Grant: Discovery Grants Program - Individual

BACKGROUND Nociception is the neural process of encoding intense somatosensory stimuli. Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Attention and working memory are cognitive processes that can regulate nociceptive signals. They can induce distraction analgesia by inhibiting nociceptive processes, or be disrupted by nociceptive stimuli, which causes pain interference. Current knowledge cannot explain these opposite effects. In addition, cognitive pain regulation was proposed to rely on spinothalamocortical and cerebrospinal pathways, but conflicting findings have been reported. This may be explained by variations in pain intensity and cognitive load, moment-to-moment fluctuations in pain-related and cognitive brain processes, and individual factors. OBJECTIVES To address these knowledge gaps, the goal of this research program is to determine the neurophysiological mechanisms underlying pain-cognition interactions using painful stimuli and validated cognitive tasks that probe selective attention and working memory. In two projects, we will examine spinal and brain activity during distraction analgesia and pain interference using two complementary electrophysiological methods. Specific objective 1: Investigate the spinothalamocortical and cerebrospinal processes underlying pain-cognition interactions; we will examine the mediation of distraction analgesia and pain interference by trial-by-trial fluctuations in spinal (nociceptive flexion reflex) and brain (electroencephalography) processes, and their moderation by individual factors. We hypothesize that pain-cognition interactions vary as a function of pain intensity and cognitive load, that they are mediated by trial-by-trial fluctuations in pain-related and cognitive responses, and moderated by pain-related and cognitive factors, in addition to sex, gender, and age. Specific objective 2: Investigate overlapping and interacting pain-related and cognitive brain networks during pain-cognition interactions to examine how brain resources are shared by pain and cognition, using magnetoencephalography. We hypothesize that within-network connectivity is modulated proportional to distraction analgesia and pain interference. We also hypothesize that neurophysiological resources are shared between the brain substrates of pain and cognition, as evidenced by changes in between-network functional connectivity proportional to distraction analgesia and pain interference. We anticipate that these effects are moderated by individual factors. SIGNIFICANCE With this innovative approach, we will show novel spinothalamocortical and cerebrospinal mechanisms underlying pain-cognition interactions. This will serve as foundations for future mechanistic studies and innovations on enhancement of normal cognitive functions for situations in which cognitive tasks are executed in the presence of salient distractors or pain, and during normal aging.