Due to economic pressures, health care delivery is being restructured in the United States. Consequently, the treatment of the alcohol withdrawal syndrome (AWS) is now occurring more frequently in outpatient settings. Benzodiazepines (BZS) have been the primary medication treatment for AWS in North American for 30 years. However, a growing number of preclinical and clinical studies suggest that the anticonvulsant carbamazepine (CBZ) is equal in overall efficacy to BZS for the treatment of AWS. Further, there are several reasons to believe that CBZ may be superior to BZS for the treatment of AWS in outpatients, including the fact that CBZ has little abuse potential and the drug does not interact with alcohol to enhance CNS depression. Moreover, given its purported """"""""anti-kindling"""""""" properties, CBZ may be more efficacious for the treatment of AWS is patients who have had a history of multiple previous detoxifications and, therefore, may be more likely to present with more serious alcohol withdrawal symptoms. The present study represents a double-blind, placebo controlled clinical trial comparing the efficacy of the BZ lorazepam, to CBZ in outpatient alcoholics who meet DSM-IV criteria for a diagnosis of uncomplicated AWS. The two medication groups will be stratified on the basis of past history of detoxifications, and will be balanced for potentially important baseline characteristics. Subjects enrolled in the study will receive medications for 5 consecutive days in a """"""""fixed dose taper"""""""" method. The will return for follow-up evaluation one week later. The primary dependent variable, severity of AWS, will be determined by the CIWA-Ar. Other dependent variables (e.g., side effect checklist, visual analog scales, cognitive assessments) will be assessed for secondary analyses, as well.
The aim of this project is to provide relevant clinical information for primary care practitioners who will be treating AWS in ambulatory outpatient settings. Additionally, information will be obtained which will enhance our scientific knowledge regarding the effects of alcohol withdrawal-induced neuronal sensitization and the efficacy of the two classes of medications for the treatment of AWS.

National Institute of Health (NIH)
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Specialized Center (P50)
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Medical University of South Carolina
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Stewart, Scott H; Reuben, Adrian; Anton, Raymond F (2018) Reply: Carbohydrate Deficient Transferrin in Patients with Cirrhosis: A Tale of Bridges. Alcohol Alcohol 53:351-352
Kearney-Ramos, Tonisha E; Lench, Daniel H; Hoffman, Michaela et al. (2018) Gray and white matter integrity influence TMS signal propagation: a multimodal evaluation in cocaine-dependent individuals. Sci Rep 8:3253
Haun, Harold L; Griffin, William C; Lopez, Marcelo F et al. (2018) Increasing Brain-Derived Neurotrophic Factor (BDNF) in medial prefrontal cortex selectively reduces excessive drinking in ethanol dependent mice. Neuropharmacology 140:35-42
Schacht, Joseph P; Voronin, Konstantin E; Randall, Patrick K et al. (2018) Dopaminergic Genetic Variation Influences Aripiprazole Effects on Alcohol Self-Administration and the Neural Response to Alcohol Cues in a Randomized Trial. Neuropsychopharmacology 43:1247-1256
McGuier, Natalie S; Rinker, Jennifer A; Cannady, Reginald et al. (2018) Identification and validation of midbrain Kcnq4 regulation of heavy alcohol consumption in rodents. Neuropharmacology 138:10-19
Nimitvilai, Sudarat; Lopez, Marcelo F; Woodward, John J (2018) Effects of monoamines on the intrinsic excitability of lateral orbitofrontal cortex neurons in alcohol-dependent and non-dependent female mice. Neuropharmacology 137:1-12
Dowdle, Logan T; Brown, Truman R; George, Mark S et al. (2018) Single pulse TMS to the DLPFC, compared to a matched sham control, induces a direct, causal increase in caudate, cingulate, and thalamic BOLD signal. Brain Stimul 11:789-796
Zamudio-Bulcock, Paula A; Homanics, Gregg E; Woodward, John J (2018) Loss of Ethanol Inhibition of N-Methyl-D-Aspartate Receptor-Mediated Currents and Plasticity of Cerebellar Synapses in Mice Expressing the GluN1(F639A) Subunit. Alcohol Clin Exp Res 42:698-705
Cannady, Reginald; Rinker, Jennifer A; Nimitvilai, Sudarat et al. (2018) Chronic Alcohol, Intrinsic Excitability, and Potassium Channels: Neuroadaptations and Drinking Behavior. Handb Exp Pharmacol 248:311
Harlan, Benjamin A; Becker, Howard C; Woodward, John J et al. (2018) Opposing actions of CRF-R1 and CB1 receptors on VTA-GABAergic plasticity following chronic exposure to ethanol. Neuropsychopharmacology 43:2064-2074

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