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Clive Harper - One of the best experts on this subject based on the ideXlab platform.
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prevalence of wernicke Korsakoff Syndrome in australia has thiamine fortification made a difference
The Medical Journal of Australia, 1998Co-Authors: Clive Harper, Therese Garrick, John M N Hilton, Ana Lara, Donna Sheedy, Jack M RaisanenAbstract:OBJECTIVE: To determine the prevalence of the Wernicke-Korsakoff Syndrome (WKS) in Australia and compare this with previous studies. DESIGN AND SETTING: Prospective autopsy study at the New South Wales Institute of Forensic Medicine, 1996-1997. METHODS: Brains of deceased people (aged over 15 years) derived from 2212 sequential autopsies performed between 1 January 1996 and 31 December 1997 were studied macroscopically and microscopically to identify cases of WKS. MAIN OUTCOME MEASURES: Standard histological criteria for WKS and any available clinical data. RESULTS: Twenty-five cases of WKS were identified (prevalence, 1.1%), mostly among the 5.9% of the 2212 people who had a history suggestive of alcohol abuse. Only four cases (16%) had been diagnosed during life. CONCLUSIONS: There has been a significant reduction in the prevalence of WKS in Australia since the introduction of thiamine enrichment of bread flour. While the prevalence is still higher than in most other Western countries, further research is needed before adding thiamine to alcoholic beverages can be recommended.
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chronic alcoholics without wernicke Korsakoff Syndrome or cirrhosis do not lose serotonergic neurons in the dorsal raphe nucleus
Alcoholism: Clinical and Experimental Research, 1996Co-Authors: Kerry G Baker, Clive Harper, Jillian J Kril, Glenda M HallidayAbstract:Despite the considerable evidence that alcoholics have perturbation of serotonergic function, there is little pathological evidence for alcohol directly affecting the nervous system. The present study aims to assess neuronal loss that occurs as a consequence of alcohol neurotoxicity in the serotonergic dorsal raphe nucleus (DRN). To that end, the brains of eight alcoholics and eight age-matched control cases were carefully screened to eliminate serious liver disease, the sequela of thiamine deficiency, Wernicke-Korsakoff Syndrome (WKS), and other pathological abnormalities. Brains were formalin-fixed for 2 weeks, cut, and then immunohistochemically stained using a monoclonal PH8 antibody specific for the rate-limiting enzyme of serotonin synthesis, tryptophan hydroxylase. The morphology of the serotonin-synthesizing neurons and their average size was similar in all cases. However, there was a reduction in the staining intensity of the reaction product in the DRN serotonergic neurons of most alcoholics. Neuronal counts on spaced serial sections revealed that there were an estimated average total of 106,100 ± 19,500 serotonergic neurons in the DRN of alcoholics and 108,300 ± 11,800 in the DRN of controls, indicating that in most alcoholics there is no reduction in the number of these neurons. Therefore, the effect of chronic alcohol consumption on the serotonergic system, in the absence of WKS or liver disease, seems to be functional rather than neuropathological.
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thiamine dependent enzyme changes in the brains of alcoholics relationship to the wernicke Korsakoff Syndrome
Alcoholism: Clinical and Experimental Research, 1993Co-Authors: Roger F. Butterworth, Jillian J Kril, Clive HarperAbstract:Chronic alcoholism results in thiamine deficiency as a consequence of poor nutrition, impaired absorption, and decreased phosphorylation to the enzyme cofactor form of the vitamin, thiamine pyrophosphate (TPP). Results of this study demonstrate significant reductions of TPP-dependent enzymes [pyruvate dehydrogenase complex, α-ketoglutarate dehydrogenase (αKGDH), and transketolase] in autopsied cerebellar vermis samples from alcoholic patients with the clinical and neuropathologically confirmed diagnosis of Wernicke-Korsakoff Syndrome (WKS). Enzyme activities in brain samples from alcoholics without WKS were within normal limits and activities of a nonthiamine-dependent enzyme, glutamate dehydrogenase, were not significantly different from control values in brain samples from alcoholics with or without WKS. These findings provide evidence, for the first time, of a direct implication of TPP-related metabolic processes in the pathogenesis of WKS. Decreased activities of αKGDH could be the trigger for a sequence of metabolic events resulting in energy compromise, and ultimately neuronal death in this Syndrome.
