November 2012

Intramuscular manual therapy for heel pain

Intramuscular manual therapy, also known as dry needling, is hypothesized to relieve pain by modifying tension in connective tissue. Limited evidence supports the use of IMT for plantar fasciitis, although further research is needed to rule out a placebo effect.

By Brent Harper, PT, DPT, DSc, OCS, FAAOMPT

Plantar fasciitis—also called runner’s heel, heel spur syndrome, painful heel syndrome, subcalcaneal pain, chronic plantar heel pain, plantar heel pain, and calcaneodynia1,2 —is the most prevalent foot pain condition experienced by adults and treated by healthcare providers (11%-15% of service visits),3 including physical therapists.1,4,5 Recent evidence suggests plantar fasciitis is a noninflammatory degenerative condition in the plantar fascia caused by repetitive microtears at the medial tubercle of the calcaneus.1,3,4,6,7 It is a form of tendinosis characterized by the presence of fibroblasts rather than inflammatory cells, degeneration of collagen, and proliferation of vascular and connective tissues, especially along the medial calcaneal tubercle.4,7

This painful condition is more aptly referred to as plantar fasciopathy (a general term for acute and chronic heel pain), plantar fasciosis (particular to chronic heel conditions), or plantar heel pain.1,3

Plantar fasciitis can be diagnosed clinically based on subjective and objective findings and without further investigation.8 Imaging is a valuable tool for confirmation of true fasciopathy, though positive imaging studies occur in the absence of plantar fasciitis pain. In their study on subjects with normal arches and flexible flatfeet, Huang et al found hypoechoic fascial thickening of 4 mm or greater in the plantar fascia of 15 of 23 flatfooted individuals (65.2%). Ten of those (43.4% of the total) had symptoms of heel pain. Therefore, thickened fascia based on ultrasonography is not an automatic diagnostic finding for plantar fasciitis.9

Figure 1. Common heel pain referral MTrPs with most likely IMT needle placement: gastrocnemius (left), abductor hallucis (top right), and quadratus plantae (lower right).

Annually, 600,000 to 2 million Americans seek care for heel pain.1-5 Painful foot and ankle conditions are associated with gait disturbances and balance difficulties.2 Geriatric patients with heel pain have an increased risk of falls during activities of daily living.2 Statistics demonstrate the negative impact of plantar heel pain on quality of life and underscore its influence on disability and function.3

Plantar fasciitis is a self-limiting condition in which 80% of cases usually resolve spontaneously within six to 18 months.1,7 The classic symptom is an intense sharp heel pain when taking the first few steps in the morning. This heel pain also may occur when standing after prolonged sitting, as a dull ache after a day on one’s feet, or as pain after vigorous exercise. Walking barefoot or in shoes with minimal arch support or running and jumping may exacerbate the symptoms. Signs include pain provocation during palpation over the medial tubercle of the calcaneus, limited ankle dorsiflexion, and impaired great toe extension. The presence of any neurological symptoms indicates an alternate etiology.10,11

Several intrinsic and extrinsic risk factors for plantar heel pain have been identified in the literature (Table 1). Riddle et al identified three independent risk factors for plantar fasciitis. These were limited ankle dorsiflexion (equinus), long hours of standing, and high body mass index (BMI > 30 kg/m2).13 In a separate study by Riddle et al, high BMI was the only correlative finding for plantar fasciitis, functional loss, and disability.14 Irving et al found correlations between plantar fasciitis and both BMI greater than 30 kg/m2 and a pronated foot posture as measured by the Foot Posture Index.15 In individuals with excessive pronation, 81% to 86% exhibit plantar heel pain symptoms.16 Other studies reported that excessive pronation, in and of itself, did not result in lower extremity abnormalities.17-19 In another study, the risk of heel pain doubled in the presence of impaired ankle dorsiflexion (less than 10°).13 As dorsiflexion range decreased, the incidence ratio dramatically increased.1,13 Despite inconsistent correlative evidence to support the most common physical impairments associated with plantar fasciitis, these may have the most clinical relevance: BMI greater than 30 kg/m2, excessive foot pronation, and limited ankle dorsiflexion.1,6,7,13-19

