Anterograde Episodic Memory in Korsakoff Syndrome

Abstract

A profound anterograde memory deficit for information, regardless of the nature of the material, is the hallmark of Korsakoff syndrome, an amnesic condition resulting from severe thiamine (vitamin B1) deficiency. Since the late nineteenth century when the Russian physician, S. S. Korsakoff, initially described this syndrome associated with “polyneuropathy,” the observed global amnesia has been a primary focus of neuroscience and neuropsychology. In this review we highlight the historical studies that examined anterograde episodic memory processes in KS, present a timeline and evidence supporting the myriad theories proffered to account for this memory dysfunction, and summarize what is known about the neuroanatomical correlates and neural systems presumed affected in KS. Rigorous study of KS amnesia and associated memory disorders of other etiologies provide evidence for distinct mnemonic component processes and neural networks imperative for normal declarative and nondeclarative memory abilities and for mnemonic processes spared in KS, from whence emerged the appreciation that memory is not a unitary function. Debate continues regarding the qualitative and quantitative differences between KS and other amnesias and what brain regions and neural pathways are necessary and sufficient to produce KS amnesia.

Salient cues improve prospective remembering in Korsakoff's syndrome

“…Planned contrasts showed that, as expected, Korsakoff individuals' PM significantly improved when highly salient cues were presented; supporting assumptions that salient cues may indeed automatically attract attention, prompt retrieval of the delayed intention, and facilitate switching to the PM task as postulated by the multiprocess framework of prospective remembering . Our findings clearly show that memory performance in Korsakoff's syndrome is moderated by executive control demands, which is in line with previous evidence showing a relation between executive function impairments and memory deficits (Fama, Pfefferbaum, & Sullivan, 2004;Oscar-Berman, 2012). Importantly, memory load was comparable across both salience conditions; with both conditions requiring participants to remember one target picture (cat or dog) and one action (press the pink button).…”

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

“…An important point is that non-Korsakoff alcoholics also exhibit thalamic and cortical changes and they show a range of neuropsychological impairments. However, Korsakoff patients exhibit disproportionate deficits at episodic memory tasks (Butters and Cermak, 1980;Pitel et al, 2008;Fama et al, 2012), consistent Victor et al's (1971) …”

The neurobiology of thalamic amnesia: Contributions of medial thalamus and prefrontal cortex to delayed conditional discrimination

“…2). It should be noted that while these tasks allow for direct comparison of animal and human performance for functions spared and impaired by amnesia, they by no means represent the full range of cognitive functions affected by WKS (Butters and Cermak, 1980;Fama et al, 2012;Oscar-Berman, 2012;Talland, 1965).…”