Human Pain Seminar Series
This series was borne out of the COVID-19 Global Pandemic, which posed significant challenges to the pain community. Its purpose was to reinforce the message that the we—those who do human pain research—are part of a community.
I put together the #WeAreAllInThisTogether COVID-19 Journal Club. It's an opportunity to connect, to remain intellectually stimulated, to learn, and to keep up with the literature.
It has evolved into a Seminar Series that highlights the work of our community, and allows members of the community at any stage of their career engage with the speakers.
We are supported by the University of Toronto Centre for the Study of Pain.
We meet over Zoom every so often - about every 3 weeks. The specifics, papers, and link to the Zoom will be posted here.
We look forward to seeing you all.
Friday, October 15, 2021, 11 am EST
Title: Characterising sensorimotor adaptation in Complex Regional Pain Syndrome
Presented by: Janet Bultitude, Senior Lecturer (Associate Professor),Psychology Department and Centre for Pain Research, University of Bath, UK.
Abstract: It has been suggested that sensorimotor conflict contributes to the maintenance of some pathological pain conditions, implying that there are problems with the adaptation processes that normally resolve such conflict. We tested whether sensorimotor adaptation is impaired in people with Complex Regional Pain Syndrome (CRPS) by characterising their adaption to lateral prismatic shifts in vision. People with unilateral upper-limb CRPS Type I (n = 17), and pain-free individuals (n = 18; matched for age, sex, and handedness) completed prism adaptation with their affected/non-dominant and non-affected/dominant arms. We examined 1) the rate at which participants compensated for the optical shift during prism exposure (i.e., strategic recalibration), 2) endpoint errors made directly after prism adaptation (sensorimotor realignment) and the retention of these errors, and 3) kinematic markers associated with strategic control. Direct comparisons between people with CRPS and controls revealed no evidence of any differences in strategic recalibration, including no evidence for differences in a kinematic marker associated with trial-by-trial changes in movement plans during prism exposure. All participants made significant endpoint errors after prism adaptation exposure, indicative of sensorimotor realignment. Overall, the magnitude of this realignment did not differ between people with CRPS and pain-free controls. However, when endpoint errors were considered separately for each hand, people with CRPS made greater errors (indicating more rather than less realignment) when using their affected hand than their non-affected hand. No such difference was seen in controls. Taken together, these findings provide no evidence of impaired strategic control or sensorimotor realignment in people with CRPS. In contrast, they provide some indication that there could be a greater propensity for sensorimotor realignment in the CRPS-affected arm, consistent with more flexible representations of the body and peripersonal space. Our study challenges an implicit assumption of the theory that sensorimotor conflict might underlie some pathological pain conditions.
Meeting ID: 814 0707 5625
Monday, October 25, 2021, 1 pm EST
Title: Classifying chronic pain using multidimensional pain-agnostic symptom assessments and clustering analysis
Presented by: Gadi Gilam, Postdoctoral Fellow (Mackey Lab), Anesthesiology, Perioperative and Pain Medicine, Stanford University, CA, USA.
Abstract: Chronic pain conditions present in various forms, yet all feature symptomatic impairments in physical, mental, and social domains. Rather than assessing symptoms as manifestations of illness, we used them to develop a chronic pain classification system. A cohort of real-world treatment-seeking patients completed a multidimensional patient-reported registry as part of a routine initial evaluation in a multidisciplinary academic pain clinic. We applied hierarchical clustering on a training subset of 11448 patients using nine pain-agnostic symptoms. We then validated a three-cluster solution reflecting a graded scale of severity across all symptoms and eight independent pain-specific measures in additional subsets of 3817 and 1273 patients. Negative affect-related factors were key determinants of cluster assignment. The smallest subset included follow-up assessments that were predicted based on baseline cluster assignment. Findings provide a cost-effective classification system that promises to improve clinical care and alleviate suffering by providing putative markers for personalized diagnosis and prognosis.
Relevant Preprint: https://www.science.org/doi/10.1126/sciadv.abj0320
Meeting ID: 884 0786 3594
Wednesday, December 1, 2021, 11 am EST
Presented by: Markus Rütgen, Postdoctoral Fellow (Lamm Lab), Social, Cognitive and Affective Neuroscience Unit, Department of Cognition, Emotion, and Methods in Psychology, University of Vienna, Austria.
