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Neuroplasticity and Predictors of Alcohol Recovery.

Seo D, Sinha R - Alcohol Res (2015)

Bottom Line: Chronic alcohol-related neuroadaptations in key neural circuits of emotional and cognitive control play a critical role in the development of, and recovery from, alcoholism.Converging evidence in the neurobiological literature indicates that neuroplastic changes in the prefrontal-striatal-limbic circuit, which governs emotion regulation and decisionmaking and controls physiological responses in the autonomic nervous system and hypothalamic-pituitary-adrenal axis system, contribute to chronic alcoholism and also are significant predictors of relapse and recovery.This paper reviews recent evidence on the neuroplasticity associated with alcoholism in humans, including acute and chronic effects, and how these neurobiological adaptations contribute to alcohol recovery, along with the discussion of relevant clinical implications and future research directions.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut.

ABSTRACT
Chronic alcohol-related neuroadaptations in key neural circuits of emotional and cognitive control play a critical role in the development of, and recovery from, alcoholism. Converging evidence in the neurobiological literature indicates that neuroplastic changes in the prefrontal-striatal-limbic circuit, which governs emotion regulation and decisionmaking and controls physiological responses in the autonomic nervous system and hypothalamic-pituitary-adrenal axis system, contribute to chronic alcoholism and also are significant predictors of relapse and recovery. This paper reviews recent evidence on the neuroplasticity associated with alcoholism in humans, including acute and chronic effects, and how these neurobiological adaptations contribute to alcohol recovery, along with the discussion of relevant clinical implications and future research directions.

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Hyperactive ventromedial prefrontal cortex (VmPFC) response to the neutral-relaxing condition, alcohol craving, and relapse risk. (A) In 45 patients with alcohol use disorder (AUD), hyperactive response in the VmPFC and anterior cingulate cortex (ACC) when they are exposed to neutrally relaxing situations during brief guided imagery was significantly associated with high alcohol craving during alcohol cue imagery (R = 0.56; R2 = 0.31, P < 0.01 whole-brain FWE corrected). (B) Estimated survival functions for time to initial alcohol relapse, showing that the more VmPFC hyperactivity during the neutral condition, the shorter the time to subsequent initial relapse and heavy drinking relapse: mean (in red) +1 (green) and +2 (gray) standard deviation (SD) above the mean, and −1 (blue) and −2 (black) SD below the mean. Cox proportional hazards regression analysis indicates that hyperactive VmPFC response during the neutral condition predicted a shorter time to initial alcohol use (χ2 = 6.39, P = 0.01; hazard ratio [HR] = 8.45, confidence interval [CI] = 1.6–44.2) as well as heavy drinking relapse (χ2 = 7.39, P < 0.01, HR = 8.68, CI = 1.8–41.2). I-B = imagery minus baseline ratings.SOURCE: This figure is reproduced with the permission of the American Medical Association (Seo et al. 2013).
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f2-arcr-37-1-143: Hyperactive ventromedial prefrontal cortex (VmPFC) response to the neutral-relaxing condition, alcohol craving, and relapse risk. (A) In 45 patients with alcohol use disorder (AUD), hyperactive response in the VmPFC and anterior cingulate cortex (ACC) when they are exposed to neutrally relaxing situations during brief guided imagery was significantly associated with high alcohol craving during alcohol cue imagery (R = 0.56; R2 = 0.31, P < 0.01 whole-brain FWE corrected). (B) Estimated survival functions for time to initial alcohol relapse, showing that the more VmPFC hyperactivity during the neutral condition, the shorter the time to subsequent initial relapse and heavy drinking relapse: mean (in red) +1 (green) and +2 (gray) standard deviation (SD) above the mean, and −1 (blue) and −2 (black) SD below the mean. Cox proportional hazards regression analysis indicates that hyperactive VmPFC response during the neutral condition predicted a shorter time to initial alcohol use (χ2 = 6.39, P = 0.01; hazard ratio [HR] = 8.45, confidence interval [CI] = 1.6–44.2) as well as heavy drinking relapse (χ2 = 7.39, P < 0.01, HR = 8.68, CI = 1.8–41.2). I-B = imagery minus baseline ratings.SOURCE: This figure is reproduced with the permission of the American Medical Association (Seo et al. 2013).

