Relevant bibliographies by topics / Korsakoff Syndrome

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Academic literature on the topic 'Korsakoff Syndrome'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Korsakoff Syndrome"

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Jacobson, R. R., C. F. Acker, and W. A. Lishman. "Patterns of neuropsychological deficit in alcoholic Korsakoff's Syndrome." Psychological Medicine 20, no. 2 (May 1990): 321–34. http://dx.doi.org/10.1017/s0033291700017633.

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SynopsisTwenty-five male and 13 female patients with alcoholic Korsakoff's syndrome (AKS) were compared with age- and sex-matched non-Korsakoff chronic alcoholics and healthy volunteers in a neuropsychological study, which included computer-administered tests of cognitive function. The performance of male Korsakoff patients was significantly inferior to that of healthy male controls, not only in tests of memory, but also in visuo-perceptual tasks with a speed or motor component, and on category sorting and verbal fluency measures. Compared with male alcoholics, the performance of male Korsakoff patients was again inferior on similar tests. Female Korsakoff patients showed more extensive deficits compared with female controls, but differed less from matched female alcoholics.The results suggest that, in addition to their amnesia, many Korsakoff patients have sustained widespread cognitive deficits, affecting particularly visuo-perceptual and abstracting functions, which are sensitive to cortical lesions. The range of deficits falls short of what may be regarded as ‘global’ in male, but probably not in female, Korsakoffs. The implications for a dual aetiology of AKS involving thiamine deficiency and other features associated with alcoholism, probably direct alcohol neurotoxicity, are discussed.
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Egger, Jos I. M., Arie J. Wester, Hubert R. A. De Mey, and Jan J. L. Derksen. "Korsakoff's syndrome on the MMPI-2." Acta Neuropsychiatrica 14, no. 5 (October 2002): 231–36. http://dx.doi.org/10.1034/j.1601-5215.2002.140506.x.

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Background:This article describes an exploratory study of MMPI-2 administration to 20 patients with Korsakoff's disease, all admitted to the Korsakoff unit of a major psychiatric hospital in the Netherlands.Methods:We compared their MMPI-2 basic profiles with those of an inpatient alcohol-dependent non-Korsakoff group. Attention was also given to content scales and some selected supplementary scales. Furthermore, we explored the differences between MMPI-2 profiles of Korsakoff patients with and without insight into oneself and one's disease.Results:Compared with both the Dutch norms and the scale means of the non-Korsakoff alcoholics, Korsakoff patients showed an extraordinary flat profile. Illness insight appeared to be related to the levels of the various scales.Discussion:The results show the potential usefulness of the MMPI-2 in the differential diagnosis of chronic alcoholism and Korsakoff's disease.
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Madeira, N., T. Santos, and J. L. Pio-Abreu. "Wernicke-Korsakoff Syndrome: A Common Yet Elusive Diagnosis." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)71095-8.

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In 1897, Murawieff proposed that a common cause was responsible for the two syndromes previously described by Carl Wernicke and Sergei Korsakoff. More than 100 years afterwards, the neuropsychiatric nosological entity known as Wernicke-Korsakoff syndrome remains one of the most significant, yet under-recognized, consequences of long-term alcohol abuse.Prompt recognition and treatment of Wernicke's encephalopathy with parenteral thiamine can prevent permanent cognitive impairment, involving severe short-term memory loss - Korsakoff's amnesic syndrome. Such condition has devastating consequences for patients, not infrequently demanding long-term institutionalization.Based on two clinical vignettes, the authors review some epidemiological, clinical and neuropathological features of Wernicke-Korsakoff syndrome, besides issues concerning differential diagnosis, treatment and prognosis.
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Mushtaq, Raheel, Sheikh Shoib, Tabindah Shah, Mudasir Bhat, Randhir Singh, and Sahil Mushtaq. "Unusual Presentation of Uncommon Disease: Anorexia Nervosa Presenting as Wernicke-Korsakoff Syndrome—A Case Report from Southeast Asia." Case Reports in Psychiatry 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/482136.