Abstract: It is not known how specific the neural mechanisms underpinning empathy for different domains are. In the present study, we set out to test whether shared neural representations between first-hand pain and empathy for pain are pain-specific or extend to empathy for unpleasant affective touch as well. Using functional magnetic resonance imaging and psychopharmacological experiments, we investigated if placebo analgesia reduces first-hand and empathic experiences of affective touch, and compared them with the effects on pain. Placebo analgesia also affected the first-hand and empathic experience of unpleasant touch, implicating domain-general effects. However, and in contrast to pain and pain empathy, administering an opioid antagonist did not block these effects. Moreover, placebo analgesia reduced neural activity related to both modalities in the bilateral insular cortex, while it specifically modulated activity in the anterior midcingulate cortex for pain and pain empathy. These findings provide causal evidence that one of the major neurochemical systems for pain regulation is involved in pain empathy, and crucially substantiates the role of shared representations in empathy.
Relevant Article: https://academic.oup.com/cercor/article/31/6/2773/6102670?login=true
Meeting ID: 839 7247 2357
Wednesday, December 7, 2021, 12 noon EST
Title: Neuroimmune signatures in human chronic pain
Presented by: Marco Loggia, Associate Professor of Radiology, Harvard Medical School and Co-Director, Center for Integrative Pain NeuroImaging (CiPNI), Pain and Neuroinflammation Imaging Laboratory, Departments of Radiology and Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, A. A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA
Abstract:Despite the plethora of preclinical studies demonstrating a role for activated microglia and astrocytes in the establishment and/or maintenance of persistent pain, our understanding of the role of neuroinflammation in human pain remains limited. This has so far prevented the translation of important preclinical observations into novel glia-targeted treatments for pain. In this talk, I will present results of a series of studies which suggest the presence of elevated levels of the 18kDa translocator protein (TSPO) in the central nervous system of patients with various chronic pain disorders. Because TSPO upregulation is highly co-localized with activated glia, our results suggest that neuroinflammation might indeed occur, and in fact may be a pervasive phenomenon that can be observed across multiple, etiologically heterogeneous human pain disorders, although in a disorder-specific spatial distribution. Identifying the role of glia in the development and maintenance of persistent pain and pain-related disability in humans will have important practical implications, and provide crucial human evidence contributing to rationale for the development of tailored interventions focused on glial modulation.
Meeting ID: 891 2422 3268
Monday, January 25, 2021, 2 pm EST
Title: Pain Reprocessing Therapy for Chronic Back Pain
Presented by: Yoni Ashar, Postdoctoral Fellow Wager Lab, University of Colorado, Boulder, USA
Abstract:Psychological treatments for chronic pain typically aim to improve functioning and quality of life, rather than targeting pain intensity directly. Here, we developed and tested Pain Reprocessing Therapy (PRT), a psychological treatment aiming to reduce or eliminate pain. PRT aims to help patients reconceptualize pain as non-dangerous and due to brain plasticity rather than bodily injury. In a randomized clinical trial of N = 151 primary chronic back pain patients, we compared PRT to placebo injection and usual care control conditions. 66% of participants randomized to PRT reported being pain-free or nearly so at post-treatment, as compared to less than 20% of controls. Treatment effects were largely maintained at 1-year follow-up. Effects of PRT were mediated by reductions in fearful beliefs that pain indicates injury and pain-related fear and avoidance. Longitudinal fMRI showed (1) reduced responses to evoked back pain in the anterior midcingulate and the anterior prefrontal cortex for PRT vs placebo; (2) reduced responses in the anterior insula for PRT vs usual care; (3) increased resting connectivity from the anterior prefrontal cortex and the anterior insula to the primary somatosensory cortex for PRT vs both control groups; and (4) increased connectivity from the anterior midcingulate to the precuneus for PRT vs usual care. We conclude that psychological treatment centered on changing patients’ beliefs about the causes and threat value of pain may provide substantial and durable pain relief for a substantial portion of people with primary CBP.
Meeting ID: 865 9029 9942