Adult Onset Simple Phonic Tic After Caudate Stroke

Total Page:16

File Type:pdf, Size:1020Kb

Adult Onset Simple Phonic Tic After Caudate Stroke ADULT ONSET PHONIC TIC AFTER CAUDATE STROKE. 765 Adult Onset Simple Phonic Tic previous lacunar infarct in the right lenticular nucleus. The magnetic resonance imaging (MRI), which included After Caudate Stroke a diffusion sequence, performed in the first week after Meritxell Gomis, MD,* Victor Puente, MD, stroke onset showed an acute lacunar infarct located in Claustre Pont-Sunyer, MD, Carlos Oliveras, MD, and the tail of the left caudate nucleus (see Fig. 1). Jaune Roquer MD, PhD During hospitalization the patient improved, and after Servei de Neurologia, Hospital del Mar, Passeig Marı´tim seven days from admission recovered. 25-29, Barcelona, Spain Within three weeks after the stroke he noticed the onset of involuntary “a” sound with no premonitory symptoms. He observed that stress exacerbated the phonic tic. He was able to suppress it voluntarily for only very short periods of time and then experienced an urge. Because of the interfer- Abstract: We describe a case of adult onset simple phonic tic after subcortical stroke involving left caudate nucleus. ence of the tic, the prosody of the patient speech was not In the acute phase of stroke the patient presented a mild normal. The patient did not present the phonic tic during right clumsiness with complete recovery one week after sleep. No motor tic was observed and he denied exposure to onset. Within 3 weeks after stroke the patient noticed the any medication or illicit drugs. Personal and family history gradual onset of involuntary simple phonic tic consisting of an “a” sound which persists. The patient did not for tics or behavioral disorders was negative. present motor tics or the typical Tourette syndrome Except for the phonic tic, the results of the patient’s co-morbidities, such as attention deficit or obsessive- physical and neurological examinations were normal, as compulsive disorder. © 2008 Movement Disorder Society were the neuropsychological tests. The MRI showed an Key words: phonic tic; subcortical stroke; Tourette syn- acute ischemic lesion involving the left caudate nucleus drome; caudate nucleus. and some previous lacunar strokes. Functional imaging using photon emission computerized tomography Motor and phonic tics are most frequently due to (SPECT) highlighted abnormal patterns of blood flow Tourette Syndrome (TS). There are, however, many and metabolism in the left basal ganglia, and in the motor other causes of tics, such as various acquired and con- cortex of the left frontal lobe. genital neurological and neuropsyquiatric disorders, or The phonic tic only partially responded to pimozide exposure to a range of drugs.1 Acute brain injury such as treatment, which the patient discontinued due to severe stroke, central trauma, and peripheral injury has been somnolence. associated with a variety of movement disorders, most DISCUSSION 2,3 frequently dystonia and tremor. Although subcortical Tics are abrupt, repetitive movements (motor tics), or 4 stroke has been described as a cause of TS, stroke as a sounds (phonic tics), that are commonly preceded by a cause of simple phonic tic has not been reported. premonitory sensation of an extreme tension discomfort We report an adult patient who presented a simple motor or other sensory phenomena.5 phonic tic three weeks after acute left caudate stroke. Motor and phonic tics are usually seen in children, most CASE REPORT frequently due to TS, but there are many other causes of 1 A 71-year-old man, right-handed, ex-smoker, and with tics. In a study evaluating tics and co-existing disorders, ϳ hypertension as a vascular risk factor, was admitted to 9% of the sample had tics associated with an effect on the the hospital due to suddenly suffering a slight clumsiness basal ganglia; and stroke represented 1.2% of these. 6 on his right side. The neurological exam showed a mild In one of the few large prospective studies evaluating right clumsiness and a gait disturbance. On admission a the involuntary abnormal movements following a stroke, CT scan did not show anomalies with the exception of a it was observed that the frequency of these movements was ϳ3.7%. Chorea was the commonest movement al- though dystonia, tremor, and parkinsonism were also This article includes supplementary video clips, available online at observed, but not tics. http://www.interscience.wiley.com/jpages/0885-3185/suppmat Although the specific etiology and pathogenesis of tics *Correspondence to: Dr. M. Gomis, Servei de Neurologı´a, Hospital del Mar, Passeig Marı´tim 25-29, 08003, Barcelona, Spain. cannot always be determined, in many cases of tics not E-mail: [email protected] related