Etiology, Treatment Options and Prognosis of Post- Lesions: Etiology, Stroke Movement Disorders

Total Page:16

File Type:pdf, Size:1020Kb

Etiology, Treatment Options and Prognosis of Post- Lesions: Etiology, Stroke Movement Disorders REVIEW ARTICLE http://dx.doi.org/10.14802/jmd.16008 / J Mov Disord 2016;9(2):63-70 pISSN 2005-940X / eISSN 2093-4939 Movement Disorders ABSTRACT Post-stroke movement disorders are uncommon, but comprise an important part of secondary move- Following ment disorders. These exert variable and hetero- geneous clinical courses according to the stroke le- sion and its temporal relationships. Moreover, the Cerebrovascular predominant stroke symptoms hinder a proper di- agnosis in clinical practice. This article describes the etiology, treatment options and prognosis of post- Lesions: Etiology, stroke movement disorders. Key Words Treatment Options Stroke; Movement disorders; Etiology; Treatment; and Prognosis Prognosis. Do-Young Kwon Department of Neurology, Korea University College of Medicine, Ansan Hospital, Ansan, Korea Received: February 4, 2016 Revised: February 23, 2016 Accepted: March 7, 2016 Corresponding author: Do-Young Kwon, MD, PhD, Department of Neurology, Korea Univer- sity College of Medicine, Ansan Hospital, 123 Jeokgeum-ro, Danwon-gu, Ansan 15355, Korea Tel: +82-31-412-5150 Fax: +82-31-412-5154 E-mail: [email protected] cc This is an Open Access article distributed under the terms of the Creative Commons Attri- bution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which per- mits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2016 The Korean Movement Disorder Society 63 JMD J Mov Disord 2016;9(2):63-70 INTRODUCTION feature significantly greater involvement of deep br- ain lesions affecting the basal ganglia, thalamus, in- Movement disorders are rare, but may present as ternal capsule, diencephalon, and mesencephalon than a consequence of stroke.1,2 Involuntary movements stroke patients without movement disorders. Strokes related to any type of stroke comprise one important in deep brain lesions are also associated with a high- part of secondary movement disorders. Post-stroke er probability of AIM (odds ratio 3.38, 95% confid- movement disorders are defined as paroxysmal, re- ence interval 1.64 to 6.99).1 For cortical lesions, the current, transient, permanent and delayed move- areas most commonly associated with post-stroke ments in the acute phase or as a delayed syndrome movement disorders include those involved in the occurring months or years after vascular events.1,3 cortical motor system, including the primary motor, Thus, movement disorder after stroke is a heteroge- supplementary motor and premotor cortical areas. neous condition. Abnormal involuntary movements The parietal cortex is also involved in processing so- (AIM) following stroke can be classified as hyper- matosensory information related to movement. How- kinetic or hypokinetic.4 Various presentations in- ever, “pure” or “isolated” stroke-related cortical move- cluding tremor, chorea-ballism, dystonia, athetosis, ment disorders are rare, as most “cortical” strokes myoclonus, ataxia, and parkinsonism have been as- also affect subcortical structures. Therefore, consid- sociated with vascular brain lesions.1,2,5,6 The time eration is needed for the possibility that many “st- course for the development of AIM attributed to ructural” cortical strokes actually have functional stroke is not easily predicted, as the course differs defects arising from lesions affecting subcortical according to the type of AIM; they can manifest with structures. Several case reports have described cor- a variety of presentations or even in the same move- tical stroke-related movement disorders, including ments.4 Similar to the typical stroke symptoms, the parietal lobe stroke with choreo-ballism,8 focal dys- duration of AIM also varies from paroxysmal and/ tonia,9,10 arm levitation due to distortion of the body or transient to persistent and progressive.1 The mani- schema and athetosis.11 Frontal lobe stroke is asso- festation of stroke varies even in the same vascular ciated with asterixis (negative myoclonus),7 second- territory.7 Accordingly, mixed movements are one of ary painless leg moving toe syndrome,12 and resting the characteristics of secondary AIM associated with and action tremor (with strokes affecting the ante- a stroke lesion with an extensive involvement. Al- rior cerebral artery territory).7,13 Structural cystic