The Posterior Cerebral Artery Syndrome
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Cognitive Emotional Sequelae Post Stroke
11/26/2019 The Neuropsychology of Objectives 1. Identify various cognitive sequelae that may result from stroke Stroke: Cognitive & 2. Explain how stroke may impact emotional functioning, both acutely and long-term Emotional Sequelae COX HEALTH STROKE CONFERENCE BRITTANY ALLEN, PHD, ABPP, MBA 12/13/2019 Epidemiology of Stroke Stroke Statistics • > 795,000 people in the United States have a stroke • 5th leading cause of death for Americans • ~610,000 are first or new strokes • Risk of having a first stroke is nearly twice as high for blacks as whites • ~1/4 occur in people with a history of prior stroke • Blacks have the highest rate of death due to stroke • ~140,000 Americans die every year due to stroke • Death rates have declined for all races/ethnicities for decades except that Hispanics have seen • Approximately 87% of all strokes are ischemic an increase in death rates since 2013 • Costs the United States an estimated $34 billion annually • Risk for stroke increases with age, but 34% of people hospitalized for stroke were < 65 years of • Health care services age • Medicines to treat stroke • Women have a lower stroke risk until late in life when the association reverses • Missed days of work • Approximately 15% of strokes are heralded by a TIA • Leading cause of long-term disability • Reduces mobility in > 50% of stroke survivors > 65 years of age Source: Centers for Disease Control Stroke Death Rates Neuropsychological Assessment • Task Engagement • Memory • Language • Visuospatial Functioning • Attention/Concentration • Executive -
Lack of Motivation: Akinetic Mutism After Subarachnoid Haemorrhage
Netherlands Journal of Critical Care Submitted October 2015; Accepted March 2016 CASE REPORT Lack of motivation: Akinetic mutism after subarachnoid haemorrhage M.W. Herklots1, A. Oldenbeuving2, G.N. Beute3, G. Roks1, G.G. Schoonman1 Departments of 1Neurology, 2Intensive Care Medicine and 3Neurosurgery, St. Elisabeth Hospital, Tilburg, the Netherlands Correspondence M.W. Herklots - [email protected] Keywords - akinetic mutism, abulia, subarachnoid haemorrhage, cingulate cortex Abstract Akinetic mutism is a rare neurological condition characterised by One of the major threats after an aneurysmal SAH is delayed the lack of verbal and motor output in the presence of preserved cerebral ischaemia, caused by cerebral vasospasm. Cerebral alertness. It has been described in a number of neurological infarction on CT scans is seen in about 25 to 35% of patients conditions including trauma, malignancy and cerebral ischaemia. surviving the initial haemorrhage, mostly between days 4 and We present three patients with ruptured aneurysms of the 10 after the SAH. In 77% of the patients the area of cerebral anterior circulation and akinetic mutism. After treatment of the infarction corresponded with the aneurysm location. Delayed aneurysm, the patients lay immobile, mute and were unresponsive cerebral ischaemia is associated with worse functional outcome to commands or questions. However, these patients were awake and higher mortality rate.[6] and their eyes followed the movements of persons around their bed. MRI showed bilateral ischaemia of the medial frontal Cases lobes. Our case series highlights the risk of akinetic mutism in Case 1: Anterior communicating artery aneurysm patients with ruptured aneurysms of the anterior circulation. It A 28-year-old woman with an unremarkable medical history is important to recognise akinetic mutism in a patient and not to presented with a Hunt and Hess grade 3 and Fisher grade mistake it for a minimal consciousness state. -
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 -
Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
A.qxd 9/29/05 04:02 PM Page 1 A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis (i.e., with dorsal column disease). Cross References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circum- stances: normal old age obesity after abdominal surgery after multiple pregnancies in acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neu- rone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis. -
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 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. -
Crossed Brainstem Syndrome Revealing
