Most practitioners have historically considered chronic pain to be largely from peripheral nociceptive input (i.e. damage or inflammation). If they consider central nervous system involvement in pain, they typically focus
entirely on psychological factors. We now understand that non-psychological central nervous system factors can markedly increase (sensitization) or decrease pain sensitivity, in that the CNS is now thought of as “setting the volume control” or gain on pain processing and determining what nociception is felt as pain. The most highly prevalent pain conditions in younger individuals are now thought to be more “central” than “peripheral,” and centralized pain or central sensitization can also be identified in subsets of individuals with any nociceptive or neuropathic pain state. This is not currently appreciated in clinical practice so there is marked overuse of treatments for acute/nociceptive pain (opioids, injections, surgery) for treating centralized pain, and underuse of non-opioid centrally-acting analgesics and non-pharmacological therapies.
You will learn to:
- Identify the underlying mechanisms responsible for chronic pain
- Identify the most effective pharmacological treatments for pain based on mechanism.
- Determine the optimal manner to incorporate non-pharmacological treatment of pain into clinical practice
Additional Questions from the Audience:
Do you believe that Neuroplasticity could play a role in treating Chronic Pain?
Yes – neuroplasticity means changing the nervous system – it occurs when people develop chronic pain, and we’re going to have to undo this to treat pain
Can you use rTMS in NP?
Yes – many studies have shown that either TMS or DCS can be helpful in treating pain
Daniel Clauw, MD
Professor of Anesthesiology, Medicine (Rheumatology) and Psychiatry, University of Michigan
Daniel Clauw, M.D. is a Professor of Anesthesiology, Medicine and Psychiatry at the University of Michigan where he also attended undergrad and medical school. He completed an internal medicine residency and rheumatology fellowship at Georgetown University, where he held roles including Chief of Rheumatology and Vice Chair of Medicine. He and his research team moved to the University of Michigan in 2002 where Dr. Clauw helped grow the clinical and translational research infrastructure, becoming the first Assistant and then Associate Dean for Clinical Research, and the first PI of the University of Michigan Clinical and Translational Sciences Award. This group has identified the critical phenotypic features of individuals whose central nervous system is amplifying or magnifying their pain, and as such has been critical in helping elucidate the importance of the central nervous system in all chronic pain conditions.
Partially funded by: