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[Sympathetic nervous system and pain: pathophysiological mechanisms]
1Physiologisches Institut, Christian-Albrechts-Universität Kiel.
Schmerz (Berlin, Germany)
|June 12, 2003
Summary
Sympathetic neurons contribute to pain and inflammation through two distinct mechanisms: nerve injury-induced chemical coupling and prostaglandin release in tissue trauma. Understanding these pathways is key to managing neuropathic pain.
Area of Science:
- Neuroscience
- Pain Research
- Autonomic Nervous System
Context:
- Sympathetic postganglionic neurons play a role in pain, hyperalgesia, and neurogenic inflammation.
- Two distinct modes of sympathetic-afferent neuron interaction exist, differing based on nerve lesion versus tissue trauma with inflammation.
Purpose:
- To differentiate the mechanisms by which sympathetic neurons influence afferent neurons in pathophysiological conditions.
- To elucidate the roles of noradrenaline, prostaglandins, and nerve growth factor in sympathetic-mediated pain and inflammation.
Summary:
- Nerve lesions induce plastic changes, leading to sympathetic-afferent chemical coupling via noradrenaline and adrenoceptors, potentially involving neurotrophic factors.
- In tissue trauma without nerve lesions, sympathetic nerve terminals mediate hyperalgesia and inflammation through prostaglandin release (PGE(2) or PGI(2)) and nerve growth factor (NGF).
- These sympathetic influences on pain and inflammation can occur through distinct molecular and cellular pathways.
Impact:
- Provides insights into the neurobiological underpinnings of neuropathic pain and inflammatory conditions.
- Identifies potential therapeutic targets for managing pain and inflammation by modulating sympathetic-afferent interactions.
- Highlights the dual role of sympathetic neurons in both nerve injury and inflammatory responses.