Alcohol withdrawal syndrome

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Alcohol Withdrawal Syndrome
Classification and external resources

Ethanol
ICD-10 F10.3, F10.4
ICD-9 291.81
DiseasesDB 3543
MedlinePlus 000764

Alcohol withdrawal syndrome is the set of symptoms seen when an individual reduces or stops alcohol consumption after prolonged periods of excessive alcohol intake. Excessive use of alcohol leads to tolerance, physical dependence, and an alcohol withdrawal syndrome. The withdrawal syndrome is largely due to the central nervous system being in a hyper-excitable state. The withdrawal syndrome can include seizures and delirium tremens and may lead to excito-neurotoxicity.[1]

Sedative-hypnotics, such as alcohol, are well known for their propensity to induce physiological dependence. Alcohol withdrawal occurs as a result of neuro-adaptation resulting from chronic exposure to alcohol. A withdrawal syndrome occurs upon declining blood levels of alcohol which can be alleviated by reintroduction of alcohol or a cross-tolerant agent. Alcohol withdrawal is characterized by neuropsychiatric excitability and autonomic disturbances similar to other sedative-hypnotic drugs. Dependence on other sedative-hypnotics increases the severity of the withdrawal syndrome.[2]

Contents

Signs and symptoms [edit]

The severity of the alcohol withdrawal syndrome can vary from mild symptoms such as mild sleep disturbances and mild anxiety to very severe and life threatening including delirium, particularly visual hallucinations in severe cases and convulsions (which may result in death).[3] These symptoms initially appear characteristically on waking, due to the fall in the blood alcohol concentration during sleep.[4] The severity of alcohol withdrawal depends on various factors including age, genetics[citation needed], and, most importantly, degree of alcohol intake and length of time the individual has been using alcohol and number of previous detoxifications.[5][6]

Progression of symptoms [edit]

Typically the severity of the symptoms experienced will depend on the amount and duration of prior alcohol consumption, as well as the number and severity of previous withdrawals. Even the most severe of these symptoms can occur in as little as 2 hours after cessation; therefore, the overall unpredictability necessitates either pre-planned hospitalization, treatment coordinated with a doctor, or at the very least fast access to medical care and a supporting system of friends or family should be introduced prior to addressing detoxification. In many cases, however, symptoms follow a reasonably predictable time frame as exampled below:[citation needed]

Six to 12 hours after the ingestion of the last drink, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea or vomiting occur. Other comparable symptoms may also exist in this period. Twelve to 24 hours after cessation, the condition may progress to such major symptoms as confusion, hallucinations (with awareness of reality), tremor, agitation, and similar ailments. It's between the 24 and 48 hour period that seizures typically may begin to emerge among the previous symptoms in the period, and this is where the serious risk of mortality begins. Although most often, the condition begins to improve past the 48 hour mark, it can sometimes continue to increase in severity to delirium tremens, characterized by hallucinations that are indistinguishable from reality, severe confusion, more seizures, high blood pressure and fever which can persist anywhere from 4 to 12 days.

Protracted withdrawal [edit]

See also: Protracted withdrawal syndrome

A protracted alcohol withdrawal syndrome occurs in many alcoholics where withdrawal symptoms continue beyond the acute withdrawal stage but usually at a subacute level of intensity and gradually decreasing with severity over time. This syndrome is also sometimes referred to as the post acute withdrawal syndrome. Some withdrawal symptoms can linger for at least a year after discontinuation of alcohol. Symptoms can include a craving for alcohol, inability to feel pleasure from normally pleasurable things (also known as anhedonia), clouding of sensorium, disorientation, nausea and vomiting or headache.[15] Insomnia is also a common protracted withdrawal symptom which persists after the acute withdrawal phase of alcohol. Insomnia has also been found to influence relapse rate. Studies have found that magnesium or trazodone can help treat the persisting withdrawal symptom of insomnia in recovering alcoholics. Insomnia can be difficult to treat in alcoholics because many of the traditional sleep aids (e.g. benzodiazepine receptor agonists and barbiturate receptor agonists) work via a GABAA receptor mechanism and are cross tolerant with alcohol. However, trazodone is not cross tolerant with alcohol.[16][17][18] The acute phase of the alcohol withdrawal syndrome can also occasionally be protracted. Protracted delirium tremens has been reported in the medical literature as a possible but unusual feature of alcohol withdrawal.[19]

