Revision as of 06:48, 19 February 2015 editWindandfire11 (talk | contribs)2 editsm Replaced w/ new "addiction" article← Previous edit | Revision as of 07:36, 19 February 2015 edit undoSeppi333 (talk | contribs)Autopatrolled, Extended confirmed users, Page movers, New page reviewers, Pending changes reviewers, Template editors35,350 edits →Rebound syndrome: WP:MEDRSNext edit → | ||
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A wide range of drugs whilst not causing a true physical dependence can still cause ] symptoms or ] during dosage reduction or especially abrupt or rapid withdrawal.<ref>{{cite journal |author=Heh CW, Sramek J, Herrera J, Costa J |title=Exacerbation of psychosis after discontinuation of carbamazepine treatment |journal=Am J Psychiatry |volume=145 |issue=7 |pages=878–9 |date=July 1988 |pmid=2898213 |doi= |url=http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=2898213}}</ref> These can include ],<ref name="pmid2262896">{{cite journal |author=Griffiths RR, Evans SM, Heishman SJ, et al. |title=Low-dose caffeine physical dependence in humans |journal=J. Pharmacol. Exp. Ther. |volume=255 |issue=3 |pages=1123–32 |date=December 1990 |pmid=2262896 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=2262896}}</ref> stimulants,<ref>{{cite journal |author=Lake CR, Quirk RS |title=CNS stimulants and the look-alike drugs |journal=Psychiatr. Clin. North Am. |volume=7 |issue=4 |pages=689–701 |date=December 1984 |pmid=6151645 |doi= |url=}}</ref><ref>{{cite journal |author=Sarampote CS, Efron LA, Robb AS, Pearl PL, Stein MA |title=Can stimulant rebound mimic pediatric bipolar disorder? |journal=J Child Adolesc Psychopharmacol |volume=12 |issue=1 |pages=63–7 |year=2002 |pmid=12014597 |doi=10.1089/10445460252943588}}</ref><ref>{{cite journal |author=Danke F |title= |language=German |journal=Psychiatr Clin (Basel) |volume=8 |issue=4 |pages=201–11 |year=1975 |pmid=1208893 |doi= |url=}}</ref><ref>{{cite journal |author=Cohen D, Leo J, Stanton T, et al. |title=A boy who stops taking stimulants for "ADHD": commentaries on a Pediatrics case study |journal=Ethical Hum Sci Serv |volume=4 |issue=3 |pages=189–209 |year=2002 |pmid=15278983 |doi= |url=}}</ref> ] drugs and ] drugs.<ref>{{cite journal |author=Chichmanian RM, Gustovic P, Spreux A, Baldin B |title= |language=French |journal=Therapie |volume=48 |issue=5 |pages=415–9 |year=1993 |pmid=8146817 |doi= |url=}}</ref> It is debated if the entire ] drug class causes true physical dependency, if only a subset does, or if none does,<ref name="isbn0-07-149430-8">{{cite book |author=Tierney, Lawrence M.; McPhee, Stephen J.; Papadakis, Maxine A. |title=Current medical diagnosis & treatment, 2008 |publisher=McGraw-Hill Medical |location= |year=2008 |page=916 |isbn=0-07-149430-8 |oclc= |doi= |accessdate=}}</ref> but all, if discontinued too rapidly, cause an acute withdrawal syndrome.<ref>{{cite web | url = http://www.bnf.org/bnf/bnf/56/3209.htm | title = Antipsychotic drugs | accessdate = 22 December 2008 | author = BNF | authorlink = British National Formulary |author2=British Medical Journal | year = 2008 | publisher = British National Formulary | location = UK}}</ref> When talking about illicit drugs rebound withdrawal is, especially with stimulants, sometimes referred to as "coming down" or "crashing". | A wide range of drugs whilst not causing a true physical dependence can still cause ] symptoms or ] during dosage reduction or especially abrupt or rapid withdrawal.<ref>{{cite journal |author=Heh CW, Sramek J, Herrera J, Costa J |title=Exacerbation of psychosis after discontinuation of carbamazepine treatment |journal=Am J Psychiatry |volume=145 |issue=7 |pages=878–9 |date=July 1988 |pmid=2898213 |doi= |url=http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=2898213}}</ref> These can include ],<ref name="pmid2262896">{{cite journal |author=Griffiths RR, Evans SM, Heishman SJ, et al. |title=Low-dose caffeine physical dependence in humans |journal=J. Pharmacol. Exp. Ther. |volume=255 |issue=3 |pages=1123–32 |date=December 1990 |pmid=2262896 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=2262896}}</ref> stimulants,<ref>{{cite journal |author=Lake CR, Quirk RS |title=CNS stimulants and the look-alike drugs |journal=Psychiatr. Clin. North Am. |volume=7 |issue=4 |pages=689–701 |date=December 1984 |pmid=6151645 |doi= |url=}}</ref><ref>{{cite journal |author=Sarampote CS, Efron LA, Robb AS, Pearl PL, Stein MA |title=Can stimulant rebound mimic pediatric bipolar disorder? |journal=J Child Adolesc Psychopharmacol |volume=12 |issue=1 |pages=63–7 |year=2002 |pmid=12014597 |doi=10.1089/10445460252943588}}</ref><ref>{{cite journal |author=Danke F |title= |language=German |journal=Psychiatr Clin (Basel) |volume=8 |issue=4 |pages=201–11 |year=1975 |pmid=1208893 |doi= |url=}}</ref><ref>{{cite journal |author=Cohen D, Leo J, Stanton T, et al. |title=A boy who stops taking stimulants for "ADHD": commentaries on a Pediatrics case study |journal=Ethical Hum Sci Serv |volume=4 |issue=3 |pages=189–209 |year=2002 |pmid=15278983 |doi= |url=}}</ref> ] drugs and ] drugs.