The construct of emotion regulation has been increasingly investigated in the last decade, and this work has important implications for advancing anxiety disorder theory. This paper reviews research demonstrating that: 1) emotion (i.e., fear and anxiety) and emotion regulation are distinct, non-redundant, constructs that can be differentiated at the conceptual, behavioral, and neural levels of analysis; 2) emotion regulation can augment or diminish fear, depending on the emotion regulation strategy employed; and 3) measures of emotion regulation explain incremental variance in anxiety disorder symptoms above and beyond the variance explained by measures of emotional reactivity. The authors propose a model by which emotion regulation may function in the etiology of anxiety disorders. The paper concludes with suggestions for future research.

There has been growing interest in the interrelations among traumatic event exposure, posttraumatic stress disorder (PTSD), and sleep problems. A wealth of research has examined the associations among these factors and there is an emerging literature focused on how sleep problems relate to both traumatic event exposure and PTSD across time. The current review provides a detailed analysis of studies pertaining to the temporal patterning of sleep problems and traumatic event-related factors (e.g., traumatic event exposure, PTSD) and draws conclusions regarding the current state of this literature. Research coalesces to suggest (1) exposure to a traumatic event can interfere with sleep, (2) PTSD is related to the development of self-reported sleep problems, but evidence is less clear regarding objective indices of sleep, and (3) limited evidence suggests sleep problems may interfere with recovery from elevated posttraumatic stress levels. Future research now needs to focus on understanding mechanisms involved in these patterns to inform the prevention and treatment of comorbid sleep problems and PTSD.

The current review critically examines the extant empirical literature focused on the associations among cigarette smoking, trauma, and posttraumatic stress. Inspection of the extant literature suggests smoking rates are significantly higher among persons exposed to a traumatic event relative to those without such exposure. Moreover, smoking rates appear particularly high among persons with posttraumatic stress disorder (PTSD). In terms of the direction of this relation, evidence most clearly suggests posttraumatic stress is involved in the development of smoking. Significantly less is known about the role of trauma and PTSD in terms of cessation outcome. Limitations of extant work, clinical implications, and key directions for future study are delineated. Keywordssmoking; posttraumatic stress; comorbidity; trauma; PTSD Cigarette smoking continues to be one of the leading preventable causes of death and disease in the U.S., resulting in healthcare costs that rank among the highest in the country [U.S. Department of Health and Human Services (USDHHS), 2004]. Large-scale efforts targeting smoking cessation have helped address this problem (USDHHS, 2000), but the negative impact of smoking is still widely evident. For example, more than 1 in 5 (22%) adults [Centers for Disease Control and Prevention (CDC), 2004] and almost 1 in 4 (24%) youth (Johnston, O'Malley, Bachman, & Schulenberg, 2004) in the U.S. currently smoke. Moreover, though smokers often are motivated to quit, the majority (approximately 90-95% of self-quitters and 60-80% of those in treatment programs) relapse (Cohen et al., 1989). Scholars have suggested smokers who fail at quitting may have unique attributes that increase their probability of smoking (Hughes, 1993;Pomerleau, 1997). Although various characteristics may increase the risk of relapse (e.g., heavier smoking levels), psychological disorders and related vulnerability factors have increasingly been recognized as playing a prominent role in quit success (Hughes, 1993;Zvolensky & Bernstein, 2005; Zvolensky, Bernstein, Marshall, & Feldner, in press).Smokers with anxiety disorders represent a common, albeit understudied, segment of the smoking population who are at heightened risk for relapse . For example, Correspondence concerning this article should be addressed to Dr. Matthew T. Feldner, Intervention Sciences Laboratory, University of Arkansas, Department of Psychology, 216 Memorial Hall, Fayetteville, AR 72701, 479-575-4256 (phone), 479-575-3219 (facsimile). Electronic mail may be sent to mfeldne@uark.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the jo...

