Neurophysiological efficiency in male and female alcoholics

Nixon, Sara Jo; Tivis, Rick; Ceballos, Natalie A.; Varner, Jerald L.; Rohrbaugh, John

doi:10.1016/s0278-5846(02)00206-3

Cited by 48 publications

(44 citation statements)

References 39 publications

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“…Influenced by the work of Parson, Glenn, and Nixon in women (Fabian & Parsons, 1983;Glenn & Parsons, 1992;Nixon, Tivis, Ceballos, Varner, & Rohrbaugh, 2002;Parsons & Nixon, 1998), we also sought a profile of impairment in alcoholic women and found that apart from static balance, alcoholic men and women showed similar deficit patterns (Sullivan, Fama, Rosenbloom, & Pfefferbaum, 2002) (Figure 1). Furthermore, neither the diffuse impairment hypothesis nor the right hemisphere hypothesis of alcoholism-related impairment was supported, conclusions reached decades ago by Tarter (Tarter, 1975) and supported by the observation of similarly impaired verbal and nonverbal skills in two samples of alcoholics (Tivis, Beatty, Nixon, & Parsons, 1995).…”

Section: Ev Sullivanmentioning

confidence: 99%

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Sullivan

2017

J Int Neuropsychol Soc

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Alcohol use disorder (AUD) has been a major cause of family, social, and personal strife for centuries, with current prevalence estimates of 14% for 12-month and 29% lifetime AUD. Neuropsychological testing of selective cognitive, sensory, and motor functions complemented with in vivo brain imaging has enabled tracking the consequences of AUD, which follows a dynamic course of development, maintenance, and recovery or relapse. Controlled studies of alcoholism reviewed herein provide evidence for disruption of selective functions involving executive, visuospatial, mnemonic, emotional, and attentional processes, response inhibition, prosody, and postural stability and brain systems supporting these functions. On a hopeful front, longitudinal study provides convincing evidence for improvement in brain structure and function following sustained sobriety. These discoveries have a strong legacy in the International Neuropsychological Society (INS), starting from its early days when assumptions regarding which brain regions were disrupted relied solely on patterns of functional sparing and impairment deduced from testing. This review is based on the symposium presentation delivered at the 2017 annual North American meeting of the INS in celebration of the 50th anniversary since its institution in 1967. In the spirit of the meeting's theme, "Binding the Past and Present," the lecture and this review recognized the past by focusing on early, rigorous neuropsychological studies of alcoholism and their influence on research currently conducted using imaging methods enabling hypothesis testing of brain substrates of observed functional deficits. (JINS, 2017, 23, 843-859)

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Section: Ev Sullivanmentioning

confidence: 99%

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Sullivan

2017

J Int Neuropsychol Soc

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“…NEUROCIRCUITRY OF ALCOHOL DEPENDENCE alcoholics are likely contributors to vulnerability for relapse by virtue of executive function impairment in disinhibition (Fein et al, 2006), impulse control (Nixon, Tivis, Ceballos, Varner, & Rohrbaugh, 2002), and conflict processing (De Rosa, Desmond, Anderson, Schulte et al, 2009).…”

Section: Brain Macrostructure: Quantitative Dtimentioning

confidence: 99%

“…The pattern of findings from these and later fMRI studies, reviewed next, provide evidence for inefficient processing by showing that alcoholics activated either a different neural network from controls (Pfefferbaum et al, 2001;Tapert et al, 2001Tapert et al, , 2004 or activated appropriate regions but more widely than controls (Desmond et al, 2003;Parks et al, 2003) in order to perform on par with controls. The "inefficient processing" hypothesis (Nixon et al, 2002) is based on the need for sharing resources between different cognitive processes and thus between different neuronal networks to compensate for compromised brain regions or systems. The disadvantage of this compensation scheme is that more resources than normal are usurped, thereby reducing free processing capacity and infringing on the opportunity for multitasking.…”

Section: Functional Brain Network Characterized With Task-activated mentioning

confidence: 99%

Human Imaging Studies of Brain Circuitry Disrupted by Alcoholism

Sullivan

Pfefferbaum

2014

Neurobiology of Alcohol Dependence

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“…Functions commonly affected involve abstract problem solving, visuospatial and verbal learning, selective memory processes, perceptual motor skills, and postural stability (Butters and Granholm, 1987;Fein et al, 1990;Nixon et al, 2002;Oscar-Berman, 2000;Sullivan et al, 2000aSullivan et al, , b, 2002. Disruption of frontopontocerebellar and cerebellothalamocortical circuitry may underlie the mainstay of these neuropsychological deficits (Sullivan, 2003;Sullivan and Pfefferbaum, 2005).…”

Section: Introductionmentioning

confidence: 99%

Interaction of Thiamine Deficiency and Voluntary Alcohol Consumption Disrupts Rat Corpus Callosum Ultrastructure

Sullivan

Stankovic

et al. 2007

Neuropsychopharmacol

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The relative roles of alcohol and thiamine deficiency in causing brain damage remain controversial in alcoholics without the WernickeKorsakoff syndrome. Experimental control over alcohol consumption and diet are impossible in humans but can be accomplished in animal models. This experiment was designed to differentiate the separate and combined effects on the macro-and ultrastructure of the corpus callosum of thiamine deficiency and voluntary alcohol consumption. Adult male alcohol-preferring (P) rats (9 chronically alcoholexposed and 9 water controls) received a thiamine-deficient diet for 2 weeks. There were four groups: five rats previously exposed to alcohol were treated with pyrithiamine (a thiamine phosphorylation inhibitor); five rats never exposed to alcohol were treated with pyrithiamine; four alcohol-exposed rats were treated with thiamine; and four rats never exposed to alcohol were treated with thiamine. On day 14, thiamine was restored in all 18 rats; 2 weeks later the 10 pyrithiamine-treated rats received intraperitoneal thiamine. The rats were perfused 61 days post-pyrithiamine treatment at age 598 days. Brains were dissected and weight and volumes were calculated. Sagittal sections were stained to measure white matter structures. The corpus callosum was examined using transmission electron microscopy to determine density of myelinated fibers, fiber diameter, and myelin thickness. The corpus callosum in the alcohol/ pyrithiamine group was significantly thinner, had greater fiber density, higher percentage of small fibers, and myelin thinning than in the alcohol/thiamine and water/thiamine groups. Several measures showed a graded effect, where the alcohol/pyrithiamine group had greater pathology than the water/pyrithiamine group, which had greater pathology than the two thiamine-replete groups. Across all 16 rats, thinner myelin sheaths correlated with higher percentage of small fibers. Myelin thickness and axon diameter together accounted for 71% of the variance associated with percentage of small fibers. Significant abnormalities in the alcohol/pyrithiamine group and lack of abnormality in the alcohol-exposed/thiamine-replete group indicate that thiamine deficiency caused white matter damage. The graded abnormalities across the dually to singly treated animals support a compounding effect of alcohol exposure and thiamine depletion, and indicate the potential for interaction between alcohol and thiamine deficiency in human alcohol-related brain damage.

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Neurophysiological efficiency in male and female alcoholics

Cited by 48 publications

References 39 publications

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Human Imaging Studies of Brain Circuitry Disrupted by Alcoholism

Interaction of Thiamine Deficiency and Voluntary Alcohol Consumption Disrupts Rat Corpus Callosum Ultrastructure

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