The science of Dry Needling and how it works!!

Physiological effects of dry needling

When a filiform needle is inserted into the muscle there a numerous physiological changes that take place to the muscle and/or fascia. On insertion of the filiform needle into ischemic tight muscle bands micro damage occurs to muscle tissue and fascia causing the production of inflammatory mediators (Leung 2012, p.267). The micro damage is due to the filiform needle bursting plasma membranes and causing neurogenic inflammation (Lund 2015). The micro damage to the muscle fibres initiates an inflammatory response increasing blood flow and oxygen to the ischemic area of the trigger point and facilitating physiological tissue healing and decreased pain (Lund 2015). Wu (2015) states that the micro damage promotes healing due to the local increase in blood flow and may be used to improve the function of muscles by decreasing muscle tension, improving range of motion, increasing coordination and decreasing pain (Cagnie 2013). When the needle enters the muscle there is a release of calcitonin gene related peptide via the axon reflex from thin sensory nerve endings, this causes vasodilation and increased blood flow to the area (Shinbara 2014, p.65). Shinbara (2014) also states that acetylcholine which gets released from cholinergic vasodilator nerves to possibly be the cause of the vasodilation. Furthermore mechanical stimulation to the endothelial tissue is believed to synthesis nitrous oxide as well as binding of vasodilators on receptors on the endothelium (Shinbara 2015). Interestingly Woehrle (2015) found that needling resulted in an increase in temperature and short term vasodilation which was similar to the subject’s pain distribution pattern when they used infrared thermovision. The response can often be seen with bright red skin surrounding the needle and a wheel may be seen post treatment (Wu 2015, p.15). The local twitch response is the contraction of the affected muscle fibres being needles which causes an involuntary spinal reflex (Cagnie 2013). When the involuntary contraction occurs the excessive acetylcholine which was released at the motor endplate gets used and the local ischemic tissue which was sustained by continuous contraction of the sarcomere relaxes as blood flushes in to the muscle fibres (Cagnie 2013). Another cause of the muscle relaxing as a result of the local twitch response is the opening of calcium ion channels allowing calcium ions to rush out and potassium to rush in (Lund 2015). This is believed to disturb the integrity of dysfunctional endplate through mechanical stimulation (Cagnie 2013). Another physiological effect of when the needle is inserted into muscle the tissue is a temperature and circulation increase which alters the cell membrane permeability which increases its ability to be affected by endogenous chemicals (Woehrle 2015).Refer to question 3. Another event that takes place when a filiform needle enters muscle is the penetration of the surrounding fascia. Leung (2011) suggests that this interrupts the fascia, distorting the continuity of the connective tissue by tugging on the elastic like fibres. This is hypothesized to activate local mechanoreceptors which then sends the initial neural signals (Leung 2011, p.263). Another part that connective tissue plays a role in is the release of adenosine phosphate compounds causing vasodilation. Lund (2015) states that the mechanical signalling through the extracellular matrix also causes vasodilation. It has also been found that if rotation of the needles occurs that the needle will grip the fibres of muscles and connective tissue causing an internal stretch of the tissues due to the production of surface tension and electrical attraction which is adequately enough to contribute to the mechanical effect of dry needling (Dommerholt 2013, p.36). Wu (2015) states that twirling of the needles winding up collagen fibres also changes the microenvironment of the interstitial tissue. The filiform needle results in mechanical stimulation of fibroblast, changing their cell shape and increasing their cross sectional area as the cell bodies spread out and expand (Lund 2015). It was observed that the remodelling of fibroblasts is important for sustaining the viscoelasticity properties of the tissue (Luind 2015). This counteracts fibrosis as seen in scar tissue and may result in dynamic changes of the actin cytoskeleton through purinergic receptors where high concentrations of purines e.g. ATP have been found close to the needle site (Lund 2015).

Neurological effects of dry needling

When a filiform needle is inserted into muscle there are numerous neurological changes and effects that take place centrally and peripherally. The peripheral changes resulting from the filiform needle entering muscle are as followed. Peripheral sensory nerve fibres locally set off action potentials around the network, known as the axon reflex which releases calcitonin gene-related peptide, an inflammatory neuropeptide (Wu 2015, p.14). This neuropeptide along with substance P activate mast cells and blood vessels resulting in blood vessel dilation and increasing muscle blood flow (Wu 2015, p.20). This causes vasodilation and it is believed that when increased blood flow occurs in the muscle that it washes out fatigued and or algesic substances which may result in improved functioning of the muscle (Shinbara 2014, p.65). In conjunction to this, action potentials also occur in the neurons of the dorsal root ganglion and afferent nerve trunk (Wu 2015, p.20). Dry needling eliciting a local twitch response also causes sympathetic cholinergic vasodilator nerves to release acetylcholine. When a filiform needle is inserted into muscle or more specifically the sensitive loci within taut bands it causes mechanical irritation via mechanoreceptors. Mechanotransduction takes place activating larger diameter alpha beta fibres and smaller diameter alpha delta fibres (Cagnie 2013). The needle is believed to disturb the pain cycle which involves peripheral nerves ascending the spinal cord to the brain areas which modulate and perceive pain, where the message then descends the spinal cord to the peripheral nerves resulting in nociception to the area (Lund 2015). These are the central changes as a result of dry needling. Leung (2012) found that needling activates brain nuclei by sending signals along the ventrolateral tract of the spinal cord modulating pain sensitisation by descending inhibition pathways. Action potentials were also found to occur in the dorsal horn of the spinal cord, neurons of dorsal root ganglion and afferent nerve trunks where Alpha beta and C-fibres are involved (Wu 2015, p.20). Alpha delta fibres and C-fibres are essential for pain modulation and the activity of the autonomic nervous system (Hong 2013, p.7). Dommerholt (2013, p.23) in particular states that it is slow conducting unmyelinated C fibre afferents. The signal passes through the spinal cord via the dorsal horn and to supraspinal centers. It is here that serotonin, glutamate, opioid and adrenergic systems are activated on the dorsal horn of the spinal cord reducing nociceptive inputs, as well as activation of diffuse noxious inhibitory control sending inhibition to the dorsal horn also reducing nociceptive inputs (Leung 2012, p.267). It was also found that activation of neural plasticity from the dorsal horn via long term potentiation and long term depression inhibits activation of C-fibres (Leung 2012, p.267). Supraspinal centers also activated correlating brain networks of the raphe nucleus, locus coeruleus, peri-aqueductal grey matter, prefrontal cortex, insula, cingulate cortex, caudate nucleus and amygdala which enhance the descending inhibition of nociception on the dorsal horn resulting in analgesia (Leung 2012). It appears that a common trend among the research is the fact that when a filiform needle is inserted into muscle peripheral nociceptive inputs travel through the ascending dorsal horn of the spinal cord and activate central inhibitory pain pathways (Fernandez-De-Las-Penas 2016, p.366).