In general, treatment for substance dependence involves a combination of several psychosocial interventions, which can be combined with pharmacological interventions. Treatment of AUDs can be preceded by a detoxification, depending on severity of alcohol dependence. Personality and Substance Misuse and Pharmacotherapy of Addiction are discussed in depth in site. A short description and discussion of psychological and pharmacological interventions in AUDs are presented below.
Detoxification: Symptoms, Medication
The first stage of treatment for alcohol dependence often consists of alcohol detoxification, in order to prevent complications during detoxification, and to diminish symptoms and adverse effects associated with detoxification. Symptoms can develop within several hours after last alcohol use, and usually show a peak 24–36 h after abstinence. Symptoms that can be experienced during alcohol detoxification are anxiety, restlessness, sleeplessness, sweating, nausea, vomiting, tremors, heightened blood pressure, and an increased heart rate. Alcohol detoxification is estimated to take a week, although sleep disturbances and psychological withdrawal symptoms can persist much longer.
Monitoring of alcohol-dependent patients during detoxification is especially relevant because serious effects as delirium, epileptic insults, or dehydration can be present. If an alcoholic delirium occurs (usually after 3–5 days of abstinence), it is characterized by severe sympathetic hyperactivity (e. g., severe perspiration, fever, tachycardia, and hypertension). Medications used in detoxification usually consist of slow-acting benzodiazepines (e. g. diazepam, clorazepine, or chlordiazepoxide), which are dosed based on symptoms or according to a fixed dose. Dosage of benzodiazepines depends on the severity of the detoxification symptoms, and should take in consideration that benzodiazepines can build up in persons with diminished liver functioning. When severe liver dysfunctioning is present, benzodiazepines with a short half-time should therefore be considered (e. g., oxazepam and lorazepam). Next to benzodiazepines, haloperidol is used to diminish restlessness and to lower the chance of epileptic insults. Thiamine and vitamin B suppletion is used to avoid the development of Wernicke’s syndrome, and should be continued for a longer period after detoxification (1 month to 3 months), depending on thiamine and vitamin B deficiencies.
A range of psychosocial interventions has been implemented in the treatment of AUDs. These interventions range from brief interventions by primary health care providers to intensive residential treatment. Brief interventions for AUDs are effective in reducing drinking levels, and regarding cost-effectiveness of brief interventions tends to be very high. A recently developed type of brief intervention, motivational interviewing [MI], is designed to enhance the readiness of individuals to change their behavior on their own and/or undertake more formal treatment. MI can be a useful intervention for drinkers who have not yet recognized the problematic nature of their drinking. There is a long history of behavioral approaches to alcohol treatment, and contingency management is a new promising approach that seems to be more effective in promoting abstinence, compared to other treatment methods ().
In cognitive behavior therapy (CBT), the focus is to learn new skills to cope with problems and to change harmful behavior patterns by employing a wide range of behavioral and cognitive techniques, although it is not clear what specific factors account for treatment effectiveness. CBT focuses on processes such as learning adaptive behavioral strategies to cope with alcohol craving and with stressful situations that result in a high chance of relapse (e. g., distraction strategies, leaving the situation, or calling a friend), and identifying and reducing irrational, erroneous, or self- defeating thought patterns about alcohol use. One type of CBT that has received considerable support is relapse prevention training where there is a strong explicit focus on situations most likely to result in relapse
Like cognitive behavioral therapies, twelve-step models provide a range of coping behaviors but view alcohol dependence as a spiritual disease and medical disease. Twelve-step programs outline 12 consecutive activities that individuals with AUDs should achieve during the recovery process. Twelve-step models view alcoholism as a disease which can be controlled, but can never be cured, and therefore, twelve-step models focus on abstinence, rather than diminishing alcohol use. Similarities between twelve-step models and CBT lie in the development of coping skills to resist alcohol craving and urges. The combination of a twelve-step program combined with CBT has not been studied extensively in randomized control trials: one study found that a combination of professional treatment and a twelve-step program led to better treatment results than a twelve-step program alone A nonrandomized trial found that a twelve-step approach was more effective. Twelve-step models seem to be more effective compared to CBT and motivational enhancement therapy in a subgroup of individuals with AUDs who have a social network which is highly supportive of drinking. This interaction is likely related to the fact that twelve-step models provide an alternative social network not supportive of drinking. More randomized controlled trials have to be done to compare potential differences in treatment effectiveness of twelve-step models and other psychosocial treatments
Family and couple therapy is sometimes employed in the treatment of AUDs, in order to engage the immediate social environment as a support system for change, and to address interpersonal communication and the role it has in the addictive behavior. A recent review reported that behavioral couple therapy was associated with better outcome (frequency of use, consequences of use, and relationship satisfaction) than individual behavioral therapy, especially at follow-up.
Pharmacological Interventions for Alcohol Dependence
Anticraving Medication (Naltrexone, Acamprosate, Topiramate)
Two anticraving medications (acamprosate, oral naltrexone, and the once-monthly injectable, extended release naltrexone) have received approval for the treatment of alcohol dependence in the USA and European countries. Acamprosate is thought to act by normalizing protracted dysregulation of NMDA-mediated glutamatergic neurotransmission, a result of chronic heavy alcohol use and withdrawal. The safety and efficacy of acamprosate have been established in several clinical trials (), although not all studies find positive effects: a large clinical trial did notfind any effects of acamprosate alone, or in combination with naltrexone and/or CBT, compared to placebo. Naltrexone is an opioid antagonist which is thought to reduce alcohol craving by blocking the mu-opioid receptors, and thereby reducing the rewarding properties of alcohol and other psychoactive substances. Naltrexone has been shown to be effective in reducing relapse and diminishing percent of drinking days, when combined with several interventions, ranging from medical management to CBT (, for a review, see). A promising off-label pharmacological intervention for alcohol dependence is topiramate, which is thought to reduce the reinforcing effects of alcohol by facilitating gamma-aminobutyric acid function and inhibiting glutaminergic pathways in the corticomesolimbic system. Several clinical trials show the efficacy of topiramate above placebo. Another off-label pharmacological intervention for AUDs that recently has been studied is baclofen, a GABA-B receptor agonist. Somefirst studies show effectiveness of baclofen over placebo, but null-findings are reported as well. Therefore, the effectiveness of baclofen has to be studied in large clinical trials to demonstrate clearly the efficacy of baclofen and to ascertain whether efficacy is in fluenced by certain AUD characteristics such as severity and alcohol dependence subtype.
Disulfiram is an FDA-approved aversive medication for treatment of alcohol dependence. It inhibits the action of aldehyde dehydrogenase, thus preventing the breakdown of alcohol into acetate, resulting in nausea, vomiting, headache, and chestpain when alcohol is taken. The mechanism of disulfiram thus is an aversive response to alcohol consumption, even at a low level of alcohol consumption. Nonadherence tends to be high to very high in clinical trials of disulfiram, and reviews suggest that supervised prescription of disulfiram is needed to increase adherence. A severe side effect of disulfiram is the rare and idiosyncratic but potentially fatal hepatotoxicity that can occur with disulfiram. For a more recent discussion on the use of disulfiram in AUDs.
Selections from the book: Joris C. Verster • Kathleen Brady Marc Galanter • Patricia Conrod Editors “Drug Abuse and Addiction in Medical Illness: Causes, Consequences and Treatment”, 2012.
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