What is the Korsakoff syndrome? - a paper in tribute to Prof Alwyn Lishman.

INTRODUCTION: Alwyn Lishman was interested in how memory research could be applied to clinical psychiatry. After a brief review of his major contributions, this paper will focus on his research on the alcoholic Korsakoff syndrome. It will consider how his findings relate to contemporary debates, particularly on how the syndrome should be defined, and its relationship to broader alcohol-induced cognitive impairments. METHODS: A review of the contribution of Alwyn Lishman, Robin Jacobson and colleagues to our knowledge of Korsakoff's syndrome, together with a review of the pertinent recent literature. RESULTS: Lishman and colleagues followed earlier authors in defining the Korsakoff syndrome in terms of disproportionate memory impairment, but they also noted a variable degree of IQ, frontal-executive, and timed visuo-spatial impairment in their cases. More recent authors have included such features in their definitions of the syndrome. Lishman also argued for a specific "alcoholic dementia". The present paper argues that recent definitions of the Korsakoff syndrome confound its core and associated features, and also fail to recognise the multifactorial basis of alcohol-related brain damage. CONCLUSIONS: Korsakoff's syndrome is best defined in terms of disproportionate memory impairment, and more widespread cognitive impairment is best encompassed within "alcohol-related brain damage".

Capacidad de predicción del inventario de temperamento y carácter de Cloninger (TCI-R) en la evolución de los trastornos por uso de alcohol / Predictive Capacity of Cloninger’s temperament and character inventory (TCI-R) in alcohol use disorder outcomes

Objetivo: se pretende investigar la capacidad de predicción del inventario de temperamento y carácter de Cloninger (TCI-R) en la evolución de los trastornos por uso de alcohol. Metodología: Es un estudio longitudinal de 237 pacientes con trastornos por uso de alcohol, en tratamiento ambulatorio y seguimiento durante seis meses, cuya personalidad fue estudiada mediante el inventario TCI-R. Se analizó la puntuación de cada una de las dimensiones del inventario TCI-R en función de su situación (retención o abandono) al final del estudio. Resultados: La muestra presentaba puntuaciones elevadas en búsqueda de novedad (BN) y evitación del daño (ED) y baja en autodirección (AD), definidas, estas últimas, como prominentes. El grupo que abandonó presentaba una puntuación significativamente (p= .004) más elevada en búsqueda de novedad (BN) que el grupo en seguimiento; además cuando la puntuación era superior al percentil 67 la probabilidad de abandonar era 1,07 veces superior. Conclusiones: El inventario de temperamento y carácter de Cloninger (TCI-R) es un buen instrumento para predecir la evolución de los pacientes con trastorno por uso de alcohol y la dimensión búsqueda de novedad (BN) está fuertemente relacionada con el abandono terapéutico

Objective: to investigate the ability to predict the outcome of alcohol use disorders through Cloninger’s temperament and character inventory (TCI-R). Methods: this is a prospective study consisting of 237 outpatients with alcohol use disorders who underwent follow-up treatment for 6 months and whose personality traits were studied using TCI-R. At the end of that period, the scores of each TCI-R trait were analyzed in terms of those who remained in treatment and those who dropped out. Results: The whole group scored highly in novelty seeking (NS) and harm avoidance (HA) and produced low scores in self-directedness (SD), these last traits are considered prominent. The drop-out group scored significantly (p=.004) higher in novelty seeking (NS) than the follow-up group. Also, when the score was higher than the 67 percentile the likelihood of abandoning the treatment was 1.07 times higher. Conclusions: Cloninger’s temperament and character inventory is a good instrument to predict the outcome of treatment of patients with alcohol use disorders and the novelty seeking (NS) dimension is strongly related to therapeutic drop-out

What does a comparison of the alcoholic Korsakoff syndrome and thalamic infarction tell us about thalamic amnesia?