le- though the frequency of AIM following stroke is low, sions with mass effects of the middle fossa involving it is important to know the possible clinical condi- the fronto-temporo-parietal area can mimic Holme’s tions, its course and symptoms and the proper man- tremor.14 Alleviation of a previous tremor is also pos- agement strategies, as these aspects could consider- sible after frontal cortical stroke.15 Some cortical ably affect a stroke patient’s quality of life as much as stroke-related movement disorders feature a laterali- the paretic stroke symptoms. This article describes ty component: bilateral cortical ptosis can occur with the etiology, treatment options and prognosis of post- a large right-side, hemispheric lesion.16,17 Secondary stroke movement disorders. restless legs syndrome (RLS) after stroke has been reported with temporo-occipital cortical lesions, as ETIOLOGY OF POST-STROKE well as with stroke affecting the basal ganglia, thala- MOVEMENT DISORDERS mus, internal capsule and pons.18 Stroke lesion location Stroke subtypes Post-stroke movement disorders can develop in A large epidemiologic study previously examined any stroke subtype and at any brain level of the mo- post-stroke movement disorders but was limited by tor circuit. In the extrapyramidal system, however, a small number of patients. However, in that study, the basal ganglia and thalamus are the primary le- basal ganglia and thalamus involvement in stroke sion sites associated with post-stroke movement was frequent.2 Overwhelmingly, the typical stroke disorders.1,4 A comparison between stroke patients symptoms that occur in the acute phase play a role and case-controls (without movement disorders) re- in overlooking combined movement disorders. In vealed that stroke patients with movement disorders one registry study that enrolled 1,500 consecutive st- 64 Management of Post-Stroke Movement Disorders Kwon DY roke patients, 59 (3.9%) developed post-stroke mo- MELAS vement disorders, with chorea as the most common Mitochondrial encephalomyopathy, lactic acido- movement disorder subtype.1 Ischemic stroke can be sis, and stroke-like episodes (MELAS) syndrome is etiologically classified as a small vessel disease, large a distinct clinical syndrome involving skeletal mus- vessel disease or cardioembolic stroke.19 Among the cles and the brain.29 As the name suggests, the most ischemic stroke subtypes, multifocal small vessel st- common movement disorder in MELAS is myoclo- roke is the most commonly associated with move- nus. Parkinsonism and gait freezing are other symp- ment disorders following stroke, and it is the leading toms associated with MELAS.30-32 Nakagaki et al.33 cause of post-stroke AIM. However, cardioembolic reported a case of chorea-ballism in MELAS that stroke and large- and medium-sized atherosclerotic might accelerate hyperglycemic movement disor- stroke are also included in the etiology of movement ders. Although brain lesions in MELAS are not con- disorders.2,20 Hemorrhagic stroke has a high proba- fined to a specific vascular territory,34 the brain pa- bility of developing post-stroke movement disor- thology might contribute to most of the related se- ders when compared to ischemic stroke. Generally condary movements. speaking, there is no specific preference to the vas- cular region or subtype in post-stroke movement Moyamoya disease disorders, with only a trend for some of the clinical Moyamoya disease is defined by progressive oc- factors described.21 Chronic small vessel disease or clusion of the internal carotid artery and arteries in Binswanger’s disease can develop into secondary the circle of Willis.35 Movement disorders in moy- parkinsonism (vascular parkinsonism). Vascular amoya disease are rare and have been reported main- parkinsonism is phenomenologically characterized ly in pediatric patients.36-38 Regardless of age, the most by bilateral slowness and rigidity, which is predom- common AIM in moyamoya disease is chorea.39 The inant in the lower extremities, causing gait problems reported occurrence in one study was 31 of 42 (67.4%) and lower-body parkinsonism.22 Subcortical small patients, which was followed by dystonia in 8 of 42 vessel pathology, rather than the typical Lewy body (17.4%) patients, with a mean age of onset of 21.4 pathology, was reported in the pathologic study of years.40 In another study, 5 of 513 pediatric patients vascular parkinsonism.23 with moyamoya disease had AIM, 4 had chorea, and one had