Research Article: Effects of Nicotine on Emotional Reactivity in PTSD and Non-PTSD Smokers: Results of a Pilot fMRI Study

Date Published: June 3, 2012

Publisher: Hindawi Publishing Corporation

Author(s): Brett Froeliger, Jean Crowell Beckham, Michelle Feldman Dennis, Rachel Victoria Kozink, Francis Joseph McClernon.


There is evidence that individuals with posttraumatic stress disorder (PTSD) may smoke in part to regulate negative affect. This pilot fMRI study examined the effects of nicotine on emotional information processing in smokers with and without PTSD. Across groups, nicotine increased brain activation in response to fearful/angry faces (compared to neutral faces) in ventral caudate. Patch x Group interactions were observed in brain regions involved in emotional and facial feature processing. These preliminary findings suggest that nicotine differentially modulates negative information processing in PTSD and non-PTSD smokers.

Partial Text

Posttraumatic stress disorder (PTSD) is associated with elevated rates of cigarette smoking (40%–63%) compared with population norms (20%–30%) [1–3]. Moreover, smokers with PTSD are significantly more likely to be “heavy” smokers (i.e., smoke >25 cigarettes/day) [4] and take larger puffs [5]. In naturalistic studies, PTSD smokers are more likely to report negative affective (NA) states as an antecedent to smoking [6] and also report significant reductions in NA following smoking [7].

This preliminary study is the first to systematically assess the effects of nicotine on neural correlates of emotional information processing in a PTSD sample. As in previous studies [17, 18], PTSD was associated with larger brain responses to emotional face stimuli in amygdala and prefrontal regions.

The present preliminary study provides novel information regarding the effects of nicotine on emotional information processing in smokers with and without PTSD. Smokers with PTSD report greater NA immediately prior to smoking [34] and greater decreases in NA following smoking [35], and these findings are consistent with the observed patterns of brain activation in the current study. Thus, our findings provide a neurobiological basis that helps explain why individuals with PTSD are at greater risk of smoking and also experience greater difficulty quitting. The present study is not without its limitations. Our sample size was small and was predominately represented by female smokers. Moreover, among the female participants, we did not obtain information regarding menstrual cycle phase in relation to the timing of each of their experimental sessions which may have added some variance to the results. Future work will examine the effects of nicotine and smoking in larger samples of smokers with PTSD, control for sex differences, and among females control for time in menstrual cycle, and relate these findings to smoking-related outcomes (e.g., smoking cessation success/failure).




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