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P.6.f.001 Diminished error processing in smokers during smoking cue exposure: an ERP study
S608
P.6.f. Addiction − Other (basic)
Methods: A functional magnetic resonance imaging (fMRI) event related cue reactivity paradigm, consisting of gambling, nicotine, and neutral pictures, was employed in 21 pathological gamblers, 17 heavy smokers, and 19 healthy controls. A twochoice button press was made during the viewing of the pictures: participants had to indicate whether a face was present on the pictures or not. Self-reported craving measures were filled out before and after the cue reactivity task. Group interactions are reported at p < 0.001, masked with the appropriate main effect at p < 0.05. Results: Pathological gamblers showed higher brain activation compared to healthy controls and heavy smokers when viewing gambling pictures compared to neutral pictures (see Figure 1 and Figure 2). Specifically, cortical brain areas related to visual information processing (the ventral and dorsal visual stream), and basal ganglia structures, (putamen, caudate nucleus) known to be related to reinforcement learning and salience, showed higher activation patterns. Subjective craving in pathological gamblers correlated positively with brain activation in left VLPFC and left insula. Whereas no overall differences between heavy smokers and controls were present, a subgroup of heavy smokers with higher scores on the Fagerstrom Test for Nicotine Dependence demonstrated higher frontal and anterior cingulate brain reactivity to nicotine pictures versus neutral pictures, compared to the healthy control group. These findings point to the persistent emotional relevance of gambling stimuli in abstinent pathological gamblers, and were accompanied by higher overall craving scores for gambling in the pathological gambling group, and higher craving scores for smoking in the heavy smokers group, compared to the healthy control group. No differences were present between the groups in reaction times to the pictures. Nicotine craving correlated with activation in left prefrontal and left amygdala when viewing smoking-related pictures in heavy smokers. Conclusions: Increased regional responsiveness to gambling pictures in brain regions linked to motivation and visual processing is present in pathological gamblers, similar to neural mechanisms underlying cue reactivity in substance dependence. Increased brain activation in related fronto-limbic brain areas was present in heavy smokers with a higher nicotine dependence score, compared to a subgroup of smokers with lower nicotine dependence scores. These findings indicate that cue responsivity at the neuronal level is still present in a group of abstinent pathological gamblers. Similar to reports in substance dependence, where brain reactivity to cues promotes relapse, this long lasting effect of gambling cues on brain activity in pathological gamblers may promote relapse in problem gambling.
P.6.f. Addiction − Other (basic) P.6.f.001 Diminished error processing in smokers during smoking cue exposure: an ERP study
conditioned smoking cues. Error processing in the brain can be measured at the electrophysiological level with two event-related potentials (ERPs), namely, the error-related negativity (ERN), reflecting automatic and initial error processing [1], and the error positivity (Pe), which is assumed to be related to the motivational significance attributed to an error [2]. Methods: 13 smokers (mean age = 20.7, 9 men) were compared with 14 non-smoking controls (mean age = 21.4, 10 men). Smokers smoked at least 10 cigarettes a day (mean = 16.8 cigarettes). FTND scores served as a measure of nicotine dependence in smokers (mean score = 5.0). ERPs were measured during the performance of an adapted Erikson Flanker task. Participants were exposed to smoking related and neutral pictures during task performance. Furthermore, impulsivity was assessed using the I7 questionnaire. Results: Smokers and non-smoking controls made comparable numbers of errors. Analyses indicated a group × post correctness interaction effect for reaction times, F(1,25) = 4.4, p = 0.045. Posthoc tests showed that the difference between post-incorrect and post-correct reaction times was significant for controls, t(13) = 4.7, p < 0.001, and not for smokers, t(12) = 1.41, ns, suggesting diminished post-error slowing in smokers. A group × performance (correct versus incorrect responses) was found for both the ERN, F(1,25) = 7.83, p = 0.01, and Pe, F(1,25) = 5.07, p < 0.05. Posthoc analyses on mean difference waves confirmed that smokers had reduced ERN and Pe waves as compared to non-smokers, t(25) = 2.80, p = 0.01 and t(25) = 2.30, p < 0.05. Impulsivity levels across groups correlated with ERN, r = 0.44, p = 0.02, but not with Pe amplitudes, such that higher impulsivity levels are related to reduced ERN amplitudes. Moreover, nicotine dependence levels correlated with ERN, r = 0.69, p 0.01, but not with Pe amplitudes, showing that higher levels of nicotine dependence are associated with reduced ERN amplitudes. Conclusion: Results of the current study showed diminished error processing in smokers during smoking cue exposure both at the behavioural and electrophysiological level. Decreased ERN and Pe amplitudes in smokers were accompanied by reduced posterror slowing. Furthermore, impulsivity levels across groups and nicotine dependence levels in smokers are associated with reduced ERN amplitudes, suggesting that multiple mechanisms contribute to reduced error processing. Since adequate error processing is required to adapt behaviour properly, reduced error processing may contribute to the development and maintenance of addictive behaviours. References [1] Falkenstein, M., Hoormann, J., Christ, S., Hohnsbein, J., 2000 ERP components on reaction errors and their functional significance: a tutorial. Biological Psychology, 87–107. [2] Ridderinkhof, K.R., Ramautar, J.R., Wijnen, J.G., 2009 To P(E) or not to P(E): a P3 like ERP component reflecting the processing of response errors. Psychophysiology 46(3), 531–538.
