Mindful emotion regulation: exploring the neurocognitive mechanisms behind mindfulness

The purpose of this paper is to review some of the psychological and neural mechanisms behind mindfulness practice in order to explore the unique factors that account for its positive impact on emotional regulation and health. After reviewing the mechanisms of mindfulness and its effects on clinical populations we will consider how the practice of mindfulness contributes to the regulation of emotions. We argue that mindfulness has achieved effective outcomes in the treatment of anxiety, depression, and other psychopathologies through the contribution of mindfulness to emotional regulation. We consider the unique factors that mindfulness meditation brings to the process of emotion regulation that may account for its effectiveness. We review experimental evidence that points towards the unique effects of mindfulness specifically operating over and above the regulatory effects of cognitive reappraisal mechanisms. A neuroanatomical circuit that leads to mindful emotion regulation is also suggested. This paper thereby aims to contribute to proposed models of mindfulness for research and theory building by proposing a specific model for the unique psychological and neural processes involved in mindful detachment that account for the effects of mindfulness over and above the effects accounted for by other well-established emotional regulation processes such as cognitive reappraisal

Uncovering the Social Deficits in the Autistic Brain. A Source-Based Morphometric Study

Autism is a neurodevelopmental disorder that mainly affects social interaction and communication. Evidence from behavioral and functional MRI studies supports the hypothesis that dysfunctional mechanisms involving social brain structures play a major role in autistic symptomatology. However, the investigation of anatomical abnormalities in the brain of people with autism has led to inconsistent results. We investigated whether specific brain regions, known to display functional abnormalities in autism, may exhibit mutual and peculiar patterns of covariance in their gray-matter concentrations. We analyzed structural MRI images of 32 young men affected by autistic disorder (AD) and 50 healthy controls. Controls were matched for sex, age, handedness. IQ scores were also monitored to avoid confounding. A multivariate Source-Based Morphometry (SBM) was applied for the first time on AD and controls to detect maximally independent networks of gray matter. Group comparison revealed a gray-matter source that showed differences in AD compared to controls. This network includes broad temporal regions involved in social cognition and high-level visual processing, but also motor and executive areas of the frontal lobe. Notably, we found that gray matter differences, as reflected by SBM, significantly correlated with social and behavioral deficits displayed by AD individuals and encoded via the Autism Diagnostic Observation Schedule scores. These findings provide support for current hypotheses about the neural basis of atypical social and mental states information processing in autism

Schema therapy for emotional dysregulation: Theoretical implication and clinical applications

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 posttraumatic 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 interactiveontogenetic 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\u2019s 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

Anxiety and its Regulation: Neural Mechanisms and Regulation Techniques According to the Experiential-Dynamic Approach

Although anxiety is not necessarily a pathological phenomenon, it can become dysregulated, causing suffering. Indeed, emotion dysregulation lies at the core of many psychopathologies. Thus, anxiety regulation is central to all effective psychological treatment. The predominant perspective on emotion regulation and dysregulation is appraisal theory, which proposes that the cognitive appraisal of an event generates an emotional response. According to Gross’s process model, any emotion can become dysregulated when the patient lacks or fails to use an appropriate regulatory strategy. Therefore, the clinician must teach the patient better regulatory strategies. The perspective we put forward departs from Gross’s model based on appraisal theory. The experiential-dynamic emotion-regulation model, EDER, grounded in affective neuroscience and modern psychodynamic psychotherapy proposes that (1) emotions precede cognition (temporal and neuroanatomical primacy), (2) emotions are not inherently dysregulated (they have specific properties of time and strength proportional to the quality of the stimulus), and (3) dysregulation derives from the combination of emotions plus conditioned anxiety, or from secondary-defensive affects, both leading to dysregulated-affective states (DASs). To regulate DAS, the clinician must regulate the dysregulating anxiety or restructure the defenses, which create defensive affects, and then help the client to fully express the underlying emotions that elicit anxiety and defenses. In this chapter, we specifically focus on dysregulated anxiety, its neural bases, and how to regulate it according to the EDER model. First, we present hypotheses and data to show the neural bases of anxiety. Then, specific strategies and techniques to regulate anxiety are explained and clinical excerpts illustrate their application

Per una metodologia della regolazione emozionale basata su principi psicodinamici.

