Hemiballismus and Choreoathetosis As a Relapse in Multiple Sclerosis: a Case Report and Review of Literature
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Hemimasticatory Spasm Treated with Botulinum Toxin
Arq Neuropsiquiatr 2002;60(2-A):288-289 HEMIMASTICATORY SPASM TREATED WITH BOTULINUM TOXIN Case report Hélio A.G. Teive1, Élcio J. Piovesan2, Francisco M.B. Germiniani3, Carlos Henrique A. Camargo3, Daniel Sá3, Rosana H. Scola4, Lineu C. Werneck5 ABSTRACT - We describe a female patient with hemimasticatory spasm, a rare movement disorder due to dysfunction of the motor trigeminal nerve of unknown origin. This patient had an excellent response to botulinum toxin therapy. KEY WORDS: hemimasticatory spasm, paroxysmal spasms, botulinum toxin. Espasmo hemimastigatório tratado com toxina botulínica: relato de caso RESUMO - Relatamos o caso de paciente feminina com espasmo hemimastigatório, distúrbio do movimento raro decorrente de disfunção da porção motora do nervo trigeminal, de etiologia desconhecida. A paciente teve excelente resposta clínica ao tratamento com toxina botulínica. PALAVRAS-CHAVE: espasmo hemimastigatório, espasmos paroxísticos, toxina botulínica. Hemimasticatory spasm (HMS) represents a rare spontaneously. She also complained of difficulty in talk- movement disorder due to a dysfunction of the mo- ing and swallowing when she had the spasms. tor trigeminal nerve of unknown origin. It is frequen- Neurological examination was normal except for in- tly misdiagnosed as hemifacial spasm, which is a tense contraction of the masseter and temporal muscles disorder due to dysfunction of the facial nerve1-3. on the right with severe facial pain when the patient had the spasms. Routine laboratory tests (WBC, biochemistry, The most striking features of HMS are the excruciat- VDRL, ERS) and ceruloplasmine were all normal. ing pain that accompanies the spasm itself and the The patient also had a previous history of irregular fact that initially masticatory movements act as a menstrual cycles and even amenorrhea for more than 1-3 trigger for the spasm . -
Perioral Twitching During Smiling - a Rare Form of Essential Tremor
Clinical Video Neurological Case Reports Published: 02 Dec, 2020 Perioral Twitching during Smiling - A Rare form of Essential Tremor Lea Pollak* Department of Neurology, Neurological Clinic, Kupat Cholim Macabi, Israel Abstract Involuntary movements of facial muscles such as jaw tremor, oromandibular dyskinesia, dystonia, facial myoclonus or hemifacial spasm are common in clinical practice. A 52-year old woman with a 15 year history of upper limb tremor complained of recent spread of the tremor to her face. On examination a moderate kinetic and action, mildly asymmetric tremor of the arms was present. On voluntary and spontaneous smiling bilateral twitching of the buccal muscles was observed. Keywords: Periorbital twitching; Essential tremor; Tardive dyskinesia Introduction Involuntary movements of facial muscles such as jaw tremor, oromandibular dyskinesia, dystonia, facial myoclonus or hemifacial spasm are common in clinical practice. Isolated tremor induced by mild contraction of smiling muscles smiling tremor is extremely rare and was reported by some authors to be associated with Parkinson disease while others related this condition to essential tremor [1-3]. Clinical Video A 52-year old woman with a 15 year history of upper limb tremor complained of recent spread of the tremor to her face. Her medical history comprised Crohn's disease treated with adalimumab and depression treated with sertraline and perphenazine during the last ten years. On examination a moderate kinetic and action, mildly asymmetric tremor of the arms was present. On voluntary and spontaneous smiling bilateral twitching of the buccal muscles was observed (video 1). The twitching disappeared on rest and forced smiling. There were no extra pyramidal signs or involuntary OPEN ACCESS movements of the jaw, lips or tongue (Figure 1). -
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. -
Isolated Corpus Callosal Infarction Secondary to Pericallosal Artery Disease Presenting As Alien Hand Syndrome N C Suwanwela, N Leelacheavasit
533 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.72.4.536 on 1 April 2002. Downloaded from SHORT REPORT Isolated corpus callosal infarction secondary to pericallosal artery disease presenting as alien hand syndrome N C Suwanwela, N Leelacheavasit ............................................................................................................................. J Neurol Neurosurg Psychiatry 2002;72:533–536 held a paper with both hands, the left hand would try to pull Two patients are described with the callosal type of alien the paper against the right. Some actions indicating mirror hand syndrome. Both presented with abnormal feelings in movement were also seen. For example, when he moved his the left upper limb and intermanual conflict without clinical right hand backwards, he felt that the left hand was pulled evidence of callosal