Pathophysiology [edit]

Chronic use of alcohol leads to changes in brain chemistry especially in the GABAergic system. Various adaptations occur such as changes in gene expression and down regulation of GABAA receptors. During acute alcohol withdrawal, changes also occur such as upregulation of alpha4 containing GABAA receptors and down regulation of alpha1 and alpha3 containing GABAA receptors. Neurochemical changes occurring during alcohol withdrawal can be minimized with drugs which are used for acute detoxification. With abstinence from alcohol and cross tolerant drugs these changes in neurochemistry gradually return towards normal.[20][21] Adaptations to the NMDA system also occur as a result of repeated alcohol intoxication and are involved in the hyper-excitability of the central nervous system during the alcohol withdrawal syndrome. Homocysteine levels which are elevated during chronic drinking increase even further during the withdrawal state and may result in excito-neurotoxicity. Alterations in ECG, in particular an increase in QT interval, and EEG abnormalities including may occur during early withdrawal.[22] Dysfunction of the hypothalamic–pituitary–adrenal axis and increased release of corticotropin-releasing hormone occur during both acute as well as protracted abstinence from alcohol and contribute to both acute and protracted withdrawal symptoms. Anhedonia/dysphoria symptoms, which can persist as part of a protracted withdrawal may be due to dopamine underactivity.[23]

Kindling [edit]

See also: Kindling (substance withdrawal)

Kindling is the phenomenon where repeated alcohol detoxifications lead to an increased severity of the withdrawal syndrome. For example, binge drinkers may initially experience no withdrawal symptoms but with each period of resumption of drinking followed by abstinence their withdrawal symptoms intensify in severity and may eventually result in full blown delirium tremens with convulsive seizures. Alcoholics who experience seizures during hospital detoxification have been found to be much more likely to have experienced more previous alcohol detoxification episodes than alcoholics who did not have seizures. Those experiencing previous detoxification are more likely to have more medically complicated alcohol withdrawal symptoms. Kindling can cause complications and may increase the risk of relapse, alcohol-related brain damage and cognitive deficits. Chronic alcohol misuse and kindling via multiple alcohol withdrawals may lead to permanent alterations in the GABAA receptors.[24]

The mechanism behind kindling is sensitization of some neuronal systems and desensitization of other neuronal systems which leads to increasingly gross neurochemical imbalances. This in turn leads to more profound withdrawal symptoms including anxiety, convulsions and neurotoxicity.[6]

Binge drinking is associated with increased impulsivity, impairments in spatial working memory and impaired emotional learning. These adverse effects are believed to be due to the neurotoxic effects of repeated withdrawal from alcohol on aberrant neuronal plasticity and cortical damage. Repeated periods of acute intoxication followed by acute detoxification has profound effects on the brain and is associated with an increased risk of seizures as well as cognitive deficits. The effects on the brain are similar to those seen in alcoholics who have been detoxified multiple times but not as severe as in alcoholics who have no history of prior detox. Thus the acute withdrawal syndrome appears to be the most important factor in causing damage or impairment to brain function. The brain regions most sensitive to harm from binge drinking are the amygdala and prefrontal cortex.[25]

People in adolescence who experience multiple withdrawals from binge drinking show impairments of long-term nonverbal memory. Alcoholics who have had two or more alcohol withdrawals show more frontal lobe cognitive dysfunction than alcoholics who have experienced one or no prior withdrawals. Kindling of neurons is the proposed cause of withdrawal related cognitive damage. Kindling from multiple withdrawals leads to accumulating neuroadaptational changes. Kindling may also be the reason for cognitive damage seen in binge drinkers.[26]

Diagnosis [edit]

Many hospitals use the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol in order to assess the level of withdrawal present and therefore the amount medication needed.[7] When overuse of alcohol is suspected but drinking history is unclear, testing for elevated values of carbohydrate-deficient transferrin and/or gammaglutamyl transferase can help make the diagnosis of alcohol overuse and dependence more clear.

Treatment [edit]

Benzodiazepines are effective for the management of symptoms as well as the prevention of seizures.[27]

Treatment of alcohol withdrawal syndrome can be managed with various pharmaceutical medications including barbiturates and clonidine. Certain vitamins are also an important part of the management of alcohol withdrawal syndrome.