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Anorexia nervosa presenting as Wernicke-Korsakoff syndrome is rare. The causes of Wernicke-Korsakoff syndrome are multiple like alcohol abuse, thyrotoxicosis, haemodialysis, severe malnutrition because of gastric carcinoma and pyloric obstruction, hyperemesis gravidarum, and prolonged parenteral feeding. We report a case of anorexia nervosa, who presented with Wernicke's encephalopathy and progressed to Korsakoff's syndrome. Knowledge, awareness, and early intervention of anorexia nervosa by mental health professionals can prevent development of Wernicke-Korsakoff syndrome.
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Jacobson, R. R., and W. A. Lishman. "Cortical and diencephalic lesions in Korsakoff's syndrome: a clinical and scan study." Psychological Medicine 20, no. 1 (February 1990): 63–75. http://dx.doi.org/10.1017/s0033291700013234.

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SYNOPSISTwenty-five male alcoholic Korsakoff patients were compared with age and sex-matched non-Korsakoff chronic alcoholics and healthy volunteers on clinical and CT brain scan parameters. The scans were assessed by planimetry, visual grading procedures and computerized analysis. Reliable measures of third ventricular size were developed.The Korsakoff patients had wider third ventricles, larger lateral ventricles and wider interhemispheric fissures than the comparison groups; but sulcal and Sylvian fissure widths were equivalent in Korsakoff and non-Korsakoff alcoholics.The results suggest that, in addition to their well-established diencephalic lesions, many Korsakoff patients have sustained widespread cerebral damage. Shrinkage in the frontal brain regions appears to be especially pronounced. The implications for a dual aetiology of alcoholic Korsakoff's syndrome involving thiamine deficiency and features associated with alcoholism, probably direct alcohol neurotoxicity, are discussed.
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Paller, Ken A., Ananth Acharya, Brian C. Richardson, Odile Plaisant, Arthur P. Shimamura, Bruce R. Reed, and William J. Jagust. "Functional Neuroimaging of Cortical Dysfunction in Alcoholic Korsakoff's Syndrome." Journal of Cognitive Neuroscience 9, no. 2 (March 1997): 277–93. http://dx.doi.org/10.1162/jocn.1997.9.2.277.

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Many neuropsychological investigations of human memory have focused on the amnesic deficits of alcoholic Korsakoff's syndrome. Structural neuroimaging suggests that the syndrome results from midline diencephalic damage, but functional neuroimaging has the potential to reveal additional neuropathology that may be responsible for cognitive dysfunction. Accordingly, high-resolution positron emission tomography (PET) was used to measure regional cerebral metabolic rates for glucose utilization in five alcoholic Korsakoff patients and nine alcoholic control subjects. Results from a continuous recognition test administered during the radiotracer uptake period indicated that all subjects performed normally with respect to immediate memory, whereas Korsakoff patients demonstrated a marked memory impairment in delayed recognition. PET results from the Korsakoff group showed a widespread decline in glucose metabolism in frontal, parietal, and cingulate regions, suggesting that these functional abnormalities in the cerebral cortex contribute to the memory impairment. Hippocampal glucose metabolism did not differ between the groups. Thus, the evidence did not support the hypothesis that parallel brain dysfunctions are responsible for the similar amnesic symptomatology after hippocampal and diencephalic damage. We hypothesize that the amnesic dysfunction of Korsakoff's syndrome depends on a disruption of thalamocortical interactions that mediate a function critical for normal memory storage.
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Oosterman, Joukje M., Maartje de Goede, Arie J. Wester, Martine J. E. van Zandvoort, and Roy P. C. Kessels. "Perspective taking in Korsakoff's syndrome: the role of executive functioning and task complexity." Acta Neuropsychiatrica 23, no. 6 (December 2011): 302–8. http://dx.doi.org/10.1111/j.1601-5215.2011.00552.x.

