Outpatient detoxification of the addicted or alcoholic patient. (1/71)

Outpatient detoxification of patients with alcohol or other drug addiction is being increasingly undertaken. This type of management is appropriate for patients in stage I or stage II of withdrawal who have no significant comorbid conditions and have a support person willing to monitor their progress. Adequate dosages of appropriate substitute medications are important for successful detoxification. In addition, comorbid psychiatric, personality and medical disorders must be managed, and social and environmental concerns need to be addressed. By providing supportive, nonjudgmental, yet assertive care, the family physician can facilitate the best possible chance for a patient's successful recovery.  (+info)

Life-threatening brain failure and agitation in the intensive care unit. (2/71)

The modern intensive care unit (ICU) has evolved into an area where mortality and morbidity can be reduced by identification of unexpected hemodynamic and ventilatory decompensations before long-term problems result. Because intensive care physicians are caring for an increasingly heterogeneous population of patients, the indications for aggressive monitoring and close titration of care have expanded. Agitated patients are proving difficult to deal with in nonmonitored environments because of the unpredictable consequences of the agitated state on organ systems. The severe agitation state that is associated with ethanol withdrawal and delirium tremens (DT) is examined as a model for evaluating the efficacy of the ICU environment to ensure consistent stabilization of potentially life-threatening agitation and delirium.  (+info)

Animal models of alcohol withdrawal. (3/71)

One diagnostic criterion of alcohol dependence is the appearance of a withdrawal syndrome when alcohol consumption ceases. Researchers have used various animal models, including isolated brain cells, slices of brain tissue, and intact animals, to study the mechanisms and manifestations of withdrawal. Results from these experimental studies have demonstrated that many consequences of withdrawal found in animals resemble those observed in humans. Such signs and symptoms of alcohol withdrawal include enhanced activity of the autonomic nervous system; body posture and motor abnormalities; hyperexcitability of the central nervous system, including sensory hyperreactivity; convulsions; anxiety; and psychological discomfort. Researchers also have used animal models to study the electrophysiological correlates of withdrawal, as well as neurobiological mechanisms underlying alcohol dependence and withdrawal.  (+info)

Alcohol's effects on sleep in alcoholics. (4/71)

Sleep problems, which can have significant clinical and economic consequences, are more common among alcoholics than among nonalcoholics. During both drinking periods and withdrawal, alcoholics commonly experience problems falling asleep and decreased total sleep time. Other measures of sleep are also disturbed. Even alcoholics who have been abstinent for short periods of time (i.e., several weeks) or extended periods of time (i.e., several years) may experience persistent sleep abnormalities. Researchers also found that alcoholics are more likely to suffer from certain sleep disorders, such as sleep apnea. Conversely, sleep problems may predispose some people to developing alcohol problems. Furthermore, sleep problems may increase the risk of relapse among abstinent alcoholics.  (+info)

Alcohol, antidepressants, and circadian rhythms. Human and animal models. (5/71)

Alcohol consumption (both acute and chronic) and alcohol withdrawal have a variety of chronobiological effects in humans and other animals. These effects are widespread, altering the circadian rhythms of numerous physiological, endocrine, and behavioral functions. Thus, some of alcohol's negative health consequences may be related to a disruption of normal physiological timing. Most studies of alcohol's chronobiological effects have been conducted under natural conditions in which environmental stimuli, such as regular cycles of light and darkness, act to coordinate circadian rhythms with the environment and with each other. However, such studies cannot distinguish between effects occurring directly on the circadian pacemaker and those occurring "downstream" from the pacemaker on the physiological control systems. Studies using animals have enabled researchers to begin to examine the effects of alcohol on circadian rhythms under so-called free-running conditions in experimental isolation from potential environmental synchronizers. These studies have provided preliminary evidence that alcohol's chronobiological effects are indeed the result of direct influences on the circadian pacemaker itself. Furthermore, the effects of alcohol on animal circadian rhythms appear similar to the effects seen during administration of antidepressant drugs. Taken together with evidence that the chronobiological effects of alcohol withdrawal in human alcoholics are reminiscent of those described in depressed patients, these observations suggest that alcohol may produce antidepressantlike effects on the circadian pacemaker. One theory suggests that the effects of alcohol on the circadian pacemaker are mediated in part by alterations in serotonin, an important chemical involved in cellular communication within the circadian system. However, other neurochemical systems also are likely to be involved.  (+info)

