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Dynamic Relational Group Psychotherapy: A Neurobiologically Informed Model of Change
Abstract
In this article we introduce a preliminary, neurobiologically informed model of group therapy that links the timing and nature of specific group interventions with hypothesized changing neurobiological needs of the group. We suggest that the observed phases of group development reflect an underlying reorganization of neuronal circuitry that occurs as members progress through a hierarchically organized treatment, and that this reorganization involves the integration and homeostatic rebalancing of subcortical and neural networks. Our preliminary Dynamic Relational model suggests that an understanding of the neurobiological processes involved in group development may help inform and direct effective group-based psychotherapy interventions.
In this paper we outline a hierarchical, phase-based model of psychotherapy to address a range of psychopathology. The proposed hierarchy of intervention is informed by emerging evidence on the modulation, integration, and homeostatic rebalancing of subcortical and neural networks involved in emotion modulation, self-referential processing, and mentalization. To illustrate our Dynamic-Relational Model, we include a case description detailing the clinical presentation and treatment goals/approaches at each phase of the intervention, and sessional vignettes to illustrate specific techniques. We suggest this model of treatment has significant implications for understanding the pathogenesis of mental disorders, and may inform prevention efforts that could potentially reduce the prevalence or burden of mental illness.
Expressive writing (EW) can be a useful supplement to psychotherapy, regardless of therapeutic orientation. In an open trial of exposure-based cognitive therapy for depression, 43 participants used EW before each session, producing 928 EW samples. Using examples from these, we discuss how EW can be used to both promote and track therapeutic change. Specifically, we review the impact of EW on therapeutic growth, via self-monitoring, increased awareness, and exposure/ emotional processing. We then discuss how EW can be used to track important predictors of change such as symptoms, therapeutic alliance, social support, avoidance, and hopelessness. We conclude by discussing potential limitations to the use of EW in therapy and by recommending specific strategies for incorporating EW into clinical practice.
Many psychiatric disorders are widely thought to involve problematic patterns of emotional reactivity and emotion regulation. Unfortunately, it has proven far easier to assert the centrality of “emotion dysregulation” than to rigorously document the ways in which individuals with various forms of psychopathology differ from healthy individuals in their patterns of emotional reactivity and emotion regulation. In the first section of this article, we define emotion and emotion regulation. In the second and third sections, we present a simple framework for examining emotion and emotion regulation in psychopathology. In the fourth section, we conclude by highlighting important challenges and opportunities in assessing and treating disorders that involve problematic patterns of emotion and emotion regulation.
Objective
Nonhuman and human studies have documented the adverse effects of early life stress (ELS) on emotion regulation and underlying neural circuitry. Less is known about how these experiences shape social processes and neural circuitry. In this study we thus investigated how ELS impacts children’s perception of, and neural response to, negative social experiences in a social exclusion paradigm (CyberBall).
Method
Twenty-five foster or adopted children with ELS (age 10.6±1.8y, 13 male) and 26 matched non-separated controls (age 10.38 ±1.7y, 12 male) took part in a CyberBall paradigm during functional magnetic resonance imaging (fMRI).
Results
During peer rejection, children with ELS reported significantly more feelings of exclusion and frustration than non-separated controls. On the neural level, children with ELS showed reduced activation in the dorsal anterior cingulate cortex (dACC) and dorsolateral prefrontal cortex (dlPFC), and reduced connectivity between dlPFC-dACC, areas previously implicated in affect regulation. Conversely, children with ELS showed increased neural activation in brain regions involved in memory, arousal, and threat-related processing (middle temporal gyrus, thalamus, ventral tegmental area) relative to controls during social exclusion. The number of separation experiences before entering the permanent family predicted reductions in fronto-cingulate recruitment. The relationship between early separations and self-reported exclusion was mediated by dlPFC activity.
Conclusion
The findings suggest that ELS leads to alterations in neural circuitry implicated in the regulation of socioemotional processes. This neural signature may underlie foster children’s differential reactivity to rejection in everyday life and could increase risk for developing affective disorders.
