Depressants alcohol

The authors concluded that antidepressants exert a modest beneficial effect for patients with combined depressive disorder and substance use disorder. They also emphasized that antidepressants are not a stand-alone treatment for depressed alcoholic patients and that concurrent therapy directly targeting the substance use disorder is also indicated. 

Anxiolytics with little abuse potential, such as buspirone, and antidepressants that have a benign side-effect profile and may reduce ethanol intake warrant careful evaluation in the treatment of anxious and depressed alcoholic patients. 

Salloum IM, Cornelius JR, Thase ME, et al Naltrexone utility in depressed alcoholics. Psychopharmacol Bull 34 111—115, 1998... 

Cornelius JR, Salloum IM, EhlerJG, et al Fluoxetine in depressed alcoholics a doubleblind, placebo-controlled trial. Arch Gen Psychiatry 54 700—705, 1997 Cornelius JR, Salloum IM, Haskett RF, et al Fluoxetine versus placebo for the marijuana use of depressed alcoholics. Addict Behav 24 111—114, 1999 Cui S-S, Bowen RC, Gu G-B, et al Prevention of cannabinoid withdrawal syndrome by lithium involvement of oxytocinergic neuronal activation. J Neurosci 21 9867— 9876, 2001... 

Depressants alcohol, barbiturates Opioids heroin, morphine, methadone... 

True Cushing s syndrome also must be distinguished from other conditions that share some clinical presentations (as well as elevated plasma cortisol concentrations), such as depression, alcoholism, obesity, and chronic illness—the so-called pseudo-Cushing s states. 

Cornelius, 1., Salloum, I., Ehler, 1. et al. Double-blind fluoxetine in depressed alcoholic smokers. Psychopharmacol. Bull. 33 165, 1997. 

Mutant mice lackingNPY showincreased anxiety-relatedbehavior (Palmiter et al. 1998) a full description of the behavioral phenotype of NPY receptor-null mutant mice is not available yet. However, data from Y2 receptor-null mutants support an anti-stress activity of NPY (Tschenett et al. 2003). In addition to the anxiolytic and anti-stress effects of NPY, a relationship to alcohol intake has been described. Voluntary ethanol consumption is increased in NPY and Yi receptor-null mutant mice, whereas either NPY overexpression or potentiation of NPY signaling through blockade of Y2 receptors suppresses rodent alcohol intake (Thiel et al. 1998,2002 Thorsell et al. 2002). Thus, in addition to anxiety and depression, alcohol dependency may be a promising clinical field for newly developed NPY receptor hgands. 

London E, Fanelh RJ, Kimes A, et al Effects of chronic nicotine on cerebral glucose utilization in the rat. Brain Res 520 208-214, 1990 Lonnqvist J, Sihvo S, Syvalahti E, et al Moclobemide and fluoxetine in atypical depression a double-blind trial. J Affect Disord 32 169-177, 1994 Loo H, Malka R, Defance R, et al Tianeptine and amitriptyline controlled double-blind trial in depressed alcoholic patients. Neuropsychobiology 19 79-85, 1988... 

In addition, abnormalities have been reported in depression, alcoholism, Alzheimer s disease, and multi-infarct dementia. It is important to note that these are statistical findings in the psychiatric research setting, and CT is not sufficiently sensitive or specific to be used as a routine diagnostic test. 

Fatalities due to acute BZD overdose alone are extremely rare. Nevertheless, fatal overdoses with triazolam in the elderly have been reported ( 192, 193). Even with ingestion of massive doses, recovery appears to be rapid and without serious complications or aftereffects ( 194, 195, 196 and 197). Combined ingestion of BZDs with other CNS depressants (alcohol, barbiturates, narcotics, orTCAs), however, may result in severe CNS and respiratory depression or hypotension. Severity of symptoms appears to depend more on the type and quantity of the other drugs than on the BZD plasma level (194, 195, 196 and 197). 

In regard to this last issue, the question of co-morbid depression associated with alcohol dependence can represent a difficult clinical picture. Whereas antidepressants may be appropriate and useful, premature intervention may be unnecessary. Dackis and colleagues ( 398), for example, found that 80% of 49 severely depressed alcoholics remitted after 2 weeks of unmedicated sobriety. They concluded that many severe depressions are alcohol-induced organic mood syndromes and improve spontaneously with abstinence. 

The role of tricyclics for depressed alcoholics has usually been limited to the period of acute withdrawal and not for longer-term maintenance. Other methodological problems with studies in this area include the following ... 

Cornelius JR, Salloum IM, Ehler JG, et al. Fluoxetine in depressed alcoholics a double-blind, placebo-controlled trial. Arch Gen Psychiatry 1997 54 700-705. 

Ethanol, also known simply as alcohol, is by far the most widely used depressant. Its structure is shown in Figure 14.34. In the United States, about a third of the population, or about 100 million people, drink alcohol. It is well established that alcohol consumption leads to about 150,000 deaths each year in the United States. The causes of these deaths are overdoses of alcohol alone, overdoses of alcohol combined with other depressants, alcohol-induced violent crime, cirrhosis of the liver, and alcohol-related traffic accidents. 

Although the BZDs have minimal depressant effects on respiration, when combined with other CNS depressants (alcohol, opioids), BZDs can cause fatal respiratory suppression. However, most non-BZD sedatives may also cause death by suppression of breathing and heart failure if taken in sufficient quantity. Benzodiazepines can also cause some degree of memory loss called anterograde amnesia—a form of amnesia that involves the formation of memories after a specific event a person with anterograde amnesia cannot remember information presented to them after ingesting the BZD, a process similar to an alcohol black-out. 

Depressive effects are increased by other CNS depressants (alcohol, MAOIs, other anticonvulsants, etc.)... 

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