Empathy is an essential component of our social lives, allowing us to understand and share other people's affective and sensory states, including pain. Evidence suggests a core neural network—including anterior insula (AI) and mid-cingulate cortex (MCC)—is involved in empathy for pain. However, a similar network is associated to empathy for non-pain affective states, raising the question whether empathy for pain is unique in its neural correlates. Furthermore, it is yet unclear whether neural correlates converge across different stimuli and paradigms that evoke pain-empathy. We performed a coordinate-based activation likelihood estimation (ALE) meta-analysis to identify neural correlates of empathy, assess commonalities and differences between empathy for pain and for non-pain negative affective states, and differences between pain-empathy evoking stimuli (i.e., facial pain expressions vs. acute pain inflictions) and paradigms (i.e., perceptual/affective vs. cognitive/evaluative paradigms). Following a systematic search, data from 128 functional brain imaging studies presenting whole-brain results of an empathy condition vs. baseline/neutral condition were extracted. Synthesizing neural correlates of empathy confirmed a core network comprising AI, MCC, postcentral gyrus, inferior parietal lobe, thalamus, amygdala, and brainstem. There was considerable overlap in networks for empathy for pain and empathy for non-pain negative affective states. Important differences also arose: empathy for pain uniquely activated bilateral mid-insula and more extensive MCC. Regarding stimuli, painful faces and acute pain inflictions both evoked the core empathy regions, although acute pain inflictions activated additional regions including medial frontal and parietal cortex. Regarding paradigms, both perceptual/affective and cognitive/evaluative paradigms recruited similar neural circuitry, although cognitive/evaluative paradigms activated more left MCC regions while perceptual/affective paradigms activated more right AI. Taken together, our findings reveal that empathy for pain and empathy for non-pain negative affective states share considerable neural correlates, particularly in core empathy regions AI and MCC. Beyond these regions, important differences emerged, limiting generalizability of findings across different affective/sensory states. Within pain-empathy studies, the core regions were recruited robustly irrespective of stimuli or instructions, allowing one to tailor designs according to specific needs to some extent, while ensuring activation of core regions.

Background The parent's role in the context of pediatric chronic pain is essential. There is growing evidence that parent psychological flexibility positively impacts child functioning. To assess parents’ abilities to respond with psychological flexibility to their child's pain, the Parent Psychological Flexibility Questionnaire (PPFQ) was developed. Here, we aim to validate the 10‐item version of the questionnaire in an English‐speaking population and to evaluate associations with parent behaviour, child pain acceptance and functioning. Methods Five hundred and seventy‐eight parent‐child dyads presenting at a pediatric pain clinic were included (92% mothers, average child age 15.2 ± 1.6 years). The PPFQ was completed by the parent. Parent and child also completed other standardized questionnaires. In addition to confirmatory factor analysis and assessments of reliability and validity of the PPFQ‐10, a mediation analysis was performed to examine the direct and indirect effects of parent psychological flexibility on child functioning. Results Confirmatory factor analysis supported the three‐factor model with subscales for Values‐Based Action, Pain Willingness and Emotional Acceptance, and the PPFQ‐10 demonstrated strong psychometric properties. After controlling for child pain, parent psychological flexibility indirectly affected child functioning through its association with both parent behaviour (i.e., protectiveness) and child pain acceptance. Conclusions Our findings provide further support for use of the PPFQ‐10 and the importance of assessing and addressing parent psychological flexibility in the context of child chronic pain. Our data show that parent psychological flexibility has an important adaptive role and can impact child functioning through two different routes, both of which can be actively targeted in treatment. Significance Our findings demonstrate that the PPFQ‐10 is an efficient measure of parent psychological flexibility, demonstrating strong psychometric properties. Furthermore, our analyses showed that parent psychological flexibility indirectly affects child functioning through associations with both adaptive parent behaviour and child functioning. Taken together, this study furthers the understanding of how parent psychological flexibility operates and affects children with chronic pain, and may inform and optimize treatments aimed at improving functioning by addressing child and parent coping.

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Among youth with chronic pain, elevated somatic symptoms across multiple body systems have been associated with greater emotional distress and functional disability and could represent poor adaptation to pain. The Children's Somatic Symptoms Inventory (formerly the Children's Somatization Inventory) is commonly used to assess somatic symptoms in children. However, no studies have evaluated the clinical usefulness of the measure in the assessment of pediatric patients with chronic pain. This study evaluated the factor structure and clinical relevance of the 24-item Children's Somatic Symptoms Inventory (CSSI-24) in youth (n = 1,150) with mixed chronic pain complaints presenting to a tertiary pain clinic. The CSSI-24 total scores were equal or superior to factor scores as indicators of patients' clinical characteristics (functional disability, pain catastrophizing, fear of pain, and anxiety and depressive symptoms) and parental catastrophizing and protective responses. Tertile-derived clinical reference points for the CSSI-24 total score (<18, low; 19−31, moderate; ≥ 32, high) significantly differed on measures of clinical characteristics and parent factors. Controlling for age, sex, pain intensity, and primary pain complaint, the high somatic symptoms group exhibited significantly greater health care use compared with the moderate and low groups. The assessment of somatic symptoms in pediatric patients with chronic pain may provide useful information regarding patients' psychosocial risk and tendency to access health services. Perspective: Clinical reference points based on the CSSI-24 total scores meaningfully differentiated youth with chronic pain on measures of emotional distress, functioning, parent catastrophizing and protective responses, and health care use. Assessing somatic symptoms could provide useful information regarding a pediatric patient's psychosocial risk, tendency to access health services, and need for enhanced care coordination.

In chronic pain, a number of brain regions involved in emotion (e.g., amygdala, hippocampus, nucleus accumbens, insula, anterior cingulate, and prefrontal cortex) show significant functional and morphometric changes. One phenotypic manifestation of these changes is pain-related fear (PRF). PRF is associated with profoundly altered behavioral adaptations to chronic pain. For example, patients with a neuropathic pain condition known as complex regional pain syndrome (CRPS) often avoid use of and may even neglect the affected body area(s), thus maintaining and likely enhancing PRF. These changes form part of an overall maladaptation to chronic pain. To examine fear-related brain circuit alterations in humans, 20 pediatric patients with CRPS and 20 sex- and age-matched healthy controls underwent functional magnetic resonance imaging (fMRI) in response to a well-established fearful faces paradigm. Despite no significant differences on self-reported emotional valence and arousal between the two groups, CRPS patients displayed a diminished response to fearful faces in regions associated with emotional processing compared to healthy controls. Additionally, increased PRF levels were associated with decreased activity in a number of brain regions including the right amygdala, insula, putamen, and caudate. Blunted activation in patients suggests that (a) individuals with chronic pain may have deficits in cognitive-affective brain circuits that may represent an underlying vulnerability or consequence to the chronic pain state; and (b) fear of pain may contribute and/or maintain these brain alterations. Our results shed new light on altered affective circuits in patients with chronic pain and identify PRF as a potentially important treatment target.