RESUMO
AIM: To determine the exact relation between the characteristics of quantitative electroencephalogram analyses and the estimators of the cognitive status in alcoholic patients undergoing withdrawal. SUBJECTS AND METHODS: The study examined 49 patients diagnosed with alcoholism (DSM-IV) after 10 days of withdrawal, as well as the correlation between the bandwidth measures from the quantitative electroencephalogram (qEEG) analysis and the characteristics of the visual and auditory cognitive evoked potentials (P300) and from the findings of the attention and memory tests. RESULTS: The patients were divided into two groups: group one, which displayed an overall increase in the delta and theta absolute powers with frontal predominance, and group two, with reduced delta and theta absolute powers. Latency of the P300 wave was delayed in patients, particularly in those in group one, but regional absence of the P300 wave was more frequent in group two. Results of attention and memory tests were abnormal in patients, especially those in group one. CONCLUSIONS: The findings in the two groups appear to reflect different stages in the progression of alcoholism: the first only involved cortical dysfunction due to metabolic causes and the second possibly had added cortical atrophy. They might also represent two types of biological response by their nervous systems to the same pathogenic agent. These findings suggest that it is advisable to conduct follow-up studies involving qEEG, cognitive tests and magnetic resonance imaging of the brain in this kind of patient.
Assuntos
Transtornos do Sistema Nervoso Induzidos por Álcool/psicologia , Alcoolismo/psicologia , Transtornos Cognitivos/induzido quimicamente , Eletroencefalografia/estatística & dados numéricos , Etanol/efeitos adversos , Síndrome de Abstinência a Substâncias/psicologia , Adulto , Transtorno Amnésico Alcoólico/fisiopatologia , Transtorno Amnésico Alcoólico/psicologia , Transtornos do Sistema Nervoso Induzidos por Álcool/fisiopatologia , Alcoolismo/fisiopatologia , Atenção , Transtornos Cognitivos/fisiopatologia , Progressão da Doença , Potenciais Evocados P300 , Feminino , Lobo Frontal/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Córtex Pré-Frontal/fisiopatologia , Tempo de Reação , Síndrome de Abstinência a Substâncias/fisiopatologiaRESUMO
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/terapiaRESUMO
This discussion has been concerned with one small corner of the anatomy of memory, namely, with the role of mammillary body lesions in the causation of the Korsakoff amnesic state. Clinical-pathologic studies, both our own (of alcoholics with the Wernicke-Korsakoff syndrome) and those of others (in patients with thalamic infarctions and neoplasms) provide unambiguous evidence that medial thalamic lesions, without additional lesions of the mammillary bodies, are quite sufficient to produce a severe and enduring amnesic state. Behavioral abnormalities in animals, insofar as they can be equated with a defect in retentive memory, tend to substantiate the observations in humans.