOGICAL MANAGEMENT Stroke and transient ischaemic attacks Peter Humphrey The management of stroke is expensive and ANATOMY accounts for about 5% of NHS hospital costs. Carotid v vertebrobasilar arterial territory Stroke is the commonest cause of severe Carotid-Classifying whether a stroke is in the physical disability. About 100 000 people territory of the carotid or vertebrobasilar suffer a first stroke each year in England and arteries is important, especially if the patient Wales. It is important to emphasise that makes a good recovery. Carotid endarterec- around 20-25% of all strokes affects people tomy is of proven value in those with carotid under 65 years of age. The annual incidence symptoms. Carotid stroke usually produces of stroke is two per 1000.' About 10% of all hemiparesis, hemisensory loss, or dysphasia. patients suffer a recurrent stroke within one Apraxia and visuospatial problems may also year. The prevalence of stroke shows that occur. If there is a severe deficit, there may there are 250 000 in England and Wales. also be an homonymous hemianopia and gaze Each year approximately 60 000 people are palsy. Episodes of amaurosis fugax or central reported to die of stroke; this represents retinal artery occlusion are also carotid about 12% of all deaths. Only ischaemic events. heart disease and cancer account for more Homer's syndrome can occur because of deaths. This means that in an "average" dis- damage to the sympathetic fibres in the trict health authority of 250 000 people, there carotid sheath. -
Clinicalguidelines
Postgrad MedJ7 1995; 71: 577-584 © The Fellowship of Postgraduate Medicine, 1995 Clinical guidelines Postgrad Med J: first published as 10.1136/pgmj.71.840.577 on 1 October 1995. Downloaded from Management of transient ischaemic attacks and stroke PRD Humphrey Summary The management of stroke and transient ischaemic attacks (TIAs) consumes The management of stroke and about 500 of NHS hospital costs. Stroke is the commonest cause of severe transient ischaemic attacks physical disability with an annual incidence of two per 1000.1 In an 'average' (TIAs) has changed greatly in the district general hospital of 250 000 people there will be 500 first strokes in one last two decades. The importance year with a prevalence of about 1500. TIAs are defined as acute, focal of good blood pressure control is neurological symptoms, resulting from vascular disease which resolve in less the hallmark of stroke preven- than 24 hours. The incidence of a TIA is 0.5 per 1000. tion. Large multicentre trials Stroke is not a diagnosis. It is merely a description of a symptom complex have proven beyond doubt the thought to have a vascular aetiology. It is important to classify stroke according value of aspirin in TIAs, warfarin to the anatomy ofthe lesion, its timing, aetiology and pathogenesis. This will help in patients with atrial fibrillation to decide the most appropriate management. and embolic cerebrovascular symptoms, and carotid endarter- Classification of stroke ectomy in patients with carotid TIAs. There seems little doubt Many neurologists have described erudite vascular syndromes in the past. Most that patients managed in acute ofthese are oflittle practical use. -
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. -
A Small Dorsal Pontine Infarction Presenting with Total Gaze Palsy Including Vertical Saccades and Pursuit
Journal of Clinical Neurology / Volume 3 / December, 2007 Case Report A Small Dorsal Pontine Infarction Presenting with Total Gaze Palsy Including Vertical Saccades and Pursuit Eugene Lee, M.D., Ji Soo Kim, M.D.a, Jong Sung Kim, M.D., Ph.D., Ha Seob Song, M.D., Seung Min Kim, M.D., Sun Uk Kwon, M.D. Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine aDepartment of Neurology, Seoul National University, Bundang Hospital A small localized infarction in the dorsal pontine area can cause various eye-movement disturbances, such as abducens palsy, horizontal conjugate gaze palsy, internuclear ophthalmoplegia, and one-and-a-half syndrome. However, complete loss of vertical saccades and pursuit with horizontal gaze palsy has not been reported previously in a patient with a small pontine lesion. We report a 67-year-old man with a small dorsal caudal pontine infarct who exhibited total horizontal gaze palsy as well as loss of vertical saccades and pursuit. J Clin Neurol 3(4):208-211, 2007 Key Words : Ophthalmoplegia, Pontine infarction, Omnipause neurons A small localized dorsal pontine infarction can to admission he had experienced sudden general produce abducens palsy, horizontal conjugate gaze weakness for approximately 20 minutes without loss palsy, internuclear ophthalmoplegia (INO), and one- of consciousness while working on his farm. The and-a-half syndrome by damaging the abducens nucleus following day, the patient experienced dysarthric and its fascicle, the paramedian pontine reticular speech and visual obscuration, and his family members formation (PPRF), or the medial longitudinal fasciculus noticed that his eyes were deviated to one side. -