No association between metabotropic glutamate receptors 7 and 8 (mGlur7 and mGlur8) gene polymorphisms and withdrawal seizures and delirium tremens in alcohol-dependent individuals. (6/71)

- Up-regulation of the glutamatergic neurotransmission from chronic ethanol intoxication may cause a hyperexcitable state during alcohol withdrawal that may lead to seizures and delirium tremens. The aim of our study was to evaluate the association between a history of alcohol withdrawal-induced seizures and delirium tremens and a mGlurR7 (Tyr433Phe); and a mGlurR8 (C2756T) metabotropic glutamate receptor polymorphism in alcoholics compared to controls. A total of 182 patients meeting DSM-IV alcohol dependence criteria and 117 controls, both groups being of German descent, were investigated. mGluR7 and mGluR8 polymorphisms were determined using polymerase chain reaction of lymphocyte DNA. History of alcohol withdrawal-induced delirium tremens and seizures were obtained using the Semi-Structured Assessment of Genetics in Alcoholism (SSAGA). Data were cross-checked with inpatients' clinical files. No significant associations were obtained between both receptor polymorphisms and alcohol withdrawal-induced seizures and delirium tremens. The negative results in this study question the role of these polymorphisms in the pathogenesis of alcohol withdrawal-induced seizures and delirium tremens.  (+info)

The effect of chronic ethanol consumption and withdrawal on mu-opioid and dopamine D(1) and D(2) receptor density in Fawn-Hooded rat brain. (7/71)

Previous studies have implicated the dopamine and opioid systems in the induction and maintenance of ethanol consumption. This study investigated, in alcohol-preferring Fawn-Hooded (FH) rats, whether chronic free-choice ethanol consumption and subsequent withdrawal cause alterations in central mu-opioid, dopamine D(1), and D(2) receptor density using autoradiography. FH rats were given a free choice between a 5% ethanol solution and tap water (n = 25) and displayed a mean ethanol consumption of 5.6 g/kg/day. A parallel group of FH rats (n = 5) only had access to tap water. Rats were then withdrawn from ethanol for 0, 1, 2, 5, or 10 days and killed by cervical dislocation and decapitation. Increases in mu-opioid receptor density were observed in the nucleus accumbens and ventral tegmental area upon withdrawal compared with the ethanol naive group. In the lateral amygdala, binding in all withdrawal groups was significantly different from the ethanol naive FH rats, and also from the chronic ethanol rats. An increase in dopamine D(1) receptor density was observed in the substantia nigra, pars reticulata in the 5- and 10-day withdrawal groups compared with ethanol naive. Accumbal dopamine D(2) receptor density (+25-30%) increased in the 10-day withdrawal group compared with both naive and chronic ethanol groups. These findings demonstrate that the opioid and dopamine systems are susceptible to modulation by chronic ethanol consumption and withdrawal in the FH rat. Furthermore, although acute ethanol withdrawal results in modulation of mu-opioid receptors, effects on dopamine receptors are delayed and only become evident 5 to 10 days after withdrawal.  (+info)

Basal and isoproterenol-stimulated cyclic-adenosine monophosphate levels in mouse hippocampus and lymphocytes during alcohol tolerance and withdrawal. (8/71)

AIMS: Basal and isoproterenol-stimulated levels of cyclic-adenosine monophosphate (cAMP) were investigated in the brain (hippocampus) and in the lymphocytes of mice rendered tolerant to, and physically dependent on, ethanol. METHODS: cAMP was measured with radioimmunoassay. Tolerance to, and physical dependence on, ethanol were induced by a 14-day ingestion of ethanol in drinking water. Upon replacing ethanol with water, ethanol withdrawal was precipitated and measured by the intensity of withdrawal-induced hyperexcitability and seizures. RESULTS: Basal (non-stimulated) levels of cAMP - both in the hippocampus and in the lymphocytes - were significantly reduced in the alcohol-drinking tolerant and physically dependent animals, but significantly increased 24 h after the onset of withdrawal. Isoproterenol resulted in a dose-dependent stimulation of cAMP in all groups investigated (control, tolerant/physically dependent, withdrawal), however, the magnitude of isoproterenol-induced net increase was significantly lower in the tolerant, and higher in the ethanol-withdrawn, animals. CONCLUSIONS: The major finding of the present experiments is that there was a significant positive correlation between basal cAMP levels in brain and lymphocytes versus the intensity of withdrawal hyperexcitability in ethanol-addicted mice.  (+info)