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History

Patients often have movement disorders that may actually represent a mixture or overlap of several dyskinesia disorders. Individuals treated with neuroleptics may demonstrate both acute and chronic effects, manifested by acute dyskinesias and tardive dyskinesia (TD). Akathisia and tics may be manifested simultaneously after long-term treatment with neuroleptics.

When a patient is seen for the first time, diagnosis of acute and chronic dyskinesias may be difficult without a careful history. Precise documentation of a patient’s complete movement history and medication history may facilitate accurate delineation of movement disorders. Therefore, a full neurologic and pharmacologic history may provide the basis for distinguishing idiopathic Tourette disorder from acute medication-induced tardive tics.

Patients and families often cannot provide accurate histories; thus, firm diagnoses may be impossible. Because acute and tardive medication effects may occur simultaneously, the distinction may be challenging in a clinical setting. Observing patients carefully on a regular basis and precisely documenting (through the use of structured rating instruments) the phenomenology and topography of movements and the pharmacologic treatments at each visit will help provide a basis for accurate future diagnosis of acute dyskinesia and TD.

Although TD has been observed after exposure to various substances (eg, levodopa, amphetamine, and metoclopramide), the prototypical TD is the orofacial (ie, buccolingual, masticatory) hyperkinesia induced by neuroleptics (antipsychotic dopamine D₂-receptor blockers). People with other movement disorders and those with diabetes mellitus are at increased risk of TD.

Neuroleptic-induced TD is characterized by choreiform, athetoid, and rhythmic movements of the tongue, jaw, trunk, and extremities that have persisted for at least 4 weeks and that began during treatment with neuroleptics or within 4 weeks of discontinuing neuroleptics. Diagnosis of neuroleptic-induced TD generally requires exposure to neuroleptics for at least 3 months. At least 1 month of exposure is typically required if the patient is aged 60 years or older. Oral and genital pain can be prominent manifestations of TD.

Neuroleptic-induced TD is excluded if symptoms and signs result from another neurologic or medical disorder, ill-fitted dentures, or other medications. For example, hyperthyroidism may manifest with choreiform movements of the limbs. Furthermore, neuroleptic-induced TD cannot be diagnosed if symptoms and signs result from an acute neuroleptic-induced movement disorder.

Antiparkinsonism agents usually do not improve neuroleptic-induced dyskinesias. Decreasing the dose of the neuroleptic may increase the movements temporarily. In some patients, increasing the dose of the neuroleptic diminishes movements, thereby masking the TD.

Although the neuroleptic dose may temporarily diminish the disorder, regular increments are needed to achieve apparent beneficial effects. Over the long term, maintaining and increasing doses of neuroleptics to mask TD may be ineffective. However, situations may exist in which masking of TD by continuing and escalating neuroleptic doses may be justified. Benefits and risks must be weighed. Neuroleptic-induced TDs are absent during sleep.

On initial examination, obtain a history of neurologic disorders that may involve the basal ganglia (eg, cerebrovascular disease, encephalitis, head trauma, and neoplasms). Obtain a family history for hereditary dyskinesias associated with Huntington disease, Wilson disease, and torsion dystonia.

Inquire about medications, including amphetamines, levodopa, and substances that may result in dyskinesias (see Etiology). Specifically note whether antiemetic medications (especially metoclopramide, prochlorperazine, and related compounds) are being administered.

Distinction from similar conditions

Unlike TD, Sydenham chorea is a disorder associated with a history of group A streptococcal infection and rheumatic fever in children. It typically affects children and adolescents 6 months or more after an infection with group A streptococci. Prompt administration of antibiotic therapy for infections with group A streptococci dramatically reduces the incidence of Sydenham chorea. The female-to-male ratio is approximately 2:1.

Sydenham chorea is characterized by the rapid onset of chorea, muscular weakness, hypotonia, dysarthria, obsessions, compulsions, and other behavioral and emotional disturbances. After an abrupt or insidious onset, Sydenham chorea worsens over 2-4 weeks and then resolves over 3–6 months. Chorea may persist after the episode has ended. One fifth of patients with Sydenham chorea experience a recurrence, typically within 2 years of the initial episode.