In this review, the clinical, neuropsychological, and neuroimaging findings in the alcoholic Korsakoff syndrome and in thalamic amnesia, resulting from focal infarction, are compared. In both disorders, there is controversy over what is the critical site for anterograde amnesia to occur-damage to the anterior thalamus/mammillo-thalamic tract has most commonly been cited, but damage to the medio-dorsal nuclei has also been advocated. Both syndromes show 'core' features of an anterograde amnesic syndrome; but retrograde amnesia is generally much more extensive (going back many years or decades) in the Korsakoff syndrome. Likewise, spontaneous confabulation occurs more commonly in the Korsakoff syndrome, although seen in only a minority of chronic cases. These differences are attributed to the greater prevalence of frontal atrophy and frontal damage in Korsakoff cases.

Pellagra encephalopathy in the context of alcoholism: review and case report.

AIMS: The aim of the study was to review and describe the Alcoholic Pellagra Encephalopathy, a severe neuropsychiatric condition caused by a combination of niacin (vitamin B3) deficiency and alcohol abuse. METHODS: PsychInfo, Medline and Embase databases were searched for peer-reviewed studies addressing this illness. RESULTS: A historical and conceptual review of the psychopathological aspects of this condition is offered, followed by the report of a patient with a history of chronic alcohol consumption showing signs of pellagra, delusions and visual hallucinations, which was treated successfully with niacin. CONCLUSION: Pellagra encephalopathy should still be considered in the differential diagnosis of acute psychotic disorders seen in the context of chronic alcoholism.

Daño cerebral relacionado con el alcohol. Situación actual y llamada a la acción / Alcohol related brain damage. State of the art and a call for action

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Signs of preclinical Wernicke's encephalopathy and thiamine levels as predictors of neuropsychological deficits in alcoholism without Korsakoff's syndrome.

The purpose of this study was to determine whether meeting historical criteria for unsuspected Wernicke's encephalopathy (WE), largely under-diagnosed in vivo, explains why some alcoholics have severe neuropsychological deficits, whereas others, with a similar drinking history, exhibit preserved performance. Demographic, clinical, alcohol related, and neuropsychological measures were collected in 56 abstinent alcoholics and 38 non-alcohol-dependent volunteers. Alcoholics were classified using the clinical criteria established by Caine et al (1997) and validated in their neuropathological study of alcoholic cases. Our alcoholics who met a single criterion were considered 'at risk for WE' and those with two or more criteria with 'signs of WE'. Whole blood thiamine was also measured in 22 of the comparison group and 28 alcoholics. Of the alcoholics examined, 27% met no criteria, 57% were at risk for WE, and 16% had signs of WE. Neuropsychological performance of the alcoholic subgroups was graded, with those meeting zero criteria not differing from controls, those meeting one criterion presenting mild-to-moderate deficits on some of the functional domains, and those meeting two or more criteria having the most severe deficits on each of the domains examined. Thiamine levels were selectively related to memory performance in the alcoholics. Preclinical signs of WE can be diagnosed in vivo, enabling the identification of ostensibly 'uncomplicated' alcoholics who are at risk for neuropsychological complications. The graded effects in neuropsychological performance suggest that the presence of signs of WE explains, at least partially, the heterogeneity of alcoholism-related cognitive and motor deficits.

Do amnesic patients with Korsakoff's syndrome use feedback when making decisions under risky conditions? An experimental investigation with the Game of Dice Task with and without feedback.

We investigated the role of feedback processing in decision making under risk conditions in 50 patients with amnesia in the course of alcoholic Korsakoff's syndrome (KS). Half of the patients were administered the Game of Dice Task (GDT) and the remaining 25 patients were examined with a modified version of the GDT in which no feedback was provided. Patients' results in the GDT and in the modified version were compared with that of 50 healthy subjects of whom 25 subjects performed the original GDT and 25 performed the modified version. While performance on the original GDT was superior to performance on the modified GDT in healthy subjects, KS patients performed similarly on both the GDT with and GDT without feedback. Performance on both task versions was correlated with categorization and set-shifting. The findings indicate that amnesic patients do not profit from receiving feedback for their decisions in explicit risk conditions.

