Benzodiazepine Treatment of the Ethanol Withdrawal Syndrome

The objective of drug treatment in ethanol withdrawal is the relief of subjective symptoms, the prevention or treatment of more serious complications such as seizures or delirium tremens, and the preparation for long-term rehabilitation with minimal hazard of new dependence problems or direct toxicity related to drug treatment. The ideal drug for alcohol withdrawal should have a rapid onset and long duration of action, wide margin of safety, metabolism not dependent on liver function, and absence of abuse potential. The various benzodiazepines offer many of these advantages; the selection of the most appropriate benzodiazepine will depend on the clinical situation. Withdrawal severity can be quickly and reliably determined upon admission by measuring breath alcohol concentration and administering an objective rating scale, such as the CIWA-A (Clinical Institute Withdrawal Assessment of Alcohol). Patients in mild ethanol withdrawal (CIWA-A<20) and without a prior history of withdrawal seizures can generally be treated conservatively (fluids, multivitamins, reassurance, antacids, thiamine). Treatment without medication offers the patient an opportunity to exercise nonpharmacological control over his or her life Read more […]

Treatment of Methamphetamine Abuse

Treatment of Methamphetamine Abuse — Lack of Evidence for the Efficacy of Any of the Models Currently in Use Traditional treatment programs based on the Minnesota Model (28-day in-patient treatment) have been shown to be ineffective for the treatment of stimulant addiction. Both the National Institute of Drug Abuse (NIDA) and the Center for Substance Abuse Treatment (CSAT) have sponsored research into the efficacy of treatments for methamphetamine (methamphetamine) abuse. A third program that has been put forward as a potentially useful model for the treatment of methamphetamine abuse is the Haight Ashbury Outpatient Model. Although the program that is currently receiving the greatest national attention, the Matrix Model, has been shown to be promising, none of these models has been effectively evaluated for its efficacy for the treatment of methamphetamine abuse. Treatment of Methamphetamine: Matrix Model of Outpatient Treatment NIDA Treatment Guidelines NIDA has published treatment guidelines for stimulant abusers that have been empirically tested and their efficacy validated. However, these manuals were developed and tested on a population of cocaine users. A recent report () identified a variety of differences Read more […]

Effects of Methamphetamine Use

Cerebral Injury and Death from Methamphetamine Use The cerebral damage caused by methamphetamine intoxication can be formidable. Prolonged use is associated with injury to the dopamine system. Essentially, continued methamphetamine use likely leads to axonic degeneration of the dopamine axon terminals in the striatum, frontal cortex, nucleus accumbens, and amygdala. Hypersensitization of neurons occurs, for example, in increasing sensitivity of D-1 receptors. It is important to note that changes in catecholamines alone cannot explain behavior in humans when they are methamphetamine intoxicated. Animal studies across several species demonstrate that high dosages of methamphetamine damage nerve cells. In rats, one high dose is enough to cause damage to neurons; prolonged administration increases the number of neurons that are killed off. In squirrels, a single dose of MDMA (which is structurally similar to methamphetamine and mescaline) in only slight doses significantly damages brain neurons that produce serotonin. Twelve to 18 months after exposure, serotonin-producing nerves grow abnormally or not at all. MDMA selectively damages serotonin neurons in virtually all species. Buffenstein et al. showed through SPECT Read more […]