Rescuing Our Warriors from Chronic Pain: A Battlefield-to-Nondeployment Means to Prevent Opioid-induced Amplification of Neuropathic Pain from Traumatic Injury
Abstract
Based on our preliminary data and a thorough review of the available scientific/clinical literature to date, we hypothesize that: (a) Trauma and opioids combine to amplify the intensity and duration of trauma-induced chronic pain. (b) This combined exposure to trauma plus opioids amplifies the creation and release of endogenous danger signals in spinal cord that create enduring release of TLR4 stimulatory substances as a consequence of cell stress/damage/death, leading to amplified trauma induced chronic pain. Objective 1. Define the response to opioids commonly used for acute pain management, when these are administered early after trauma, prior to development of neuropathic pain Objective 2. Define the response to opioids and non-opioids commonly used for neuropathic pain management, when these treatments are administered later after trauma, after development of neuropathic pain Objective 3. Define whether the deleterious effects on neuropathic pain observed in Aims 1 and 2 can be prevented by targeting TLR4 andP2X7Objective 4. Define whether the deleterious effects of analgesics, and positive effects of co-administered TLR4/P2X7 antagonists, extend beyond neuropathic pain to other indices of disability
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2017
- Accession Number
- AD1045555
Entities
People
- Linda R. Watkins
- Peter M. Grace
- Suzanne M. Fulgham
Organizations
- University of Colorado Boulder