Opioid Abuse Medication

  • Author: Adrian Preda, MD; Chief Editor: Eduardo Dunayevich, MD   more...
 
Updated: Feb 29, 2012
 

Medication Summary

The goals of pharmacotherapy are to treat the addiction of the chemical substances that cause them.

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Opioid analgesics

Class Summary

Two uses for opioid analgesics are as follows: (1) Oral substitution therapy or maintenance therapy or opioid agonist therapy (OAT) refers to substitution of an oral opioid for injected heroin, with the goal of reducing harmful behaviors associated with heroin use. (2) Detoxification, or controlled withdrawal with the goal of abstinence, is based on the principle of cross-tolerance in which one opioid is replaced with another and then slowly withdrawn.

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Methadone (Dolophine)

 

Inhibits ascending pain pathways, diminishing the perception of and response to pain. There are inpatient facilities and a few, specialized, licensed, outpatient, drug treatment programs that provide opioid detoxification using methadone. Also a preferred agent for opioid agonist maintenance. Some experts feel that laboratory measures of plasma levels should be used to adjust the dose and that 400 ng/mL seems sufficient to stop craving and drug hunger.

Benefits include good treatment retention, psychosocial adjustment, and reduced criminal activity.

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Buprenorphine (Subutex)

 

Partial opioid agonist and potent antagonist, is a potent analgesic that can be administered once a day to block withdrawal symptoms. A dose of 0.6-1.2 mg/d of buprenorphine tapered over 3 days is found superior to a 5 day clonidine regimen in controlling early withdrawal symptoms. Proposed as an alternative to methadone for heroin detoxification and maintenance.

Used sublingually for the initial detoxification treatment of opioid addiction. Produces agonist/antagonist effects at the opioid mu receptor. The agonist effect is limited by a ceiling effect (ie, higher doses [>12-16 mg] do not produce more analgesia). The sublingual product is called Subutex.

8 mg SL is comparable to 30-60 mg oral methadone on suppressing heroin use and subject retention; in low doses, produces morphinelike effects but reaches its ceiling at about 12 mg; has abuse potential, but this potential is low compared with other opioids

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Buprenorphine and naloxone (Suboxone)

 

Used sublingually for the maintenance detoxification treatment (unsupervised phase) of opioid dependence following induction with sublingual buprenorphine (Subutex). Contains both buprenorphine (an opiate agonist/antagonist) and the opiate antagonist naloxone. Naloxone has been added to guard against intravenous abuse of buprenorphine by individuals physically dependent on opiates.

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Antidotes for opioids

Class Summary

Inhibit opioid effects by inhibiting opioid agonists at receptor sites.

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Naltrexone (ReVia, Vivitrol)

 

Used in combination with clonidine for rapid (4-5 d) detoxification.

Very effective long-acting opioid antagonist that was thought to be an ideal maintenance agent because it blocks receptor sites and, hence, opioid reinforcing properties. However, clinical results are not very promising when compared with methadone maintenance. Craving may continue during naltrexone maintenance. For groups of patients such as health care professionals or business executives for whom external incentives to stay away from drugs are important, naltrexone therapy has been very effective.

Indicated for prevention of relapse to opioid dependence following opioid detoxification.

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Naloxone (Narcan)

 

Pure opioid antagonist. Used to reverse opioid intoxication.

If patients do not respond to multiple doses of naloxone, consider alternative causes of unconsciousness. Need of ongoing substance abuse treatment should be established while caring for overdose.

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Alpha 2 adrenergic agonists

Class Summary

Used primarily for the treatment of hypertension.

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Clonidine (Catapres)

 

May reduce norepinephrine release. In opioid withdrawal, seems to be most effective in suppressing autonomically mediated signs and symptoms of abstinence but less effective for subjective symptoms.

Used in higher doses for detoxification than for treating hypertension. Benzodiazepine may be beneficial as adjuvant therapy for muscle cramps and insomnia. Clonidine also has anticraving effect for opioids. Clonidine in combination with naltrexone, which is a potent long-acting narcotic antagonist, also is referred to be as rapid detoxification. This approach is designed to shorten the time course of withdrawal to 5 d. Clonidine alone and in combination has been demonstrated to be feasible in primary care settings as an outpatient.

Treatment is initiated after confirmation of physical dependence by naloxone challenge test.

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Contributor Information and Disclosures
Author

Adrian Preda, MD  Health Sciences Associate Professor of Psychiatry and Human Behavior, University of California Irvine School of Medicine

Adrian Preda, MD is a member of the following medical societies: International Congress of Schizophrenia Research, Schizophrenia International Research Society, and Society of Biological Psychiatry

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

Eduardo Dunayevich, MD  Adjunct Assistant Professor, Department of Psychiatry, University of Cincinnati; Clinical Research Physician, Neuroscience, Lilly Research Laboratories

Eduardo Dunayevich, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Ziaur Rehman, MD, Suzan Khoromi, MD, James E Douglas, MD, Steven A Adelman, MD, and William J Meehan, MD, PhD to the development and writing of this article.

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Schematic diagram of the brain-reward circuitry of the mammalian (laboratory rat) brain with sites at which various abusable substances appear to act to enhance brain-reward and, thus, to induce drug-taking behavior and possibly drug craving. Courtesy William & Wilkins Substance Abuse by Eliot L Gardner.KEY - Nucleus accumbens (Acc), ventral tegmental area (VTA), amygdala (AMYG), locus ceruleus (LC), dopaminergic mesolimbic system (DA), ventral pallidum (VP), noradrenergic fibers (NF), enkephalinergic outflow (ENK), frontal cortex (FCX), GABAergic inhibitory fiber system (GABA), dynorphinergic outflow (DYN),component of reward circuitry preferentially activated by electrical intracranial self-stimulation (ICSS).
 
 
 
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