Thursday, September 22nd
4:30pm-6:00pm EDT


Topical Workshop




715 A

Neurobiological Mechanisms and Clinical Relevance of Stress-pain Interactions

The relationship between stress and pain is complex and multi-layered. Stress has been known to produce hyperalgesic and hypoalgesic effects depending on various factors. Individual reactions to pain (e.g., catastrophizing) can trigger a psycho-neuro-endocrine response that negatively impacts pain. Multiple brain pathways (e.g., thalamocorticoamygdala) and systems (e.g., endogenous opioid and cannabinoid systems) are central to the mediation or modulation of pain and stress responses and for intensifying endocrine responses, fear extinction and recruiting the involvement of other brain structures. This symposium will provide a comprehensive overview of the bi-directional interactions of pain and stress from multiple perspectives. First, preclinical and animal models of stress-pain interactions, such as fear-conditioned analgesia and anxiety/depression-related hyperalgesia will be discussed, with a focus on the endocannabinoid and endogenous opioid systems. Second, examples of human research on stress-induced analgesia and the role of endogenous opioid mechanisms will be discussed. Last, an integrative model of stressful characteristics of pain (novelty, unpredictability, threat to ego and sense of control) that can help us understand some of the psycho-behavioral responses observed in chronic pain patients will be presented.


4:30pm EDT6:00pm EDT

Exploring Triggers of the Stress Response and its Association with Pain Outcomes in Various Chronic Pain Populations

Tracks: Mechanisms
Categories: Topical Workshop
Presented By: Gabrielle Page

It is well documented that pain generates stress and is influenced by stress. There is a vast body of literature documenting the role of numerous psychosocial factors in the development/maintenance of chronic pain. However these factors are rarely examined in conjunction with specific characteristics of pain that might directly influence the extent to which pain is perceived as threatening.

The general stress literature converges on 4 distinctive characteristics that trigger an acute cortisol response: Sense of Control, social-evaluative Threat (ego), Unpredictability, and Novelty (i.e. “STUN”).  This presentation will review evidence that these stress characteristics adequately capture the stressful nature of pain and might interact with individual psychosocial predispositions to influence one’s appraisal and mal(adaptive) psychological responses to pain . These characteristics will be presented in a new theoretical understanding of pain that might allow for a true integration of psychosocial models and neuro-psycho-endocrinological mechanisms of pain.

4:30pm EDT6:00pm EDT

Interactions Between Pain and Stress: Role of the Cannabinoid and Opioid Systems

Tracks: Mechanisms
Categories: Topical Workshop
Presented By: Prof. David Finn

Pain and affective state interact reciprocally, whereby the latter can both influence, and be influenced by, the pain experience. Dr. Finn will present recent research aimed at elucidating supraspinal neurochemical and receptor mechanisms involved in (1) hyperalgesia associated with negative affect (anxiety/depression), (2) fear-induced analgesia and (3) pain-induced negative affect. He will present research employing animal models including the Wistar-Kyoto rat model of hyperalgesia associated with negative affect and a rat model of fear-conditioned analgesia, coupled with behavioural pharmacology, optogenetics, and neurochemical and molecular analyses of the endogenous cannabinoid and opioid systems. He will also discuss the role of novel endocannabinoid-related targets including peroxisome proliferator-activated receptors, and consider clinical relevance and implications.

4:30pm EDT6:00pm EDT

Stress-Induced Analgesia: An Evaluation of Effects on Pain Tolerance, Temporal Summation of Pain and the Role of Endogenous Opioid Mechanisms

Tracks: Mechanisms
Categories: Topical Workshop

Acute stress attenuates pain (stress-induced analgesia; SIA) but mechanisms remain debated. SIA effects on temporal summation of pain (TSP), a dynamic evoked pain measure indexing central sensitization, have been little studied. We tested whether acute laboratory stressors reduce pain perception and TSP and whether endogenous opioid (EO) mechanisms contributed. Participants (N=84) attended two laboratory sessions, receiving either oral naltrexone (50mg; opioid antagonist) or placebo (randomized, counterbalanced order). In each session, participants underwent two evoked pain stimuli (cold pressor test [CPT], heat pain) and a heat pain TSP protocol, once after extended rest and once after public speaking and mental arithmetic stressors. Stress attenuated pain perception (SIA) as indicated by significantly increased CPT tolerance; these SIA effects were abolished by opioid blockade. We observed significant SIA on initial pain ratings in the TSP protocol but not TSP slope (index of central sensitization). This SIA effect occurred in high stress responders only. Results demonstrate that endogenous opioids mediate effects of acute stress on static evoked pain responses, although this effect may be qualified by type of evoked pain stimulus. SIA does not influence central sensitization itself, but may exaggerate TSP values based on difference scores in TSP protocols by lowering initial ratings.


Prof. Mustafa al'Absi

University of Minnesota

Prof. David Finn

Professor and Head of Pharmacology and Therapeutics, Co-Director of the Centre for Pain Research
National University of Ireland Galway

Gabrielle Page

Assistant professor
Université de Montréal