DOCSLIB.ORG

Neuroleptic Malignant Syndrome: Case Report and Discussion

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Neuroleptic Malignant Syndrome: Case Report and Discussion PRACTICE Neuroleptic malignant syndrome: case report and discussion Geethan J. Chandran, John R. Mikler, David L. Keegan Abstract tion and cardiac troponin levels. Other laboratory results, including electrolyte levels, were normal. WE REPORT A CASE INVOLVING AN 81-YEAR-OLD man with schizoaffec- The patient was observed for the night. The next morn- tive disorder who presented with neuroleptic malignant syndrome ing his Parkinsonian features and elevated temperature per- (NMS) after an increase in his neuroleptic dose. NMS, a rare but sisted, and he was found to have bilateral hyporeflexia. The potentially fatal complication of neuroleptic medications (e.g., loxapine therapy was stopped because neuroleptic malig- antipsychotics, sedatives and antinauseants), is characterized by nant syndrome (NMS) was suspected. That afternoon the hyperthermia, muscle rigidity, an elevated creatine kinase level CK level climbed to 2574 U/L. The next day, the patient and autonomic instability. The syndrome often develops after a had increased rigidity and his temperature rose to 39.3°C. sudden increase in dosage of the neuroleptic medication or in A septic workup yielded normal results, but the urine myo- states of dehydration. Treatment is mainly supportive and in- cludes withdrawal of the neuroleptic medication and, possibly, globin test result was positive. A firm diagnosis of NMS administration of drugs such as dantrolene and bromocriptine. was made, and therapy with dantrolene (70 mg intra- Complications of NMS include acute renal failure and acute res- venously) was started and about 24 hours later was changed piratory failure. Given the widespread prescription of neuroleptics to bromocriptine (2.5 mg 3 times daily). by physicians in a variety of fields, all physicians need to be able Within a few days, the patient’s NMS symptoms im- to recognize and appropriately manage NMS. proved and his CK level returned to normal. As his symp- toms resolved, the bromocriptine dose was tapered off. In order to control his ongoing psychotic symptoms, the pa- Case tient was prescribed olanzapine (2.5 mg once daily) because of its lower reported rate of NMS. He was also given ser- An 81-year-old man with a history of schizoaffective dis- traline (25 mg once daily) to control his depressive symp- order presented to hospital with increasing auditory hallu- toms. After 5 weeks, his depressive and psychotic symptoms cinations, persecutory delusions and depressive symptoms, improved considerably, and he was discharged from hospi- including suicidal ideation. He was admitted to hospital and tal without further complications. given loxapine (10mg every morning, 50 mg every evening) for his psychotic symptoms and methotrimeprazine (10 mg Comments once daily) for sleep disturbance. Two weeks earlier he had been prescribed venlafaxine by his family physician and had NMS is an uncommon but serious complication of been experiencing some symptomatic hypotensive episodes neuroleptic medications. It was first described in 1967 as as a result. He had also been taking levothyroxine (0.1 mg “akinetic hypertonic syndrome.” 1,2 The frequency of the syn- once daily) and procyclidine (2.5 mg once daily). drome ranges from 0.07% to 2.2% among patients receiving Within 3 days after admission, the methotrimeprazine neuroleptic medications.1 The mortality is 10%–30%.1 therapy was stopped because of somnolence and the loxa- NMS likely results from a complex interaction between pine dose increased to 65 mg/d at bedtime. Twelve hours the neuroleptic medication and a susceptible host. Two the- after this change, the patient had diaphoresis, tremulous- ories have been proposed to explain the syndrome: central ness, urinary incontinence and some cognitive impairment. dopamine receptor blockade and skeletal muscle defect. In His temperature was elevated (38.3°C), and although nor- the first theory, the dopaminergic receptor antagonism by motensive (blood pressure 124/84 mm Hg) he had tachy- neuroleptics may interfere with dopamine’s normal role in cardia (heart rate 128 beats/min) and exhibited Parkinson- central thermoregulation. Heat is produced from serotonin ian features, including tremor, rigidity and unsteady gait. stimulation in the hypothalamus, and dopamine inhibits this An electrocardiogram revealed no acute ischemic changes. process. Dopaminergic blockade therefore leads to less inhi- Laboratory investigation revealed mild leukocytosis (leuko- bition of serotonin stimulation and contributes to the hy- cyte count 11.7 × 109/L), with a shift to the left (neutrophil perthermia seen in NMS.3 To support this theory, there count 9.9 × 109/L). His aspartate aminotransferase level