to TS a clear anatomical-clinical relationship can be Received 15 May 2007; Revised 21 December 2007; Accepted 24 established. The association of tics with well-documented December 2007 Published online 8 February 2008 in Wiley InterScience (www. lesions involving the basal ganglia suggests that these sub- interscience.wiley.com). DOI: 10.1002/mds.21955 cortical structures play an important role in the genesis of Movement Disorders, Vol. 23, No. 5, 2008 766 M. GOMIS ET AL. dence linking sound production and excitability changes in the motor cortex is of interest.13 In our case, brain MRI showed an acute lesion in the left basal ganglia specifically in the tail of the caudate nucleus suggesting that the tic was secondary to this lacunar stroke. The SPECT, however, showed abnormal patterns of blood flow, not only in the left basal ganglia but also in the motor area of the left frontal lobe. It is possible, therefore, that disinhibition of the cortico-stri- atal-thalamic-cortical circuitry plays a role in its patho- genesis.12,14 Legends to the Video The video shows the simple phonic tic of the patient. The neurological examination, with the exception of the tic was normal. During the video we asked to suppress the tic, and after this the patient had an urge. REFERENCES 1. Mejia NI, Jankovic J. Secondary tics and tourettism. Rev Bras Psiquiatr 2005;27:11-17. 2. Jankovic J. Can peripheral trauma induce dystonia and other move- FIG. 1. Diffusion weighted magnetic resonance imaging (DW MRI) ment disorders? Yes! Mov Disord 2001;16:7-12. of the patient showing an acute stroke in left caudate nucleus. 3. Schrag A, Trimble M, Quinn N, Bhatia K. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain 2004;127:2360-2372. secondary tics.7 Stroke affecting the basal ganglia has been 4. Kwak CH, Jankovic J. Tourettism and dystonia after subcortical stroke. Mov Disord 2002;17:821-825. reported as producing symptoms otherwise typical of TS. 5. Jankovic J. TouretteЈs syndrome. N Engl J Med 2001;345:1184-1192. We have shown, however, that an isolated simple phonic tic 6. Alarco´n F, Zijlmans JCM, Duen˜as G, Cevallos N. Post-stroke could be a consequence of subcortical stroke involving the movement disorders: report of 56 patients. J Neurol Neurosurg basal ganglia, specifically the caudate nucleus. In the liter- Psychiatry 2004;75:1568-1574. 7. Jankovic J. Differential diagnosis and etiology of tics. Adv Neurol ature there is a case report of an isolated simple phonic tic 2001;85:15-29. related to multiple sclerosis.8 8. MA Lana-Peixoto AL. Teixeira and the Brazilian Committee for Studies9-10 have demonstrated that reduced caudate Treatment and Reserch in Multiple Sclerosis (BCTRIMS). Simple phonic tic in multiple sclerosis. Mult Scler 2002;8:510-511. nucleus volumes might be a good candidate marker for a 9. Bloch MH, Leckman JF, Zhu H, Peterson BS. Caudate volumes in trait abnormality in the structure of the basal ganglia in childhood predict symtom severity in adults with Tourette syn- people with TS compared with healthy subjects. It has drome. Neurology 2005;65:1253-1258. also been shown that caudate volume in children with TS 10. Peterson BS, Thomas P, Kane MJ, et al. Basal Ganglia volumes in patients with Gilles de la Tourette syndrome. Arch Gen Psychiatry can predict symptom severity of tic and obsessive-com- 2003;60:415-424. pulsive symptoms in early adulthood. 11. Peterson BS. Neuroimaging studies of TouretteЈs syndrome: a Functional MRI studies during periods of suppression decade of progress. In: Cohen DJ, Jankovic J, Goetz CG, editors. TouretteЈs syndrome. Philadelphia: Lippincott Williams and have shown decreased neuronal activity in the ventral Wilkins; 2001. p 179-196. globus pallidus, putamen, and thalamus, and increased 12. Eidelberg D, Moeller JR, Antonini A, et al. The metabolic anatomy activity in cortical areas normally involved in the inhi- of TouretteЈs syndrome. Neurology 1997;48:927-934. bition of unwanted impulses.11 Previous neuroimaging 13. Sparing R, Meister IG, Wienemann M, Buelte D, Staedtgen M, Boroojerdi B. Task-dependent modulation of functional connec- studies of TS using PET (positron emission tomography) tivity between hand motor cortices and neuronal networks under- have shown decreased metabolic activity in the caudate lying language and music: a transcranial magnetic stimulation and thalamic areas10 and studies using SPECT have also study in humans. Eur J Neurosci 2007;25:319-323. 14. Stern E, Silbersweig DA, Chee KY, et al. A functional neuroanat- identified frontal lobe metabolic differences between TS omy of tics in Tourette syndrome. Arch Gen Psychiatry and healthy subjects.12 The fact that there is some evi- 2000;57:741-748. Movement Disorders, Vol. 23, No. 5, 2008.
