Clonidine belongs to a class of drugs called central alpha-adrenergic agonists. In the United States, clonidine tablets are sold under the brand name Catapres and clonidine skin patches are sold under the brand name Catapres-TTS. The tablets are also available generically. There is also an injectable form that is administered directly into the spinal cord for the treatment of postoperative pain.
Clonidine tablets and patches are approved by the United States Food and Drug Administration (FDA) for the treatment of high blood pressure. However, clonidine has been found to be useful in the treatment of alcohol, opiate, and nicotine withdrawal syndromes, attention-deficit/hyperactivity disorder (ADHD), and Tourette's syndrome, one of the tic disorders .
Clonidine was synthesized in 1960s and was initially tested as a nasal decongestant. In the United States, clonidine was first used to treat hypertension although it has also been investigated for treatment of different neuropsychiatric disorders. Clonidine works on specific nerve cells in the brain that are responsible for lowering blood pressure, slowing heart rate, and decreasing the body's reaction to the withdrawal of chemicals like alcohol, opiates, cocaine, and nicotine. Because of this, clonidine is often used to treat the symptoms of drug, alcohol, and nicotine withdrawal.
Clonidine is beneficial in opiate withdrawal because it treats symptoms that are commonly associated with that condition (watery eyes and nose, diarrhea, irritability). For this condition, clonidine is often used alone. For the treatment of alcohol withdrawal, clonidine is usually combined with benzodiazepine tranquilizers such as Librium, Valium, Xanax, or Ativan.
Several studies of treatment for smoking cessation showed patients treated with clonidine had decreased nicotine craving. Clonidine skin patches appear to be more effective than tablets in this condition. Both dermal patches and tablets are effective in the treatment of Tourette's syndrome and ADHD.
Clonidine tablets are available in 0.1-mg, 0.2-mg, and 0.3-mg strengths. Clonidine skin patches are available in 0.1-mg, 0.2-mg, and 0.3-mg per day patches. Each patch lasts seven days.
Dosages of 0.4–0.6 mg have been used for the treatment of alcohol withdrawal. Total daily dosage for the treatment of opiate withdrawal range between 0.5 and 1.4 mg, depending on the stage as well as the severity of withdrawal symptoms. If the clonidine patch is used to treat nicotine withdrawal symptoms, dosages that deliver 0.1–.2 mg daily are used. For oral therapy (tablets), a total dosage of 0.2–0.4 mg daily is taken in divided doses.
Pediatric doses of clonidine are calculated based on the child's body weight. Clonidine dosage for ADHD in children is 5 micrograms per kilogram of body weight per day orally in four divided doses. Children who require a daily dosage of 0.2 mg usually can use the 0.3 mg dermal patch. If ADHD is associated with sleep disturbances, low to moderate doses of clonidine can be taken at bedtime. Oral doses in children with Tourette's syndrome range from 3 to 6 micrograms per kilogram of body weight per day divided into two to four even doses.
Clonidine should not be used by people who have a known allergy to this drug. If a person has underlying depression, clonidine should be used with caution and under close physician supervision.
Clonidine should not be abruptly withdrawn but rather, slowly decreased over several days to avoid withdrawal symptoms. Withdrawal symptoms include increases in blood pressure, irritability, nervousness, insomnia , and headache. Because of the possibility of withdrawal, clonidine should not be used in patients who are unwilling or unable to follow the prescribing information.
Clonidine should be used only with caution and close physician supervision in patients with chronic renal failure, coronary artery disease, and in patients with preexisting eye problems. Often people with kidney disease should take a reduced dosage. Clonidine should not be used by pregnant women, except in the rare case where the benefits of taking clonidine outweigh the risks to the developing fetus.
The most common side effect associated with clonidine is dizziness associated with sudden changes in position such as standing up rapidly. In order to avoid this, atients should stand up slowly. People using the dermal patch may develop rash, hair loss, a burning sensation on the skin, or other skin irritations where the patch is applied. Switching to tablets may not completely eliminate these skin problems, however.
