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

RESUMO

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.


Assuntos
Acidose/etiologia , Intoxicação Alcoólica , Emergências , Hipoglicemia/etiologia , Acidose/epidemiologia , Acidose/terapia , Transtorno Amnésico Alcoólico/epidemiologia , Transtorno Amnésico Alcoólico/etiologia , Transtorno Amnésico Alcoólico/metabolismo , Intoxicação Alcoólica/complicações , Intoxicação Alcoólica/epidemiologia , Intoxicação Alcoólica/metabolismo , Saúde Global , Humanos , Hipoglicemia/epidemiologia , Hipoglicemia/terapia , Incidência , Fatores de Risco , Taxa de Sobrevida/tendências
2.
Am J Geriatr Psychiatry ; 17(7): 542-55, 2009 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-19546653

RESUMO

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.


Assuntos
Transtorno Amnésico Alcoólico/etiologia , Consumo de Bebidas Alcoólicas/efeitos adversos , Alcoolismo/complicações , Doença de Alzheimer/etiologia , Transtornos Cognitivos/etiologia , Demência Vascular/etiologia , Demência/etiologia , Idoso , Idoso de 80 Anos ou mais , Transtorno Amnésico Alcoólico/diagnóstico , Transtorno Amnésico Alcoólico/epidemiologia , Transtorno Amnésico Alcoólico/psicologia , Consumo de Bebidas Alcoólicas/epidemiologia , Consumo de Bebidas Alcoólicas/psicologia , Alcoolismo/epidemiologia , Alcoolismo/psicologia , Doença de Alzheimer/diagnóstico , Doença de Alzheimer/epidemiologia , Doença de Alzheimer/psicologia , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/epidemiologia , Transtornos Cognitivos/psicologia , Comorbidade , Estudos Transversais , Demência/diagnóstico , Demência/epidemiologia , Demência/psicologia , Demência Vascular/diagnóstico , Demência Vascular/epidemiologia , Demência Vascular/psicologia , Seguimentos , Humanos , Risco
3.
Artigo em Inglês | MEDLINE | ID: mdl-17828626

RESUMO

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.


Assuntos
Transtorno Amnésico Alcoólico/complicações , Alcoolismo/complicações , Transtornos da Memória/etiologia , Adulto , Fatores Etários , Idoso , Transtorno Amnésico Alcoólico/etiologia , Análise de Variância , Feminino , Previsões , Humanos , Inteligência/fisiologia , Masculino , Pessoa de Meia-Idade , Testes Neuropsicológicos
6.
Hosp Med ; 60(3): 169-72, 1999 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-10476237

RESUMO

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'.


Assuntos
Alcoolismo , Depressores do Sistema Nervoso Central/envenenamento , Etanol/envenenamento , Transtornos Psicóticos , Transtorno Amnésico Alcoólico/etiologia , Delirium por Abstinência Alcoólica/etiologia , Alcoolismo/psicologia , Alcoolismo/terapia , Diagnóstico Duplo (Psiquiatria) , Transtornos da Alimentação e da Ingestão de Alimentos/etiologia , Humanos , Transtornos do Humor/etiologia , Psicoses Alcoólicas/etiologia , Transtornos Psicóticos/etiologia , Transtornos Psicóticos/terapia , Suicídio/estatística & dados numéricos , Deficiência de Tiamina/complicações
7.
Inf. psiquiatr ; 18(3): 70-4, jul.-set. 1999.
Artigo em Português | LILACS | ID: lil-268928

RESUMO

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


Assuntos
Humanos , Transtornos Cognitivos/etiologia , Transtornos da Memória , Fases do Sono , Transtornos do Sono-Vigília , Transtornos Intrínsecos do Sono/fisiopatologia , Acetilcolina/efeitos adversos , Antagonistas Colinérgicos/efeitos adversos , Ansiolíticos/efeitos adversos , Sonhos , Hipnóticos e Sedativos/efeitos adversos , Antagonistas dos Receptores Histamínicos H1/efeitos adversos , Psicotrópicos/efeitos adversos , Síndromes da Apneia do Sono , Distúrbios do Início e da Manutenção do Sono , Transtorno Amnésico Alcoólico/etiologia
8.
Fortschr Neurol Psychiatr ; 66(10): 450-8, 1998 Oct.
Artigo em Alemão | MEDLINE | ID: mdl-9825250

RESUMO

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.


Assuntos
Idoso/psicologia , Alcoolismo/terapia , Transtorno Amnésico Alcoólico/etiologia , Transtorno Amnésico Alcoólico/terapia , Alcoolismo/complicações , Alcoolismo/diagnóstico , Alcoolismo/psicologia , Delusões/etiologia , Delusões/terapia , Alucinações/etiologia , Alucinações/terapia , Humanos , Síndrome , Encefalopatia de Wernicke/etiologia , Encefalopatia de Wernicke/terapia
9.
Prog Neurobiol ; 56(4): 385-431, 1998 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-9775400

RESUMO

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.


Assuntos
Transtornos Relacionados ao Uso de Álcool/fisiopatologia , Alcoolismo/complicações , Etanol/efeitos adversos , Degeneração Neural/induzido quimicamente , Doenças do Sistema Nervoso/induzido quimicamente , Acetilcolina/fisiologia , Adaptação Fisiológica , Transtorno Amnésico Alcoólico/etiologia , Consumo de Bebidas Alcoólicas/efeitos adversos , Animais , Apoptose , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Condicionamento Clássico , Depressão/induzido quimicamente , Depressão/fisiopatologia , Modelos Animais de Doenças , Dopamina/fisiologia , Tolerância a Medicamentos , Etanol/toxicidade , Humanos , Degeneração Neural/fisiopatologia , Óxido Nítrico/fisiologia , Estresse Oxidativo , Receptores de N-Metil-D-Aspartato/fisiologia , Síndrome de Abstinência a Substâncias/etiologia , Deficiência de Tiamina/induzido quimicamente , Deficiência de Tiamina/complicações , Ácido gama-Aminobutírico/fisiologia
10.
Alcohol Alcohol ; 33(4): 317-36, 1998.
Artigo em Inglês | MEDLINE | ID: mdl-9719389

RESUMO

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.