<ref>{{cite journal |author=Chichmanian RM, Gustovic P, Spreux A, Baldin B |title= |language=French |journal=Therapie |volume=48 |issue=5 |pages=415–9 |year=1993 |pmid=8146817 |doi= |url=}}</ref> It is debated if the entire ] drug class causes true physical dependency, if only a subset does, or if none does,<ref name="isbn0-07-149430-8">{{cite book |author=Tierney, Lawrence M.; McPhee, Stephen J.; Papadakis, Maxine A. |title=Current medical diagnosis & treatment, 2008 |publisher=McGraw-Hill Medical |location= |year=2008 |page=916 |isbn=0-07-149430-8 |oclc= |doi= |accessdate=}}</ref> but all, if discontinued too rapidly, cause an acute withdrawal syndrome.<ref>{{cite web | url = http://www.bnf.org/bnf/bnf/56/3209.htm | title = Antipsychotic drugs | accessdate = 22 December 2008 | author = BNF | authorlink = British National Formulary |author2=British Medical Journal | year = 2008 | publisher = British National Formulary | location = UK}}</ref> When talking about illicit drugs rebound withdrawal is, especially with stimulants, sometimes referred to as "coming down" or "crashing". | ||
Some drugs, like ] and ], describe the drug category and not the mechanism. The individual agents and drug classes in the anticonvulsant drug category act at many different receptors and it is not possible to generalize their potential for physical dependence or incidence or severity of ] as a group so need to be looked at individually. ] as a group however are known to cause tolerance to the anti-seizure effect.<ref>{{cite journal |author=Wolfgang Löscher and Dieter Schmidt |title=Experimental and Clinical Evidence for Loss of Effect (Tolerance) during Prolonged Treatment with Antiepileptic Drugs|journal=Epilepsia|volume=47 |issue=8 |pages=1253–1284 |date=August 2006 | doi=10.1111/j.1528-1167.2006.00607.x |pmid=16922870}}</ref> ] drugs, which have an important use as antidepressants, |
Some drugs, like ] and ], describe the drug category and not the mechanism. The individual agents and drug classes in the anticonvulsant drug category act at many different receptors and it is not possible to generalize their potential for physical dependence or incidence or severity of ] as a group so need to be looked at individually. ] as a group however are known to cause tolerance to the anti-seizure effect.<ref>{{cite journal |author=Wolfgang Löscher and Dieter Schmidt |title=Experimental and Clinical Evidence for Loss of Effect (Tolerance) during Prolonged Treatment with Antiepileptic Drugs|journal=Epilepsia|volume=47 |issue=8 |pages=1253–1284 |date=August 2006 | doi=10.1111/j.1528-1167.2006.00607.x |pmid=16922870}}</ref> ] drugs, which have an important use as antidepressants, engender a ] that manifests with physical side effects. E.g., There have been case reports of a discontinuation syndrome with ] (Effexor).<ref name="Quaglio G, Schifano F, Lugoboni F 2008 1572–4"/> | ||
==See also== | ==See also== |
Revision as of 07:36, 19 February 2015
Addiction and dependence glossary | |
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Physical dependence refers to a state resulting from chronic use of a drug that has produced tolerance and where negative physical symptoms of withdrawal result from abrupt discontinuation or dosage reduction. Physical dependence can develop from low-dose therapeutic use of certain medications such as benzodiazepines, opioids, antiepileptics and antidepressants, as well as misuse of recreational drugs such as alcohol, opioids, and benzodiazepines. The higher the dose used, the greater the duration of use, and the earlier age use began are predictive of worsened physical dependence and thus more severe withdrawal syndromes. Acute withdrawal syndromes can last days, weeks or months, and protracted withdrawal syndrome, also known as "post-acute withdrawal syndrome" or "PAWS" - a low-grade continuation of some of the symptoms of acute withdrawal, typically in a remitting-relapsing pattern, that often results in relapse into active addiction and prolonged disability of a degree to preclude the possibility of lawful employment - can last for months, years, or, in relatively common to extremely rare cases, depending on individual factors, indefinitely. Protracted withdrawal syndrome is noted to be most often caused by benzodiazepines, but is also present in a majority of cases of alcohol and opioid addiction, especially that of a long-term, high-dose, adolescent-beginning, or chronic-relapsing nature (viz. a second or third addiction after withdrawal from the self-same substance of dependence). Withdrawal response will vary according to the dose used, the type of drug used, the duration of use, the age of the patient, the age of first use, and the individual person.