was have been reported cases of conditions resembling NMS in elevated (82 U/L), and his creatine kinase (CK) level was patients with Parkinson’s disease who had no history of the markedly elevated (1145 U/L), with normal CK MB frac- syndrome and in whom therapy with levodopa–carbidopa CMAJ • SEPT. 2, 2003; 169 (5) 439 © 2003 Canadian Medical Association or its licensors P RACTICE NMS.18 There seems to be no significant difference in the Box 1: Neuroleptic medications associated duration of clinical symptoms with long-acting neuroleptics 18 with neuroleptic malignant syndrome compared with short-acting ones. Psychomotor agitation (NMS)* preceding the onset of symptoms is a significant clinical manifestation in patients who are at risk of NMS.15,19 Dehy- Typical neuroleptics Atypical neuroleptics dration with the concomitant use of neuroleptics has been • Haloperidol (+++) Clozapine (+) implicated as a risk factor for the syndrome, because the de- • Chlorpromazine (++) Olanzapine (+) creased blood volume induces peripheral vasoconstriction and impairs heat dissipation. NMS can often be prevented • Fluphenazine, long Quetiapine (+) by ensuring that patients receiving neuroleptics are well hy- acting (++) Risperidone (+) drated. Other risk factors for NMS include stress, humidity • Fluphenazine (++) and concomitant use of lithium, anticholinergic agents or • Levomepromazine (+) some antidepressants.9 • Loxapine (+) Many diagnostic criteria have been proposed for NMS, but because of its variable presentation, no single set of cri- *+ = rarely associated with NMS, +++ = more commonly associated with NMS.1,8–14 teria is used universally. Some clinical manifestations are described in Box 2.1,9,20 The symptoms usually develop over 24 to 72 hours and can last from 1 to 44 days (about 10 days on average).13 There is no typical sequence of symp- and amantadine was abruptly stopped.4 Because central toms, but extrapyramidal symptoms usually occur before thermoregulation is mediated by noradrenergic, dopamin- autonomic ones.17 Hyperthermia, rigidity and recent initia- ergic, serotoninergic and cholinergic pathways, it is unlikely tion of drug therapy with one or more neuroleptics are that the syndrome is due to central dopaminergic blockade common features of NMS. alone.1 Furthermore, dopamine may directly inhibit skeletal The differential diagnosis of NMS is described in muscle contraction, and therefore dopamine blockade may Box 3.1,10,12,20,21 A thorough history taking, physical examina- result in increased skeletal muscle contraction.5 tion and laboratory investigations, including leukocyte In the second theory, NMS is believed to share a patho- count with differential, renal function tests, and measure- physiology with malignant hyperthermia.6 The symptoms ment of electrolyte, serum CK, urine myoglobin and serum of hyperthermia, rigidity and elevated CK levels are com- lithium concentrations, should be performed. An electro- mon to both conditions, as is the response to the peripheral encephalogram, CT scan of the head and lumbar puncture muscle relaxant, dantrolene. Furthermore, both conditions should also be considered to rule out other causes. produce abnormal in vitro contractility test results.1,7 As has For treatment, it is essential to recognize the symptoms been found in patients with malignant hyperthermia, in and to stop the neuroleptic therapy immediately. Support- vitro investigations of patients with NMS have revealed ive therapy, such as fever reduction, hydration and nutri- multiple defects in skeletal muscle, usually associated with increased calcium release from the sarcoplasmic reticulum.5 Box 2: Clinical manifestations of NMS Most neuroleptic medications have some risk of NMS associated with them Physical findings • Opisthotonos† 1,8–14 (Box 1). Even atypical neuroleptics • Abnormal blood pressure • Positive Babinski’s sign previously thought to have less risk, such (typically hypertension)* 13,14 8 • Tachycardia* as olanzapine and quetiapine, have • Altered level of consciousness* been associated with reported cases of • Tachypnea* • Chorea NMS. A rapid change in neuroleptic dose • Trismus‡ 15 • Diaphoresis* is a major risk factor for the syndrome, Laboratory findings especially if it occurs within 5 days before • Fever (temperature > 38.5°C)* ↑ the onset of symptoms,16 and the risk can • Generalized tonic-clonic • Creatine kinase level* persist for 20 days or more after discontin- seizures • Leukocytosis, with shift to the left* uing the neuroleptic therapy.1 NMS most • Muscle rigidity* • Myoglobinuria* often occurs after the initiation or increase • Mutism • ↑ Transaminase levels in dose of neuroleptics, but rarely it can occur after the sudden discontinuation of *Common finding. 17 †Extreme hyperextension of the body in which the head and heels are bent backward and the the drug therapy.
