David E. Evans

Nicotine self‐medication of cognitive‐attentional processing

This article selectively reviews research concerning nicotines effects on cognition, including the neurobiological mechanism for these effects, task and experimental features that may be important for elucidating these effects, and why these effects may have amplified motivational significance among smokers with cognitive deficit. Nicotine has effects on various cognitive processes, though most studies in humans have focused on the amelioration of cognitive deficits experienced during drug withdrawal. The direct cognitive‐enhancing effect of nicotine remains a controversial topic. The relationship between attentional and non‐attentional cognitive effects of nicotine is discussed in the context of cognitive self‐medication. Further research should include theory‐driven examination of cognitive effects of nicotine, and develop targeted smoking cessation programs based on an improved understanding of the role of cognitive self‐medication in high‐risk individuals.

Neurocognitive variation in smoking behavior and withdrawal: genetic and affective moderators.

A burgeoning literature suggests that attentional factors are associated with smoking behavior (e.g. direct nicotine effects and smoking withdrawal). This study examined differences in attentional processing between nonsmokers, satiated smokers and overnight nicotine‐deprived smokers by comparing the amplitude of the P300 (P3) component of the event‐related brain potential (ERP) elicited during a go–nogo task. We also examined the moderating effects of a common dopamine receptor genotype and state negative affect (SNA) on this ERP index of attention. Nonsmokers relative to smokers had greater nogo P3 amplitude. Carrying the A1 allele at the dopamine receptor D2 (DRD2) Taq1A polymorphism site moderated the effects of withdrawal on nogo P3 amplitude, suggesting the A1 allele is a vulnerability marker for withdrawal‐related attentional deficits. Increased SNA also predicted attenuated P3 amplitude among deprived smokers. These findings suggest that DRD2 status and SNA moderate the effects of smoking status and withdrawal on neurocognitive variation during attentional processing. This research contributes to a better understanding of the role of individual differences and attentional processing in smoking behavior.

Attentional bias for smoking and affective stimuli: a Stroop task study.

Prior research has demonstrated attentional biases to smoking-related cues among smokers, and several lines of research suggest strong ties between smoking and negative affect. The authors tested attentional biases to both smoking and affective cues in 27 smokers using an emotional Stroop paradigm, and examined the relationship between these forms of attentional bias. Findings indicated significant attentional biases to smoking-related and negative-affect words, but not positive-affect words. In addition, there was a significant correlation between the degree of attentional bias to smoking and negative-affect words. These data provide evidence of a close association between smoking-related and affective cue processing from a cognitive perspective. Potential theoretical and clinical implications for these findings are discussed.

Nicotine Deprivation Influences P300 Markers of Cognitive Control

Studies suggest that reduced cognitive control due to nicotine withdrawal may have a critical role in promoting tobacco use. The P3 family of event-related brain potential (ERP) components is thought to serve as markers of cognitive control processes. Unfortunately, existing research that examines the effects of nicotine deprivation on P3 amplitude has been marred by small sample sizes and other design limitations. The present study sought to determine the effects of nicotine deprivation on P3b and P3a amplitudes, which index task relevant target detection and orienting responses to novelty, respectively. A secondary aim was to examine self-reported trait cognitive control as a moderator of nicotine deprivation-induced reductions in P3b and P3a amplitudes. In all, 121 nicotine-dependent smokers attended two experimental sessions following 12-h smoking/nicotine deprivation. In a counterbalanced manner, participants smoked nicotine cigarettes during one session and placebo cigarettes during the other session. Findings indicated that nicotine deprivation reduced P3b amplitude (p<0.00001) during a three-stimulus oddball task independent of trait cognitive control. In contrast, nicotine deprivation reduced P3a only among participants who scored lower on measures of trait cognitive control. Implications for conceptualizing risk for nicotine dependence, and its treatment, are discussed.