Beucler et al. BMC Neurology (2021) 21:204 https://doi.org/10.1186/s12883-021-02223-7 CASE REPORT Open Access Crossed brainstem syndrome revealing bleeding brainstem cavernous malformation: an illustrative case Nathan Beucler1,2* , Sébastien Boissonneau1,3, Aurélia Ruf4, Stéphane Fuentes1, Romain Carron3,5 and Henry Dufour1,6 Abstract Background: Since the nineteenth century, a great variety of crossed brainstem syndromes (CBS) have been described in the medical literature. A CBS typically combines ipsilateral cranial nerves deficits to contralateral long tracts involvement such as hemiparesis or hemianesthesia. Classical CBS seem in fact not to be so clear-cut entities with up to 20% of patients showing different or unnamed combinations of crossed symptoms. In terms of etiologies, acute brainstem infarction predominates but CBS secondary to hemorrhage, neoplasm, abscess, and demyelination have been described. The aim of this study was to assess the proportion of CBS caused by a bleeding episode arising from a brainstem cavernous malformation (BCM) reported in the literature. Case presentation: We present the case of a typical Foville syndrome in a 65-year-old man that was caused by a pontine BCM with extralesional bleeding. Following the first bleeding episode, a conservative management was decided but the patient had eventually to be operated on soon after the second bleeding event. Discussion: A literature review was conducted focusing on the five most common CBS (Benedikt, Weber, Foville, Millard-Gubler, Wallenberg) on Medline database from inception to 2020. According to the literature, hemorrhagic BCM account for approximately 7 % of CBS. Microsurgical excision may be indicated after the second bleeding episode but needs to be carefully weighted up against the risks of the surgical procedure and openly discussed with the patient. -
High-Yield Neuroanatomy
LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page i Aptara Inc. High-Yield TM Neuroanatomy FOURTH EDITION LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page ii Aptara Inc. LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page iii Aptara Inc. High-Yield TM Neuroanatomy FOURTH EDITION James D. Fix, PhD Professor Emeritus of Anatomy Marshall University School of Medicine Huntington, West Virginia With Contributions by Jennifer K. Brueckner, PhD Associate Professor Assistant Dean for Student Affairs Department of Anatomy and Neurobiology University of Kentucky College of Medicine Lexington, Kentucky LWBK110-3895G-FM[i-xviii].qxd 8/14/08 5:57 AM Page iv Aptara Inc. Acquisitions Editor: Crystal Taylor Managing Editor: Kelley Squazzo Marketing Manager: Emilie Moyer Designer: Terry Mallon Compositor: Aptara Fourth Edition Copyright © 2009, 2005, 2000, 1995 Lippincott Williams & Wilkins, a Wolters Kluwer business. 351 West Camden Street 530 Walnut Street Baltimore, MD 21201 Philadelphia, PA 19106 Printed in the United States of America. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at 530 Walnut Street, Philadelphia, PA 19106, via email at [email protected], or via website at http://www.lww.com (products and services). -
True and False Localization in Neuro- Ophthalmology—A Report of Two Cases
Case Report Neuro-ophthalmology True and False Localization in Neuro- ophthalmology—a Report of Two Cases Jared Raabe,1 Lance J Lyons,2 Bayan Al Othman,3 Andrew G Lee3,4,5,6 1. University of Texas Medical Branch, School of Medicine, Galveston, TX, USA; 2. Department of Ophthalmology & Visual Sciences, University of Texas Medical Branch, Galveston, TX, USA; 3. Department of Ophthalmology, Blanton Eye Institute, Houston Methodist Hospital, Houston, TX, USA; 4. Departments of Ophthalmology, Neurology, and Neurosurgery, Weill Cornell Medicine, New York, NY, USA; 5. Section of Ophthalmology, University of Texas MD Anderson Cancer Center, Houston, TX, USA; 6. Department of Ophthalmology, The University of Iowa Hospitals and Clinics, Iowa City, IA, USA his report of two cases describes two patients who each had ocular motor cranial neuropathies in addition to a second neurologic finding that usually, in combination, hold localizing value. One of these cases localized as anticipated, and the other case demonstrated Ta false localizing sign. We detail these two cases and review the localizing value of various combinations of neurologic signs. Keywords The Parkinson sign is classically described as a sixth nerve palsy and an ipsilateral Horner syndrome Oculomotor palsy, Horner syndrome, ocular motor that localizes to the cavernous sinus. 1,2 The localizing value of any afferent and efferent (e.g., Horner cranial nerve, Parkinson sign, cavernous sinus, syndrome) pupillary finding with an ipsilateral ocular motor cranial neuropathy merits revisiting the anisocoria, relative afferent pupillary defect Parkinson sign.3,4 For example, a unilateral pupil-sparing cranial nerve III palsy with an ipsilateral Disclosure: Jared Raabe, Lance Lyons, smaller pupil (rather than a larger pupil), a normal pupillary light reaction, an anisocoria worse in the Bayan Al Othman, and Andrew Lee have no dark (ocular sympathetic pupil dilation problem), and absence of aberrant regeneration suggests a relevant conflicts of interest to declare. -
26 Aphasia, Memory Loss, Hemispatial Neglect, Frontal Syndromes and Other Cerebral Disorders - - 8/4/17 12:21 PM )
