In this review, we present a survey on Korsakoff’s syndrome (KS), a residual syndrome in patients who suffered from a Wernicke encephalopathy (WE) that is predominantly characterized by global amnesia, and in more severe cases also by cognitive and behavioral dysfunction. We describe the history of KS and its definition, its epidemiology, and the lack of consensus criteria for its diagnosis. The cognitive and behavioral symptoms of KS, which include anterograde and retrograde amnesia, executive dysfunction, confabulation, apathy, as well as affective and social-cognitive impairments, are discussed. Moreover, recent insights into the underlying neurocognitive mechanisms of these symptoms are presented. In addition, the evidence so far on the etiology of KS is examined, highlighting the role of thiamine and alcohol and discussing the continuity hypothesis. Furthermore, the neuropathology of KS is reviewed, focusing on abnormalities in the diencephalon, including the mammillary bodies and thalamic nuclei. Pharmacological treatment options and nonpharmacological interventions, such as those based on cognitive rehabilitation, are discussed. Our review shows that thiamine deficiency (TD) is a crucial factor in the etiology of KS. Although alcohol abuse is by far the most important context in which TD occurs, there is no convincing evidence for an essential contribution of ethanol neurotoxicity (EN) to the development of WE or to the progression of WE to KS. Future research on the postmortem histopathological analysis of brain tissues of KS patients is crucial for the advancement of our knowledge of KS, especially for associating its symptoms with lesions in various thalamic nuclei. A necessary requirement for the advancement of studies on KS is the broad acceptance of a comprehensive definition and definite diagnostic criteria. Therefore, in this review, we propose such a definition of KS and draft outlines for prospective diagnostic criteria.

Introduction and Aims Cognitive impairments in substance use disorder predict treatment outcome and are assumed to differ between substances. They often go undetected, thus the current study focuses on the prevalence of and differences in cognitive functioning across substances by means of a cognitive screen at the early stage of addiction treatment. Design and Methods The Montreal Cognitive Assessment was administered to outpatients seeking treatment for substance use disorder. Patient characteristics (age, years of regular use, polysubstance use, severity of dependence/abuse, depression, anxiety and stress) were also taken into account. Results A total of 656 patients were included (n = 391 used alcohol, n = 123 used cannabis, n = 100 used stimulants and n = 26 used opioids). The prevalence of cognitive impairments was 31%. Patients using alcohol had a lower total‐ and memory domain score than those using cannabis. Patients using opioids scored lower on visuospatial abilities than those using cannabis or stimulants. Younger patients scored higher than older patients. No effect was found for the other investigated characteristics. Discussion and Conclusions Given the high prevalence of cognitive impairments, standard screening at an early stage of treatment is important to determine the course of treatment and maximise treatment outcome. Caution is needed in interpreting results about opioids due to an underrepresentation of this patient group, and more research is needed on the effect of age on Montreal Cognitive Assessment performance.

Objectives: The Montreal Cognitive Assessment (MoCA) is a cognitive screen, available in three alternate versions. Aims of the current study were to examine the effects of age, education and intelligence on MoCA performance and to determine the alternate-form equivalence and test-retest reliability of the MoCA, in a group of healthy participants. Method: In 210 participants, two MoCA versions and an estimator for premorbid intelligence were administered at two time points. Results: Age, education and estimated premorbid intelligence correlated significantly with the total score (MoCA-TS) and the Memory Index Score (MoCA-MIS). Systematic differences between MoCA version 7.1 and alternate versions 7.2 and 7.3 were only found for the items animal naming, abstract reasoning and sentence repetition. Test-retest reliability of the MoCA-TS was good between 7.1 and 7.2 (ICC: 0.64) and excellent between 7.1 and 7.3 (ICC: 0.82). For the MoCA-MIS, coefficients were poor (ICC: 0.32) to fair (ICC: 0.48), respectively. Conclusion: Adequate norms are needed that take the effects of age, education and intelligence on MoCA performance into account. All three MoCA versions are largely equivalent based on MoCA-TS and the test-retest reliabilities show that this score is suitable to monitor cognitive change over time. Comparisons of the domain-specific scores should be interpreted with caution. KEY POINTS The MoCA total score is a reliable cognitive measure. All three MoCA versions are largely equivalent. Age, education and intelligence are predictors of MoCA performance in healthy participants. Future studies should focus on collecting normative data for age, education and intelligence for use in clinical practice.