Neural reward and punishment sensitivity in cigarette smokers

BACKGROUND Nicotine addiction remains a major public health problem but the neural substrates of addictive behavior remain unknown. One characteristic of smoking behavior is impulsive choice, selecting the immediate reward of smoking despite the potential long-term negative consequences. This suggests that drug users, including cigarette smokers, may be more sensitive to rewards and less sensitive to punishment. METHODS We used event-related potentials (ERPs) to test the hypothesis that smokers are more responsive to reward signals and less responsive to punishment, potentially predisposing them to risky behavior. We conducted two experiments, one using a reward prediction design to elicit a Medial Frontal Negativity (MFN) and one using a reward- and punishment-motivated flanker task to elicit an Error Related Negativity (ERN), ERP components thought to index activity in the cortical projection of the dopaminergic reward system. RESULTS AND CONCLUSIONS The smokers had a greater MFN response to unpredicted rewards, and non-smokers, but not smokers, had a larger ERN on punishment motivated trials indicating that smokers are more reward sensitive and less punishment sensitive than nonsmokers, overestimating the appetitive value and underestimating aversive outcomes of stimuli and actions.

7 mg nicotine patch fails to enhance P300 neural indices of cognitive control among nonsmokers.

Nicotine administration facilitates and nicotine deprivation reduces cognitive control in smokers. Importantly, nicotine effects on cognition may reinforce smoking behavior, especially among individuals who have cognitive deficits. The target P300 (P3b) and distracter P300 (P3a) are well-validated electrocortical markers of attention- and memory-related cognitive control processes. Nicotine deprivation has been shown to reduce P3b/P3a amplitudes. The current study sought to examine the direct effects of nicotine on P3b/P3a amplitudes among nonsmokers. It was hypothesized that nicotine would increase P3b and P3a amplitudes, and that individuals lower on trait cognitive control would show greater nicotine-induced increases. 78 nonsmokers attended two separate experimental sessions, during which they performed the P3b/P3a evoking 3-stimulus oddball task following nicotine (7-mg) or placebo patch administration. Nicotine did not enhance P3b or P3a amplitudes, nor did trait cognitive control moderate the influence of nicotine on these indices. Nicotine-induced changes in P3 amplitudes may be limited to nicotine deprivation and/or nonsmokers may be fundamentally different with respect to the influence of nicotine on P3b/P3a indices of cognitive control. Directions for future research that may further examine the effects of nicotine on P3b/P3a independent of withdrawal reversal are discussed.

The Smoking N-Back: A Measure of Biased Cue Processing at Varying Levels of Cognitive Load

INTRODUCTION Recent cognitive models of drug addiction have emphasized attentional bias to drug-related cues. This bias manifests as increased accessibility to affect-laden drug-related content relative to less emotionally evocative stimuli and ideation. We examined whether biased processing of smoking-related content would differentially affect performance on a cognitive task as a function of smoking status and task complexity. METHODS Twenty-one smokers and 15 nonsmokers completed increasingly difficult 1-, 2-, and 3-back versions of the Smoking N-back task. RESULTS There were no reaction time effects that included smoking status nor was there an effect for accuracy on the 1-back task. However, smokers showed poorer accuracy on matched trials relative to nonmatched trials for smoking words on the 2- and 3-back tasks, which involve more effortful cognitive processing. Among nonsmokers, this effect was present within the 3-back condition only. CONCLUSIONS These findings suggest that cognitive bias to drug-related cues may be modulated by task complexity. Future research on cognitive bias should better account for this factor. Additional research will be needed to validate these findings by controlling for various potential confounds (e.g., nicotine withdrawal, task fatigue) as well as determine the clinical relevance of cognitive bias across varying levels of task complexity.

Measuring smoking-related preoccupation and compulsive drive: evaluation of the obsessive compulsive smoking scale.

