Several lines of research have illustrated that negative environments can precipitate psychopathology, particularly in the context of relatively increased biological risk, while social resources can buffer the effects of these environments. However, little research has examined how social resources might buffer proximal biological risk for psychopathology or the neurobiological pathways through which such buffering may be mediated. Here we report that the expression of trait anxiety as a function of threat-related amygdala reactivity is moderated by perceived social support, a resource for coping with adversity. A significant positive correlation between amygdala reactivity and trait anxiety was evident in individuals reporting below average levels of support but not in those reporting average or above average levels. These results were consistent across multiple measures of trait anxiety and were specific to anxiety in that they did not extend to measures of broad negative or positive affect. Our findings illuminate a biological pathway, namely moderation of amygdala-related anxiety, through which social support may confer resilience to psychopathology. Moreover, our results indicate that links between neural reactivity and behavior are not static but rather may be contingent on social resources.
"Moreover, amygdala activation in response to happy facial expression was associated with the personality trait extraversion (Canli et al., 2002; Canli, 2004), that might have some associations with generalized self-efficacy. Furthermore, PSS was found to moderate the relation between amygdala activity in response to fearful and angry facial expressions and anxiety trait, such that only low PSS predicted the relation between amygdala activity and anxiety trait (Hyde et al., 2011). Taken together, these different findings call for future studies that will enable their integration into a single comprehensive framework using diverse methodologies to measure functional signal in face related regions and the connectivity between these regions, as well as genetic, self and face processing measures. "
[Show abstract][Hide abstract] ABSTRACT: The aim of the proposed theoretical model is to illuminate personal and interpersonal resilience by drawing from the field of emotional face perception. We suggest that perception/recognition of emotional facial expressions serves as a central link between subjective, self-related processes and the social context. Emotional face perception constitutes a salient social cue underlying interpersonal communication and behavior. Because problems in communication and interpersonal behavior underlie most, if not all, forms of psychopathology, it follows that perception/recognition of emotional facial expressions impacts psychopathology. The ability to accurately interpret one's facial expression is crucial in subsequently deciding on an appropriate course of action. However, perception in general, and of emotional facial expressions in particular, is highly influenced by individuals' personality and the self-concept. Herein we briefly outline well-established theories of personal and interpersonal resilience and link them to the neuro-cognitive basis of face perception. We then describe the findings of our ongoing program of research linking two well-established resilience factors, general self-efficacy (GSE) and perceived social support (PSS), with face perception. We conclude by pointing out avenues for future research focusing on possible genetic markers and patterns of brain connectivity associated with the proposed model. Implications of our integrative model to psychotherapy are discussed.
Frontiers in Human Neuroscience 08/2014; 8:602. DOI:10.3389/fnhum.2014.00602 · 3.63 Impact Factor
"Associations of FFM-Psychopathy and FFM-APD scores with amygdala reactivity were examined in regressions using IBM SPSS statistics v.20. Consistent with past studies (e.g., Hyde et al., 2011) gender was controlled for in all regressions given its main effect on amygdala reactivity in this sample (see Table 1). 1 In all regression analyses, extracted amygdala reactivity values were regressed first on APD or psychopathy scores separately, and then onto APD and psychopathy scores simultaneously to assess for overlapping versus unique relationships between psychopathy and APD dimensions and amygdala reactivity. As APD and psychopathy trait scores demonstrated a high correlation (see Table 1), collinearity was a concern and thus tolerance was monitored with scores below 0.10 considered problematic (Cohen, Cohen, West, & Aiken, 2003). "
[Show abstract][Hide abstract] ABSTRACT: Previous studies have emphasized that antisocial personality disorder (APD) and psychopathy overlap highly but differ critically in several features, notably negative emotionality (NEM) and possibly amygdala reactivity to social signals of threat and distress. Here we examined whether dimensions of psychopathy and APD correlate differentially with NEM and amygdala reactivity to emotional faces. Testing these relationships among healthy individuals, dimensions of psychopathy and APD were generated by the profile matching technique of Lynam and Widiger (2001), using facet scales of the NEO Personality Inventory-Revised, and amygdala reactivity was measured using a well-established emotional faces task, in a community sample of 103 men and women. Higher psychopathy scores were associated with lower NEM and lower amygdala reactivity, whereas higher APD scores were related to greater NEM and greater amygdala reactivity, but only after overlapping variance in APD and psychopathy was adjusted for in the statistical model. Amygdala reactivity did not mediate the relationship of APD and psychopathy scores to NEM. Supplemental analyses also compared other measures of factors within psychopathy in predicting NEM and amygdala reactivity and found that Factor 2 psychopathy was positively related to NEM and amygdala reactivity across measures of psychopathy. The overall findings replicate seminal observations on NEM in psychopathy by Hicks and Patrick (2006) and extend this work to neuroimaging in a normative population. They also suggest that one critical way in which APD and psychopathy dimensions may differ in their etiology is through their opposing levels of NEM and amygdala reactivity to threat. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
"Extracting parameter estimates from functional clusters activated by our fMRI paradigm, rather than clusters specifically correlated with our independent variables of interest, precludes the possibility of any correlation coefficient inflation that may result when an explanatory covariate is used to select a region of interest
. We have used this more conservative and rigorous analytic strategy in recent studies
[Show abstract][Hide abstract] ABSTRACT: Background
Recent laboratory studies employing an extended sleep deprivation model have mapped sleep-related changes in behavior onto functional alterations in specific brain regions supporting emotion, suggesting possible biological mechanisms for an association between sleep difficulties and deficits in emotion regulation. However, it is not yet known if similar behavioral and neural changes are associated with the more modest variability in sleep observed in daily life.
We examined relationships between sleep and neural circuitry of emotion using the Pittsburgh Sleep Quality Index and fMRI data from a widely used emotion regulation task focusing on cognitive reappraisal of negative emotional stimuli in an unselected sample of 97 adult volunteers (48 women; mean age 42.78±7.37 years, range 30–54 years old).
Emotion regulation was associated with greater activation in clusters located in the dorsomedial prefrontal cortex (dmPFC), left dorsolateral prefrontal cortex (dlPFC), and inferior parietal cortex. Only one subscale from the Pittsburgh Sleep Quality Index, use of sleep medications, was related to BOLD responses in the dmPFC and dlPFC during cognitive reappraisal. Use of sleep medications predicted lesser BOLD responses during reappraisal, but other aspects of sleep, including sleep duration and subjective sleep quality, were not related to neural activation in this paradigm.
The relatively modest variability in sleep that is common in the general community is unlikely to cause significant disruption in neural circuits supporting reactivity or regulation by cognitive reappraisal of negative emotion. Use of sleep medication however, may influence emotion regulation circuitry, but additional studies are necessary to determine if such use plays a causal role in altering emotional responses.
Biology of Mood and Anxiety Disorders 12/2012; 2(1):22. DOI:10.1186/2045-5380-2-22
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.