M. Luijten1 ° , I.H.A. Franken1 . 1 Erasmus University Rotterdam, Institute of Psychology, Rotterdam, The Netherlands
P.6.f.002 Hypericum perforatum, nicotine patches and combination hypericum perforatum/nicotine patches for smoking cessation
Purpose: Deficits in error processing may contribute to the continuation of impulsive behaviours such as smoking despite negative consequences. Error processing deficits in smokers may be more pronounced during smoking cue exposure, as limited capacity may be available to monitor ongoing behaviour. Furthermore, enhanced impulsivity levels may be associated with diminished error processing. The present study aimed to investigate error processing deficits in smokers in a challenging environment including
M. Kras1 ° , C. Stough1 , A. Scholey1 , C. Kure1 , D. Camfield1 . 1 Swinburne University, Brain Sciences Institute, Melbourne, Australia Purpose: There are several treatments available for smoking cessation. However current treatments are only mildly efficacious and have side effects [1]. Research suggests that Hypericum Perforatum Extract (Ze117) influences the dopamine reward pathways [2],
P.6.f. Addiction − Other (basic)
Methods: A functional magnetic resonance imaging (fMRI) event related cue reactivity paradigm, consisting of gambling, nicotine, and neutral pictures, was employed in 21 pathological gamblers, 17 heavy smokers, and 19 healthy controls. A twochoice button press was made during the viewing of the pictures: participants had to indicate whether a face was present on the pictures or not. Self-reported craving measures were filled out before and after the cue reactivity task. Group interactions are reported at p < 0.001, masked with the appropriate main effect at p < 0.05. Results: Pathological gamblers showed higher brain activation compared to healthy controls and heavy smokers when viewing gambling pictures compared to neutral pictures (see Figure 1 and Figure 2). Specifically, cortical brain areas related to visual information processing (the ventral and dorsal visual stream), and basal ganglia structures, (putamen, caudate nucleus) known to be related to reinforcement learning and salience, showed higher activation patterns. Subjective craving in pathological gamblers correlated positively with brain activation in left VLPFC and left insula. Whereas no overall differences between heavy smokers and controls were present, a subgroup of heavy smokers with higher scores on the Fagerstrom Test for Nicotine Dependence demonstrated higher frontal and anterior cingulate brain reactivity to nicotine pictures versus neutral pictures, compared to the healthy control group. These findings point to the persistent emotional relevance of gambling stimuli in abstinent pathological gamblers, and were accompanied by higher overall craving scores for gambling in the pathological gambling group, and higher craving scores for smoking in the heavy smokers group, compared to the healthy control group. No differences were present between the groups in reaction times to the pictures. Nicotine craving correlated with activation in left prefrontal and left amygdala when viewing smoking-related pictures in heavy smokers. Conclusions: Increased regional responsiveness to gambling pictures in brain regions linked to motivation and visual processing is present in pathological gamblers, similar to neural mechanisms underlying cue reactivity in substance dependence. Increased brain activation in related fronto-limbic brain areas was present in heavy smokers with a higher nicotine dependence score, compared to a subgroup of smokers with lower nicotine dependence scores. These findings indicate that cue responsivity at the neuronal level is still present in a group of abstinent pathological gamblers. Similar to reports in substance dependence, where brain reactivity to cues promotes relapse, this long lasting effect of gambling cues on brain activity in pathological gamblers may promote relapse in problem gambling.
