Stuart Derbyshire
Stuart is faculty in the psychology department at NUS and also at the A*-STAR Clinical Imaging Research Centre (CIRC). His current work involves both theoretical and empirical research on the nature of pain. In particular, Stuart is examining the possible causes of a rising incidence of pain and somatic illness in the absence of identifiable pathology and in the context of improving health and longevity. Consequently, his research abuts psychology, cognitive science, and philosophical ethics.
How has functional imaging informed our understanding of pain and hypnosis?
Pain is typically understood as a simple reaction to injury or disease. That understanding, however, fails to account for the times we are injured but do not experience pain, or for the many patients that appear to be perfectly healthy and yet experience pain. Patients with pain but without injury or disease have posed a major challenge to medicine. Early functional imaging studies demonstrated that brain areas responsive to physically noxious stimuli are also activated by hypnotic suggestion of the same physically noxious stimulus. This finding informed our understanding of pain by demonstrating that brain regions known to mediate pain could also generate pain without a physically noxious stimulus. Thus the finding provided a potential mechanism for pain being created in otherwise healthy patients.
Subsequent studies also demonstrated that patients with chronic pain in the absence of obvious injury or disease could also modulate their pain with hypnotic suggestion. That modulation was related to linear changes in the activation of brain areas associated with pain. Suggestions with a hypnotic induction produced larger changes in brain activity than those without; a finding more compatible with state than non-state theories of hypnosis. More recently we have demonstrated large changes in pain report in normal volunteers modulating experimental heat pain with and without a hypnotic suggestion. Again, brain activation changes were stronger after the induction. The brain activation pattern, however, was not linear with changes in pain report. Instead areas associated with pain increased when pain was modulated down and when pain was modulated up by suggestion. These findings imply a very different mechanism of suggested pain modulation in controls experiencing heat pain compared with patients experiencing chronic pain. That is not something we would have suspected, or could have tested, based on the behavioural data alone.
