Cases reported "Alcohol Amnestic Disorder"

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1/14. An atypical neuropsychological profile of a korsakoff syndrome patient throughout the follow-up.

    The basis of amnesia in alcoholic Wernicke-korsakoff syndrome (WKS) has been generally associated with diencephalic lesions and more specifically with lesions of the anterior thalamic nuclei. These brain structures are considered to be involved in encoding/consolidation processes of episodic memory. However, frontal lobe damage responsible for executive function deficits has also been documented. The present report details the nature and extent of amnesia in an alcoholic patients with WKS and which appears to be mainly due to frontal lobe (executive) deficits.
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2/14. Memory disorder in Korsakoff's psychosis: a neuropathological and neuropsychological investigation of two cases.

    Neuropathological findings in the brains of two alcoholic patients with Korsakoff's psychosis are reported. Their memory defects had been studied in detail quantitatively over a period of nine years in one case and three years in the other, relevant details of which are presented. Both patients had had a relatively pure long-term memory impairment in the absence of other cognitive deficits and in the absence of a short-term memory impairment. Their retrograde amnesia for public events and famous faces had been measured and found to have extended backwards over at least twenty-five years. There was severe impairment in anterograde recognition memory for both verbal and non-verbal material. On a newly prepared memory quotient battery both patients had scored well below the bottom of the normal scale (less than 60, where 100 is the mean with a standard deviation of /- 15). Both patients had also shown the characteristic differential improvement in retention when tested by cued recall and also the characteristic 'prior learning effect', i.e. normal retention of one list of words when tested by cued recall but impaired retention of a second list sharing the same cues as the first list. There had been a slight but significant deterioration in intelligence in one of the patients in the two years prior to his death, although his IQ still fell within the normal range. The other patient remained undeteriorated until his death, and his IQ also was close to an estimated measure of his premorbid IQ. In the brains of both patients there was marked gliosis, shrinkage and discolouration bilaterally in the medial nuclei of the mammillary bodies. In addition there was a thin band of gliosis bilaterally between the wall of the third ventricle and the medial dorsal nucleus, the rostral limit lying anterior to the medial dorsal nucleus. In the patient with no intellectual deterioration these were the only pathological changes that were seen. In neither patient was there evident local loss of nerve cells, gliosis or any other qualitative evidence of abnormality in the hippocampi, the white matter of the temporal lobes or the greater part of the medial dorsal nuclei, although it is difficult to be certain whether there was any overlap between the band of gliosis and the most medial region of the medial dorsal nueleus and other adjacent thalamic nuclei. In the other patient there was also a small zone of softening in the cerebellum and an increase in astrocytes in other regions of the cerebral hemispheres, including the basal ganglia, amygdala, and brain-stem, but without noticeable loss of cells. The question of the minimal lesion for the alcoholic Korsakoff amnesic state, and some aspects of the related anatomy, is discussed in the context of other reports in the literature which are, however, difficult to assess in the absence of details of the specificity, severity and character of the memory disorders.
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3/14. Wernicke-korsakoff syndrome of nonalcoholic origin.

    We describe a patient who developed a severe loss of memory following intravenous feeding and intestinal surgery. The pattern of both anterograde and retrograde memory impairment and frontal pathology is shown to be comparable with that observed in patients with Wernicke-korsakoff syndrome of an alcoholic etiology. The data strengthen the view that the essential characteristics of the Wernicke-korsakoff syndrome are not dependent on a prior history of chronic alcoholism. Implications of these data for the interpretation of alcoholic Wernicke-korsakoff syndrome are considered.
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4/14. Characteristics of the memory loss of a patient with Wernicke-Korsakoff's syndrome without alcoholism.

    The memory loss in alcoholic Wernicke-korsakoff syndrome has been well characterized. However, it has been suggested that some of the neuropsychological defects seen in these patients are due to frontal lobe dysfunction resulting from chronic alcohol abuse. The present report details the nature and extent of the amnesia in a Wernicke-Korsakoff patient who did not have a history of alcoholism. In spite of her normal performance on measures of frontal lobe function, this patient showed many characteristics similar to those seen in alcoholic Wernicke-korsakoff syndrome including a graded loss of remote memories and abnormal semantic information processing. Thus, the extent of the "core" features of this amnesic syndrome may be greater than was previously thought.
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5/14. Regional cerebral blood flow during alcoholic blackout.