RationaleTobacco use for many people is compulsive in nature. Compelling theories of how smoking becomes compulsive exist but are largely based on extrapolation from neuroscience findings. Research on smokers is impeded, in part, by a lack of instruments that specifically measure compulsive smoking.ObjectiveThis study evaluated the measurement structure and validity of the Obsessive Compulsive Smoking Scale (OCSS), a ten-item questionnaire designed to measure compulsive smoking.MethodsParticipants were 239 daily smokers (≥1 cigarette/day), including 142 students at a public university in Chicago and 97 veterans treated at the VA Boston Healthcare System. The OCSS and questionnaires measuring current and past smoking, cigarette craving, automatic smoking, and nicotine dependence were administered.ResultsFactor analysis with maximum likelihood extraction and oblique rotation revealed two correlated underlying factors, interpreted as “Preoccupation with Smoking” and “Compulsive Drive.” The measurement structure was consistent across students and veterans, and confirmed in an independent sample of adults (n = 95). Veterans exhibited higher OCSS scores (full scale and subscales) than students. Across groups, higher OCSS scores were positively correlated with smoking intensity, craving, and nicotine dependence. OCSS full-scale and compulsive drive scores, but not smoking preoccupation scores, were inversely correlated with past month smoking reduction and minutes since last cigarette.ConclusionsThe OCSS is a valid and reliable inventory for measuring the degree to which daily smokers are preoccupied with smoking and engage in compulsive tobacco use, and may be useful for advancing understanding of core smoking phenotypes or for tailoring cessation therapies.

Smokers exhibit biased neural processing of smoking and affective images.

OBJECTIVE There has been growing interest in the role that implicit processing of drug cues can play in motivating drug use behavior. However, the extent to which drug cue processing biases relate to the processing biases exhibited to other types of evocative stimuli is largely unknown. The goal of the present study was to determine how the implicit cognitive processing of smoking cues relates to the processing of affective cues using a novel paradigm. METHOD Smokers (n = 50) and nonsmokers (n = 38) completed a picture-viewing task, in which participants were presented with a series of smoking, pleasant, unpleasant, and neutral images while engaging in a distractor task designed to direct controlled resources away from conscious processing of image content. Electroencephalogram recordings were obtained throughout the task for extraction of event-related potentials (ERPs). RESULTS Smokers exhibited differential processing of smoking cues across 3 different ERP indices compared with nonsmokers. Comparable effects were found for pleasant cues on 2 of these indices. Late cognitive processing of smoking and pleasant cues was associated with nicotine dependence and cigarette use. CONCLUSIONS Results suggest that cognitive biases may extend across classes of stimuli among smokers. This raises important questions about the fundamental meaning of cognitive biases, and suggests the need to consider generalized cognitive biases in theories of drug use behavior and interventions based on cognitive bias modification. (PsycINFO Database Record

Nicotine-induced cortical activation among nonsmokers with moderation by trait cognitive control

RationaleConsiderable research suggests that nicotine enhances cognitive control-related processes (e.g., attention, memory) among nicotine-deprived smokers, both in terms of behavior and neural indices (e.g., ERP, slow-wave EEG). Nicotine may also increase cognitive control among nonsmokers, and this may vary as a function of trait cognitive control. It is important to examine the effects of nicotine on cognitive control-related processes among nonsmokers as these effects may provide a path for the initiation of smoking.ObjectivesThe objectives of the study were to examine in nonsmokers (1) the effect of nicotine on resting cortical activity, an indirect measure of cognitive control, and (2) trait cognitive control as a moderator of nicotine-induced cortical activity changes.MethodEighty participants were given placebo and 7-mg nicotine patches in separate sessions for this counter-balanced, double-blind, within-subject study. Resting cortical activity was measured with EEG for a 3-min period with eyes opened.ResultsAverage alpha-1 band power density values in frontal and central regions were lower during the nicotine versus placebo condition, which provides evidence of nicotine-induced cortical activation. Furthermore, those with lower self-reported cognitive control exhibited greater nicotine-induced reductions in alpha-1 power density values.ConclusionsThese individual differences in nicotine-induced cortical activation are consistent with a model of nicotine self-medication whereby individuals with lower cognitive control may find smoking more reinforcing via amelioration of related cognitive deficits.