Clonidine can cause dry mouth, constipation, nausea, daytime sleepiness, weakness, and lethargy. These side effects may take several weeks to disappear. In some cases, these side effects can be eliminated with dosage readjustment. In addition, clonidine may cause eye dryness, loss of sex drive, and decreased sexual activity.
If patients experience weight gain in the beginning of therapy, they can expect this side effect to decline over a period of several days to weeks.
Clonidine's blood pressure-lowering effects may be enhanced by other drugs that lower blood pressure. Conversely, the blood pressure-lowering effects of clonidine may be negated by many antidepressants.
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"Clonidine." Gale Encyclopedia of Mental Disorders. . Encyclopedia.com. (December 17, 2017). http://www.encyclopedia.com/psychology/encyclopedias-almanacs-transcripts-and-maps/clonidine
"Clonidine." Gale Encyclopedia of Mental Disorders. . Retrieved December 17, 2017 from Encyclopedia.com: http://www.encyclopedia.com/psychology/encyclopedias-almanacs-transcripts-and-maps/clonidine
While not itself life-threatening, the opioid Withdrawal syndrome is extremely unpleasant and contributes to further opioid use and relapse. Heroin addicts report that the acute withdrawal syndrome begins in approximately eight hours after their last injection and includes the following: craving for the drug, anxiety, perspiration, perspiration with hot and cold flashes, tearing of the eyes and nose, restlessness, problems sleeping, problems falling asleep, goose bumps, aching bones and muscles, loss of appetite, nausea, vomiting, diarrhea, abdominal cramps, spontaneous yawning, and a group of symptoms called flu-like.
During the later years of the nineteenth century and early years of the twentieth, some cures for this opioid withdrawal syndrome have been far worse than the withdrawal itself—with some actually causing death. Soon after it became available in the mid-nineteenth century, injectable Morphine was proposed as a treatment for opium eating; then heroin or Cocaine were, in the late nineteenth century, proposed as cures for morphine addiction. From the mid-twentieth century until the 1970s, most medical treatment of the opioid withdrawal syndrome involved either gradual reduction of the dose of opioid or the substitution of Methadone, followed by its gradual reduction. In 1978, Gold and coworkers proposed that the nonopiate antihypertensive clonidine could be an effective nonopiate treatment for opiate withdrawal distress. The scientific basis for the proposition that clonidine would be useful was based on the hypothesis that the opiate withdrawal syndrome was caused by hyperactivity or hyperexcitability of a specific brain nucleus composed of noradrenergic neurons, called the locus coeruleus (LC). There was considerable neuroscientific research to support this withdrawal hypothesis and the rationale for the efficacy of clonidine.
Since 1977/78, clonidine has been tried in numerous inpatient and outpatient opioid addict populations worldwide and studied by researchers in numerous well-controlled studies. In virtually all studies, clonidine has been shown to be a safe and effective nonopioid treatment that could control several aspects of opioid withdrawal. Clonidine, while having opiate-like effects in reversing several aspects of opiate withdrawal, is not an opiate and is therefore not subject to the burdensome regulatory Controls that have been placed on the use of opioids. Clonidine has its most demonstrable effects on autonomic elements of opioid withdrawal: sweating, gastrointestinal complaints (cramps, diarrhea, nausea), and elevated blood pressure. It does not have substantial capacity to alleviate muscle aches, insomnia, or craving for opioids.
Research and clinical experiences since the original discoveries have (1) supported the notion of LC hyperactivity as one of the neural substrates for the opioid withdrawal syndrome; (2) supported the efficacy of clonidine—establishing clonidine detoxification as one of the standard treatments for adult opioid addicts—and extended it to neonates (newborns) and to alcohol, nicotine, and other drug withdrawals that share a preponderance of behaviours with opioid withdrawal; (3) demonstrated that abstinence could be maintained by some opioid addicts and that others could benefit from antagonist therapy with Naltrexone, thanks to clonidine or accelerated clonidine-naltrexone detoxification; (4) led to considerable progress in the understanding of the critical cellular event causing LC hyperactivity in opioid withdrawal and hypoactivity in the presence of clonidine or opioid agonists; and (5) led to the rapidly expanding clinical armamentarium available to treat addicts on the basis of rodent and primate studies.