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Oosterman JM, de Goede M, Wester AJ, van Zandvoort MJE, Kessels RPC. Perspective taking in Korsakoff's syndrome: the role of executive functioning and task complexity.Objective: The ability to make inferences about knowledge, thoughts and feelings of others, i.e. perspective taking, is a key element of social cognition. Clinical observations indicate that Korsakoff patients may have impairments in social cognition, but studies are scarce. Also, executive dysfunction is present in Korsakoff patients, which may hamper perspective taking directly.Methods: Twenty-three patients with Korsakoff's syndrome and 15 healthy matched controls were examined on a story comprehension task, in which inferences had to be made that either relied on perspective taking or not. The effects of task complexity were taken into account and executive function was assessed using an extensive neuropsychological test battery.Results: The performance of Korsakoff patients declined with increasing complexity, but the pattern of decline for perspective-taking and non-perspective-taking stories was similar compared to that of the control group. Furthermore, the performance decline with increasing task complexity was directly related to the overall decline in executive functioning.Conclusion: Executive dysfunction, not deficits in perspective taking per se, appears to underlie difficulties in story comprehension in patients with Korsakoff's syndrome.
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Evers, Kathinka. "Korsakoff Syndrome." International Journal of Applied Philosophy 13, no. 2 (1999): 193–208. http://dx.doi.org/10.5840/ijap199913217.

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Zhou, Yongxing, Derrick Fox, Abhishek Anand, Amal Elhaj, Arushi Kapoor, Faranak Najibi, Han Kim, Roger Weir, and Annapurni Jayam-Trouth. "Artery of Percheron Infarction as an Unusual Cause of Korsakoff’s Syndrome." Case Reports in Neurological Medicine 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/927809.

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The Korsakoff syndrome is defined as “an abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient.” Confabulation refers to false or erroneous memories arising, not deliberately, in the context of a neurological amnesia and is often thought of as pathognomonic of the Korsakoff syndrome. Although the exact pathophysiology is unknown, various studies have identified brain lesions in the thalami, mammillary bodies, and frontal cortex. We report a case of a 68-year-old male presenting with acute altered mental status on July 16, 2015. The neuropsychological dysfunctions included prominent Korsakoff’s syndrome, which became apparent when the altered mental status resolved. Amnesia was accompanied by prominent confabulation, disorientation, and lack of insight into his own disability. Neuroradiological data indicated that the intralaminar and dorsomedial nuclei in bilateral thalami were infarcted by occlusion of the artery of Percheron. We believe that ours is one of few reported cases of Korsakoff syndrome in a patient with infarction involving the territory of the artery of Percheron. We conclude that bilateral thalamic lesions could cause Korsakoff’s syndrome and the intralaminar and dorsomedial nuclei might be important structures in the pathogenesis of confabulation.
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Oyama, Hirofumi, Toshiko Mabuchi, Masahiro Niwa, Yoshihisa Kida, Takayuki Tanaka, Kazuo Yoshida, Takanori Iwakoshi, Ryuji Kitamura, Satoshi Maezawa, and Tatsuya Kobayashi. "Traumatic Korsakoff syndrome." Journal of Clinical Neuroscience 5, no. 4 (October 1998): 441–44. http://dx.doi.org/10.1016/s0967-5868(98)90284-3.

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Dissertations / Theses on the topic "Korsakoff Syndrome"

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Chancellay, Léon. "Contribution à l'étude de la psychose polynévritique thèse pour le doctorat en médecine présentée et soutenue le mercredi 15 mai 1901 /." Paris : BIUM, 2004. http://www.bium.univ-paris5.fr/histmed/medica/cote?TPAR1901x367.

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Konishi, Kyoto. "The cognitive profile of elderly Korsakoff's syndrome patients /." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116028.

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Korsakoff's syndrome (KS) is characterized by the acute onset of a severe anterograde memory impairment and a less pronounced retrograde amnesia. In addition to deficits in memory, executive function, visuo-spatial abilities, and visuo-perception are impaired. The main structures involved in the neuropathology of KS are the mammillary bodies and the thalamus. It is generally assumed that KS is a stable amnesic condition, and little research has been done in studying the effects of aging on the syndrome.
A group of elderly KS patients were evaluated on a large battery of neuropsychological tests to examine general cognitive function, memory, attention, visuo-spatial ability, and executive function. Their performance was compared to age-matched Alzheimer's disease patients and healthy controls. Results showed that there is an interaction between age and KS, with exaggerated deficits seen in memory and executive function, as well as new deficits in semantic memory.
To better understand KS, the thesis provides a review focusing on human, English language studies published between the years 1995 and 2008. Updates on the current findings of treatment and prevention, genetics and prevalence, neuropathology, and neuropsychology including memory and frontal function are provided. In addition, comparison studies of KS to other neurological disorders are summarized.
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Pitel, Anne-Lise. "Les troubles cognitifs dans l'alcoolisme chronique avec et sans syndrome de Korsakoff : analyse neuropsychologique et remédiation cognitive." Caen, 2007. http://www.theses.fr/2007CAEN1494.

