Disorders of Cerebellum
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Reframing Psychiatry for Precision Medicine
Reframing Psychiatry for Precision Medicine Elizabeth B Torres 1,2,3* 1 Rutgers University Department of Psychology; [email protected] 2 Rutgers University Center for Cognitive Science (RUCCS) 3 Rutgers University Computer Science, Center for Biomedicine Imaging and Modelling (CBIM) * Correspondence: [email protected]; Tel.: (011) +858-445-8909 (E.B.T) Supplementary Material Sample Psychological criteria that sidelines sensory motor issues in autism: The ADOS-2 manual [1, 2], under the “Guidelines for Selecting a Module” section states (emphasis added): “Note that the ADOS-2 was developed for and standardized using populations of children and adults without significant sensory and motor impairments. Standardized use of any ADOS-2 module presumes that the individual can walk independently and is free of visual or hearing impairments that could potentially interfere with use of the materials or participation in specific tasks.” Sample Psychiatric criteria from the DSM-5 [3] that does not include sensory-motor issues: A. Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive, see text): 1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions. 2. Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures; to a total lack of facial expressions and nonverbal communication. -
Cerebellar Atrophy with Long-Term Phenytoin (Pht) Use: Case Report
REVIEWS CASE REPORTS CEREBELLAR ATROPHY WITH LONG-TERM PHENYTOIN (PHT) USE: CASE REPORT Jamir P. Rissardo, Ana L.F. Caprara, Juliana O.F. Silveira Departament of Neurology, Federal University of Santa Maria, RS, Brazil Federal University of Santa Maria Health Sciences Center – Camobi Street, Km 09 – Universitary Campus Santa Maria/RS – 97105-900 ABSTRACT Cerebellar atrophy can be found with long-term phenytoin (PHT) use or acute phenytoin intoxication. PHT may cause cerebellar symptoms, such as nystagmus, diplopia, dysarthria and ataxia. Clinical manifestations may be persistent. We report a case of a 41-year-old male who presented with cerebellar dysfunction and cerebellar atrophy after long- term phenytoin use. He had ataxic gait, preserved strength, commuting deep refl exes, dysmetria, dysdiadochocine- sia, scanning speech and somnolence. Cranial computed tomography revealed enlargement of inter follicular cere- brospinal fl uid spaces in cerebellum and also a slight enlargement of the fourth ventricle, suggesting signs of cerebellar volumetric reduction. PHT was withdrawn. Six months later, he presented improvement in his condition; he had atypical gait, mild dysmetria, diadochokinesia and normal speech. In conclusion, clinicians should be vigilant with patients on phenytoin. If the patient has cerebellar signs with a correspondent clinical history of phenytoin intoxication CT scan should be helpful as an initial cerebellar assessment. Keywords: phenytoin, ataxia, cerebellum, atrophy INTRODUCTION CASE REPORT C erebellar atrophy can be found with long-term A 41-year-old male admitted to our hospital pre- phenytoin (PHT) use (1), acute phenytoin intoxica- senting acute ataxia and scanning speech, for 20 tion (2,9), normal aging brain and alcohol abuse days. -
TWITCH, JERK Or SPASM Movement Disorders Seen in Family Practice
TWITCH, JERK or SPASM Movement Disorders Seen in Family Practice J. Antonelle de Marcaida, M.D. Medical Director Chase Family Movement Disorders Center Hartford HealthCare Ayer Neuroscience Institute DEFINITION OF TERMS • Movement Disorders – neurological syndromes in which there is either an excess of movement or a paucity of voluntary and automatic movements, unrelated to weakness or spasticity • Hyperkinesias – excess of movements • Dyskinesias – unnatural movements • Abnormal Involuntary Movements – non-suppressible or only partially suppressible • Hypokinesia – decreased amplitude of movement • Bradykinesia – slowness of movement • Akinesia – loss of movement CLASSES OF MOVEMENTS • Automatic movements – learned motor behaviors performed without conscious effort, e.g. walking, speaking, swinging of arms while walking • Voluntary movements – intentional (planned or self-initiated) or externally triggered (in response to external stimulus, e.g. turn head toward loud noise, withdraw hand from hot stove) • Semi-voluntary/“unvoluntary” – induced by inner sensory stimulus (e.g. need to stretch body part or scratch an itch) or by an unwanted feeling or compulsion (e.g. compulsive touching, restless legs syndrome) • Involuntary movements – often non-suppressible (hemifacial spasms, myoclonus) or only partially suppressible (tremors, chorea, tics) HYPERKINESIAS: major categories • CHOREA • DYSTONIA • MYOCLONUS • TICS • TREMORS HYPERKINESIAS: subtypes Abdominal dyskinesias Jumpy stumps Akathisic movements Moving toes/fingers Asynergia/ataxia -