This article discusses how recent studies of the right brain, which is dominant for the implicit, nonverbal, intuitive, holistic processing of emotional information and social interactions, can elucidate the neurobiological mechanisms that underlie the relational foundations of psychotherapy. Utilizing the interpersonal neurobiological perspective of regulation theory, I describe the fundamental role of the early developing right brain in relational processes, throughout the life span. I present interdisciplinary evidence documenting right brain functions in early attachment processes, in emotional communications within the therapeutic alliance, in mutual therapeutic enactments, and in therapeutic change processes. This work highlights the fact that the current emphasis on relational processes is shared by, cross-fertilizing, and indeed transforming both psychology and neuroscience, with important consequences for clinical psychological models of psychotherapeutic change. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
Neuroimaging measures of behavioral and emotional dysregulation can yield biomarkers denoting developmental trajectories of psychiatric pathology in youth. We aimed to identify functional abnormalities in emotion regulation (ER) neural circuitry associated with different behavioral and emotional dysregulation trajectories using latent class growth analysis (LCGA) and neuroimaging.
A total of 61 youth (9-17 years) from the Longitudinal Assessment of Manic Symptoms study, and 24 healthy control youth, completed an emotional face n-back ER task during scanning. LCGA was performed on 12 biannual reports completed over 5 years of the Parent General Behavior Inventory 10-Item Mania Scale (PGBI-10M), a parental report of the child's difficulty regulating positive mood and energy.
There were two latent classes of PGBI-10M trajectories: high and decreasing (HighD; n = 22) and low and decreasing (LowD; n = 39) course of behavioral and emotional dysregulation over the 12 time points. Task performance was >89% in all youth, but more accurate in healthy controls and LowD versus HighD (p < 0.001). During ER, LowD had greater activity than HighD and healthy controls in the dorsolateral prefrontal cortex, a key ER region, and greater functional connectivity than HighD between the amygdala and ventrolateral prefrontal cortex (p's < 0.001, corrected).
Patterns of function in lateral prefrontal cortical-amygdala circuitry in youth denote the severity of the developmental trajectory of behavioral and emotional dysregulation over time, and may be biological targets to guide differential treatment and novel treatment development for different levels of behavioral and emotional dysregulation in youth.
Mindfulness training aims to impact emotion regulation. Generalized anxiety disorder (GAD) symptoms can be successfully addressed through mindfulness-based interventions. This preliminary study is the first to investigate neural mechanisms of symptom improvements in GAD following mindfulness training. Furthermore, we compared brain activation between GAD patients and healthy participants at baseline. 26 patients with a current DSM-IV GAD diagnosis were randomized to an 8-week Mindfulness Based Stress Reduction (MBSR, N = 15) or a stress management education (SME, N = 11) active control program. 26 healthy participants were included for baseline comparisons. BOLD response was assessed with fMRI during affect labeling of angry and neutral facial expressions. At baseline, GAD patients showed higher amygdala activation than healthy participants in response to neutral, but not angry faces, suggesting that ambiguous stimuli reveal stronger reactivity in GAD patients. In patients, amygdala activation in response to neutral faces decreased following both interventions. BOLD response in ventrolateral prefrontal regions (VLPFC) showed greater increase in MBSR than SME participants. Functional connectivity between amygdala and PFC regions increased significantly pre- to post-intervention within the MBSR, but not SME group. Both, change in VLPFC activation and amygdala-prefrontal connectivity were correlated with change in Beck Anxiety Inventory (BAI) scores, suggesting clinical relevance of these changes. Amygdala-prefrontal connectivity turned from negative coupling (typically seen in down-regulation of emotions), to positive coupling; potentially suggesting a unique mechanism of mindfulness. Findings suggest that in GAD, mindfulness training leads to changes in fronto-limbic areas crucial for the regulation of emotion; these changes correspond with reported symptom improvements.
