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Figure 1.
T1-weighted axial magnetic resonance image with signal hyperintensity in the putamen, caudate, and globus pallidus in a patient with hyperglycemic hemichorea.

T1-weighted axial magnetic resonance image with signal hyperintensity in the putamen, caudate, and globus pallidus in a patient with hyperglycemic hemichorea.

Figure 2.
Fluid-attenuated inversion recovery (A) and diffusion-weighted (B) axial magnetic resonance imaging sequences demonstrating typical findings of anoxic brain injury including signal hyperintensity affecting the basal ganglia, thalamus, and cortical ribbon.

Fluid-attenuated inversion recovery (A) and diffusion-weighted (B) axial magnetic resonance imaging sequences demonstrating typical findings of anoxic brain injury including signal hyperintensity affecting the basal ganglia, thalamus, and cortical ribbon.

Figure 3.
Photographs demonstrating dystonia affecting the head and neck. The dystonic posture is complex, consisting of rotational torticollis, anterocollis, and shoulder elevation.

Photographs demonstrating dystonia affecting the head and neck. The dystonic posture is complex, consisting of rotational torticollis, anterocollis, and shoulder elevation.

Table 1. 
Clinical Definitions of Hyperkinetic Movement Disorders
Clinical Definitions of Hyperkinetic Movement Disorders
Table 2. 
Etiologies of Acute-Onset Chorea
Etiologies of Acute-Onset Chorea
Table 3. 
Treatment of Hyperkinetic Movement Disorders
Treatment of Hyperkinetic Movement Disorders
1.
Genel  FArslanoglu  SUran  NSaylan  B Sydenham's chorea: clinical findings and comparison of the efficacies of sodium valproate and carbamazepine regimens. Brain Dev 2002;24 (2) 73- 76
PubMedArticle
2.
Shiffman  RN Guideline maintenance and revision: 50 years of the Jones criteria for diagnosis of rheumatic fever. Arch Pediatr Adolesc Med 1995;149 (7) 727- 732
PubMedArticle
3.
Terreri  MTRARoja  SCLen  CAFaustino  PCRoberto  AMHilário  MO Sydenham's chorea: clinical and evolutive characteristics. Sao Paulo Med J 2002;120 (1) 16- 19
PubMedArticle
4.
Carapetis  JRCurrie  BJ Rheumatic fever in a high incidence population: the importance of monoarthritis and low grade fever. Arch Dis Child 2001;85 (3) 223- 227
PubMedArticle
5.
de Teixeira  ALCardoso  FMaia  DP  et al.  Frequency and significance of vocalizations in Sydenham's chorea. Parkinsonism Relat Disord 2009;15 (1) 62- 63
PubMedArticle
6.
Weiner  SGNormandin  PA Sydenham chorea: a case report and review of the literature. Pediatr Emerg Care 2007;23 (1) 20- 24
PubMedArticle
7.
Stollerman  GH Rheumatic fever in the 21st century. Clin Infect Dis 2001;33 (6) 806- 814
PubMedArticle
8.
Harries-Jones  RGibson  JG Successful treatment of refractory Sydenham's chorea with pimozide. J Neurol Neurosurg Psychiatry 1985;48 (4) 390
PubMedArticle
9.
Nyman  MDurling  ULundell  A Chorea gravidarum. Acta Obstet Gynecol Scand 1997;76 (9) 885- 886
PubMedArticle
10.
Birbeck  GL Chorea gravidarum. Kaplan  PWNeurologic Disease in Women. New York, NY Demos Medical Publishing2006;355- 358
11.
Palanivelu  LM Chorea gravidarum. J Obstet Gynaecol 2007;27 (3) 310
PubMedArticle
12.
Levine  JSBranch  DWRauch  J The antiphospholipid syndrome. N Engl J Med 2002;346 (10) 752- 763
PubMedArticle
13.
Pekmezović  TSvetel  MRistić  A  et al.  Incidence of vascular hemiballism in the population of Belgrade. Mov Disord 2004;19 (12) 1469- 1472
PubMedArticle
14.
Dewey  RB  JrJankovic  J Hemiballism-hemichorea: clinical and pharmacologic findings in 21 patients. Arch Neurol 1989;46 (8) 862- 867
PubMedArticle
15.
Ghika-Schmid  FGhika  JRegli  FBogousslavsky  J Hyperkinetic movement disorders during and after acute stroke: the Lausanne Stroke Registry. J Neurol Sci 1997;146 (2) 109- 116
PubMedArticle
16.
Ristic  AMarinkovic  JDragasevic  NStanisavljevic  DKostic  V Long-term prognosis of vascular hemiballismus. Stroke 2002;33 (8) 2109- 2111
PubMedArticle
17.
Oh  SHLee  KYIm  JHLee  MS Chorea associated with non-ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1-weighted brain MRI study: a meta-analysis of 53 cases including four present cases. J Neurol Sci 2002;200 (1-2) 57- 62
PubMedArticle
18.
Handley  AMedcalf  PHellier  KDutta  D Movement disorders after stroke. Age Ageing 2009;38 (3) 260- 266
PubMedArticle
19.
Timmermann  LGross  JButz  MKircheis  GHäussinger  DSchnitzler  A Mini-asterixis in hepatic encephalopathy induced by pathologic thalamo-motor-cortical coupling. Neurology 2003;61 (5) 689- 692
PubMedArticle
20.
Burn  DJBates  D Neurology and the kidney. J Neurol Neurosurg Psychiatry 1998;65 (6) 810- 821
PubMedArticle
21.
Wijdicks  EFMParisi  JESharbrough  FW Prognostic value of myoclonus status in comatose survivors of cardiac arrest. Ann Neurol 1994;35 (2) 239- 243
PubMedArticle
22.