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. -
A Dictionary of Neurological Signs
FM.qxd 9/28/05 11:10 PM Page i A DICTIONARY OF NEUROLOGICAL SIGNS SECOND EDITION FM.qxd 9/28/05 11:10 PM Page iii A DICTIONARY OF NEUROLOGICAL SIGNS SECOND EDITION A.J. LARNER MA, MD, MRCP(UK), DHMSA Consultant Neurologist Walton Centre for Neurology and Neurosurgery, Liverpool Honorary Lecturer in Neuroscience, University of Liverpool Society of Apothecaries’ Honorary Lecturer in the History of Medicine, University of Liverpool Liverpool, U.K. FM.qxd 9/28/05 11:10 PM Page iv A.J. Larner, MA, MD, MRCP(UK), DHMSA Walton Centre for Neurology and Neurosurgery Liverpool, UK Library of Congress Control Number: 2005927413 ISBN-10: 0-387-26214-8 ISBN-13: 978-0387-26214-7 Printed on acid-free paper. © 2006, 2001 Springer Science+Business Media, Inc. All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, Inc., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dis- similar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to propri- etary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omis- sions that may be made. -
Full Text (PDF)
RESIDENT & FELLOW SECTION Clinical Reasoning: Section Editor An 82-year-old man with worsening gait John J. Millichap, MD Sheena Chew, MD SECTION 1 neck and left leg cramps. He denied bowel or bladder Ivana Vodopivec, MD, An 82-year-old man with hypothyroidism presented symptoms. PhD with difficulty walking. The patient was previously healthy, playing com- Aaron L. Berkowitz, MD, One year prior to presentation, he noticed that his petitive sports at the national level into his late 70s. PhD legs occasionally “froze” when initiating walking. His His only medication was levothyroxine. gait progressively worsened over the year. He devel- oped balance difficulty, tripping and falling twice Question for consideration: Correspondence to without loss of consciousness. In the 4 months prior Dr. Chew: to presentation, he started using a cane, a rolling 1. What examination findings would help to localize [email protected] walker, then a wheelchair. He reported occasional the etiology of his abnormal gait? GO TO SECTION 2 From the Department of Neurology, Brigham and Women’s Hospital (S.C., I.V., A.L.B.), and Department of Neurology, Massachusetts General Hospital (S.C.), Harvard Medical School, Boston. Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article. e246 © 2017 American Academy of Neurology ª 2017 American Academy of Neurology. Unauthorized reproduction of this article is prohibited. SECTION 2 arm dysdiadochokinesia and right leg dysmetria, but The neurologic basis of gait spans the entire neuraxis, no left-sided or truncal ataxia. -
Ataxia and Tremor in People with Multiple Sclerosis (MS)
for health professionals Ataxia and tremor in people with multiple sclerosis (MS) Freecall: 1800 042 138 www.msaustralia.org.au MS PRACTICE // ATAXIA AND TREMOR IN PEOPLE WITH MULTIPLE SCLEROSIS Ataxia and tremor in people with multiple sclerosis (MS) Ataxia and tremor are common yet difficult symptoms to manage in people with MS ― often requiring the involvement of a multidisciplinary team. Early intervention is important in order to address both the functional and psychological issues associated with these symptoms. Freecall: 1800 042 138 www.msaustralia.org.au MS PRACTICE // ATAXIA AND TREMOR IN PEOPLE WITH MULTIPLE SCLEROSIS 01 Contents Page 1.0 Definitions 02 2.0 Incidence and impact 3.0 Pathophysiology and clinical characteristics 3.1 Ataxia 3.2 Tremor 03 4.0 Assessment 5.0 Management 04 5.1 Physiotherapy 5.2 Pharmacotherapy 05 5.3 Surgical intervention 06 6.0 Summary Freecall: 1800 042 138 www.msaustralia.org.au MS PRACTICE // AtaXIA AND TREMOR IN PEOPLE WITH MULTIPLE SCLEROSIS 02 1.0 Definitions Ataxia Tremor Ataxia is a term used to describe a number of Tremor is defined as a rhythmic, involuntary, oscillating abnormal movements that may occur during the movement of a body part. There are two main execution of voluntary movements. They include, but classifications of tremor ― resting tremor and action are not limited to, incoordination, delay in movement, tremor. Resting tremor is present in a body part that dysmetria (inaccuracy in achieving a target), is completely supported against gravity and is not dysdiadochokinesia (inability -