dystonia. The symptoms improved in all MOVEMENT DISORDERS IN cases after bypass surgery, suggesting that cerebral SPECIFIC STROKE SYNDROMES ischemia even in the absence of stroke lesions might be a pathogenic mechanism in moyamoya disease.37 CADASIL Another retrospective review study of 316 surgical- Cerebral autosomal dominant arteriopathy with ly treated children with moyamoya disease report- subcortical infarcts and leukoencephalopathy (CA- ed that 10 (3.2%) children had chorea that resolved DASIL) is a progressive vascular disease character- following the revascularization surgery. The same ized by migraine headache, stroke syndromes, and authors postulated that dysfunction of the basal gan- dementia.24
Recommended publications
  • Moyanioya Syndrome*
    Rey. Argent. Neuroc. 2005; 19: 31 Actualización MOYANIOYA SYNDROME* Edward R. Smith, MD, R. Michael Scott, MD Department of Neurosurgery, The Children's Hospital, Boston RESUMEN El síndrome de Moyamoya es una vasculopatía caracterizada por la estenosis crónica y progresiva de la arteria carótida interna intracraneal. El diagnóstico se realiza en base a hallazgos clínicos y radiológicos que incluyen la muy característica estenosis de la carótida interna con un importante desarrollo de circulación colateral. Los pacientes adultos con Moyamoya con frecuencia se presentan con cuadros hemorrágicos. En cambio, los niños usualmente presentan ataques isquémicos transitorios (AIT) o infartos isquémicos y en ellos es frecuente un diagnóstico más tardío del síndrome Moyamoya. La progresión de la enfermedad puede ser lenta con eventos intermitentes o puede ser fulminante, con un rápido deterioro neurológico. Cualquiera sea laforma de evolucionar, el síndrome de Moyamoya suele presentar un empeoramiento clínico y radiológico progresivo en los pacientes no tratados. La cirugía es recomendada para el tratamiento de pacientes con eventos isquémicos cerebrales recurrentes o progresivos que presentan una reducción de la reserva de perfusión cerebral. Múltiples técnicas operatorias han sido descriptas con el propósito de prevenir injurias cerebrales isquémicas mediante un aumento del flujo sanguíneo colateral en áreas corticales hipoperfundidas utilizando la circulación carotídea externa como vascularización donante. Este trabajo discute las diferentes formas terapéuticas con un énfasis especial en la utilización de la sinangiosis pial como método de revascularización indirecta. La utilización de la sinangiosis pial es unaforma de revascularización cerebral efectiva y durable en el síndrome de Moyamoya y debe ser considerada como una forma primaria de tratamiento de esta entidad, especialmente en la población infantil.
    [Show full text]
  • Physiology of Basal Ganglia Disorders: an Overview
    LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES SILVERSIDES LECTURE Physiology of Basal Ganglia Disorders: An Overview Mark Hallett ABSTRACT: The pathophysiology of the movement disorders arising from basal ganglia disorders has been uncer­ tain, in part because of a lack of a good theory of how the basal ganglia contribute to normal voluntary movement. An hypothesis for basal ganglia function is proposed here based on recent advances in anatomy and physiology. Briefly, the model proposes that the purpose of the basal ganglia circuits is to select and inhibit specific motor synergies to carry out a desired action. The direct pathway is to select and the indirect pathway is to inhibit these synergies. The clinical and physiological features of Parkinson's disease, L-DOPA dyskinesias, Huntington's disease, dystonia and tic are reviewed. An explanation of these features is put forward based upon the model. RESUME: La physiologie des affections du noyau lenticulaire, du noyau caude, de I'avant-mur et du noyau amygdalien. La pathophysiologie des desordres du mouvement resultant d'affections du noyau lenticulaire, du noyau caude, de l'avant-mur et du noyau amygdalien est demeuree incertaine, en partie parce qu'il n'existe pas de bonne theorie expliquant le role de ces structures anatomiques dans le controle du mouvement volontaire normal. Nous proposons ici une hypothese sur leur fonction basee sur des progres recents en anatomie et en physiologie. En resume, le modele pro­ pose que leurs circuits ont pour fonction de selectionner et d'inhiber des synergies motrices specifiques pour ex£cuter Taction desiree. La voie directe est de selectionner et la voie indirecte est d'inhiber ces synergies.