Recommended publications
  • Final Program
    FINAL PROGRAM 2nd Pan American Parkinson’s Disease and Movement Disorders Congress JUNE 22-24, 2018 MIAMI, FLORIDA, USA www.pascongress2018.org Table of Contents About MDS ...............................................................................................................................................................................................................................................2 About MDS-PAS Section ...........................................................................................................................................................................................................................3 Continuing Medical Education (CME) Information ....................................................................................................................................................................................4 Hilton Miami Downtown Floor Plan .........................................................................................................................................................................................................4 Schedule-At-A-Glance .............................................................................................................................................................................................................................5 Session Definitions ...................................................................................................................................................................................................................................6
    [Show full text]
  • Tourrete-Syndrome.Pdf
    ISSN : 2376-0249 International Journal of Volume 2 • Issue 8• 1000360 Clinical & Medical Imaging August, 2015 http://dx.doi.org/10.4172/2376-0249.1000360 Case Blog Title: Tourrete Syndrome Rajarshi Sannigrahi1, Ajay Manickam1*, Shaswati Sengupta1, Jayanta saha1, SK Basu1 and Sunetra Mondal2 1Department of ENT and Head Neck Surgery, RG Kar Medical College and Hospital, Kolkata, India 2Vivekananda institute of medical science. Kolkata India Introduction Tourette syndrome is an inherited neuropsychiatric disorder with onset in childhood; it is characterized by multiple motor tics and at least one vocal tic. The occurrence of tics wax and wane with time can be suppressed voluntarily and are frequently preceded by a premonitory urge. Tourette is defined as a part of spectrum of tic disorders which include provisional, transient or persistent tics. The prevalence of tourrete is 0.4% to 3.8% among children between 5 to 18 years [1]. The tourette syndrome can be associated with use of obscene words and derogatory remarks but this is present in only a few cases [2]. Eye blinking, coughing, throat clearing, sniffing and facial movements are the common type of tics. Tourrete does not affect intelligence or life expectancy. To urrete is often associated with comorbid condition such as attention deficit hyperactivity disorder (ADHD) and obsessive compulsive disorder(OCD). These conditions often cause more functional impairment than the tics. Case Study 6 year old female patient presented in the ENT opd with recurrent sore throat. On examination bilateral tonsillitis was seen. During examination frequent blinking of eyes, grimacing, frowning and frequent protrusion of tongue was observed.
    [Show full text]
  • Tourette's Syndrome
    Tourette’s Syndrome CHRISTOPHER KENNEY, MD; SHENG-HAN KUO, MD; and JOOHI JIMENEZ-SHAHED, MD Baylor College of Medicine, Houston, Texas Tourette’s syndrome is a movement disorder most commonly seen in school-age children. The incidence peaks around preadolescence with one half of cases resolving in early adult- hood. Tourette’s syndrome is the most common cause of tics, which are involuntary or semi- voluntary, sudden, brief, intermittent, repetitive movements (motor tics) or sounds (phonic tics). It is often associated with psychiatric comorbidities, mainly attention-deficit/hyperac- tivity disorder and obsessive-compulsive disorder. Given its diverse presentation, Tourette’s syndrome can mimic many hyperkinetic disorders, making the diagnosis challenging at times. The etiology of this syndrome is thought to be related to basal ganglia dysfunction. Treatment can be behavioral, pharmacologic, or surgical, and is dictated by the most incapacitating symp- toms. Alpha2-adrenergic agonists are the first line of pharmacologic therapy, but dopamine- receptor–blocking drugs are required for multiple, complex tics. Dopamine-receptor–blocking drugs are associated with potential side effects including sedation, weight gain, acute dystonic reactions, and tardive dyskinesia. Appropriate diagnosis and treatment can substantially improve quality of life and psychosocial functioning in affected children. (Am Fam Physician. 2008;77(5):651-658, 659-660. Copyright © 2008 American Academy of Family Physicians.) ▲ Patient information: n 1885, Georges Gilles de la Tourette normal context or in inappropriate situa- A handout on Tourette’s described the major clinical features tions, thus calling attention to the person syndrome, written by the authors of this article, is of the syndrome that now carries his because of their exaggerated, forceful, and provided on p.
