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Empathy is significantly influenced by the identification of others' emotions. In a recent study, we have found increased activation in the anterior insular cortex (aIns) that could be attributed to affect sharing rather than perceptual saliency, when seeing another person genuinely experiencing pain as opposed to merely acting to be in pain. In that prior study, effective connectivity between aIns and the right supramarginal gyrus (rSMG) was revealed to represent what another person really feels. In the present study, we used a similar paradigm to investigate the corresponding neural signatures in the domain of empathy for disgust - with participants seeing others genuinely sniffing unpleasant odors as compared to pretending to smell something disgusting (in fact the disgust expressions in both conditions were acted for reasons of experimental control). Consistent with the previous findings on pain, we found stronger activations in aIns associated with affect sharing for genuine disgust (inferred) compared with pretended disgust. However, instead of rSMG we found engagement of the olfactory cortex. Using dynamic causal modeling (DCM), we estimated the neural dynamics of aIns and the olfactory cortex between the genuine and pretended conditions. This revealed an increased excitatory modulatory effect for genuine disgust compared to pretended disgust. For genuine disgust only, brain-to-behavior regression analyses highlighted a link between the observed modulatory effect and a few empathic traits. Altogether, the current findings complement and expand our previous work, by showing that perceptual saliency alone does not explain responses in the insular cortex. Moreover, it reveals that different brain networks are implicated in a modality-specific way when sharing the affective experiences associated with pain vs. disgust.

Empathy for pain engages both shared affective responses and self-other distinction. In this study, we addressed the highly debated question of whether neural responses previously linked to affect sharing could result from the perception of salient affective displays. Moreover, we investigated how the brain network involved in affect sharing and self-other distinction underpinned our response to a pain that is either perceived as genuine or pretended (while in fact both were acted for reasons of experimental control). We found stronger activations in regions associated with affect sharing (anterior insula [aIns] and anterior mid-cingulate cortex) as well as with affective self-other distinction (right supramarginal gyrus [rSMG]), in participants watching video clips of genuine vs. pretended facial expressions of pain. Using dynamic causal modeling, we then assessed the neural dynamics between the right aIns and rSMG in these two conditions. This revealed a reduced inhibitory effect on the aIns to rSMG connection for genuine pain compared to pretended pain. For genuine pain only, brain-to-behavior regression analyses highlighted a linkage between this inhibitory effect on the one hand, and pain ratings as well as empathic traits on the other. These findings imply that if the pain of others is genuine and thus calls for an appropriate empathic response, neural responses in the aIns indeed seem related to affect sharing and self-other distinction is engaged to avoid empathic over-arousal. In contrast, if others merely pretend to be in pain, the perceptual salience of their painful expression results in neural responses that are down-regulated to avoid inappropriate affect sharing and social support., eLife digest Empathy enables us to share and understand the emotional states of other people, often based on their facial expressions. This empathic response involves being able to distinguish our own emotional state from someone else’s, and it is influenced by how we recognize that person’s emotion. In real life, knowing and identifying whether the facial expression we are witnessing reflects genuine or pretended pain is particularly important so that we can appropriately react to someone’s emotions and avoid unnecessary personal distress. How our brains manage to do this is still heavily debated. Two areas, the anterior insular (aIns for short) and the mid-cingulate cortex, appear to be activated when someone ‘feels’ someone else’s pain. However, these regions might just automatically be triggered by vivid emotional facial expressions, regardless of whether we really respond to that pain. To examine this question, Zhao et al. measured brain activity as healthy adults watched video clips of people either feeling or pretending to feel pain. The activation of aIns was particularly related to the emotional component that someone shared with another person’s genuine pain, but not to pretended pain. This suggests that neurons in the aIns track a truly empathic response when seeing someone who is actually experiencing pain. Effective connectivity analyses which reflect how brain areas ‘crosstalk’ also revealed distinct patterns when people viewed expressions of genuine, as opposed to pretended pain. Zhao et al. focused on the interactions between the alns and the right supramarginal gyrus, a brain region which helps to distinguish another person’s emotions from our own. This crosstalk tracked others’ feelings when participants viewed expressions of genuine but not of pretended pain. Put together, these findings provide a more refined model of empathy and its neural underpinnings. This will help further our understanding of conditions such as autism or depression, in which a person’s social skills and emotional processing are impaired.

