The study of emotional states has recently received considerable attention within the cognitive and neural sciences. However, limited work has been done to synthesize this growing body of literature ...within a coherent hierarchical, neuro-cognitive framework. In this article, we review evidence pertaining to three interacting hierarchical neural systems associated with the generation, perception and regulation of one's own emotional state. In the framework we propose, emotion generation proceeds through a series of appraisal mechanisms - some of which appear to require more cognitively sophisticated computational processing (and hence more time) than others - that ultimately trigger iterative adjustments to one's bodily state (as well as to the modes of processing in other cognitive systems). Perceiving one's own emotions then involves a multi-stage interoceptive/somatosensory process by which these body state patterns are detected and assigned conceptual emotional meaning. Finally, emotion regulation can be understood as a hierarchical control system that, at various levels, modulates autonomic reactions, appraisal mechanisms, attention, the contents of working memory, and goal-directed action selection. We highlight implications this integrative model may have for competing theories of emotion and emotional consciousness and for guiding future research.
The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago. In our neurovisceral integration model we have tried to build on this pioneering work. In ...the present paper we further elaborate our model. Specifically we review recent neuroanatomical studies that implicate inhibitory GABAergic pathways from the prefrontal cortex to the amygdala and additional inhibitory pathways between the amygdala and the sympathetic and parasympathetic medullary output neurons that modulate heart rate and thus heart rate variability. We propose that the default response to uncertainty is the threat response and may be related to the well known negativity bias. We next review the evidence on the role of vagally mediated heart rate variability (HRV) in the regulation of physiological, affective, and cognitive processes. Low HRV is a risk factor for pathophysiology and psychopathology. Finally we review recent work on the genetics of HRV and suggest that low HRV may be an endophenotype for a broad range of dysfunctions.
Since Freud, clinicians have understood that disturbing memories contribute to psychopathology and that new emotional experiences contribute to therapeutic change. Yet, controversy remains about what ...is truly essential to bring about psychotherapeutic change. Mounting evidence from empirical studies suggests that emotional arousal is a key ingredient in therapeutic change in many modalities. In addition, memory seems to play an important role but there is a lack of consensus on the role of understanding what happened in the past in bringing about therapeutic change. The core idea of this paper is that therapeutic change in a variety of modalities, including behavioral therapy, cognitive-behavioral therapy, emotion-focused therapy, and psychodynamic psychotherapy, results from the updating of prior emotional memories through a process of reconsolidation that incorporates new emotional experiences. We present an integrated memory model with three interactive components - autobiographical (event) memories, semantic structures, and emotional responses - supported by emerging evidence from cognitive neuroscience on implicit and explicit emotion, implicit and explicit memory, emotion-memory interactions, memory reconsolidation, and the relationship between autobiographical and semantic memory. We propose that the essential ingredients of therapeutic change include: (1) reactivating old memories; (2) engaging in new emotional experiences that are incorporated into these reactivated memories via the process of reconsolidation; and (3) reinforcing the integrated memory structure by practicing a new way of behaving and experiencing the world in a variety of contexts. The implications of this new, neurobiologically grounded synthesis for research, clinical practice, and teaching are discussed.
The hierarchical basis of neurovisceral integration Smith, Ryan; Thayer, Julian F.; Khalsa, Sahib S. ...
Neuroscience and biobehavioral reviews,
April 2017, 2017-Apr, 2017-04-00, 20170401, Letnik:
75
Journal Article
Recenzirano
•Neurovisceral integration (NVI) theory has received considerable empirical support.•A detailed model of the functional neuroanatomy underlying NVI findings is lacking.•We describe an eight-level ...neural hierarchy underlying NVI and cardiac vagal control.•The interactions within this hierarchy may implement predictive coding computations.•Implications for understanding physiology, emotion, and cognition are discussed.