    [Show full text]
  • 2018 Celebration of Research
    UNIVERSITY OF FLORIDA COLLEGE OF MEDICINE 2018 Celebration of Research Welcome from the Dean The annual University of Florida College of Medicine Celebration of Research affords me the opportunity to say Thank You. Thank you for the late nights, the papers written and reviewed, the grant proposals that have been funded and those that will be resubmitted, the patience that you have shown with the varied hurdles placed in the pathway of research. But most importantly, thank you for the passion that you employ to move the boundary of science knowledge forward. Your research vision and the work of your research teams are appreciated and valued. The discoveries and inventions that result from the basic, translational, population and clinical research at our university are transforming medicine. Thank you for your dedication to creating a healthier future for all. The College of Medicine stands proudly behind your efforts. Michael L. Good, MD Dean, UF College of Medicine Celebration of Research 3 POSTER SESSION & RECEPTION Monday, February 19, 2018 5:30pm – 8:30pm Stephen C. O’Connell Center Slow down and smell the roses The 2018 Celebration is already here. Where did the year go? 2017 was indeed another remarkable year of continued growth and progress for research within the College of Medicine, and 2018 is already off to a great start. We have all been running and seem a bit out of breath. Now it is time to slow down and appreciate the breadth and depth of the College of Medicine’s research endeavors and recognize how our research is directed at fundamental, timely, and significant areas of human health.
    [Show full text]
  • Tourette Syndrome in Children
    Focus | Clinical Tourette syndrome in children Valsamma Eapen, Tim Usherwood UP TO 20% OF CHILDREN exhibit rapid jerky peak severity at the age of approximately movements (motor tics) that are made 10–12 years, and typically improve by without conscious intention as part of a adolescence or thereafter.6 Background Gilles de la Tourette syndrome (GTS), developmental phase that often lasts a few 1 characterised by motor and vocal tics, weeks to months. Similarly, involuntary has a prevalence of approximately 1% sounds, vocalisations or noises (vocal or Clinical features in school-aged children. Commonly phonic tics) such as coughing and even In addition to simple motor and vocal/ encountered comorbidities of GTS brief screams or shouts may be observed in phonic tics, complex tics may be present include attention deficit hyperactivity some children for brief periods of time. Tics (Table 1). Some complex tics – such as disorder (ADHD) and obsessive- lasting for a few weeks to months are known spitting, licking, kissing, etc – may be compulsive behaviour/disorder (OCB/ OCD). Genetic factors play an important as ‘transient tic disorder’. When single misunderstood or misinterpreted and part in the aetiology of GTS, and family or multiple motor or vocal tics – but not a may result in the young person getting members may exhibit tics or related combination of both – have been present in trouble, especially if these tics include disorders such as ADHD, OCB or OCD. for more than one year, the term ‘chronic involuntary and inappropriate obscene tic disorder’ is used. When both (multiple) gesturing (copropraxia) or copying the Objective The aim of this article is to present a motor and (one or more) vocal tics have been movements of other people (echopraxia).
