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.
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.
- Content Type Journal Article
- Category Review
- Pages 1-12
- DOI 10.1007/s11065-012-9207-0
- Authors
- Rosemary Fama, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine (MC5723), 401 Quarry Road, Stanford, CA 94305-5723, USA
- Anne-Lise Pitel, INSERM, U1077, 14033 Caen, France
- Edith V. Sullivan, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine (MC5723), 401 Quarry Road, Stanford, CA 94305-5723, USA
- Journal Neuropsychology Review
- Online ISSN 1573-6660
- Print ISSN 1040-7308