Mentions: Recent evidence in humans suggests that excessive, chronic alcohol consumption may lead to hyperexcitability of neurons in the CNS, which, in turn, plays a role in alcohol addiction and recovery (Porjesz and Begleiter 2003; Seo et al. 2013; Sinha et al. 2011). Indeed, studies have found hyperactive CNS and electroencephalogram (EEG) responses in people with AUD, including increased excitatory neurotransmission associated with long-term alcohol use and hyperactive EEG responses in the frontal regulatory regions (Bauer 2001; Porjesz and Begleiter 2003). Studies also have found that alcohol-related neuronal adaptations on basal-state physiology, including upregulated ANS and HPA axis systems, underlie high alcohol craving, poor clinical outcome, and relapse vulnerability by disrupting physiological arousal (Breese et al. 2011; Seo et al. 2013; Sinha et al. 2011). In addition, a recent fMRI study found significant associations between hyperactive brain response during a relaxed state and susceptibility to alcohol craving and relapse in AUD patients who were engaged in treatment and 4 to 8 weeks abstinent. In this study, hyperactivity during relaxation in the VmPFC/ACC, but no other region, was associated with greater alcohol craving when subjects were presented with alcohol cues (figure 2A). In addition, the VmPFC/ACC hyperactivity predicted a shorter time to subsequent initial relapse and heavy-drinking relapse (figure 2B), as well as more alcohol use during a 90-day follow-up period (Seo et al. 2013). These findings highlight the important role of basal-state hyperactivity and integrity of VmPFC function in recovery from chronic alcoholism.


Neuroplasticity and Predictors of Alcohol Recovery.

Seo D, Sinha R - Alcohol Res (2015)

Hyperactive ventromedial prefrontal cortex (VmPFC) response to the neutral-relaxing condition, alcohol craving, and relapse risk. (A) In 45 patients with alcohol use disorder (AUD), hyperactive response in the VmPFC and anterior cingulate cortex (ACC) when they are exposed to neutrally relaxing situations during brief guided imagery was significantly associated with high alcohol craving during alcohol cue imagery (R = 0.56; R2 = 0.31, P < 0.01 whole-brain FWE corrected). (B) Estimated survival functions for time to initial alcohol relapse, showing that the more VmPFC hyperactivity during the neutral condition, the shorter the time to subsequent initial relapse and heavy drinking relapse: mean (in red) +1 (green) and +2 (gray) standard deviation (SD) above the mean, and −1 (blue) and −2 (black) SD below the mean. Cox proportional hazards regression analysis indicates that hyperactive VmPFC response during the neutral condition predicted a shorter time to initial alcohol use (χ2 = 6.39, P = 0.01; hazard ratio [HR] = 8.45, confidence interval [CI] = 1.6–44.2) as well as heavy drinking relapse (χ2 = 7.39, P < 0.01, HR = 8.68, CI = 1.8–41.2). I-B = imagery minus baseline ratings.SOURCE: This figure is reproduced with the permission of the American Medical Association (Seo et al. 2013).
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4476600&req=5