    [Show full text]
  • Psychological, Pharmaceutical Or Neurosurgical
    PSYCHOLOGICAL, PHARMACEUTICAL OR NEUROSURGICAL: A META-ANALYSIS OF TREATMENTS FOR TOURETTE'S SYNDROME Emmett W. McGinley This thesis is submitted in partial fulfillment of the requirements of the Research Honors Program in the Department of Psychology Marietta College Marietta, Ohio April 18, 2008 This Research Honors thesis has been approved for the Department of Psychology and the Honors and Investigative Studies Committee by __________________________________ _________ Faculty thesis advisor Date __________________________________ _________ Thesis committee member Date 2 Introduction George Gilles de la Tourette, a neurobiologist who worked with Sigmund Freud, was the first to describe the condition now known as Tourette's syndrome (TS) (Olson, 2004). While working in France in 1885, George Gilles de la Tourette discovered similar symptoms among his patients including motor tics, coprolalia, and echolalia. These observations led to his discovery of the most widely known and most severe of disorders within the DSM classification of “Tic Disorders” (Sadock & Sadock, 2003). TS is generally believed to occur in about 1 in every 2000 people (Cohen, Leckman & Shaywitz, 1984), with consistent symptomalogy across cultural boundaries (Robertson, 2000). Tic disorders occur in a continuum with less problematic tic disorders such as transient tic disorder on one end and more severe types such as Tourette’s Syndrome on the other (Peterson, Campise, & Azrin, 1994). According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), Tourette's Syndrome or “Tourette's Disorder” is classified by multiple motor and vocal tics that occur numerous times a day within a period of one year (Diagnostic, 2000). The DSM- IV-TR defines tics as “A sudden, rapid, recurrent, non-rhythmic, stereotyped motor movement or vocalization” (Diagnostic, 2000).
    [Show full text]
  • Do Maternal/Paternal Child Relationships Have a Similar Pattern When the Child Has Tourette's Syndrome? a Case Study
    Electronic Journal for Inclusive Education Volume 1 Number 7 Electronic Journal for Inclusive Article 5 Education Vol. 1, No. 7 (Winter 2004) Winter 2004 Do Maternal/Paternal Child Relationships Have a Similar Pattern When the Child Has Tourette's Syndrome? A Case Study Judy Olson Ph.D. [email protected] Follow this and additional works at: https://corescholar.libraries.wright.edu/ejie Part of the Curriculum and Instruction Commons, Curriculum and Social Inquiry Commons, Disability and Equity in Education Commons, Special Education Administration Commons, and the Special Education and Teaching Commons Repository Citation Olson, J. (2004). Do Maternal/Paternal Child Relationships Have a Similar Pattern When the Child Has Tourette's Syndrome? A Case Study, Electronic Journal for Inclusive Education, 1 (7). This Article is brought to you for free and open access by CORE Scholar. It has been accepted for inclusion in Electronic Journal for Inclusive Education by an authorized editor of CORE Scholar. For more information, please contact [email protected]. Olson: Do Maternal/Paternal Child Relationships Have a Similar Pattern W RELATIONSHIPS WHEN CHILD HAS TOURETTE’S SYNDROME Do Maternal/Paternal Child Relationships Have a Similar Pattern When the Child has Tourette’s Syndrome? A Case Study. Dr. Judy Olson Bemidji State University Bemidji, MN Presented Oxford Roundtable Pembroke College March, 2003 Abstract Although I did not realize it at the time, my first experiences in parenting evolved around a child who was diagnosed with onset pervasive developmental disorder by age five. Due to his hyperactivity, he was prescribed Ritalin. Within two weeks after being given this medication, he developed motor and vocal tics and was diagnosed with Tourette’s syndrome (TS) by the time he reached nine years of age.