Wijdicks  EFMHijdra  AYoung  GBBassetti  CLWiebe  SQuality Standards Subcommittee of the American Academy of Neurology, Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2006;67 (2) 203- 210
PubMedArticle
23.
Levy  DECaronna  JJSinger  BHLapinski  RHFrydman  HPlum  F Predicting outcome from hypoxic-ischemic coma. JAMA 1985;253 (10) 1420- 1426
PubMedArticle
24.
Lance  JWAdams  RD The syndrome of intention or action myoclonus as a sequel to hypoxic encephalopathy. Brain 1963;86111- 136
PubMedArticle
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Werhahn  KJBrown  PThompson  PDMarsden  CD The clinical features and prognosis of chronic posthypoxic myoclonus. Mov Disord 1997;12 (2) 216- 220
PubMedArticle
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Obeso  JAArtieda  JRothwell  JCDay  BThompson  PMarsden  CD The treatment of severe action myoclonus. Brain 1989;112 (pt 3) 765- 777
PubMedArticle
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Río  JMontalbán  JPujadas  FAlvarez-Sabín  JRovira  ACodina  A Asterixis associated with anatomic cerebral lesions: a study of 45 cases. Acta Neurol Scand 1995;91 (5) 377- 381
PubMedArticle
28.
Snider  LASeligman  LDKetchen  BR  et al.  Tics and problem behaviors in schoolchildren: prevalence, characterization, and associations. Pediatrics 2002;110 (2, pt 1) 331- 336
PubMedArticle
29.
Erenberg  GCruse  RPRothner  AD Gilles de la Tourette's syndrome: effects of stimulant drugs. Neurology 1985;35 (9) 1346- 1348
PubMedArticle
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Fras  I Gilles de la Tourette's syndrome: effects of tricyclic antidepressants. N Y State J Med 1978;78 (8) 1230- 1232
PubMed
31.
Gatto  EPikielny  RMicheli  F Fluoxetine in Tourette's syndrome. Am J Psychiatry 1994;151 (6) 946- 947
PubMed
32.
Tourette's Syndrome Study Group, Treatment of ADHD in children with tics: a randomized controlled trial. Neurology 2002;58 (4) 527- 536
PubMedArticle
33.
Marras  CAndrews  DSime  ELang  AE Botulinum toxin for simple motor tics: a randomized, double-blind, controlled clinical trial. Neurology 2001;56 (5) 605- 610
PubMedArticle
34.
Goetz  CGKlawans  HL Gilles de la Tourette syndrome and compressive neuropathies. Ann Neurol 1980;8 (4) 453
PubMedArticle
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Krauss  JKJankovic  J Severe motor tics causing cervical myelopathy in Tourette's syndrome. Mov Disord 1996;11 (5) 563- 566
PubMedArticle
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Jankovic  JPenn  AS Severe dystonia and myoglobinuria. Neurology 1982;32 (10) 1195- 1197
PubMedArticle
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Manji  HHoward  RSMiller  DH  et al.  Status dystonicus: the syndrome and its management [published correction appears in Brain. 2000;123(pt 2):419]. Brain 1998;121 (pt 2) 243- 252
PubMedArticle
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Mariotti  PFasano  AContarino  MF  et al.  Management of status dystonicus: our experience and review of the literature. Mov Disord 2007;22 (7) 963- 968
PubMedArticle
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Zorzi  GMarras  CNardocci  N  et al.  Stimulation of the globus pallidus internus for childhood-onset dystonia. Mov Disord 2005;20 (9) 1194- 1200
PubMedArticle
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Dalvi  AFahn  SFord  B Intrathecal baclofen in the treatment of dystonic storm. Mov Disord 1998;13 (3) 611- 612
PubMedArticle
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Diederich  NJGoetz  CG Drug-induced movement disorders. Neurol Clin 1998;16 (1) 125- 139
PubMedArticle
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Pierre  JM Extrapyramidal symptoms with atypical antipsychotics: incidence, prevention and management. Drug Saf 2005;28 (3) 191- 208
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van Harten  PNHoek  HWKahn  RS Acute dystonia induced by drug treatment. BMJ 1999;319 (7210) 623- 626
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Campbell  D The management of acute dystonic reactions. Aust Prescriber 2001;24 (1) 19- 20
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Gupta  AKRoy  DRConlan  ESCrawford  AH Torticollis secondary to posterior fossa tumors. J Pediatr Orthop 1996;16 (4) 505- 507
PubMedArticle
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Kumandaş  SPer  HGümüş  H  et al.  Torticollis secondary to posterior fossa and cervical spinal cord tumors: report of five cases and literature review. Neurosurg Rev 2006;29 (4) 333- 338
PubMedArticle
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Grisel  P Enucleation de l'atlas et torticolis nasopharyngien. Presse Med 1930;3850- 53
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Yu  KKWhite  DRWeissler  MCPillsbury  HC Nontraumatic atlantoaxial subluxation (Grisel syndrome): a rare complication of otolaryngological procedures. Laryngoscope 2003;113 (6) 1047- 1049
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Neurological Review
June 2011