    Regional cerebral blood flow was measured during alcoholic blackout in a 61-year-old man with a blood-alcohol level of 0.38%. The mean flow level was found to be elevated by about 30-60% compared to repeated studies during long-term abstinence. The regional pattern did not change greatly. Increases of mean regional cerebral blood flow have previously been reported during social drinking and in Wernicke-Korsakoff's syndrome. A common disturbance of subcortical activation systems is hypothesized.
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6/14. Attempted clinical application of a technique for promoting robust free recall to a case of alcoholic Korsakoff's syndrome.

    A case study is reported which attempted to teach personal orienting information (i.e., recent history) to an amnesic male patient. The structured cuing methods reported by Kovner, Mattis, and Pass (1985, Journal of Clinical and Experimental neuropsychology, 7, 395-411) were adopted. This involves structured presentation and cuing of target words embedded in a narrative. Some patients eventually are able to freely recall large amounts of material presented in this way. In the present case, the patient received 30 training sessions over 8 weeks. The material to be remembered was 10 target words pertaining to recent personal history. These words were embedded in accompanying storyline. The patient's immediate recall at the end of each session improved to some extent over the training period. However, delayed recall for the material remained nil throughout. Twelve months after the last training session the patient showed some "implicit" retention of the material. The findings are contrasted with Kovner et al.'s dramatic results and discussed.
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keywords = alcoholic
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7/14. Amnestic-confabulatory syndrome in hydrocephalic dementia and Korsakoff's psychosis in alcoholism.

    The clinical course of six alcoholics with Korsakoff's psyter shunt operation. The initial clinical state as well as the symptom improvement showed important similarities between the Korsakoff group and the hydrocephalic dementia group, who improved after shunt operation. Fantastic confabulation and appraxia were only observed in the hydrocephalic dementia group. Psychometrically, both groups showed a similar degree of improvement of the initially impaired verbal memory while only the hydrocephalic dementia group showed impairment of spatial abilities indicating a constructional apraxia. It is suggested that the similarities of the two conditions are related to dysfunction of diencephalic and temporal-limbic structures. The constructional and general apraxia as well as the fantastic confabulation in hydrocephalic dementia indicate a cortical, especially frontal cortical, dysfunction in this disorder.
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keywords = alcoholic
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8/14. Fat embolism syndrome in delirium tremens.

    delirium tremens in a common feature in the alcoholic population. The Fat embolism Syndrome (FES) is characterized by fever, encephalopathy, respiratory failure and skin petechiae. Fat embolism has been associated with alcoholics but the diagnosis was apparent only at autopsy. We present an alcoholic male who developed delirium tremens unresponsive to therapy, followed by features of the FES. Asterixis and Korsakoff's psychosis are newly described features of this syndrome. Corticosteroids were a definitive therapy in this case.
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keywords = alcoholic
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9/14. Wernicke-korsakoff syndrome after subtotal gastrectomy.

    A case of Wernicke-korsakoff syndrome is a nonalcoholic patient after gastric surgery provides support for the theory that nutritional deficiencies play an important part in the pathogenesis of the disease.
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10/14. Wernicke-Korsakov syndrome lesions in coronial necropsies.

    The clinical and pathological features of the Wernicke-Korsakov syndrome are described in 12 cases in which the syndrome had not been recognised before death. In a 1 year period there were 9 cases (5.3%) among 169 necropsies ordered by the coroner in unexpected or unexplained non-violent death. The characteristic brain lesions were grossly apparent in 5 cases and identified only histologically in 7 cases. The findings suggest that in cases of coma or patients found dead who might have been alcoholics, adequate postmortem examination of the brain is likely to demonstrate the lesions of the Wernicke-Korsakov syndrome in a significant number.
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keywords = alcoholic
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