Decision Making, Impulse Control and Loss of Willpower to Resist Drugs: A Neurocognitive Perspective

Institute for the Neurological Study of Emotion and Creativity, Department of Psychology, University of Southern California, Los Angeles, California 90089-2520, USA.
Nature Neuroscience (Impact Factor: 16.1). 12/2005; 8(11):1458-63. DOI: 10.1038/nn1584
Source: PubMed


Here I argue that addicted people become unable to make drug-use choices on the basis of long-term outcome, and I propose a neural framework that explains this myopia for future consequences. I suggest that addiction is the product of an imbalance between two separate, but interacting, neural systems that control decision making: an impulsive, amygdala system for signaling pain or pleasure of immediate prospects, and a reflective, prefrontal cortex system for signaling pain or pleasure of future prospects. After an individual learns social rules, the reflective system controls the impulsive system via several mechanisms. However, this control is not absolute; hyperactivity within the impulsive system can override the reflective system. I propose that drugs can trigger bottom-up, involuntary signals originating from the amygdala that modulate, bias or even hijack the goal-driven cognitive resources that are needed for the normal operation of the reflective system and for exercising the willpower to resist drugs.

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    • "The construct of impulsivity includes a variety of different components, most generally classified as cognitive/choice impulsivity and motor/action impulsivity (Bechara, Damasio, & Damasio, 2000; Hamilton et al., 2015a; 2015b). Cognitive/choice impulsivity reflects suboptimal choices in the face of delayed contingencies or potential rewards and is measured in the laboratory with decision-making and/or delay discounting paradigms (Hamilton et al., 2015b), on which individuals with heroin dependence have shown functional impairments (Bechara, 2005; Kirby & Petry, 2004). Motor/action impulsivity refers to the inability to inhibit a prepotent motor response (Dougherty et al., 2003), measured in the laboratory with response inhibition paradigms such as continuous performance tasks (Dougherty et al., 2003) or stop signal tasks (Logan & Cowan, 1994). "
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    ABSTRACT: Objectives: Heroin dependence is associated with deficits in impulsivity, which is also a core feature of ADHD. This study aimed to explore the association between childhood ADHD symptoms and cognitive and motor impulsivity among abstinent individuals with a history of heroin dependence. Methods: Thirty-two abstinent Bulgarian males with a history of heroin dependence participated in the study. Self-rated childhood ADHD symptoms were obtained using the Wender-Utah Rating Scale. Cognitive impulsivity was measured using the Iowa Gambling Task (IGT), an index of impulsive decision-making and the Delayed Reward Discounting Task (DRDT), a measure of inter-temporal choice. Motor impulsivity was indexed with the Stop Signal Task (SST), a measure of response inhibition. Results: Participants, whose average age was 27.66 years (SD = 2.7), had an average ADHD symptom score of 36.6 (SD = 18.6), roughly 7 years (SD = 2.9) of heroin use, and been abstinent for just over a year (M = 402.5 days, SD = 223.8). Linear regression analyses revealed that self-reported ADHD symptoms predicted impulsive decision-making (IGT), but not delayed discounting (DRDT) or response inhibition (SST). Conclusions: Self-reported childhood ADHD symptoms do not uniformly predict impulsivity among abstinent individuals with heroin dependence. Results suggest the IGT may be more sensitive to externalizing psychopathology among individuals with heroin dependence than other measures of impulsivity.
    Journal of Dual Diagnosis 10/2015; DOI:10.1080/15504263.2015.1104482 · 0.80 Impact Factor
    • "Chronic drug use is known to alter various neurotransmitter systems and synaptic structure within these networks, leading to impairments in motivational drive and sensitized conditioned responses to drug-related cues (Kalivas & Volkow 2005), including cue-induced craving for the substance (Wise 1988; Berridge & Robinson 1998; Kauer & Malenka 2007). 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 "
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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
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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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