apraxia or frontal lobe dysfunction back in the same manner. On examination, he was alert. such as motor deficit or reflexive grasping. Imaging studies Motor power of the arms and legs was full. There was no pin- disclosed subacute infarction in the body and splenium of prick sensory loss or inattention, on double simultaneous the corpus callosum due to pericallosal artery disease. stimulation test. Proprioceptive sense was normal. He could These patients were unique in their presentation as a not identify his left hand fingers or objects placed in his left callosal type of alien hand syndrome secondary to ischae- hand with his eyes closed, but was able to do so under visual mic stroke. observation. There was no apraxia of the left hand on verbal command, in imitation, and in actual object use. Frontal lobe releasing signs such as reflexive grasping, palmomental reflex, and snout reflex were absent. -
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. -
Dystonia and Chorea in Acquired Systemic Disorders
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.4.436 on 1 October 1998. Downloaded from 436 J Neurol Neurosurg Psychiatry 1998;65:436–445 NEUROLOGY AND MEDICINE Dystonia and chorea in acquired systemic disorders Jina L Janavs, Michael J AminoV Dystonia and chorea are uncommon abnormal Associated neurotransmitter abnormalities in- movements which can be seen in a wide array clude deficient striatal GABA-ergic function of disorders. One quarter of dystonias and and striatal cholinergic interneuron activity, essentially all choreas are symptomatic or and dopaminergic hyperactivity in the nigros- secondary, the underlying cause being an iden- triatal pathway. Dystonia has been correlated tifiable neurodegenerative disorder, hereditary with lesions of the contralateral putamen, metabolic defect, or acquired systemic medical external globus pallidus, posterior and poste- disorder. Dystonia and chorea associated with rior lateral thalamus, red nucleus, or subtha- neurodegenerative or heritable metabolic dis- lamic nucleus, or a combination of these struc- orders have been reviewed frequently.1 Here we tures. The result is decreased activity in the review the underlying pathogenesis of chorea pathways from the medial pallidus to the and dystonia in acquired general medical ventral anterior and ventrolateral thalamus, disorders (table 1), and discuss diagnostic and and from the substantia nigra reticulata to the therapeutic approaches. The most common brainstem, culminating in cortical disinhibi- aetiologies are hypoxia-ischaemia and tion. Altered sensory input from the periphery 2–4 may also produce cortical motor overactivity medications. Infections and autoimmune 8 and metabolic disorders are less frequent and dystonia in some cases. To date, the causes. Not uncommonly, a given systemic dis- changes found in striatal neurotransmitter order may induce more than one type of dyski- concentrations in dystonia include an increase nesia by more than one mechanism. -
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. -
New Zealand Data Sheet 1
New Zealand Data Sheet 1. PRODUCT NAME Motetis 25 mg tablet 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each Motetis 25 mg tablets contains 25 mg of tetrabenazine. Excipient(s) with known effect Contains lactose monohydrate. For the full list of excipients, see Section 6.1. 3. PHARMACEUTICAL FORM Yellow, round, flat tablet with a score line on one side. The tablet can be divided into equal halves. 4. CLINICAL PARTICULARS 4.1. Therapeutic indications Movement disorders associated with organic central nervous system conditions, such as Huntington's chorea, hemiballismus and senile chorea. Tetrabenazine is also indicated for the treatment of moderate to severe tardive dyskinesia, which is disabling and/or socially embarrassing. The condition should be persistent despite withdrawal of antipsychotic therapy, or in cases where withdrawal of antipsychotic medication is not a realistic option; also, where the condition persists despite reduction in dosage of antipsychotic medication or switching to atypical antipsychotic medication. 4.2. Dose and method of administration Dose Proper dosing of tetrabenazine involves careful titration of therapy to determine an individualised dose for each patient. When first prescribed, tetrabenazine therapy should be titrated slowly over several weeks to allow the identification of a dose for chronic use that reduces chorea and is well tolerated. Movement disorders Dosage and administration are variable and only a guide is given. An initial starting dose of 25 mg three times a day is recommended. This can be increased by 25 mg a day every three (3) or four (4) days until 200 mg per day is being given or the limit of tolerance, as dictated by unwanted effects, is reached, whichever is the lower dose. -
Essential Tremor of the Voice Vs. Spasmodic Dysphonia by Michael M
