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There have been few direct examinations of the volitional control of emotional responses to provocative stimuli in PTSD. To address this gap, an emotion regulation task was administered to 27 Operation Enduring Freedom/Operation Iraqi Freedom combat veterans and 23 healthy controls. Neutral and aversive photographs were presented to participants who did or did not employ emotion regulation strategies. Objective indices included corrugator electromyogram, the late positive potential, and the electrocardiogram. On uninstructed trials, participants with PTSD exhibited blunted cardiac reactivity rather than the exaggerated cardioacceleratory responses seen in trauma cue reactivity studies. On interleaved regulation trials, no measure evidenced group differences in voluntary emotion regulation. Persons with PTSD may not differ from normals in their capacity to voluntarily regulate normative emotional responses to provocative stimuli in the laboratory, though they may nevertheless respond differentially on uninstructed trials and endorse symptoms of dyscontrol pathognomonic of the disorder outside of the laboratory.

This paper reports the results of a study that administered an emotion regulation task to Operation Enduring Freedom/Operation Iraqi Freedom veterans diagnosed with posttraumatic stress disorder (27) and to healthy controls (23). Seated movement and postural responses were transduced with a sensitive accelerometer attached to the underside of a low-mass cantilevered chair. Consistent with prior studies in which subjects stood on force plates, aversive photographs induced attenuation of nondirectional movement in patients and controls. Regarding seated postural responses, controls leaned towards neutral photographs and away from aversive ones, while participants with PTSD did the opposite. Regulation had no impact on seated movement but was associated with a seated postural withdrawal from the computer screen.

Studies of cognitive reappraisal have demonstrated that reinterpreting a stimulus can alter emotional responding, yet few studies have examined the durable effects associated with reinterpretation-based emotion regulation strategies. Evidence for the enduring effects of emotion regulation may be found in clinical studies that use cognitive restructuring (CR) techniques in cognitive-behavioral therapy (CBT) to alleviate anxiety. These techniques are based on cognitive theories of anxiety that suggest these disorders arise from biased cognitions; therefore, changing a person's thoughts will elicit durable changes in an individual's emotional responses. Despite the considerable success of CBT for anxiety disorders, durable effects associated with emotion regulation have not been thoroughly examined in the context of a laboratory paradigm. The goal of this study was to determine whether CR, a technique used in CBT and similar to cognitive reappraisal, could attenuate conditioned fear responses, and whether the effect would persist over time (24 hr). We conditioned participants using images of snakes or spiders that were occasionally paired with a mild shock to the wrist while we obtained subjective fear reports and electrodermal activity (EDA). After conditioning, half of the participants were randomly assigned to CR training aimed at decreasing their emotional response to the shock and the conditioned stimuli, while the other half received no such training. All participants returned 24 hr later to repeat the conditioning session. Compared with control participants, CR participants demonstrated a reduction in fear and EDA across sessions. These findings suggest that CR has durable effects on fear responding.

Cognitive emotion regulation has been widely shown in the laboratory to be an effective way to alter the nature of emotional responses. Despite its success in experimental contexts, however, we often fail to use these strategies in everyday life where stress is pervasive. The successful execution of cognitive regulation relies on intact executive functioning and engagement of the prefrontal cortex, both of which are rapidly impaired by the deleterious effects of stress. Because it is specifically under stressful conditions that we may benefit most from such deliberate forms of emotion regulation, we tested the efficacy of cognitive regulation after stress exposure. Participants first underwent fear-conditioning, where they learned that one stimulus (CS+) predicted an aversive outcome but another predicted a neutral outcome (CS−). Cognitive regulation training directly followed where participants were taught to regulate fear responses to the aversive stimulus. The next day, participants underwent an acute stress induction or a control task before repeating the fear-conditioning task using these newly acquired regulation skills. Skin conductance served as an index of fear arousal, and salivary α-amylase and cortisol concentrations were assayed as neuroendocrine markers of stress response. Although groups showed no differences in fear arousal during initial fear learning, nonstressed participants demonstrated robust fear reduction following regulation training, whereas stressed participants showed no such reduction. Our results suggest that stress markedly impairs the cognitive regulation of emotion and highlights critical limitations of this technique to control affective responses under stress.

l i r t a P H p n U s p t s e c i t F or more than a century, psychologists and psychiatrists have sought to understand the biological bases of mental disorders, with a view to fashioning more effective treatments. Advances in functional neuroimaging have made it possible for clinical researchers to make significant strides towards realizing this long-held goal, allowing them to do the following: 1) characterize differences in neural responses between patients with various psychiatric conditions and healthy subjects (HS), and 2) examine the neural correlates of psychosocial and biologic treatments. One particular target of investigation has been the anxiety disorders, which constitute the most common family of psychiatric disorders, with a lifetime prevalence of 28.8% (1). Compared with HS, patients with anxiety disorders demonstrate hyperactivity in the insula and amygdala, key regions in the fear network (2,3). In addition to shared features, there are important differences among anxiety disorders. For example, hypoactivation in the rostral anterior cingulate cortex (ACC), dorsal ACC, ventromedial prefrontal cortex (PFC), and thalamus is more characteristic of posttraumatic stress disorder than social anxiety disorder (SAD) or specific phobias (2). In contrast, hyperactivation in the amygdalae and insular cortex is found more frequently in SAD and specific phobias than in posttraumatic stress disorder (2). Related research examining the neural correlates of psychosocial treatments for anxiety disorders has found that cognitive behavioral therapy (CBT) decreases blood flow to the amygdala and the medial temporal lobe in patients with SAD during an anxiety-inducing task (4). Research in patients with specific phobias has demonstrated that CBT leads to reduced activation in the anterior insula and increased activation in the dorsolateral PFC (4). These findings suggest that the neural mechanisms underlying anxiety may be specific to each disorder and that the mechanisms associated with change during CBT may be disorder specific as well. Despite the wealth of research examining the neural correlates of anxiety disorders, surprisingly little is known about the neurobiology of panic disorder (PD). Panic disorder is marked by internally generated threat, vegetative symptoms, and sudden extreme anxiety (3). Maladaptive associative learning is thought to play a role in the etiology of PD, and research has shown that patients with PD extrapolate learned fears to related stimuli (5). Agoraphobia (the avoidance of situations in which escape or assistance may not be possible) commonly co-occurs with panic disorder (PD/A) (6). The neural correlates of PD/A are not well described, but one positron emission tomography study found that, compared with HS, PD/A patients displayed higher levels of glucose uptake in the bilateral amygdala, hippocampus, and thalamus (among other regions) (7), providing evidence for the role of the fear network in PD/A. Only two studies have investigated the neural correlates of CBT for PD/A