    [Show full text]
  • Drug-Induced Movement Disorders
    Expert Opinion on Drug Safety ISSN: 1474-0338 (Print) 1744-764X (Online) Journal homepage: https://www.tandfonline.com/loi/ieds20 Drug-induced movement disorders Dénes Zádori, Gábor Veres, Levente Szalárdy, Péter Klivényi & László Vécsei To cite this article: Dénes Zádori, Gábor Veres, Levente Szalárdy, Péter Klivényi & László Vécsei (2015) Drug-induced movement disorders, Expert Opinion on Drug Safety, 14:6, 877-890, DOI: 10.1517/14740338.2015.1032244 To link to this article: https://doi.org/10.1517/14740338.2015.1032244 Published online: 16 May 2015. Submit your article to this journal Article views: 544 View Crossmark data Citing articles: 4 View citing articles Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=ieds20 Review Drug-induced movement disorders Denes Za´dori, Ga´bor Veres, Levente Szala´rdy, Peter Klivenyi & † 1. Introduction La´szlo´ Vecsei † University of Szeged, Albert Szent-Gyorgyi€ Clinical Center, Department of Neurology, Faculty of 2. Methods Medicine, Szeged, Hungary 3. Drug-induced movement disorders Introduction: Drug-induced movement disorders (DIMDs) can be elicited by 4. Conclusions several kinds of pharmaceutical agents. The major groups of offending drugs include antidepressants, antipsychotics, antiepileptics, antimicrobials, antiar- 5. Expert opinion rhythmics, mood stabilisers and gastrointestinal drugs among others. Areas covered: This paper reviews literature covering each movement disor- der induced by commercially available pharmaceuticals. Considering the mag- nitude of the topic, only the most prominent examples of offending agents were reported in each paragraph paying a special attention to the brief description of the pathomechanism and therapeutic options if available. Expert opinion: As the treatment of some DIMDs is quite challenging, a pre- ventive approach is preferable.
    [Show full text]
  • Complete Issue (PDF)
    JUNE 2018 AJNR VOLUME 39 • PP 993–1191 JUNE 2018 THE JOURNAL OF DIAGNOSTIC AND VOLUME 39 INTERVENTIONAL NEURORADIOLOGY NUMBER 6 WWW.AJNR.ORG Multisite concordance of DSC for brain tumors Comparison of 3T intracranial vessel wall sequences Ophthalmic artery collaterals in Moyamoya disease Official Journal ASNR • ASFNR • ASHNR • ASPNR • ASSR Low-profile Visualized Intraluminal Support Stent Deployment. Refined. Braided Coil Assist Stents with High Neck Coverage, Excellent Visibility and Improved Conformability* Aneurysm Therapy Solutions For more information or a product demonstration, contact your local MicroVention representative: MicroVention Worldwide Innovation Center PH +1.714.247.8000 35 Enterprise *Humanitarian Device: Authorized by Federal Law for use with bare platinum Aliso Viejo, CA 92656 USA embolic coils for the treatment of unruptured, wide neck (neck ≥ 4 mm or dome to neck ratio < 2), intracranial, saccular aneurysms arising from a parent MicroVention UK Limited PH +44 (0) 191 258 6777 vessel with a diameter ≥ 2.5 mm and ≤ 4.5 mm. The effectiveness of this device MicroVention Europe, S.A.R.L. PH +33 (1) 39 21 77 46 for this use has not been demonstrated. MicroVention Deutschland GmbH PH +49 211 210 798-0 microvention.com MICROVENTION and LVIS are registered trademarks of MicroVention, Inc. • Refer to Instructions for Use, contraindications and warnings for additional information. Federal (USA) law restricts this device for sale by or on the order of a physician. ©2018 MicroVention, Inc. Jan. 2018 Now you have 24 hours to make a lifetime of difference in stroke patients like Nora The Trevo Retriever is the only device cleared to reduce disability in stroke patients up to 24 hours from time last seen well.
    [Show full text]
  • Radiologic-Clinical Correlation Hemiballismus
    Radiologic-Clinical Correlation Hemiballismus James M. Provenzale and Michael A. Schwarzschild From the Departments of Radiology (J.M.P.), Duke University Medical Center, Durham, and f'leurology (M.A.S.), Massachusetts General Hospital, Boston Clinical History derived from the Greek word meaning "to A 65-year-old recently retired surgeon in throw," because the typical involuntary good health developed disinhibited behavior movements of the affected limbs resemble over the course of a few months, followed by the motions of throwing ( 1) . Such move­ onset of unintentional, forceful flinging move­ ments usually involve one side of the body ments of his right arm and leg. Magnetic res­ (hemiballismus) but may involve one ex­ onance imaging demonstrated a 1-cm rim­ tremity (monoballism), both legs (parabal­ enhancing mass in the left subthalamic lism), or all the extremities (biballism) (2, 3). region, which was of high signal intensity on The motions are centered around the shoul­ T2-weighted images (Figs 1A-E). Positive der and hip joints and have a forceful, flinging serum human immunodeficiency virus anti­ quality. Usually either the arm or the leg is gen and antibody titers were found, with predominantly involved. Although at least mildly elevated cerebrospinal fluid toxo­ some volitional control over the affected plasma titers. Anti-toxoplasmosis treatment limbs is still maintained, the involuntary with sulfadiazine and pyrimethamine was be­ movements typically can be checked by the gun, with resolution of the hemiballistic patient for only a few moments ( 1). The movements within a few weeks and decrease movements are usually continuous but may in size of the lesion.
