Correlations between orbitofrontal dysfunction and tobacco smoking

Spinella, Marcello

doi:10.1080/1355621021000005964

Cited by 78 publications

(72 citation statements)

References 27 publications

(17 reference statements)

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“…Relative to non-smokers, smokers have been found to be impaired on behavioural indices of impulse control in oculomotor (antisaccade), go/no-go, and delayed alternation tasks (e.g. Spinella, 2002), to take more risks in decision-making (Lejuez et al, 2003) and to show abnormally strong preferences for immediate or certain rewards over larger but delayed or less certain rewards (delay or probability discounting; e.g. Bickel et al, 1999;Mitchell, 1999;Reynolds et al, 2004).…”

Section: Response Inhibition / Inhibitory Controlmentioning

confidence: 99%

Relapse to smoking during unaided cessation: clinical, cognitive and motivational predictors

et al. 2010

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Rationale: Neurobiological models of addiction suggest that abnormalities of brain reward circuitry distort salience attribution and inhibitory control processes, which in turn contribute to high relapse rates. Objectives:To determine whether impairments of salience attribution and inhibitory control predict relapse in a pharmacologically unaided attempt at smoking cessation.Methods: 141 smokers were assessed on indices of nicotine consumption / dependence (e.g. the FTND, cigarettes per day, salivary cotinine), and three trait impulsivity measures. After overnight abstinence they completed experimental tests of cue reactivity, attentional bias to smoking cues, response to financial reward, motor impulsiveness, and response inhibition (antisaccades). They then started a quit attempt with follow-up after 7 days, 1 month, and 3 months; abstinence was verified via salivary cotinine levels ≤ 20ng/ml. Results:Relapse rates at each point were 52.5%, 64% and 76.3%. The strongest predictor was pre-cessation salivary cotinine; other smoking / dependence indices did not explain additional outcome variance and neither did trait impulsivity. All experimental indices except responsivity to financial reward significantly predicted one week outcome. Salivary cotinine, attentional bias to smoking cues and antisaccade errors explained unique as well as shared variance. At one and three months, salivary cotinine, motor impulsiveness and cue reactivity were all individually predictive; the effects of salivary cotinine and motor impulsiveness were additive.Conclusions: These data provide some support for the involvement of abnormal cognitive and motivational processes in sustaining smoking dependence and suggest that they might be a focus of interventions, especially in the early stages of cessation.2

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Section: Response Inhibition / Inhibitory Controlmentioning

confidence: 99%

Relapse to smoking during unaided cessation: clinical, cognitive and motivational predictors

et al. 2010

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“…For example, adult smoking has been associated with both impulsive choice (Bickel et al, 1999;Mitchell, 1999) as well as deficits in inhibitory control when compared to nonsmokers (Mitchell, 1999;Skinner et al, 2004;Spinella, 2002). However, whether impulsivity in adult smokers results from nicotine exposure, or alternatively, is a preexisting vulnerability trait predisposing individuals to initiate and maintain smoking is as yet unclear.…”

Section: Adolescent Nicotine Exposure and Impulsivitymentioning

confidence: 99%

Long-Lasting Cognitive Deficits Resulting from Adolescent Nicotine Exposure in Rats

Counotte

Spijker

Burgwal

et al. 2008

Neuropsychopharmacol

151

134

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Adolescence is a developmental period, during which the brain and particularly medial prefrontal cortical (mPFC) regions thereof have not fully matured. Because epidemiological data have suggested that adolescent nicotine use may result in disturbances in cognitive function in adulthood, we investigated the long-term effects of adolescent nicotine exposure in rats. Male Wistar rats were exposed to either nicotine (three times daily, 0.4 mg/kg s.c.) or saline for 10 days during (postnatal day (PND) 34-43) or following (PND 60-69) adolescence. After 5 weeks during adulthood, separate groups of animals were tested in operant paradigms taxing attention and distinct measures of impulsivity. Visuospatial attention and impulsive action were tested in the five-choice serial reaction time task, whereas impulsive choice was assessed in the delayed reward task. Our data show that adolescent, but not postadolescent, nicotine exposure affects cognitive performance in adulthood and results in diminished attentional performance and increments in impulsive action, while leaving impulsive choice intact. This altered cognitive performance appeared to be associated with enhanced releasability of dopamine in the mPFC. Together, these data suggest that adolescence is a time window during which the brain is vulnerable to long-lasting cognitive disturbances resulting from nicotine exposure.

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“…In a study examining antisaccade performance in smokers, Spinella (2002) found that smokers commit more inhibition errors than do non-smokers. Further, Chung et al (2011) found that adolescents diagnosed with substance use disorder committed more inhibition errors in a rewarded antisaccade task than did those without a history of substance abuse.…”

Section: Cross-sectional Comparisons Campanella and Colleaguesmentioning

confidence: 99%