Clinical Implications

Tissue injury and inflammation lead to the production and release of mediators that affect nerves by changing ion channel expression, thereby contributing to sensitization. This development of hyperalgesia can be blunted by antagonizing such mediators, such as nerve growth factor, or blocking their second messenger systems. While results obtained in animal experiments are promising, unwanted effects on other systems (e.g., immune function) have limited the use of this approach in humans.

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