Symptoms
Physical dependence can manifest itself in the appearance of both physical and psychological symptoms which are caused by physiological adaptions in the central nervous system and the brain due to chronic exposure to a substance. Symptoms which may be experienced during withdrawal or reduction in dosage include increased heart rate and/or blood pressure, sweating, and tremors. More serious withdrawal symptoms such as confusion, seizures, and visual hallucinations indicate a serious emergency and the need for immediate medical care. Sedative hypnotic drugs such as alcohol, benzodiazepines, and barbiturates are the only commonly available substances that can be fatal in withdrawal due to their propensity to induce withdrawal convulsions. Abrupt withdrawal from other drugs, such as opioids can cause an extremely physiologically and psychologically painful withdrawal that is very rarely fatal in patients of general good health and with medical treatment, but is more often fatal in patients with weakened cardiovascular systems; toxicity is generally caused by the often-extreme increases in heart rate and blood pressure (which can be treated with clonidine), or due to arrhythmia due to electrolyte imbalance caused by the inability to eat, and constant diarrhea and vomiting (which can be treated with loperamide and ondansetron respectively) associated with acute opioid withdrawal, especially in longer-acting substances where the diarrhea and emesis can continue unabated for weeks, although life-threatening complications are extremely rare, and nearly non-existent with proper medical management. Dependence itself and chronic intoxication on psychostimulants can cause mild-to-moderate neurotoxic effects due to hyperthermia and generation of free radicals. This is treated with discontinuation; life-threatening complications are nonexistent.
Treatment
Treatment for physical dependence depends upon the drug being withdrawn and often includes administration of another drug, especially for substances that can be dangerous when abruptly discontinued. Physical dependence is usually managed by a slow dose reduction over a period of weeks, months or sometimes longer depending on the drug, dose and the individual. A physical dependence on alcohol is often managed with a cross tolerant drug, such as long acting benzodiazepines to manage the alcohol withdrawal symptoms.
Drugs that cause physical dependence
- All µ-opioids with any (even slight) agonist effect, such as (partial list) morphine, heroin, codeine, oxycodone, buprenorphine, nalbuphine, methadone, and fentanyl, but not agonists specific to non-µ opioid receptors, such as salvinorin A (a k-opioid agonist), nor opioid antagonists or inverse agonists, such as naltrexone (a universal opioid inverse agonist)
- All GABA agonists and positive allosteric modulators of both the GABA-A ionotropic receptor and GABA-B metabotropic receptor subunits, of which the following drugs are examples (partial list):
- alcohols such as ethyl alcohol (alcoholic beverage) (cf. alcohol dependence, alcohol withdrawal, delirium tremens)
- barbiturates such as phenobarbital, sodium thiopental and secobarbital
- benzodiazepines such as diazepam (Valium), lorazepam (Ativan), and alprazolam (Xanax) (see benzodiazepine dependence and benzodiazepine withdrawal syndrome)
- nonbenzodiazepines (z-drugs) such as zopiclone and zolpidem.
- gamma-hydroxybutyric acid (GHB) and 1,4-butanediol
- carisoprodol (Soma) and related carbamates (tybamate and meprobamate)
- baclofen (Lioresal) and its non-chlorinated analogue phenibut
- chloral hydrate
- glutethimide
- clomethiazole
- methaqualone (Quaalude)
- gabapentin (Neurontin) and pregabalin (Lyrica), calcium channel modifiers that affect GABA
- antiepileptic drugs such as valproate, lamotrigine, tiagabine, vigabatrin, carbamazepine and oxcarbazepine, and topiramate
- possibly neuroleptic drugs such as clozapine, risperidone, olanzapine, haloperidol, thioridazine, etc.
