Symposium
Complementary Integrative Rehabilitation Medicine
Clinical Practice
Health Services Research
Neuroplasticity
Pain Rehabilitation
Peter Behel, MA
Biofeedback Provider
Kaiser Permanente
Santa Rosa, CA, United States
J.P. (Jack) Ginsberg, PhD, Licensed Clinical Psychologist
Faculty member
Saybrook University
Columbia, SC, United States
Meghan Varner, PT, DPT
Owner, Health Coach
Guide2Resilience
Richmond, Virginia, United States
Biofeedback is an evidence-based method of restoring autonomic functioning through targeted regulation. While this methodology has successfully been applied to an assortment of stress-related health concerns over the years, recent findings related to pain signal transmission have placed autonomic dysfunction at the heart of the disordered pain signaling that characterizes chronic pain. Not only has this served to increase recognition of the critical role that autonomic dysregulation plays in generating amplified pain, hyperalgesia, and central sensitization, but the ensuing inflammatory cascading is linked to neurogenic inflammation, action potential propagation and joint hypermobility. This symposium focusses on how the larger footprint associated with dysregulated autonomic functioning leads to a broader platform in applying biofeedback towards autonomic rehabilitation.
Nociception refers to the transfer of pain signals from the periphery to the spinal cord by dedicated neurons called nociceptors. Research has determined that the release of norepinephrine enhances nociceptor activity in various pathological conditions. These affects are related to a link between nociceptor sensitization and sympathetic excitation, to the extent that sympathetic activation increases nociceptive functioning. The degree to which adrenoreceptors are involved in nociceptive coupling provides a basis for autonomic plasticity. This maladaptive neuroplasticity is based on sympathetically-induced nociceptor hyperexcitability, and the resulting synaptic dysfunction is responsible for inducing nociceptive priming, a persistent hyperfunctional state that represents the hallmark of central sensitization.
Not only has this aberrant neuronal excitability become recognized as its own pain phenotype (nociplastic) , it has additionally been determined that actual tissue penetration is not necessarily required to release the nociceptive/ inflammatory cascade typically associated with pain. The recognition of this hyperexcitability phenotype has essentially redefined the multiplicity of parameters contained within a normative stress response, and has increased recognition that moderating persistent sympathetic activation occupies a greater rehabilitation platform than the isolated application of biofeedback might suggest.