Fetal cerebrovascular resistance is influenced by several factors in the setting of intact autoregulation to allow for normal cerebral blood flow and oxygenation. Maternal hyperoxygenation (MH) allows for acute alterations in fetal physiology and can be a tool to test cerebrovascular reactivity in late-gestation fetuses. In this study, we utilized MH to evaluate cerebrovascular reactivity in fetuses with specific congenital heart disease (CHD).This was a cross-sectional study of fetuses with complex CHD compared to controls without CHD. CHD cases were grouped according to physiology into: left-sided obstructive lesion (LSOL), right-sided obstructive lesion (RSOL) or dextro-transposition of the great arteries (d-TGA). Subjects underwent MH testing during the third-trimester fetal echocardiogram. The pulsatility index (PI) was calculated for the fetal middle cerebral artery (MCA), umbilical artery (UA) and branch pulmonary artery (PA). The change in PI from baseline to during MH was compared between each CHD group and controls.Sixty pregnant women were enrolled (CHD, n = 43; control, n = 17). In the CHD group, there were 27 fetuses with LSOL, seven with RSOL and nine with d-TGA. Mean gestational age was 33.9 (95% CI, 33.6-34.2) weeks. At baseline, MCA-PI Z-score was lowest in the LSOL group (-1.8 (95% CI, -2.4 to -1.2)) compared with the control group (-0.8 (95% CI, -1.3 to -0.3)) (P = 0.01). In response to MH, MCA-PI Z-score increased significantly in the control and d-TGA groups but did not change significantly in the LSOL and RSOL groups. The change in MCA-PI Z-score was significantly higher in the control group than in the LSOL group (0.9 (95% CI, 0.42-1.4) vs 0.12 (95% CI, -0.21 to 0.45); P = 0.03). This difference was more pronounced in the LSOL subgroup with retrograde aortic arch flow. Branch PA-PI decreased significantly in response to MH in all groups, with no difference in the change from baseline to MH between the groups, while UA-PI was unchanged during MH compared with at baseline.The fetal cerebrovascular response to MH varies based on the underlying CHD diagnosis, suggesting that cardiovascular physiology may influence the autoregulatory capacity of the fetal brain. Further studies are needed to determine the clinical implications of these findings on long-term neurodevelopment in these at-risk children. © 2020 International Society of Ultrasound in Obstetrics and Gynecology.

The endogenous opioid system is strongly involved in the modulation of pain. However, the potential role of this system in perceiving painful facial expressions from others has not been sufficiently explored as of yet. To elucidate the contribution of the opioid system to the perception of painful facial expressions, we conducted a double‐blind, within‐subjects pharmacological functional magnetic resonance imaging (fMRI) study, in which 42 participants engaged in an emotion discrimination task (pain vs. disgust expressions) in two experimental sessions, receiving either the opioid receptor antagonist naltrexone or an inert substance (placebo). On the behavioral level, participants less frequently judged an expression as pain under naltrexone as compared to placebo. On the neural level, parametric modulation of activation in the (putative) right fusiform face area (FFA), which was correlated with increased pain intensity, was higher under naltrexone than placebo. Regression analyses revealed that brain activity in the right FFA significantly predicted behavioral performance in disambiguating pain from disgust, both under naltrexone and placebo. These findings suggest that reducing opioid system activity decreased participants' sensitivity for facial expressions of pain, and that this was linked to possibly compensatory engagement of processes related to visual perception, rather than to higher level affective processes, and pain regulation., The behavioral and neural findings of this psychopharmacological fMRI study shed light on a causal role of the opioid system in the discrimination of painful facial expressions, paving the way for further exploration of clinical implications in the domains of pain diagnosis and treatment, on the one hand, and future research on the relationship between basic socio‐perceptual processing and empathy, on the other.

Introduction Complete ureteral avulsion is one of the most serious complications of ureteroscopy. The aim of this report was to look for a good solution to full-length complete ureteral avulsion. Case presentation A 40-year-old man underwent ureteroscopic management. Full-length complete avulsion of ureter occurred during ureteroscopy. Pyeloureterostomy plus greater omentum investment outside the avulsed ureter and ureterovesical anastomosis were performed 6 hours after ureteral avulsion. The patient was followed-up during 34 months. Double-J tube was removed at 3 months after operation. Twenty three months after the first operation, the patient developed hydronephrosis because of a new ureter upside stone, then rigid ureteroscopy and holmium laser lithotripsy were used successfully. Conclusion Pyeloureterostomy plus greater omentum investment outside the avulsed ureter and ureterovesical anastomosis may be a good choice for full-length complete ureteral avulsion.