In recent years, an explosion of neuroimaging studies has examined cognitive reappraisal, an emotion regulation strategy that involves changing the way one thinks about a stimulus in order to change its affective impact. Existing models broadly agree that reappraisal recruits frontal and parietal control regions to modulate emotional responding in the amygdala, but they offer competing visions of how this is accomplished. One view holds that control regions engage ventromedial prefrontal cortex (vmPFC), an area associated with fear extinction, that in turn modulates amygdala responses. An alternative view is that control regions modulate semantic representations in lateral temporal cortex that indirectly influence emotion-related responses in the amygdala. Furthermore, while previous work has emphasized the amygdala, whether reappraisal influences other regions implicated in emotional responding remains unknown. To resolve these questions, we performed a meta-analysis of 48 neuroimaging studies of reappraisal, most involving downregulation of negative affect. Reappraisal consistently 1) activated cognitive control regions and lateral temporal cortex, but not vmPFC, and 2) modulated the bilateral amygdala, but no other brain regions. This suggests that reappraisal involves the use of cognitive control to modulate semantic representations of an emotional stimulus, and these altered representations in turn attenuate activity in the amygdala.
Applied relaxation (AR), originally developed by Lars-Göran Öst, is a long-standing, efficacious treatment for generalized anxiety disorder (GAD). While newer treatments are continuing to be developed, AR remains one of the most efficacious treatments for GAD. However, AR has received less in-depth attention more recently, particularly in terms of potential mechanisms of action. This article is written to honor the development and history of AR and to highlight the ways that it has continued to be adapted. In this article, AR treatment strategies are presented, which include: noticing early signs of anxiety, learning relaxation skills, and applying relaxation at the first sign of anxiety. Then, additional adaptations to AR are presented along with recommendations of how AR may be enhanced by understanding potential mechanisms of change. Finally, recommendations are made for the continued evolution of AR as a powerful and efficacious treatment for GAD.
There is a high degree of intra-individual variation in how individuals respond to stress. This becomes evident when exploring the development of posttraumatic symptoms or stress-related disorders after exposure to trauma. Whether or not an individual develops posttraumatic symptoms after experiencing a traumatic event is partly dependent on a person's resilience. Resilience can be broadly defined as the dynamic process encompassing positive adaptation within the context of significant adversity. Even though research into the neurobiological basis of resilience is still in its early stages, these insights can have important implications for the prevention and treatment of stress-related disorders. Neuroimaging studies contribute to our knowledge of intra-individual variability in resilience and the development of posttraumatic symptoms or other stress-related disorders. This review provides an overview of neuroimaging findings related to resilience. Structural, resting-state, and task-related neuroimaging results associated with resilience are discussed. There are a limited number of studies available and neuroimaging research of resilience is still in its infancy. The available studies point at brain circuitries involved in stress and emotion regulation, with more efficient processing and regulation associated with resilience.
Empathy involves affective, cognitive, and emotion regulative components. The affective component relies on the sharing of emotional states with others and is discussed here in relation to the human Mirror System. On the other hand, the cognitive component is related to understanding the mental states of others and draws upon literature surrounding Theory of Mind (ToM). The final component, emotion regulation, depends on executive function and is responsible for managing the degree to which explicit empathic responses are made. This mini-review provides information on how each of the three components is individually affected by group membership and how this leads to in-group bias.
The amygdala has been repeatedly implicated in emotional processing of both positive and negative-valence stimuli. Previous studies suggest that the amygdala response to emotional stimuli is lower when the subject is in a meditative state of mindful-attention, both in beginner meditators after an 8-week meditation intervention and in expert meditators. However, the longitudinal effects of meditation training on amygdala responses have not been reported when participants are in an ordinary, non-meditative state. In this study, we investigated how 8 weeks of training in meditation affects amygdala responses to emotional stimuli in subjects when in a non-meditative state. Healthy adults with no prior meditation experience took part in 8 weeks of either Mindful Attention Training (MAT), Cognitively-Based Compassion Training (CBCT; a program based on Tibetan Buddhist compassion meditation practices), or an active control intervention. Before and after the intervention, participants underwent an fMRI experiment during which they were presented images with positive, negative, and neutral emotional valences from the IAPS database while remaining in an ordinary, non-meditative state. Using a region-of-interest analysis, we found a longitudinal decrease in right amygdala activation in the Mindful Attention group in response to positive images, and in response to images of all valences overall. In the CBCT group, we found a trend increase in right amygdala response to negative images, which was significantly correlated with a decrease in depression score. No effects or trends were observed in the control group. This finding suggests that the effects of meditation training on emotional processing might transfer to non-meditative states. This is consistent with the hypothesis that meditation training may induce learning that is not stimulus- or task-specific, but process-specific, and thereby may result in enduring changes in mental function.
