Psychology

Cognitive models of chronic pain emphasize the critical role of pain catastrophizing in attentional bias to pain-related stimuli. The aim of this study was (a) to investigate the relationship between pain catastrophizing and the ability to inhibit selective attention to pain-related faces (attentional bias); and (b) to determine whether attentional control moderated this relationship. One hundred and ten pain-free participants completed the anti-saccade task with dynamic facial expressions, specifically painful, angry, happy, and neutral facial expressions and questionnaires including a measure of pain catastrophizing. As predicted, participants with high pain catastrophizing had significantly higher error rates for antisaccade trials with pain faces relative to other facial expressions, indicating a difficulty disinhibiting attention towards painful faces. In moderation analyses, data showed that attentional control moderated the relationship between attentional bias to pain faces and pain catastrophizing. Post-hoc analyses demonstrated that it was shifting attention (not focusing) that accounted for this effect. Only for those with high self-reported ability to shift attention was there a significant relationship between catastrophizing and attentional bias to pain. These findings confirm that attentional control is necessary for an association between attentional bias and catastrophizing to be observed, which may explain the lack of relationships between attentional bias and individual characteristics, such as catastrophizing, in prior research.

Chronic pain negatively affects psychological functioning including self-perception. Self-compassion may improve self-related functioning in patients with chronic pain but understanding of the neural mechanisms is limited. In this study, twenty patients with chronic low back pain read negative self-related situations and were instructed to be either self-reassuring or self-critical while undergoing fMRI. Patients rated their feelings of self-reassurance and self-criticism during each condition, and brain responses were contrasted with neutral instructions. Trait self-compassion measures (SCS) were also acquired. Brain activations during self-criticism and self-reassurance were localized to prefrontal, self- and emotion-processing areas, such as medial prefrontal cortex, dorsolateral prefrontal cortex (dlPFC), dorsal anterior cingulate cortex and posterior cingulate cortex. Self-reassurance resulted in more widespread and stronger activations relative to self-criticism. Patients then completed a brief self-compassion training (8 contact hours, 2 weeks home practice). Exploratory pre-post comparisons in thirteen patients found that feelings of self-criticism were significantly reduced and brain activations were greater in the anterior insula and prefrontal cortical regions such as dlPFC. Pre-post increases in dlPFC activation correlated with increased self-compassion (SCS), suggesting that early self-compassion skills might primarily target self-criticism via dlPFC upregulation. Future controlled studies on self-compassion training in chronic pain populations should extend these results.

Using a nationally representative sample of adults and pain definitions consistent with the United States National Pain Strategy, we examined the associations of pain and cognitive impairment (CI) with each other and with measures of health status, physical impairment, social impairment, health care utilization, and dissatisfaction with health care.

Abdominal pain, frequent in patients with chronic pancreatitis (CP), has a negative impact on quality of life (QOL). Psychiatric comorbidities including anxiety and depression are associated with pain, but their prevalence and effects on QOL in CP have not been quantified. We studied the prevalence of anxiety and depression in patients with CP and their associated patient and disease characteristics and impact on QOL.

Several recent studies suggest that placebos administered without deception (i.e., non-deceptive placebos) can help people manage a variety of highly distressing clinical disorders and nonclinical impairments. However, whether non-deceptive placebos represent genuine psychobiological effects is unknown. Here we address this issue by demonstrating across two experiments that during a highly arousing negative picture viewing task, non-deceptive placebos reduce both a self-report and neural measure of emotional distress, the late positive potential. These results show that non-deceptive placebo effects are not merely a product of response bias. Additionally, they provide insight into the neural time course of non-deceptive placebo effects on emotional distress and the psychological mechanisms that explain how they function.

Chronic pain is common in those with substance use disorders (SUDs) and predicts poorer addiction treatment outcomes. A critical challenge for addiction treatment is to develop effective methods to improve pain-related and substance use-related outcomes for those in treatment for SUDs.

Nocebo hyperalgesia refers to increases in perceived pain that putatively result from negative expectations regarding a nocebo stimulus (eg, an inert treatment, compared with no treatment). The precise cognitive-emotional factors contributing to the origins of nocebo effects are poorly understood. We aimed to test the effects of experimentally induced pain-related fear on the acquisition and extinction of nocebo hyperalgesia in healthy participants (N = 72). Acquisition and extinction of nocebo hyperalgesia were compared between a group receiving standard nocebo conditioning (Control group) and 2 groups receiving distinct fear inductions: high intensity of pain stimulations (High-pain group) or a threat manipulation (High-threat group). During nocebo acquisition, the Control and High-threat groups were administered thermal pain stimulations of moderate intensity paired with sham electrical stimulation (nocebo trials), whereas high pain intensity was administered to the High-pain group. During extinction, equivalent pain intensities were administered across all trials. Pain-related fear was measured by eyeblink startle electromyography and self-report. Nocebo hyperalgesia occurred in all groups. Nocebo effects were significantly larger in the High-pain group than those in the Control group. This effect was mediated by self-reported fear, but not by fear-potentiated startle. Groups did not differ in the extinction rate. However, only the High-pain group maintained significant nocebo responses at the end of extinction. Anticipatory pain-related fear induced through a threat manipulation did not amplify nocebo hyperalgesia. These findings suggest that fear of high pain may be a key contributor to the amplification of nocebo hyperalgesia, only when high pain is experienced and not when it is merely anticipated.

Fibromyalgia (FM) is a complex pain condition where the pathophysiological and molecular mechanisms are not fully elucidated. The primary aim of this study was to investigate the plasma proteome profile in women with FM compared to controls. The secondary aim was to investigate if plasma protein patterns correlate with the clinical variables pain intensity, sensitivity, and psychological distress. Clinical variables/background data were retrieved through questionnaires. Pressure pain thresholds (PPT) were assessed using an algometer. The plasma proteome profile of FM (n = 30) and controls (n = 32) was analyzed using two-dimensional gel electrophoresis and mass spectrometry. Quantified proteins were analyzed regarding group differences, and correlations to clinical parameters in FM, using multivariate statistics. Clear significant differences between FM and controls were found in proteins involved in inflammatory, metabolic, and immunity processes. Pain intensity, PPT, and psychological distress in FM had associations with specific plasma proteins involved in blood coagulation, metabolic, inflammation and immunity processes. This study further confirms that systemic differences in protein expression exist in women with FM compared to controls and that altered levels of specific plasma proteins are associated with different clinical parameters.