Load more

Recommended publications
  • 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.
    [Show full text]
  • Acute and Chronic Chorea in Childhood Donald L
    Acute and Chronic Chorea in Childhood Donald L. Gilbert, MD, MS This review discusses diagnostic evaluation and management of chorea in childhood. Chorea is an involuntary, hyperkinetic movement disorder characterized by continuous, jerky, or flowing movement fragments, with irregular timing and direction. It tends to be enhanced by voluntary actions and generally causes interference with fine motor function. The diagnostic evaluation begins with accurate classification of the movement disorder followed by consideration of the time course. Most previously healthy children presenting with acute/subacute chorea have an autoimmune etiology. Chronic chorea usually occurs as part of encephalopathies or diseases causing more global neurologic symptoms. We review the management of acute/subacute and chronic choreas, with special emphasis on Sydenham chorea and benign hereditary chorea. Semin Pediatr Neurol 16:71–76 © 2009 Published by Elsevier Inc. horea is a nonpatterned, involuntary, hyperkinetic genetic chorea, will be emphasized. Paroxysmal movement Cmovement disorder. It is continuous, variable in speed, disorders involving chorea will not be discussed but are re- unpredictable in timing and direction, and flowing or jerky in viewed elsewhere.4 As the phenomenology of chorea over- appearance.1 Chorea may be accompanied by athetosis or laps in acute and chronic choreas, most features of the neu- ballism. Athetosis is also continuous but the rate is slower. rologic examination will be discussed under acute chorea. Athetosis often accompanies dystonia or occurs in symptom- atic chorea and may be referred to as choreoathetosis. Ballism designates larger amplitude, flinging, proximally generated Acute Chorea movements. It rarely occurs in isolation in children but can accompany chorea.
    [Show full text]
  • Wilson's Disease
    Reprinted with permission from Thieme Medical Publishers (Semin Neurol. 2007 April;27(2):123-132) Homepage at www.thieme.com Wilson’s Disease Ronald F. Pfeiffer, M.D.1 ABSTRACT Wilson’s disease is an autosomal-recessive disorder caused by mutation in the ATP7B gene, with resultant impairment of biliary excretion of copper. Subsequent copper accumulation, first in the liver but ultimately in the brain and other tissues, produces protean clinical manifestations that may include hepatic, neurological, psychiatric, oph- thalmological, and other derangements. Genetic testing is impractical because of the multitude of mutations that have been identified, so accurate diagnosis relies on judicious use of a battery of laboratory and other diagnostic tests. Lifelong palliative treatment with a growing stable of medications, or with liver transplantation if needed, can successfully ameliorate or prevent the progressive deterioration and eventual death that would otherwise inevitably ensue. This article discusses the epidemiology, genetics, pathophysi- ology, clinical features, diagnostic testing, and treatment of Wilson’s disease. KEYWORDS: Ceruloplasmin, copper, Wilson’s disease, penicillamine, zinc Although he was not the first to recognize the EPIDEMIOLOGY disease process,1 in a doctoral thesis of more than 200 Wilson’s disease is a rare autosomal-recessive disorder. A pages published in Brain in 1912, S. A. Kinnier Wilson prevalence rate of 30 cases per million (or one per masterfully provided the first detailed, coherent descrip- 30,000) and a birth incidence rate of one per 30,000 to 12–15 tion of both the clinical and pathological details of the 40,000 are often quoted. It has been estimated that entity that now bears his name.2 Many other individuals there are 600 cases of Wilson’s disease in the United 14 have embellished and expanded our understanding of States and that 1% of the population are carriers.