    [Show full text]
  • Characteristics of Moyamoya Disease in the Older Population: Is It Possible to Define a Typical Presentation and Optimal Therapeutical Management?
    Journal of Clinical Medicine Review Characteristics of Moyamoya Disease in the Older Population: Is It Possible to Define a Typical Presentation and Optimal Therapeutical Management? Ignazio G. Vetrano 1,* , Anna Bersano 2 , Isabella Canavero 2, Francesco Restelli 1, Gabriella Raccuia 1, Elisa F. Ciceri 3, Giuseppe Faragò 3, Andrea Gioppo 3, Morgan Broggi 1 , Marco Schiariti 1, Laura Gatti 4 , Paolo Ferroli 1 and Francesco Acerbi 1,5 1 Department of Neurosurgery, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; [email protected] (F.R.); [email protected] (G.R.); [email protected] (M.B.); [email protected] (M.S.); [email protected] (P.F.); [email protected] (F.A.) 2 Cerebrovascular Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; [email protected] (A.B.); [email protected] (I.C.) 3 Interventional Neuroradiology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; [email protected] (E.F.C.); [email protected] (G.F.); [email protected] (A.G.) 4 Cellular Neurobiology Laboratory, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; [email protected] 5 Experimental Microsurgical Laboratory, Fondazione IRCCS Istituto Neurologico Carlo Besta, Citation: Vetrano, I.G.; Bersano, A.; 20133 Milan, Italy Canavero, I.; Restelli, F.; Raccuia, G.; * Correspondence: [email protected] Ciceri, E.F.; Faragò, G.; Gioppo, A.; Broggi, M.; Schiariti, M.; et al. Abstract: Whereas several studies have been so far presented about the surgical outcomes in terms of Characteristics of Moyamoya Disease mortality and perioperative complications for elderly patients submitted to neurosurgical treatments, in the Older Population: Is It Possible the management of elderly moyamoya patients is unclear.
    [Show full text]
  • Movement Disorders After Brain Injury
    Movement Disorders After Brain Injury Erin L. Smith Movement Disorders Fellow UNMC Department of Neurological Sciences Objectives 1. Review the evidence behind linking brain injury to movement disorders 2. Identify movement disorders that are commonly seen in persons with brain injury 3. Discuss management options for movement disorders in persons with brain injury Brain Injury and Movement Disorders: Why They Happen History • James Parkinson’s Essay on the Shaking Palsy • Stated that PD patients had no h/o trauma • “Punch Drunk Syndrome” in boxers (Martland, 1928) • Parkinsonian features after midbrain injury (Kremer 1947) • 7 pts, Varying etiology of injury • Many more reports have emerged over time History Chronic Traumatic Encephalopathy (CTE) • Dementia pugilistica (1920s) • Chronic, repeated head injury (30%) • Football players • Mike Webster, 2005 • Boxers • Other “combat” sports • Domestic violence • Military background • Many neurological sx • Dx on autopsy • Taupoathy Linking Brain Injury to Movement Disorders Timeline Injury Anatomy Severity Brain Injury and Movement Disorders Typically severe injury • Neurology (2018) • Rare after mild-moderate • 325,870 veterans injury • Half with TBI (all severities) Pre-existing movement • 12-year follow-up disorders may be linked • 1,462 dx with PD • Parkinson’s Disease (PD) • 949 had TBI • Caveats: • Mild TBI = 56% increased • Incidence is overall low risk of PD • Environmental factors • Mod-Severe TBI = 83% also at play increased risk of PD • Not all data supports it Timeline: Brain Injury
    [Show full text]
  • History-Of-Movement-Disorders.Pdf
    Comp. by: NJayamalathiProof0000876237 Date:20/11/08 Time:10:08:14 Stage:First Proof File Path://spiina1001z/Womat/Production/PRODENV/0000000001/0000011393/0000000016/ 0000876237.3D Proof by: QC by: ProjectAcronym:BS:FINGER Volume:02133 Handbook of Clinical Neurology, Vol. 95 (3rd series) History of Neurology S. Finger, F. Boller, K.L. Tyler, Editors # 2009 Elsevier B.V. All rights reserved Chapter 33 The history of movement disorders DOUGLAS J. LANSKA* Veterans Affairs Medical Center, Tomah, WI, USA, and University of Wisconsin School of Medicine and Public Health, Madison, WI, USA THE BASAL GANGLIA AND DISORDERS Eduard Hitzig (1838–1907) on the cerebral cortex of dogs OF MOVEMENT (Fritsch and Hitzig, 1870/1960), British physiologist Distinction between