Pantothenate kinase-associated neurodegeneration (PKAN) (Hallervorden-Spatz disease) occurs in patients aged 10–15 years, a different age group than that of persons with TD. PKAN is an extremely rare, progressive neurogenetic disorder with autosomal recessive inheritance associated with dementia and death (approximately 20 y after onset). It is characterized by rigidity, dystonia, choreoathetosis, spasticity, foot deformity, and intellectual deterioration. It is associated with excessive iron deposition in the basal ganglia that can be observed on MRI.

Assessment tools

Differentiate neuroleptic-induced TD from spontaneous dyskinesias and mannerisms of psychosis and other mental disorders.^[32] Several rating scales have been developed to identify the presence and severity of TD.^{[33, 34, 35, 36, 37, 38]}

The most widely used instrument is the Abnormal Involuntary Movement Scale (AIMS) developed by the Psychopharmacology Research Branch of the National Institute of Mental Health.^[39] Because the AIMS can be readily administered in a few minutes, it is recommended in patients receiving treatment with substances that may cause TD. Administer the AIMS at baseline before the institution of pharmacotherapy to document any movements present, then at least every 3 months thereafter during the course of treatment.

Part of the AIMS assessment includes observation of the patient when he or she is distracted by other activities. Patients may suppress movements while concentrating intensely. Therefore, administration of the AIMS can be supplemented by requesting that the patient perform additional tasks during the assessment. Movements may then be demonstrated when the patient is concentrating on the additional tasks.

For example, during the administration of item 5 of the AIMS assessment, have the patient sit in a chair with hands on knees, legs slightly apart, and feet flat on the floor. Examine the entire body for movements while the patient is in this position, then ask the patient to count backwards from 30.

In addition, during item 5 of the AIMS, ask the patient to sit with hands hanging unsupported (between the legs if male, or hanging over the knees if female and wearing a dress). Observe the hands and other body areas, then request that the patient describe in detail the path traveled that day. Ask the patient where the trip started, what streets were traveled, where turns were made, where the trip terminated, and what floor and room were entered. These procedures stimulate the patient and may provoke the appearance of movement disorders.

The AIMS may be modified to allow repeated brief assessments during the course of a single patient examination to check for possible effects of interventions. In other words, by administering the modified AIMS regularly after the administration of a treatment, the time course of abnormal movements may be regularly recorded and plotted.^[40]

To assess the appropriateness of treatment with antipsychotic medication,^{[33, 34, 41]} the Psychoactive Medication Quality Assurance Rating Survey (PQRS) can be used at initial assessment and then repeated annually,^[42] and the PQRS Screening Criteria can be repeated monthly.^[43]

Specific tardive dyskinesias

Specific TDs resulting from long-term use of dopamine antagonists (eg, orofacial dyskinesia, tardive akathisia, tardive blepharospasm, tardive dystonia, tardive myoclonus, and tardive tics) may occur concurrently.

Tardive akathisia is manifested by repetitive tapping, squirming, and marching movements. It occurs as the dose of the dopamine antagonist is decreased after long-term treatment. People with akathisia complain of inner restlessness and the inability to remain still. Unlike other movement disorders, akathisia can be diagnosed solely on the basis of the patient’s subjective symptoms in the absence of any objective signs. The Hillside Akathisia Scale is often helpful.

Blepharospasm (repetitive, forceful, sustained contraction of the orbicularis oculi) may occur as an isolated finding. When it occurs in conjunction with dystonia of the lower face, jaw, and neck, it is referred to as Meige syndrome. Although blepharospasm has been reported with dopaminergic and sympathomimetic agents and antihistamines, it has also been associated with long-term treatment with dopamine antagonists.

Tardive blepharospasm is defined as the presence of repetitive sustained contractions of the orbicularis oculi that have lasted for at least 1 month and that developed during or within 3 months of the discontinuance of treatment with dopamine antagonists (in the absence of other disease or familial causes). Symptoms of tardive blepharospasm fluctuate. Fatigue, anxiety, work, and light exacerbate tardive blepharospasm, whereas rest and sleep relieve it.

