Effects of cigarette smoking and abstinence on Stroop task performance.

RATIONALE: Smokers report enhanced concentration after cigarette smoking and difficulty concentrating when abstinent from smoking. These perceived effects may contribute to smoking cessation failures, and if so, clarification of their cognitive bases could inform treatment strategies. Selective attention may be important in this regard, but earlier literature presents inconsistent findings on how smoking abstinence and resumption of smoking influence this cognitive function. OBJECTIVES: We aimed to compare smokers and nonsmokers on selective attention, and in smokers, to test the effects of overnight abstinence from smoking and of acute smoking on selective attention. MATERIALS AND METHODS: Smokers and nonsmokers (n = 43) performed a Stroop test (two test days, two test blocks per day). Smokers participated after overnight abstinence and also within 1-h of ad libitum smoking. Smokers each smoked a cigarette between test blocks on each day; nonsmokers did not. RESULTS: Smokers demonstrated longer response latencies for both congruent and incongruent stimuli after overnight than brief abstinence, but no deficit specifically related to selective attention. Whereas nonsmokers showed no changes in performance in the second test block, smoking between blocks reduced the Stroop effect when smokers were abstinent overnight. CONCLUSIONS: These data are consistent with the hypothesis that abstinence from smoking among nicotine-dependent individuals has deleterious effects on cognitive performance, but do not indicate that selective attention is adversely effected. Improvement in selective attention after terminating abstinence with one cigarette may also contribute to smokers' perceived enhanced ability to concentrate after smoking.

Attenuation of cue-induced cigarette craving and anterior cingulate cortex activation in bupropion-treated smokers: a preliminary study.

In untreated smokers, exposure to cigarette-related cues increases both the intensity of cigarette craving and relative glucose metabolism of the perigenual/ventral anterior cingulate cortex (ACC). Given that treatment with bupropion HCl reduces overall cigarette craving levels in nicotine dependent subjects, we performed a preliminary study of smokers to determine if bupropion HCl treatment attenuates cue-induced cigarette craving and associated brain metabolic activation. Thirty-seven, otherwise healthy smokers (20 untreated and 17 who had received open-label treatment with bupropion HCl) underwent two (18)F-fluorodeoxyglucose positron emission tomography scanning sessions in randomized order--one when presented with neutral cues and the other when presented with cigarette-related cues. Bupropion-treated smokers had smaller cigarette cue-induced increases in craving scores on the Urge to Smoke (UTS) Scale and less activation of perigenual/ventral ACC metabolism from the neutral to the cigarette cue scan than untreated smokers. Thus, in addition to its known effects on spontaneous cigarette craving and withdrawal symptoms, bupropion HCl diminishes cue-induced cigarette craving and appears to attenuate cigarette cue-induced ACC activation. These results are consistent with the known effects of bupropion HCl, including its enhancement of catecholaminergic neurotransmission.

Differences between smokers and nonsmokers in regional gray matter volumes and densities.

BACKGROUND: Magnetic resonance imaging (MRI) studies have demonstrated large-scale brain abnormalities in cigarette smokers, such as ventricular enlargement and atrophy. Converging lines of evidence point to functional differences between smokers and nonsmokers in specific brain regions, namely the lateral prefrontal cortex (PFC), anterior cingulate cortex (ACC), ventral striatum, and thalamus. Using MRI, we examined these regions for differences in gray matter between smokers and nonsmokers. METHODS: Thirty-six otherwise healthy adults (19 smokers and 17 nonsmoking control subjects) underwent three-dimensional Fourier-transform spoiled-gradient-recalled acquisition MRI of the brain. Both hand-drawn regions of interest and the computer program voxel-based morphometry were used to assess group differences in regional gray matter volumes and densities, respectively. RESULTS: Smokers had smaller gray matter volumes and lower gray matter densities than nonsmokers in the PFC bilaterally, along with smaller volumes in the left dorsal ACC and lower gray matter densities in the right cerebellum. Smokers also had negative associations between pack-year smoking history and PFC gray matter densities. CONCLUSIONS: Smokers and nonsmokers differed in regional gray matter in brain areas previously linked with nicotine dependence. These findings might reflect effects of chronic smoking, predisposing traits that lead to smoking, or some combination of these factors.

Brain metabolic changes during cigarette craving.

