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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a group of 85 men with alcohol dependence syndrome occurrence of depressive symptoms was examined and the intensification of psychomotor activation disorders was assessed. 60% of patients showed symptoms of depression during alcohol intoxication. Relationship between the intensification of depressive symptoms and psychomotor activity disorders was testified.
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PMID:[Depressive disorders with psychomotor activity in patients with alcohol dependence syndrome]. 129 6

Causes of death in 8 of 235 drunkenness offenders each followed up for two years, have been described. The subjects followed up were a heterogenous population of alcohol abusers. The majority were alcohol dependent irregular heavy drinkers. The main causes of death were suicide, road traffic accident, domestic accident, liver cirrhosis, hypothermia (from exposure) and ischaemic heart disease. More than one cause of death was listed in all cases. Chronic alcoholism was frequently listed. Depression was another sub-ordinate cause of death. The overall observed rate of mortality was 30 times the expected rate which was many times higher than those reported by earlier workers for alcoholics generally. These findings were discussed and it was concluded that drunkenness offenders are a particular at risk sub group of alcoholics. In view of the appreciable post mortem blood alcohol levels, it was further concluded that chronic alcoholism and the actual state of being drunk were the two major causes of death in this group of alcohol abusers.
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PMID:Causes of mortality in drunkenness offenders followed-up for 2 years. 130 84

The overall high rates of drug use found among Indian youth may be accounted for in part by lack of educational and employment opportunity and other endemic problems of Indian reservations. Individual drug involvement is most highly related to membership in drug-using peer clusters; but because of physical isolation, links between drug use and close friends are weaker for Indian youth, and family influence is felt more strongly. Anxiety, depression, and low self-esteem are not related to drug involvement, but angry youth are more likely to have drug-involved peers. Risk factors for Indian youth are low family caring, age first drunk, poor school adjustment, weak family sanctions against drugs, positive attitudes toward alcohol use, risk of school dropout, father not at home, and poor religious identification.
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PMID:Characteristics of Indian youth and drug use. 142 May 41

The behavior and environment of individuals are key determinants of both unintentional and intentional injuries in childhood and adolescence. These two determinants often interact so that certain behaviors lead to different injury outcomes depending on the environmental context of the injury. For example, depression is more likely to lead to suicide in the presence of alcohol intoxication. Alcohol intoxication is much more likely to lead to the choice of a firearm in a suicide attempt. Children with poor pedestrian crossing skills are far more likely to be hit in a busy urban intersection than in a safer location. The science of injury control has attempted to learn more about both the behavioral, environmental, and agent characteristics that lead to injury. Each of these dimensions offers opportunities for injury prevention or amelioration of the outcome. Despite increasing knowledge about how certain behaviors are associated with specific types of injuries, there has been only limited success achieved by attempts to modify behavior, particularly by persuasion or education. More success has been derived by legislative mandates. The most success, particularly in the prevention of unintentional injury, has been achieved by modification of the environments and the agents that are most often associated with injury. Because intentional injuries involve extremely complex and aberrant behavior, there is a persistent concern that attempts to modify the environment (e.g., handgun control) will be overridden by those with a high level of intent, i.e., they will seek another method. Although this may be true for carefully premeditated acts, suicide attempts and assaults by youth are usually precipitated by an acute stressor that depends on the availability of a weapon at that immediate time. While we develop more sophisticated psychosocial epidemiologic models that accurately predict violent behavior, we must continue to analyze aspects of intentional injuries that offer an opportunity to reduce the injury severity after the injury has occurred. Pediatricians and other health providers of children have played three important historical roles in the field of injury control. As clinicians, we have a unique opportunity to discuss these concerns with our patients and use our influence to attempt to modify individual behavior and inform about risks. As investigators, pediatricians have been important advocates of research initiatives to use the same epidemiologic methods used to study infectious diseases and cancer and apply them to the study of injury. Finally, pediatricians have played a critical public policy role in the evolution of injury control. Pediatricians have been at the helm behind most legislative initiatives to reduce injury among all people.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Injury control in childhood. 157 54

Flumazenil acts as an antidote for pharmacological and toxic effects due to benzodiazepines. Several isolated observations and short uncontrolled series have also suggested a possible effect against the impairment of consciousness induced by pure alcohol intoxication. Patients admitted in the emergency department with coma related to acute alcohol (ALC) or pure benzodiazepine (BZD) intoxication were randomized and treated blindly with either placebo or 1 mg flumazenil. A modified Glasgow score was used to observe the evolution of consciousness. In the 18 ALC patients, 1 mg flumazenil was not more effective than placebo, whereas it appeared to be very active in the BZD group. However, an open administration of higher doses of flumazenil (2-5 mg) in 11 ALC patients, whose condition had not initially improved, was followed by clear improvement of consciousness in five of them. Flumazenil, administered at a dose usually active against BZD sedation, does not improve CNS depression induced by ALC intoxication. Higher doses could be more effective in some patients, but it should also be verified in a placebo-controlled trial.
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PMID:Efficacy of flumazenil in acute alcohol intoxication: double blind placebo-controlled evaluation. 167 45