    [Show full text]
  • Abnormal Eye Movements in Three Types of Chorea
    DOI: 10.1590/0004-282X20160109 VIEW AND REVIEW Abnormal eye movements in three types of chorea Anormalidades dos movimentos oculares em três tipos de coreia Tiago Attoni1, Rogério Beato2, Serge Pinto3, Francisco Cardoso2 ABSTRACT Chorea is an abnormal movement characterized by a continuous flow of random muscle contractions. This phenomenon has several causes, such as infectious and degenerative processes. Chorea results from basal ganglia dysfunction. As the control of the eye movements is related to the basal ganglia, it is expected, therefore, that is altered in diseases related to chorea. Sydenham’s chorea, Huntington’s disease and neuroacanthocytosis are described in this review as basal ganglia illnesses that can present with abnormal eye movements. Ocular changes resulting from dysfunction of the basal ganglia are apparent in saccade tasks, slow pursuit, setting a target and anti-saccade tasks. The purpose of this article is to review the main characteristics of eye motion in these three forms of chorea. Keywords: chorea; eye movements; Huntington disease; neuroacanthocytosis. RESUMO Coreia é um movimento anormal caracterizado pelo fluxo contínuo de contrações musculares ao acaso. Este fenômeno possui variadas causas, como processos infecciosos e degenerativos. A coreia resulta de disfunção dos núcleos da base, os quais estão envolvidos no controle da motricidade ocular. É esperado, então, que esta esteja alterada em doenças com coreia. A coreia de Sydenham, a doença de Huntington e a neuroacantocitose são apresentadas como modelos que têm por característica este distúrbio do movimento, por ocorrência de processos que acometem os núcleos da base. As alterações oculares decorrentes de disfunção dos núcleos da base se manifestam em tarefas de sacadas, perseguição lenta, fixação de um alvo e em tarefas de antissacadas.
    [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]
  • Physical and Occupational Therapy
    Physical and Occupational Therapy Huntington’s Disease Family Guide Series Physical and Occupational Therapy Family Guide Series Reviewed by: Suzanne Imbriglio, PT Edited by Karen Tarapata Deb Lovecky HDSA Printing of this publication was made possible through an educational grant provided by The Bess Spiva Timmons Foundation Disclaimer Statements and opinions in this book are not necessarily those of the Huntington’s Disease Society of America, nor does HDSA promote, endorse, or recommend any treatment mentioned herein. The reader should consult a physician or other appropriate healthcare professional concerning any advice, treatment or therapy set forth in this book. © 2010, Huntington’s Disease Society of America All Rights Reserved Printed in the United States No portion of this publication may be reproduced in any way without the expressed written permission of HDSA. Contents Introduction Movement Disorders in HD 4 Cognitive Disorders 8 The Movement Disorder and Nutrition 9 Physical Therapy in Early Stage HD Pre-Program Evaluation 11 General Physical Conditioning for Early Stage HD 14 Cognitive Functioning and Physical Therapy 16 Physical Therapy in Mid-Stage HD Assessment in Mid-Stage HD 17 Functional Strategies for Balance and Seating 19 Physical Therapy in Later Stage HD Restraints and Specialized Seating 23 Accommodating the Cognitive Disorder in Later Stage HD 24 Occupational Therapy in Early Stage HD Addressing the Cognitive Disability 26 Safety in the Home 28 Occupational Therapy in Mid-Stage HD Problems and Strategies 29 Occupational Therapy in Later Stage HD Contractures 33 Hope for the Future 34 Introduction Understanding Huntington’s Disease Huntington’s Disease (HD) is a hereditary neurological disorder that leads to severe physical and mental disabilities.
    [Show full text]
  • Movement Disorders and AIDS: a Review
    Parkinsonism and Related Disorders 10 (2004) 323–334 www.elsevier.com/locate/parkreldis Review Movement disorders and AIDS: a review Winona Tsea,*, Maria G. Cersosimob, Jean-Michel Graciesa, Susan Morgelloc, C. Warren Olanowa, William Kollera aDepartment of Neurology, Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1052, New York, NY 10029, USA bDepartment of Neurology, University of Buenos Aires, Buenos Aires, Argentina cDepartment of Pathology, Mount Sinai Medical Center, New York, NY, USA Abstract Movement disorders are a potential neurologic complication of acquired immune deficiency syndrome (AIDS), and may sometimes represent the initial manifestation of HIV infection. Dopaminergic dysfunction and the predilection of HIV infection to affect subcortical structures are thought to underlie the development of movement disorders such as parkinsonism in AIDS patients. In this review, we will discuss the clinical presentations, etiology and treatment of the various AIDS-related hypokinetic and hyperkinetic movement disorders, such as parkinsonism, chorea, myoclonus and dystonia. This review will also summarize current concepts regarding the pathophysiology of parkinsonism in HIV infection. q 2004 Elsevier Ltd. All rights reserved. Keywords: Parkinsonism; AIDS; Human immunodeficiency virus; Movement disorders; Dopamine; Chorea Contents 1. Introduction............................................................................. 324 2. Tremor ................................................................................ 324 2.1.