Benzodiazepines [edit]

Benzodiazepines, such as diazepam or lorazepam, are the most commonly used drug for the treatment of alcohol withdrawal and are generally safe and effective in suppressing alcohol withdrawal signs. Chlordiazepoxide and diazepam are the benzodiazepines most commonly used in alcohol detoxification.[28] Benzodiazepines can be life saving, particularly if delirium tremens appears during alcohol withdrawal.[29] Benzodiazepines should only be used short term in alcoholics who aren't already dependent on benzodiazepines as benzodiazepines share cross tolerance with ethanol and there is a risk of replacing the addiction with a benzodiazepine dependence or worse still adding an additional addiction. Furthermore, disrupted GABA benzodiazepine receptor function is part of alcohol dependence and chronic benzodiazepines may prevent full recovery from alcohol induced mental effects.[30][31] Benzodiazepines have the problem of increasing cravings for alcohol in problem alcohol consumers and they also increase the volume of alcohol consumed by problem drinkers.[32] The combination of benzodiazepines and alcohol can amplify the adverse psychological effects of each other causing enhanced depressive effects on mood and increase suicidal actions and are generally contraindicated except for alcohol withdrawal.[33]

Antipsychotics [edit]

Antipsychotic agents, such as haloperidol, are sometimes used for alcohol withdrawal as an add-on to first-line measures such as benzodiazepines to control agitation or psychosis.[7] Antipsychotics may potentially worsen alcohol withdrawal effects (or other CNS depressant withdrawal states) as they lower the seizure threshold and can worsen withdrawal effects. Clozapine, olanzapine or low potency phenothiazines (e.g. chlorpromazine) are particularly risky; if used, extreme caution is required.[34] There is also concern for this class of drugs prolonging the QT interval, sometimes leading to fatal heart dysrhythmias.

Anticonvulsants [edit]

Some evidence indicates that topiramate[22] carbamazepine and other anticonvulsants are effective in the treatment of alcohol withdrawal however, research is limited.[22][35] A Cochrane review similarly reported that the evidence to support the role of anticonvulsants over benzodiazepines in the treatment of alcohol withdrawal is not statistically significant and noted significant weaknesses in the studies available and recommended further research. The Cochrane Review did note however, that paraldehyde combined with chloral hydrate showed superiority over chlordiazepoxide with regard to incidence of life threatening side effects and also noted that carbamazapine may have advantages for certain symptoms.[36] The advantages of carbamazapine demonstrated in one trial are less rebound withdrawal symptoms and appears to have a higher success rate for abstinence from alcohol post detoxification compared to benzodiazepines.[37]

Baclofen [edit]

Baclofen has been shown to be as effective as diazepam in uncomplicated alcohol withdrawal syndrome.[38]

Barbiturates [edit]

Barbiturates are superior to diazepam in the treatment of severe alcohol withdrawal syndromes such as delirium tremens but equally effective in milder cases of alcohol withdrawal.[39]

Clomethiazole [edit]

Clomethiazole (Heminevrin) is a non-benzodiazepine sedative-hypnotic with anticonvulsant effects which is active on the barbiturate site of the GABA-A receptor. Clomethiazole also inhibits the enzyme alcohol dehydrogenase, which is responsible for breaking down alcohol in the body. This slows the rate of elimination of alcohol from the body, which helps to relieve the sudden effects of alcohol withdrawal in alcoholics.

Clonidine [edit]

Clonidine has demonstrated superior clinical effects in the suppression of alcohol withdrawal symptoms in a head to head comparison study with the benzodiazepine drug chlordiazepoxide.[40][41][42]

Ethanol [edit]

Alcohol (ethanol) itself at low doses, but only when given intravenously by medical personnel, has been found to be superior to chlordiazepoxide in the detoxification of alcohol dependent patients. Low dose ethanol as a means of weaning alcoholics from alcohol was found to produce less profound sleep disturbances during withdrawal.[43] Low dose ethanol has been found to reduce treatment time, improve the failure rate from 20% down to 7% and increase retention in treatment centers with an increased rate of alcoholics attending substance misuse clinics after detoxification.[44]

Flumazenil [edit]

Flumazenil, which has shown some promise in the management of the benzodiazepine withdrawal syndrome has also demonstrated benefit in a research study in reducing anxiety withdrawal related symptomatology during alcohol withdrawal.[45]

Trazodone [edit]

Trazodone has demonstrated efficacy in the treatment of the alcohol withdrawal syndrome. It may have particular use in withdrawal symptoms, especially insomnia, persisting beyond the acute withdrawal phase.[17][18][46]

Caffeine [edit]

Caffeine has been shown to upregulate GABA receptors although high doses can cause caffeine poisoning and nervous system damage.