Essential Tremor (ET) Essential Tremor of the Voice vs. Spasmodic Dysphonia By Michael M. Johns, MD (pictured below)- Director at Emory Voice Center, Emory University, Atlanta, GA and member of the IETF Medical Advisory Board, and Madeleine Pethan, MS, CCC-SLP - Speech Pathologist at Emory Voice Center Introduction box, is not the only structure which can cause essential tremor of the voice. Tremor of the voice can be caused Certain neurologic conditions can cause people to have when any of the structures in the speech system is problems with their voice. These voice problems can affected. Essential tremor of the voice may be caused often lead to more difficulty communicating throughout by tremor in the soft palate, tongue, pharynx, or even daily life. It is important that patients with neurological muscles of respiration. Extralaryngeal tremor (i.e., out- voice disorders are evaluated by an otolaryngologist, or side the voice box) has been reported in up to as many ENT doctor, in addition to their neurologist to determine as 93% of patients with diagnosed essential tremor of the diagnosis and discuss treatment options. Many the voice. Similarly, most patients with essential tremor patients with essential tremor also experience essential of the voice also have tremor affecting their hands, leg, tremor of the voice. Essential tremor of the voice can chin, or trunk. often be confused with another neurologic voice disor- der known as spasmodic dysphonia. Essential tremor seems to be associated with aging, al- though the reasons are still inconclusive. Most studies What is Essential Tremor? report average age of onset from the late 40s to early 50s. -
Movement Disorder Emergencies 1 4 Robert L
Movement Disorder Emergencies 1 4 Robert L. Rodnitzky Abstract Movement disorders can be the source of signifi cant occupational, social, and functional disability. In most circumstances the progression of these disabilities is gradual, but there are circumstances when onset is acute or progression of a known movement disorders is unexpectedly rapid. These sudden appearances or worsening of abnormal involuntary movements can be so severe as to be frightening to the patient and his family, and disabling, or even fatal, if left untreated. This chapter reviews movement disorder syndromes that rise to this level of concern and that require an accurate diagnosis that will allow appropriate therapy that is suffi cient to allay anxiety and prevent unnecessary morbidity. Keywords Movement disorders • Emergencies • Acute Parkinsonism • Dystonia • Stiff person syndrome • Stridor • Delirium severe as to be frightening to the patient and his Introduction family, and disabling, or even fatal, if left untreated. This chapter reviews movement disor- Movement disorders can be the source of signifi - der syndromes that rise to this level of concern cant occupational, social, and functional disabil- and that require an accurate diagnosis that will ity. In most circumstances the progression of allow appropriate therapy that is suffi cient to these disabilities is gradual, but there are circum- allay anxiety and prevent unnecessary morbidity. stances when onset is acute or progression of a known movement disorders is unexpectedly rapid. These sudden appearances or worsening Acute Parkinsonism of abnormal involuntary movements can be so The sudden or subacute onset of signifi cant par- R. L. Rodnitzky , MD (*) kinsonism, especially akinesia, is potentially very Neurology Department , Roy J. -
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 -
Review of Systems Reason for Visit Past Gynecologic
REVIEW OF SYSTEMS Patient Name Date DOB Height Weight REASON FOR VISIT Why are you seeing the doctor today? ________________________________________________________________________________________ Have you been treated for this problem in the past? Yes No If yes, please explain ______________________________________________________________________________________________________ Have you had any recent radiology or laboratory studies? Yes No If yes, please indicate where, when, and type of study __________________________________________________________________________ PAST GYNECOLOGIC HISTORY Please indicate if you have received treatment for the conditions below, or if you are currently receiving treatment. Yes No Yes No Abnormal Pap HPV (Human Papillomavirus) Other Gynecologic Problems _______________________________________________________________________________________________ Are there any other medical problems that we should be aware of? ______________________________________________________________ _________________________________________________________________________________________________________________________ Are you currently pregnant or could you possibly be pregnant? Yes No Date of Last Menstrual Period ____________________/ / Do you/have you taken female hormones? Yes No Oral contraceptives? Yes No Type of contraception: _____________________________ Total number of: Pregnancies ________ Term Births ________ Pre-Term Births ________ Elective Abortions ________ Miscarriages ________ C-sections ________ REVIEW OF