Pain Signal Transmission and Centralized Sensitization: The Role of Synaptic Plasticity

Friday, November 11, 2022

1:00 PM – 2:15 PM

Presenter(s)

Peter A. Behel, MA

Professor
Sonoma State University
Santa Rosa, California, United States

Slides
JP (Jack) Ginsberg, PhD; Licensed Clinical Psychologist/Neuropsychologist; VA Research Health Scientist (Ret.)

Research Assistant Professor
School of Medicine, University of South Carolina
Columbia, South Carolina, United States

Slides

Nociception is the process of transmitting pain signals from the periphery to the central nervous system (CNS). In instances involving chronic pain, this process is facilitated by unmyelinated c fibers. The conduction of these small diameter fibers is influenced by autonomic nervous system output, and autonomic dysregulation has been associated with persistent pain in instances where there are no identifiable nerve injuries or lesions. Regulating autonomic output has been a mainstay of this author's chronic pain clinical practice for over 20 years, and reports of significant pain reduction have become reasonably commonplace. This presentation will focus on the mechanics involved with facilitating this process, and discuss the implications that are relevant to PTSD.

Learning Objectives:

Upon completion of this presentation, participants will be able to define peripheral sensitization as a lowering of the threshold at which pan is received.
Upon completion of this symposia, participants will be able to determine that when pain becomes chronic, pain signal transmission become facilitated by unmyelinated nerve endings called c fibers.
Upon completion of this symposia, participants will be able to determine that the excitatory neurotransmitter glutamate coexists with the neuropeptide substance P.
Upon completion of this presentation, participants will be able to determine that substance P is colocalized with the neuromodulator calcitonin gene-related peptide (CGRP).
Upon completion of this Symposia, the participant will be able to determine that hyperalgesia represents an exaggerated response to pain stimulation.