Alcoholic Korsakoff’s Syndrome

Evert, Denise L.

doi:10.1007/978-1-4899-1857-4_14

Cited by 16 publications

(21 citation statements)

References 63 publications

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“…Chronic heavy alcohol use in humans has been associated with differences in neuroanatomy and brain physiology as well as deficits of perception, learning and memory (Oscar-Berman M, 1997, George et al, 2001, Agartz et al, 2003, Harper et al, 2003, Pfefferbaum et al, 2009, Spreckelmeyer et al, 2011). While cognitive function is generally thought to improve in adult humans after extended abstinence from alcohol (Rosenbloom et al, 2004, Fein et al, 2006, Kopera et al, 2012), some cognitive deficits appear to persist after the cessation of alcohol consumption [see (Fein et al, 1990) for review] and the extent of any recovery may be related to age, length of abstinence and whether periods of abstinence were interrupted by alcohol consumption (Rourke and Grant, 1999, Munro et al, 2000, Zinn et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Chronic periadolescent alcohol consumption produces persistent cognitive deficits in rhesus macaques

Wright¹,

Taffe²

2014

Neuropharmacology

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Background Although human alcoholics exhibit lasting cognitive deficits, it can be difficult to definitively rule out pre-alcohol performance differences. For example, individuals with a family history of alcoholism are at increased risk for alcoholism and are also behaviorally impaired. Animal models of controlled alcohol exposure permit balanced group assignment, thereby ruling out the effects of pre-existing differences. Methods Periadolescent male rhesus macaques (N=5) consumed alcohol during 200 drinking sessions (M-F) across a 10-month period (mean daily alcohol consumption: 1.38 g/kg/day). A control group (N=5) consumed a fruit-flavored vehicle during the same period. Spatial working memory, visual discrimination learning and retention and response time behavioral domains were assessed with subtests of the Monkey CANTAB (CAmbridge Neuropsychological Test Automated Battery). Results Spatial working memory performance was impaired in the alcohol group after 120 drinking sessions (6 mo) in a manner that depended on retention interval. The chronic alcohol animals were also impaired in retaining a visual discrimination over 24 hrs when assessed 6-8 weeks after cessation of alcohol drinking. Finally, the presentation of distractors in the response time task impaired the response time and accuracy of the chronic alcohol group more than controls after 6 months of alcohol cessation. Conclusions Chronic alcohol consumption over as little as 6 months produces cognitive deficits, with some domains still affected after acute (6-8 wks) and lasting (6 mo) discontinuation from drinking. Animals were matched on alcohol preference and behavioral performance prior to exposure, thus providing strong evidence for the causal role of chronic alcohol in these deficits.

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Section: Introductionmentioning

confidence: 99%

Chronic periadolescent alcohol consumption produces persistent cognitive deficits in rhesus macaques

Wright¹,

Taffe²

2014

Neuropharmacology

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“…The cognitive decline seen in AAD patients is more variable than that reported in WKS patients. Cognitive deficits on frontal cortical-dependent tasks has been observed in alcoholics with and without WKS (Dirksen, Howard, Cronin-Golomb, & Oscar-Berman, 2006; Gansler et al, 2000; Oscar-Berman & Evert, 1997; Oscar-Berman et al, 2004). Beyond tests of memory, WKS patients were impaired on tests of fluency, cognitive flexibility, and perseverative responding.…”

Section: Introductionmentioning

confidence: 99%

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Vetreno

Hall

Savage

2011

Neurobiology of Learning and Memory

126

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Chronic alcoholism is associated with impaired cognitive functioning. Over 75% of autopsied chronic alcoholics have significant brain damage and over 50% of detoxified alcoholics display some degree of learning and memory impairment. However, the relative contributions of different etiological factors to the development of alcohol-related neuropathology and cognitive impairment are questioned. One reason for this quandary is that both alcohol toxicity and thiamine deficiency result in brain damage and cognitive problems. Two alcohol-related neurological disorders, alcohol-associated dementia and Wernicke-Korsakoff syndrome have been modeled in rodents. These pre-clinical models have elucidated the relative contributions of ethanol toxicity and thiamine deficiency to the development of dementia and amnesia. What is observed in these models-from repeated and chronic ethanol exposure to thiamine deficiency-is a progression of both neural and cognitive dysregulation. Repeated binge exposure to ethanol leads to changes in neural plasticity by reducing GABAergic inhibition and facilitating glutamatergic excitation, longterm chronic ethanol exposure results in hippocampal and cortical cell loss as well as reduced hippocampal neurotrophin protein content critical for neural survival, and thiamine deficiency results in gross pathological lesions in the diencephalon, reduced neurotrophic protein levels, and neurotransmitters levels in the hippocampus and cortex. Behaviorally, after recovery from repeated or chronic ethanol exposure there is impairment in working or episodic memory that can recover with prolonged abstinence. In contrast, after thiamine deficiency there is severe and persistent spatial memory impairments and increased perseverative behavior. The interaction between ethanol and thiamine deficiency does not produce more behavioral or neural pathology, with the exception of reduction of white matter, than long-term thiamine deficiency alone.

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“…In neuroimaging studies in which alcoholics demonstrated diminished metabolic activity of frontal areas, this reduction often was associated with neuropsychological impairment of frontal functioning (Oscar-Berman and Evert 1997; Oscar-Berman 2000; Sullivan 2000). Neuropsychological findings indicate that KS patients exhibit signs of frontal-system damage including perseveration, disinhibition, apathy, and personality changes.…”

Section: Introductionmentioning

confidence: 99%

Patterns of prefrontal dysfunction in alcoholics with and without Korsakoff's syndrome, patients with Parkinson's disease, and patients with rupture and repair of the anterior communicating artery

Dirksen¹,

Howard²,

Cronin‐Golomb³

et al. 2006

Neuropsychiatric Disease and Treatment

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Alcoholic Korsakoff’s Syndrome

Cited by 16 publications

References 63 publications

Chronic periadolescent alcohol consumption produces persistent cognitive deficits in rhesus macaques

Chronic periadolescent alcohol consumption produces persistent cognitive deficits in rhesus macaques

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Patterns of prefrontal dysfunction in alcoholics with and without Korsakoff's syndrome, patients with Parkinson's disease, and patients with rupture and repair of the anterior communicating artery

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