Michael Costigan PhD

"Mechanisms of Neuropathic Pain"






9:00 am

Saturday, January 21, 2012

International Academy of Endodontics, Annual Meeting

The Fairmont Hotel

Dallas, Texas




Neuropathic pain is triggered by identifiable lesions to the somatosensory nervous system, whether physical trauma, through disease or chemical toxicity. These injuries alter structure and function of the sensory neurons so that pain occurs spontaneously and responses to noxious and innocuous stimuli are pathologically amplified. The pain is an expression of maladaptive plasticity within the nociceptive system, a series of changes must be considered a disease in their own right and treated as such, not just the unfortunate consequence of the precipitating condition. Toward this goal we are defining mechanisms, both clinical and molecular, which will aid in accurate syndrome diagnosis and aid new therapy discovery. Multiple alterations distributed widely across the nervous system contribute to complex pain phenotypes. These alterations include ectopic generation of action potentials, facilitation and disinhibition of synaptic transmission, loss of synaptic connectivity and formation of new synaptic circuits, and neuroimmune interactions. Although neural lesions are necessary, they are not sufficient to generate neuropathic pain; genetic polymorphisms, gender, and age all influence the risk of developing persistent pain. I will discuss how genetics influences alter chronic pain risk in patients. Modern treatment needs to move from merely suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk, tangible examples of how this is being done will be discussed.


Learning objectives

Understand neuropathic pain as a standalone disease, with its own mechanisms and risks.

Understand current chronic neuropathic pain treatment profiles and how we hope to develop these in the future.