Deep dry needling (DDN) is an invasive procedure in which an acupuncture needle is inserted into the skin and muscle. DDN is directed at myofascial trigger points (MTrPs), which are defined as “hyper-irritable spots in skeletal muscle that are associated with a hypersensitive palpable nodule in a taut band”. MTrPs may consist of multiple contraction knots, which are thought to be due to an excessive release of acetylcholine (ACh) from select motor endplates, and can be divided into active and latent MTrPs. Active MTrPs can spontaneously trigger local pain in the vicinity of the MTrP, or they can refer pain or paraesthesia to more distant locations. They cause muscle weakness, a range of motion restrictions, and several autonomic phenomena. Latent MTrPs do not trigger local or referred pain without being stimulated, but they may alter muscle activation patterns and contribute to limited range of motion.

At Maple Motion Chartered Physiotherapy we use DDN very successfully to treat a number of musculoskeletal disorders. Often the active trigger points may only be a secondary manifestation of an underlying injury. Your chartered physiotherapist will be able to use DDN to help treat this symptom of your underlying condition and then assess and treat for the ‘route cause’ of you issue. High performing athletes can develop active trigger points in response to the high training loads they endure and so can benefit from DDN to release tight tissue and allow them to train to their full potential.


Diagnostically, DDN can assist in differentiating between pain that originates from a joint, an entrapped nerve, or a muscle. Mechanical stimulation or deformation of a sensitized MTrP can reproduce the patient’s pain and may assist in the differential diagnostic process. One of the unique features of MTrPs is the local twitch response (LTR), which is an involuntary spinal cord reflex contraction of the muscle fibers in a taut band following palpation or needling of the band or MtrP.


Despite a growing body of literature exploring the etiology and pathophysiology of MTrPs, the exact mechanisms of DDN remain elusive. Possible explanations of its efficacy include normalisation of the chemical environment of the active MTrP or lengthening of the cytoskeletal structures secondary to induced stretch reflexes