    [Show full text]
  • Psychiatry for Neurologists C URRENT CLINICAL NEUROLOGY
    Psychiatry for Neurologists C URRENT CLINICAL NEUROLOGY Daniel Tarsy, MD, SERIES EDITOR Psychiatry for Neurologists, edited by Dilip V. Jeste and Joseph H. Friedman, 2006 Diagnostic Criteria in Neurology, edited by Alan J. Lerner, 2006 Status Epilepticus: A Clinical Perspective, edited by Frank W. Drislane, 2005 Thrombolytic Therapy for Acute Stroke, Second Edition, edited by Patrick D. Lyden, 2005 Parkinson’s Disease and Nonmotor Dysfunction, edited by Ronald F. Pfeiffer and Ivan Bodis-Wollner, 2005 Movement Disorder Emergencies: Diagnosis and Treatment, edited by Steven J. Frucht and Stanley Fahn, 2005 Inflammatory Disorders of the Nervous System: Pathogenesis, Immunology, and Clinical Management, edited by Alireza Minagar and J. Steven Alexander, 2005 Neurological and Psychiatric Disorders: From Bench to Bedside, edited by Frank I. Tarazi and John A. Schetz, 2005 Multiple Sclerosis: Etiology, Diagnosis, and New Treatment Strategies, edited by Michael J. Olek, 2005 Seizures in Critical Care: A Guide to Diagnosis and Therapeutics, edited by Panayiotis N. Varelas, 2005 Vascular Dementia: Cerebrovascular Mechanisms and Clinical Management, edited by Robert H. Paul, Ronald Cohen, Brian R. Ott, Stephen Salloway, 2005 Atypical Parkinsonian Disorders: Clinical and Research Aspects, edited by Irene Litvan, 2005 Handbook of Neurocritical Care, edited by Anish Bhardwaj, Marek A. Mirski, and John A. Ulatowski, 2004 Handbook of Stroke Prevention in Clinical Practice, edited by Karen L. Furie and Peter J. Kelly, 2004 Clinical Handbook of Insomnia, edited by Hrayr P. Attarian, 2004 Critical Care Neurology and Neurosurgery, edited by Jose I. Suarez, 2004 Alzheimer’s Disease: A Physician’s Guide to Practical Management, edited by Ralph W. Richter and Brigitte Zoeller Richter, 2004 Field of Vision: A Manual and Atlas of Perimetry, edited by Jason J.
    [Show full text]
  • Treatment of Patients with Obsessive-Compulsive Disorder
    PRACTICE GUIDELINE FOR THE Treatment of Patients With Obsessive-Compulsive Disorder WORK GROUP ON OBSESSIVE-COMPULSIVE DISORDER Lorrin M. Koran, M.D., Chair Gregory L. Hanna, M.D. Eric Hollander, M.D. Gerald Nestadt, M.D. Helen Blair Simpson, M.D., Ph.D. This practice guideline was approved in October 2006 and published in July 2007. A guideline watch, summarizing significant developments in the scientific literature since publication of this guide- line, may be available in the Psychiatric Practice section of the American Psychiatric Association (APA) Web site at www.psych.org. Dr. Koran has received research grants from Forest Pharmaceuticals, Pfizer, Eli Lilly, Ortho-McNeil, Somaxon, and Jazz Pharmaceuticals. He has received honoraria from the Forest Pharmaceuticals Speakers Bureau and the Pfizer Speakers Bureau. He has received consultant fees from Cypress Bioscience. Dr. Hanna reports no competing interests. Dr. Hollander has received research grants from the National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, the National Institute on Drug Abuse, the Office of Orphan Products Development of the U.S. Food and Drug Administration, Pfizer, GlaxoSmithKline, Wyeth, Eli Lilly, Janssen, and Abbott. He has served on advisory boards for Forest Pharmaceuticals, Abbott, and Somaxon. Dr. Nestadt reports no competing inter- ests. Dr. Simpson reports no competing interests. The Executive Committee on Practice Guidelines has reviewed this guideline and found no evidence of influence from these relationships. Suggested citation: American Psychiatric Association. Practice guideline for the treatment of patients with obsessive-compulsive disorder. Arlington, VA: American Psychiatric Association, 2007. Available online at http//www.psych.org/psych_pract/treatg/pg/ prac_ guide.cfm.
    [Show full text]
  • Neurobehavioural Correlates of Abnormal Repetitive Behaviour
    Behavioural Neurology, 1991,4, 113-119 Neurobehavioural Correlates of Abnormal Repetitive Behaviour R. A. FORD Springfield Hospital Glenbumie Road, London SW17, UK Correspondence to: Warlingham Park Hospital, Warlingham, Surrey CR3 9YR, UK Conditions in which echolalia and echopraxia occur are reviewed, followed by an attempt to elicit possible mechanisms of these phenomena. A brief description of stereotypical and perseverative behaviour and obsessional phenomena is given. It is suggested that abnormal repetitive behaviour may occur partly as a result of central dopaminergic dysfunction. Introduction Repetition of the motor activities or language of another person is usually under voluntary control; if it becomes an involuntary process it may be indicative of an underlying disease process. Echophenomena is a term which encompasses echolalia and echopraxia. Echolalia is the repetition of another individual's speech, and does not usually serve a communicative purpose. Echopraxia is the repetition of another individual's motor activities, and is usually non-goal-directed. Echolalia is found in conditions in which there is an abnormality or immaturity of communicative processes, such as in acquired deafness, during normal childhood speech development, transcor­ tical aphasias and childhood autism. Echolalia and echopraxia are fre­ quently found together in conditions such as catatonia, Gilles de la Tourette syndrome and the hyperekplexias. Other phenomena characterized by an excessive tendency to repetition are mannerisms, stereotyped behaviour and perseveration. Stereotyped behaviour has been defined as repetitive, non­ goal-directed actions which are carried out in a uniform way. If the particular behaviour is thought to be goal-directed, it is classified as a mannerism (Fish, 1974), although the distinction between the two is an artificial one.