Assuntos
Psicoses Alcoólicas/etiologia , Psicoses Alcoólicas/terapia , Deficiência de Vitaminas do Complexo B/complicações , Deficiência de Vitaminas do Complexo B/terapia , Transtorno Amnésico Alcoólico/etiologia , Transtorno Amnésico Alcoólico/terapia , Humanos , Pelagra/etiologia , Pelagra/terapia , Deficiência de Tiamina/complicações , Deficiência de Tiamina/terapia , Deficiência de Vitamina B 6/complicações , Deficiência de Vitamina B 6/terapia , Encefalopatia de Wernicke/etiologia , Encefalopatia de Wernicke/terapia
13.
Rev Environ Health ; 12(3): 201-13, 1997.
Artigo em Inglês | MEDLINE | ID: mdl-9406291

RESUMO

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.


Assuntos
Alcoolismo/fisiopatologia , Etanol/efeitos adversos , Adulto , Idoso , Transtorno Amnésico Alcoólico/etiologia , Alcoolismo/complicações , Alcoolismo/psicologia , Alcoolismo/terapia , Progressão da Doença , Etanol/metabolismo , Etanol/farmacologia , Saúde da Família , Feminino , Transtornos do Espectro Alcoólico Fetal/etiologia , Humanos , Recém-Nascido , Masculino , Pessoa de Meia-Idade , Gravidez
14.
Alcohol Alcohol ; 32(3): 281-5, 1997.
Artigo em Inglês | MEDLINE | ID: mdl-9199729

RESUMO

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.


Assuntos
Transtorno Amnésico Alcoólico/epidemiologia , Comparação Transcultural , População Urbana/estatística & dados numéricos , Adulto , Idoso , Transtorno Amnésico Alcoólico/etiologia , Transtorno Amnésico Alcoólico/prevenção & controle , Estudos Transversais , Relação Dose-Resposta a Droga , Feminino , Humanos , Incidência , Infusões Intravenosas , Masculino , Pessoa de Meia-Idade , Admissão do Paciente/estatística & dados numéricos , Estudos Retrospectivos , Fatores de Risco , Escócia/epidemiologia , Tiamina/administração & dosagem , Tiamina/efeitos adversos , Encefalopatia de Wernicke/epidemiologia , Encefalopatia de Wernicke/etiologia , Encefalopatia de Wernicke/prevenção & controle
15.
Postgrad Med J ; 73(855): 27-31, 1997 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-9039406

RESUMO

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.


Assuntos
Transtorno Amnésico Alcoólico/fisiopatologia , Doenças Metabólicas/fisiopatologia , Encefalopatia de Wernicke/fisiopatologia , Transtorno Amnésico Alcoólico/etiologia , Transtorno Amnésico Alcoólico/história , Transtorno Amnésico Alcoólico/patologia , Transtorno Amnésico Alcoólico/terapia , Alcoolismo/complicações , História do Século XIX , Humanos , Doenças Metabólicas/etiologia , Doenças Metabólicas/história , Doenças Metabólicas/patologia , Doenças Metabólicas/terapia , Prognóstico , Síndrome , Tiamina/uso terapêutico , Deficiência de Tiamina/complicações , Encefalopatia de Wernicke/etiologia , Encefalopatia de Wernicke/história , Encefalopatia de Wernicke/patologia , Encefalopatia de Wernicke/terapia
16.
Artigo em Russo | MEDLINE | ID: mdl-9424341

RESUMO

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.


Assuntos
Giro do Cíngulo/irrigação sanguínea , Malformações Arteriovenosas Intracranianas/diagnóstico , Adolescente , Adulto , Transtorno Amnésico Alcoólico/diagnóstico , Transtorno Amnésico Alcoólico/etiologia , Hemorragia Cerebral/diagnóstico , Hemorragia Cerebral/etiologia , Criança , Feminino , Giro do Cíngulo/cirurgia , Atividade Nervosa Superior , Humanos , Malformações Arteriovenosas Intracranianas/complicações , Malformações Arteriovenosas Intracranianas/cirurgia , Masculino , Transtornos da Memória/diagnóstico , Transtornos da Memória/etiologia , Pessoa de Meia-Idade , Testes Neuropsicológicos , Neuropsicologia , Síndrome
17.
Clin Chim Acta ; 255(1): 13-25, 1996 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-8930410

RESUMO

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.


Assuntos
Transtorno Amnésico Alcoólico/etiologia , Encéfalo/enzimologia , Complexo Cetoglutarato Desidrogenase/metabolismo , Complexo Piruvato Desidrogenase/metabolismo , Ácido Pirúvico/metabolismo , Deficiência de Tiamina/enzimologia , Encefalopatia de Wernicke/etiologia , Animais , Química Encefálica , Feminino , Hipotálamo/química , Ácido Láctico/metabolismo , Mesencéfalo/química , Mitocôndrias/enzimologia , Consumo de Oxigênio , Piritiamina , Ratos , Ratos Sprague-Dawley , Especificidade por Substrato , Tálamo/química , Deficiência de Tiamina/induzido quimicamente , Fatores de Tempo
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