Previous studies have shown a decrease in sensitivity to noxious thermal stimuli to the limb following focal photobiomodulation (PBM) of the sural nerve. The mechanism by which PBM blocks nociceptive transmission in the sural nerve is unknown. We tested two possible theories for neural inhibition using computational models (NEURON simulation environment). First, the beading phenomenon known as varicosities observed with PBM and second, the observations that nitric oxide or other reactive oxygen species are increased following PBM. Other groups have shown that nitric oxide can block unmyelinated and demyelinated axons by blocking sodium current. We hypothesize that the size increase observed with PBM in vivo is not sufficient to block action potentials, and the results indicate that increasing the axon diameter to block action potentials requires diameter increases much larger than those observed in vivo, suggesting varicosities cannot be solely responsible for the block phenomenon. However, the role of nitric oxide on sodium current is expected to reduce the action potential magnitude enough to cause the block effect, and this mechanism of block merits further investigation.
Previous meta-analyses of photobiomodulation (PBM) parameters have reported correlations between effect size and emitter parameters, but the trends are not robust enough to prospectively predict doses that will yield a significant effect. A meta-analysis of PBM dosing protocols on peripheral nerves with 800 – 840 nm wavelength light was performed using Monte Carlo photon propagation models to elucidate clearer trends between dose and effect. We then tested various doses of PBM applied directly at exposed hindlimb nerve in a rodent pain model. A single application of PBM at the nerve reduced pain associated with heat-sensitive fibers for approximately 7 days.
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