Developmental Neuroscience Division, Department of Psychiatry, College of Physicians and Surgeons, Columbia University, 1051 Riverside Dr, Unit 40, New York, NY 10032. .Psychosomatic Medicine (Impact Factor: 3.47). 08/2012; 74(7):717-27. DOI: 10.1097/PSY.0b013e3182688e8b
Somatoform pain is a highly prevalent, debilitating condition and a tremendous public health problem. Effective treatments for somatoform pain are urgently needed. The etiology of this condition is, however, still unknown. On the basis of a review of recent basic and clinical research, we propose one potential mechanism of symptom formation in somatoform pain and a developmental theory of its pathogenesis. Emerging evidence from animal and human studies in developmental neurobiology, cognitive-affective neuroscience, psychoneuroimmunology, genetics, and epigenetics, as well as that from clinical and treatment studies on somatoform pain, points to the existence of a shared neural system that underlies physical and social pain. Research findings also show that nonoptimal early experiences interact with genetic predispositions to influence the development of this shared system and the ability to regulate it effectively. Interpersonal affect regulation between infant and caregiver is crucial for the optimal development of these brain circuits. The aberrant development of this shared neural system during infancy, childhood, and adolescence may therefore ultimately lead to an increased sensitivity to physical and social pain and to problems with their regulation in adulthood. The authors critically review translational research findings that support this theory and discuss its clinical and research implications. Specifically, the proposed theory and research review suggest that psychotherapeutic and/or pharmacological interventions that foster the development of affect regulation capacities in an interpersonal context will also serve to more effectively modulate aberrantly activated neural pain circuits and thus be of particular benefit for the treatment of somatoform pain.
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ABSTRACT: Functional somatic symptoms (FSS) are common in children and adolescents, but explanatory models that synthesize research findings are lacking. This article reviews the studies published from January 2012 to March 2013 that investigate the neurophysiological mechanisms that may underlie FSS. Studies from diverse medical disciplines suggest that FSS are associated with functional differences in hypothalamic-pituitary-adrenal function, imbalances in vagal-sympathetic tone, upregulation of immune-inflammatory function, and primed cognitive-emotional responses that serve to amplify reactivity to threatening stimuli, thereby contributing to the subjective experience of somatic symptoms. FSS appear to reflect dysregulations of the stress system. When seemingly disparate research findings are interpreted together within an overarching 'stress-system' framework, a coherent explanatory model begins to emerge.Current opinion in psychiatry 07/2013; 13(5). DOI:10.1097/YCO.0b013e3283642ca0 · 3.94 Impact Factor
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ABSTRACT: To test the potential mediation effect of psychosomatic symptoms on the relationship between parents' history of childhood physical victimization and current risk for child physical maltreatment. Data from the Portuguese National Representative Study of Psychosocial Context of Child Abuse and Neglect were used. Nine-hundred and twenty-four parents completed the Childhood History Questionnaire, the Psychosomatic Scale of the Brief Symptom Inventory, and the Child Abuse Potential Inventory. Mediation analysis revealed that the total effect of the childhood physical victimization on child maltreatment risk was significant. The results showed that the direct effect from the parents' history of childhood physical victimization to their current maltreatment risk was still significant once parents' psychosomatic symptoms were added to the model, indicating that the increase in psychosomatic symptomatology mediated in part the increase of parents' current child maltreatment risk. The mediation analysis showed parents' psychosomatic symptomatology as a causal pathway through which parents' childhood history of physical victimization exerts its effect on increased of child maltreatment risk. Somatization-related alterations in stress and emotional regulation are discussed as potential theoretical explanation of our findings. A cumulative risk perspective is also discussed in order to elucidate about the mechanisms that contribute for the intergenerational continuity of child physical maltreatment.Journal of psychosomatic research 08/2013; 75(2):178-83. DOI:10.1016/j.jpsychores.2013.04.001 · 2.74 Impact Factor
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ABSTRACT: Emotions elicited by interpersonal versus non-interpersonal experiences have different effects on neurobiological functioning in both animals and humans. However, the extent to which the brain circuits underlying interpersonal and non-interpersonal emotions are distinct still remains unclear. The goal of our study was to assess whether different neural circuits are implicated in the processing of arousal and valence of interpersonal versus non-interpersonal emotions. During functional magnetic resonance imaging, participants imagined themselves in emotion-eliciting interpersonal or non-interpersonal situations and then rated the arousal and valence of emotions they experienced. We identified (1) separate neural circuits that are implicated in the arousal and valence dimensions of interpersonal versus non-interpersonal emotions, (2) circuits that are implicated in arousal and valence for both types of emotion, and (3) circuits that are responsive to the type of emotion, regardless of the valence or arousal level of the emotion. We found extensive recruitment of limbic (for arousal) and temporal-parietal (for valence) systems associated with processing of specifically interpersonal emotions compared to non-interpersonal ones. The neural bases of interpersonal and non-interpersonal emotions may, therefore, be largely distinct.Social neuroscience 09/2013; 8(5):474-88. DOI:10.1080/17470919.2013.833984 · 2.66 Impact Factor
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