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Dry needling

Trigger Point Massage

Dry Needling of Trigger Points and Myofacial Release

We use dry needling frequently in the accompaniment with Real Time Ultrasound to attain improved fascicular gliding of the myofascia, The mechanism of action involves a cascade of events from the release of nitrous oxide and pro- and anti-inflammatory substances to the release of endogenous opioids leading to the reduction in pain and muscle spasm. Primarily, this gives the brain a new reference point of relaxation. Combined with massage and joint mobilisations it becomes immediately apparent that joint tissue compression is  much relieved by dry needling, allowing the opportunity for passive movement to lubricate the joint. The relaxed state of muscles (which were in spasm) allows the re-education of the appropriate 'timing' and synergies within and between muscles.

Dry Needling has been shown to result in significant improvements of muscular endurance of knee extensors and hip flexion that persisted 4 wk posttreatment as well as a short-term improvement of muscular endurance of knee flexors in the intragroup analysis of soccer players. Compared with placebo, DN showed a significant effect on hip flexion that persisted 4 wk posttreatment. Compared with a nontreatment control, DN also significantly improved maximum force of knee extensors also 4 wk posttreatment. Compared with a nontreatment control, placebo laser combined with water pressure massage resulted in a small but statistically significant improvement of hip flexion range of motion at treatment end and 4 wk posttreatment (Haser et al 2017 Medicine & Science in Sports & Exercise . 49(2):378-383)


Liu et al. (Arch Phys Med Rehabil. 2015;96(5):944–55) systematically reviewed the effect of DN for TrP associated with neck and shoulder pain, showing a specific and significant short- and medium-term effect. Current studies also suggest that DN may be helpful in reducing pain in the upper quarter and craniofacial region (Curr Pain Headache Rep. 2014;18(8):437) and plantar heel region (Phys Ther. 2014;94(8):1083–94).

Shah et al. (Arch Phys Med Rehabil. 2008;89(1):16–23: J Bodyw Mov Ther. 2008;12(4):371–84) found higher concentrations of substance P (SP), calcitonin gene–related peptide, bradykinin, 5-hydroxytryptamine/serotonin, norepinephrine, tumor necrosis factor α, and interleukin 1β in myofascial TrP. After DN, SP and calcitonin gene–related peptide concentrations significantly dropped corresponding with less clinical tenderness and pain of TrP. Besides the mechanical tissue stimulus with a change in the milieu of local inflammatory parameters (Curr Pain Headache Rep. 2012;16(5):407–12), remote reduction of inflammatory neuromediators such as SP may also be responsible for the effect of DN (Biomed Res Int. 2014;2014:982121).

Trigger Point Massage


 Trigger Point palpation

Trigger point - gluteus medius

  Trigger point - gluteus medius

Trigger Points : piriformis, gluteus maximus, quadratus lumborum, levator ani

Trigger Points : piriformis, gluteus maximus, quadratus lumborum, levator ani

Trigger Point - adductor magnus. Note the anal referral which is common amongst cyclists who use the adductors to power hip extension

Trigger Point - adductor magnus. Note the anal referral which is common amongst cyclists who use the adductors to power hip extension

Trigger Points : Obtrator Internus and pelvic floor

Trigger Points : Obturator Internus and pelvic floor

Trigger point - iliopsoas

Trigger point - iliopsoas

It should be noted that we treat many other trigger points in other parts of the body besides the ones illustrated.


Biochemistry of trigger points


Trigger Point Massage

Comparison of normal, latent and active trigger point physiology using microdialysis in the upper trapezius muscle (Shah et al 2005). These researchers also found similar results for Bradykinin, Calcitonin Gene Related Peptide (CGRP), Substance P, Tumor Necrosis Factor alpha, and Interleukin 1beta. Additionally, reduced pH levels were also seen in areas of active trigger points.

The biomechanics of plyometric (eccentric-concentric) exercise which can give rise to trigger points.

