Frontal Lobe Changes in Alcoholism: A Review of the Literature

Moselhy, Hamdy F.; Georgiou, George K.; Kahn, Ashraf

doi:10.1093/alcalc/36.5.357

Cited by 479 publications

(380 citation statements)

References 121 publications

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“…Numerous targeted lesion studies in rats and monkeys have shown that working memory performance depends on the mPFC (24), and alcohol dependence produces long-term impairment in PFC function in humans (25,26). The present results showed that rats with a history of escalation of alcohol intake in a binge-drinking model exhibited impairments in mPFC function during withdrawal, showing that mPFC dysfunction may appear early during the transition from alcohol abuse to alcohol dependence; also, these results suggest that repeated binge and withdrawal episodes in young adults may sensitize the mPFC to additional dysfunction and possibly facilitate the transition to alcohol dependence.…”

Section: Discussionmentioning

confidence: 99%

Recruitment of medial prefrontal cortex neurons during alcohol withdrawal predicts cognitive impairment and excessive alcohol drinking

George

Sanders

Freiling

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

218

178

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Chronic intermittent access to alcohol leads to the escalation of alcohol intake, similar to binge drinking in humans. Converging lines of evidence suggest that impairment of medial prefrontal cortex (mPFC) cognitive function and overactivation of the central nucleus of the amygdala (CeA) are key factors that lead to excessive drinking in dependence. However, the role of the mPFC and CeA in the escalation of alcohol intake in rats with a history of binge drinking without dependence is currently unknown. To address this issue, we examined FBJ murine osteosarcoma viral oncogene homolog (Fos) expression in the mPFC, CeA, hippocampus, and nucleus accumbens and evaluated working memory and anxiety-like behavior in rats given continuous (24 h/d for 7 d/wk) or intermittent (3 d/wk) access to alcohol (20% vol/vol) using a two-bottle choice paradigm. The results showed that abstinence from alcohol in rats with a history of escalation of alcohol intake specifically recruited GABA and corticotropin-releasing factor (CRF) neurons in the mPFC and produced working memory impairments associated with excessive alcohol drinking during acute (24-72 h) but not protracted (16 -68 d) abstinence. Moreover, abstinence from alcohol was associated with a functional disconnection of the mPFC and CeA but not mPFC and nucleus accumbens. These results show that recruitment of a subset of GABA and CRF neurons in the mPFC during withdrawal and disconnection of the PFC-CeA pathway may be critical for impaired executive control over motivated behavior, suggesting that dysregulation of mPFC interneurons may be an early index of neuroadaptation in alcohol dependence.A lcoholism is a chronic relapsing disorder associated with compulsive drinking, loss of control over intake, and emergence of a negative emotional state during abstinence from the drug (1). Although no known animal model of addiction fully emulates the condition in humans, some models are better suited for the investigation of specific elements of the addiction process in a clinically relevant manner. Recently, an animal model of alcohol binge drinking with good face and predictive validity for what may be considered a transition to alcoholism has been reintroduced (2, 3). Rats given extended (24 h/d) and intermittent (every other day) choice access to ethanol escalate their intake of alcohol over the course of 2-4 wk in a binge-like pattern (2-6), and alcohol drinking using this paradigm was reduced by two drugs approved by the US Food and Drug Administration for the treatment of alcoholism (i.e., naltrexone and acamprosate) (2). Moreover, escalation of alcohol drinking using this model is associated with decreased dopamine levels in the nucleus accumbens after 24 h of abstinence (7), decreased endocannabinoid signaling in the dorsolateral striatum (8), and activation of FBJ murine osteosarcoma viral oncogene homolog B (ΔFosB) in the nucleus accumbens core, dorsolateral striatum, and orbitofrontal cortex.Converging lines of evidence from human and animal studies suggest that impairm...

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Section: Discussionmentioning

confidence: 99%

Recruitment of medial prefrontal cortex neurons during alcohol withdrawal predicts cognitive impairment and excessive alcohol drinking

George

Sanders

Freiling

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

218

178

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“…Prior structural neuroimaging studies in alcoholism have focused principally on global atrophic changes in cerebral cortex, white-matter, and cerebellum, plus local effects in hippocampus (62), demonstrating volume reduction (21)(22)(23)63). Smaller right amygdalae have been reported in relatives of alcoholics (56).…”

Section: Discussionmentioning

confidence: 99%

Decreased Volume of the Brain Reward System in Alcoholism

Makris

Oscar‐Berman

Jaffin

et al. 2008

Biological Psychiatry

345

327

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Background-Reinforcement of behavioral responses involves a complex cerebral circuit engaging specific neuronal networks that are modulated by cortical oversight systems affiliated with emotion, memory, judgment, and decision making (collectively referred to in this study as the "extended reward and oversight system" or "reward-network"). We examined whether rewardnetwork brain volumes are reduced in alcoholics, and how volumes of subcomponents within this system are correlated with memory and drinking-history.

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“…Therefore individuals with suppressed delta and theta responses are likely to show deficits in cognitive functions that are mediated by these oscillatory processes. There is ample neuropsychological evidence that supports this view, by demonstrating a wide range of cognitive deficits in the domain of executive functions (including attention, working memory, encoding and retrieval processes) in alcoholics and high risk individuals (Fein et al, 1990;Moselhy et al, 2001;Nixon and Tivis, 1997;Ratti et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Delta and theta oscillations as risk markers in adolescent offspring of alcoholics

Rangaswamy

Jones

Porjesz

et al. 2007

International Journal of Psychophysiology

117

136

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Background-Visual P300 is consistently lower in alcohol dependent individuals, their offspring and subjects at risk. Delta and theta event related oscillations (ERO) are the major contributors to the P300 signal. The total and evoked power in delta and theta bands in the 300 to 700 millisecond post-stimulus window (corresponding to the zone of P3 maxima) was compared between adolescent offspring of alcoholics (high-risk) and age-matched normal controls (low-risk), to assess the utility of the risk markers.Methods-EEG was recorded during the performance of visual oddball task. The S-Transform algorithm decomposed the EEG signals into different frequency bands and the group differences in total and evoked power in the oscillatory responses during the P300 time window (300 to 700 ms) were analyzed using a multivariate design. Similar analysis was performed on P300 peak amplitudes for the target.Results-The high-risk group showed significantly lower parietal post-stimulus evoked and total power in the delta band for targets. A decrease in total power was seen centrally and parietally in theta band. The P300 peak amplitude in the parietal electrodes was also significantly lower in the high-risk group.Conclusions-The decreased total theta power and total and evoked delta power for visual targets in high risk individuals may serve as an endophenotypic marker in the development of alcoholism and other disinhibitory disorders. The differences seen between the offspring of alcoholics and controls may have a cholinergic basis. The ERO measures appear to be more robust than the P300 amplitude in differentiating the groups.

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Frontal Lobe Changes in Alcoholism: A Review of the Literature

Cited by 479 publications

References 121 publications

Recruitment of medial prefrontal cortex neurons during alcohol withdrawal predicts cognitive impairment and excessive alcohol drinking

Recruitment of medial prefrontal cortex neurons during alcohol withdrawal predicts cognitive impairment and excessive alcohol drinking

Decreased Volume of the Brain Reward System in Alcoholism

Delta and theta oscillations as risk markers in adolescent offspring of alcoholics

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