Movement Disorders Emergencies Part 2Hyperkinetic Disorders

Author Affiliations

Author Affiliations: Department of Neurology, University of Maryland School of Medicine, Baltimore (Drs Robottom and Weiner); and Movement Disorders Program, Emory University School of Medicine, Atlanta, Georgia (Dr Factor).

 

David E.PleasureMD

Arch Neurol. 2011;68(6):719-724. doi:10.1001/archneurol.2011.117
Abstract

Although movement disorders do not usually present as neurologic emergencies, there are times when the abrupt onset of an unusual movement abnormality results in emergency department or intensive care unit consultations. Part 1 of this review discussed hypokinetic movement disorders emergencies. Part 2 provides a diagnostic approach to the recognition and treatment of hyperkinetic movement disorders emergencies by identifying phenomenology and reviewing common etiologies.

Movement disorders most often have an insidious onset and a slowly progressive course and are not associated with emergency situations. In part 1, we addressed hypokinetic movement disorders emergencies focusing on drug-induced emergencies and acute complications of Parkinson disease. Part 2 focuses on the phenomenology of hyperkinetic movement disorders (chorea, ballism, myoclonus, and dystonia) as the key to appropriate recognition and treatment in the emergent situation. Key clinical features of hyperkinetic movement disorders are presented in Table 1.