Trigger points have been classically associated with plyometric type of exercise where muscles lengthen during eccentric contraction which although it damages cytoskeletal is considered adaptive in the formation of new sarcomeres. Investigations into eccentric exercise revealed pain 8 hours after initial exercise which was maximal 48 hours later (Newham, Mills, Q uigley, Edwards 1983).   These investigators found low frequency fatigue 10 minutes after a 20 minute period of stepping (Newham et al 1983).  Additionally, they demonstrated progressive increases in IEMG during the exercise in the rectus femoris (160% increase) and vastus medialis (140% increase) in the eccentric contracting leg (Newham et al 1983).  Mechanical damage to the sarcoplasmic reticulum resulting in less calcium release for each excitatory action potential was suggested as the cause of the low frequency fatigue (Newham et al 1983).

Trigger Point Massage

However, a number of sites in the myofibrillar complex such as reduce binding sensitivity and capacity of Troponin C for calcium, altered troponin-tropomysosin interaction to impaired binding and force generation by actin and myosin have been implicated in impaired force generation (Green 1990).  Indeed, in the absence of any association between relaxation rates and Calcium kinetics raises support for the notion of a rate-limiting process controlling the relaxation of fatigued muscles being located in the contractile proteins (Hill et al 2001).  During fatigue the relaxation times can be prolonged as much as 50% (Bigland-Ritchie et al 1986) thus resulting in increased force generation during submaximal stimulation due to tetanic fusion despite a substantial fall in the maximum tetanic force (Bigland-Ritchie et al 1986).   


The initial overall loss of force production seen may be due to Desmin and Titan damage (Lieber & Friden 2002).  Desmin acts as an extra-sarcomeric mechanical stabilizer between adjacent Z discs and the attachment to the costomere at the sarcolemma (Lieber, Shah & Fridén 2002).  The costomere complex contains Talin, Vinculin & Dystrophin which attach to the trans-sarcolemmal proteins Integrin and Dystrophin associated proteins.  These proteins allow the lateral transmission of force from actin to the basal lamina containing type IV collagen which is contiguous with the endomysium (Kovanen 2002).  Desmin loss after eccentric exercise can occur within 5 minutes, possibly as a result of increased intracellular Calcium leading to Calpain activation and selective hydrolysis of intermediate filament network (Lieber & Fridén 2002).  This may result in the ‘popping of sarcomeres' of different length thereby potentially loosing their myofilament overlap of actin and myosin (Lieber & Fridén 2002).  Hence, reduced force production would be expected.  Additionally, the release of matrix metalloproteinase (MMP) which may degrade the extramyocellular type IV collagen (Korskinen, Kovanen, Komulainen et al 1996).  However, this effect occurs many days after exercise (Korskinen et al 1996) and could even effect torque production 28 days after exercise (Lieber & Fridén 2002).  This has significant implications in exercise training prescription. 

flash file created by Martin Krause 2003

Titan molecules span the gap between the ends of the thick filaments and Z-bands. At the 2007 MPA conference in Cairns, Rob Herbert, provided the AJP oration whereby he explained the significance of Titan as a major determinant of extensibility in muscle fibres. Additionally, he stated that Titan is differentially expressed in human skeletal muscle as short stiff fibres and long compliant fibres.

  • Costomeres are 15 different proteins
  • Low oxidative muscles have a tendency to tear during eccentric exercise
  • Loss of desmin proceeds loss of fibronectin membrane
  • Fibre strain results in increased intracellular and extracellular calcium which ?may lead to desmin hydrolysis through calpaine?
  • Sarcomere shortening occurs to the detriment of tendon lengthening
  • Excitation-contractile coupling may be the area disrupted rather than pure sarcomere disruption
  • Structural changes of the disruption of the cytoskeleton include dystrophin (sublaminal membrane protein), sometimes desmin and titin, whereas alpha actin is always OK ?suggesting that calpaine is not the enzyme responsible for protein dysruption?
  • Creatine Kinase has no correlation with these cytoskeletal changes
  • Inflammatory process important for tissue cleaning and remodelling
  • Mechanism for muscle adaptation may be myosin gene regulation - heavy chain myosin isoform upregulation
  • Oxygen into the Mitochondria and through the electron transfer chain (ETC) results in ATP use of 20% for power and 80% for heat, therefore people producing less heat may be producing more power?
  • Slow twitch muscle fibre concentration varies with the years of training
  • Cycling cadence velocity at peak efficiency for slow twitch muscle fibres is 80rpm