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the locus coeruleus and memory a study of chronic alcoholics with and without the memory impairment of Korsakoff s psychosis
Brain Research, 1992Co-Authors: Glenda M Halliday, Clive Harper, Jane EllisAbstract:The loss of noradrenergic locus coeruleus neurons has been identified as the possible critical lesion inducing amnesia in alcoholic patients with the Wernicke-Korsakoff Syndrome. The present study aims to test this hypothesis by quantifying the number of pigmented locus coeruleus neurons in 4 alcoholics with the Wernicke-Korsakoff Syndrome, 5 alcoholics with Wernicke's encephalopathy alone but no amnesia, and 1 alcoholic and 5 age-matched controls with no neurological disorders. Apart from an increased vascularity in the locus coeruleus of alcoholics, no significant differences in the number, morphology or distribution of pigmented locus coeruleus neurons was noted between any of the groups analysed. There was a significant correlation between the number of locus coeruleus neurons and brain weight. These data demonstrate that neither alcohol neurotoxicity nor thiamine deficiency result in a reduction in the number of pigmented cells in the locus coeruleus and refute the hypothesis that locus coeruleus cell loss is critical for the amnesia in the Wernicke-Korsakoff Syndrome.
Peter Bartenstein - One of the best experts on this subject based on the ideXlab platform.
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increased cerebellar pet glucose metabolism corresponds to ataxia in wernicke Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Klaus Mann, Lutz G. Schmidt, Hartmut Luddens, Georg Winterer, Thomas Siessmeier, Peter BartensteinAbstract:Aims: To investigate a possible relationship between cerebellar glucose metabolism and recovery from ataxia in the first months of acute Wernicke–Korsakoff Syndrome. Methods: Two cases of alcoholic Wernicke–Korsakoff Syndrome were followed up with the clinical status and cerebral glucose metabolism over a 4- and 9-month period. Results: Initially both patients showed severe ataxia and elevated cerebellar glucose metabolism that decreased corresponding to the restitution of stance and gait. Conclusion: Increased cerebellar glucose metabolism at the onset of the illness may reflect the reorganization process of disturbed motor skills and may indicate cerebellar plasticity. ( Received 25 July 2003; first notified 12 September 2003; in revised form 20 October 2003; accepted 20 October 2003 )
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persistence of disturbed thalamic glucose metabolism in a case of wernicke Korsakoff Syndrome
Psychiatry Research-neuroimaging, 2003Co-Authors: Andreas Fellgiebel, Armin Scheurich, Lutz G. Schmidt, Thomas Siessmeier, Peter BartensteinAbstract:Abstract We report the case of a 40-year-old alcoholic male patient, hospitalized with an acute ataxia of stance and gait, ocular muscle weakness with nystagmus and a global apathetic-confusional state. After admission, an amnestic Syndrome with confabulation was also observed and diagnosis of Wernicke–Korsakoff Syndrome was made. Under treatment with intravenous thiamine, the patient recovered completely from gaze weakness and ataxia, whereas a severe amnestic Syndrome persisted. Fluorodeoxyglucose (FDG) positron emission tomography (PET) showed bilateral thalamic and severe bilateral temporal–parietal hypometabolism resembling a pattern typical for Alzheimer's disease. Longitudinal assessment of the alcohol-abstinent and thiamine-substituted patient revealed improvements of clinical state and neuropsychological performance that were paralleled by recovered cerebral glucose metabolism. In contrast to metabolic rates that increased between 7.1% (anterior cingulate, left) and 23.5% (parietal, left) in cortical areas during a 9-month remission period, thalamic glucose metabolism remained severely disturbed over time (change: left +0.2%, right +0.3%).
Pierre Maurage - One of the best experts on this subject based on the ideXlab platform.
