Function and Dysfunction of Prefrontal Brain Circuitry in Alcoholic Korsakoff’s Syndrome

Abstract

The signature symptom of alcohol-induced persisting amnestic disorder, more commonly referred to as alcoholic Korsakoff’s syndrome (KS), is anterograde amnesia, or memory loss for recent events, and until the mid 20th Century, the putative brain damage was considered to be in diencephalic and medial temporal lobe structures. Overall intelligence, as measured by standardized IQ tests, usually remains intact. Preservation of IQ occurs because memories formed before the onset of prolonged heavy drinking — the types of information and abilities tapped by intelligence tests — remain relatively well preserved compared with memories recently acquired. However, clinical and experimental evidence has shown that neurobehavioral dysfunction in alcoholic patients with KS does include nonmnemonic abilities, and further brain damage involves extensive frontal and limbic circuitries. Among the abnormalities are confabulation, disruption of elements of executive functioning and cognitive control, and emotional impairments. Here, we discuss the relationship between neurobehavioral impairments in KS and alcoholism-related brain damage. More specifically, we examine the role of damage to prefrontal brain systems in the neuropsychological profile of alcoholic KS.

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?

“…There is often concomitant cortical atrophy, especially frontally; and there may be loss of large neurons in the superior frontal cortex, hypothalamus and cerebellum, loss of prefrontal white matter, and neuronal dendritic shrinkage (Victor et al, 1989;Torvik et al, 1982;Harper et al, 1987Harper et al, , 1988Harper and Corbett, 1990;Harper, 2009). The finding of concomitant frontal changes is consistent with the neuropsychological finding of associated executive impairments (Kopelman, 1991;Van Oort and Kessels, 2009;Oscar-Berman, 2012).…”

Neurocognitive, psychosocial and functional status of individuals with alcohol-related brain damage (ARBD) on admission to specialist residential care

“…Therefore, the findings also provide evidence for executive dysfunction in ARBD, which is in line with recent postulations that ARBD is not solely associated with anterograde amnesia (Van Oort and Kessels, 2009;Maharasingam et al, 2013;Brion et al, 2014). The neurocognitive profile observed in this study reflects current knowledge about the structural brain abnormalities that are associated with ARBD, including damage to the brain regions underpinning memory, such as the mammillary bodies, anterior thalamus, mammilothalamic tract and hippocampus, as well as damage to the prefrontal brain circuitry involved in executive functions such as behavioural inhibition (Kril & Harper, 2012;Oscar-Berman, 2012;Zahr, Kaufman & Harper, 2011).…”