Tardive dystonia occurs in 1–2% of individuals during long-term treatment with dopamine antagonists. It must be differentiated from acute dystonia, which occurs in the first days of neuroleptic treatment or after an increase in the dose. Tardive dystonia presents as fixed posturing of the face and neck (eg, anterocollis, retrocollis, torticollis), extremities, and trunk. It may be either localized, involving one or more body parts, or generalized. Unlike TD, tardive dystonia may improve with anticholinergic medication.

Unlike TD, torsion dystonia is an inherited disorder with childhood onset that typically occurs in people of Ashkenazi Jewish descent.

Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.

Tardive tourettism resembles Tourette syndrome^[44] and presents during or after treatment with dopamine antagonists. Typically, it begins in individuals older than 21 years, whereas Tourette syndrome commonly presents by the age of 7 years. Tardive tourettism is characterized by frequent, multiple motor and vocal tics, echolalia, echopraxia, coprolalia, and copropraxia. Tics may be suppressed temporarily while inner tension builds; this inner tension is relieved by an explosion of tics. Tardive tourettism may occur with other TDs.

Tardive tremor is a hyperkinetic movement disorder associated with long-term treatment with dopamine antagonists. Kuo and Jankovic have reported the occurrence of tardive gait as a tardive dyskinesia.^[45]

Next: Physical Examination

Physical Examination

As noted, neuroleptic-induced orofacial hyperkinesia is the prototypical form of tardive dyskinesia (TD). It is characterized by irregular movements of variable amplitude and low frequency. TD is expressed in the tongue, cheeks, mandible, perioral area, and other regions of the face, fingers, and toes. Various facial movements are observed. TD may be observed in the upper face with excessive blinking and brow wrinkling.

Orofacial dyskinesias appear as involuntary, repetitive, and stereotyped facial grimacing with twisting or protrusion of the tongue. The individual may initially be unaware of these movements until family and friends draw attention to them. Puckering, smacking, opening, and closing of the lips may occur constantly. The person may appear to be chewing or sucking on items. The movements resemble those of people with ill-fitting dentures.

Inquire about the use of dentures. Inquire if the person is aware of movements in the mouth, face, hands, and feet. Ask if dentures or teeth bother the patient. The tongue may protrude briefly out of the lips. If asked to hold the tongue in a protruded position, the person may be unable to maintain protrusion for longer than 1 second. Although the individual may attempt to disguise the movements by placing the hand to the mouth, in time, the movements become constant during waking hours and cannot be suppressed by the patient.

TD is commonly associated with involuntary athetoid movements (slow, snakelike writhing) of the extremities, including wiggling, twisting, and tapping the fingers and toes. To perform a full assessment, ask the individual to remove shoes and socks so that the movements of the toes and feet can be observed fully. Movements typically become constant during waking hours. Often, the individual cannot suppress them for longer than 1 second.

Guitar- and piano-playing movements and other flexion and extension movements of the fingers or wrists can be observed. Flexion and extension movements of the ankles and toes are characteristic. Dyskinetic movements of the neck, trunk, and pelvis are occasionally seen. Jerking movements of the abdomen and diaphragm, resulting in respiratory irregularity, may occur.

Neuroleptic-induced TD is present at rest and diminishes or subsides when the affected body part is activated. For example, squeezing the hand of another person often eliminates finger dyskinesias, tongue protrusion commonly reduces tongue dyskinesias, and mouth opening diminishes orofacial dyskinesias. Simply pointing out these movements and asking the patient to stop can reduce the movements. For example, orofacial movements may be stopped by placing the patient’s fingers on his or her lips.

Neuroleptic-induced TD is increased when the patient’s attention is drawn away from the movements, as when the examiner asks the patient to move a different body part. For example, finger dyskinesias may be increased by asking the patient to walk with arms resting comfortably at the sides. Asking the patient to repeatedly touch the thumb to each finger sequentially in both hands may amplify TD in the tongue and the face. Provocative distracting movements may be necessary to induce movement in mild TD. Distraction is a key component of the AIMS.^[46]

Tardive akathisia includes the presence of subjective symptoms of restlessness and the urge to move. It refers to the inability to sit down or remain still. People with tardive akathisia exhibit constant pacing and moving of the hands and feet. They typically shift their weight from one foot to the other when standing and swing their legs when sitting.