The differential effectiveness of group psychotherapy was estimated in a meta-analysis of 111 experimental and quasi-experimental studies published over the past 20 years. A number of client, therapist, group, and methodological variables were examined in an attempt to determine specific as well as generic effectiveness. Three different effect sizes were computed: active versus wait list, active versus alternative treatment, and pre- to posttreatment improvement rates. The active versus wait list overall effect size (0.58) indicated that the average recipient of group treatment is better off than 72% of untreated controls. Improvement was related to group composition, setting, and diagnosis. Findings are discussed within the context of what the authors have learned about group treatment, meta-analytic studies of the extant group literature, and what remains for future research. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
One of the core symptoms of borderline personality disorder (BPD) is the instability in interpersonal relationships. This might be related to existent differences in mindreading between BPD patients and healthy individuals.
We examined the behavioural and neurophysiological (fMRI) responses of BPD patients and healthy controls (HC) during performance of the 'Reading the Mind in the Eyes' test (RMET).
Mental state discrimination was significantly better and faster for affective eye gazes in BPD patients than in HC. At the neurophysiological level, this was manifested in a stronger activation of the amygdala and greater activity of the medial frontal gyrus, the left temporal pole and the middle temporal gyrus during affective eye gazes. In contrast, HC subjects showed a greater activation in the insula and the superior temporal gyri.
These findings indicate that BPD patients are highly vigilant to social stimuli, maybe because they resonate intuitively with mental states of others.
It is obvious that emotions are real, but the question is what kind of "real" are they? In this article, I outline a theoretical approach where emotions are a part of social reality. I propose that physical changes (in the face, voice, and body, or neural circuits for behavioral adaptations like freezing, fleeing, or fighting) transform into an emotion when those changes take on psychological functions that they cannot perform by their physical nature alone. This requires socially shared conceptual knowledge that perceivers use to create meaning from these physical changes (as well as the circuitry that supports this meaning making). My claim is that emotions are, at the same time, socially constructed and biologically evident. Only when we understand all the elements that construct emotional episodes, in social, psychological, and biological terms, will we understand the nature of emotion.
Bipolar disorder (BP) is characterized by a dysfunction of mood, alternating between states of mania/hypomania and depression. Thus, the primary abnormality appears to be an inability to regulate emotion, the result of which is emotional extremes. The purpose of this paper is to review the current functional magnetic resonance imaging (fMRI) literature on adult patients with BP using emotion processing or regulation paradigms.
A search was conducted on PubMed using the keywords: bipolar disorder, fMRI, mania, bipolar depression, bipolar euthymia, emotion, and amygdala. Only those studies that were conducted in adult patients using an emotion activation task were included in the final review.
Using tasks that assess neural functioning during emotion processing and emotion regulation, many fMRI studies have examined BP subjects during mania and euthymia. Fewer fMRI studies have been conducted during depression, and fewer still have included the same subjects in multiple mood states. Despite these limitations, these studies have demonstrated specific abnormalities in frontal-limbic regions. Using a variety of paradigms, investigators have specifically evaluated the amygdala (a structure within the limbic system known to be critical for emotion) and the prefrontal cortex (PFC) (a region known to have a regulatory function over the limbic system).
These investigations reveal that amygdala activation varies as a function of mood state, while the PFC remains persistently hypoactivated across mood states. Emotional dysregulation and lability in mania and depression may reflect disruption of a frontal-limbic functional neuroanatomical network.
The ability to cognitively regulate emotional responses to aversive events is important for mental and physical health. Little is known, however, about neural bases of the cognitive control of emotion. The present study employed functional magnetic resonance imaging to examine the neural systems used to reappraise highly negative scenes in unemotional terms. Reappraisal of highly negative scenes reduced subjective experience of negative affect. Neural correlates of reappraisal were increased activation of the lateral and medial prefrontal regions and decreased activation of the amygdala and medial orbito-frontal cortex. These findings support the hypothesis that prefrontal cortex is involved in constructing reappraisal strategies that can modulate activity in multiple emotion-processing systems.
