Several recent neuroimaging studies have examined the neuroanatomical correlates of normal emotional states, such as happiness, sadness, fear, anger, anxiety, and disgust; however, no previous study has examined the emotional state of guilt.
In the current study, we used positron emission tomography and the script-driven imagery paradigm to study regional cerebral blood flow (rCBF) during the transient emotional experience of guilt in eight healthy male participants. In the Guilt condition, participants recalled and imagined participating in a personal event involving the most guilt they had ever experienced. In the Neutral condition, participants recalled and imagined participating in an emotionally neutral personal event.
In the Guilt versus Neutral comparison, rCBF increases occurred in anterior paralimbic regions of the brain: bilateral anterior temporal poles, anterior cingulate gyrus, and left anterior insular cortex/inferior frontal gyrus.
These results, along with those of previous studies, are consistent with the notion that anterior paralimbic regions of the brain mediate negative emotional states in healthy individuals.
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"). Hence not surprisingly, IFG activity is also often observed in social interaction paradigms and interpreted as contributing to mentalizing or perspective-taking processes (Beyer et al. 2013; Polosan et al. 2011). Our IFG connectivity cluster was on the left hemisphere around Brodmann area 47, matching a region activated by script-induced guilt (Shin et al. 2000), and an empathy-related peak identified by Liakakis et al. (2011). A recent study found that VS-IFG connectivity induced by happy faces was lower as a function of autistic traits in healthy adults (Sims et al. 2014). "
[Show abstract][Hide abstract] ABSTRACT: Social neuroscience studies have shown that the ventral striatum (VS), a highly reward-sensitive brain area, is activated when participants win competitive tasks. However, in these settings winning often entails both avoiding punishment and punishing the opponent. It is thus unclear whether the rewarding properties of winning are mainly associated to punishment avoidance, or if punishing the opponent can be additionally gratifying. In the present paper we explored the neurophysiological correlates of each outcome, aiming to better understand the development of aggression episodes. We previously introduced a competitive reaction time task that separates both effects: in half of the won trials, participants can physically punish their opponent (active trials), whereas in the other half they can only avoid a punishment (passive trials). We performed functional connectivity analysis seeded in the VS to test for differential network interactions in active compared to passive trials. The VS showed greater connectivity with areas involved in reward valuation (orbitofrontal cortex), arousal (dorsal thalamus and posterior insula), attention (inferior occipital gyrus), and motor control (supplementary motor area) in active compared to passive trials, whereas connectivity between the VS and the inferior frontal gyrus decreased. Interindividual variability in connectivity strength between VS and posterior insula was related to aggressive behavior, whereas connectivity between VS and supplementary motor area was related to faster reaction times in active trials. Our results suggest that punishing a provoking opponent when winning might adaptively favor a "competitive state" in the course of an aggressive interaction.
Brain Imaging and Behavior 03/2015; DOI:10.1007/s11682-015-9370-z · 4.60 Impact Factor
"Nonetheless, several brain regions have been consistently implicated and the activation of these regions have also been observed for the experience of negative affect, physical pain, and 'social pain' (Shackman et al., 2011; Eisenberger, 2012). For instance, anticipating and imagining a guilt-evoking situation activate the anterior cingulate cortex (ACC), the anterior insula (AI) and the lateral orbitofrontal cortex (LOFC) (Shin et al., 2000; Basile et al., 2011; Chang et al., 2011; Wagner et al., 2011). These activations may reflect an 'unpleasant arousal akin to anxiety' (Tennen and Herzberger, 1987), such as the anxiety over being socially excluded (Baumeister et al., 1994). "
[Show abstract][Hide abstract] ABSTRACT: People feel bad for inflicting harms upon others; this emotional state is termed interpersonal guilt. In this study, the participant
played multiple rounds of a dot-estimation task with anonymous partners while undergoing fMRI. The partner would receive pain
stimulation if the partner or the participant or both responded incorrectly; the participant was then given the option to
intervene and bear a proportion of pain for the partner. The level of pain voluntarily taken and the activations in anterior
middle cingulate cortex (aMCC) and bilateral anterior insula (AI) were higher when the participant was solely responsible
for the stimulation (Self_Incorrect) than when both committed an error (Both_Incorrect). Moreover, the gray matter volume
in the aMCC predicted the individual’s compensation behavior, measured as the difference between the level of pain taken in
the Self_Incorrect and Both_Incorrect conditions. Furthermore, a mediation pathway analysis revealed that activation in a
midbrain region mediated the relationship between aMCC activation and the individual’s tendency to compensate. These results
demonstrate that the aMCC and the midbrain nucleus not only play an important role in experiencing interpersonal guilt, but
also contribute to compensation behavior.
Social Cognitive and Affective Neuroscience 08/2014; 9(8):1150-1158. DOI:10.1093/scan/nst090 · 7.37 Impact Factor
"Other regions where BP patients and control subjects differed included bilateral temporal and right insular cortex and posterior parietal and occipital cortices. Insular cortex activations have been shown to be sensitive to the negative salience of the stimuli  with higher responses during transient induction of sadness  and in a wide range of negative experiences in healthy and psychiatric populations  including the experience of guilt . "
[Show abstract][Hide abstract] ABSTRACT: Objectives. Patients affected by bipolar disorder (BP) and major depressive disorder (UP) share the susceptibility to experience depression and differ in their susceptibility to mania, but clinical studies suggest that the biological substrates of the two disorders could influence the apparently similar depressive phases. The few brain imaging studies available described different brain metabolic and neural correlates of UP and BP. Methods. We studied the BOLD neural response to a moral valence decision task targeting the depressive biases in information processing in 36 subjects (14 BP, 11 UP, and 11 controls). Results. Main differences between UP and controls and between UP and BP were detected in left ventrolateral prefrontal cortex (PFC, BA 47). Neural responses of BP patients differed from those of control subjects in multiple brain areas, including anterior cingulate cortex (ACC) and medial PFC, bilateral dorsolateral PFC, temporal cortex and insula, and parietal and occipital cortex. Conclusions. Our results are in agreement with hypotheses of dysfunctions in corticolimbic circuitries regulating affects and emotions in mood disorders and suggest that specific abnormalities, particularly in ventrolateral PFC, are not the same in UP and BP depression.