The neurovisceral integration (NVI) model was originally proposed to account for observed relationships between peripheral physiology, cognitive performance, and emotional/physical health. This model has also garnered a considerable amount of empirical support, largely from studies examining cardiac vagal control. However, recent advances in functional neuroanatomy, and in computational neuroscience, have yet to be incorporated into the NVI model. Here we present an updated/expanded version of the NVI model that incorporates these advances. Based on a review of studies of structural/functional anatomy, we first describe an eight-level hierarchy of nervous system structures, and the contribution that each level plausibly makes to vagal control. Second, we review recent work on a class of computational models of brain function known as “predictive coding” models. We illustrate how the computational dynamics of these models, when implemented within our proposed vagal control hierarchy, can increase understanding of the relationship between vagal control and both cognitive performance and emotional/physical health. We conclude by discussing novel implications of this updated NVI model for future research.
•Unconscious emotion (UE) remains largely unexplored neuroscientifically.•UE may involve reactions to a situation that are not selected for conscious access.•UE might plausibly be maintained via ...top-down (TMs) or bottom-up (BMs) mechanisms.•TMs may involve thought substitution, suppression, or biased attention.•BMs may involve arousal-induced inhibition of concept-level emotion representations.
While psychiatry and clinical psychology have long discussed the topic of unconscious emotion, and its potentially explanatory role in psychopathology, this topic has only recently begun to receive attention within cognitive neuroscience. In contrast, neuroscientific research on conscious vs. unconscious processes within perception, memory, decision-making, and cognitive control has seen considerable advances in the last two decades. In this article, we extrapolate from this work, as well as from recent neural models of emotion processing, to outline multiple plausible neuro-cognitive mechanisms that may be able to explain why various aspects of one’s own emotional reactions can remain unconscious in specific circumstances. While some of these mechanisms involve top-down or motivated factors, others instead arise due to bottom-up processing deficits. Finally, we discuss potential implications that these different mechanisms may have for therapeutic intervention, as well as how they might be tested in future research.
•Low emotional awareness (EA) is associated with multiple clinical conditions.•The neurocomputational processes underlying EA are poorly understood.•We present a deep active inference model of EA ...that can simulate these processes.•This model illustrates 7 distinct mechanisms whereby aberrant processing produces low EA.•This may offer distinct targets that could inform individualized treatment selection.
Emotional awareness (EA) is recognized as clinically relevant to the vulnerability to, and maintenance of, psychiatric disorders. However, the neurocomputational processes that underwrite individual variations remain unclear. In this paper, we describe a deep (active) inference model that reproduces the cognitive-emotional processes and self-report behaviors associated with EA. We then present simulations to illustrate (seven) distinct mechanisms that (either alone or in combination) can produce phenomena – such as somatic misattribution, coarse-grained emotion conceptualization, and constrained reflective capacity – characteristic of low EA. Our simulations suggest that the clinical phenotype of impoverished EA can be reproduced by dissociable computational processes. The possibility that different processes are at work in different individuals suggests that they may benefit from distinct clinical interventions. As active inference makes particular predictions about the underlying neurobiology of such aberrant inference, we also discuss how this type of modelling could be used to design neuroimaging tasks to test predictions and identify which processes operate in different individuals – and provide a principled basis for personalized precision medicine.
•Affective Neuroscience (AN) involves more invasive approaches in animals.•Cognitive Neuroscience (CN) involves less invasive approaches to emotion in humans.•AN and CN often promote discordant views ...on the neural basis of emotional experience.•AN, unlike CN, holds that subcortical processes alone are sufficient for conscious emotion.•Future experiments we describe may be required to integrate these perspectives.
The “affective” and “cognitive” neuroscience approaches to understanding emotion (AN and CN, respectively) represent potentially synergistic, but as yet unreconciled, theoretical perspectives, which may in part stem from the methods that these distinct perspectives routinely employ—one focusing on animal brain emotional systems (AN) and one on diverse human experimental approaches (CN). Here we present an exchange in which each approach (1) describes its own theoretical perspective, (2) offers a critique of the other perspective, and then (3) responds to each other’s critique. We end with a summary of points of agreement and disagreement, and describe possible future experiments that could help resolve the remaining controversies. Future work should (i) further characterize the structure/function of subcortical circuitry with respect to its role in generating emotion, and (ii) further investigate whether sub-neocortical activations alone are sufficient (as opposed to merely necessary) for affective experiences, or whether subsequent cortical representation of an emotional response is also required.