Differenti modelli di psicoterapia provenienti dai più svariati orientamenti teorici hanno nel tempo incorporato principi e tecniche per migliorare la regolazione emozionale del paziente. Tuttavia, nell’ambito della psicoterapia psicodinamica, un chiaro tentativo di integrazione con le conoscenze derivanti dalla scienza della regolazione emozionale non è ancora stato fatto. Noi crediamo che la scienza psicodinamica possa offrire interessanti riflessioni su: 1) cosa debba essere regolato durante la regolazione emozionale e 2) come ciò debba essere fatto (strategie e tecniche). In linea con i principi psicodinamici, noi sosteniamo che la regolazione debba essere rivolta a due aspetti fondamentali di ogni condizione psicopatologica: l’eccessiva ansia elicitata dall’emergere di emozioni; e gli affetti difensivi, ovvero stati affettivi secondari creati dall’utilizzo di meccanismi di difesa patologici che sostituiscono e coprono le emozioni originarie. Lo scopo della terapia è di regolare questi stati affettivi (regolazione emozionale propriamente detta, RE), e nel frattempo aiutare il paziente ad accedere, elaborare ed esprimere  le emozioni primarie o reattive allo stimolo (esperienza emozionale, EE). Dopo alcune considerazioni teoriche, verrà proposta una metodologia di regolazione emozionale basata su principi psicodinamici ed esperienziali e una serie di tecniche che il clinico può utilizzare nel trattamento degli stati affettivi disregolati, e che lo sperimentatore può testare nel laboratorio.</p

Dysregulated Anxiety and Dysregulating Defenses: Toward an Emotion Regulation Informed Dynamic Psychotherapy

One of the main objectives of psychotherapy is to address emotion dysregulation that causes pathological symptoms and distress in patients. Following psychodynamic theory, we propose that in humans, the combination of emotions plus conditioned anxiety due to traumatic attachment can lead to dysregulated affects. Likewise, defenses can generate and maintain dysregulated affects (altogether Dysregulated Affective States, DAS). We propose the Experiential-Dynamic Emotion Regulation methodology, a framework to understand emotion dysregulation by integrating scientific evidence coming from the fields of affective neuroscience and Experiential-Dynamic Psychotherapy aimed at resolving DAS. This method and the techniques proposed can be integrated within other approaches. Similarities and differences with the Cognitive model of emotion regulation and cognitive-behavioral approaches are discussed within the paper

Neurochemical Correlates of Brain Atrophy in Fibromyalgia Syndrome: A Magnetic Resonance Spectroscopy and Cortical Thickness Study.

(1) Background: Recently, a series of clinical neuroimaging studies on fibromyalgia (FM) have shown a reduction in cortical volume and abnormally high glutamate (Glu) and glutamate + glutamine (Glx) levels in regions associated with pain modulation. However, it remains unclear whether the volumetric decreases and increased Glu levels in FM are related each other. We hypothesized that higher Glu levels are related to decreases in cortical thickness (CT) and volume in FM patients. (2) Methods: Twelve females with FM and 12 matched healthy controls participated in a session of combined 3.0 Tesla structural magnetic resonance imaging (MRI) and single-voxel MR spectroscopy focused on the thalami and ventrolateral prefrontal cortices (VLPFC). The thickness of the cortical and subcortical gray matter structures and the Glu/Cr and Glx/Cr ratios were estimated. Statistics included an independent t-test and Spearman's test. (3) Results: The Glu/Cr ratio of the left VLPFC was negatively related to the CT of the left inferior frontal gyrus (pars opercularis (p = 0.01; r = -0.75) and triangularis (p = 0.01; r = -0.70)). Moreover, the Glx/Cr ratio of the left VLPFC was negatively related to the CT of the left middle anterior cingulate gyrus (p = 0.003; r = -0.81). Significantly lower CTs in FM were detected in subparts of the cingulate gyrus on both sides and in the right inferior occipital gyrus (p < 0.001). (4) Conclusions: Our findings are in line with previous observations that high glutamate levels can be related, in a concentration-dependent manner, to the morphological atrophy described in FM patients