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L'objectif de cette thèse était de mieux comprendre les effets de la consommation chronique d’alcool sur la cognition et plus particulièrement sur la mémoire. Les résultats de nos études ont montré, chez les alcooliques non-Korsakoff (AL), une véritable atteinte de la mémoire épisodique, peu liée aux dysfonctionnements exécutifs. Ces troubles neuropsychologiques se normalisaient avec l'abstinence alors que la reprise même limitée de la consommation d’alcool entrainait une dégradation cognitive. Les mêmes composantes de la mémoire épisodique et de la mémoire de travail étaient altérées chez les AL et les patients Korsakoff (SK). Les SK présentaient toutefois des troubles plus sévères de la mémoire épisodique et de certaines fonctions exécutives. Les systèmes esclaves de la mémoire de travail et les autres fonctions exécutives évaluées étaient altérés de manière similaire dans les deux groupes d'alcooliques. Concernant les répercussions de ces troubles cognitifs sur les capacités à acquérir de nouvelles informations complexes, l'apprentissage des catégories et des caractéristiques de nouveaux concepts et de la procédure de résolution de la tour de Toronto était ralenti chez les AL. L'acquisition des noms des concepts, particulièrement difficile, était toutefois possible chez les AL grâce à l'utilisation de l'apprentissage sans erreur. Les capacités d'apprentissage sémantique des SK étaient différemment altérées selon la nature des informations à acquérir. Enfin, le ralentissement de la dynamique d’apprentissage procédural cognitif des SK entrainait l'absence d'automatisation de la procédure, malgré un niveau de performance final équivalent à celui des sujets contrôles
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Roland, Jessica Justine. "Hippocampal and striatal acetylcholine efflux during learning in diencephalic-lesioned rats." Diss., Online access via UMI:, 2005.

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Alexander-Kaufman, Kimberley Louise. "Proteomics of the human alcoholic brain: Implications for the pathophysiology of alcohol-related brain damage." The University of Sydney, 2008. http://hdl.handle.net/2123/2692.

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Doctor of Philosophy (PhD)
Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. These optimized techniques were then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.
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Maillard, Angéline. "Atteintes cognitives et cérébrales dans le trouble de l'usage d'alcool et le syndrome de Korsakoff : valeur pronostique, évolution et prise en charge Prognosis factors of low-risk drinking and relapse in alcohol use disorder : a multimodal analysis Short-term neuropsychological recovery in alcohol use disorder : a retrospective clinical study Is there cognitive and brain changes over time in Korsakoff's syndrome ? Neuropsychological deficits in alcohol use disorder : impact on treatmen The effect of alcohol withdrawal syndrome severity on sleep, brain and cognition." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC017.