    [Show full text]
  • Secondary Tics and Tourettism Tiques Secundários E Touretismo
    11 ORIGINAL ARTICLE Secondary tics and tourettism Tiques secundários e touretismo Nicte I Mejia,1 Joseph Jankovic1 Original version accepted in English Abstract Motor and phonic tics are most frequently due to Tourette syndrome, but there are many other causes of tics. We analyzed data on 155 patients with tics and co-existent disorders (101M/54F; mean age 40.5 ± 20.2 years). Fourteen (9.0%) patients had tics associated with an insult to the basal ganglia, such as head trauma (N = 4, 2.5%), stroke (N = 2, 1.2%), encephalitis (N = 3, 1.9%) and other causes. In addition, certain drugs, toxins, and post-infectious causes were associated with tics. Rarely, peripheral injury can cause movement disorders, including tics (N = 1, 0.6%). Pervasive developmental disorders, including Asperger’s syndrome (N = 13, 8.3%), mental retardation (N = 4, 2.5%), autism (N = 3, 1.9%), and Savant’s syndrome (N = 1, 0.6%), also may be associated with tics, as noted in 21 of the 155 patients (13.5%). Genetic and chromosomal disorders, such as Down’s syndrome 5 (3.2%), neuroacanthocytosis (N = 2, 1.2%), and Huntington’s disease (N = 1, 0.6%), were associated with tics in 16 patients (10.3%). We have also examined the co-existence of tics and other movement disorders such as dystonia (N = 31, 20.0%) and essential tremor (N = 17, 10.9%). Sixteen (10.3%) patients presented psychogenic tics, and one (0.6%) psychogenic tics and dystonia; conversely, Tourette syndrome preceded the onset of psychogenic dystonia (N = 1, 0.6%), and psychogenic tremor (N = 1, 0.6%) in two patients.
    [Show full text]
  • Tardive Syndromes
    Tardive Syndromes Eoin Mulroy1, Bettina Balint1, 2, Kailash P Bhatia1 1 Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London WC1N, 3BG 2 Department of Neurology, University Hospital, Heidelberg, Germany Corresponding Author: Eoin Mulroy [email protected] Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London WC1N 3BG Phone: 02034567890 Word count: 4141 Abstract Dopamine receptor blocking antipsychotics, first introduced to clinical practice in 1952, were hailed as a panacea in the treatment of a number of psychiatric disorders. Within 5 years however, this notion was to be shattered by the recognition of both acute and chronic drug-induced movement disorders which can accompany their administration. Tardive syndromes, denoting the delayed onset of movement disorders following administration of dopamine receptor blocking (and also other) drugs, comprise diverse manifestations ranging from the classic oro-bucco-lingual dyskinesia, through dystonic craniocervical and trunk posturing to abnormal breathing patterns. Despite having been an important part of clinical movement disorder practice for over 60 years, the pathophysiologic basis of tardive syndromes remains poorly understood and the optimal treatment approach remains unclear. This review summarises the current state of knowledge relating to tardive syndromes, and provides clinicians with pragmatic, clinically focused guidance with which to tackle the disorder. Introduction Movement disorders occurring as a direct iatrogenic consequence of the administration of dopamine receptor blocking neuroleptic drugs were first reported in 1957, five years after their introduction into psychiatric practice. The year 1964 saw their first collective description as a ‘tardive’ (drawn from the latin tardus, meaning late) phenomenon [1], reflecting their delayed onset following medication administration, in contrast to ‘acute’ dystonic reactions, which can also occur following dopaminergic blockade.
    [Show full text]