P.6.f. Addiction − Other (basic) P.6.f.001 Diminished error processing in smokers during smoking cue exposure: an ERP study
conditioned smoking cues. Error processing in the brain can be measured at the electrophysiological level with two event-related potentials (ERPs), namely, the error-related negativity (ERN), reflecting automatic and initial error processing [1], and the error positivity (Pe), which is assumed to be related to the motivational significance attributed to an error [2]. Methods: 13 smokers (mean age = 20.7, 9 men) were compared with 14 non-smoking controls (mean age = 21.4, 10 men). Smokers smoked at least 10 cigarettes a day (mean = 16.8 cigarettes). FTND scores served as a measure of nicotine dependence in smokers (mean score = 5.0). ERPs were measured during the performance of an adapted Erikson Flanker task. Participants were exposed to smoking related and neutral pictures during task performance. Furthermore, impulsivity was assessed using the I7 questionnaire. Results: Smokers and non-smoking controls made comparable numbers of errors. Analyses indicated a group × post correctness interaction effect for reaction times, F(1,25) = 4.4, p = 0.045. Posthoc tests showed that the difference between post-incorrect and post-correct reaction times was significant for controls, t(13) = 4.7, p < 0.001, and not for smokers, t(12) = 1.41, ns, suggesting diminished post-error slowing in smokers. A group × performance (correct versus incorrect responses) was found for both the ERN, F(1,25) = 7.83, p = 0.01, and Pe, F(1,25) = 5.07, p < 0.05. Posthoc analyses on mean difference waves confirmed that smokers had reduced ERN and Pe waves as compared to non-smokers, t(25) = 2.80, p = 0.01 and t(25) = 2.30, p < 0.05. Impulsivity levels across groups correlated with ERN, r = 0.44, p = 0.02, but not with Pe amplitudes, such that higher impulsivity levels are related to reduced ERN amplitudes. Moreover, nicotine dependence levels correlated with ERN, r = 0.69, p 0.01, but not with Pe amplitudes, showing that higher levels of nicotine dependence are associated with reduced ERN amplitudes. Conclusion: Results of the current study showed diminished error processing in smokers during smoking cue exposure both at the behavioural and electrophysiological level. Decreased ERN and Pe amplitudes in smokers were accompanied by reduced posterror slowing. Furthermore, impulsivity levels across groups and nicotine dependence levels in smokers are associated with reduced ERN amplitudes, suggesting that multiple mechanisms contribute to reduced error processing. Since adequate error processing is required to adapt behaviour properly, reduced error processing may contribute to the development and maintenance of addictive behaviours. References [1] Falkenstein, M., Hoormann, J., Christ, S., Hohnsbein, J., 2000 ERP components on reaction errors and their functional significance: a tutorial. Biological Psychology, 87–107. [2] Ridderinkhof, K.R., Ramautar, J.R., Wijnen, J.G., 2009 To P(E) or not to P(E): a P3 like ERP component reflecting the processing of response errors. Psychophysiology 46(3), 531–538.
M. Luijten1 ° , I.H.A. Franken1 . 1 Erasmus University Rotterdam, Institute of Psychology, Rotterdam, The Netherlands
P.6.f.002 Hypericum perforatum, nicotine patches and combination hypericum perforatum/nicotine patches for smoking cessation
Purpose: Deficits in error processing may contribute to the continuation of impulsive behaviours such as smoking despite negative consequences. Error processing deficits in smokers may be more pronounced during smoking cue exposure, as limited capacity may be available to monitor ongoing behaviour. Furthermore, enhanced impulsivity levels may be associated with diminished error processing. The present study aimed to investigate error processing deficits in smokers in a challenging environment including
M. Kras1 ° , C. Stough1 , A. Scholey1 , C. Kure1 , D. Camfield1 . 1 Swinburne University, Brain Sciences Institute, Melbourne, Australia Purpose: There are several treatments available for smoking cessation. However current treatments are only mildly efficacious and have side effects [1]. Research suggests that Hypericum Perforatum Extract (Ze117) influences the dopamine reward pathways [2],