What brain regions are involved in regulating behavior when the emotional consequence of a stimulus changes from harmful to harmless? One way to address this question is to study the neural mechanisms underlying extinction of Pavlovian fear conditioning, an important form of emotional regulation that has direct relevance to the treatment of human fear and anxiety disorders. In fear extinction, the capacity of a conditioned stimulus to elicit fear is gradually reduced by repeatedly presenting it in the absence of any aversive consequence. In recent years there has been a dramatic increase in research on the brain mechanisms of fear extinction. One region that has received considerable attention as a component of the brain's extinction circuitry is the medial prefrontal cortex (mPFC). In the present article, we review the historical foundations of the modern notion that the mPFC plays a critical role in emotional regulation, a literature that was largely responsible for studies that explored the role of the mPFC in fear extinction. We also consider the role of the mPFC in a broader neural circuit for extinction that includes the amygdala and hippocampus.
The study of human anxiety disorders has benefited greatly from functional neuroimaging approaches. Individual studies, however, vary greatly in their findings. The authors searched for common and disorder-specific functional neurobiological deficits in several anxiety disorders. The authors also compared these deficits to the neural systems engaged during anticipatory anxiety in healthy subjects.
Functional magnetic resonance imaging and positron emission tomography studies of posttraumatic stress disorder (PTSD), social anxiety disorder, specific phobia, and fear conditioning in healthy individuals were compared by quantitative meta-analysis. Included studies compared negative emotional processing to baseline, neutral, or positive emotion conditions.
Patients with any of the three disorders consistently showed greater activity than matched comparison subjects in the amygdala and insula, structures linked to negative emotional responses. A similar pattern was observed during fear conditioning in healthy subjects. Hyperactivation in the amygdala and insula were, of interest, more frequently observed in social anxiety disorder and specific phobia than in PTSD. By contrast, only patients with PTSD showed hypoactivation in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex-structures linked to the experience and regulation of emotion.
This meta-analysis allowed us to synthesize often disparate findings from individual studies and thereby provide neuroimaging evidence for common brain mechanisms in anxiety disorders and normal fear. Effects unique to PTSD furthermore suggested a mechanism for the emotional dysregulation symptoms in PTSD that extend beyond an exaggerated fear response. Therefore, these findings help refine our understanding of anxiety disorders and their interrelationships.
Background:
Bipolar disorder (BD) is a severe, disabling and life-threatening illness. Disturbances in emotion and affective processing are core features of the disorder with affective instability being paralleled by mood-congruent biases in information processing that influence evaluative processes and social judgment. Several lines of evidence, coming from neuropsychological and imaging studies, suggest that disrupted neural connectivity could play a role in the mechanistic explanation of these cognitive and emotional symptoms. The aim of the present study is to investigate the effective connectivity in a sample of bipolar patients.
Methods:
Dynamic causal modeling (DCM) technique was used to study 52 inpatients affected by bipolar disorders consecutively admitted to San Raffaele hospital in Milano and forty healthy subjects. A face-matching task was used as activation paradigm.
Results:
Patients with BD showed a significantly reduced endogenous connectivity in the DLPFC to Amy connection. There was no significant group effect upon the endogenous connection from Amy to ACC, from ACC to Amy and from DLPFC to ACC.
Conclusions:
Both DLPFC and ACC are part of a network implicated in emotion regulation and share strong reciprocal connections with the amygdale. The pattern of abnormal or reduced connectivity between DLPFC and amygdala may reflect abnormal modulation of mood and emotion typical of bipolar patients.
Collectively, functional neuroimaging studies implicate frontal-limbic dysfunction in the pathophysiology of posttraumatic stress disorder (PTSD), as reflected by altered amygdala reactivity and deficient prefrontal responses. These neural patterns are often elicited by social signals of threat (fearful/angry faces) and traumatic reminders (combat sounds, script-driven imagery). Although PTSD can be conceptualized as a disorder of emotion dysregulation, few studies to date have directly investigated the neural correlates of volitional attempts at regulating negative affect in PTSD.
