PAIN-CENTRAL SENSITIZATION, MECHANISMS

From NeuroRehab.wiki

SUMMARY

1. High-intensity and/or prolonged nociceptor activation in association with injury and inflammation ⟹ NMDA receptor activation ⟹ central sensitisation.

2. This leads to increased intracellular Ca2+ ⟹ changes in gene expression and associated phenotypic shifts in dorsal horn nociceptive neurons.

3. NMDA receptor activation underlies dorsal horn wind-up and manifests as a broadening of sensory fields and allodynia associated with secondary hyperalgesia.

4. Central sensitization similarly occurs at higher CNS synapses and is similar to long-term potentiation (LTP) that underlies memory formation in hippocampal networks.

5. Such strengthened nociceptive networks may persist after healing of peripheral injury.

6. NMDA receptor antagonists (ketamine) attenuate central sensitization but their efficacy may be limited by inhibition of higher CNS synapses involved in conscious processing and memory.


Reference(s)

Hudspith, M.J. (2019). Anatomy, physiology and pharmacology of pain. Anaesthesia & Intensive Care Medicine, 20(8), pp.419–425. doi:https://doi.org/10.1016/j.mpaic.2019.05.008.
Cifu, D.X. (2020). Braddom’s physical medicine and rehabilitation. Elsevier. Get it on Amazon.
Cuccurullo, S. (2019). Physical medicine and rehabilitation board review. New York: Demosmedical. Get it on Amazon.
O’Young, B., Young, M.A. and Stiens, S.A. (2008). Physical Medicine and Rehabilitation Secrets. Mosby. Get it on Amazon.