Recovery of Hippocampus-Related Functions in Chronic Alcoholics During Monitored Long-Term Abstinence

Bartels, Claudia; Kunert, Hanns Jürgen; Stawicki, Sabina; Kröner‐Herwig, Birgit; Ehrenreich, Hannelore; Krampe, Henning

doi:10.1093/alcalc/agl104

Cited by 66 publications

(65 citation statements)

References 94 publications

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“…These findings echo both earlier and more recent controlled studies of memory recovery with short-term or sustained sobriety showing a range of recovery, from little to extensive, after short-term (e.g., 1 week) to long-term (e.g., 1 year or more) sustained abstinence from alcohol (e.g., Bartels et al, 2007;Bates, Voelbel, Buckman, Labouvie, & Barry, 2005;Bell, Vissicchio, & Weinstein, 2016;Butters & Cermak, 1980;Fabian & Parsons, 1983; 852 E.V. Sullivan Leber, Jenkins, & Parsons, 1981;Mann, Gunther, Stetter, & Ackermann, 1999;Pitel et al, 2009;Rosenbloom et al, 2004;Rourke & Grant, 1999;Yohman, Parsons, & Leber, 1985) (for reviews, see Oscar-Berman et al, 2014;Pitel, Eustache, & Beaunieux, 2014).…”

Section: Recovery Of Component Processes Of Memory Functions With Alcsupporting

confidence: 89%

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: Recovery Of Component Processes Of Memory Functions With Alcsupporting

confidence: 89%

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Sullivan

2017

J Int Neuropsychol Soc

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“…For example, compensatory responses to chronic ethanol exposure, such as increased cell surface expression of NR subunits, contribute to increased excitability and a loss of GABAergic tone during ethanol withdrawal (Alele & Devaud et al, 2005;Davidson et al, 1995;Maler et al, 2005;Prendergast et al, 2000). Such effects are likely to contribute to neurotoxicity, hippocampal deficits, cognitive problems, and possibly cueinduced craving during withdrawal (Bartels et al, 2007;Prendergast et al, 2004;Schneider et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

Potentiation of N-methyl-d-aspartate receptor-mediated neuronal injury during methamphetamine withdrawal in vitro requires co-activation of IP3 receptors

et al. 2008

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Recent findings suggest that methamphetamine (METH) functions acutely to inhibit N-methyl-Daspartate (NMDA) receptor function. Protracted withdrawal from METH exposure may increase the sensitivity of NMDA receptors to agonist exposure, promoting neuronal excitability. However, the relevance of METH effects on NMDA receptor activity with regard to neuronal viability has not been studied. The present studies examined the effects of protracted METH exposure (6 or 7 days; 1.0-100 μM) and withdrawal (1 or 7 days) on NMDA receptor-dependent neurotoxicity, determined with use of the non-vital fluorescent marker propidium iodide, in organotypic slice cultures of male and female rats. Prolonged exposure to METH (100 μM) produced only modest toxicity in the granule cell layer of the dentate gyrus. Withdrawal from METH exposure (1 or 7 days) did not produce overt neuronal injury in any region of slice cultures. Exposure to NMDA (5 μM) produced marked neurotoxicity in the CA1 pyramidal cell layer. Neither co-exposure to METH nor 1 day of METH withdrawal in combination with NMDA exposure altered NMDA-induced neurotoxicity. In contrast, protracted withdrawal from METH exposure (7 days) was associated with a marked (~400%) increase in NMDA-induced neurotoxicity in CA1 region pyramidal cells. This potentiation of neurotoxicity was prevented by co-exposure to the selective NMDA receptor antagonist 5-2-amino-5-phoshonovaleric acid (20 μM) and was markedly attenuated by co-exposure of slices to xestospongin C (1 μM), an antagonist of IP 3 receptors. The results of the present studies suggest that long-term METH withdrawal functionally sensitizes the NMDA receptor to agonist exposure and requires the co-activation of NMDA and IP 3 receptors.

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“…Reduction of hippocampal volume in alcoholics is reversible after short periods of abstinence (White et al 2000). Similarly, hippocampal dependent cognitive functions have shown reversibility after comparable periods of abstinence (Bartels et al 2006).…”

Section: Neural Systems Affected and Concomitant Neurobehavioral Defimentioning

confidence: 99%

Alcohol: Effects on Neurobehavioral Functions and the Brain

2007

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Alcoholism results from an interplay between genetic and environmental factors, and is linked to brain defects and associated cognitive, emotional, and behavioral impairments. A confluence of findings from neuroimaging, physiological, neuropathological, and neuropsychological studies of alcoholics indicate that the frontal lobes, limbic system, and cerebellum are particularly vulnerable to damage and dysfunction. An integrative approach employing a variety of neuroscientific technologies is essential for recognizing the interconnectivity of the different functional systems affected by alcoholism. In that way, relevant experimental techniques can be applied to assist in determining the degree to which abstinence and treatment contribute to the reversal of atrophy and dysfunction.

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Recovery of Hippocampus-Related Functions in Chronic Alcoholics During Monitored Long-Term Abstinence

Cited by 66 publications

References 94 publications

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Contributions to Understanding the Neuropsychology of Alcoholism: An INS Legacy

Potentiation of N-methyl-d-aspartate receptor-mediated neuronal injury during methamphetamine withdrawal in vitro requires co-activation of IP3 receptors

Alcohol: Effects on Neurobehavioral Functions and the Brain

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