Using functional magnetic resonance imaging and a well-validated task involving cognitive regulation of negative affect via reappraisal and known to engage prefrontal cortical regions, the authors compared brain activation in veterans with PTSD (n = 21) and without PTSD (n = 21, combat-exposed controls/CEC), following military combat trauma experience during deployments in Afghanistan or Iraq. The primary outcome measure was brain activation during cognitive reappraisal (i.e., decrease negative affect) as compared to passive viewing (i.e., maintain negative affect) of emotionally evocative content of aversive images RESULTS: The subjects in both groups reported similar successful reduction in negative affect following reappraisal. The PTSD group engaged the dorsolateral prefrontal cortex (dlPFC) during cognitive reappraisal, albeit to a lesser extent than the CEC group. Although the amygdala was engaged in both groups during passive viewing of aversive images, neither group exhibited attenuation of amygdala activation during cognitive reappraisal.
Veterans with combat-related PTSD showed less recruitment of the dlPFC involved in cognitive reappraisal, suggesting focal and aberrant neural activation during volitional, self-regulation of negative affective states.
Borderline personality disorder (BPD) is a severe mental disorder, characterized by pronounced deficits in emotion regulation, cognitive disturbances including dissociation, impulsivity, and interpersonal disturbances. Over the last decades, neuroimaging has become one of the most important methods to investigate neurobiological alterations possibly underlying core features of BPD. The aim of our article is to provide an overview of the latest neuroimaging research in BPD focusing on functional and structural MRI studies published since 2010. Findings of these studies are depicted and discussed referring to central domains of BPD psychopathology. On a neurochemical level, altered function in neurotransmitter systems including the serotonin, glutamate, and GABA systems was observed in patients with BPD. On a neural level, individuals with BPD showed structural and functional abnormalities in a fronto-limbic network including regions involved in emotion processing (e.g., amygdala, insula) and frontal brain regions implicated in regulatory control processes (e.g., anterior cingulate cortex, medial frontal cortex, orbitofrontal cortex, and dorsolateral prefrontal cortex). Limbic hyperreactivity and diminished recruitment of frontal brain regions may yield a link between disturbed emotion processing and other core features of BPD such as impulsivity and interpersonal disturbances. To clarify whether findings are specific to BPD, comparisons with other clinical groups are needed.
A brief history of the development of research on group work is presented in the context of the evolution of group practice.
This paper reviews the foundation for a role of the human anterior insular cortex (AIC) in emotional awareness, defined as the conscious experience of emotions. We first introduce the neuroanatomical features of AIC and existing findings on emotional awareness. Using empathy, the awareness and understanding of other people's emotional states, as a test case, we then present evidence to demonstrate: 1) AIC and anterior cingulate cortex (ACC) are commonly coactivated as revealed by a meta-analysis; 2) AIC is functionally dissociable from ACC; 3) AIC integrates stimulus-driven and top-down information; and 4) AIC is necessary for emotional awareness. We propose a model in which AIC serves two major functions: integrating bottom-up interoceptive signals with top-down predictions to generate a current awareness state; and providing descending predictions to visceral systems that provide a point of reference for autonomic reflexes. We argue that AIC is critical and necessary for, emotional awareness. J. Comp. Neurol., 2013. © 2013 Wiley Periodicals, Inc.
In this study, we examined changes in attachment style as measured by the Relationship Scales Questionnaire before and after six weeks of intensive group psychotherapy. We also investigated whether changes in attachment style were associated with changes in interpersonal functioning. Results indicated that participants showed increases in secure attachment and decreases in fearful attachment and, to a lesser degree, preoccupied attachment styles. Change was not found in the dismissive attachment style. Changes in Secure and/or Fearful (but not Preoccupied) attachment styles were related to changes in interpersonal functioning on seven of the eight subscales of the Inventory of Interpersonal Problems. Overall findings suggest intensive group psychotherapy programs show promise for reducing attachment pathology and improving interpersonal functioning. Assessing differential responsiveness to psychotherapy may help us align our interventions to better address differing attachment styles through modifications in focus and approach.
Research on brain areas involved in experiencing emotion and physical pain is abundant; however, psychological pain has received little attention in studies of the brain. The purpose of this systematic review was to provide an overview of studies on brain function related to psychological pain. The review was limited to studies in which participants experienced actual psychological pain or recalled a significant autobiographical event that may be assumed to have involved psychological pain. Based on results of the studies (N = 18), a tentative neural network for psychological pain is proposed that includes the thalamus, anterior and posterior cingulate cortex, the prefrontal cortex, cerebellum, and parahippocampal gyrus. Results indicated that grief may be a more accurate exemplar of psychological pain than recalled sadness, with indications of greater arousal during psychological pain. The proposed neural network for psychological pain overlaps to some extent with brain regions involved in physical pain, but results suggest a markedly reduced role for the insula, caudate, and putamen during psychological pain. Psychological pain is well known for its association with depression and as a precursor of suicidal behavior. Thus, identification of brain areas involved in psychological pain may help guide development of interventions to decrease mortality and morbidity.
