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IntroductionSmoking urges are fundamental aspects of nicotine dependence that contribute significantly to drug use and postquit relapse. Recent evidence has indicated that damage to the insular cortex disrupts smoking behaviors and claims to reduce urges associated with nicotine use, although tools that assess urge have yet to be used to validate these findings. We examined the effect of insular versus non-insular damage on urge using a well-accepted urge scale.MethodsThis 3-month observational prospective cohort study consisted of 156 current smokers hospitalized for acute ischemic stroke (38 with insular infarctions, 118 with non-insular infarctions). During hospitalization, the Questionnaire of Smoking Urges (QSU)-brief was assessed retrospectively based on experiences before the stroke (baseline, T0), prospectively immediately following the stroke (T1) and once more via telephone at 3-month follow-up (T2), with higher scores indicating greater urge. Bivariate statistics and multivariable linear regression were used to evaluate differences in QSU-brief scores, relative to baseline, between exposure groups, controlling for age, baseline dependence, stroke severity, use of nicotine replacement, and damage to other mesocorticolimbic regions.ResultsA greater reduction in QSU-brief score was seen in the insular group compared to the non-insular group from T0 to T1 (covariate-adjusted difference in means of -1.15, 95% CI: -1.85, -0.44) and similarly from T0 to T2 (covariate-adjusted difference in means of -0.93, 95% CI: -1.79, -0.07).ConclusionsThese findings confirm the potential role of the insula in regulating nicotine-induced urges and support the growing evidence of its novelty as a key target for smoking cessation interventions.ImplicationsHuman lesioning studies that evaluate the insula's involvement in maintaining nicotine addiction make inferences of the insula's role in decreasing urge, but do not use validated instruments that directly assess urges. This study corroborates prior findings using the continuous Questionnaire of Smoking Urges to quantify changes in urge from before lesion onset to immediate and 3-month follow-up time points.

Emotional deficits have been widely described in alcohol-dependence, but several subtle and critical emotional decoding abilities remain to be investigated. In particular, the ability of alcohol-dependent individuals to process emotionally ambiguous facial stimuli, which are more frequent in everyday life than full emotional facial expressions, remains poorly understood. The present study used a categorical perception paradigm to evaluate the identification of mixed emotional facial expressions among alcohol-dependent participants.Nineteen recently detoxified participants with alcohol-dependence and 19 healthy controls were presented with facial stimuli depicting four emotional facial expressions (happy, angry, sad, and neutral), morphed along continua between each possible pair of emotions. Participants had to indicate the predominant emotion within the randomly presented facial stimuli. For each emotional category, a logistic function that estimated the percentage of identification according to the morph steps was adjusted for each participant's data.While there was no significant group difference regarding the response slope (p = 0.502, ηp2 = 0.014), the identification threshold was significantly increased in alcohol-dependent participants compared to controls (p = 0.007, ηp2 = 0.204), independently of the emotional category.The categorical perception of emotional facial expression per se appeared preserved in alcohol-dependence, but alcohol-dependent participants exhibited a bias in emotional facial expression decoding characterized by a global under-identification. This study is the first to evidence a deficit of alcohol-dependent individuals in the processing of ambiguous emotional facial expressions by using this emotional continuum paradigm measuring the categorical perception effect.

BACKGROUND:Recent evidence suggests that the insular cortex may play an important role in cognitive and emotional processes that facilitate drug use but it is unclear whether changes to the insula would result in sustained abstinence. To better understand the role of the insula in maintaining abstinence, we examined quitting patterns in smokers with acute damage to their insula relative to other regions.DESIGN:Prospective cohort study with 3month follow-up, beginning June 2013 and ending May 2014.SETTING:Three acute care hospitals in Rochester, NY.PARTICIPANTS:One-hundred-fifty-six current smokers hospitalized for acute ischemic stroke; 38 with insular infarctions and 118 with non-insular infarctions, assessed by 3 neuroradiologists.MEASUREMENTS:Self-reported smoking status (seven-day point prevalence and continuous abstinence), complete abstinence from any nicotine product, and disruption of smoking addiction (defined by criteria on smoking status, difficulty of quitting, and urge) were assessed at three months post-stroke. Time to relapse (in days) after discharge was also assessed.RESULTS:Insular damage was associated with increased odds of three-month continuous abstinence (OR=3.71, 95% CI: 1.59, 8.65) and complete cessation from any nicotine product (OR=2.72, 95% CI: 1.19, 6.22). Average time to relapse was longer in the insular-damaged group (17.50days, SD=19.82) relative to non-insular damage (10.42days, SD=18.49). Among quitters, insular damage was also associated with higher relative odds of experiencing a disruption of addiction compared to non-insular damage (adjusted OR=5.60, 95% CI: 1.52, 20.56).CONCLUSIONS:These findings support the potential role of the insular cortex in maintaining smoking and nicotine abstinence. Further research is needed to establish whether the insula may be a novel target for smoking cessation interventions.

BACKGROUND AND AIMS:Current pharmacotherapies for tobacco dependence are generally well tolerated, but have relatively high rates of relapse. They target primarily the brains' mesocorticolimbic 'reward' pathway. However, recent evidence suggests that the insular cortex, a central cerebral hemispheric region historically overlooked in addiction models, may also play an important role in cognitive and emotional processes that facilitate drug use. We examined whether insular versus non-insular damage from ischemic stroke attenuated acute withdrawal from cigarette smoking and reduced the likelihood of nicotine replacement therapy (NRT) use during hospitalization.DESIGN:Data were derived from a longitudinal study with 3 months' follow-up, beginning June 2013 and ending May 2014.SETTING:Three acute care hospitals in Rochester, NY, USA.PARTICIPANTS:One-hundred and fifty-six current smokers hospitalized for acute ischemic stroke (38 with insular infarctions and 118 with non-insular infarctions, assessed by three neuroradiologists).MEASUREMENTS:The Wisconsin Smoking Withdrawal Scale (WSWS) and Minnesota Nicotine Withdrawal Scale (MNWS) were administered during hospitalization (a period of forced abstinence) to assess the frequency and severity of withdrawal symptoms. NRT use was also assessed during hospitalization.FINDINGS:On average, smokers with insular damage had a lower WSWS score during admission [mean=5.89, standard deviation (SD)=4.72] compared with those with non-insular damage (mean=9.20, SD=4.71; P<0.001) [covariate-adjusted difference in means of -3.12, 95% confidence interval (CI)=-4.97, -1.27]. A similar difference was also noted when the MNWS was used (P=0.02). Furthermore, participants with insular lesions appeared to be less likely to use NRT during admission compared with those with non-insular lesions [odds ratio (OR)=0.72, 95% CI=0.32, 1.64].CONCLUSIONS:Current smokers with damage to their insular cortex brain region appear to experience fewer and less severe tobacco withdrawal symptoms, and appear to be less likely to require nicotine replacement therapy during hospitalization, compared with smokers with non-insular damage. These findings support the potential role of the insular cortex in regulating withdrawal during abstinence, a motivator responsible for the maintenance of addictive behaviors.