cortex, white matter, David Ferrier’s (1843–1928) stimulation and ablation and subcortical nuclei experiments on rabbits, cats, dogs and primates begun in 1873 (Ferrier, 1876), and Jackson’s careful clinical The distinction between cortex, white matter, and sub- and clinical-pathologic studies in people (late 1860s cortical nuclei was appreciated by Andreas Vesalius and early 1870s) that the role of the motor cortex was (1514–1564) and Francisco Piccolomini (1520–1604) in appreciated, so that by 1876 Jackson could consider the the 16th century (Vesalius, 1542; Piccolomini, 1630; “motor centers in Hitzig and Ferrier’s region ...higher Goetz et al., 2001a), and a century later British physician in degree of evolution that the corpus striatum” Thomas Willis (1621–1675) implicated the corpus
    [Show full text]
  • Part Ii – Neurological Disorders
    Part ii – Neurological Disorders CHAPTER 14 MOVEMENT DISORDERS AND MOTOR NEURONE DISEASE Dr William P. Howlett 2012 Kilimanjaro Christian Medical Centre, Moshi, Kilimanjaro, Tanzania BRIC 2012 University of Bergen PO Box 7800 NO-5020 Bergen Norway NEUROLOGY IN AFRICA William Howlett Illustrations: Ellinor Moldeklev Hoff, Department of Photos and Drawings, UiB Cover: Tor Vegard Tobiassen Layout: Christian Bakke, Division of Communication, University of Bergen E JØM RKE IL T M 2 Printed by Bodoni, Bergen, Norway 4 9 1 9 6 Trykksak Copyright © 2012 William Howlett NEUROLOGY IN AFRICA is freely available to download at Bergen Open Research Archive (https://bora.uib.no) www.uib.no/cih/en/resources/neurology-in-africa ISBN 978-82-7453-085-0 Notice/Disclaimer This publication is intended to give accurate information with regard to the subject matter covered. However medical knowledge is constantly changing and information may alter. It is the responsibility of the practitioner to determine the best treatment for the patient and readers are therefore obliged to check and verify information contained within the book. This recommendation is most important with regard to drugs used, their dose, route and duration of administration, indications and contraindications and side effects. The author and the publisher waive any and all liability for damages, injury or death to persons or property incurred, directly or indirectly by this publication. CONTENTS MOVEMENT DISORDERS AND MOTOR NEURONE DISEASE 329 PARKINSON’S DISEASE (PD) � � � � � � � � � � �
    [Show full text]
  • Hemiballismus: /Etiology and Surgical Treatment by Russell Meyers, Donald B
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.13.2.115 on 1 May 1950. Downloaded from J. Neurol. Neurosurg. Psychiat., 1950, 13, 115. HEMIBALLISMUS: /ETIOLOGY AND SURGICAL TREATMENT BY RUSSELL MEYERS, DONALD B. SWEENEY, and JESS T. SCHWIDDE From the Division of Neurosurgery, State University of Iowa, College ofMedicine, Iowa City, Iowa Hemiballismus is a relatively uncommon hyper- 1949; Whittier). A few instances are on record in kinesia characterized by vigorous, extensive, and which the disorder has run an extended chronic rapidly executed, non-patterned, seemingly pur- course (Touche, 1901 ; Marcus and Sjogren, 1938), poseless movements involving one side of the body. while in one case reported by Lea-Plaza and Uiberall The movements are almost unceasing during the (1945) the abnormal movements are said to have waking state and, as with other hyperkinesias con- ceased spontaneously after seven weeks. Hemi- sidered to be of extrapyramidal origin, they cease ballismus has also been known to cease following during sleep. the supervention of a haemorrhagic ictus. Clinical Aspects Terminology.-There appears to be among writers on this subject no agreement regarding the precise Cases are on record (Whittier, 1947) in which the Protected by copyright. abnormal movements have been confined to a single features of the clinical phenomena to which the limb (" monoballismus ") or to both limbs of both term hemiballismus may properly be applied. sides (" biballismus ") (Martin and Alcock, 1934; Various authors have credited Kussmaul and Fischer von Santha, 1932). In a majority of recorded (1911) with introducing the term hemiballismus to instances, however, the face, neck, and trunk as well signify the flinging or flipping character of the limb as the limbs appear to have been involved.