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 ................................................................................................................. -
Supranuclear Gaze Palsy and Opsoclonus After Diazinon Poisoning T-W Liang, L J Balcer, D Solomon, S R Messé, S L Galetta
677 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.5.677 on 1 May 2003. Downloaded from SHORT REPORT Supranuclear gaze palsy and opsoclonus after Diazinon poisoning T-W Liang, L J Balcer, D Solomon, S R Messé, S L Galetta ............................................................................................................................. J Neurol Neurosurg Psychiatry 2003;74:677–679 Brain magnetic resonance imaging was normal. Nerve con- A 52 year old man developed a supranuclear gaze palsy duction studies and EMG with repetitive stimulation were and opsoclonus after Diazinon poisoning. The diagnosis normal. Organophosphate poisoning was confirmed by low was confirmed by low plasma and red blood cell levels of plasma and red blood cell cholinesterase activity, 0.1 cholinesterase activity and urine mass spectroscopy. IU/ml (normal 5.2 to 12.8 IU/ml) and 2.2 IU/ml (normal 6.2 to Saccadic control may be mediated in part by acetylcho- 10.3 IU/ml), respectively. Treatment with atropine and line. Opsoclonus in the setting of organophosphate intoxi- pralidoxime was initiated over the next 10 days. On day 15 of cation may occur as a result of cholinergic excess which the hospital course, he became more responsive and on day 17 overactivates the fastigial nuclei. he was extubated. Neurological examination at this time showed mild diffuse weakness and tremor. His voluntary eye movements were full and his ocular flutter had resolved. His wife brought in a sample of liquid found in his garage arious central eye movement abnormalities have been which proved to be Diazinon. Diazinon was also detected in 12 described after organophosphate poisoning. -
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. -
The One-And-A-Half Syndrome. Clinical Correlation with a Pontine Lesion Demonstrated by Nuclear Magnetic Resonance Imaging in a Case of Multiple Sclerosis
Br J Ophthalmol: first published as 10.1136/bjo.72.7.515 on 1 July 1988. Downloaded from British Journal of Ophthalmology, 1988, 72, 515-517 The one-and-a-half syndrome. Clinical correlation with a pontine lesion demonstrated by nuclear magnetic resonance imaging in a case of multiple sclerosis C N MARTYN AND D KEAN From the University Departments of Medicine and Radiology, Royal Infirmary, Edinburgh SUMMARY Nuclear magnetic resonance (NMR) imaging has been used to visualise a localised area of demyelination in the dorsal pons of a patient who presented with an unusual disorder of eye movements, namely, the one-and-a-half syndrome. Judged clinically the patient made a nearly complete recovery, but little change was apparent in the NMR image six months later. The unusual and remarkable disorder of eye move- eye movements in response to head turning. A ment consisting of a lateral gaze palsy in one direction contralateral internuclear ophthalmoplegia was and an internuclear ophthalmoplegia in the other was present: the left eye failed to adduct past the midline, probably first described by Freeman et al. and later and horizontal jerking nystagmus was apparent in the dubbed the one-and-a-half syndrome by Fisher.2 In abducting right eye. Up-gaze was incomplete with the fully developed syndrome one eye is in the gaze-evoked upbeat nystagmus, and convergence midline and completely fails to move horizontally was impaired. Figs. 1-3 illustrate the horizontal gaze while the other can only abduct. Fisher attributed the palsies. There was an incomplete left-sided facial syndrome to a single unilateral lesion affecting the palsy of lower motor neurone type, and taste http://bjo.bmj.com/ centre for conjugate lateral gaze in the paramedian sensation was lost on the left side of the tongue.