Cocaine-Related Psychiatric Disorders Medication

  • Author: Christopher P Holstege, MD; Chief Editor: David Bienenfeld, MD   more...
 
Updated: Jun 9, 2011
 

Medication Summary

Cocaine induces 10 psychiatric disorders described in DSM-IV-TR. Treatment of each disorder varies. Benzodiazepines are the drugs of choice for acute cocaine intoxication with extreme agitation. Pharmacologic therapy depends on presenting signs and symptoms (eg, treat chest pain with oxygen, benzodiazepines, aspirin, and nitroglycerin). All possible pharmacotherapies for various cocaine-induced medical conditions are beyond the scope of this article. For a complete review of treating cocaine-induced nonpsychiatric effects, refer to Toxicity, Cocaine.

Avoid use of beta-blockers because of the unopposed alpha-agonist activity. The mood shifts, abnormal sleep and even delusions associated with acute cocaine intoxication or withdrawal often are transient and do not require medications. Persistent mood disorders with mania may be treated with lithium, whereas antidepressants are advocated for mood disorders with depressive features. Antipsychotics are advocated to treat persistent psychotic disorders.

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Benzodiazepines

Class Summary

Bind specific benzodiazepine receptor on GABA-receptor complex, thereby increasing GABA affinity for its receptor. Increase the frequency of chlorine channel opening in response to GABA binding. GABA receptors are chlorine channels that mediate postsynaptic inhibition, resulting in postsynaptic neuron hyperpolarization. The final result is a sedative-hypnotic effect that counteracts the stimulant effect of cocaine.

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Diazepam (Valium)

 

Depresses all levels of CNS (eg, limbic and reticular formation) possibly by increasing activity of GABA. Individualize dose and increase cautiously to avoid adverse effects.

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Lorazepam (Ativan)

 

Sedative hypnotic with short onset of effects and relatively long half-life. Increases action of GABA (ie, major inhibitory neurotransmitter in brain). May depress all levels of CNS, including limbic and reticular formation.

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Midazolam (Versed)

 

Short-acting benzodiazepine used for acute or short-term sedation. Also exhibits amnestic effects.

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Antipsychotic agents

Class Summary

High-potency antipsychotic agents in the butyrophenone class (eg, haloperidol, droperidol) are used for rapid sedation. Easily titrated and cause less sedation and orthostasis; however, they cause extrapyramidal symptoms more often than lower-potency agents. Used short term to rapidly control psychosis.

Newer antipsychotics (eg, risperidone, olanzapine, quetiapine) are used for long-term management. Improvements over earlier antipsychotics include fewer anticholinergic effects and less dystonia, parkinsonism, and tardive dyskinesia. Affect dopamine and serotonin receptors.

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Haloperidol (Haldol)

 

DOC for acute psychosis. Parenteral dosage form may be admixed in same syringe with 2 mg lorazepam for better anxiolytic effects.

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Droperidol (Inapsine)

 

DOC for severely disturbed and/or violent patient. Faster acting and more sedating than haloperidol but more likely to cause hypotension. May exert antipsychotic activity through dopaminergic system. Evidence suggests it alters dopamine action in CNS.

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Risperidone (Risperdal)

 

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

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Olanzapine (Zyprexa)

 

May inhibit serotonin, muscarinic, and dopamine effects.

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Quetiapine (Seroquel)

 

May act by antagonizing dopamine and serotonin effects.

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Antidepressants

Class Summary

While numerous antidepressants are currently available, selective serotonin reuptake inhibitors (SSRIs) provide many advantages over past antidepressants. MAOIs should be avoided in mood disorders with depressive features. MAOIs are lethal if patient relapses from abstinence and combines them with cocaine.

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Citalopram (Celexa)

 

Enhances serotonin activity by selective reuptake inhibition at the neuronal membrane.

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Fluoxetine (Prozac)

 

Selectively inhibits presynaptic serotonin reuptake with minimal or no effect on reuptake of norepinephrine or dopamine.

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Fluvoxamine (Luvox)

 

Inhibits neuronal serotonin reuptake. Does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors, thus has fewer adverse effects than TCAs.

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Paroxetine (Paxil)

 

Alternative DOC. Potent selective inhibitor of neuronal serotonin reuptake. Weak effect on norepinephrine and dopamine neuronal reuptake.

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Sertraline (Zoloft)

 

Selectively inhibits presynaptic serotonin reuptake.

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Venlafaxine (Effexor)

 

Inhibits neuronal serotonin and norepinephrine reuptake. Also causes beta-receptor down-regulation.

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Contributor Information and Disclosures
Author

Christopher P Holstege, MD  Associate Professor of Emergency Medicine and Pediatrics, University of Virginia School of Medicine; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Center; Associate Medical Toxicology Fellowship Director, Veterans Affairs Department of Health

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, European Association of Poisons Centres and Clinical Toxicologists, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Lori Holstege, MD  Assistant Clinical Professor, Department of Psychiatry, Michigan State University

Lori Holstege, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: Nothing to disclose.

Nathan P Charlton, MD  Fellow in Medical Toxicology, University of Virginia, Blue Ridge Poison Center

Nathan P Charlton, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, South Carolina Medical Association, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Barry I Liskow, MD  Professor of Psychiatry, Vice Chairman, Psychiatry Department, Director, Psychiatric Residency Program, University of Kansas School of Medicine; Director, Psychiatric Outpatient Clinic, The University of Kansas Medical Center

Disclosure: Nothing to disclose.

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

Harold H Harsch, MD  Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin

Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: lilly Honoraria Speaking and teaching; Forest Labs None None; Pfizer Grant/research funds Speaking and teaching; Northstar None None; Novartis Grant/research funds research; Pfizer Honoraria Speaking and teaching; Sunovion Speaking and teaching; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research; Merck Honoraria Speaking and teaching

Chief Editor

David Bienenfeld, MD  Professor of Psychiatry, Vice-Chair and Director of Residency Training, Department of Psychiatry, Wright State University, Boonshoft School of Medicine

David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry

Disclosure: Nothing to disclose.

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