Abstract

Korsakoff’s syndrome (KS) is a chronic neuropsychiatric disorder caused by alcohol abuse and thiamine deficiency. Patients with KS show restricted autonomy due to their severe declarative amnesia and executive disorders. Recently, it has been suggested that procedural learning and memory are relatively preserved in KS and can effectively support autonomy in KS. In the present review we describe the available evidence on procedural learning and memory in KS and highlight advances in memory rehabilitation that have been demonstrated to support procedural memory. The specific purpose of this review was to increase insights in the available tools for successful memory rehabilitation and give suggestions how to apply these tools in clinical practice to increase procedural learning in KS. Current evidence suggests that when memory rehabilitation is adjusted to the specific needs of KS patients, this will increase their ability to learn procedures and their typically compromised autonomy gets enhanced.

Highlights

  • Korsakoff’s syndrome (KS) is a chronic neuropsychiatric disorder that is caused by thiamine deficiency

  • The aim of the present review was to give an overview of procedural learning and memory in KS to disentangle what processes are preserved

  • The currently available evidence suggests that patients with KS are able to learn procedures, the extent of learning is highly task dependent

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Summary

Introduction

Korsakoff’s syndrome (KS) is a chronic neuropsychiatric disorder that is caused by thiamine deficiency. The most common cause of thiamine deficiency is alcoholism, with around 90 % of the deficiencies associated with alcohol abuse (Harper et al 1986; Thomson et al 2002; Kopelman et al 2009). Around 15 % of the chronic alcoholics have neurological signs of KS (Kril and Harper 2012). In KS, there is a temporally-graded memory deficits for remote memory (retrograde amnesia) which characteristically extends back many years or decades (Kopelman et al 1999). The cognitive problems in KS are caused by diencephalic atrophy of the brain, with damage to the anterior nucleus of the thalamus, the mammillary bodies and the corpus callosum as the most common features of KS that are not caused by the direct neurotoxic effects of alcohol (see Fig. 1 for the anatomical localization of the most common brain abnormalities in KS). (Paller et al 1997; Kopelman 1995; Kopelman 2002; Sullivan and Pfefferbaum 2009; Kril and Harper 2012; Pitel et al 2012; Jung et al 2012)

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