This is part 2 in a series of blog posts where I am sharing key highlights I took away from presentations, by Professor Cesar Fernandez de Las Penas, at the recent annual Spring Conference of the BMAS.
Part 1 can be viewed here...
With regards dry needling ‘mechanisms of action’ two main hypotheses were discussed:
Firstly a mechanical mechanism whereby the needle tip ‘destroys’ the dysfunctional motor end plate resulting in deactivation of the MTrP. This hypothesis is supported by evidence which shows a 60-70% decrease in local electrical activity within the end plate zone after dry needling. A certain amount of muscle damage has also be shown to occur, however 28 hours after dry needling the muscle morphology is restored to normal based on histological analysis. The normalisation of motor end plate activity after dry needling may partly explain a reduction in local muscle tone, amelioration of the local twitch response and improved muscle function.
The effects of fascial stimulation while dry needling are as yet unclear. It is suggested a signalling effect may occur as the needle gets temporarily trapped by the fascia en route to the muscle tissue, resulting in a form of healing mechanotransduction.
A sensory mechanism was then discussed whereby the sensory stimulatory effects of dry needling may result in an anti-nociceptive effect mediated locally and centrally. This may be related to a local release of ATP and CGRP and a reduction in the levels of MTrP related nociceptive sensitising substances including bradykinin and substance P. Segmental pain modulatory effects may also occur which has been shown to have a bilateral effect. Furthermore dry needling a MTrP in a forearm extensor muscle resulted in a decrease in MTrP activity within the upper trapezius muscle. This may indicate more remote central effects; possibly involving the descending pain inhibitory system.
Until part 3, take care.
Simon.