CLONIDINE SHORTENS DETOXIFICATION
Detoxification of opioid addicts with clonidine has been used to facilitate the transition from chronic opioid administration to naltrexone (a long-acting opioid Antagonist) or to drug-free status. Naltrexone possesses opioid-blocking action at all opioid-receptor sites in the body and brain, rather than having an affinity for a specific type of opioid receptor. It is a useful medication for those patients willing to take it to prevent relapse. When recovering addicts take naltrexone, they make opioid effects unavailable to themselves. The affinity of naltrexone for the receptors is such that they are unable to feel the effects of heroin, methadone, or other exogenous opioids. While the original clonidine treatment protocol of Gold and his colleagues (1978a, b) facilitated the initiation of naltrexone by avoiding the extra ten-day wait required after the last methadone, an accelerated detoxification protocol has been developed using naltrexone and clonidine simultaneously. Since clonidine reduces precipitated withdrawal as well as the withdrawal that results from simply discontinuing chronic opioid administration, total withdrawal and naltrexone induction time has been shortened to six days with little loss in success rate (Charney, Heninger, & Kleber, 1986).
OTHER NEW USES
Clonidine has been tried with varying success in a number of medical problems where the behaviors, signs, and/or symptoms resemble those seen in opiate withdrawal or following LC electrical or chemical stimulation to a certain degree. Clonidine has also been tried in humans on the basis of noradrenergic hyperactivity in generalized and panic Anxiety; obsessive-compulsive symptomatology; Gilles de La Tourette's syndrome; mania; Attention Deficit Disorder; narcolepsy; neuroleptic-induced akathisia; Alcohol withdrawal and Nicotine withdrawal; and phaeochromocytoma. Clonidine's Analgesic effects have been rediscovered and given orally, transdermally (skin patches), epidurally (into the area around the spinal canal), and parenterally (by injection)—to decrease anesthetic requirements and to effect less respiratory depression than Opioids alone.
Using clonidine for withdrawal distress allows the brain to reestablish normal homeostatic patterns when given as part of a long-term recovery program. It allows patients sufficient motivation to achieve and sustain drug-free existence.
(See also: Opioid Complications and Withdrawal )
Charney, D. S., Heninger, G. R., & Kleber, H. D. (1986). The combined use of clonidine and naltrexone as a rapid, safe and effective treatment of abrupt withdrawal from methadone. American Journal of Psychiatry, 143, 817-831.
Gold, M. S. (1991). The good news about drugs and alcohol. New York: Villard Books.
Gold, M. S., Redmond, D. E., & Kleber, H. D. (1978a). Clonidine in opiate withdrawal. Lancet I, 929-930.
Gold, M. S., Redmond, D. E., & Kleber, H. D. (1978). Clonidine blocks acute opiate symptoms. Lancet II, 599-602.
Jaffe J. H. (1990). Drug addiction and drug abuse. In A. G. Gilman, et al. (Eds.), Goodman and Gilman's the pharmacological basis of therapeutics, 8th ed. New York: Pergamon.
Mark S. Gold
"Clonidine." Encyclopedia of Drugs, Alcohol, and Addictive Behavior. . Encyclopedia.com. (December 17, 2017). http://www.encyclopedia.com/education/encyclopedias-almanacs-transcripts-and-maps/clonidine
"Clonidine." Encyclopedia of Drugs, Alcohol, and Addictive Behavior. . Retrieved December 17, 2017 from Encyclopedia.com: http://www.encyclopedia.com/education/encyclopedias-almanacs-transcripts-and-maps/clonidine
"clonidine." A Dictionary of Nursing. . Encyclopedia.com. (December 17, 2017). http://www.encyclopedia.com/caregiving/dictionaries-thesauruses-pictures-and-press-releases/clonidine
"clonidine." A Dictionary of Nursing. . Retrieved December 17, 2017 from Encyclopedia.com: http://www.encyclopedia.com/caregiving/dictionaries-thesauruses-pictures-and-press-releases/clonidine