- commonly prescribed antidepressants such as the selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) (cf. SSRI/SNRI withdrawal syndrome)
- blood pressure medications, including beta blockers such as propanolol and alpha-adrenergic agonists such as clonidine
- androgenic-anabolic steroids
- glucocorticoids
Rebound syndrome
Main article: Rebound effectA wide range of drugs whilst not causing a true physical dependence can still cause withdrawal symptoms or rebound effects during dosage reduction or especially abrupt or rapid withdrawal. These can include caffeine, stimulants, steroidal drugs and antiparkinsonian drugs. It is debated if the entire antipsychotic drug class causes true physical dependency, if only a subset does, or if none does, but all, if discontinued too rapidly, cause an acute withdrawal syndrome. When talking about illicit drugs rebound withdrawal is, especially with stimulants, sometimes referred to as "coming down" or "crashing".
Some drugs, like anticonvulsants and antidepressants, describe the drug category and not the mechanism. The individual agents and drug classes in the anticonvulsant drug category act at many different receptors and it is not possible to generalize their potential for physical dependence or incidence or severity of rebound syndrome as a group so need to be looked at individually. Anticonvulsants as a group however are known to cause tolerance to the anti-seizure effect. SSRI drugs, which have an important use as antidepressants, engender a discontinuation syndrome that manifests with physical side effects. E.g., There have been case reports of a discontinuation syndrome with venlafaxine (Effexor).
See also
- Addiction
- Addiction recovery groups
- Alcohol withdrawal syndrome
- Benzodiazepine dependence
- Benzodiazepine withdrawal syndrome
- Discontinuation syndrome
- Drug and Alcohol Dependence (academic journal)
- Drug tolerance
- Psychological dependence
- Rebound insomnia
- Substance dependence
References
- Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274.
- Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 15 (4): 431–443. PMC 3898681. PMID 24459410.
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
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Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder. - "Definition of physical dependence - NCI Dictionary of Cancer Terms". Retrieved 2015-02-18.
- "All about Addiction". Medical News Today. Retrieved 2015-02-18.
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{{cite journal}}
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- Heh CW, Sramek J, Herrera J, Costa J (July 1988). "Exacerbation of psychosis after discontinuation of carbamazepine treatment". Am J Psychiatry. 145 (7): 878–9. PMID 2898213.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - Griffiths RR, Evans SM, Heishman SJ; et al. (December 1990). "Low-dose caffeine physical dependence in humans". J. Pharmacol. Exp. Ther. 255 (3): 1123–32. PMID 2262896.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - Lake CR, Quirk RS (December 1984). "CNS stimulants and the look-alike drugs". Psychiatr. Clin. North Am. 7 (4): 689–701. PMID 6151645.
- Sarampote CS, Efron LA, Robb AS, Pearl PL, Stein MA (2002). "Can stimulant rebound mimic pediatric bipolar disorder?". J Child Adolesc Psychopharmacol. 12 (1): 63–7. doi:10.1089/10445460252943588. PMID 12014597.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - Danke F (1975). "". Psychiatr Clin (Basel) (in German). 8 (4): 201–11. PMID 1208893.
- Cohen D, Leo J, Stanton T; et al. (2002). "A boy who stops taking stimulants for "ADHD": commentaries on a Pediatrics case study". Ethical Hum Sci Serv. 4 (3): 189–209. PMID 15278983.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - Chichmanian RM, Gustovic P, Spreux A, Baldin B (1993). "". Therapie (in French). 48 (5): 415–9. PMID 8146817.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - Tierney, Lawrence M.; McPhee, Stephen J.; Papadakis, Maxine A. (2008). Current medical diagnosis & treatment, 2008. McGraw-Hill Medical. p. 916. ISBN 0-07-149430-8.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - BNF; British Medical Journal (2008). "Antipsychotic drugs". UK: British National Formulary. Retrieved 22 December 2008.
- Wolfgang Löscher and Dieter Schmidt (August 2006). "Experimental and Clinical Evidence for Loss of Effect (Tolerance) during Prolonged Treatment with Antiepileptic Drugs". Epilepsia. 47 (8): 1253–1284. doi:10.1111/j.1528-1167.2006.00607.x. PMID 16922870.
External links
Psychoactive substance-related disorders | |||||
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