Neurovascular Anatomy (2): Posterior Circulation Anatomy
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Cerebellar Ataxia
CEREBELLAR ATAXIA Dr. Waqar Saeed Ziauddin Medical University, Karachi, Pakistan What is Ataxia? ■ Derived from a Greek word, ‘A’ : not, ‘Taxis’ : orderly Ataxia is defined as an inability to maintain normal posture and smoothness of movement. Types of Ataxia ■ Cerebellar Ataxia ■ Sensory Ataxia ■ Vestibular Ataxia Cerebellar Ataxia Cerebrocerebellum Spinocerebellum Vestibulocerebellum Vermis Planning and Equilibrium balance Posture, limb and initiating and posture eye movements movements Limb position, touch and pressure sensation Limb ataxia, Eye movement dysdiadochokinesia, disorders, Truncal and gait Dysmetria dysarthria nystagmus, VOR, ataxia hypotonia postural and gait. Gait ataxia Types of Cerebellar Ataxia • Vascular Acute Ataxia • Medications and toxins • Infectious etiologies • Atypical Infectious agents • Autoimmune disorders • Primary or metastatic tumors Subacute Ataxia • Paraneoplastic cerebellar degeneration • Alcohol abuse and Vitamin deficiencies • Systemic disorders • Autosomal Dominant Chronic • Autosomal recessive Progressive • X linked ataxias • Mitochondrial • Sporadic neurodegenerative diseases Vascular Ataxia ▪ Benedikt Syndrome It is a rare form of posterior circulation stroke of the brain. A lesion within the tegmentum of the midbrain can produce Benedikt Syndrome. Disease is characterized by ipsilateral third nerve palsy with contralateral hemitremor. Superior cerebellar peduncle and/or red nucleus damage in Benedikt Syndrome can further lead in to contralateral cerebellar hemiataxia. ▪ Wallenberg Syndrome In -
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. -
Full Disclosures
RESIDENT & FELLOW SECTION Clinical Reasoning: Section Editor An unusual case of subacute Mitchell S.V. Elkind, MD, MS encephalopathy Neal Parikh, MD SECTION 1 revealed wide-based gait and lower extremity dysmet- Alexander E. Merkler, A 52-year-old previously healthy man presented with 8 ria. Relevant laboratory evaluation revealed only a MD months of progressive cognitive decline. He complained C-reactive protein of 1.79 (normal 0–0.99). Natalie T. Cheng, MD of months of confusion, fatigue, depression, hypersom- Brain MRI obtained in Morocco 2 months prior Hediyeh Baradaran, MD nolence, headaches, and, subsequently, urinary inconti- to presentation had demonstrated bilateral thalamic Halina White, MD nence and unsteady gait. His family reported that he T2 hyperintensities and patchy enhancement in the Dana Leifer, MD spoke of his deceased mother as if she were alive. His right medial temporal lobe, midbrain, and basal gan- executive deficits progressed, leading to termination of glia. A right thalamic biopsy obtained in Morocco his employment and a motor vehicle accident. He had revealed “inflammatory cells” without evidence Correspondence to was evaluated and treated in Morocco before presenting of malignancy. Dr. Leifer: to our institution for further care. [email protected] Questions for consideration: Mental status examination was notable for slowed mentation and dyscalculia but was otherwise normal. 1. How can thalamic injury cause encephalopathy? Motor, sensory, and deep tendon reflex examination 2. What is the differential diagnosis for bilateral tha- results were normal. Cerebellar and gait examination lamic MRI abnormalities? GO TO SECTION 2 From the Departments of Neurology (N.P., A.E.M., N.T.C., H.W., D.L.) and Radiology (H.B.), Weill Cornell Medical Center, New York, NY. -
Management of Vertical Gaze Paresis from an Artery of Percheron Infarction
Abstract title: Management of Vertical Gaze Paresis from an Artery of Percheron Infarction. Abstract: A patient presents with vertical gaze paresis (down gaze > up gaze), a ‘drunk’ feeling when in a visually stimulating environment, speech impairment and memory impairment all stemming from a recent Artery of Percheron Infarction. Case History 40 year old white male Chief vision complaints on July 15, 2016: o Vertical gaze difficulty down gaze > up gaze o ‘Drunk’ feeling when in a visually stimulating environment (supermarket, crowd) Eye exam from 2015 was unremarkable o No glasses Rx was given o Patient has never worn glasses before Patient currently on Plavix and Lipitor medications Patient medical history: unremarkable, no prior medical issues o After event patient had speech impairment and mild memory impairment Pertinent findings Recent diagnosis of Artery of Percheron infarction (May 29, 2016) o Magnetic Resonance Imaging/Magnetic Resonance Angiogram images are available for viewing Poor convergence (27 cm) o Poor convergence even when adjusted for age Very low amplitude of accommodation for age: 2 D o Avg Amps for 40 yo = 5 D o Min Amps for 40 yo = 1.67 D Restricted down gaze > up gaze on EOM testing BCVA 20/20 OD/OS o Low Hyperopic Rx found o Minimal reading Rx found o Patient appreciated better vision with trial of glasses with manifest Rx Mild Meibomian Gland Dysfunction Posterior: unremarkable Blood work was negative except mildly elevated Protein S Differential diagnosis and reasons excluded Primary: ‘Top of the -
Topical Diagnosis in Neurology
V Preface In 2005 we publishedacomplete revision of Duus’ Although the book will be useful to advanced textbook of topical diagnosis in neurology,the first students, also physicians or neurobiologists inter- newedition since the death of its original author, estedinenriching their knowledge of neu- Professor PeterDuus, in 1994.Feedbackfromread- roanatomywith basic information in neurology,oR ers wasextremelypositive and the book wastrans- for revision of the basics of neuroanatomywill lated intonumerous languages, proving that the benefit even morefromit. conceptofthis book wasasuccessful one: combin- This book does notpretend to be atextbook of ing an integrated presentation of basic neu- clinical neurology.That would go beyond the scope roanatomywith the subject of neurological syn- of the book and also contradict the basic concept dromes, including modern imaging techniques. In described above.Firstand foremostwewant to de- this regard we thank our neuroradiology col- monstratehow,onthe basis of theoretical ana- leagues, and especiallyDr. Kueker,for providing us tomical knowledge and agood neurological exami- with images of very high quality. nation, it is possible to localize alesion in the In this fifthedition of “Duus,” we have preserved nervous system and come to adecision on further the remarkablyeffective didactic conceptofthe diagnostic steps. The cause of alesion is initially book,whichparticularly meets the needs of medi- irrelevant for the primarytopical diagnosis, and cal students. Modern medical curricula requirein- elucidation of the etiology takes place in asecond tegrative knowledge,and medical studentsshould stage. Our book contains acursoryoverviewofthe be taught howtoapplytheoretical knowledge in a major neurologicaldisorders, and it is notintended clinical settingand, on the other hand, to recognize to replace the systematic and comprehensive clinical symptoms by delving intotheir basic coverage offeredbystandardneurological text- knowledge of neuroanatomyand neurophysiology. -
The Artery of Percheron Megan Quetsch, Sureshkumar Nagiah , Stephen Hedger
Case report BMJ Case Rep: first published as 10.1136/bcr-2020-238681 on 11 January 2021. Downloaded from Stroke masquerading as cardiac arrest: the artery of Percheron Megan Quetsch, Sureshkumar Nagiah , Stephen Hedger General Medicine, Flinders SUMMARY level of consciousness. The patient was extubated Medical Centre, Bedford Park, The artery of Percheron (AOP) is a rare arterial variant 24 hours later, with her GCS improving to 13–14 South Australia, Australia of the thalamic blood supply. Due to the densely packed over the next day. collection of nuclei it supplies, an infarction of the Correspondence to AOP can be devastating. Here we highlight a patient Dr Sureshkumar Nagiah; INVESTIGATIONS sureshkumar. nagiah@ health. who had an AOP stroke in the community, which was sa. gov. au initially managed as cardiac arrest. AOP strokes most CT of the brain and CT angiogram (CTA) were often present with vague symptoms such as reduced performed at the regional hospital 3 hours after Accepted 11 December 2020 conscious level, cognitive changes and confusion without the acute onset of symptoms. CT scan showed no obvious focal neurology, and therefore are often missed evidence of ischaemic damage. CTA showed no at the initial clinical assessment. This case highlights the filling defects, significant stenosis or aneurysmal importance of recognising an AOP stroke as a cause of changes. Blood tests, including complete blood otherwise unexplained altered consciousness level and examination, renal function, electrolytes, C reac- the use of MRI early in the diagnostic work- up. tive protein and creatine kinase were normal. Telemetry showed normal sinus rhythm. Electro- encephalogram showed no evidence of seizure activity. -
