Altered neural correlates of affective processing after internet-delivered cognitive behavior therapy for social anxiety disorder

BackgroundApart from a progressive decline of motor functions, Parkinson’s disease (PD) is also characterized by non-motor symptoms, including disturbed processing of emotions. This study aims at assessing emotional processing and its neurobiological correlates in PD with the focus on how medicated Parkinson patients may achieve normal emotional responsiveness despite basal ganglia dysfunction.MethodsNineteen medicated patients with mild to moderate PD (without dementia or depression) and 19 matched healthy controls passively viewed positive, negative, and neutral pictures in an event-related blood oxygen level-dependent functional magnetic resonance imaging study (BOLD-fMRI). Individual subjective ratings of valence and arousal levels for these pictures were obtained right after the scanning.ResultsParkinson patients showed similar valence and arousal ratings as controls, denoting intact emotional processing at the behavioral level. Yet, Parkinson patients showed decreased bilateral putaminal activation and increased activation in the right dorsomedial prefrontal cortex (PFC), compared to controls, both most pronounced for highly arousing emotional stimuli.ConclusionsOur findings revealed for the first time a possible compensatory neural mechanism in Parkinson patients during emotional processing. The increased medial PFC activity may have modulated emotional responsiveness in patients via top-down cognitive control, therewith restoring emotional processing at the behavioral level, despite striatal dysfunction. These results may impact upon current treatment strategies of affective disorders in PD as patients may benefit from this intact or even compensatory influence of prefrontal areas when therapeutic strategies are applied that rely on cognitive control to modulate disturbed processing of emotions.

Social anxiety disorder (SAD) is characterized at a neurobiological level by disrupted activity in emotion regulation neural circuitry. Previous work has demonstrated amygdala hyperreactivity and disrupted prefrontal responses to social cues in individuals with SAD (Kim et al., 2011). While exposure-based psychological treatments effectively reduce SAD symptoms, not all individuals respond to treatment. Better understanding of the neural mechanisms involved offers the potential to improve treatment efficacy. In this study, we investigated functional connectivity in emotion regulation neural circuitry in a randomized controlled treatment trial for SAD. Participants with SAD underwent fMRI scanning while performing an implicit emotion regulation task prior to treatment (n=62). Following 12 weeks of cognitive behavioral therapy, acceptance and commitment therapy, or wait-list, participants completed a second scan (n=42). Psychophysiological interaction analyses using amygdala seed regions demonstrated differences between SAD and healthy control participants (HC; n=16) in right amygdala-vmPFC connectivity. SAD participants demonstrated more negative amygdala-to-vmPFC connectivity, compared to HC participants, an effect that was correlated with SAD symptom severity. Post-treatment symptom reduction was correlated with altered amygdala-to-vm/vlPFC connectivity, independent of treatment type. Greater symptom reduction was associated with more negative amygdala-to-vm/vlPFC connectivity. These findings suggest that effective psychological treatment for SAD enhances amygdala-prefrontal functional connectivity.

At the time of writing (December, 2013), a search for cognitive bias modification (CBM) in SCOPUS yields 113 results. Tellingly, the earliest of the articles found by this rather crude search appear in 2009, clustering around the special issue on CBM in the Journal of Abnormal Psychology that year (Koster et al. 2009). While the term CBM had been used in the literature prior to this, and in fact research into CBM (albeit not always using this exact term) had been steadily gathering momentum since the first studies were published in 2000, there has clearly been an explosion in research on CBM in the years since. What has happened in this period? Over the past 4 years, CBM research has been on an exciting journey, with many twists and turns, ups and downs. This special issue seeks to provide an overview of this journey, and a glimpse of the road-or roads-ahead. But where to begin? The journey did not start in 2009, nor even a decade earlier when the dominant CBM paradigms were first described. To fully make sense of this journey, and all the twists in this travellers' tale, we must go back further still.Once upon a time … during the cognitive era of psychology … researchers embarked on the great adventure of exploring the 'cognitive landscape' of emotional pathology … an extremely challenging landscape…. After a few years, the first landmarks were established: cognitive biases in emotional disorders. But what did they signify? It seemed that such selective information-processing biases were crucial factors in the etiology, maintenance, and relapse of various types of emotional disorders. Hence, many cognitive theories built on this discovery in order to account for emotional pathology (e. Cognitive biases reflect a general processing advantage for disorder-relevant information. The findings of cognitive-experimental research indicate that emotional disorders are (roughly) characterized by three types of biases, i.e., biases in attention, interpretation, and memory. To illustrate, depressed or anxious individuals are, compared to healthy individuals, more likely to attend to negative cues, interpret ambiguity in a more negative manner, and selectively recall negative information (for a review, see Mathews and MacLeod 2005). According to the assumptions put forward by cognitive theories, the functional relationship between biases and emotional pathology can be described as follows: Biases are accompanied by various dysfunctional cognitions, which in turn activate dysfunctional emotional and behavioral responses. Due to the reinforcing connection between cognitions, emotions, and behavior, a 'psychopathological downward spiral' becomes activated in vulnerable individuals, possibly resulting in anxiety-or depression-related symptoms.In parallel to the development of measures to assess biases in attention, interpretation, and memory, researchers started to investigate whether it is also possible to modify biased cognitive processes. This work was motivated by the question of the causal nature of these biases: while the...