The Korsakoff Syndrome: Clinical Aspects, Psychology and Treatment

Kopelman, Michael; Thomson, Allan D.; Guerrini, Irene; Marshall, E. Jane

doi:10.1093/alcalc/agn118

Cited by 389 publications

(302 citation statements)

References 49 publications

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“…; DSM-5; American Psychiatric Association, APA, 2013) alcohol-induced major neurocognitive disorder, as established by neurological, psychiatric, neuroradiological, and neuropsychological examinations. In addition, the criteria for alcoholic Korsakoff's syndrome had to be met: A history of malnutrition or thiamine deficit with evidence of a history of Wernicke encephalopathy, and a disproportionate memory disorder (Kopelman, Thomson, Guerrini, & Marshall, 2009). The disproportionate memory disorder was reflected in the performance of all patients on the CVLT: A total of 98.1% of the participants were impaired (i.e., more than 1.5 standard deviations of the mean) on their overall performance on Trials 1-5, and 94.2% of the participants showed rapid forgetting after delayed testing as compared to a representative norm group.…”

Section: Participantsmentioning

confidence: 99%

Intrusions and provoked and spontaneous confabulations on memory tests in Korsakoff’s syndrome

Rensen

Oosterman

Walvoort

et al. 2016

Journal of Clinical and Experimental Neuropsychology

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Introduction: Intrusions on verbal memory tests have been used as an index for clinical confabulation. Severe memory impairments in combination with executive dysfunction have been suggested to be the underlying mechanism of confabulation, but to date, this relation is unclear. The aim of this study was (a) to examine the relation between (different types of) intrusions and confabulations in a large sample of confabulating patients with Korsakoff's syndrome (KS) and (b) to investigate whether different measures of executive functioning and memory performance are related to provoked and spontaneous confabulation. Method: The Dutch version of the California Verbal Learning Test (CVLT) and various executive function and memory tests were administered to a group of 51 confabulating patients with KS. Professional caregivers rated the severity of provoked and spontaneous confabulation behavior of the patients using the Nijmegen-Venray Confabulation List-20 (NVCL-20). Results: The total number of intrusions on the CVLT was not related to either provoked or spontaneous confabulation scores. None of the CVLT intrusion scores correlated significantly with any of the confabulation scores, but we did find small-to-medium, positive correlations between unrelated intrusions and both provoked confabulations and spontaneous confabulation. Provoked confabulation behavior was associated with executive dysfunction and poorer memory performances. Spontaneous confabulation was not related to performance on measures of executive function and memory. Conclusions: The total number of intrusions on verbal memory tests and clinical confabulations appear to be different phenomena. Only unrelated intrusions produced on the CVLT might possibly be related to confabulations. The production of provoked, but not spontaneous, confabulation is associated with executive dysfunction and memory deficits.

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Section: Participantsmentioning

confidence: 99%

Intrusions and provoked and spontaneous confabulations on memory tests in Korsakoff’s syndrome

Rensen

Oosterman

Walvoort

et al. 2016

Journal of Clinical and Experimental Neuropsychology

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“…All Korskoff patients suffer medial diencephalic pathology that includes the medial mammillary bodies (e.g., Victor et al 1971;Mair et al 1979;Harding et al 2000), and almost every case has severe recognition memory deficits (Aggleton and Shaw 1996). There remains, however, the problem that in this condition there is often additional pathology outside the diencephalon (Victor et al 1971;Kopelman et al 2009). Consequently, it is necessary to focus on those very few cases of diencephalic amnesia, including Korsakoff's syndrome, where the pathology seems confined to the diencephalon and where specific recognition memory deficits have been established.…”

Section: Does Selective Diencephalic Pathology Impair Recognition Memmentioning

confidence: 99%

“…Some cases with the poorest recognition memory are those with Korsakoff's syndrome. In this disorder, there is often both cell loss in multiple diencephalic sites and extensive cortical dysfunction (e.g., Kopelman et al 2009). 4.…”