Sensorineural Hearing Loss Due to Vertebrobasilar Artery Ischemia
logy & N ro eu u r e o N p h f y o s l i a o l n o r Ohki, J Neurol Neurophysiol 2013, S8 g u y o J Journal of Neurology & Neurophysiology ISSN: 2155-9562 DOI: 10.4172/2155-9562.S8-005 ReviewResearch Article Article OpenOpen Access Access Sensorineural Hearing Loss Due to Vertebrobasilar Artery Ischemia– Illustrative Case and Literature Review Masafumi Ohki* Department of Otolaryngology, Saitama Medical Center, Japan Abstract Acute sensorineural hearing loss is commonly caused by peripheral vestibulocochlear disorders such as sudden deafness, Meniere’s disease, and Ramsay Hunt syndrome, but is rarely due to infarction of the vertebrobasilar artery. In this report, a case of right anterior inferior cerebellar artery syndrome presenting with sudden deafness and vertigo is described in order to feature acute sensorineural hearing loss due to vertebrobasilar artery ischemia, and sensorineural hearing loss due to vertebrobasilar artery ischemia is reviewed and discussed. A 79-year-old man presented with right acute sensorineural hearing loss preceded by occasional, minute-long periods of dizziness without cranial neural symptoms other than vestibulocochlear symptoms. Magnetic resonance imaging (MRI) revealed infarction of the right anterior inferior cerebellar artery territory. The vertebrobasilar artery supplies the vestibulocochlear organ, brainstem, and cerebellum, whose abnormalities are related to vestibulocochlear symptoms. Vertigo is a major symptom associated with vertebrobasilar artery ischemia. Further, acute sensorineural hearing loss is caused by hypoperfusion of the vertebrobasilar artery. Vertigo and/or acute sensorineural hearing loss could be a prodrome of subsequent infarction of the vertebrobasilar artery territory. The artery most often responsible for acute sensorineural hearing loss is the anterior inferior cerebellar artery, whereas ischemia of the basilar artery, the posterior inferior cerebellar artery, and the superior cerebellar artery rarely cause acute sensorineural hearing loss. -
THE SYNDROMES of the ARTERIES of the BRAIN and SPINAL CORD Part 1 by LESLIE G
65 Postgrad Med J: first published as 10.1136/pgmj.29.328.65 on 1 February 1953. Downloaded from THE SYNDROMES OF THE ARTERIES OF THE BRAIN AND SPINAL CORD Part 1 By LESLIE G. KILOH, M.D., M.R.C.P., D.P.M. First Assistant in the Joint Department of Psychological Medicine, Royal Victoria Infirmary and University of Durham Introduction general circulatory efficiency at the time of the Little interest is shown at present in the syn- catastrophe is of the greatest importance. An dromes of the arteries of the brain and spinal cord, occlusion, producing little effect in the presence of and this perhaps is related to the tendency to a normal blood pressure, may cause widespread minimize the importance of cerebral localization. pathological changes if hypotension co-exists. Yet these syndromes are far from being fully A marked discrepancy has been noted between elucidated and understood. It must be admitted the effects of ligation and of spontaneous throm- that in many cases precise localization is often of bosis of an artery. The former seldom produces little more than academic interest and ill effects whilst the latter frequently determines provides Protected by copyright. nothing but a measure of personal satisfaction to infarction. This is probably due to the tendency the physician. But it is worth recalling that the of a spontaneous thrombus to extend along the detailed study of the distribution of the bronchi affected vessel, sealing its branches and blocking and of the pathological anatomy of congenital its collateral circulation, and to the fact that the abnormalities of the heart, was similarly neglected arterial disease is so often generalized. -
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 .................................................................................................................