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.

Figure 1

Component processes of memory. In KS, declarative (explicit) memory components (in the red box) are impaired while nondeclarative (implicit) memory components (in the green box) are relatively spared. This review focuses on anterograde episodic memory processes.

Figure 2

A number of theories have been proposed to identify the principal mechanisms responsible for the amnesia of KS.

Figure 3

Gray matter brain abnormalities in Korsakoff syndrome (KS), ′uncomplicated′ alcoholism (AL), and shared between KS and AL. Brain data were collected on a high-resolution T1-weighted MRI (1.5-T Signa Advantage Echospeed; General Electric) and analyzed according to the VBM5 toolbox (SPM5; Wellcome Department of Cognitive Neurology, Institute of Neurology, London, UK). Gray matter volumes in 11 patients with KS and 34 patients with AL were compared with 25 control subjects (corrected for False Discovery Rate, p<0.05). Gray matter abnormalities in KS compared with control subjects are reported in red, those in AL in yellow, and the overlap between the patterns of brain volume deficits on the two groups in orange. Brain regions involved in episodic memory, including medial temporal lobes, thalami, mammillary bodies and cingulate gyri are damaged in both patient groups. Quantitatively, the thalami and mammillary bodies were more severely damaged in KS than in AL. See Pitel et al. 2012 for more details.