HYPERKINETIC DISORDERS
Chorea

Chorea consists of involuntary, irregular, purposeless movements that “flow” into one another in a random fashion. Though often referred to separately, the distinction between chorea, athetosis, ballismus, and dystonia is somewhat arbitrary and relates more to speed, amplitude, and duration of the movement rather than underlying pathology. A combination of these movements is often encountered in a single patient. Chorea may result from toxic/metabolic, vascular, and infectious/inflammatory disorders and may be acute in onset. Sydenham chorea is the most common cause of acquired, childhood-onset chorea.1 Sydenham chorea is the neurologic manifestation of rheumatic fever and is sufficient to make the diagnosis of rheumatic fever.2 Its incidence has declined dramatically with the widespread availability of penicillin; nevertheless, Sydenham chorea remains prevalent in areas where access to health care is limited.3,4 In addition to chorea, which may be generalized or hemichorea, additional features of Sydenham chorea include behavioral changes (obsessions, compulsions, hyperactivity, and emotional lability), weakness, hypotonia, and, rarely, vocalizations.5 Symptoms may begin abruptly, from 1 to 6 months after streptococcal pharyngitis.6 The diagnosis is made clinically, though elevated antistreptolysin O antibody titers are supportive. Treatment with penicillin may prevent the cardiac complications of rheumatic fever and is sometimes continued for several years as prophylaxis.7 If Sydenham chorea requires treatment, 1 prospective, nonrandomized trial suggested that valproic acid or carbamazepine may be used.1 Based on observational data, dopamine receptor blockers or dopamine depleters are also recommended.8

Chorea gravidarum usually begins in the first or early second trimester.9 Chorea may be unilateral or bilateral, often involving the face as well as the limbs. Dysarthria is common.10 Chorea usually resolves by the third trimester or disappears within hours after delivery.11 Although chorea gravidarum is rarely an emergency, it is likely that neurologists will encounter this entity in the context of an emergent inpatient consultation on a maternity ward.

The antiphospholipid syndrome may result in acute generalized chorea. Antiphospholipid syndrome may be primary or secondary to systemic lupus erythematosus. Antiphospholipid syndrome is thought to be the most common cause of chorea gravidarum in industrialized nations.12 Rarely is chorea the sole manifestation of antiphospholipid syndrome, but a high index of suspicion is important because of the other potentially catastrophic manifestations (eg, deep venous thrombosis, pulmonary emboli, stroke, thrombotic microangiopathy, thrombocytopenia, and hemolytic anemia) that could occur with failure to diagnose and treat antiphospholipid syndrome.12 Other metabolic causes include hyperthyroidism and hyperglycemia (Table 2).

Hemichorea-Hemiballism

Hemiballism refers to large-amplitude, flinging movements of one side of the body that can be violent. As hemiballismus resolves over days to weeks, the movements often become choreiform. Historically, the most common cause of hemiballism was stroke involving the subthalamic nucleus. However, this etiology is rare, with an annual incidence of less than 1 per 100 000 in a population-based study from Belgrade, Serbia.13 Although stroke remains the most common cause, only a minority of cases have lesions within the contralateral subthalamic nucleus.1416 The second most commonly reported cause of hemiballism is nonketotic hyperglycemia. With this disorder, chorea, or ballism, may be unilateral or bilateral. It occurs more in women,17 and it may be the initial presentation of diabetes mellitus. Magnetic resonance T1-weighted images demonstrate hyperintensity in the putamen, caudate nucleus, and globus pallidus17 (Figure 1). Magnetic resonance imaging findings result from ischemic injury due to hyperviscosity and regional metabolic failure. Like hemiballism secondary to stroke, the movements typically subside over a period of months. In some patients, abnormal movements reverse when the glucose level is normalized. Resolution of magnetic resonance imaging signal change correlates with clinical improvement in chorea.17 If treatment is required (eg, violent, self-injurious, exhausting, or distressing movements), dopamine receptor blockers or dopamine depleters such as tetrabenazine or reserpine are used (Table 3). Because the movements usually resolve over time,18 medication should be tapered after 3 months and the patient, reevaluated.

Myoclonus

Myoclonus consists of sudden, brief shocklike movements that may be due to muscle contraction (positive myoclonus) or loss of muscle tone (negative myoclonus or asterixis). Neurologists are often emergently consulted in the intensive care unit to see patients with myoclonus as a result of toxic/metabolic derangements or cerebral anoxia. It is also seen in serotonin syndrome and neuroleptic malignant syndrome. Medications including monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, opiates, levodopa, gabapentin, triptans, lysergic acid diethylamide (LSD), amphetamines, cocaine, and 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) may cause myoclonus. Hepatic and uremic encephalopathies are the most common metabolic derangements resulting in myoclonus and asterixis.19,20