Akathisia can be objectively and readily assessed in clinical settings by using the Hillside Akathisia Scale.^{[47, 48, 49]} For this evaluation, examine the patient with his or her feet bare and hands exposed so that movements of the extremities can be observed. Ask the patient to sit, stand, and lie still for 2 minutes in each position.

In each patient position, inquire about the presence of a sensation of inner restlessness and an urge to move. After the patient has maintained the designated position for a full minute, ask, “Do you feel restless inside? Do you have the urge to move? Are you able to keep your feet still?” If the patient responds that these sensations are present, ask him or her to quantify the magnitude of the urge to move as mild, moderate, or severe.^{[47, 48, 49]}

In addition, ask if the urge to move is distressing. If the patient is experiencing distress, ask him or her to quantify the feeling as mild, moderate, or severe. For clinical assessments, the patient may be assessed in the sitting and standing positions only; assessment in the lying position may be omitted. Score the evaluation at the conclusion of the assessment session.^{[47, 49]} Perform this assessment at the initial evaluation and then regularly throughout the course of treatment to determine beneficial and adverse effects.^{[47, 49]}

Tardive blepharospasm manifests with findings similar to those of other forms of blepharospasm. Repetitive, forceful, and sustained contractions of the orbicularis oculi are observed. Dyskinetic blinking may occur.

Unlike tardive dystonia, torsion dystonia is characterized by twisting and sustained contractions of muscles resulting in rapid, repetitive, distressing movements. Torsion dystonia usually begins with inversion of the foot and spasm of the proximal limb muscles, resulting in gait abnormalities. Scoliosis, torticollis, and tortipelvis may occur in torsion dystonia. Patients may experience considerable impairment in performing activities of daily living. Spasmodic torticollis presents in adults and is characterized by torticollis, anterocollis, or retrocollis.

Tardive tics may be observed in affected patients. Because the patient may suppress the tics temporarily, they may not be observed during the initial encounter.

Tardive tremor manifests as involuntary rhythmic sinusoidal movements of limbs, head, neck, or voice. Tardive tremors are persistent. Unlike cerebellar tremors, which are present on voluntary motion and not at rest, and psychogenic tremors, which diminish during the course of long examinations, tardive tremors are usually present at rest and with voluntary movement.

The presence of dementia in a patient in whom TD is suspected merits consideration of Huntington disease, Wilson disease, or a central nervous system (CNS) neoplasm. The presence of hemiparesis, asymmetric reflexes, and other focal deficits indicates the need for further assessment to exclude structural brain lesions.

The presence of jaundice, hepatomegaly, abdominal pain, or Kayser-Fleischer rings in the cornea requires further assessment to exclude Wilson disease. Kayser-Fleischer rings may be observed best with a slit-lamp examination. Ophthalmologic consultation is mandatory for patients in whom Wilson disease is suspected.

Wilson disease is characterized by the presence of choreiform movements, tremors, diminished dexterity, marked rigidity, dystonia, dysarthria, and neuropsychiatric manifestations. The presenting manifestation may be psychosis. Check serum ceruloplasmin and the copper transporter gene in every patient in whom Wilson disease is suspected. The onset of movement disorders in patients younger than 50 years merits ruling out Wilson disease, a treatable disorder.

Tachycardia, sweating, and a goiter suggest hyperthyroidism. TD may coexist with other neuroleptic-induced movement disorders, including parkinsonism (manifested by tremor, rigidity, and bradykinesia). Distinguish TD from acute dystonic reactions induced by medications and from neuroleptic withdrawal dyskinesias. Unlike TDs, withdrawal dyskinesias remit within a month after discontinuance of neuroleptics.

Postural instability is common in Huntington disease but uncommon in neuroleptic-induced TD. Unlike TD, Huntington disease appears with chorea in the face and the proximal extremities. The term chorea implies a dancelike distinctive gait.

