OUTPATIENT ALCOHOL DETOXIFICATION:
Alcohol detoxification is medically supervised withdrawal. Medically supervised withdrawal is accomplished by giving a long acting drug that works on the same receptor system as alcohol. The drug is given in tapering doses down over a period of time. The class of drugs called benzodiazepines are used for outpatient detox from alcohol. However, alcohol and benzodiazepines are both sedatives, so caution must be used since combining the two can result in overdose.
ALCOHOL WITHDRAWAL IS A SERIOUS MEDICAL CONDITION:
Alcohol withdrawal should be taken very seriously and treated with caution. The first and most important reason for detox is to try and prevent life threatening complications. Two life-threatening complications of alcohol withdrawal are grand-mal withdrawal seizures and delirium tremens (“DT’s”). Delirium tremens is alcohol withdrawal with hallucinations and unstable vital signs. Outpatient medical detox from alcohol is not safe for everyone. If you are interested in outpatient detoxification from alcohol, Dr. Siegel will assess your safety for this type of treatment. Please note that the first appointment is an evaluation only. Medications are never prescribed at the first appointment. Please also note that you must stay with a responsible adult friend or family member for the first 24 to 48 hours of your detox. That person will be administering your medication to you.
DO I ACTUALLY NEED DETOX?:
With prolonged and heavy use of alcohol people develop physical dependence and a characteristic withdrawal syndrome will develop if the blood alcohol level progressively decreases. In order to develop a serious withdrawal syndrome, the body needs to have a substantial physical dependence on alcohol. Alcohol withdrawal is diagnosed for the most part by hand tremors, abnormal vital signs (elevated heart rate and elevated blood pressure), nausea, vomiting, and feelings of anxiousness, agitation, and irritability. Isolated complaints of anxiety and irritability are not symptoms that require treatment with a benzodiazepine taper. These symptoms do require treatment with other types of medications, which do not have the risk of overdose when combining a benzodiazepine with alcohol in the event of a relapse.
STOP OR MODERATE YOUR DRINKING:
There are now a number of different medications that are available to help people reduce or stop their drinking. They work in a variety ways to modulate the neurobiological adaptations that come from chronic alcohol use and help with the transition back to a more normal state when alcohol use is stopped or reduced. Unfortunately, only 10 to 20% of people will have a clinically meaningful response to any given medication. However, just because you do not respond to one medication doesn’t mean that you won’t respond to another. The reasons for this are unclear, but may be due to genetic differences. So there is an element of trial and error in medical therapies and it’s important not to get discouraged. Most people find one of these medications works well for them.
NALTREXONE
Alcohol increases the release of opioid peptides. These bind to the same receptor that is stimulated by narcotic pain medications such as Percocet and Vicodin. Activating this receptor causes a release of dopamine in the brain. Naltrexone is an opioid-receptor blocker that is used in the treatment of alcohol dependence. It is believed that naltrexone works by reducing the positive reinforcing effects of alcohol leading to decreased gratification from drinking and fewer cravings. Naltrexone has been shown to decrease the amount and frequency of drinking.
CAMPRAL (acamprosate)
Campral was specifically developed for the treatment of alcoholism. It acts at GABA-A and glutamate receptors. Its effects on glutamate and GABA-A transmission compensate for the neurobiological derangement produced by stopping drinking. It has been demonstrated to be effective in preventing relapse in studies conducted worldwide. In addition to its effect on abstinence, some studies and reviews have found that it reduces heavy drinking in those patients who do relapse. It is most effective when started immediately after detox.
BACLOFEN
Numerous case studies have been published indicating the effectiveness of baclofen in patients with alcohol use disorder. However, some randomized controlled trials have yielded conflicting results. Although data are mixed regarding baclofen’s efficacy in alcohol use disorder, they are consistent in terms of safety. Extensive information on baclofen's safety is available from its widespread use for the treatment of spasticity for decades. The administration of baclofen is considered to be safe in patients affected by alcohol use disorder.
Baclofen's primary mechanism of action for alcohol dependence is presumed to be the reduction of the reinforcing properties of alcohol by suppressing alcohol-stimulated dopamine release. The effects of baclofen at GABA-B receptors located in reward pathway inhibit alcohol-induced firing of dopamine neurons and of the alcohol-stimulated dopamine release, resulting into the reduction of reinforcing properties of alcohol and drugs. Baclofen's effects have been shown to not be due to muscle-relaxation or sedation, but rather as a result of its ability to reduce the desire for alcohol.
In addition, GABA-B receptors are highly expressed in structures involved in the mediation of anxiety, while activation of GABA-B receptors in these structures might reduce anxiety. Evidence from various clinical studies shows that baclofen reduced anxiety in alcohol use disorder subjects. Analyses in one of the trials found that treatment with baclofen was most effective in patients with comorbid anxiety. Baclofen may also influence the subjective expression of craving and risk of relapse by suppressing associated anxiety. Thus, besides dampening the reinforcing properties of alcohol through the suppression of alcohol-stimulated dopamine release, baclofen's effects on drinking may also be due to the relief of anxiety symptoms.
ANTICONVULSANTS
A number of anticonvulsants are used in the treatment of alcohol dependence based on their mechanisms of action such as strengthening of GABA mediated neurotransmission, inhibition of glutamate activity (achieved by blocking the excitatory effects of glutamate receptors and suppressing glutamate release) and blocking of calcium channels, decreasing alcohol-induced dopamine release. On the basis of these effects, anticonvulsant drugs can modulate the craving or can alter the subjective effects of alcohol, thereby reducing the risk of relapse.
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