1 Aphasia, Memory Loss, 26 Hemispatial Neglect, Frontal Syndromes and Other Cerebral Disorders M.-Marsel Mesulam CHAPTER The cerebral cortex of the human brain contains ~20 billion neurons spread over an area of 2.5 m2. The primary sensory and motor areas constitute 10% of the cerebral cortex. The rest is subsumed by modality- 26 selective, heteromodal, paralimbic, and limbic areas collectively known as the association cortex (Fig. 26-1). The association cortex mediates the Aphasia, Memory Hemispatial Neglect, Frontal Syndromes and Other Cerebral Disorders Loss, integrative processes that subserve cognition, emotion, and comport- ment. A systematic testing of these mental functions is necessary for the effective clinical assessment of the association cortex and its dis- eases. According to current thinking, there are no centers for “hearing words,” “perceiving space,” or “storing memories.” Cognitive and behavioral functions (domains) are coordinated by intersecting large-s- cale neural networks that contain interconnected cortical and subcortical components. Five anatomically defined large-scale networks are most relevant to clinical practice: (1) a perisylvian network for language, (2) a parietofrontal network for spatial orientation, (3) an occipitotemporal network for face and object recognition, (4) a limbic network for explicit episodic memory, and (5) a prefrontal network for the executive con- trol of cognition and comportment. Investigations based on functional imaging have also identified a default mode network, which becomes activated when the person is not engaged in a specific task requiring attention to external events. The clinical consequences of damage to this network are not yet fully defined. THE LEFT PERISYLVIAN NETWORK FOR LANGUAGE AND APHASIAS The production and comprehension of words and sentences is depen- FIGURE 26-1 Lateral (top) and medial (bottom) views of the cerebral dent on the integrity of a distributed network located along the peri- hemispheres. -
Balin Bhatia Gadolinium Deposition Basal Ganglia
T1 weighted basal ganglia hyperintensities due to gadolinium deposition – a cautionary note Bettina Balint, MD1,2 and Kailash P. Bhatia, MD, FRCP1 1 Sobell Department of Motor Neuroscience and Movement Disorders UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom 2 Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany Corresponding author: Prof Kailash P. Bhatia Sobell Department of Motor Neuroscience and Movement Disorders UCL Institute of Neurology Queen Square WC1G 3BG London U.K. Tel: +44 02034488723 Email: [email protected] Correspondence Word count: 585; Character count title: 91; number of references: 5; number of figures: 0; Supplemental Data: 0 Disclosures: Dr Balint reports no conflict of interest. Prof Bhatia reports no conflict of interest. Full disclosures for the past 12 months unrelated to the present manuscript: K.P.B. receives royalties from Oxford University Press and a stipend for MDCP editorship, holds grants from NIHR RfPB, MRC Welcome Strategic grant (WT089698), PD UK (Ref. no.: G-1009) and Horizon 2020 EC grant Propag- Aging. He has received honoraria/financial support to speak/attend meetings or serve on advisory boards from Ipsen, Merz, Allergan, Teva Lundbeck pharmaceutical companies. Gadolinium-based contrast agents (GBCAs) have been widely used in clinical MR imaging since the late 1980ies. Overall, they were considered safe, apart from the well-known risk of nephrogenic systemic fibrosis, which could be counteracted by limitation of their use in patients with renal insufficiency. Now however, there have been a number of publications describing the dose-dependent deposition of Gadolinium in the brain, manifesting as high signal intensities on non-enhanced T1-weighted images particularly in the dentate nucleus and globus pallidus, but also in the thalamus and the pons.1-3 Gadolinium is a rare-earth metal. -
Definition of Stroke/Brain Attack
Definition of Stroke/Brain Attack Stroke II: • A syndrome caused by disruption in the flow of Diagnosis, Evaluation, and Prevention blood to part of the brain due to either: – occlusion of a blood vessel • ischemic stroke Lenore N. Joseph, MD – rupture of a blood vessel Neurology Service Chief, McGuire VAMC • hemorrhagic stroke Assistant Professor of Neurology • The interruption in blood flow deprives the brain VCU Health System of nutrients and oxygen resulting in injury to cells Medical College of Virginia in the affected vascular territory of the brain 1 2 Stroke: The Problem Stroke: The Problem • Third leading cause of death in US • Among 6 month or longer survivors: – after heart disease and cancer – 48% have a hemiparesis • 740,000 new strokes each year – 22% cannot walk • 4.5 million stroke survivors – 24-53% report complete or partial • Leading cause of disability in adults in US dependence for activities • $45.5 billion per year in the USA – 12-18% are aphasic • 1 of 6 Americans will be affected – 32% are clinically depressed – only 10% fully recover 3 4 Symptoms of Brain Attack: Symptoms of Brain Attack: Teach your patients! Teach your patients! • Sudden weakness, paralysis, or numbness of: • Sudden unexplained dizziness –face – especially when associated with other – arm and the leg on one or both sides of the neurologic symptoms body – unsteadiness • Sudden loss of speech, or difficulty speaking or – sudden falls understanding speech • Sudden severe headache and/or loss of • Sudden dimness or loss of vision consciousness –