Article

Impulsivity, frontal lobes and risk for addiction

Bowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
Pharmacology Biochemistry and Behavior (Impact Factor: 2.78). 06/2009; 93(3):237-47. DOI: 10.1016/j.pbb.2009.04.018
Source: PubMed

ABSTRACT

Alcohol and substance abuse disorders involve continued use of substances despite negative consequences, i.e. loss of behavioral control of drug use. The frontal-cortical areas of the brain oversee behavioral control through executive functions. Executive functions include abstract thinking, motivation, planning, attention to tasks and inhibition of impulsive responses. Impulsiveness generally refers to premature, unduly risky, poorly conceived actions. Dysfunctional impulsivity includes deficits in attention, lack of reflection and/or insensitivity to consequences, all of which occur in addiction [Evenden JL. Varieties of impulsivity. Psychopharmacology (Berl) 1999;146:348-361.; de Wit H. Impulsivity as a determinant and consequence of drug use: a review of underlying processes. Addict Biol 2009;14:22-31]. Binge drinking models indicate chronic alcohol damages in the corticolimbic brain regions [Crews FT, Braun CJ, Hoplight B, Switzer III RC, Knapp DJ. Binge ethanol consumption causes differential brain damage in young adolescent rats compared with adult rats. Alcohol Clin Exp Res 2000;24:1712-1723] causing reversal learning deficits indicative of loss of executive function [Obernier JA, White AM, Swartzwelder HS, Crews FT. Cognitive deficits and CNS damage after a 4-day binge ethanol exposure in rats. Pharmacol Biochem Behav 2002b;72:521-532]. Genetics and adolescent age are risk factors for alcoholism that coincide with sensitivity to alcohol-induced neurotoxicity. Cortical degeneration from alcohol abuse may increase impulsivity contributing to the development, persistence and severity of alcohol use disorders. Interestingly, abstinence results in bursts of neurogenesis and brain regrowth [Crews FT, Nixon K. Mechanisms of neurodegeneration and regeneration in alcoholism. Alcohol Alcohol 2009;44:115-127]. Treatments for alcoholism, including naltrexone pharmacotherapy and psychotherapy may work through improving executive functions. This review will examine the relationships between impulsivity and executive function behaviors to changes in cortical structure during alcohol dependence and recovery.