Fibroblasts and Loose Connective Tissue

At the APA conference in Sydney during October 2009, Dr Helene Longevin presented her research into the effects of stretching subcutaneous tissue. Superficial and deep fascia are composed of loose and dense connective tissue layers. The loose layers allow dense layers to glide past one another. This tissue contains abundant fibroblasts, immune cells and neurovascular bundles. A 20% static stretch of loose connective tissue for 30minutes significantly increases the size of fibroblasts in vivo and in vitro. Although this mechanism remains unclear it is hypothesised to be due to microtubule reorganisation (Beta-tubulin). Inhibition of growth kinase and Roc prevents the cells from spreading out. Actine polymerisation occurs at the leading edge. Fibro-attraction occurs whereby fibroblasts push forward at it's front edge, whilst retracting the rear (through Rho). Both Rac and Rho are activated simultaneously. The fibroblasts microtubule assembly contributes to connective tissue (C.T) relaxation, which means that tense in connective tissue is actively regulated. Viscoelastic response of loose connective tissue is influenced by specific cytoskeletal inhibitors. Rac increases the equilibrium force. Active C.T tensioin regulation may occur normally in response to sustained chnages in tissue length (e.g. hift in body position). This role may be to prevent sustained mechanical stimulation of other cells within the C.T (immune cells, nerve fibres, blood vessels).

The dense C.T fibroblasts don't respond to stretch due to the stiff matrix preventing the fibroblasts from receiving any strain. Scarring due to injury causes an increase in dense C.T which can be pevented by 10minutes, 2 times per day for 1 week in a suspended tail animal model. The combination of reduced movement and inflammation is a recipe for fibrosis. R-T US can be used as feedback during dry needling to observe C.T movement. In people suffering low back pain the fascial layers are less fluid and less differentiated. Additionally, people with LBP have hicker perivascular C.T. Involuntary muscle spasms may decrease the relative C.T motion during passive movement. Conversely, increased C.T thickness, stiffness and/or viscosity may affect the passive stiffness and range of movement of adjacent muscles.

Trigger Point Massage

Intrinsic tension within C.T will have profound effects in the cells within it such as blood vessel precursors stimulating angiogenesis. Similarly, immune cells may be affected by this tension. High amplitude or repetitive tissue stretch may cause injury but can also increase C.T strength. Low amplitude stretch within or slightly beyond the usual ROM may help maintain appropriate mibility and dynamic tissue response. Hence this may represent strong evidence for STM, dry needling, joint mobilisations, muscle energy technqiues, strain-counterstrain techniques and training with Whole Body Vibration.

Trigger Point Massage

Additionally, myofascial release techniques and Kinesiotaping can also be employed in order to restore optimal movement function.

Publications into trigger point therapy include 

  • Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Shah JP et al (2008) Arch Phys Med Rehabil, 89, 16 -23.
  • Integrated Dry Needling with new concepts of myofascial pain, muscle physiology and sensitization. Shah JP In : Contemporary Pain Medicine, Integrative Pain Medicine, The Science and Practice of Complementary nd Alternative Medicine in Pain Management. Ed Audette & Bailey, Human Press, Totowa, NJ
  • An explanation of Simons' integrated hypothesis of trigger point formation. Gerwin RD, Doomerholt J, Shah JP (2004). Current Pain and Headache reports, 8, 468-475
  • Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: an application of muscle pain concepts to myofascial pain syndrome. Shah JA & Gilliams EA (2008). J of Bodywork and Movement Therapies, 12, 371-384
  • An in-vivo microanalytial technique for measuring the local biochemical milieu of human skeletal muscle. Shah JP et al (2005) J Appl Physiol, 99, 1977-1984

Updated : 20 February 2017


Trending @ Back in B Physio

  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups. In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 18 May 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More
  • Mon 07 Nov 2016

    Pilates – with Brunna Cardoso

    Pilates – with Brunna Cardoso Martin is pleased to welcome the bubbly Brunna Cardoso to Back in Business Physiotherapy for Pilates Classes in February 2017.  Brunno is an experienced pilates instructor and has had several years experience training with pilates instructors in Brazil. Read more Read More

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Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected