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1.
Emerg Med Clin North Am ; 32(2): 293-301, 2014 May.
Article in English | MEDLINE | ID: mdl-24766933

ABSTRACT

Ethanol intoxication and ethanol use are associated with a variety of metabolic derangements encountered in the Emergency Department. In this article, the authors discuss alcohol intoxication and its treatment, dispel the myth that alcohol intoxication is associated with hypoglycemia, comment on electrolyte derangements and their management, review alcoholic ketoacidosis, and end with a section on alcoholic encephalopathy.


Subject(s)
Acidosis/etiology , Alcoholic Intoxication , Emergencies , Hypoglycemia/etiology , Acidosis/epidemiology , Acidosis/therapy , Alcohol Amnestic Disorder/epidemiology , Alcohol Amnestic Disorder/etiology , Alcohol Amnestic Disorder/metabolism , Alcoholic Intoxication/complications , Alcoholic Intoxication/epidemiology , Alcoholic Intoxication/metabolism , Global Health , Humans , Hypoglycemia/epidemiology , Hypoglycemia/therapy , Incidence , Risk Factors , Survival Rate/trends
2.
Am J Geriatr Psychiatry ; 17(7): 542-55, 2009 Jul.
Article in English | MEDLINE | ID: mdl-19546653

ABSTRACT

The relationships between alcohol consumption and dementia and cognitive decline were investigated in a systematic review including meta-analyses of 15 prospective studies. Follow-ups ranged from 2 to 8 years. Meta-analyses were conducted on samples including 14,646 participants evaluated for Alzheimer disease (AD), 10,225 participants evaluated for vascular dementia (VaD), and 11,875 followed for any type of dementia (Any dementia). The pooled relative risks (RRs) of AD, VaD, and Any dementia for light to moderate drinkers compared with nondrinkers were 0.72 (95% CI = 0.61-0.86), 0.75 (95% CI = 0.57-0.98), and 0.74 (95% CI = 0.61-0.91), respectively. When the more generally classified "drinkers," were compared with "nondrinkers," they had a reduced risk of AD (RR = 0.66, 95% CI = 0.47-0.94) and Any dementia (RR = 0.53, 95% CI = 0.53-0.82) but not cognitive decline. There were not enough data to examine VaD risk among "drinkers." Those classified as heavy drinkers did not have an increased risk of Any dementia compared with nondrinkers, but this may reflect sampling bias. Our results suggest that alcohol drinkers in late life have reduced risk of dementia. It is unclear whether this reflects selection effects in cohort studies commencing in late life, a protective effect of alcohol consumption throughout adulthood, or a specific benefit of alcohol in late life.


Subject(s)
Alcohol Amnestic Disorder/etiology , Alcohol Drinking/adverse effects , Alcoholism/complications , Alzheimer Disease/etiology , Cognition Disorders/etiology , Dementia, Vascular/etiology , Dementia/etiology , Aged , Aged, 80 and over , Alcohol Amnestic Disorder/diagnosis , Alcohol Amnestic Disorder/epidemiology , Alcohol Amnestic Disorder/psychology , Alcohol Drinking/epidemiology , Alcohol Drinking/psychology , Alcoholism/epidemiology , Alcoholism/psychology , Alzheimer Disease/diagnosis , Alzheimer Disease/epidemiology , Alzheimer Disease/psychology , Cognition Disorders/diagnosis , Cognition Disorders/epidemiology , Cognition Disorders/psychology , Comorbidity , Cross-Sectional Studies , Dementia/diagnosis , Dementia/epidemiology , Dementia/psychology , Dementia, Vascular/diagnosis , Dementia, Vascular/epidemiology , Dementia, Vascular/psychology , Follow-Up Studies , Humans , Risk
3.
Article in English | MEDLINE | ID: mdl-17828626

ABSTRACT

This article compared alcoholics and healthy controls on the Buschke Selective Reminding Task. Alcoholics demonstrated deficits in memory and learning when compared to healthy controls, even when controlling for age. Examination of the alcoholic sample initially showed that age predicted memory deficits; however, age was no longer a significant predictor once the number of years of heavy drinking was entered into the regression equation. Findings suggest a direct link or mechanism of action between alcohol use and memory impairments, above and beyond effects of age or education.


Subject(s)
Alcohol Amnestic Disorder/complications , Alcoholism/complications , Memory Disorders/etiology , Adult , Age Factors , Aged , Alcohol Amnestic Disorder/etiology , Analysis of Variance , Female , Forecasting , Humans , Intelligence/physiology , Male , Middle Aged , Neuropsychological Tests
6.
Hosp Med ; 60(3): 169-72, 1999 Mar.
Article in English | MEDLINE | ID: mdl-10476237

ABSTRACT

Alcohol and psychiatric disorder have a complicated relationship. Certain important psychiatric syndromes arise from the toxic effects of alcohol and thiamine deficiency. Liver disease and hypoglycaemia are also associated with their own psychiatric syndromes. Many psychiatric patients also turn to alcohol as an easily available 'medication'.


Subject(s)
Alcoholism , Central Nervous System Depressants/poisoning , Ethanol/poisoning , Psychotic Disorders , Alcohol Amnestic Disorder/etiology , Alcohol Withdrawal Delirium/etiology , Alcoholism/psychology , Alcoholism/therapy , Diagnosis, Dual (Psychiatry) , Feeding and Eating Disorders/etiology , Humans , Mood Disorders/etiology , Psychoses, Alcoholic/etiology , Psychotic Disorders/etiology , Psychotic Disorders/therapy , Suicide/statistics & numerical data , Thiamine Deficiency/complications
7.
Inf. psiquiatr ; 18(3): 70-4, jul.-set. 1999.
Article in Portuguese | LILACS | ID: lil-268928

ABSTRACT

É feita uma revisäo sobre o sono, sua arquitetura normal e as relaçöes existentes entre esta atividade, a memória e as funçöes cognitivas. As hipóteses que vinculam a memória ao sono REM e ao sono näo-REM säo avaliadas quanto à possível funçäo "consolidadora" desta atividade sobre a memória recente e aprendizado. Condiçöes de transtorno de sono ou situaçöes de supressäo de sono REM ou näo-REM que podem alterar as funçöes cognitivas säo criticamente analisadas. O papel desempenhado pela hipoxemia cerebral em condiçöes como a apnéia de sono é revisto quanto às disfunçöes cognitivas e seu retorno à normalidade uma vez que seja instituído tratamento eficaz. As correlaçöes entre narcolepsia, memória e cogniçäo säo também analisadas. As disfunçöes mnêmicas e cognitivas causadas por hipnoindutores, benzodiazepínicos e antidepressores säo revistas e discutidas


Subject(s)
Humans , Cognition Disorders/etiology , Memory Disorders , Sleep Stages , Sleep Wake Disorders , Sleep Disorders, Intrinsic/physiopathology , Acetylcholine/adverse effects , Cholinergic Antagonists/adverse effects , Anti-Anxiety Agents/adverse effects , Dreams , Hypnotics and Sedatives/adverse effects , Histamine H1 Antagonists/adverse effects , Psychotropic Drugs/adverse effects , Sleep Apnea Syndromes , Sleep Initiation and Maintenance Disorders , Alcohol Amnestic Disorder/etiology
8.
Fortschr Neurol Psychiatr ; 66(10): 450-8, 1998 Oct.
Article in German | MEDLINE | ID: mdl-9825250

ABSTRACT

Alcohol abuse and alcohol dependence are frequent disorders in the elderly. The disorders often develop as a response to burdensome life events which have to be treated specifically. Old alcoholics often respond well to age-specific interventions, if co-existing depressive symptoms are also treated. Because of the non-specific nature of the initial symptoms, the majority of the elderly alcoholics remain unrecognised during the diagnostic process. This review, therefore, gives a synopsis of clinical clues to alcoholism and associated psychic complications in elderly patients. Psychic complications in persistent alcoholism include Wernicke-Korsakow's syndrome, symptom patterns of delusions and hallucinations and specific types of organic brain syndromes.