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Le trouble de l’usage d’alcool (TUAL) est associé à des atteintes cérébrales et cognitives. Ces altérations empêchent les patients de bénéficier des prises en charges psychosociales et augmentent le risque de rechute. Une réversibilité de ces atteintes est possible avec l’abstinence et a été mise en évidence dans le TUAL. En revanche, les patients présentant un syndrome de Korsakoff (SK) ont une amnésie antérograde sévère qui est considérée comme irréversible, même si l’évolution cognitive et cérébrale de ces patients est peu documentée. L’objectif de cette thèse est donc d’étudier la valeur pronostique, l’évolution ainsi que la prise en charge des atteintes cognitives et cérébrales dans le TUAL et le SK. Nos résultats montrent que l’alexithymie et les altérations des systèmes limbique et fronto-cérébelleux observés post-sevrage sont des facteurs de mauvais pronostic du statut addictologique au cours de l’année post-sevrage. Nous montrons qu’après le sevrage, un court séjour en soins de suite et de réadaptation permet une amélioration, voire même une normalisation des fonctions cognitives. Une prise en charge intensive, incluant des ateliers de stimulation cognitive pendant ce séjour, semble favoriser la récupération. Nos résultats ont mis en évidence que chez les patients SK, les déficits sévères de mémoire épisodique sous-tendus par des altérations du circuit de Papez, persistent avec le temps. Les atteintes des fonctions exécutives et du circuit fronto-cérébelleux peuvent récupérer de manière limitée. Ces résultats soulignent la nécessité d’évaluer les atteintes cognitives et cérébrales ayant une valeur pronostique pour la rechute. Ils indiquent également l’importance d’adapter la prise en charge afin de favoriser la récupération cognitive dans le TUAL ou de compenser les troubles mnésiques persistants et invalidants dans le SK
Alcohol use disorder (AUD) is characterized by brain damage and cognitive deficits. These alterations hinder AUD patients to benefit from psychosocial treatment and increase the risk of relapse. It is now clear that cognitive deficits and brain abnormalities can be reversible with drinking cessation in AUD. However, patients with Korsakoff’s syndrome (KS) are described as exhibiting a severe anterograde amnesia supposed to persist over time, even though longitudinal studies in KS patients are very rare. The objective of this thesis is to examine the prognostic value, changes over time, and rehabilitation of the cognitive impairments and brain alterations in AUD and KS. Our results suggest that alexithymia, as well as alteration of limbic and frontocerebellar systems observed early in abstinence, contribute to a poor prognosis regarding alcohol status within the year following detoxification. We highlight that, after detoxification, a short stay as inpatient in a convalescent home favors cognitive improvement, and even a return to a normal level of performance. During this stay, an intensive care including neuropsychological training seems to favor the recovery. Finally, our results indicate that in KS patients, severe memory impairments, sustained by Papez circuit alterations, persist over time. Executive deficits and damage of the fronto-cerebellar circuit may recover but to a limited extent. These results emphasize the need to assess cognitive and brain alteration that have a prognostic value regarding treatment outcome. Results also encourage adapting treatment to favor recovery in AUD, or to compensate for persisting memory impairments in KS
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Roland, Jessica Justine. "Septohippocampal system modulation in an animal model of diencephalic amnesia." Diss., Online access via UMI:, 2008.

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Laniepce, Alice. "Modifications du sommeil associées à la consommation chronique et excessive d'alcool : liens avec les altérations cérébrales structurales et les troubles cognitifs Neuropsychological and neuroimaging examinations of self‐reported sleep quality in alcohol use disorder with and without Korsakoff's syndrome Sleep architecture and episodic memory performance in alcohol use disorder with and without Korsakoff syndrome The effect of alcohol withdrawal severity on sleep, brain and cognition Dissociating thalamic alterations in alcohol use disorder defines specificity of Korsakoff's syndrome Cerebellar hypermetabolism in alcohol use disorder: compensatory mechanism or maladaptive plasticity ? Alcohol use disorder : permanent and transient effects on the brain and neuropsychological functions Effects of sleep and age on prospective memory consolidation Troubles cognitifs dans l'alcoolodépendance Repérage des troubles cognitifs liés à l’alcool." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMC039.