Section: Toward a Model Of Diencephalic Contributions To Recognition mentioning

confidence: 99%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

137

111

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Both clinical investigations and studies with animals reveal nuclei within the diencephalon that are vital for recognition memory (the judgment of prior occurrence). This review seeks to identify these nuclei and to consider why they might be important for recognition memory. Despite the lack of clinical cases with circumscribed pathology within the diencephalon and apparent species differences, convergent evidence from a variety of sources implicates a subgroup of medial diencephalic nuclei. It is supposed that the key functional interactions of this subgroup of diencephalic nuclei are with the medial temporal lobe, the prefrontal cortex, and with cingulate regions. In addition, some of the clinical evidence most readily supports dual-process models of recognition, which assume two independent cognitive processes (recollective-based and familiarity-based) that combine to direct recognition judgments. From this array of information a "multi-effect multinuclei" model is proposed, in which the mammillary bodies and the anterior thalamic nuclei are of preeminent importance for recollective-based recognition. The medial dorsal thalamic nucleus is thought to contribute to familiarity-based recognition, but this nucleus, along with various midline and intralaminar thalamic nuclei, is also assumed to have broader, indirect effects upon both recollective-based and familiarity-based recognition.Clinical studies repeatedly show that diencephalic pathology can impair recognition memory. Even so, there is no agreed locus within the diencephalon responsible for this memory loss and, hence, no agreed mechanism to explain the impairment. The present review examines both clinical and animal findings, and from this information a multi-effect multi-nuclei (MEMN) model emerges to explain the contributions of the diencephalon to recognition memory.At the outset, it is necessary to refine the focus of this review and to define some of its principal terms. The diencephalon comprises the thalamus and hypothalamus but, as will be explained, only the more medial parts of the diencephalon will be considered in detail. Recognition memory refers to the ability to detect whether a stimulus (e.g., a word, face, picture, object, or sound) has previously been encountered. As a consequence, this review is not about item identification (sometimes also confusingly referred to as recognition). Likewise, conditions that have broad disruptive effects on cognition, e.g., dementia, will not be considered even though recognition is typically impaired. Distinctions will be made between "item recognition," where the task is to determine if an individual item is novel or familiar, and "associative recognition," where all the individual items being experienced are familiar, but their particular combination is novel. A further, distinct ability is "recency" discrimination-the ability to determine which of two familiar stimuli has been experienced more recently. Both studies of amnesia and electrophysiological recordings show how recency memory and recogniti...

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“…The natural history of this syndrome presents two different stages: a) the Wernicke's Encephalopathy (WE), the acute phase of the syndrome which needs a prompt treatment by the reintegration of thiamine and b) the Korsackoff's psychosis, considered the chronic evolution of the neurological condition [1]. The majority of the clinical cases are related to a persistent alcoholic abuse [2], but it is not infrequent to find cases nonalcohol dependent [3].…”

Section: Introductionmentioning

confidence: 99%

“…The WE is characterized by a classic triad: encephalopathy, oculomotor dysfunction and gait ataxia. Rarely the whole triad is present in the same patient [1,5]. Therefore, the clinical diagnosis is hard; as a consequence, the syndrome is still significantly missed.…”

Section: Introductionmentioning

confidence: 99%

Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

Becilli¹,

Pagano²,

Mallio³

et al. 2017

J Blood Lymph

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Wernicke-Korsackoff Syndrome is a potentially fatal neurological complication caused by a deficiency of thiamine. The clinical diagnosis is a challenge and the syndrome is frequently misdiagnosed. In this paper we describe the case of a young man affected by T-ALL and ileotyphlitis who developed Wernicke's Encephalopathy after a month of total parenteral nutrition. Neurological symptomatology, consisting of confusion, nystagmus on lateral gaze, impairment of consciousness state, prosopagnosia and weakness in the four limbs, appeared progressively. An MRI of brain permitted to confirm the diagnosis and high-dose thiamine reintegrating therapy was started obtaining complete resolution of the syndrome.

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The Korsakoff Syndrome: Clinical Aspects, Psychology and Treatment

Cited by 389 publications

References 49 publications

Intrusions and provoked and spontaneous confabulations on memory tests in Korsakoff’s syndrome

Intrusions and provoked and spontaneous confabulations on memory tests in Korsakoff’s syndrome

Unraveling the contributions of the diencephalon to recognition memory: A review

Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

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