Magnesium [edit]

Magnesium appears to be effective in the treatment of alcohol withdrawal related cardiac arrhythmias. It is ineffective in controlling other symptoms of alcohol withdrawal.[47]

Nitrous Oxide [edit]

Nitrous oxide has been shown to be an effective and safe treatment for alcohol withdrawal.[48] Over 20,000 cases of the alcoholic withdrawal state have been successfully treated with psychotropic analgesic nitrous oxide (PAN) in South Africa and Finland. In 1992 it was officially approved for the treatment of addictive withdrawal states by the medical authorities in South Africa. Consequently, patients receiving it can claim a refund from their medical insurance. The gas therapy reduces the use of highly addictive sedative medications (like benzopdiazepines and barbiturates) by over 90%. The technique thus reduces the danger of secondary addiction to benzodiazepines, which can be a real problem amongst alcoholics who have been treated with these agents. <http://www.sabri.org.za/>

Vitamins [edit]

The prophylactic administration of thiamine intravenously is recommended before starting any carbohydrate containing fluids or food. Alcoholics are often deficient in various nutrients which can cause severe complications during alcohol withdrawal such as the development of Wernicke syndrome. The vitamins of most importance in alcohol withdrawal are thiamine and folic acid. To help to prevent Wernicke syndrome alcoholics should be administered a multivitamin preparation with sufficient quantities of thiamine and folic acid. Vitamins should always be administered before any glucose is administered otherwise Wernicke syndrome can be precipitated.[49]

Prevention of brain damage [edit]

Failure to manage the alcohol withdrawal syndrome appropriately can lead to permanent brain damage or death.[50] It has been proposed that brain damage due to alcohol withdrawal may be prevented by the administration of NMDA antagonists, calcium antagonists, and glucocorticoid antagonists.[51] The NMDA antagonist acamprosate reduces excessive glutamate rebound thereby suppressing excitotoxicity and potential withdrawal related neurotoxicity.[52] A cheaper, non prescription substance would be dextromethorphan, which is metabolized into dextrothrophan, which has calcium channel and NMDA blocking effects. Any NMDA antagonist is likely to be of benefit in alcohol withdrawal, due to the upregulated nature of ligand gated calcium channels due to the downregulated GABAA Cl- channel.

Substances impairing recovery [edit]

Continued use of benzodiazepines may impair recovery from psychomotor and cognitive impairments from alcohol.[53] Cigarette smoking may slow down or interfere with recovery of brain pathways in recovering alcoholics.[54]

See also [edit]

References [edit]