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En amont du développement de complications neurologiques sévères telles que le syndrome de Korsakoff (SK), les patients présentant un Trouble de l’Usage d’Alcool (TUAL) présentent des altérations cérébrales et cognitives de nature et de sévérité variables, ainsi que des troubles du sommeil. Bien qu’il soit clairement établi que le sommeil contribue au fonctionnement cérébral et cognitif, son implication comme facteur explicatif des atteintes cérébrales et cognitives dans le TUAL reste peu documentée. L’objectif de cette thèse était de préciser les modifications (subjectives et objectives) du sommeil chez les patients TUAL et SK, et leurs liens avec la structure cérébrale et le fonctionnement cognitif. Nos résultats montrent que la plainte de sommeil doit être interprétée au regard de la sévérité des atteintes cérébrales et cognitives chez les patients TUAL et SK. De plus, nous montrons qu’une proportion élevée de patients présentent des apnées du sommeil. Chez les patients SK, une atteinte spécifique du sommeil paradoxal est observée, associée à la sévérité des difficultés mnésiques. Enfin, chez les patients TUAL, nous montrons le rôle particulier de la sévérité du syndrome de sevrage dans l’atteinte du sommeil lent profond, et son impact sur le fonctionnement cérébral et cognitif. Ainsi, il semble exister des similarités et des différences dans l’architecture du sommeil de ces deux formes cliniques (TUAL et SK). Ces modifications de sommeil dépendraient de la sévérité du sevrage et seraient impliquées dans la physiopathologie des atteintes structurales et cognitives liées à l’alcool. Ces résultats soulignent la nécessité d’évaluer et de prendre charge à la fois le sevrage et les modifications du sommeil des patients TUAL afin d’améliorer le pronostic des patients à la sortie des services hospitaliers
Well before the development of severe alcohol-related neurological complications such as Korsakoff’s syndrome (KS), patients with Alcohol Use Disorder (AUD) exhibit variable brain damage and cognitive deficits, as well as sleep disturbances. Although it is well established that sleep contributes to brain and cognitive functioning, its involvement in brain damage and cognitive deficits in AUD remains poorly understood. The objective of this thesis was to investigate subjective and objective sleep quality in AUD and KS patients, and its relationships with brain structure and function. Our results show that sleep complaint must be interpreted with regard to the severity of brain alterations and cognitive impairments in AUD and KS patients. Moreover, we showed a high prevalence of sleep apnea in these patients. REM sleep abnormalities are specifically observed in KS patients and related to the severity of memory deficits. Regarding AUD patients, we highlight the contribution of the severity of withdrawal syndrome in slow wave sleep decrease, and its effects on brain and cognitive functioning. Hence, similarities and differences of sleep architecture have been found in the two clinical forms (AUD and KS). These sleep modifications could depend on the severity of alcohol withdrawal and be involved in the pathophysiology of alcohol-related structural brain damage and cognitive impairment. These results encourage evaluating and managing both alcohol withdrawal and sleep modifications to improve patients’ prognosis at discharge from Addiction department
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Kopelman, Michael D. "Psychological studies of the memory deficits in Alzheimer-type dementia and the alcoholic Korsakoff syndrome, and a comparison with the effect of cholinergic blockade in healthy subjects." Thesis, King's College London (University of London), 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265845.

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Anzalone, Steven J. "Cholinergic cortical dysfunction in an animal model of diencephalic amnesia." Diss., Online access via UMI:, 2009.

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Books on the topic "Korsakoff Syndrome"

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Lévesque, Isabelle. Le syndrome de Korsakoff. Paris: Editions de Minuit, 1994.

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1911-, Adams Raymond D., and Collins George H. 1927-, eds. The Wernicke-Korsakoff syndrome and related neurologic disorders due to alcoholism and malnutrition. 2nd ed. Philadelphia, PA: F.A. Davis Co., 1989.

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Döblin, Alfred. Geda chtnissto rungen bei der Korsakoffschen Psychose. Berlin: Tropen Verlag, 2006.

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Schaade, Gudrun. Ergotherapeutische Behandlungsansätze bei Demenz und dem Korsakow-Syndrom. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-48811-9.

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Schnider, Armin. The history of confabulation. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198789680.003.0002.

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The interest in confabulations has a long history. Starting with Korsakoff’s early reports of pseudo-reminiscences in alcoholic and malnourished patients and Kraepelin’s description of fantastic confabulations in psychosis and syphilis, this chapter examines a rich literature which documented in fine detail the various presentations and causes of confabulations. Korsakoff syndrome was recognized as the combination of amnesia, disorientation, and confabulation. Authors soon distinguished between different forms of confabulation. From the beginning, they speculated about the mechanisms and indeed anticipated most of the currently proposed models. The chapter finishes with a table comparing old and new terminology of the proposed mechanisms.
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Misulis, Karl E., and E. Lee Murray. Nutritional Deficiencies and Toxicities. Edited by Karl E. Misulis and E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0029.