Myofascial trigger points

Myofascial trigger points (MTrPs) have been proposed as a possible cause of plantar fasciitis symptoms. MTrPs are hyperirritable spots with hard hypersensitive palpable nodules located in taut bands within muscles. When these points are compressed or spontaneously provoked, predictable patterns of pain can occur in a distal region, called a referred pain zone.20-22

MTrP formation can result from many factors, including trauma, overstress, overuse, psychological stress, and joint dysfunction.23 MTrPs are either active (symptomatic) or latent (asymptomatic). Active trigger points can spontaneously produce local pain, referred pain, or paresthesia while latent trigger points cause pain symptoms only when stimulated. The hallmark characteristics of MTrPs include motor, sensory, and autonomic phenomena and hyperexcitability of the central nervous system.20-22,24 Gerwin et al demonstrated statistically significant inter-rater reliability for MTrPs as a reliable clinical sign as long as the examiners are trained to identify the features of a trigger point.25 Of note, the authors suggested that even when symptom provocation is negative with manual palpations, a local twitch response (LTR), pain reproduction, and referred pain are often elicited by placing a needle into the MTrP.25

Local twitch responses, a type of spinal reflex in which muscle fibers within the MTrP contract abruptly, seem to be exclusive to MTrPs and occur when one is stimulated through manual or needle palpations.23,26 There is a clinical correlation between eliciting an LTR during treatment and a positive outcome.24

The best known and most studied of the primary theoretical models for the etiology of MTrPs is the integrated hypothesis of the trigger point model.23,26 According to this theory, an MTrP is a multifactorial phenomenon composed of biochemical, biomechanical, and neurophysiological factors that interact to produce sensory, autonomic, and motor symptoms. In normal resting muscle there should be minimal to no measurable electrical activity, but taut bands seem to spontaneously produce electrical activity.

Spontaneous electrical activity (SEA) is characteristic of MTrPs. On electromyography (EMG), SEA results in endplate noise. One hypothesis for SEA and the resulting endplate noise is excess acetylcholine (ACh) in the neuromuscular junction. This ACh release may be due to the tension the MTrP produces on the integrins (cellular proteins that bind connective tissue),27,28 resulting in focal muscle fiber contractions.29 As the cycle perpetuates, ACh is released without direct alpha-motor neuron activity. The elevated levels of ACh result in continuous muscle contraction, which initiates SEA, by causing the sodium channels located in the sarcoplasmic reticulum to remain open, allowing an influx of excess calcium into the intracellular region.23,26-28

The more irritable an active MTrP is, the greater the prevalence of SEA. Higher SEA amplitudes have been correlated with lowered pressure-pain thresholds.30 Theoretically, active MTrPs impair descending inhibition, causing central sensitization. They also may impair motor coordination, resulting in excessive coactivation of muscle antagonists, which may lead to a reorganization of the motor control strategy and, therefore, to muscle overload with increased nociception.29

The dorsal horn and central nervous system may develop neuroplastic alterations secondary to MTrP nociception. The biochemical inflammatory mediators surrounding MTrPs activate muscle nociceptors. These chemicals, compounded by the mechanical tension, compression, friction, or vibratory actions of the MTrP, irritate the associated peripheral nerves, leading to peripheral sensitization. The cascading nociceptive damage accumulates until it affects the dorsal horn, causing central sensitization—a form of neuroplasticity that leads to hyperalgesia and allodynia. Eventually, this leads to local ischemia and hypoxia, which stimulates even greater amounts of ACh. The lack of oxygen in the muscle tissue causes hyperacidity in surrounding musculature, which may excite additional nociceptive input to the dorsal horn, furthering the central sensitization process.31 This results in an amplified pain reaction, pain from normally non-noxious stimuli, a diminished pressure-pain threshold, and a wide-ranging hyperalgesic pain field.27,28,31,32

Central sensitization, a type of neuroplasticity, is a dynamic process by which the brain interprets pain and is prevalent in many pain syndromes. This phenomenon involves phenotypic switches and structural modifications of the dorsal horn, leading to increased membrane excitability, reduced inhibitory communication, and increased synaptic efficiency.33 Once the dorsal horn is sensitized, it amplifies nociceptive inputs, both somatic and visceral, from areas sharing segmental innervations. Pain signals are fired with increased rapidity or spontaneity to the thalamus and cerebral cortex.27 The result is a pain response from previously nonpainful stimuli. The involved innervating segment is now facilitated or sensitized.32