  1. ^ Hughes JR (February 2009). "Alcohol withdrawal seizures". Epilepsy Behav 15 (2): 92–7. doi:10.1016/j.yebeh.2009.02.037. PMID 19249388. 
  2. ^ Dart, Richard C. (1 December 2003). Medical Toxicology (3rd ed.). USA: Lippincott Williams & Wilkins. pp. 139–140. ISBN 978-0-7817-2845-4. 
  3. ^ a b c d e f g h i j Harada K (1993). "Emotional condition in alcohol withdrawal acute psychosis". Seishin Shinkeigaku Zasshi 95 (7): 523–9. PMID 8234534. 
  4. ^ Gelder et al,2005 p188. Psychiatry 3rd Ed. oxford:New York.
  5. ^ Liskow BI; Rinck C, Campbell J, DeSouza C (September 1989). "Alcohol withdrawal in the elderly". J Stud Alcohol 50 (5): 414–21. PMID 2779242. 
  6. ^ a b Howard C. Becker (1998). "Kindling in Alcohol Withdrawal" (PDF). Alcohol Health & Research World (NIAAA) 22 (1). Archived from the original on 2010-11-14. 
  7. ^ a b c d e f g h i j k l m n o p Bayard M, McIntyre J, Hill KR, Woodside J (March 2004). "Alcohol withdrawal syndrome". Am Fam Physician 69 (6): 1443–50. PMID 15053409. Archived from the original on 2010-11-14. 
  8. ^ Cowley DS (January 24, 1992). "Alcohol abuse, substance abuse, and panic disorder". Am J Med 92 (1A): 41S–48S. doi:10.1016/0002-9343(92)90136-Y. PMID 1346485. 
  9. ^ Muralidharan K; Rajkumar RP, Ananthapadmanabha Rao S, Benegal V (2007). "Catatonia as a Presenting Feature of Alcohol Withdrawal: A Case Report". Prim Care Companion J Clin Psychiatry 9 (6): 465. doi:10.4088/PCC.v09n0611a. PMC 2139932. PMID 18185829. 
  10. ^ Burov YV; Treskov VG, Vedernikova NN, Shevelyova OS (May 1986). "Types of alcohol withdrawal syndrome and dexamethasone suppression test". Drug Alcohol Depend 17 (1): 81–8. doi:10.1016/0376-8716(86)90039-6. PMID 3720534. 
  11. ^ Abitan J; Sigrist O (8-15). "[Treatment of alcohol withdrawal symptoms: a clinical study (author's transl)]". Semaine des Hôpitaux 55 (21–22): 1105–7. PMID 225818. 
  12. ^ Peppers MP (January–February 1996). "Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease". Pharmacotherapy 16 (1): 49–57. PMID 8700792. 
  13. ^ Fruensgaard K (February 1976). "Withdrawal psychosis: a study of 30 consecutive cases". Acta Psychiatr Scand 53 (2): 105–18. doi:10.1111/j.1600-0447.1976.tb00065.x. PMID 3091. 
  14. ^ Gann H; Feige B, Hohagen F, van Calker D, Geiss D, Dieter R (September 1, 2001). "Sleep and the cholinergic rapid eye movement sleep induction test in patients with primary alcohol dependence". Biol Psychiatry 50 (5): 383–90. doi:10.1016/S0006-3223(01)01172-6. PMID 11543743. 
  15. ^ Martinotti G; Nicola MD, Reina D, Andreoli S, Focà F, Cunniff A, Tonioni F, Bria P, Janiri L (2008). "Alcohol protracted withdrawal syndrome: the role of anhedonia". Subst Use Misuse 43 (3–4): 271–84. doi:10.1080/10826080701202429. PMID 18365930. 
  16. ^ Hornyak M; Haas P, Veit J, Gann H, Riemann D (November 2004). "Magnesium treatment of primary alcohol-dependent patients during subacute withdrawal: an open pilot study with polysomnography". Alcohol Clin Exp Res 28 (11): 1702–9. doi:10.1097/01.ALC.0000145695.52747.BE. PMID 15547457. 
  17. ^ a b Le Bon O; Murphy JR, Staner L, Hoffmann G, Kormoss N, Kentos M, Dupont P, Lion K, Pelc I, Verbanck P (August 2003). "Double-blind, placebo-controlled study of the efficacy of trazodone in alcohol post-withdrawal syndrome: polysomnographic and clinical evaluations". J Clin Psychopharmacol 23 (4): 377–83. doi:10.1097/01.jcp.0000085411.08426.d3. PMID 12920414. 
  18. ^ a b Borras L; de Timary P, Constant EL, Huguelet P, Eytan A (November 2006). "Successful treatment of alcohol withdrawal with trazodone". Pharmacopsychiatry 39 (6): 232. doi:10.1055/s-2006-951385. PMID 17124647. 
  19. ^ Miller FT (Mar-April 1994). "Protracted alcohol withdrawal delirium". J Subst Abuse Treat 11 (2): 127–30. doi:10.1016/0740-5472(94)90029-9. PMID 8040915. 