Pseudoathetosis in the Spectrum of Alcoholic Neurotoxicity: Presentation and Management
Nachane & Nayak: Pseudoathetosis 154 Case Report Pseudoathetosis in the spectrum of alcoholic neurotoxicity: presentation and management Hrishikesh B. Nachane1, Ajita S. Nayak2 1Assistant Professor, Department of Psychiatry, T.N.M.C. and B.Y.L. Nair Ch. Hospital, Mumbai 2Professor and Head, Department of Psychiatry, K.E.M. Hospital and Seth G.S. Medical college, Mumbai Corresponding author: Hrishikesh Nachane Email – [email protected] ABSTRACT Pseudoathetosis, a proprioceptive abnormality, refers to a movement disorder consisting of involuntary, slow, writhing movements of the fingers. Although many causes for pseudoathetosis have been documented previously, such as multiple sclerosis, myelitis, leprosy, vitamin B12 deficiency, trauma, etc. it has not been previously described in a case of alcohol use disorder. A 50 years old man with chronic alcoholism presented to us with cognitive impairment, cerebellar signs and slow writhing movements of his fingers. Upon detailed investigations, no vitamin deficiency was detected. The patient was managed with a combination of nutritional supplementation, Memantine and Quetiapine, and had complete reversal of pseudoathetosis. The authors imply that pseudoathetosis can be a presentation of alcoholic neurotoxicity, co-occurring with cortico-cerebellar dysfunction, and can manifest irrespective of nutritional status of the patient. Key words: Pseudoathetosis, alcohol, neurotoxicity (Paper received – 5th January 2020, Peer review completed – 20th February 2020) (Accepted – 28th February 2020) INTRODUCTION With increase in alcohol consumption across India, there has been a steady rise in alcohol related complications [1]. The spectrum of alcoholic neurotoxicity is vast: covering dementia, Wernicke-Korsakoff syndrome, myelopathy to peripheral neuropathy. These conditions are not only challenging to diagnose, but downright difficult to treat [2]. -
Handbook on Clinical Neurology and Neurosurgery
Alekseenko YU.V. HANDBOOK ON CLINICAL NEUROLOGY AND NEUROSURGERY FOR STUDENTS OF MEDICAL FACULTY Vitebsk - 2005 УДК 616.8+616.8-089(042.3/;4) ~ А 47 Алексеенко Ю.В. А47 Пособие по неврологии и нейрохирургии для студентов факуль тета подготовки иностранных граждан: пособие / составитель Ю.В. Алексеенко. - Витебск: ВГМ У, 2005,- 495 с. ISBN 985-466-119-9 Учебное пособие по неврологии и нейрохирургии подготовлено в соответствии с типовой учебной программой по неврологии и нейрохирургии для студентов лечебного факультетов медицинских университетов, утвержденной Министерством здравоохра нения Республики Беларусь в 1998 году В учебном пособии представлены ключевые разделы общей и частной клиниче ской неврологии, а также нейрохирургии, которые имеют большое значение в работе врачей общей медицинской практики и системе неотложной медицинской помощи: за болевания периферической нервной системы, нарушения мозгового кровообращения, инфекционно-воспалительные поражения нервной системы, эпилепсия и судорожные синдромы, демиелинизирующие и дегенеративные поражения нервной системы, опу холи головного мозга и черепно-мозговые повреждения. Учебное пособие предназначено для студентов медицинского университета и врачей-стажеров, проходящих подготовку по неврологии и нейрохирургии. if' \ * /’ L ^ ' i L " / УДК 616.8+616.8-089(042.3/.4) ББК 56.1я7 б.:: удгритний I ISBN 985-466-119-9 2 CONTENTS Abbreviations 4 Motor System and Movement Disorders 5 Motor Deficit 12 Movement (Extrapyramidal) Disorders 25 Ataxia 36 Sensory System and Disorders of Sensation -
Neurology and the Liver