Cerebral anoxia may result in 2 distinct myoclonic syndromes, myoclonus status epilepticus and postanoxic myoclonus (Figure 2). Myoclonus status epilepticus may begin in the hours immediately after a cerebral anoxic event. This occurs in approximately 30% of comatose adult survivors of cardiac arrest.21 The presence of myoclonus status epilepticus, defined as “spontaneous, repetitive, unrelenting, generalized multifocal myoclonus involving the face, limbs, and axial musculature in comatose patients,” is ominous.22 The chance of good recovery in this setting is exceedingly low,23 and the likelihood of any outcome other than a poor one is 0% (95% confidence interval, 0%-8.8%).22 A “poor outcome” is defined as death or persisting unconsciousness after 1 month or death, persisting unconsciousness, or severe disability requiring full nursing care after 6 months. Postanoxic myoclonus (Lance-Adams syndrome24) usually occurs after recovery from an anoxic event. The action myoclonus seen after recovery from anoxia is generated by abnormal cortical discharges. At rest, the movements are absent, but with muscle activation, they can become disabling. This syndrome may improve over years.25 If a patient requires treatment, clonazepam, primidone, valproic acid, or levetiracetam may be used (Table 3). Successful treatment may require a combination of agents.26 The acute onset of focal asterixis or myoclonus should prompt the search for an underlying structural lesion, usually located in the contralateral thalamus.27

Tics

Tics are either brief paroxysmal movements or vocalizations that are sometimes accompanied by a premonitory urge. They may be stereotyped and, unlike other hyperkinetic movements, may be voluntarily suppressed for a short period.

Motor tics are common in schoolchildren, with a prevalence of 3.2% to 9.6%.28 Even though it is rare for tics to present as an emergency, 2 situations may bring a patient with a tic disorder for emergency evaluation: tic exacerbation and neurologic compromise secondary to tics. Tic disorders wax and wane and some factors lead to marked exacerbation of tic severity including fatigue, stress (physical or emotional), infection, and medications. When this occurs, the dramatic increase in severity (amplitude, violence, or frequency) may be quite alarming to patients and their families. Medications used to treat comorbid conditions (eg, attention-deficit/hyperactivity disorder or obsessive-compulsive disorder), such as stimulants29 and antidepressants,30,31 are often reported to exacerbate tics, although a controlled trial did not confirm this.32 In the emergency department, tics should be diagnosed, and potential exacerbating factors including psychiatric ones should be identified and removed. Pharmacologic treatment, if needed, can be initiated. Initial treatment for debilitating tics uses a neuroleptic or a dopamine-depleting agent (Table 3). Patients with focal tics may benefit from botulinum toxin injections, but this treatment is not helpful emergently.33 Neurologic compromise secondary to tics is uncommon; however, severe tics can cause both compressive neuropathies34 and cervical myelopathy.35

Status Dystonicus

Patients with primary and secondary dystonia can rarely experience acute worsening with generalized, severe, dystonic spasms called dystonic storm or status dystonicus.36 These unremitting dystonic spasms may be life threatening. Reported precipitants for status dystonicus include infection, medication changes, and trauma. The unremitting dystonic spasms may lead to hyperpyrexia, dehydration, respiratory failure, and rhabdomyolysis with renal failure.37 Most patients require intensive care unit admission because orally administered agents are insufficient to arrest the dystonic spasms. The usual therapeutic approach is to use combinations of agents including anticholinergics, benzodiazepines, catecholamine-depleting agents, and dopamine receptor blockers.37,38 Extreme cases may require general anesthesia or paralyzing agents. Refractory cases may respond to neurosurgical intervention, either pallidotomy or deep brain stimulation of the globus pallidus interna, although this surgery is not an emergent procedure.39 Intrathecal baclofen therapy has been used successfully in some patients with status dystonicus.40

Acute Dystonic Reaction

Acute dystonic reaction is most commonly seen after exposure to dopamine receptor blockers, both neuroleptics and antiemetics. Dystonia begins within 24 hours of exposure, and 90% of reactions occur within 5 days.41 Acute dystonic reactions are less common than tardive dyskinesia or drug-induced parkinsonism, affecting approximately 6% of patients exposed to “typical” neuroleptics and 1% to 2% of those exposed to “atypical” neuroleptics.42 Clinical manifestations are diverse, usually affecting the head and neck (Figure 3). Laryngeal dystonia, blepharospasm, cervical dystonia, oculogyric crisis, and focal limb dystonia have all been reported. Acute dystonic reactions are more common in young men,43 while tardive dyskinesia and drug-induced parkinsonism are more common in elderly individuals.42 Treatment with an intravenous anticholinergic agent, such as benztropine mesylate (1-2 mg) or diphenhydramine (25-50 mg), is very effective (Table 3). Because of the possibility of a reoccurrence, a short oral course of an anticholinergic (4-7 days) may be necessary.42 After an acute dystonic reaction, patients are at higher risk for future dystonic reactions when exposed to other dopamine receptor blockers.44