Functional neuroimaging investigations of major depressive disorder can advance both the neural theory and treatment of this debilitating illness. Inconsistency of neuroimaging findings and the use of region-of-interest approaches have hindered the development of a comprehensive, empirically informed neural model of major depression. In this context, the authors sought to identify reliable anomalies in baseline neural activity and neural response to affective stimuli in major depressive disorder.
The authors applied voxel-wise, whole-brain meta-analysis to neuroimaging investigations comparing depressed to healthy comparison groups with respect to baseline neural activity or neural response to positively and/or negatively valenced stimuli.
Relative to healthy subjects, those with major depression had reliably higher baseline activity, bilaterally, in the pulvinar nucleus. The analysis of neural response studies using negative stimuli showed greater response in the amygdala, insula, and dorsal anterior cingulate cortex and lower response in the dorsal striatum and dorsolateral prefrontal cortex in individuals with major depressive disorder than in healthy subjects.
The meta-analytic results support an elegant and neuroanatomically viable model of the salience of negative information in major depressive disorder. In this proposed model, high baseline pulvinar activity in depression first potentiates responding of the brain's salience network to negative information; next, and owing potentially to low striatal dopamine levels in depression, this viscerally charged information fails to propagate up the cortical-striatal-pallidalthalamic circuit to the dorsolateral prefrontal cortex for contextual processing and reappraisal.
We aimed to study the neural processing of emotion-denoting words based on a circumplex model of affect, which posits that all emotions can be described as a linear combination of two neurophysiological dimensions, valence and arousal. Based on the circumplex model, we predicted a linear relationship between neural activity and incremental changes in these two affective dimensions.
Using functional magnetic resonance imaging, we assessed in 10 subjects the correlations of BOLD (blood oxygen level dependent) signal with ratings of valence and arousal during the presentation of emotion-denoting words.
Valence ratings correlated positively with neural activity in the left insular cortex and inversely with neural activity in the right dorsolateral prefrontal and precuneus cortices. The absolute value of valence ratings (reflecting the positive and negative extremes of valence) correlated positively with neural activity in the left dorsolateral and medial prefrontal cortex (PFC), dorsal anterior cingulate cortex, posterior cingulate cortex, and right dorsal PFC, and inversely with neural activity in the left medial temporal cortex and right amygdala. Arousal ratings and neural activity correlated positively in the left parahippocampus and dorsal anterior cingulate cortex, and inversely in the left dorsolateral PFC and dorsal cerebellum.
We found evidence for two neural networks subserving the affective dimensions of valence and arousal. These findings clarify inconsistencies from prior imaging studies of affect by suggesting that two underlying neurophysiological systems, valence and arousal, may subserve the processing of affective stimuli, consistent with the circumplex model of affect.
Humans have the ability to control negative affect and perceived fear. Nevertheless, it is still unclear whether this affect regulation capacity relies on a common neural mechanism in different experimental domains. Here, we sought to identify commonalities in regulatory brain activation in the domains of fear extinction, placebo, and cognitive emotion regulation. Using coordinate-based activation-likelihood estimation meta-analysis we intended to elucidate concordant hyperactivations and the associated deactivations in the three experimental domains, when human subjects successfully diminished negative affect. Our data show that only one region in the ventromedial prefrontal cortex (VMPFC) controlled negative affective responses and reduced the degree of subjectively perceived unpleasantness independent of the experimental domain. This down-regulation of negative affect was further accompanied by a concordant reduction of activation in the left amygdala. Finally, the soothing effect of placebo treatments and cognitive reappraisal strategies, but not extinction retrieval, was specifically accompanied by a coherent hyperactivation in the anterior cingulate and the insular cortex. Collectively, our data strongly imply that the human VMPFC may represent a domain-general controller of perceived fear and aversiveness that modulates negative affective responses in phylogenetically older structures of the emotion processing system. In addition, higher-level regulation strategies may further engage complementary neural resources to effectively deal with the emotion-eliciting events.