Confabulations in alcoholic Korsakoff patients.

Besides forgetting, memory is also prone to distortions, errors and illusions. Confabulation is one type of memory distortion that may occur in cases of brain damage. Although confabulations are described anecdotally in patients with alcoholic Korsakoff syndrome (KS), there are few systematic investigations of the presence and nature of these types of false memories in KS. Moreover, it is unclear whether KS patients' confabulations evenly affect all types of memories, or whether certain memory domains are more susceptible. Our study attempted to clarify two questions: first, whether confabulations are a critical feature of the cognitive impairment associated with long-term KS in a large sample of patients (N=42). Second, we investigated which memory domain is most likely affected by confabulations in KS. To elicit confabulations, we used a Confabulation Interview containing questions from different memory domains. We found that KS patients overall confabulated more compared to a group of healthy subjects. Furthermore, we found that patients confabulated most within the episodic/autobiographical memory domain. Our results imply that besides pronounced memory deficits typically associated with KS, confabulation can also be regarded as a clinical feature of the disease. The preponderance of episodic confabulation obtained here by using a standardized test, confirms anecdotic reports that KS patients confabulate in everyday life mainly with respect to their personal past and present. Thus, for a detailed description of the memory profile of KS patients, the screening of confabulation tendencies may be a useful supplementary clinical tool.

Memory deficits among alcoholics: performance on a selective reminding task.

This article compared alcoholics and healthy controls on the Buschke Selective Reminding Task. Alcoholics demonstrated deficits in memory and learning when compared to healthy controls, even when controlling for age. Examination of the alcoholic sample initially showed that age predicted memory deficits; however, age was no longer a significant predictor once the number of years of heavy drinking was entered into the regression equation. Findings suggest a direct link or mechanism of action between alcohol use and memory impairments, above and beyond effects of age or education.

De la calle a su país: una reflexión sobre el papel facilitador de las nuevas tecnologías / For the street to her country: a reflection onthe facilitating role of new technologies

Se presenta el caso de una paciente inmigrante ingresada en la Unidad de Agudos de Psiquiatría con un trastorno amnésico alcohólico, deficiente dominio del castellano y nulo apoyo social, en el que las nuevas tecnologías y la informatización en la asistencia sanitaria resultan determinantes para una resolución satisfactoria

We present a case of an inmigrant inpatient diagnosed of alcoholic amnestic disorder, with deficient use of Spanish languaje and lack of social support, in which new technologies and computerization in health care are determining for satisfactory outcome

Dissociation of remote and anterograde memory impairment and neural correlates in alcoholic Korsakoff syndrome.

Alcoholic Korsakoff's syndrome (KS) is marked by remote memory impairment together with characteristic profound anterograde memory deficits. Despite previous studies of memory processes in KS, questions remain regarding the nature and severity of these impairments and identification of brain systems that underlie these different memory impairments. This study examined remote and anterograde memory function in 5 KS patients in comparison with 8 patients with Alzheimer's disease (AD) and 24 normal control subjects (NC). In addition, relationships between memory performance and regional brain volumes were examined in the KS group. Overall, the KS group showed severe impairment on both remote and anterograde memory measures, performing at the level of the AD group on most measures. Differences were observed on the pattern of temporal gradient for verbal recognition, with KS exhibiting a more steeply graded rate of decline over the most recent period examined. Severity of the remote memory deficit in KS was not associated with severity of anterograde memory deficit. Examination of brain structure-function relationships in the KS subjects revealed that photo naming of remote historical information was related to posterior cortical white matter volumes but not hippocampal volumes; sequencing was related to prefrontal but not hippocampal volumes. By contrast, a measure of anterograde memory for nonverbal visual material showed a relationship to hippocampal but not regional cortical white matter volumes. This set of dissociations, which parallels that observed in our earlier study of AD, is now documented in KS and provides further evidence that these separate cortical and limbic brain systems are principal neural substrates of the remote and anterograde memory and sequencing deficits in KS.

