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Chorea in Adults Medication

  • Author: Stephanie M Vertrees, MD; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Oct 24, 2014
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Antipsychotic agents

Class Summary

Block dopamine receptors and appear to have antispasmodic effects.

Haloperidol (Haldol)

 

Useful in treatment of irregular spasmodic movements of limbs or facial muscles.

Fluphenazine (Prolixin)

 

Blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in brain. Exhibits strong alpha-adrenergic and anticholinergic effects. May depress reticular activating system.

Clozapine (Clozaril)

 

New atypical neuroleptic medication available in 25- and 100-mg tab. Blocks norepinephrine, serotonergic, cholinergic, histamine, and dopaminergic receptors. Mechanism of action still unclear. Affinity for mesolimbic D4 dopamine receptor accounts for striking effects in control of behavioral and psychiatric symptoms with low incidence of extrapyramidal symptoms. Histamine receptor blockade accounts for increased incidence of sleep disturbances.

Olanzapine (Zyprexa)

 

May inhibit serotonin, muscarinic, and dopamine effects.

Risperidone (Risperdal)

 

Binds to dopamine D2-receptor with 20 times lower affinity than for 5-HT2 receptor. Improves negative symptoms of psychoses and reduces incidence of extrapyramidal adverse effects.

Quetiapine (Seroquel)

 

May act by antagonizing dopamine and serotonin effects.

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Dopamine depleting agents

Class Summary

Deplete CNS of dopamine, thereby reducing chorea.

Reserpine

 

Depletes norepinephrine and epinephrine, which, in turn, depress sympathetic nerve functions.

Tetrabenazine (Xenazine)

 

Depletes neurotransmitter stores of dopamine, serotonin, and noradrenaline within nerve cells in the brain, thereby altering transmission of electric signals from the brain that control movement by reversibly inhibiting vesicular monoamine transporter 2 (VMAT2).

Efficacy and safety established in a randomized, double-blind, placebo-controlled, multicenter study. Patients treated with tetrabenazine had significant improvement in chorea compared with those treated with placebo. Additional studies support this effect. Indicated for chorea associated with Huntington disease.

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Benzodiazepines

Class Summary

Demonstrated to reduce GABA concentrations in the caudate, putamen, substantia nigra, and globus pallidus. By analogy, increased GABA activity might ameliorate chorea.

Clonazepam (Klonopin, Rivotril)

 

Developed as antiepileptic, hypnotic, and anxiolytic used as adjunct for treatment of chorea. Belongs to benzodiazepine group, increasing GABAergic transmission in CNS. Reaches peak plasma concentration at 2-4 h after oral or rectal administration.

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Anticonvulsants

Class Summary

May help by various neuropharmacological mechanisms. Valproate is a GABAergic agent and thus it may help in the same way as benzodiazepines. Main mechanism of action of carbamazepine appears to be stabilization of inactivated state of voltage-gated sodium channels. This may reduce neuronal firing in many systems and therefore may nonspecifically reduce abnormal movements in some patients.

Valproic acid (Depacon, Depakote, Depakote ER)

 

Off-label therapy sometimes helpful in reducing choreiform movements and ameliorating disruptive behavior (eg, behavior induced by anger) in patients with HD. Dosages and other information mentioned is taken from dosages used for epilepsy because dosages for HD are not clearly established. Chemically unrelated to other drugs used to treat seizure disorders. Although mechanism of action not established, its activity may be related to increased brain levels of GABA or enhanced GABA action. Also may potentiate postsynaptic GABA responses, affect potassium channel, or have direct membrane-stabilizing effect.

For conversion to monotherapy, concomitant AED dosage ordinarily can be reduced by approximately 25% q2wk. This reduction may be started at initiation of therapy or delayed by 1-2 wk if concern that seizures are likely to occur with reduction. Monitor patients closely for increased seizure frequency during this period.

As adjunctive therapy, divalproex sodium may be added to patient's regimen at 10-15 mg/kg/d. Dosage may be increased by 5-10 mg/kg/d qwk to achieve optimal clinical response. Ordinarily, optimal clinical response achieved at daily doses of < 60 mg/kg/d.

Depakote Sprinkle Capsules (daily doses >250 mg should be divided bid/tid) and Depakote ER (once-daily formulation) are convenient dosage forms used in adults and children >10 y.

Carbamazepine (Carbatrol, Tegretol, Epitol)

 

Has been of symptomatic help in chorea, particularly in Sydenham chorea and chorea gravidarum, but also in other types. Dosage recommendations and cautions are essentially the same in this off-label use as for the more common indication of seizures.

When used as an anticonvulsant, mechanism of action may involve depressing activity in nucleus ventralis anterior of thalamus, resulting in reduction of polysynaptic responses and blocking posttetanic potentiation. Reduces sustained high-frequency repetitive neural firing. Potent enzyme inducer that can induce own metabolism. Due to potentially serious blood dyscrasias, undertake benefit-to-risk evaluation before drug instituted. Therapeutic plasma levels are 4-12 mcg/mL for analgesic and antiseizure response. Peak serum levels in 4-5 h. Half-life (serum) in 12-17 h with repeated doses. Metabolized in liver to active metabolite (ie, epoxide derivative) with half-life of 5-8 h. Metabolites excreted through feces and urine.

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Contributor Information and Disclosures
Author

Stephanie M Vertrees, MD Fellow in Public Health, Weill Cornell Medical College-Hospital for Special Surgery Fellowship in Medical Ethics; Fellow in Neuromuscular Medicine, Hospital for Special Surgery

Stephanie M Vertrees, MD is a member of the following medical societies: American Academy of Neurology, American Medical Womens Association

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

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 College of Medicine

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

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

Additional Contributors

Stephen T Gancher, MD Adjunct Associate Professor, Department of Neurology, Oregon Health Sciences University

Stephen T Gancher, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, International Parkinson and Movement Disorder Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Eric Dinnerstein, MD, Maria Alejandra Herrera, MD, and Nestor Galvez-Jimenez, MD, MSc, MHA, to the development and writing of this article.

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