f2-arcr-37-1-143: Hyperactive ventromedial prefrontal cortex (VmPFC) response to the neutral-relaxing condition, alcohol craving, and relapse risk. (A) In 45 patients with alcohol use disorder (AUD), hyperactive response in the VmPFC and anterior cingulate cortex (ACC) when they are exposed to neutrally relaxing situations during brief guided imagery was significantly associated with high alcohol craving during alcohol cue imagery (R = 0.56; R2 = 0.31, P < 0.01 whole-brain FWE corrected). (B) Estimated survival functions for time to initial alcohol relapse, showing that the more VmPFC hyperactivity during the neutral condition, the shorter the time to subsequent initial relapse and heavy drinking relapse: mean (in red) +1 (green) and +2 (gray) standard deviation (SD) above the mean, and −1 (blue) and −2 (black) SD below the mean. Cox proportional hazards regression analysis indicates that hyperactive VmPFC response during the neutral condition predicted a shorter time to initial alcohol use (χ2 = 6.39, P = 0.01; hazard ratio [HR] = 8.45, confidence interval [CI] = 1.6–44.2) as well as heavy drinking relapse (χ2 = 7.39, P < 0.01, HR = 8.68, CI = 1.8–41.2). I-B = imagery minus baseline ratings.SOURCE: This figure is reproduced with the permission of the American Medical Association (Seo et al. 2013).
Mentions: Recent evidence in humans suggests that excessive, chronic alcohol consumption may lead to hyperexcitability of neurons in the CNS, which, in turn, plays a role in alcohol addiction and recovery (Porjesz and Begleiter 2003; Seo et al. 2013; Sinha et al. 2011). Indeed, studies have found hyperactive CNS and electroencephalogram (EEG) responses in people with AUD, including increased excitatory neurotransmission associated with long-term alcohol use and hyperactive EEG responses in the frontal regulatory regions (Bauer 2001; Porjesz and Begleiter 2003). Studies also have found that alcohol-related neuronal adaptations on basal-state physiology, including upregulated ANS and HPA axis systems, underlie high alcohol craving, poor clinical outcome, and relapse vulnerability by disrupting physiological arousal (Breese et al. 2011; Seo et al. 2013; Sinha et al. 2011). In addition, a recent fMRI study found significant associations between hyperactive brain response during a relaxed state and susceptibility to alcohol craving and relapse in AUD patients who were engaged in treatment and 4 to 8 weeks abstinent. In this study, hyperactivity during relaxation in the VmPFC/ACC, but no other region, was associated with greater alcohol craving when subjects were presented with alcohol cues (figure 2A). In addition, the VmPFC/ACC hyperactivity predicted a shorter time to subsequent initial relapse and heavy-drinking relapse (figure 2B), as well as more alcohol use during a 90-day follow-up period (Seo et al. 2013). These findings highlight the important role of basal-state hyperactivity and integrity of VmPFC function in recovery from chronic alcoholism.

Bottom Line: Chronic alcohol-related neuroadaptations in key neural circuits of emotional and cognitive control play a critical role in the development of, and recovery from, alcoholism.Converging evidence in the neurobiological literature indicates that neuroplastic changes in the prefrontal-striatal-limbic circuit, which governs emotion regulation and decisionmaking and controls physiological responses in the autonomic nervous system and hypothalamic-pituitary-adrenal axis system, contribute to chronic alcoholism and also are significant predictors of relapse and recovery.This paper reviews recent evidence on the neuroplasticity associated with alcoholism in humans, including acute and chronic effects, and how these neurobiological adaptations contribute to alcohol recovery, along with the discussion of relevant clinical implications and future research directions.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut.

ABSTRACT
Chronic alcohol-related neuroadaptations in key neural circuits of emotional and cognitive control play a critical role in the development of, and recovery from, alcoholism. Converging evidence in the neurobiological literature indicates that neuroplastic changes in the prefrontal-striatal-limbic circuit, which governs emotion regulation and decisionmaking and controls physiological responses in the autonomic nervous system and hypothalamic-pituitary-adrenal axis system, contribute to chronic alcoholism and also are significant predictors of relapse and recovery. This paper reviews recent evidence on the neuroplasticity associated with alcoholism in humans, including acute and chronic effects, and how these neurobiological adaptations contribute to alcohol recovery, along with the discussion of relevant clinical implications and future research directions.

Show MeSH
Related in: MedlinePlus