The etiological development of MTrPs is multifactorial. It may include direct trauma, eccentric, submaximal concentric and low-level muscle contraction loads, and altered intramuscular pressure distribution. One proposed etiological rational is the so-called Cinderella hypothesis,23 from low-level muscle loads, is based on Henneman’s size principle, in which type I tonic muscle fibers are recruited before type II phasic muscle fibers. (The nod to the folk-tale heroine comes from a version of the story that calls her the first to rise and the last to go to bed.)

The continuous neuronal firing of tonic muscle fibers leads to a local metabolic overload with an increased release of calcium and inflammatory mediators. Local hypoxia and ischemia occur secondary to the resultant increase in intramuscular pressure. The increased muscle tissue tension may influence MTrP taut band development and its surrounding connective tissue cytoskeletal matrix. Both direct and indirect acute trauma overload may injure the sarcoplasmic reticulum or the muscle cell membrane. The more studied theoretical etiology is the integrated trigger point hypothesis, an expansion of the energy crisis model. In this theory, the SEA is secondary to MTrPs and is considered endplate noise, as discussed previously in this paper.23

The result of either overload hypotheses is elevated calcium release, decreased adenosine triphosphate (ATP), and impairment of the calcium pump, which further elevates intracellular calcium concentrations (an energy crisis hypothesis). A decrease of the pH of the local tissues and local hypoxia occurs secondary to repetitive overloading of the muscle tissues.23

Travell and Simons suggested plantar heel pain may be related to MTrPs of the lower extremities.20 MTrPs that may refer to the heel include those located in the gastrocnemius, soleus, tibialis posterior, abductor hallucis, flexor digitorum brevis, and quadratus plantae.20 The abductor hallucis, flexor digitorum brevis, and quadratus plantae are in the same region as the plantar fascia and may directly cause plantar fasciitis pain.20 (Figure 1)

Therapeutic implications

Research has failed to reach a consensus regarding invasive and noninvasive management strategies for plantar heel pain. Nonsurgical treatment options include gastrocnemius and plantar fascia stretches, manual manipulation of the gastrocnemius soft tissue trigger points, use of supportive footwear, over-the-counter or custom foot orthoses, taping, night splints, steroid injections, shock wave therapy, acetic acid iontophoresis, dexamethasone iontophoresis for short-term benefit, and oral anti-inflammatory drugs.1-5,7

Acupuncture is sometimes recommended as a treatment option; however, treatment sites vary from acupoints (acupuncture points) at the pain site to acupoints at nonlocal general pain control locations.1,34 For example, traditional acupuncture theory utilizes acupoints of the upper extremity to treat pain conditions of the lower extremity, and vice versa.34 Traditional acupuncture theory has not provided a specific acupoint for treating heel pain.34

Although intramuscular manual therapy (IMT), also known as dry needling, is a relatively new therapeutic intervention in the US, European health care providers have utilized it for many years. IMT is an invasive procedure in which an acupuncture needle is inserted into the skin and muscle.22,23 IMT seems to be efficacious when used to treat active MTrPs.36,37 The mechanism of action for IMT is unknown, but research continues to delve into questions related to the MTrPs in musculoskeletal and myofascial pain conditions.22,31,36,38-41 The application of IMT appears to be safe when performed by a trained clinician, but adverse events can occur. For plantar fasciitis, these may include local soreness, pain, bleeding, bruising, or all of these at the needle injection site.37,42

It is theorized23,26 that dry needling biochemically, biomechanically, and neurophysiologically modifies tension in connective tissue and thereby resets the sarcomere length. This may disrupt the spontaneous ACh release and thus diminish or abolish SEA. The needle’s mechanical effect may cause muscle and connective tissue to electrically polarize (mechanotransduction), which may also facilitate a normalization of the electrical activity in the muscle tissue.23,26 Theoretically, the remodeling of the connective tissue and the changes in the electrical activity within the nervous system removes the amplification effect of stimuli to the dorsal horn and potentially reverses the previous neuroplastic changes.28 When rabbit MTrPs were dry needled with a resulting LTR, the neuromuscular junction had an immediate SEA reduction and an almost immediate chemical normalization.26,35

