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Background and aims Previous research on pain and cognition has largely focused on non-social cognitive outcomes (e.g. attention, problem solving). This study examines the relationship between pain and stereotyping, which constitutes a fundamental dimension of social cognition. Drawing on dual process theories of cognition, it was hypothesized that higher levels of pain would increase stereotyped judgments based on ethnicity and age. The hypothesis was tested in conjunction with experimentally induced pain (Study 1) and clinical pain (Study 2). Methods In Study 1, experimental pain was induced with the cold pressor method on a between-subjects basis. Participants (n = 151) completed a judgment task that assessed to what extent they relied on stereotypes (ethnic and age) when estimating other people's cognitive performance. In Study 2, 109 participants with clinical, musculoskeletal pain completed the same stereotype judgment task. Correlations between stereotyped judgments and various pain qualities (intensity, interference with daily activities, duration, and persistence) were performed. Results In Study 1, pain induced participants did not form significantly more stereotyped judgments compared to pain-free participants. However, higher reported pain intensity was associated with more ethnically stereotyped judgments. In Study 2, there were no significant correlations between different aspects of clinical pain and stereotyped judgments. Conclusions The results provide weak support for the hypothesis that pain increases stereotyped judgments. This was the case for both experimentally induced pain and clinical pain. The present study is the first to investigate the link between pain and stereotyping, suggesting that stereotypical judgments may be a social cognitive outcome that is relatively unaffected by pain. Implications The results have practical implications for the clinic, for example, where chronic pain patients may not have greater difficulties interacting with health care professionals that are members of a stereotyped social group (e.g. ethnic).
Learn More >The dorsal root (DRG) and trigeminal (TG) ganglia contain cell bodies of sensory neurons of spinal and trigeminal systems, respectively. They are homologs of each other; however, differences in how the two systems respond to injury exist. Trigeminal nerve injuries rarely result in chronic neuropathic pain (NP). To date, no genes involved in the differential response to nerve injury between the two systems have been identified. We examined transcriptional changes involved in the development of trigeminal and spinal NP.
Learn More >Sensory perceptions are coded by complex neural dynamics of regional communication in the brain. Thus, sensory abnormalities such as chronic pain may occur when neural dynamics go awry. Previous studies of cross-network dynamic functional connectivity in chronic pain identified abnormalities but were based on functional MRI which only captures slow temporal features. Here we conducted a magnetoencephalography (MEG) study to investigate fine temporal dynamics of aberrant cross-regional and cross-network communication of the dynamic pain connectome in patients with chronic pain. We also introduced a novel measure, dynamic functional coupling, to quantify the variability of brain communication. The study was performed in 33 people who had chronic pain associated with multiple sclerosis and 30 healthy controls. We found that patients with chronic pain exhibited abnormalities in cross-network functional coupling across multiple frequency bands (theta, alpha, beta, gamma), between the salience network and 3 other networks: the ascending nociceptive pathway, descending anti-nociceptive pathway, and the default mode network. However, these cross-network abnormalities involved different frequency bands in patients with neuropathic versus non-neuropathic chronic pain. Furthermore, cross-network abnormalities were linked to pain severity and pain interference. Our findings implicate broadband cross-network abnormalities as hallmark features of chronic pain in multiple sclerosis.
Learn More >Morphine-3-glucuronide (M3G), the main metabolite of morphine, has been implicated in the development of tolerance and of opioid-induced hyperalgesia, both limiting the analgesic use of morphine. We evaluated the acute and chronic effects of M3G and morphine as well as development of antinociceptive cross-tolerance between morphine and M3G after intrathecal administration and assessed the expression of pain-associated neurotransmitter substance P in the spinal cord. Sprague-Dawley rats received intrathecal M3G or morphine twice daily for 6 days. Nociception and tactile allodynia were measured with von Frey filaments after acute and chronic treatments. Substance P levels in the dorsal horn of the spinal cord were determined by immunohistochemistry after 4-day treatments. Acute morphine caused antinociception as expected, whereas acute M3G caused tactile allodynia, as did both chronic M3G and morphine. Chronic M3G also induced antinociceptive cross-tolerance to morphine. M3G and morphine increased substance P levels similarly in the nociceptive laminae of the spinal cord. This study shows that chronic intrathecal M3G sensitises animals to mechanical stimulation and elevates substance P levels in the nociceptive laminae of the spinal cord. Chronic M3G also induces antinociceptive cross-tolerance to morphine. Thus, chronic M3G exposure might contribute to morphine-induced tolerance and opioid-induced hyperalgesia.
Learn More >The dorsal root ganglia is a key structure in nociception and chronic pain disorders. Several gene expression studies of dorsal root ganglia in pre-clinical pain models have been performed, but it is unclear if consistent gene changes are identifiable. We, therefore, compared several recent RNA-Seq datasets on the whole dorsal root ganglia in rodent models of nerve injury. Contrary to previous findings, we show hundreds of common differentially expressed genes and high positive correlation between studies, despite model and species differences. We also find, in contrast to prior studies, that 60% of the common rodent gene response after injury is likely to occur in nociceptors of the dorsal root ganglia. Substantial expression changes are observed at a one-week time-point, with smaller changes in the same genes at a later three to four-week time-point. However, a subset of genes shows a similar magnitude of changes at both early and late time-points, suggesting their potential involvement in the maintenance of chronic pain. These genes are centred around suppression of endogenous opioid signalling. Reversal of this suppression could allow endogenous and exogenous opioids to exert their analgesic functions and may be an important strategy for treating chronic pain disorders. Currently used drugs, such as amitriptyline and duloxetine, do not appear to appropriately modulate many of the critical pain genes and indeed may transcriptionally suppress endogenous opioid signalling further.
Learn More >Atopic dermatitis (AD) is a widespread, chronic skin disease associated with aberrant allergic inflammation. Current treatments involve either broad or targeted immunosuppression strategies. However, enhancing the immune system to control disease remains untested. We demonstrate that patients with AD harbor a blood natural killer (NK) cell deficiency that both has diagnostic value and improves with therapy. Multidimensional protein and RNA profiling revealed subset-level changes associated with enhanced NK cell death. Murine NK cell deficiency was associated with enhanced type 2 inflammation in the skin, suggesting that NK cells play a critical immunoregulatory role in this context. On the basis of these findings, we used an NK cell-boosting interleukin-15 (IL-15) superagonist and observed marked improvement in AD-like disease in mice. These findings reveal a previously unrecognized application of IL-15 superagonism, currently in development for cancer immunotherapy, as an immunotherapeutic strategy for AD.
Learn More >To investigate clinical characteristics and treatment patterns in persistent post-traumatic headache attributed to mild traumatic brain injury.
Learn More >Natural killer cells collaborate with type 2 immune cells to modulate atopic dermatitis pathogenesis (Mack , this issue).
Learn More >Interleukin 13 (IL-13) is a central pathogenic mediator driving multiple features of atopic dermatitis (AD) pathophysiology.
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