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Nutritional disorders are often encountered in hospital neurology practice, especially deficiencies of vitamins B1 and B12. Medical conditions can predispose to nutritional disorders. This chapter discusses the presentation, diagnosis, and management of B12 deficiency, B1 deficiency, protein-energy malnutrition, folate deficiency especially in the context of pregnancy, B6 deficiency, B6 toxicity, copper deficiency, and vitamin D deficiency. Wernicke encephalopathy and Korsakoff syndrome are also discussed.
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Schnider, Armin. Aetiologies and anatomy of confabulation. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198789680.003.0004.

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What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.
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Das Korsakow-Syndrom - Eine Annäherung: Theorie, Therapie, Praxis, Diskussion. München, Germany: GRIN Verlag, 2010.

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Schaade, Gudrun, and J. Wojnar. Ergotherapeutische Behandlungsansätze bei Demenz und dem Korsakow-Syndrom. Springer, 2016.

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Karen, Bellenir, ed. Alcoholism sourcebook: Basic consumer health information about the physical and mental consequences of alcohol abuse, including liver disease, pancreatitis, Wernicke-Korsakoff syndrome (alcoholic dementia), fetal alcohol syndrome, heart disease, kidney disorders, gastrointestinal problems, and immune system compromise, and featuring facts about addiction, detoxification, alcohol withdrawal, recovery, and the maintenance of sobriety, along with a glossary and directories of resources for further help and information. Detroit: Omnigraphics, 2000.

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Book chapters on the topic "Korsakoff Syndrome"

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Böhm, Markus, Thomas A. Luger, Cem Evereklioglu, Mark Berneburg, Thomas Schwarz, Irene Guerrini, Allan D. Thomson, et al. "Wernicke Korsakoff Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 2239–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3231.

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Sharp, Christopher S., and Kimberly D. Nordstrom. "Wernicke-Korsakoff Syndrome." In Quick Guide to Psychiatric Emergencies, 147–50. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58260-3_27.

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Lafleche, Ginette, and Mieke Verfaellie. "Wernicke-Korsakoff Syndrome." In Encyclopedia of Clinical Neuropsychology, 3716–20. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1164.

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Greenberg, David A., and Ivan Diamond. "Wernicke—Korsakoff Syndrome." In Alcohol and the Brain, 295–314. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_12.

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Lafleche, Ginette, and Mieke Verfaellie. "Wernicke-Korsakoff Syndrome." In Encyclopedia of Clinical Neuropsychology, 2699–702. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1164.

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Lafleche, Ginette, and Mieke Verfaellie. "Wernicke-Korsakoff Syndrome." In Encyclopedia of Clinical Neuropsychology, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1164-2.

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Akhouri, Shweta. "Wernicke–Korsakoff Syndrome." In The Palgrave Encyclopedia of Critical Perspectives on Mental Health, 1–3. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-12852-4_74-1.

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Kunze, Klaus, Michael A. DeGeorgia, and Michael N. Diringer. "Wernicke’s Encephalopathy (Wernicke-Korsakoff Syndrome)." In Neurocritical Care, 840–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87602-8_76.

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Héroux, Maryse, and Roger F. Butterworth. "Animal Models of the Wernicke-Korsakoff Syndrome." In Animal Models of Neurological Disease, II, 95–131. Totowa, NJ: Humana Press, 1992. http://dx.doi.org/10.1385/0-89603-211-6:95.

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Hochhalter, Angela K., Whitney A. Sweeney, Lisa M. Savage, Bruce L. Bakke, and J. Bruce Overmier. "Using animal models to address the memory deficits of Wernicke-Korsakoff syndrome." In Animal research and human health: Advancing human welfare through behavioral science., 281–92. Washington: American Psychological Association, 2001. http://dx.doi.org/10.1037/10441-018.

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Conference papers on the topic "Korsakoff Syndrome"

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Hoblyn, J., Tayler Sulse, Emma Mae Huston, Melanie Ryberg, P. Byrne, and Kieran O’Driscoll. "41 Korsakoff’s syndrome: neurocognitive domains impairments and potential therapeutic interventions." In The British Neuropsychiatry Association – Annual Meeting. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/jnnp-2019-bnpa.41.

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