ABSTRACT
We investigate the Fe, C, N, O, Mg, Al, Si, K, Ca, Ce, and Nd abundances of 2283 red giant stars in 31 globular clusters from high-resolution spectra observed in both the Northern and ...Southern hemisphere by the SDSS-IV APOGEE-2 survey. This unprecedented homogeneous data set, largest to date, allows us to discuss the intrinsic Fe spread, the shape, and statistics of Al-Mg and N-C anti-correlations as a function of cluster mass, luminosity, age, and metallicity for all 31 clusters. We find that the Fe spread does not depend on these parameters within our uncertainties including cluster metallicity, contradicting earlier observations. We do not confirm the metallicity variations previously observed in M22 and NGC 1851. Some clusters show a bimodal Al distribution, while others exhibit a continuous distribution as has been previously reported in the literature. We confirm more than two populations in ω Cen and NGC 6752, and find new ones in M79. We discuss the scatter of Al by implementing a correction to the standard chemical evolution of Al in the Milky Way. After correction, its dependence on cluster mass is increased suggesting that the extent of Al enrichment as a function of mass was suppressed before the correction. We observe a turnover in the Mg-Al anticorrelation at very low Mg in ω Cen, similar to the pattern previously reported in M15 and M92. ω Cen may also have a weak K-Mg anticorrelation, and if confirmed, it would be only the third cluster known to show such a pattern.
There are two broad themes in psychosomatic medicine research that relate emotions to physical disease outcomes. Theme 1 holds that self-reported negative affect has deleterious effects and ...self-reported positive affect has salubrious effects on health. Theme 2 holds that interference with the experience or expression of negative affect has adverse health consequences. From the perspective of self-report these two traditions appear contradictory. A key thesis of this paper is that the foundational distinction in cognitive neuroscience between explicit (conscious) and implicit (unconscious) processes, corresponding to Themes 1 and 2, respectively, provides a unifying framework that makes empirical research on unconscious emotional processes more tractable. A psychological model called "levels of emotional awareness" is presented first that places implicit and explicit emotional processes on a cognitive-developmental continuum. This model holds that the ability to become consciously aware of one's own feelings is a cognitive skill that goes through a developmental process similar to that which Piaget described for other cognitive functions. Empirical findings using the Levels of Emotional Awareness Scale are presented. A parallel hierarchical model of the neural substrates of emotional awareness is presented next supported by recent neuroimaging and lesion work. The evidence presented in this review suggests that the neural substrates of implicit and explicit emotional processes are distinct, that the latter have a modulatory effect on the former, and that at the neural level Theme 1 and Theme 2 phenomena share critical similarities. The implications of this psychobiological model for research in psychosomatic medicine are discussed.
We describe a new type of agnosia consisting of an impairment in the ability to mentally represent or know what one is feeling. Freud the neurologist coined the term "agnosia" in 1891 before creating ...psychoanalysis in 1895 but the term has not been previously applied to the domain of affective processing. We propose that the concept of "affective agnosia" advances the theory, measurement and treatment of what is now called "alexithymia," meaning "lack of words for emotion." We trace the origin of the alexithymia construct and discuss the strengths and limitations of extant research. We review evidence that the ability to represent and put emotions into words is a developmental achievement that strongly influences one's ability to experience, recognize, understand and use one's own emotional responses. We describe the neural substrates of emotional awareness and affective agnosia and compare and contrast these with related conditions. We then describe how this expansion of the conceptualization and measurement of affective processing deficits has important implications for basic emotion research and clinical practice.
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