We examined tryptophan and serotonin (5-hydroxytryptamine) levels in the blood after consumption of alcohol. Forty-five minutes after drinking, whole blood serotonin concentration was significantly reduced, whereas no changes were observed in tryptophan level. The diurnal rhythm of 5-HT in subjects who the day before had drunk alcohol was quite different from the control group, but very similar to that of patients with depression. The results strongly suggest that the mechanism of depression after alcohol drinking may be related to serotonin.
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PMID:Alcohol-induced depression: involvement of serotonin. 187 77

Cases of alcohol intoxication in children are common; they are encountered every day in Finland. Studies other than case studies of alcohol intoxication in children are few. Metabolic acidosis was a frequent finding in juvenile alcohol intoxication. Capillary or arterial blood pH was below normal (less than 7.36) in 61.4% of patients and bicarbonate (less than 22) in 55.3% of patients. pCO2 was varied; the higher the blood alcohol concentration the higher the pCO2. Metabolic acidosis and blood pH correlated with the blood alcohol concentration and consciousness. The lower the blood pH the higher the serum glucose. Hypoglycemia is the most common reported symptom in children under 5 years of age. In the present study three patients were slightly hypoglycemic. Hypokalemia was the most important change (in 12.2%) in serum electrolytes. Alcohol intoxication causes metabolic acidosis and respiratory depression in children. Metabolic acidosis reduces consciousness.
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PMID:Acute alcohol intoxications in children treated in hospital. 223 82

Moderate alcohol intoxication in man, a ubiqitious social event, causes acute but reversible myocardial depression, the mechanism of which is unknown. We investigated whether this depression could be due to a direct effect of ethanol on the process of electromechanical coupling by simultaneously measuring the transmembrane action potential and contraction, or the cytosolic calcium transient (via aequorin photoluminescence) and contraction in isolated ferret right ventricular papillary muscle. Ethanol, in concentrations that are similar to plasma levels in man during intoxication (0.15 vol %), depressed the force of contraction approximately 10%. The step in the electromechanical process that was affected appeared to be the calcium-myofilament interaction, as there was no change in the transmembrane action potential or cytosolic calcium transient. This inhibition was quickly reversed by removal of the ethanol from the perfusate. On the other hand, higher concentrations of ethanol produced changes in contraction, the calcium transient, and the action potential, suggesting multiple levels of inhibition of electromechanical coupling. Increasing the perfusate calcium or use of the calcium channel agonist, BAY-K 8644, increased cytosolic calcium to near maximum but had little effect on contractility, confirming that the relationship between calcium and the myofilaments had been altered. These data suggest that the acute depression in ventricular function seen with alcohol consumption may be due to a direct effect on electromechanical coupling through inhibition of the calcium myofilament interaction.
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PMID:Mechanism of myocardial contractile depression by clinical concentrations of ethanol. A study in ferret papillary muscles. 233 1

The effects of spontaneous respiration and mechanical ventilation were examined by investigating the interaction between elevated intracranial pressure and alcohol intoxication. Ethanol (200 ml 48%) was infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (group 1), 7 young pigs with elevated cerebral pressure during spontaneous respiration (group 2), and 4 young pigs without elevated cerebral pressure during spontaneous respiration (group 3). While the behavior of intracranial pressure during mechanical ventilation in the animals from group 1 was inhomogeneous with a tendency to rise (29-34 mmHg), cerebral pressure (28-55 mmHg) increased drastically in the animals from group 2. This increase was associated with a sharp rise of Pa,CO2 (37.6-73.3 mmHg) and a decrease of Pa,O2 (74 mmHg to 13 mmHg). None of the animals in group 2 survived. Pa,CO2 also rose in alcoholized animals without elevated cerebral pressure (group 3) (41.9-63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory center. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure generally avoided.
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PMID:The respiratory aspect of the treatment of brain injury associated with acute alcohol intoxication--results of an animal experiment. 303 60

The effects of spontaneous respiration and mechanical ventilation on ICP were examined by investigating the interaction between elevated pressure and alcohol intoxication. 200 ml ethanol 48% were infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (Group 1), 7 young pigs with elevated intracranial pressure during spontaneous respiration (Group 2), and 4 young pigs without elevated intracranial pressure during spontaneous respiration (Group 3). While the behaviour of intracranial pressure during mechanical ventilation in the animals from Group 1 was inhomogeneous with a tendency to rise (29 mmHg to 34 mmHg), intracranial pressure (28 mmHg to 55 mmHg) increased dramatically in Group 2. This increase was associated with a sharp rise of paCO2 (37.6 mmHg to 73.3 mmHg) and a decline of paO2 (74 mmHg to 13 mmHg). None of the animals in Group 2 survived. paCO2 also rose in alcoholized animals without elevated ICP (Group 3) (41.9 mmHg to 63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in Group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory centre. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure can be generally avoided.
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PMID:[Effect of various types of artificial respiration on raised intracranial pressure, associated with acute alcoholic intoxication]. 310 36


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