IMT is intended to be an adjunct to other therapy procedures, such as therapeutic exercises and soft tissue and/or joint mobilization and manipulation. Placement of the needle varies from a shallow depth of insertion (called superficial dry needling, and referring to stopping just prior to penetrating the muscle) to deep penetration (called deep dry needling, targeting the offending MTrP).23,26 Presently, no studies have been conducted to determine the optimal dosage for IMT needle application, which in practice can range from seconds to minutes. Nor does the literature delineate the optimal protocol following needle placement: it may be left stationary or manipulated with pistoning or twirling in one or both directions. Targeted muscle may be electrically stimulated using devices directly attached to the needle to elicit motor contractions of muscles local to the needle insertion site.

Cotchett et al conducted a systematic review of MTrPs associated with plantar heel pain and the effectiveness of treating with either dry needling or injection.43 The authors found few studies on this topic, and those identified were rife with limited evidence and methodological defects such as inconsistencies in identification of muscles treated, unspecified muscles treated, undefined size and type of needles used, number of needles inserted, depth of needle insertion, duration of and response to needle insertion, and limited or unstated diagnostic criteria used to identify MTrPs.43

Cummings and White performed a systematic review of needling therapies, including both dry needling and wet needling (injections), for MTrP pain. Marked improvements were shown when the MTrP was needled, regardless of needling method. Unfortunately, the clinical trials lacked rigor and, therefore, the reviewers concluded the current literature neither supports nor refutes the efficacy of dry needling. Further research is required to investigate the efficacy of IMT beyond the placebo effect.41 This review did not include any studies in which needling was performed for plantar fasciitis conditions. Shah et al demonstrated dramatic and almost instantaneous biochemical changes at the site of dry needle insertion.31,38,39 Several studies have reported biochemical and neurophysiological benefits with local MTrP needling and nonlocal pain modulating acupoint needling.34,40,41,44

Figure 2. Fascial manipulation points include the lateral head of the gastrocnemius (top left) and the insertion of the posterior tibialis over the navicular bone (top right). Treatment at these two sites is depicted in the two lower images.

Srbely et al44 postulated that needling tissues sharing segmental innervation, or a common neurologic link (e.g., the supraspinatus and infraspinatus share C5 innervation whereas the gluteus medius does not), would have greater antinociceptive effects. They found that IMT in the supraspinatus trigger point resulted in a greater reduction in pain sensitivity in the linked infraspinatus than in the gluteus medius. They determined that stimulating an MTrP within a muscle with shared segmental innervation might directly reduce the degree of central sensitization. They proposed that segmental inhibitory effects evoked by the stimulation of the needle at the MTrP mediate the antinociceptive effects, suggesting that MTrPs may be important portals of entry for segmental neuromodulation.

This physiological response has been observed in another study, as well. Hyuk et al found evidence suggesting that less pain reduction occurred when dry needling was applied solely at the local peripheral pain site than when additional dry needling was applied at a corresponding paraspinal segment.45 In another study Hyuk et al found that dry needling was as effective as lidocaine injection in MTrPs in the upper trapezius muscle.46 Although there is mounting empirical evidence supporting its general effectiveness, there is limited evidence specifically supporting dry needling as a primary interventional strategy for plantar fasciitis.


More recent researchers such as Ingberg et al,47-51 Langevin et al,52-54 Schleip et al,55-57 Stecco et al,58-60 and others61,62 have suggested that fascial connective tissue may play a prominent role in a variety of myo­fascial pain syndromes. With needle grasp (a phenomenon in which the tissue surrounding the needle contracts, making it difficult to withdraw the needle, and observable as a tenting effect of the skin), there may be a mechanical coupling between the needle and the fascial connective tissue that may transmit a mechanical signal to the fascial connective tissue via mechanotransduction.52-54 This phenomenon may be enhanced by needle manipulation such as twisting or rotation. After two twirls of the needle, the fascia will adhere to the needle, producing tension on the fascia and mechanically stimulating the nervous system.