    [Show full text]
  • Chorea and Related Disorders R Bhidayasiri, D D Truong
    527 Postgrad Med J: first published as 10.1136/pgmj.2004.019356 on 8 September 2004. Downloaded from REVIEW Chorea and related disorders R Bhidayasiri, D D Truong ............................................................................................................................... Postgrad Med J 2004;80:527–534. doi: 10.1136/pgmj.2004.019356 Chorea refers to irregular, flowing, non-stereotyped, Other inherited causes are also discussed in more detail later in this review. In secondary chorea, random, involuntary movements that often possess a tardive syndromes are the most common causes, writhing quality referred to as choreoathetosis. When mild, related to long term use of dopamine blocking chorea can be difficult to differentiate from restlessness. agents. Choreiform movements can also result from structural brain lesions, mainly in the When chorea is proximal and of large amplitude, it is striatum, although most cases of secondary called ballism. Chorea is usually worsened by anxiety and chorea do not demonstrate any specific struc- stress and subsides during sleep. Most patients attempt to tural lesions. disguise chorea by incorporating it into a purposeful HEREDITARY CAUSES OF CHOREA activity. Whereas ballism is most often encountered as Huntington’s disease hemiballism due to contralateral structural lesions of the Huntington’s disease, the most common cause of chorea, is an autosomal dominant disorder subthalamic nucleus and/or its afferent or efferent caused by an expansion of an unstable trinucleo- projections, chorea may be the expression of a wide range tide repeat near the telomere of chromosome 4.12 of disorders, including metabolic, infectious, inflammatory, Each offspring of an affected family member has a 50% chance of having inherited the fully vascular, and neurodegenerative, as well as drug induced penetrant mutation.
    [Show full text]
  • Movement Disorders Emergencies Part 1 Hypokinetic Disorders
    NEUROLOGICAL REVIEW SECTION EDITOR: DAVID E. PLEASURE, MD Movement Disorders Emergencies Part 1 Hypokinetic Disorders Bradley J. Robottom, MD; William J. Weiner, MD; Stewart A. Factor, DO ovement disorders usually do not require emergent intervention; nevertheless, there are acute/subacute clinical settings in which the neurologist is consulted. It is in these circumstances that the neurologist must be prepared to accurately diagnose and properly treat the patient. We have reviewed the literature regarding move- Mment disorder emergencies and divided them into hypokinetic (part 1) and hyperkinetic (part 2) presentations. In part 1, drug-induced syndromes including neuroleptic malignant syndrome, par- kinsonism hyperpyrexia syndrome, and serotonin syndrome will be discussed. Emergency com- plications related to the management of Parkinson disease, including falling, motor fluctuations, and psychiatric issues, will also be reviewed. Arch Neurol. 2011;68(5):567-572 Movement disorders often have an insidi- DRUG-INDUCED MOVEMENT ous onset and slow progression and are not DISORDER EMERGENCIES often associated with emergency situa- tions. However, neurologists may be called Neuroleptic Malignant Syndrome on to diagnose and treat evolving move- ment disorders or acute complications of Neuroleptic malignant syndrome, first de- existing diseases in the emergency depart- scribed in 1960,2 is an iatrogenic disorder re- ment or intensive care unit. Such situa- sulting from exposure to drugs that block tions meet the working definition of an dopamine
    [Show full text]
  • Diagnosing Chronic Fatigue Syndrome (CFS) Alias Myalgic Encephalomyelitis (ME), Fibromyalgia
    04 September 2013, Finn E. Somnier, M.D., D. Sc. (Med.), neurologist Diagnosing chronic fatigue syndrome (CFS) Alias Myalgic encephalomyelitis (ME), fibromyalgia There is no test for chronic fatigue syndrome (CFS), but there are clear guidelines to help doctors diagnose it. National Institute for Health and Care Excellence (NICE) guidelines (clinical guidelines CG53 issued August 2007) for diagnosing CFS In addition to the presence of fatigue, all of the following criteria must apply: it is new or had a clear starting point (it has not been a lifelong problem) it is persistent and/or recurrent it is unexplained by other conditions it substantially reduces the amount of activity someone can do it feels worse after physical activity The patient should also have one or more of these symptoms: difficulty sleeping, or insomnia muscle or joint pain without inflammation headaches painful lymph nodes that are not enlarged sore throat poor mental function, such as difficulty thinking symptoms getting worse after physical or mental exertion feeling unwell or having flu-like symptoms dizziness or nausea heart palpitations, without heart disease For more information, read the NICE guidelines on CFS; and/or National Guideline Clearinghouse: Chronic fatigue syndrome/myalgic encephalomyelitis. A primer for clinical practitioners This diagnosis should be confirmed by a clinician after other conditions have been ruled out, and the above symptoms have persisted for at least four months in an adult and three months in a child or young person. However, it can take a long time for the condition to be diagnosed, as other conditions that cause similar symptoms need to be ruled out first.