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imbalance between cognitive systems in alcohol dependence and Korsakoff Syndrome an exploration using the alcohol flanker task
Journal of Clinical and Experimental Neuropsychology, 2018Co-Authors: Melanie Brion, Valerie Dormal, Severine Lannoy, Serge Mertens, Philippe De Timary, Pierre MaurageAbstract:ABSTRACTBackground: Alcohol-dependent individuals (ALC) simultaneously present decreased inhibitory control and increased attention towards alcohol-related cues. The dual-process models have proposed that these symptoms reflect an imbalance between prefrontal/reflective and limbic/automatic systems, respectively leading to cognitive dysfunctions in executive processes and to alcohol-related bias. However, most previous research has focused on a separate exploration of these systems among ALC, and the direct measure of their interactions remains to be conducted. Moreover, no study has explored the evolution of this imbalance across the successive stages of alcohol-related disorders, and particularly in Korsakoff Syndrome (KS), the most frequent neurological complication of alcohol-dependence.Method: Ten KS, 14 ALC, and 14 matched control participants performed a modified Flanker task, the “Alcohol Flanker Task,” based on congruent, incongruent, and neutral conditions with alcohol-related stimuli. This task...
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crossmodal processing of emotions in alcohol dependence and Korsakoff Syndrome
Cognitive Neuropsychiatry, 2017Co-Authors: Melanie Brion, Severine Lannoy, Anne-lise Pitel, Fabien Dhondt, Donald A Davidoff, Pierre MaurageAbstract:ABSTRACTIntroduction: Decoding emotional information from faces and voices is crucial for efficient interpersonal communication. Emotional decoding deficits have been found in alcohol-dependence (ALC), particularly in crossmodal situations (with simultaneous stimulations from different modalities), but are still underexplored in Korsakoff Syndrome (KS). The aim of this study is to determine whether the continuity hypothesis, postulating a gradual worsening of cognitive and brain impairments from ALC to KS, is valid for emotional crossmodal processing.Methods: Sixteen KS, 17 ALC and 19 matched healthy controls (CP) had to detect the emotion (anger or happiness) displayed by auditory, visual or crossmodal auditory-visual stimuli. Crossmodal stimuli were either emotionally congruent (leading to a facilitation effect, i.e. enhanced performance for crossmodal condition compared to unimodal ones) or incongruent (leading to an interference effect, i.e. decreased performance for crossmodal condition due to discor...
Andreas Fellgiebel - One of the best experts on this subject based on the ideXlab platform.
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increased cerebellar pet glucose metabolism corresponds to ataxia in wernicke Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Klaus Mann, Lutz G. Schmidt, Hartmut Luddens, Georg Winterer, Thomas Siessmeier, Peter BartensteinAbstract:Aims: To investigate a possible relationship between cerebellar glucose metabolism and recovery from ataxia in the first months of acute Wernicke–Korsakoff Syndrome. Methods: Two cases of alcoholic Wernicke–Korsakoff Syndrome were followed up with the clinical status and cerebral glucose metabolism over a 4- and 9-month period. Results: Initially both patients showed severe ataxia and elevated cerebellar glucose metabolism that decreased corresponding to the restitution of stance and gait. Conclusion: Increased cerebellar glucose metabolism at the onset of the illness may reflect the reorganization process of disturbed motor skills and may indicate cerebellar plasticity. ( Received 25 July 2003; first notified 12 September 2003; in revised form 20 October 2003; accepted 20 October 2003 )
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persistence of disturbed thalamic glucose metabolism in a case of wernicke Korsakoff Syndrome
Psychiatry Research-neuroimaging, 2003Co-Authors: Andreas Fellgiebel, Armin Scheurich, Lutz G. Schmidt, Thomas Siessmeier, Peter BartensteinAbstract:Abstract We report the case of a 40-year-old alcoholic male patient, hospitalized with an acute ataxia of stance and gait, ocular muscle weakness with nystagmus and a global apathetic-confusional state. After admission, an amnestic Syndrome with confabulation was also observed and diagnosis of Wernicke–Korsakoff Syndrome was made. Under treatment with intravenous thiamine, the patient recovered completely from gaze weakness and ataxia, whereas a severe amnestic Syndrome persisted. Fluorodeoxyglucose (FDG) positron emission tomography (PET) showed bilateral thalamic and severe bilateral temporal–parietal hypometabolism resembling a pattern typical for Alzheimer's disease. Longitudinal assessment of the alcohol-abstinent and thiamine-substituted patient revealed improvements of clinical state and neuropsychological performance that were paralleled by recovered cerebral glucose metabolism. In contrast to metabolic rates that increased between 7.1% (anterior cingulate, left) and 23.5% (parietal, left) in cortical areas during a 9-month remission period, thalamic glucose metabolism remained severely disturbed over time (change: left +0.2%, right +0.3%).