Subject(s)
Aged/psychology , Alcoholism/therapy , Alcohol Amnestic Disorder/etiology , Alcohol Amnestic Disorder/therapy , Alcoholism/complications , Alcoholism/diagnosis , Alcoholism/psychology , Delusions/etiology , Delusions/therapy , Hallucinations/etiology , Hallucinations/therapy , Humans , Syndrome , Wernicke Encephalopathy/etiology , Wernicke Encephalopathy/therapy
9.
Prog Neurobiol ; 56(4): 385-431, 1998 Nov.
Article in English | MEDLINE | ID: mdl-9775400

ABSTRACT

In this review first we evaluate evidence on the role of the neurobiological alterations induced by chronic ethanol consumption in the development of ethanol tolerance, dependence and withdrawal. Secondly, we describe the neuropathological consequences of chronic ethanol on cognitive functions and on brain structures. Chronic alcohol consumption can induce alterations in the function and morphology of most if not all brain systems and structures. While tolerance mechanisms are unlikely to contribute to the neuroadaptive changes associated with ethanol dependence, it is otherwise clear that repeated high, intoxicating doses of ethanol trigger those neuroadaptive processes that lead to dependence and contribute to the manifestation of the abstinence syndrome upon withdrawal. An unbalance between inhibitory and excitatory neurotransmission is the most prominent neuroadaptive process induced by chronic ethanol consumption. Due to the diffuse glutamatergic innervation to all brain structures, the neuroadaptive alterations in excitatory neurotransmission can affect the function of most if not all of neurotransmitter systems. The expression of the withdrawal syndrome is the major causal factor for the onset and development of the neuropathological alterations. This suggests a link between the neuroadaptive mechanisms underlying the development of ethanol dependence and those underlying the functional and structural alterations induced by chronic ethanol. In animals and humans, specific alterations occur in the function and morphology of the diencephalon, medial temporal lobe structures, basal forebrain, frontal cortex and cerebellum, while other subcortical structures, such as the caudate nucleus, seem to be relatively spared. The neuropathological alterations in the function of mesencephalic and cortical structures are correlated with impairments in cognitive processes. In the brain of alcoholics, the prefrontal cortex and its subterritories seem particularly vulnerable to chronic ethanol, whether Korsakoff's syndrome is present or not. Due to the role of these cortical structures in cognitive functions and in the control of motivated behavior, functional alterations in this brain area may play an important role in the onset and development of alcoholism.


Subject(s)
Alcohol-Related Disorders/physiopathology , Alcoholism/complications , Ethanol/adverse effects , Nerve Degeneration/chemically induced , Nervous System Diseases/chemically induced , Acetylcholine/physiology , Adaptation, Physiological , Alcohol Amnestic Disorder/etiology , Alcohol Drinking/adverse effects , Animals , Apoptosis , Brain/drug effects , Brain/metabolism , Brain/pathology , Conditioning, Classical , Depression/chemically induced , Depression/physiopathology , Disease Models, Animal , Dopamine/physiology , Drug Tolerance , Ethanol/toxicity , Humans , Nerve Degeneration/physiopathology , Nitric Oxide/physiology , Oxidative Stress , Receptors, N-Methyl-D-Aspartate/physiology , Substance Withdrawal Syndrome/etiology , Thiamine Deficiency/chemically induced , Thiamine Deficiency/complications , gamma-Aminobutyric Acid/physiology
10.
Alcohol Alcohol ; 33(4): 317-36, 1998.
Article in English | MEDLINE | ID: mdl-9719389

ABSTRACT

Alcohol misuse and alcohol withdrawal are associated with a variety of neuropsychiatric syndromes, some of which are associated with significant morbidity and mortality. B vitamin deficiency is known to contribute to the aetiology of a number of these syndromes, and B vitamin supplementation thus plays a significant part in prophylaxis and treatment. In particular, the Wernicke Korsakoff syndrome (WKS). due to thiamine deficiency, is a common condition in association with alcohol misuse, and is associated with high morbidity and mortality. Nicotinamide deficiency may result in a rarer condition, alcoholic pellagra encephalopathy, which often has a similar clinical presentation to WKS. This review considers the role of B vitamins in the aetiology and treatment of neuropsychiatric syndromes associated with alcohol misuse, with particular emphasis on WKS.


Subject(s)
Psychoses, Alcoholic/etiology , Psychoses, Alcoholic/therapy , Vitamin B Deficiency/complications , Vitamin B Deficiency/therapy , Alcohol Amnestic Disorder/etiology , Alcohol Amnestic Disorder/therapy , Humans , Pellagra/etiology , Pellagra/therapy , Thiamine Deficiency/complications , Thiamine Deficiency/therapy , Vitamin B 6 Deficiency/complications , Vitamin B 6 Deficiency/therapy , Wernicke Encephalopathy/etiology , Wernicke Encephalopathy/therapy
13.
Rev Environ Health ; 12(3): 201-13, 1997.
Article in English | MEDLINE | ID: mdl-9406291

ABSTRACT

This paper explores the metabolic consequences of alcohol misuse and identifies the pathophysiological reasons why alcohol, no matter what quantity is taken regularly, is not beneficial for the normal functioning of most body systems. Although moderate ethanol consumption may reduce stress and the risk of coronary heart disease, ethanol also exerts a direct toxicological effect because it interferes with hepatic metabolism and immune functions. Liver transplantation may be necessary for end-stage liver disease in alcoholics. A causal effect between alcohol intake and several cancers has been reported. Both environmental and genetic factors are involved in the susceptibility to alcoholism. An explanation of alcohol dependence as a family disease is introduced to shed light on the magnitude of its collateral effects on the family and on the community as a whole. The adverse effects of alcohol on pregnant women and the fetus are also discussed. To provide awareness of the effectiveness of community efforts, we examined the possible intervention strategies and the role of community care in this regard.


Subject(s)
Alcoholism/physiopathology , Ethanol/adverse effects , Adult , Aged , Alcohol Amnestic Disorder/etiology , Alcoholism/complications , Alcoholism/psychology , Alcoholism/therapy , Disease Progression , Ethanol/metabolism , Ethanol/pharmacology , Family Health , Female , Fetal Alcohol Spectrum Disorders/etiology , Humans , Infant, Newborn , Male , Middle Aged , Pregnancy
14.
Alcohol Alcohol ; 32(3): 281-5, 1997.
Article in English | MEDLINE | ID: mdl-9199729

ABSTRACT

A retrospective analysis of all admissions between 1990 and 1995 in a population of 160,000 identified 47 new cases of Korsakoff's psychosis only seven of which were preceded by Wernicke's encephalopathy. There was a higher ratio of females to males, relative to admissions for severe alcohol dependence. It postulated that the increasing incidence may be related to the warning of anaphylaxis and subsequent withdrawal of high-potency parenteral multivitamins with thiamine.


Subject(s)
Alcohol Amnestic Disorder/epidemiology , Cross-Cultural Comparison , Urban Population/statistics & numerical data , Adult , Aged , Alcohol Amnestic Disorder/etiology , Alcohol Amnestic Disorder/prevention & control , Cross-Sectional Studies , Dose-Response Relationship, Drug , Female , Humans , Incidence , Infusions, Intravenous , Male , Middle Aged , Patient Admission/statistics & numerical data , Retrospective Studies , Risk Factors , Scotland/epidemiology , Thiamine/administration & dosage , Thiamine/adverse effects , Wernicke Encephalopathy/epidemiology , Wernicke Encephalopathy/etiology , Wernicke Encephalopathy/prevention & control
15.
Postgrad Med J ; 73(855): 27-31, 1997 Jan.
Article in English | MEDLINE | ID: mdl-9039406

ABSTRACT

Alcohol abuse is one of the most serious problems in public health and the Wernicke-Korsakoff syndrome is one of the gravest consequences of alcoholism. The pathology is often undiagnosed in its less evident presentations, therefore an accurate diagnostic approach is a critical step in treatment planning. Treatment is based on restoration of thiamine, although this is insufficient to prevent the psychological decline of a great number of patients. The cognitive impact of the pathology is derived from the interaction of alcoholic neurotoxicity, thiamine deficiency and personal susceptibility. In this article, the literature concerning Wernicke-Korsakoff syndrome is reviewed.