Real-time fMRI neurofeedback (rtfMRI-nf) is an emerging approach for studies and novel treatments of major depressive disorder (MDD). EEG performed simultaneously with an rtfMRI-nf procedure allows an independent evaluation of rtfMRI-nf brain modulation effects. Frontal EEG asymmetry in the alpha band is a widely used measure of emotion and motivation that shows profound changes in depression. However, it has never been directly related to simultaneously acquired fMRI data. We report the first study investigating electrophysiological correlates of the rtfMRI-nf procedure, by combining the rtfMRI-nf with simultaneous and passive EEG recordings. In this pilot study, MDD patients in the experimental group (n = 13) learned to upregulate BOLD activity of the left amygdala using an rtfMRI-nf during a happy emotion induction task. MDD patients in the control group (n = 11) were provided with a sham rtfMRI-nf. Correlations between frontal EEG asymmetry in the upper alpha band and BOLD activity across the brain were examined. Average individual changes in frontal EEG asymmetry during the rtfMRI-nf task for the experimental group showed a significant positive correlation with the MDD patients' depression severity ratings, consistent with an inverse correlation between the depression severity and frontal EEG asymmetry at rest. The average asymmetry changes also significantly correlated with the amygdala BOLD laterality. Temporal correlations between frontal EEG asymmetry and BOLD activity were significantly enhanced, during the rtfMRI-nf task, for the amygdala and many regions associated with emotion regulation. Our findings demonstrate an important link between amygdala BOLD activity and frontal EEG asymmetry during emotion regulation. Our EEG asymmetry results indicate that the rtfMRI-nf training targeting the amygdala is beneficial to MDD patients. They further suggest that EEG-nf based on frontal EEG asymmetry in the alpha band would be compatible with the amygdala-based rtfMRI-nf. Combination of the two could enhance emotion regulation training and benefit MDD patients.

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Posttraumatic stress disorder (PTSD) is a chronic and disabling neuropsychiatric disorder characterized by insufficient top-down modulation of the amygdala activity by the prefrontal cortex. Real-time fMRI neurofeedback (rtfMRI-nf) is an emerging method with potential for modifying the amygdala-prefrontal interactions. We report the first controlled emotion self-regulation study in veterans with combat-related PTSD utilizing rtfMRI-nf of the amygdala activity. PTSD patients in the experimental group (EG, n = 20) learned to upregulate blood‑oxygenation-level-dependent (BOLD) activity of the left amygdala (LA) using the rtfMRI-nf during a happy emotion induction task. PTSD patients in the control group (CG, n = 11) were provided with a sham rtfMRI-nf. The study included three rtfMRI-nf training sessions, and EEG recordings were performed simultaneously with fMRI. PTSD severity was assessed before and after the training using the Clinician-Administered PTSD Scale (CAPS). The EG participants who completed the study showed a significant reduction in total CAPS ratings, including significant reductions in avoidance and hyperarousal symptoms. They also exhibited a significant reduction in comorbid depression severity. Overall, 80% of the EG participants demonstrated clinically meaningful reductions in CAPS ratings, compared to 38% in the CG. No significant difference in the CAPS rating changes was observed between the groups. During the first rtfMRI-nf session, functional connectivity of the LA with the orbitofrontal cortex (OFC) and the dorsolateral prefrontal cortex (DLPFC) was progressively enhanced, and this enhancement significantly and positively correlated with the initial CAPS ratings. Left-lateralized enhancement in upper alpha EEG coherence also exhibited a significant positive correlation with the initial CAPS. Reduction in PTSD severity between the first and last rtfMRI-nf sessions significantly correlated with enhancement in functional connectivity between the LA and the left DLPFC. Our results demonstrate that the rtfMRI-nf of the amygdala activity has the potential to correct the amygdala-prefrontal functional connectivity deficiencies specific to PTSD.

The present study examines the relation between posttraumatic stress symptom severity and motives for marijuana use among 103 (55 women) young adult marijuana users (current) who reported experiencing at least one traumatic event in their lifetime. As expected, after covarying for the theoretically relevant variables of frequency of past 30-day marijuana use, number of cigarettes smoked per day, and volume of alcohol consumed, posttraumatic stress symptom severity was significantly related to marijuana use coping motives, but no other motives for marijuana use. Results are discussed in relation to better understanding the role of coping-motivated marijuana use among young adults experiencing posttraumatic stress.