Journal of Neurology, Neurosurgery, and Psychiatry 1997;63:279–293 279 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.63.3.279 on 1 September 1997. Downloaded from NEUROLOGY AND MEDICINE Neurology and the liver E A Jones, K Weissenborn Neurological syndromes commonly occur in pathy associated with increased portal- patients with liver disease. A neurological syn- systemic shunting in the absence of drome associated with a liver disease may be a unequivocal evidence of hepatocellular complication of the disease, it may be induced insuYciency—for example, shunting second- by a factor that also contributes to the ary to a congenital portal-systemic shunt, disease—for example, alcohol—or it may have extrahepatic portal hypertension or portal no relation to the presence of the liver disease. hypertension due to hepatic fibrosis (for exam- Neurological deficits associated with liver ple, schistosomiasis). disease may aVect the CNS, the peripheral Subclinical hepatic encephalopathy is the nervous system, or both. This review focuses term applied to a patient with chronic liver dis- on syndromes characterised by altered CNS ease (for example, cirrhosis) when routine function associated with structural liver dis- neurological examination is normal, but appli- eases. Space does not permit consideration of cation of psychometric or electrophysiological peripheral neuropathies associated with liver tests discloses abnormal brain function that disease (for example, xanthomatous peripheral can be reversed by eVective treatment for neuropathy), diseases of childhood that aVect hepatic encephalopathy.8 the liver and CNS (for example, Reye’s Fulminant hepatic failure and subfulminant syndrome), or neurological consequences of (or late onset) hepatic failure are terms used copyright. -
A Dictionary of Neurological Signs.Pdf
A DICTIONARY OF NEUROLOGICAL SIGNS THIRD EDITION A DICTIONARY OF NEUROLOGICAL SIGNS THIRD EDITION A.J. LARNER MA, MD, MRCP (UK), DHMSA Consultant Neurologist Walton Centre for Neurology and Neurosurgery, Liverpool Honorary Lecturer in Neuroscience, University of Liverpool Society of Apothecaries’ Honorary Lecturer in the History of Medicine, University of Liverpool Liverpool, U.K. 123 Andrew J. Larner MA MD MRCP (UK) DHMSA Walton Centre for Neurology & Neurosurgery Lower Lane L9 7LJ Liverpool, UK ISBN 978-1-4419-7094-7 e-ISBN 978-1-4419-7095-4 DOI 10.1007/978-1-4419-7095-4 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2010937226 © Springer Science+Business Media, LLC 2001, 2006, 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. -
EMG Analysis of Patients with Cerebellar Deficits'
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.38.12.1163 on 1 December 1975. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry, 1975, 38, 1163-1169 EMG analysis of patients with cerebellar deficits' MARK HALLETT, BHAGWAN T. SHAHANI, AND ROBERT R. YOUNG2 From the Department ofNeurology and the Laboratory of Clinical Neurophysiology, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts, U.S.A. SYNOPSIS EMGs from biceps and triceps were recorded during stereotyped elbow flexion tasks performed by 20 patients fulfilling clinical criteria for 'cerebellar deficits' and the data were com- pared with previously established normal standards. In a fast flexion task, 15 of 18 patients showed prolongation of the initial biceps and/or triceps components, and it is suggested that this abnormality might be an elemental feature of dysmetria. Ten of 14 patients showed the normal pattern of smooth flexion indicating that, with cerebellar deficits, smooth movements are better pre- served than fast movements. The timing of the cessation of triceps activity before the initiation of biceps activity in an alternating movement was abnormal in 12 of 16 patients; this abnormality might be an elemental feature of dysdiadochokinesia. guest. Protected by copyright. Careful behavioural observations of animals and there may be a single or few elemental abnormali- humans with lesions of cerebellum or cerebellar ties that underlie them all. A detailed study of pathways have documented a variety of motor simple movements might more easily reveal deficits (Holmes, 1939), analysis of which may such elemental abnormalities. lead to a better understanding of normal cere- We have previously defined several stereo- bellar physiology.