Risto Vataja - One of the best experts on this subject based on the ideXlab platform.
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Korsakoff Syndrome in Non-alcoholic Psychiatric Patients. Variable Cognitive Presentation and Impaired Frontotemporal Connectivity
Frontiers Media S.A., 2018Co-Authors: Georgios Nikolakaros, Timo Kurki, Janina Paju, Sokratis G. Papageorgiou, Risto Vataja, Tuula IlonenAbstract:Background: Non-alcoholic Wernicke's encephalopathy and Korsakoff Syndrome are greatly underdiagnosed. There are very few reported cases of neuropsychologically documented non-alcoholic Korsakoff Syndrome, and diffusion tensor imaging (DTI) data are scarce.Methods: We report clinical characteristics and neuropsychological as well as radiological findings from three psychiatric patients (one woman and two men) with a history of probable undiagnosed non-alcoholic Wernicke's encephalopathy and subsequent chronic memory problems.Results: All patients had abnormal neuropsychological test results, predominantly in memory. Thus, the neuropsychological findings were compatible with Korsakoff Syndrome. However, the neuropsychological findings were not uniform. The impairment of delayed verbal memory of the first patient was evident only when the results of the memory tests were compared to her general cognitive level. In addition, the logical memory test and the verbal working memory test were abnormal, but the word list memory test was normal. The second patient had impaired attention and psychomotor speed in addition to impaired memory. In the third patient, the word list memory test was abnormal, but the logical memory test was normal. All patients had intrusions in the neuropsychological examination. Executive functions were preserved, except for planning and foresight, which were impaired in two patients. Conventional MRI examination was normal. DTI showed reduced fractional anisotropy values in the uncinate fasciculus in two patients, and in the corpus callosum and in the subgenual cingulum in one patient.Conclusions: Non-alcoholic Korsakoff Syndrome can have diverse neuropsychological findings. This may partly explain its marked underdiagnosis. Therefore, a strong index of suspicion is needed. The presence of intrusions in the neuropsychological examination supports the diagnosis. Damage in frontotemporal white matter tracts, particularly in the uncinate fasciculus, may be a feature of non-alcoholic Korsakoff Syndrome in psychiatric patients
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Non-alcoholic Korsakoff Syndrome in psychiatric patients with a history of undiagnosed Wernicke's encephalopathy
Journal of the Neurological Sciences, 2016Co-Authors: Georgios Nikolakaros, Tuula Ilonen, Timo Kurki, Janina Paju, Sokratis G. Papageorgiou, Risto VatajaAbstract:Wernicke's encephalopathy is often undiagnosed, particularly in non-alcoholics. There are very few reports of non-alcoholic patients diagnosed with Korsakoff Syndrome in the absence of a prior diagnosis of Wernicke's encephalopathy and no studies of diffusion tensor imaging in non-alcoholic Korsakoff Syndrome. We report on three non-alcoholic psychiatric patients (all women) with long-term non-progressive memory impairment that developed after malnutrition accompanied by at least one of the three Wernicke's encephalopathy manifestations: ocular abnormalities, ataxia or unsteadiness, and an altered mental state or mild memory impairment. In neuropsychological examination, all patients had memory impairment, including intrusions. One patient had mild cerebellar vermis atrophy in MRI taken after the second episode of Wernicke's encephalopathy. The same patient had mild hypometabolism in the lateral cortex of the temporal lobes. Another patient had mild symmetrical atrophy and hypometabolism of the superior frontal lobes. Two patients were examined with diffusion tensor imaging. Reduced fractional anisotropy values were found in the corona radiata in two patients, and the uncinate fasciculus and the inferior longitudinal fasciculus in one patient. Our results suggest that non-alcoholic Korsakoff Syndrome is underdiagnosed. Psychiatric patients with long-term memory impairment may have Korsakoff Syndrome and, therefore, they should be evaluated for a history of previously undiagnosed Wernicke's encephalopathy.
