Project

Insights into mechanisms and influencing factors of central pain modulation

Duration
01 January 2021 → Ongoing
Funding
Regional and community funding: Special Research Fund
Research disciplines
  • Medical and health sciences
    • Diagnostics not elsewhere classified
    • Neurophysiology
    • Electrophysiology
Keywords
pain pain modulation pain processing
 
Project description

Chronic pain is the most debilitating symptom in many medical conditions, including chronic low back pain and fibromyalgia. A key mechanism responsible for the persistence of pain complaints, despite the fact that no patho-anatomical pain sources can be identified, is the dysfunction of the pain processing pathways located in the central nervous system. The presence of long-lasting pain and nociceptive input will cause the central nervous system to adapt its strategies to modulate pain. There are various pain-modulating mechanisms in the body that can either inhibit and diminish the pain or facilitate and amplify the pain via the descending and ascending pathways, and their effect can be assessed by means of quantitative sensor testing. Examples of such measures are evaluation of the nociceptive withdrawal reflex to evaluate spinal hyperexcitability and evaluation of conditioned pain modulation to evaluate the pain-inhibits-pain mechanism. Several studies have already shown that these pain processing strategies and their measurements can be influenced by modifiable (e.g. physical activity, sleep, etc.) and non-modifiable (e.g. age, gender, ethnicity, etc.) factors and that these effects should be taken into account when using and interpreting the related measures. In addition, the mechanisms of these processes and their dysfunction in chronic pain populations has not been fully unravelled. For these reasons, this research project will investigate the mechanisms and influencing factors of endogenous pain modulation. Underlying mechanisms and influencing factors such as genetic predisposition, supraspinal control, and psychosocial mechanisms will be investigated in a healthy population with normal endogenous pain modulation and in pain patients with dysfunctional endogenous pain modulation.