The fascia may significantly impact this mechanotransduction due to its ability to contract, similar to a smooth muscle contraction, meaning the fascia may be another contractile element (in addition to muscle) with the potential to effect symptomatic changes. This bioten- segrity of fascial tissue results in micro- and macro-changes. Needle placement may induce mechanical tension and chemical signaling, which may influence local biochemistry, including alkalizing the pH and reducing inflammatory mediators.31,38,39 This, in turn, may affect the neurophysiological responses of the nervous system at the dorsal horn and higher centers that may influence muscular resting tone, usually reducing it. These muscular tonal changes may affect the anatomical biomechanics of multiple regions through alterations in systemic tension and compressional loads.47-62 (Figure 2)

The idea that any treatment technique can directly change mechanotransduction and biotensegrity, influence local cellular changes by inducing a biomechanical effect on the arthrology and myology, and indirectly affect nervous system regulation of mechanoreceptors is new and not well studied. According to Stecco,58 restriction of specific anatomical locations in the fascia can influence human biomechanics. Stecco58 identified fascial congestion points that appear to result directly in plantar fascial symptoms. It is interesting that some of these points are located at, or proximate to, traditional acupuncture points. This may be one scientific explanation for the physiological mechanisms underlying acupuncture: specifically, the induction of mechanotransduction through needle placement within the fascial connective tissue. This would not be consistent with traditional acupuncture theory.63 The overlap of specific fascial points to acupuncture points is not discussed in the literature, however, the degree of overlap between trigger points and acupoints ranges from 18% to 70%.23,64-66

Of interest, referred pain sites from MTrPs may not be specific points but rather may be more reflective of a muscle in general.23,64-66 The lack of specific trigger point sites makes it difficult to correlate them with specific acupoints. Referred pain may be reflective of muscle or fascial tissue with segmentally linked innervation, either of which could result in a similar distribution of referred pain symptoms.

At present, the literature is in its infancy regarding fascial connective tissue and its direct and indirect influence on the biochemical, neurophysiological, and biomechanical systems of the human body. The histology, physiology, arthrology, myology, and neurology that govern human function may be interconnected components, any of which may affect tension and compression within the body. The expression of these forces, biotensegrity, may be a key component in understanding micro- and macropathophysiology. IMT may be one method by which to influence these reactions to make local and global changes in multiple body regions.47-62


There are limited methodologically sound randomized clinical trials measuring the effectiveness of dry needling for plantar fasciitis. There is limited evidence linking site-specific shared innervation tissue sites or distal site needle insertion techniques with improved plantar fasciitis symptoms. Despite this lack of evidence, many clinicians have championed the dramatic clinical results of IMT. Unfortunately, clinical observations provide only anecdotal evidence. It is clear that further research regarding IMT is required to more fully understand and appreciate this treatment procedure. The pathophysiological scientific rationale will continue to be debated until further evidence is provided.

Various concepts have been proposed, the most studied of which is the integrated trigger point hypothesis. IMT may affect SEA, endplate noise, ACh, pH, and other inflammatory factors, producing a clinical effect. A recent hypothesis involves the manipulation and/or stimulation of fascial planes at specific fascial points or locations in the human body, yet, to date, the author has not identified any studies linking outcomes to IMT performed at these fascial points. One could hypothesize multiple methods by which mechanotransduction might create temporary and lasting micro- and macropathophysio-anatomical changes in human biokinesiology in a closed biotensegrity system.

Applying this hypothesis via the mechanism of IMT to plantar fasciitis may be a paradigm shift in therapeutic treatment options. In the present literature, there is a lack of quality studies demonstrating IMT efficacy beyond the placebo effect, specifically for those with plantar fasciitis. Despite the lack of randomized clinical trials for IMT, there is mounting empirical, anecdotal, and clinical evidence that seem to support its clinical efficacy. Furthermore, studies have usually failed to address IMT dosage and procedural application or have done so using parameters that are varied and inconsistent. Further methodologically sound studies with consistent parameters for needle application should be conducted to validate IMT as a treatment option for plantar fasciitis.

Brent Harper, PT, DPT, DSc, OCS, FAAOMPT, is an assistant professor in the Department of Physical Therapy at Radford University in Radford, VA.

Disclosure: The author has received grant/research support from the Waldron College of Health and Human Services at Radford University.

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