BACKGROUND: In functional brain imaging studies, exposure to cues related to cocaine, opiates, and alcohol in dependent individuals is associated with activation of the anterior cingulate gyrus, amygdala, orbitofrontal cortex, and dorsolateral prefrontal cortex. Craving for these substances positively correlates with activity in the orbitofrontal cortex, dorsolateral prefrontal cortex, and anterior insula. The objective of this study was to determine changes in regional cerebral glucose metabolism and correlations between craving and regional metabolism in heavy cigarette smokers exposed to cigarette-related cues. METHODS: Twenty heavy smokers (who smoked > or =20 cigarettes per day) and 20 nonsmoking control subjects underwent 2 fluorine 18-fluorodeoxyglucose positron emission tomography scans 10 days apart in randomized order: one while watching a videotape that presented cigarette-related cues and handling a cigarette, and the other while watching an educational (nature) videotape and handling a neutral object (pen). RESULTS: From the neutral to the cigarette cue scan, heavy smokers had greater increases than nonsmoking controls in relative glucose metabolism in the perigenual anterior cingulate gyrus spanning the midline. Significant positive correlations were found between intensity of craving and metabolism in the orbitofrontal cortex, dorsolateral prefrontal cortex, and anterior insula bilaterally. An unexpected positive association was found between craving and metabolism in the right sensorimotor cortex. CONCLUSIONS: Brain regions associated with arousal, compulsive repetitive behaviors, sensory integration, and episodic memory are activated during exposure to cigarette-related cues and cigarette craving. These regional brain activations and associations with craving are similar to findings with other addictive substances.

Smoking cessation in methadone maintenance.

AIMS: To evaluate relapse prevention (relapse prevention) and contingency management (contingency management) for optimizing smoking cessation outcomes using nicotine replacement therapy for methadone-maintained tobacco smokers. DESIGN: Experimental, 2 (relapse prevention)x2 (contingency management) repeated measures design using a platform of nicotine replacement therapy featuring a 2-week baseline period, followed by randomization to 12 weeks of treatment, and 6- and 12-month follow-up visits. SETTING: Three narcotic treatment centers in Los Angeles. PARTICIPANTS: One hundred and seventy-five participants who met all inclusion and no exclusion criteria. INTERVENTION: Participants received 12 weeks of nicotine replacement therapy and assignment to one of four conditions: patch-only, relapse prevention + patch, contingency management + patch and relapse prevention + contingency management + patch. MEASUREMENTS: Thrice weekly samples of breath (analyzed for carbon monoxide) and urine (analyzed for metabolites of opiates and cocaine) and weekly self-reported numbers of cigarettes smoked. FINDINGS: Participants (73.1%) completed 12 weeks of treatment. During treatment, those assigned to receive contingency management showed statistically higher rates of smoking abstinence than those not assigned to receive contingencies (F3,4680=6.3, P=0.0003), with no similar effect observed for relapse prevention. At follow-up evaluations, there were no significant differences between conditions. Participants provided more opiate and cocaine-free urines during weeks when they met criteria for smoking abstinence than during weeks when they did not meet these criteria (F1,2054=14.38, P=0.0002; F1,2419=16.52, P<0.0001). CONCLUSIONS: Contingency management optimized outcomes using nicotine replacement therapy for reducing cigarette smoking during treatment for opiate dependence, although long-term effects are not generally maintained. Findings document strong associations between reductions in cigarette smoking and reductions in illicit substance use during treatment.

Modulating tobacco smoking rates by dopaminergic stimulation and blockade.

This study was designed to demonstrate that dopaminergic stimulation would result in decreased smoking behavior and nicotine intake, whereas dopaminergic blockade would result in increased smoking behavior and nicotine intake, in the same subjects. In prior human studies, a dopaminergic antagonist, haloperidol, increased smoking and/or nicotine intake, and a dopamine agonist, bromocriptine, decreased smoking. The smoking behavior of 20 heavy smokers was observed on two separate visits in a randomized, double-blind, repeated-measures-within-subject design. In the drug-reversal design, either bromocriptine (2.5 mg) or haloperidol (2.0 mg) was administered at each 5-h session, during which subjects smoked their own cigarettes ad libitum. Smoking topography was measured using a thermistor flow detector apparatus. Subjects smoked their cigarettes faster (p<0.05) and total puffing time was greater (p<0.05) with haloperidol than with bromocriptine. There was a trend for both a shorter latency to smoke (p<0.10, one-tailed) during time of expected peak drug concentration and for a shorter inter-cigarette interval with haloperidol than with bromocriptine (p<0.10, one-tailed). Shiffman-Jarvik Withdrawal Scale craving subscale scores increased significantly more with haloperidol than with bromocriptine (p<0.05). Mean Profile of Mood States (POMS) scores differed significantly for only one subscale (Confusion: bromocriptine>haloperidol; p<0.05). These data support the hypothesis that nicotine mediates reinforcement from smoking via dopamine, and that smoking behavior can be manipulated within the same subjects in opposite directions by alternately stimulating and blocking dopamine.