    [Show full text]
  • The Paroxysmal Dyskinesias
    The Paroxysmal Dyskinesias Kailash Bhatia Institute of Neurology Queen Square, London UK Note: 2008 Course Slides The Paroxysmal Dyskinesias A heterogeneous and rare group of disorders characterised by recurrent brief episodes of abnormal involuntary movements (Interictally the patient is usually normal) Movements may be chorea, ballism, dystonia, or a combination Diagnosis is often missed Paroxysmal Dyskinesias -Historical Aspects • Gowers (1885)- called it epilepsy! • Mount and Reback (1940)- first clear description 23 yr/male with an AD inherited condition, attacks of choreo- athetosis lasting 5 mins to hours, provoked by alcohol, coffee, tea, fatigue and smoking • “Paroxysmal dystonic choreoathetosis” (PDC) • Other similar families- (Forsmann 1961, Lance 1963, Richard and Barnet, 1968, Fink et al, 1997, Jarman et al, 2000) Paroxysmal dyskinesias -Historical aspects •Kertesz (1967) – new term (Paroxysmal “kinesigenic” choreoathetosis: An entity within the paroxysmal choreo-athetosis syndrome. Description of 10 cases including 1 autopsied) • Attacks were induced by sudden movement (i.e. kinesigenic ) and were very brief • Response to antiepileptics Paroxysmal Dyskinesias- Historical Aspects • Lance 1977 - a new form of paroxysmal dyskinesia in a family • Affected members had attacks of dystonia lasting 5-30 minutes provoked by prolonged exercise (not sudden movement) • Paroxysmal exercise-induced dystonia (PED) Paroxysmal Dyskinesias- Classification Lance (1977)- “the time factor” • PKC-sudden, brief (secs-5mins), movement induced attacks
    [Show full text]
  • The Clinical Approach to Movement Disorders Wilson F
    REVIEWS The clinical approach to movement disorders Wilson F. Abdo, Bart P. C. van de Warrenburg, David J. Burn, Niall P. Quinn and Bastiaan R. Bloem Abstract | Movement disorders are commonly encountered in the clinic. In this Review, aimed at trainees and general neurologists, we provide a practical step-by-step approach to help clinicians in their ‘pattern recognition’ of movement disorders, as part of a process that ultimately leads to the diagnosis. The key to success is establishing the phenomenology of the clinical syndrome, which is determined from the specific combination of the dominant movement disorder, other abnormal movements in patients presenting with a mixed movement disorder, and a set of associated neurological and non-neurological abnormalities. Definition of the clinical syndrome in this manner should, in turn, result in a differential diagnosis. Sometimes, simple pattern recognition will suffice and lead directly to the diagnosis, but often ancillary investigations, guided by the dominant movement disorder, are required. We illustrate this diagnostic process for the most common types of movement disorder, namely, akinetic –rigid syndromes and the various types of hyperkinetic disorders (myoclonus, chorea, tics, dystonia and tremor). Abdo, W. F. et al. Nat. Rev. Neurol. 6, 29–37 (2010); doi:10.1038/nrneurol.2009.196 1 Continuing Medical Education online 85 years. The prevalence of essential tremor—the most common form of tremor—is 4% in people aged over This activity has been planned and implemented in accordance 40 years, increasing to 14% in people over 65 years of with the Essential Areas and policies of the Accreditation Council age.2,3 The prevalence of tics in school-age children and for Continuing Medical Education through the joint sponsorship of 4 MedscapeCME and Nature Publishing Group.
    [Show full text]