  20. ^ Sanna, E; Mostallino, Mc; Busonero, F; Talani, G; Tranquilli, S; Mameli, M; Spiga, S; Follesa, P; Biggio, G (December 17, 2003). "Changes in GABA(A) receptor gene expression associated with selective alterations in receptor function and pharmacology after ethanol withdrawal". Journal of Neuroscience 23 (37): 11711–24. ISSN 0270-6474. PMID 14684873. Archived from the original on 2010-11-14. 
  21. ^ Idemudia SO, Bhadra S, Lal H (June 1989). "The pentylenetetrazol-like interoceptive stimulus produced by ethanol withdrawal is potentiated by bicuculline and picrotoxinin". Neuropsychopharmacology 2 (2): 115–22. doi:10.1016/0893-133X(89)90014-6. PMID 2742726. 
  22. ^ a b c Hughes, JR. (Jun 2009). "Alcohol withdrawal seizures". Epilepsy Behav 15 (2): 92–7. doi:10.1016/j.yebeh.2009.02.037. PMID 19249388. 
  23. ^ Heilig M, Egli M, Crabbe JC, Becker HC (April 2010). "Acute withdrawal, protracted abstinence and negative affect in alcoholism: are they linked?". Addict Biol 15 (2): 169–84. doi:10.1111/j.1369-1600.2009.00194.x. PMC 3268458. PMID 20148778. 
  24. ^ Malcolm RJ (2003). "GABA systems, benzodiazepines, and substance dependence". J Clin Psychiatry. 64 Suppl 3: 36–40. PMID 12662132. 
  25. ^ Stephens, DN.; Duka, T. (Oct 2008). "Cognitive and emotional consequences of binge drinking: role of amygdala and prefrontal cortex". Philos Trans R Soc Lond B Biol Sci 363 (1507): 3169–79. doi:10.1098/rstb.2008.0097. PMC 2607328. PMID 18640918. 
  26. ^ Courtney, KE; Polich, J (Jan 2009). "Binge Drinking in Young Adults: Data, Definitions, and Determinants". Psychol Bull 135 (1): 142–56. doi:10.1037/a0014414. PMC 2748736. PMID 19210057. 
  27. ^ Amato L, Minozzi S, Vecchi S, Davoli M (2010). "Benzodiazepines for alcohol withdrawal". In Amato, Laura. Cochrane Database Syst Rev 3 (3): CD005063. doi:10.1002/14651858.CD005063.pub3. PMID 20238336. 
  28. ^ Ebell MH (April 2006). "Benzodiazepines for alcohol withdrawal". Am Fam Physician 73 (7): 1191. PMID 16623205. [dead link]
  29. ^ Wolf KM, Shaughnessy AF, Middleton DB (1993). "Prolonged delirium tremens requiring massive doses of medication". J Am Board Fam Pract 6 (5): 502–4. PMID 8213241. 
  30. ^ Toki S, Saito T, Nabeshima A, Hatta S, Watanabe M, Takahata N (February 1996). "Changes in GABAA receptor function and cross-tolerance to ethanol in diazepam-dependent rats". Alcohol. Clin. Exp. Res. 20 (1 Suppl): 40A–44A. doi:10.1111/j.1530-0277.1996.tb01726.x. PMID 8659687. 
  31. ^ Rassnick S, Krechman J, Koob GF (April 1993). "Chronic ethanol produces a decreased sensitivity to the response-disruptive effects of GABA receptor complex antagonists". Pharmacol. Biochem. Behav. 44 (4): 943–50. doi:10.1016/0091-3057(93)90029-S. PMID 8385785. 
  32. ^ Ziegler PP (August 2007). "Alcohol use and anxiety". Am J Psychiatry 164 (8): 1270; author reply 1270–1. doi:10.1176/appi.ajp.2007.07020291. PMID 17671296. Archived from the original on 2010-11-14. 
  33. ^ Ebadi, Manuchair (23 October 2007). "Alphabetical presentation of drugs". Desk Reference for Clinical Pharmacology (2nd ed.). USA: CRC Press. p. 512. ISBN 978-1-4200-4743-1. 
  34. ^ Prince V; Turpin KR (June 1, 2008). "Treatment of alcohol withdrawal syndrome with carbamazepine, gabapentin, and nitrous oxide". Am J Health Syst Pharm 65 (11): 1039–47. doi:10.2146/ajhp070284. PMID 18499876. 
  35. ^ Minozzi, S.; Amato, L.; Vecchi, S.; Davoli, M.; Minozzi, Silvia (2010). "Anticonvulsants for alcohol withdrawal" (PDF). In Minozzi, Silvia. Cochrane Database Syst Rev 3 (3): CD005064. doi:10.1002/14651858.CD005064.pub3. PMID 20238337. Archived from the original on 2010-11-14. 
