%0 Journal Article
%T Effects of Nicotine on Emotional Reactivity in PTSD and Non-PTSD Smokers: Results of a Pilot fMRI Study
%A Brett Froeliger
%A Jean Crowell Beckham
%A Michelle Feldman Dennis
%A Rachel Victoria Kozink
%A Francis Joseph McClernon
%J Advances in Pharmacological Sciences
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/265724
%X 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. 1. Introduction Posttraumatic stress disorder (PTSD) is associated with elevated rates of cigarette smoking (40%¨C63%) compared with population norms (20%¨C30%) [1¨C3]. 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]. A hallmark phenotype of individuals with PTSD is increased psychophysiological responsivity and NA to idiopathic trauma-related stimuli [8]. Furthermore, individuals with PTSD exhibit aberrant responding to nonspecific, negative emotional stimuli [9]. For instance, individuals with PTSD exhibit biased attention to negative emotional information [10, 11]. Moreover, compared to non-PTSD trauma survivors, PTSD survivors have increased electrocortical responses to sad faces [12]. It has been proposed [13, 14] that dysregulated emotional information processing in PTSD is due to hyperresponsiveness of the amygdala¡ªa region subserving negative emotional information processes [15]¡ªand also hyporesponsiveness of medial prefrontal cortices¡ªa region involved in cognitive control of emotional responses [16]. Support for this hypothesis comes from fMRI studies of PTSD patients showing increased reactivity to fearful faces in amygdala as compared to controls [17, 18] coincident with decreased reactivity in medial prefrontal regions [18]. Laboratory studies show that smoking and nicotine reduces distraction caused by negative stimuli [19] and electrocortical responses [20] to these stimuli among smokers. Moreover, neuroimaging studies show that nicotine acts on limbic (e.g., amygdala) and prefrontal brain areas that subserve emotional information processing [21¨C23]. Despite evidence regarding smoking/PTSD interactions, no neuroimaging studies to date have
%U http://www.hindawi.com/journals/aps/2012/265724/