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Available from: Charlotte A Boettiger
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    • "I MPAIRED CONTROL PERTAINS to addiction (American Psychiatric Association, 2013), and neurobiological models suggest that impulsivity mediated by frontostriatal circuits plays a critical role in the development and maintenance of addictive behavior, including alcohol use disorder (AUD; Crews and Boettiger, 2009; Fineberg et al., 2014; No€ el et al., 2013; Potenza and de Wit, 2010; Verdejo-Garc ıa et al., 2008). Although the link between heightened impulsivity and AUD is well established, the exact relationships remain unclear (Dick et al., 2010; Lejuez et al., 2010). "
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    ABSTRACT: Background: Although there is considerable support for the relationship between impulsivity and alcohol dependence, little is known about the impact of neurocognitive aspects of impulsivity on treatment outcome. The aim of this study was to prospectively investigate the impact of neurocognitive impulsivity at treatment onset on treatment completion. Methods: Forty-three alcohol-dependent patients entering inpatient treatment for alcohol dependence completed neurocognitive measures of impulsivity at the beginning of treatment. Assessments included prototypical measures of impulsive action (Go/No-go task [GNG] and Stop Signal Task [SST]) and impulsive choice (Delay Discounting Test [DDT], and Iowa Gambling Task). According to treatment outcomes, patients were divided into a patient group with regular treatment completion (e.g., with planned discharges, and without relapse during treatment) or irregular treatment course (e.g., premature and unplanned termination of treatment, "dropout," and/or relapse). Results: Results show that, relative to patients completing treatment in a regular fashion (regular treatment completers [RTC]; 67%), those with an irregular course of treatment (relapse and/or dropout) (irregular treatment completers [ITC]; 33%) had significantly poorer GNG response inhibition performance (p = 0.011), and showed a trend toward greater delay discounting (DDT; p = 0.052) at treatment onset. Additional logistic regression analyses identified poor GNG response inhibition performance as a significant predictor for an irregular treatment course (GNG: p = 0.021; DDT: p = 0.067), particularly for relapse (GNG: p = 0.023). Conclusions: Neurocognitive impulsivity impacts upon treatment completion and appears sensitive for the prediction of relapse and dropout in alcohol-dependent patients. Poorer GNG response inhibition and a tendency toward steeper discounting of delayed rewards should be regarded as neurocognitive risk factors, which can be identified early in the course of alcohol dependence treatment.
    Preview · Article · Dec 2015 · Alcoholism Clinical and Experimental Research
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    • "It is also important to note that low P3 is not unique to alcoholics and their high risk relatives, but is also found in individuals with one or more externalizing disorders or disinhibitory conditions (Carlson et al., 1999; Hill and Shen, 2002; Iacono et al., 2002; Iacono et al., 2003; Iacono and McGue, 2006; Patrick et al., 2006; Carlson et al., 2007; Hicks et al., 2007; Iacono et al., 2008; Patrick, 2008; Gilmore et al., 2010a; Gilmore et al., 2010b, 2012). As reported by several studies, an underlying feature among risk propensity, externalizing disorders and alcoholism is the concept of "impulsivity", which is a conglomerate of personality traits that can result in premature, unduly risky and poorly conceived actions, and is known to be closely related to disinhibitory traits and clinical vulnerability (Gorenstein and Newman, 1980; Martin et al., 1994; Olson et al., 1999; Krueger and Piasecki, 2002; Hall et al., 2007; Kamarajan et al., 2007; Crews and Boettiger, 2009; Romer et al., 2009). Interestingly, P3 amplitude has been found to be either negatively correlated with impulsivity or lower in high impulsive subjects regardless of having a diagnosis of alcoholism and/or related disorders (Justus et al., 2001; Moeller et al., 2004; Chen et al., 2007; Ruchsow et al., 2008; Kamarajan et al., 2010). "
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    ABSTRACT: Background: Individuals at high risk to develop alcoholism often manifest neurocognitive deficits as well as increased impulsivity. The goal of the present study is to elucidate reward processing deficits, externalizing disorders, and impulsivity as elicited by electrophysiological, clinical and behavioral measures in subjects at high risk for alcoholism from families densely affected by alcoholism in the context of brain maturation across age groups and gender. Methods: Event-related potentials (ERPs) and current source density (CSD) during a monetary gambling task (MGT) were measured in 12-25 year old offspring (N = 1864) of families in the Collaborative Study on the Genetics of Alcoholism (COGA) Prospective study; the high risk (HR, N = 1569) subjects were from families densely affected with alcoholism and the low risk (LR, N = 295) subjects were from community families. Externalizing disorders and impulsivity scores were also compared between LR and HR groups. Results: HR offspring from older (16-25 years) male and younger (12-15 years) female subgroups showed lower P3 amplitude than LR subjects. The amplitude decrement was most prominent in HR males during the loss condition. Overall, P3 amplitude increase at anterior sites and decrease at posterior areas were seen in older compared to younger subjects, suggesting frontalization during brain maturation. The HR subgroups also exhibited hypofrontality manifested as weaker CSD activity during both loss and gain conditions at frontal regions. Further, the HR subjects had higher impulsivity scores and increased prevalence of externalizing disorders. P3 amplitudes during the gain condition were negatively correlated with impulsivity scores. Conclusions: Older male and younger female HR offspring, compared to their LR counterparts, manifested reward processing deficits as indexed by lower P3 amplitude and weaker CSD activity, along with higher prevalence of externalizing disorders and higher impulsivity scores. Significance: Reward related P3 is a valuable measure reflecting neurocognitive dysfunction in subjects at risk for alcoholism, as well as to characterize reward processing and brain maturation across gender and age group.
    Full-text · Article · Sep 2015 · International Journal of Psychophysiology
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    • "Furthermore, the findings suggest that other than cognitive control, automatic processes guiding our behavior seem to remain rather intact/ unaffected. The obtained paradoxical results obtained therefore reconcilable with findings showing that ethanol intoxication compromises cognitive control functions (Crews and Boettiger 2009; Anderson et al. 2011). A limitation of the study is that only male subjects were examined and no neurophysiological data were obtained. "
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    ABSTRACT: Binge drinking is an increasing problem in Western societies, but we are still only beginning to unravel the effects of binge drinking on a cognitive level. While common sense suggests that all cognitive functions are compromised during high-dose ethanol intoxication, several studies suggest that the effects might instead be rather specific. Moreover, some results suggest that the degrees of automaticity and complexity of cognitive operations during response control modulate effects of binge drinking. However, this has not been tested in detail. In the current study, we therefore parametrically modulate cognitive/“mental” workload during response inhibition and examine the effects of high-dose ethanol intoxication (~1.1 ‰) in n = 18 male participants. The results suggest that detrimental effects of high-dose ethanol intoxication strongly depend on the complexity of processes involved in response inhibition. The results revealed strong effects (η 2 = .495) and are in line with findings showing that even high doses of ethanol have very specific effects on a cognitive level. Opposed to common sense, more complex cognitive operations seem to be less affected by a high-dose ethanol intoxication. Complementing this, high-dose ethanol intoxication is increasingly detrimental for action control, as stronger automated response tendencies are in charge and need to be controlled. Binge-like ethanol intoxication may take a heavier toll on cognitive control processes than on automated responses/response tendencies. Therefore, ethanol effects are more pronounced in supposedly “easier” control conditions because those facilitate the formation of automated response tendencies.
    Full-text · Article · Jun 2015 · Archives of Toxicology
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