  36. ^ Malcolm R; Myrick H, Roberts J, Wang W, Anton RF, Ballenger JC (May 2002). "The Effects of Carbamazepine and Lorazepam on Single versus Multiple Previous Alcohol Withdrawals in an Outpatient Randomized Trial". J Gen Intern Med 17 (5): 349–55. doi:10.1046/j.1525-1497.2002.10201.x. PMC 1495040. PMID 12047731. 
  37. ^ Addolorato G; Leggio L, Abenavoli L, Agabio R, Caputo F, Capristo E, Colombo G, Gessa GL, Gasbarrini G (March 2006). "Baclofen in the treatment of alcohol withdrawal syndrome: a comparative study vs diazepam". Am J Med 119 (3): 276.e13–8. doi:10.1016/j.amjmed.2005.08.042. PMID 16490478. 
  38. ^ Kramp P; Rafaelsen OJ (August 1978). "Delirium tremens: a double-blind comparison of diazepam and barbital treatment". Acta Psychiatr Scand 58 (2): 174–90. doi:10.1111/j.1600-0447.1978.tb06930.x. PMID 358756. 
  39. ^ Baumgartner GR (January 1988). "Clonidine versus chlordiazepoxide in acute alcohol withdrawal: a preliminary report". South Med J 81 (1): 56–60. doi:10.1097/00007611-198801000-00012. PMID 3276009. 
  40. ^ Baumgartner GR; Rowen RC (July 1987). "Clonidine vs chlordiazepoxide in the management of acute alcohol withdrawal syndrome". Arch Intern Med 147 (7): 1223–6. doi:10.1001/archinte.147.7.1223. PMID 3300587. 
  41. ^ Björkqvist SE (October 1975). "Clonidine in alcohol withdrawal". Acta Psychiatr Scand 52 (4): 256–63. doi:10.1111/j.1600-0447.1975.tb00041.x. PMID 1103576. 
  42. ^ Funderburk FR; Allen RP, Wagman AM (March 1978). "Residual effects of ethanol and chlordiazepoxide treatments for alcohol withdrawal". J Nerv Ment Dis 166 (3): 195–203. doi:10.1097/00005053-197803000-00005. PMID 205633. 
  43. ^ Dissanaike S; Halldorsson A, Frezza EE, Griswold J (August 2006). "An ethanol protocol to prevent alcohol withdrawal syndrome". J Am Coll Surg 203 (2): 186–91. doi:10.1016/j.jamcollsurg.2006.04.025. PMID 16864031. 
  44. ^ Little HJ (July 1991). "The benzodiazepines: anxiolytic and withdrawal effects". Neuropeptides. 19 Suppl: 11–4. doi:10.1016/0143-4179(91)90077-V. PMID 1679209. 
  45. ^ Roccatagliata G; Albano C, Maffini M, Farelli S (1980). "Alcohol withdrawal syndrome: treatment with trazodone". Int Pharmacopsychiatry 15 (2): 105–10. PMID 6108298. 
  46. ^ Wilson A, Vulcano B (1984). "A double-blind, placebo-controlled trial of magnesium sulfate in the ethanol withdrawal syndrome". Alcohol. Clin. Exp. Res. 8 (6): 542–5. doi:10.1111/j.1530-0277.1984.tb05726.x. PMID 6393805. 
  47. ^ Gillman, MA; Lichtigfeld FJ (1991). "Placebo and analgesic nitrous oxide for treatment of the alcohol withdrawal state.". Brit J Psychiatry 159: 672–675. 
  48. ^ Hugh Myrick; Raymond F Anton (1998). "Treatment of Alcohol Withdrawal" (PDF). Alcohol Health & Research World (niaaa) 22 (1). Archived from the original on 2010-11-14. 
  49. ^ Hanwella R, de Silva V (June 2009). "Treatment of alcohol dependence". Ceylon Med J 54 (2): 63–5. PMID 19670554. 
  50. ^ Hunt, WA. (November–December 1993). "Are binge drinkers more at risk of developing brain damage?". Alcohol 10 (6): 559–61. doi:10.1016/0741-8329(93)90083-Z. PMID 8123218. 
  51. ^ De Witte P, Littleton J, Parot P, Koob G (2005). "Neuroprotective and abstinence-promoting effects of acamprosate: elucidating the mechanism of action". CNS Drugs 19 (6): 517–37. PMID 15963001. 
  52. ^ Gitlow, Stuart (1 October 2006). Substance Use Disorders: A Practical Guide (2nd ed.). USA: Lippincott Williams and Wilkins. pp. 95–96. ISBN 978-0-7817-6998-3. 
  53. ^ Durazzo TC, Meyerhoff DJ (2007). "Neurobiological and neurocognitive effects of chronic cigarette smoking and alcoholism". Front. Biosci. 12 (8–12): 4079–100. doi:10.2741/2373. PMID 17485360. Archived from the original on 2010-11-14. 
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