Cognitive impairment in substance abuse.

Conventional wisdom, and even well-reasoned theoretical mechanisms, suggests that the chronic use of psychoactive substances would impair cognitive functioning of individuals. This article summarizes the research literature with regard to specific drugs of abuse. Undoubtedly, acute intoxication and immediate and protracted withdrawal produce transient alterations of cognitions that can persist for weeks to months. Some subtle residual effects remain for up to 1 year for certain drugs. Evidence of irreversible effects is less clear. Even subtle lingering effects can impact treatment efforts, yet they often go undetected or unaddressed.

Hippocampal volume deficits in alcoholic Korsakoff's syndrome.

OBJECTIVE: To examine whether the amnesic syndrome of alcoholic Korsakoff's syndrome (KS) originates from pathology of the hippocampus and not solely the diencephalon. METHODS: The authors studied 5 patients with KS and two comparison groups: 20 patients with Alzheimer's disease (AD) with known bilateral hippocampal volume loss and 36 healthy control subjects. The authors used quantitative MRI to characterize the hippocampus and comparison brain structures (temporal cortex, lateral ventricles, temporal horns, and third ventricle). RESULTS: Relative to healthy control subjects, the KS and AD groups had comparable, significant bilateral hippocampal volume deficits. Although both patient groups also had extensive volume abnormalities in temporal lobe cortical gray matter, temporal horns, and lateral and third ventricles, declarative memory test performance was selectively related to hippocampal volumes in KS and not to any of the comparison volumes. CONCLUSIONS: The characteristic memory deficit of Korsakoff's syndrome involves hippocampal and diencephalic pathology.

Word familiarity influences word-stem completion in amnesic patients.

The effect of familiarity to word-stem completion priming in amnesic patients was studied. A smaller priming effect of low familiarity of words in amnesic patients indicated that the process of lexical access may be involved in word-stem completion in amnesic patients.

The assessment of cognitive procedural learning in amnesia: why the tower of Hanoi has fallen down.

The Tower of Hanoi has been widely accepted as an evaluation of cognitive procedural learning in amnesia but inconsistent findings have raised questions about the nature of the learning process involved in this task. This article presents the performance of a hippocampal amnesic, MS, who, showing poor learning across daily sessions of a formal evaluation, subsequently solved the puzzle through spontaneous use of a declarative-level strategy (the odd-even rule), suggesting that his primary approach to the task was the deployment of declarative solution-searching strategies. The presented data suggest normal learning within daily sessions, but subnormal learning across daily sessions due to the forgetting of acquired declarative information. It is suggested that tasks that are potentially solvable by an algorithm or rule, as is the Tower of Hanoi, be regarded as inappropriate for use in cognitive procedural assessments.

When true recognition suppresses false recognition: evidence from amnesic patients.

False recognition occurs when people mistakenly claim that a novel item is familiar. After studying lists of semantically related words, healthy controls show extraordinarily high levels of false recognition to nonstudied lures that are semantic associates of study list words. In previous experiments, we found that both Korsakoff and non-Korsakoff amnesic patients show reduced levels of false recognition to semantic associates, implying that the medial temporal/diencephalic structures that are damaged in amnesic patients are involved in the encoding and/or retrieval of information that underlies false recognition. These data contrast with earlier results indicating greater false recognition in Korsakoff amnesics than in control subjects. The present experiment tests the hypothesis that greater or lesser false recognition of semantic associates in amnesic patients, relative to normal controls, can be demonstrated by creating conditions that are more or less conducive to allowing true recognition to suppress false recognition. With repeated presentation and testing of lists of semantic associates, control subjects and both Korsakoff and non-Korsakoff amnesics showed increasing levels of true recognition across trials. However, control subjects exhibited decreasing levels of false recognition across trials, whereas Korsakoff amnesic patients showed increases across trials and non-Korsakoff amnesics showed a fluctuating pattern. Consideration of signal detection analyses and differences between the two types of amnesic patients provides insight into how mechanisms of veridical episodic memory can be used to suppress false recognition.

