Goldstein RZ, Volkow ND. Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications. Nat Rev Neurosci 12: 652-669

Medical Department, Brookhaven National Laboratory, Upton, New York 11973, USA.
Nature Reviews Neuroscience (Impact Factor: 31.43). 11/2011; 12(11):652-69. DOI: 10.1038/nrn3119
Source: PubMed


The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.

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    • "Furthermore, dysfunction of higher cortical areas responsible for the regulation of motivational drives, including the lateral orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), dorsolateral prefrontal cortex (dlPFC) and dorsal anterior cingulate cortex (ACC) (Bechara 2005; Koob & Volkow 2010), may aid in the progression to compulsive substance use in later stages of addiction potentially by synergizing deficiencies in the function of the reward/motivation system (Lubman, Yücel & Pantelis 2004; Kalivas 2009). Given the strong evidence for neurological alterations at the basis of drug dependence (e.g., Goldstein & Volkow 2011; Parvaz et al. 2011; Volkow et al. 2012), functional INVITED REVIEW doi:10.1111/adb.12314 © 2015 Society for the Study of Addiction Addiction Biology bs_bs_banner magnetic resonance imaging (fMRI) represents an important tool in translating these preclinical insights to brain function in humans affected by addictive disorders. "
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    ABSTRACT: Given the strong evidence for neurological alterations at the basis of drug dependence, functional magnetic resonance imaging (fMRI) represents an important tool in the clinical neuroscience of addiction. fMRI cue-reactivity paradigms represent an ideal platform to probe the involvement of neurobiological pathways subserving the reward/motivation system in addiction and potentially offer a translational mechanism by which interventions and behavioral predictions can be tested. Thus, this review summarizes the research that has applied fMRI cue-reactivity paradigms to the study of adult substance use disorder treatment responses. Studies utilizing fMRI cue-reactivity paradigms for the prediction of relapse and as a means to investigate psychosocial and pharmacological treatment effects on cue-elicited brain activation are presented within four primary categories of substances: alcohol, nicotine, cocaine and opioids. Lastly, suggestions for how to leverage fMRI technology to advance addiction science and treatment development are provided.
    Addiction Biology 10/2015; DOI:10.1111/adb.12314 · 5.36 Impact Factor
    • "In neuroimaging studies, cortical volume and activity in regions associated with cognitive control, such as dorsolateral prefrontal cortex (DLPFC) (Miller and Cohen, 2001), have been shown to predict selection of larger-later over smaller-sooner rewards (McClure et al., 2004; Bjork et al., 2009; Kim and Lee, 2011; Peters and Büchel, 2011; Gianotti et al., 2012; van den Bos and McClure, 2013). Moreover, disorders associated with impulsivity, such as gambling and addiction, have been associated with increased rates of delay discounting (Bickel et al., 2007) and impaired cognitive control (Goldstein and Volkow, 2011). "
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    ABSTRACT: Recent findings suggest that the dorsolateral prefrontal cortex (DLPFC), a region consistently associated with impulse control, is vulnerable to transient suppression of its activity and attendant functions by excessive stress and/or cognitive demand. Using functional magnetic resonance imaging, we show that a capacity-exceeding cognitive challenge induced decreased DLPFC activity and correlated increases in the preference for immediately available rewards. Consistent with growing evidence of a link between working memory capacity and delay discounting, the effect was inversely proportional to baseline performance on a working memory task. Subjects who performed well on the working memory task had unchanged, or even decreased, delay discounting rates, suggesting that working memory ability may protect cognitive control from cognitive challenge.
    NeuroImage 09/2015; 124. DOI:10.1016/j.neuroimage.2015.09.027 · 6.36 Impact Factor
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    • "Substantially weakened PFC function could, in turn, further disinhibit limbic-striatal responses especially under challenging situations, including stress and exposure to alcohol-related cues. In addition, given the crucial role of the PFC in inhibitory control and decisionmaking (Bechara 2005; Goldstein and Volkow 2011), altered PFC function could result in an inability to inhibit compulsive alcohol seeking and poor decisionmaking when confronted with the choice to return to drinking and continued alcohol use despite negative consequences, thereby aggravating the relapse cycle. "
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    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.
    Alcohol research : current reviews 09/2015; 37(1):143-152.
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