The development of TD in people with schizophrenia is associated with the development of cognitive impairment.^[50]

Assessment tools

Characterization and classification of TDs and other movement disorders are facilitated by the administration of the Movement Disorders Checklist by trained raters to score the presence or absence of traits of movements. Each discrete movement is rated separately on its own page. This checklist can be readily used by practitioners in clinical settings.

With dichotomous random variables (ie, indicator functions), algorithms in the form of linear regression equations express the relationships among dyskinesias and other movement disorders. The formulation can be expressed as a Venn diagram (see the image below).

Tardive dyskinesia. Venn diagram of the classification of movement disorders.

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As the diagram indicates, every case of akathisia is also a case of stereotypy, and therefore, the presence of akathisia implies the presence of stereotypy. Some cases of chorea can be classified as akathisia and stereotypy, whereas other cases of chorea can be classified as myoclonus. In addition, some cases of tics can also be classified as myoclonus. Some cases of dystonia can be classified as akathisia.

The Venn diagram also indicates that tic is entirely separate and distinct from akathisia, chorea, dystonia, stereotypy, and tremor. Furthermore, the diagram demonstrates that tremor is distinct from the other movement disorders.

The presence of stereotypies can be readily assessed by using the Timed Stereotypies Rating Scale.^[51]

Observe the patient with his or her feet bare and hands exposed. Ask him or her to sit still in a chair for 10 minutes. Place a check mark on the score sheet the first time each movement occurs during each 30-second interval of the observation period. The timing can be established by playing a recording containing a series of 30-second intervals adding up to 10 minutes (listen to the audio file below). The recording may be played live in the patient’s presence. To avoid distracting the patient, the examiner may listen through headphones.

Audio segment (MP3)

Another option is to record the patient on video for at least 10 minutes and then to rate the video later, using an audio recording of 30-second segments adding up to 10 minutes. Optimally, the patient is rated both live and on video. The live rater notes the seconds on the image of the video screen of the videocamera to determine each 30-second segment of the 10-minute observation period. The video recording is rated by examiners who are blind to the status of the patient. Test-retest reliability can thus be determined by assessing the ratings of the live and video sessions.

Video recordings often miss crucial events, such as a tear or a jerk. The score sheet contains blank spaces for other head/neck stereotypies in items 21 and 22 and for other stereotypies in items 49-60 at the end of the form, where additional patient movements (eg, extending arms at the elbow or extending legs at the knee) can be added. Additional patient utterances (eg, grunts, snorts, throat clearing, vowels, syllables, words, sentences) can also be added in the blank spaces for other stereotypies in items 49–60.

If the sessions are recorded on video, the recordings may be played back frame by frame to facilitate the observation of each occurrence of every stereotypy.

Because some of the terms of the Timed Stereotypies Rating Scale may not be well known, some further definitions are provided. Item 9, the bonbon sign, is present when the patient presses the tip of the tongue against the cheek as if tasting a piece of candy in the mouth. Item 48, the Bronx cheer, is a colloquial euphemism for a sound occurring when air is forcefully expressed through tightly closed lips resembling the noise of a flatulent retort.

Differential Diagnoses

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Media Gallery

Diagnostic criteria for neuroleptic-induced tardive dyskinesia.
Tardive dyskinesia. Venn diagram of the classification of movement disorders.

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Table 1. Classic Characterization of Pyramidal and Extrapyramidal Systems
Table 2. Medications Causing Tardive Dyskinesia
Table 3. Nonneuroleptic Medications Linked to Dyskinesias

Table 1. Classic Characterization of Pyramidal and Extrapyramidal Systems

Characteristic	Pyramidal	Extrapyramidal
Anatomy	Precisely demarcated pathways from cortex to muscle	Hypothesized pathways among basal ganglia and other structures of the central nervous system
Physiologic movements	Voluntary	Involuntary
Pathologic movements	Paralysis, paresis, hyperreflexia, and spasticity	Akathisia, athetosis, ballismus, chorea, dystonia, myoclonus, stereotypy, tic, and tremor

Table 2. Medications Causing Tardive Dyskinesia

Category	Agents
Antipsychotic agents (ie, neuroleptics)	Butyrophenones: droperidol, haloperidol, dibenzodiazepines, loxapine Diphenylbutylpiperidines: pimozide Indolones: molindone Phenothiazines: chlorpromazine, fluphenazine, mesoridazine, perphenazine, thioridazine, trifluoperazine Thioxanthenes: thiothixene
Newer atypical antipsychotic agents (sporadically linked to TDs)	Olanzapine Quetiapine Risperidone Paliperidone Amisulpride
TD = tardive dyskinesia.