The nucleus basalis (Ch4) in the alcoholic Wernicke-Korsakoff syndrome: reduced cell number in both amnesic and non-amnesic patients.

BACKGROUND: The cholinergic nucleus basalis (Ch4) is an exclusive site of neurofibrillary degeneration in alcoholic patients with Wernicke's encephalopathy. AIM: To test the hypothesis that the loss of Ch4 neurons contributes to the memory disorder, Korsakoff's psychosis, commonly seen in Wernicke's encephalopathy. METHODS: Magnocellular basal forebrain neurons were quantified in alcoholic patients with Wernicke's encephalopathy, both with and without Korsakoff's psychosis, and neurologically asymptomatic alcoholic and non-alcoholic controls. Because amnesic and non-amnesic patients with Wernicke's encephalopathy share common periventricular lesions, both thiamine deficient groups as well as alcoholic patients with no neurological complications were included to determine the lesion specific to memory impairment. RESULTS: Ch4 cell number did not differ significantly between alcoholic and non-alcoholic controls and there was no correlation between cell number and lifetime alcohol intake. However, Ch4 cell number in all groups was significantly correlated with the volume of its major projection target, the cerebral cortex. Ch4 cell number in the non-amnesic Wernicke's encephalopathy group was significantly below controls (24%), with cell number in patients with Korsakoff's psychosis 21% below controls. There was considerable overlap in cell number between groups. On discriminant analysis, there was significantly greater cell loss in three non-amnesic patients with Wernicke's encephalopathy than in some patients with Korsakoff's psychosis. The nonamnesic patient with the greatest cell loss was impaired on attentional tasks. CONCLUSION: Whereas neurons in the nucleus basalis are at risk in thiamine deficient alcoholic patients, cell loss is minor and does not account for the profound memory disorder.

[Pyloric stenosis complicated by Wernicke-Korsakoff syndrome]. / Estenosis pilórica complicada con el síndrome de Wernicke-Korsakoff.

The Wernicke-Korsakoff syndrome (WKS) is a picture of oculomotor alterations, ataxia and confusion presented in chronic alcoholics. It has more rarely been described in non alcoholic patients with malnutrition. The case of a patient with ulcerous peptic disease of long evolution who consulted for a picture compatible with WKS following clinical manifestations of repeated vomiting secondary to complete pyloric stenosis is presented. The peculiarity of the picture and the convenience of prevention in malnourished patients receiving intravenous glucose sera is discussed.

Apolipoprotein E epsilon 4 allele distribution in Wernicke-Korsakoff syndrome with or without global intellectual deficits.

Recent genetic studies show that the apolipoprotein E (ApoE) epsilon 4 allele is a risk factor for Alzheimer's disease (AD). Whether this allele is associated with other dementing diseases is the next important question. The information could provide a clue to the pathogenetic role of ApoE. In the present study, patients with Wernicke-Korsakoff syndrome (WKS) of alcoholic etiology were divided into two groups according to the severity of intellectual deficits, i.e., those of "classical" Korsakoff patients with preserved intellectual function other than amnesia and those with global intellectual deficits. Genotyping showed that the frequency of ApoE epsilon 4 allele was significantly higher in the patients with global deficits, suggesting the involvement of this allele in the intellectual decline of WKS. In contrast, distributions of other two markers, alpha 1-antichymotrypsin and presenilin-1, did not differ between the two groups. These results added further support to the notion that the consequence of acute insult to the brain is influenced by the ApoE genotype, and suggested ApoE's role in the development of a certain group of "alcoholic dementia."