Electrophysiological correlates of self-related processing in adults with autism.

The term "self-bias" refers to the human propensity to prioritize self- over other-related stimuli and is believed to influence various stages of the processing stream. By means of event-related potentials (ERPs), it was recently shown that the self-bias in a shape-label matching task modulates early as well as later phases of information processing in neurotypicals. Recent claims suggest autism-related deficits to specifically impact later stages of self-related processing; however, it is unclear whether these claims hold based on current findings. Using the shape-label matching task while recording ERPs in individuals with autism can clarify which stage of self-related processing is specifically affected in this condition. Therefore, this study sought to investigate the temporal course of self-related processing in adults with and without autism. Thirty-two adults with autism and 27 neurotypicals completed a shape-label matching task while ERPs were concomitantly recorded. At the behavioral level, results furnished evidence for a comparable self-bias across groups, with no differences in task performance between adults with and without autism. At the ERP level, the two groups showed a similar self-bias at early stages of self-related information processing (the N1 component). Conversely, the autism group manifested a lessened differentiation between self- and other-related stimuli at later stages (the parietal P3 component). In line with recent claims of later phases of self-related processing being altered in autism, we found an equivalent self-bias between groups at an early, sensory stage of processing, yet a strongly diminished self-bias at a later, cognitive stage in adults with autism.

The relevance of familiarity in the context of self-related information processing.

Humans are inclined to preferentially process self-related content, referred to as the "self-bias." Different paradigms have been used to study this effect. However, not all paradigms included a familiar other condition (but rather an unfamiliar other condition), needed to differentiate self-specific effects from the impact of familiarity. The primary goal of our study was to test the suitability for studying the self-bias of two paradigms that provide robust measures of salience effects-that is, the Repetition Blindness (RB) effect and the Emotional Stroop (ES) interference-while addressing the familiarity confound. We further explored whether self-bias effects were related to autism symptomatology, as a reduced self-bias in autism has been reported in previous research. In an online procedure, 82 adults performed an RB task and an ES task in a counterbalanced order, while being presented with both self- and familiar other-related stimuli. Results of both frequentist and Bayesian analyses did not provide evidence in favour of a specific self-bias on either task: we found no significant modulation of the RB effect, nor of the ES interference, for the own versus a close other's name. Moreover, no link with autism symptomatology was found. Tackling a crucial shortcoming from earlier studies, our investigation raises awareness on the importance of accounting for familiarity when investigating self-related processing.

A comparison of self-bias measures across cognitive domains.

BACKGROUND: The 'self-bias'-i.e., the human proneness to preferentially process self-relevant stimuli-is thought to be important for both self-related and social processing. Previous research operationalized the self-bias using different paradigms, assessing the size of the self-bias within a single cognitive domain. Recent studies suggested a reduced self-bias in autism, yet findings are inconsistent. The lack of consensus across existing studies may result from variation in paradigms and cognitive domains tested. Therefore, the primary goal of the current study was to investigate whether self-biases found across cognitive domains (i.e., perception, memory, attention) are related or independent. The secondary goal was to explore the relationship between these self-biases and the extent of autistic traits in a neurotypical sample. METHODS: In an online procedure, 99 Dutch-speaking adults performed three self-processing tasks in counterbalanced order-i.e., the shape-label matching task (perception), the trait adjectives task (memory) and the visual search task (attention)-and completed two self-report measures of ASD symptomatology, i.e., AQ-10 and SRS-A. To control for level of familiarity, self-, close other- and famous other-relevant stimuli were included in each task. Repeated measures ANOVAs were conducted for each task, and both frequentist as well as Bayesian analyses were applied to investigate the correlational patterns between self-bias measures. RESULTS: We observed significant correlations of the self-bias magnitude between memory and attention, as well as attention and perception. However, Bayesian analysis provided only weak support for the latter association. Further, the size of the self-bias was not significantly related across memory and perception. No significant correlation between autistic traits and the self-bias magnitude was found for any of the three tasks, with Bayesian analyses strongly favoring the null hypothesis. CONCLUSIONS: In contrast with the view of a 'unidimensional' self-bias, our findings provide evidence for a heterogeneous and multifaceted self consisting of a variety of related and unrelated aspects. None of the self-bias indices were found to relate to autistic traits in our neurotypical sample.

Anxiety Regulation: From Affective Neuroscience to Clinical Practice.

According to psychoanalysis, anxiety signals a threat whenever a forbidden feeling emerges. Anxiety triggers defenses and maladaptive behaviors, thus leading to clinical problems. For these reasons, anxiety regulation is a core aspect of psychodynamic-oriented treatments to help clients. In the present theoretical paper, we review and discuss anxiety generation and dysregulation, first from a neural point of view, presenting findings from neuroimaging and psychophysiological studies. The aim is to trace parallels with psychodynamic theories of anxiety. Then, we discuss the psychological mechanisms and neural bases of emotion regulation in the laboratory, and possible neurobiological mechanisms of anxiety regulation in psychotherapy. We describe two different approaches to emotion/anxiety regulation, one based on the standard cognitive model of emotion regulation, the other based on psychodynamic principles and affective neuroscience. We then illustrate in detail a dynamic experiential approach to regulation. This model claims that emotions arise before cognition and are not inherently dysregulated. Dysregulation emerges from co-occurrences of emotions and associated anxiety. Technical consequences of this model are discussed and include strategies to regulate anxiety.

A Dual Route Model for Regulating Emotions: Comparing Models, Techniques and Biological Mechanisms.

The aim of this article is to present recent applications of emotion regulation theory and methods to the field of psychotherapy. The term Emotion Regulation refers to the neurocognitive mechanisms by which we regulate the onset, strength, and the eventual expression of our emotions. Deficits in the regulation of emotions have been linked to most, if not all, psychiatric disorders, with patients presenting either dysregulated emotions, or dysfunctional regulatory strategies. We discuss the implications of regulating emotions from two different theoretical perspectives: the Cognitive Emotion Regulation (CER), and the Experiential-Dynamic Emotion Regulation (EDER) model. Each proposes different views on how emotions are generated, dysregulated and regulated. These perspectives directly influence the way clinicians treat such problems. The CER model views emotional dysregulation as due to a deficit in regulation mechanisms that prioritizes modifying or developing cognitive skills, whilst the EDER model posits emotional dysregulation as due to the presence of dysregulatory mechanisms that prioritizes restoring natural regulatory processes. Examples of relevant techniques for each model are presented including a range of cognitive-behavioral, and experiential (including both dynamic and cognitive) techniques. The aim of the paper is to provide a toolbox from which clinician may gain different techniques to enhance and maintain their patient's capacity for emotional regulation. Finally, the biological mechanisms behind the two models of emotion regulation are discussed as well as a proposal of a dual route model of emotion regulation.