    [Show full text]
  • Effect of Deutetrabenazine on Chorea Among Patients with Huntington Disease a Randomized Clinical Trial
    Research Original Investigation Effect of Deutetrabenazine on Chorea Among Patients With Huntington Disease A Randomized Clinical Trial Huntington Study Group Editorial page 33 IMPORTANCE Deutetrabenazine is a novel molecule containing deuterium, which attenuates Supplemental content at CYP2D6 metabolism and increases active metabolite half-lives and may therefore lead to jama.com stable systemic exposure while preserving key pharmacological activity. CME Quiz at jamanetworkcme.com OBJECTIVE To evaluate efficacy and safety of deutetrabenazine treatment to control chorea associated with Huntington disease. DESIGN, SETTING, AND PARTICIPANTS Ninety ambulatory adults diagnosed with manifest Huntington disease and a baseline total maximal chorea score of 8 or higher (range, 0-28; lower score indicates less chorea) were enrolled from August 2013 to August 2014 and randomized to receive deutetrabenazine (n = 45) or placebo (n = 45) in a double-blind fashion at 34 Huntington Study Group sites. INTERVENTIONS Deutetrabenazine or placebo was titrated to optimal dose level over 8 weeks and maintained for 4 weeks, followed by a 1-week washout. MAIN OUTCOMES AND MEASURES Primary end point was the total maximal chorea score change from baseline (the average of values from the screening and day-0 visits) to maintenance therapy (the average of values from the week 9 and 12 visits) obtained by in-person visits. This study was designed to detect a 2.7-unit treatment difference in scores. The secondary end points, assessed hierarchically, were the proportion of patients who achieved treatment success on the Patient Global Impression of Change (PGIC) and on the Clinical Global Impression of Change (CGIC), the change in 36-Item Short Form– physical functioning subscale score (SF-36), and the change in the Berg Balance Test.
    [Show full text]
  • Diagnosis in the Neuroleptic Malignant Syndrome
    Jefferson Journal of Psychiatry Volume 4 Issue 1 Article 10 January 1986 Diagnosis in the Neuroleptic Malignant Syndrome James H. Dallman, MD, CPT, MC Letterman Army Medical Center, San Francisco California Follow this and additional works at: https://jdc.jefferson.edu/jeffjpsychiatry Part of the Psychiatry Commons Let us know how access to this document benefits ouy Recommended Citation Dallman, MD, CPT, MC, James H. (1986) "Diagnosis in the Neuroleptic Malignant Syndrome," Jefferson Journal of Psychiatry: Vol. 4 : Iss. 1 , Article 10. DOI: https://doi.org/10.29046/JJP.004.1.011 Available at: https://jdc.jefferson.edu/jeffjpsychiatry/vol4/iss1/10 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Jefferson Journal of Psychiatry by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. Brief Clinical Reports Diagnosis in the Neuroleptic Malignant Syndrome James H. Dallman, M.D.,C.P.T., M.C. INTRODUCTION Neuroleptic ma lignant syndrome (NMS) is an uncommon, potentially lethal complication of treatment with antipsychotic medication. First described in America n journals by De lay and Deniker in 1968 (1), this syndrome has been reported for many years in th e European andJapanese literature.
    [Show full text]