RESUMO
The term emotional dysregulation refers to an impaired ability to regulate unwanted emotional states. Scientific evidence supports the idea that emotional dysregulation underlies several psychological disorders as, for example: personality disorders, bipolar disorder type II, interpersonal trauma, anxiety disorders, mood disorders and post-traumatic stress disorder. Emotional dysregulation may derive from early interpersonal traumas in childhood. These early traumatic events create a persistent sensitization of the central nervous system in relation to early life stressing events. For this reason, some authors suggest a common endophenotypical origin across psychopathologies. In the last 20 years, cognitive behavioral therapy has increasingly adopted an interactive-ontogenetic view to explain the development of disorders associated to emotional dysregulation. Unfortunately, standard Cognitive Behavior Therapy (CBT) methods are not useful in treating emotional dysregulation. A CBT-derived new approach called Schema Therapy (ST), that integrates theory and techniques from psychodynamic and emotion focused therapy, holds the promise to fill this gap in cognitive literature. In this model, psychopathology is viewed as the interaction between the innate temperament of the child and the early experiences of deprivation or frustration of the subject's basic needs. This deprivation may lead to develop early maladaptive schemas (EMS), and maladaptive Modes. In the present paper we point out that EMSs and Modes are associated with either dysregulated emotions or with dysregulatory strategies that produce and maintain problematic emotional responses. Thanks to a special focus on the therapeutic relationship and emotion focused-experiential techniques, this approach successfully treats severe emotional dysregulation. In this paper, we make several comparisons between the main ideas of ST and the science of emotion regulation, and we present how to conceptualize pathological phenomena in terms of failed regulation and some of the ST strategies and techniques to foster successful regulation in patients.
RESUMO
The cognitive avoidance model of worry assumes that worry has the adaptive function to keep under control the physiological arousal associated with anxiety. This study aimed to test this model by the use of a fear induction paradigm in both pathological and healthy individuals. Thirty-one pathological worriers and 36 healthy controls accepted to be exposed to a fear induction paradigm (white noise) during three experimental conditions: worry, distraction, and reappraisal. Skin conductance (SCR) and heart rate variability (HRV) were measured as indices of sympathetic and parasympathetic nervous system functioning. Worriers showed increased sympathetic and decreased parasympathetic activation during the worry condition compared to non-worriers. There were no differences between groups for the distraction and reappraisal conditions. SCRs to the white noises during worry were higher in worriers versus controls throughout the entire worry period. Intolerance of uncertainty - but not metacognitive beliefs about worry - was a significant moderator of the relationship between worry and LF/HF-HRV in pathological worriers. Results support the cognitive avoidance model in healthy controls, suggesting that worry is no longer a functional attitude when it becomes the default/automatic and pathological response.