Acute Torticollis

Acute nontraumatic torticollis occurs more commonly in children than adults and should be considered a medical emergency. While this disorder is unlikely to be a primary neurologic condition (dystonia), neurologists may be asked to evaluate the patient. Conditions that present with torticollis in children include posterior fossa tumors,45 cervical cord tumors,46 and infection. Acute infectious torticollis, or Grisel syndrome,47 may follow a number of infections including pharyngitis, tonsillitis, mastoiditis, or other infections involving the head or neck. It is secondary to atlantoaxial rotatory subluxation secondary to infection involving the soft tissue surrounding the cervical spine. The majority of cases described have been in patients younger than 13 years.48 Physical examination may reveal painful, fixed torticollis that occurred following an infection or recent surgical procedure in the head and neck area.49 Sudeck sign may be present, in which the spinous process of the axis is palpable in the contralateral neck.50 Prompt recognition and treatment decrease the rate of neurologic complications, which nonetheless occur in 15% of cases.51 Initial management of the patient with acute torticollis should include treatment of infection and cervical immobilization followed by imaging of the head and neck with computed tomography or magnetic resonance imaging to look for an underlying space-occupying lesion or orthopedic abnormality.52

CONCLUSIONS

Although movement disorders are often not regarded as emergencies, we have reviewed acute onset of chorea/hemiballismus, dystonic storm, neuroleptic malignant syndrome, altered cognitive states and falling in Parkinson disease, parkinsonism hyperpyrexia syndrome, and serotonin syndrome, all of which can be seen in emergency department and intensive care unit consultation. A systematic approach to these problems that emphasizes the identification of the phenomenology as the key to making the diagnosis and beginning the correct treatment is outlined. These disorders are uncommon and few if any randomized controlled trials have been conducted, so treatment recommendations are based on clinical experience reported in the literature.

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Article Information

Correspondence: Bradley J. Robottom, MD, Department of Neurology, University of Maryland School of Medicine, 110 S Paca St, 3-S-128, Baltimore, MD 21201 (brobottom@som.umaryland.edu).

Accepted for Publication: May 10, 2010.

Author Contributions:Study concept and design: Robottom, Factor, and Weiner. Analysis and interpretation of data: Weiner. Drafting of the manuscript: Robottom and Weiner. Critical revision of the manuscript for important intellectual content: Factor. Administrative, technical, and material support: Robottom and Weiner. Study supervision: Weiner.

Financial Disclosure: Dr Robottom has received clinical research support from Chelsea Therapeutics and Solvay Pharmaceuticals and served as an investigator for clinical trials sponsored by the National Institute of Neurological Disorders and Stroke, Westat, Elan Pharmaceuticals, and Medivation. Dr Weiner reports receiving research support from Santhera, Boehringer Ingelheim, and the National Institutes of Health and has served in advisory or consulting roles for Santhera, Novartis, GlaxoSmithKline, and Boehringer Ingelheim. Dr Factor reports receiving grant support from Teva, Ipsen, and Schering-Plough and has served as a consultant to UCB, Allergan, Lundbeck, and Boehringer Ingelheim.

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PubMedArticle
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PubMedArticle
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PubMedArticle
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Dewey  RB  JrJankovic  J Hemiballism-hemichorea: clinical and pharmacologic findings in 21 patients. Arch Neurol 1989;46 (8) 862- 867
PubMedArticle
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Ghika-Schmid  FGhika  JRegli  FBogousslavsky  J Hyperkinetic movement disorders during and after acute stroke: the Lausanne Stroke Registry. J Neurol Sci 1997;146 (2) 109- 116
PubMedArticle
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PubMedArticle
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Oh  SHLee  KYIm  JHLee  MS Chorea associated with non-ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1-weighted brain MRI study: a meta-analysis of 53 cases including four present cases. J Neurol Sci 2002;200 (1-2) 57- 62
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