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
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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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    • "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.
    International Journal of Psychophysiology 09/2015; DOI:10.1016/j.ijpsycho.2015.09.005 · 2.88 Impact Factor
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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 (η2 = .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.
    Archives of Toxicology 06/2015; DOI:10.1007/s00204-015-1565-y · 5.98 Impact Factor
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    • "While cognitive functions comprise a wide variety of different cognitive abilities, cognitive control, often referred to as impulsivity, is also considered in the scientific literature (de Wit 2009; Fernandez-Serrano et al. 2011; Jones et al. 2013) as a multi-dimensional construct including processes of attentional control, response inhibition and decision making (delay discounting ). While Dougherty et al. (2008) include impaired response initiation as an important component of impulsivity, meaning that ADP respond rapidly before a stimulus is completely processed, other authors (Crews & Boettiger 2009; Fernandez-Serrano et al. 2011) emphasize in expansion of the above-mentioned aspects of cognitive control functions the importance of reversal learning in relation to addiction. "
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    ABSTRACT: Recent models of the development of addiction propose a transition from a pleasure-driven to a heavily automatized behaviour, marked by a loss of cognitive control. This study investigated the deficits in different components of cognitive functions including behavioural inhibition in response to alcohol-related stimuli in alcohol-dependent patients (ADP) and healthy controls (HC). The aims of the study were to identify which particular cognitive functions are impaired in ADP. Furthermore, we analysed the association between cognitive deficits and relapse rates and the reversibility of cognitive deficits under abstinence in a 6-month follow-up period. Ninety-four recently detoxified ADP and 71 HC completed the cognitive tasks as well as questionnaire measures assessing drinking behaviour and personality traits. Compared with HC, ADP showed poorer performance in response initiation, response inhibition, complex-sustained attention and executive functions. Impairment in response inhibition was a significant predictor for relapse, yet the strongest predictor was the interaction between the number of previous detoxifications and response-inhibition deficits. The results of a moderation analysis showed that patients with many previous detoxifications and large deficits in response inhibition showed the highest relapse risk. These findings indicate that interventions should take into account inhibitory deficits especially in ADP with a high number of previous detoxifications. © 2015 Society for the Study of Addiction.
    Addiction Biology 02/2015; DOI:10.1111/adb.12229 · 5.36 Impact Factor
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