Subject(s)
Alcohol Amnestic Disorder/physiopathology , Metabolic Diseases/physiopathology , Wernicke Encephalopathy/physiopathology , Alcohol Amnestic Disorder/etiology , Alcohol Amnestic Disorder/history , Alcohol Amnestic Disorder/pathology , Alcohol Amnestic Disorder/therapy , Alcoholism/complications , History, 19th Century , Humans , Metabolic Diseases/etiology , Metabolic Diseases/history , Metabolic Diseases/pathology , Metabolic Diseases/therapy , Prognosis , Syndrome , Thiamine/therapeutic use , Thiamine Deficiency/complications , Wernicke Encephalopathy/etiology , Wernicke Encephalopathy/history , Wernicke Encephalopathy/pathology , Wernicke Encephalopathy/therapy
16.
Article in Russian | MEDLINE | ID: mdl-9424341

ABSTRACT

There was performed clinical and neurophysiological observation of 41 patients with arteriovenous malformations (AVM) of gyrus cinguli. Disorders of memory appeared to be the main manifestations before the operation in 38 patients, moreover they had the features of Korsakov's syndrome in 5 patients. Autonomic and epileptic-like fits weren't quite characteristic. Memory impairment was observed in 23 from 38 patients after operation, however there weren't found any qualitatively new disorders. The first appearance of Korsakov's syndrome after operation was found in 3 patients. The degree of the increase of memory impairment correlated with the degree of the destruction of the gyrus cinguli as well as with the massivity of AVM passing into corpus callosum. Qualitative analysis of amnestic syndromes revealed that practically all the patients had the alteration of the selectivity of the memory traces, inability to keep in mind the meaning of the tale. It was accompanied by an absence of criticism toward patients' own defects. Similar signs of disorders had close resemblance with amnestic defects of the patients with frontal damages. That testified the significance of both damages of frontal lobes and their connections in formation of clinical pattern in human.


Subject(s)
Gyrus Cinguli/blood supply , Intracranial Arteriovenous Malformations/diagnosis , Adolescent , Adult , Alcohol Amnestic Disorder/diagnosis , Alcohol Amnestic Disorder/etiology , Cerebral Hemorrhage/diagnosis , Cerebral Hemorrhage/etiology , Child , Female , Gyrus Cinguli/surgery , Higher Nervous Activity , Humans , Intracranial Arteriovenous Malformations/complications , Intracranial Arteriovenous Malformations/surgery , Male , Memory Disorders/diagnosis , Memory Disorders/etiology , Middle Aged , Neuropsychological Tests , Neuropsychology , Syndrome
18.
Clin Chim Acta ; 255(1): 13-25, 1996 Nov 15.
Article in English | MEDLINE | ID: mdl-8930410

ABSTRACT

Pyrithiamine-induced thiamin deficiency has been used in rat as an experimental form of Wernicke-Korsakoff encephalopathy, a disease associated with chronic alcoholism. Although the main etiological factor is known to be the lack of thiamin, the biochemical mechanisms involved in the pathogenesis remain unclear. Thiamin-dependent enzymes were studied in brain mitochondria: alpha-ketoglutarate dehydrogenase activity exhibited 40% reduction, whereas pyruvate dehydrogenase did not change significantly. Polarographic recordings of mitochondrial respiration revealed a decreased State 3, when using pyruvate/malate, alpha-ketoglutarate or glutamine as a substrate, but the respiration rates remained unchanged with glutamate or succinate. This fall in pyruvate oxidation may be due to the impairment of alpha-ketoglutarate dehydrogenase, which follows pyruvate dehydrogenase in the metabolic pathway. A time course of lactate concentration showed dramatic increases in thalamus, mid brain, hypothalamus and colliculli, consistent with the anatomopathological findings. No increases were found before the onset of neurological symptoms.


Subject(s)
Alcohol Amnestic Disorder/etiology , Brain/enzymology , Ketoglutarate Dehydrogenase Complex/metabolism , Pyruvate Dehydrogenase Complex/metabolism , Pyruvic Acid/metabolism , Thiamine Deficiency/enzymology , Wernicke Encephalopathy/etiology , Animals , Brain Chemistry , Female , Hypothalamus/chemistry , Lactic Acid/metabolism , Mesencephalon/chemistry , Mitochondria/enzymology , Oxygen Consumption , Pyrithiamine , Rats , Rats, Sprague-Dawley , Substrate Specificity , Thalamus/chemistry , Thiamine Deficiency/chemically induced , Time Factors
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