Table 3. Nonneuroleptic Medications Linked to Dyskinesias

Category	Agents
Anticholinergics	Benzhexol Biperiden Ethopropazine Orphenadrine Procyclidine
Antidepressants	MAOIs: phenelzine SSRIs: fluoxetine, sertraline Trazodone TCAs: amitriptyline, amitriptyline-perphenazine, amoxapine, doxepin, imipramine
Antiemetics	Metoclopramide Prochlorperazine
Antiepileptic drugs	Carbamazepine Ethosuximide Phenobarbital Phenytoin
Antihistamines	Various
Antihistaminic decongestants	Combinations of antihistamines and sympathomimetics
Antimalarials	Chloroquine
Antiparkinson agents	Bromocriptine Carbidopa-levodopa Levodopa
Anxiolytics	Alprazolam
Biogenic amines	Dopamine
Mood stabilizers	Lithium
Oral contraceptives	Estrogens
Stimulants	Amphetamine Methylphenidate Caffeine
MAOI = monoamine oxidase inhibitor; SSRI = selective serotonin reuptake inhibitor; TCA = tricyclic antidepressant.

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Author

James Robert Brasic, MD, MPH, MS, MA Assistant Professor, Russell H Morgan Department of Radiology and Radiological Science and Neurology, Division of Nuclear Medicine and Molecular Imaging, Assistant Professor, Department of Neurology, Johns Hopkins University School of Medicine

James Robert Brasic, MD, MPH, MS, MA is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, International Parkinson and Movement Disorder Society, Society for Neuroscience, Society of Nuclear Medicine and Molecular Imaging

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Johns Hopkins University School of Medicine; New York City Health and Hospitals/Bellevue, New York University Langone Health Serve(d) as a speaker or a member of a speakers bureau for: Society of Nuclear Medicine and Molecular Imaging, Maryland Regional Council of Child and Adolescent Psychiatry Received research grant from: National Institutes of Health, Johns Hopkins University School of Medicine, Intellectual & Developmental Disabilities Research Center (U54 HD079123) at the Kennedy Krieger Institute Received income in an amount equal to or greater than $250 from: Gerson Lehrman Group; Guidepost Received royalty from Medscape for other.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Bioserenity, Catalyst, Ceribell, Eisai, Jazz, LivaNova, Neurelis, Neuropace, SK Life Science Science, Sunovion, Takeda, UCB Serve(d) as a speaker or a member of a speakers bureau for: Catalyst, Jazz, LivaNova, Neurelis, SK Life Science, Stratus, UCB Received research grant from: Cerevel Therapeutics; Ovid Therapeutics; Neuropace; Jazz; SK Life Science, Xenon Pharmaceuticals, UCB, Marinus, Longboard.

Acknowledgements

Brian Bronson, MD Staff Physician, Department of Psychiatry, New York University Medical Center

Disclosure: Nothing to disclose.

Tristen T Chun Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine

Disclosure: Nothing to disclose.

Nestor Galvez-Jimenez, MD, MSc, MHA Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida

Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society

Disclosure: Nothing to disclose.

Daniel H Jacobs MD, FAAN, Associate Professor of Neurology, University of Florida College of Medicine; Director for Stroke Services, Orlando Regional Medical Center

Daniel H Jacobs is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience

Disclosure: Teva Pharmaceutical Grant/research funds Consulting; Biogen Idex Grant/research funds Independent contractor; Serono EMD Royalty Speaking and teaching; Pfizer Royalty Speaking and teaching; Berlex Royalty Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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