This article introduces the systems-centered concept of the "group mind" by linking systems-centered thinking and interpersonal neurobiology, building on Siegel's definition of mind as the process of regulating the flow of energy and information. Functional subgrouping, the systems-centered group method for resolving conflicts, discriminates and integrates the flow of energy and information within and between group members, subgroups, and the group-as-a-whole, thus potentiating survival, development, and transformation. This article uses the interpersonal neurobiological framework to discuss functional subgrouping as a tool for developing the group mind: considering how functional subgrouping facilitates emotional regulation, creates a secure relational context, and potentiates neural integration.
Cognitive-behavioural interventions have been shown to change brain functioning. We used an emotional linguistic go/nogo functional magnetic resonance imaging (fMRI) design to determine changes of brain activation patterns of panic disorder (PD) patients following short-term psychodynamic inpatient treatment. Nine PD patients underwent fMRI before and after treatment; 18 healthy controls were scanned twice at the same interval (4 weeks). In the go/nogo design, responses to panic-specific negative words were compared with linguistically matched positive and neutral words. According to hypotheses, patients rated affective words more strongly than controls and selectively recalled negative vs. positive/neutral words. Before treatment, high limbic (hippocampus and amygdala) activation was accompanied by low prefrontal activation to negative words. Inhibition-related activation patterns indicated difficulties of behavioural regulation in emotional context. At treatment termination, panic-related symptoms had improved significantly, and fronto-limbic activation patterns were normalized. Our results indicate that short-term psychodynamic treatment leads to changes in fronto-limbic circuitry not dissimilar to previous findings on cognitive-behavioural treatments.
The response-focused emotion regulation style 'Expressive suppression' has been associated with symptoms of lower psychological well-being and increased function magnetic resonance imaging (fMRI) activation of the sublenticular extended amygdala (SLEA) in patients with major depression. Extending prior studies on active emotion regulation, we were interested in effects of habitual emotion regulation on neurobiology. Thirty subjects with either relatively high or low suppression scores as assessed with the Emotion Regulation Questionnaire without symptoms of clinical depression participated in the study. They were instructed to expect and then perceive emotionally unpleasant, pleasant or neutral stimuli selected from the International Affective Picture System that were announced by a congruent cue during fMRI. In the subjects with high suppression scores, decreased activation of the orbital medial prefrontal cortex (oMFC) when expecting negative pictures and increased activation of the SLEA upon presentation of neutral stimuli were found. Subclinical depression ratings independently of suppression scores in the healthy subjects were positively correlated with brain activation in the SLEA when expecting negative pictures. SLEA hyperactivity may represent an emotional responsivity that involves less successful habitual emotion regulation and a tendency to depressed mood in healthy subjects, as shown in patients with major depression. Decreased anticipatory oMFC activation may parallel a lack of antecedent emotion regulation in subjects with high suppression scores, representing another neurobiological predictor of lower mental well-being.
Psychoanalysis, the science of unconscious processes, has recently undergone a significant transformation. Self psychology, derived from the work of Heinz Kohut, represents perhaps the most important revision of Freud's theory as it has shifted its basic core concepts from an intrapsychic to a relational unconscious and from a cognitive ego to an emotion-processing self. As a result of a common interest in the essential, rapid, bodily based, affective processes that lie beneath conscious awareness, a productive dialogue is now occurring between psychoanalysis and neuroscience. Here I apply this interdisciplinary perspective to a deeper understanding of the nonconscious brain/mind/body mechanisms that lie at the core of self psychology. I offer a neuropsychoanalytic conception of the development and structuralization of the self, focusing on the experience-dependent maturation of the emotion-processing right brain in infancy. I then articulate an interdisciplinary model of attachment trauma and pathological dissociation, an early forming defense against overwhelming affect that is a cardinal feature of self-psychopathologies. I end with some thoughts on the mechanism of the psychotherapeutic change process and suggest that self psychology is, in essence, a psychology of the unique functions of the right brain and that a rapprochement between psychoanalysis and neuroscience is now at hand.