The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Peter Bartenstein - One of the best experts on this subject based on the ideXlab platform.
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CASE REPORT INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN Wernicke-Korsakoff Syndrome
2020Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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.
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INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN Wernicke–Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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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increased cerebellar pet glucose metabolism corresponds to ataxia in Wernicke Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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, Thomas Siessmeier, Lutz G. Schmidt, Armin Scheurich, 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%).
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persistence of disturbed thalamic glucose metabolism in a case of Wernicke Korsakoff Syndrome
Psychiatry Research-neuroimaging, 2003Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Lutz G. Schmidt, Armin Scheurich, 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%).
Jack M Raisanen - 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, Donna Sheedy, Ana I. Lara, Therese Garrick, John M N Hilton, Jack M RaisanenAbstract:Objective To determine the prevalence of the Wernicke-Korsakoff Syndrome (WKS) in Australia and compare this with previous studies.
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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, Donna Sheedy, Therese Garrick, John M N Hilton, Ana Lara, 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.
Andreas Fellgiebel - One of the best experts on this subject based on the ideXlab platform.
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CASE REPORT INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN Wernicke-Korsakoff Syndrome
2020Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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.
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INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN Wernicke–Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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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increased cerebellar pet glucose metabolism corresponds to ataxia in Wernicke Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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, Thomas Siessmeier, Lutz G. Schmidt, Armin Scheurich, 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%).
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persistence of disturbed thalamic glucose metabolism in a case of Wernicke Korsakoff Syndrome
Psychiatry Research-neuroimaging, 2003Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Lutz G. Schmidt, Armin Scheurich, 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%).
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, Donna Sheedy, Ana I. Lara, Therese Garrick, John M N Hilton, Jack M RaisanenAbstract:Objective To determine the prevalence of the Wernicke-Korsakoff Syndrome (WKS) in Australia and compare this with previous studies.
-
prevalence of Wernicke Korsakoff Syndrome in australia has thiamine fortification made a difference
The Medical Journal of Australia, 1998Co-Authors: Clive Harper, Donna Sheedy, Therese Garrick, John M N Hilton, Ana Lara, 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.
Thomas Siessmeier - One of the best experts on this subject based on the ideXlab platform.
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CASE REPORT INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN Wernicke-Korsakoff Syndrome
2020Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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.
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INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN Wernicke–Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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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increased cerebellar pet glucose metabolism corresponds to ataxia in Wernicke Korsakoff Syndrome
Alcohol and Alcoholism, 2004Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Hartmut Lüddens, Lutz G. Schmidt, Georg Winterer, Klaus Mann, 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, Thomas Siessmeier, Lutz G. Schmidt, Armin Scheurich, 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%).
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persistence of disturbed thalamic glucose metabolism in a case of Wernicke Korsakoff Syndrome
Psychiatry Research-neuroimaging, 2003Co-Authors: Andreas Fellgiebel, Thomas Siessmeier, Lutz G. Schmidt, Armin Scheurich, 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%).
