part0034

In clinical practice, trigger point (TrP) release methods cover several manual therapies aimed at eliminating or inactivating TrPs. The latter are mainly described as hypersensitive spots in a taut band of a skeletal muscle painful on stimulation that elicit referred pain (Simons et al. 1999). TrP release methods include direct techniques such as massage, ischemic compression, TrP pressure release, or strain–counterstrain (Dommerholt & McEvoy 2010), and also indirect interventions, e.g. spray and stretch, passive stretching, muscle energy techniques (MET), neuromuscular approaches and/or myofascial induction. Direct techniques are those targeted at connective tissues related to the TrP by applying pressure directly over the TrP, whereas indirect techniques are those targeted at connective tissues related to the taut band and surrounding tissues, including fascia (Dommerholt & McEvoy 2010). An alternative release method is TrP dry needling (TrP-DN; Dommerholt & Fernández-de-las-Peñas 2013). This technique inserts acupuncture filiform and fine needles into the TrP area with the aim of inactivating the TrP. All TrP release methods are complementary because they usually act on different connective tissue levels, including the taut band, TrP area, muscle tissue, and surrounding fascia. In fact, clinicians usually combine different TrP release methods in the same session into a multimodal treatment approach.

Throughout history TrPs have been referred to by different names (myogelosis, fibrositis, etc.). Although various definitions of TrPs are used among different disciplines, the most commonly accepted definition maintains that ‘TrPs are hypersensitive spots in a taut band of a skeletal muscle that are painful on compression, stretch, overload or contraction of the tissue which respond with a referred pain’ (Simons et al. 1999). Based on their clinical experience, different authors have modified TrP release methods (Simons et al. 1999, Chaitow 2007, Fernández-de-las-Peñas et al. 2011). Different TrP release methods, depending on the amount of pressure applied, presence/absence of pain, duration of the application, position of the tissue (shortened or lengthened), or presence/absence of active contraction of the affected (agonist) or surrounding (antagonist) tissues, are clinically proposed for TrP treatment (Fernández-de-las-Peñas & Pilat 2011).

• Finally, recent theories also include mechanisms to the surrounding fascial tissue as it is suggested that TrP release methods, including TrP-DN, can change viscoelastic properties or behavior of the fascial tissue (Langevin 2013). The interaction between TrPs and fascia is based on the premise that muscle perimysium has a high density of myofibroblasts, a common cell found in connective tissue (Schleip et al. 2005), and the role of hyaluronanic acid in myofascial pain (Stecco et al. 2011).

Some systematic reviews have found moderate evidence supporting the use of some TrP release methods for immediate pain relief of TrPs (Vernon & Schneider 2009, Gay et al. 2013) and limited evidence for long-term pain relief; however, it is difficult to draw any clinical conclusion since most studies have investigated single modalities, whereas multimodal approaches are usually used by clinicians. More recent studies have reported that the integration of TrP release methods, including TrP-DN, within multimodal manual therapy programs is effective for some chronic pain conditions such as plantar heel pain, ankle sprain, fibromyalgia syndrome, neck pain, migraine, etc. Future studies are needed to determine the efficacy of TrP release methods included in a biopsychosocial treatment of chronic pain. For instance, it has been observed that a combination of TrP-DN and neuroscience education was more effective than TrP-DN alone for the management of low back pain (Téllez-García et al. 2015).

Rather than explaining TrP as a local pathological/anatomical muscle problem, current theories focus on the nociceptive nature of TrPs and their role in perpetuating sensitization mechanisms. The clinical aims of any TrP release method are the inactivation of muscle-associated sensory and motor symptoms and the decrease of nociceptive barrage to the CNS (Fernández-de-las-Peñas et al. 2011). TrP release methods are applied by numerous healthcare professionals, including osteopaths, physicians, chiropractics, physical therapists, dentists, or massage therapists, among others, dependent upon the country and local jurisdictional regulations.

All TrP release methods aim to inactivate active TrPs. The first step in the clinical reasoning process to determine which TrP release method should be used, is the accurate diagnosis of a TrP. In fact, correct TrP diagnosis requires manual ability, training and clinical practice to develop a high degree of reliability in the clinical examination. Typical signs and symptoms include: 1) presence of a hyperirritable spot in a palpable taut band in a skeletal muscle (when accessible to palpation); 2) palpable local twitch response on snapping palpation or DN of the TrP area (when possible); and 3) presence of referred pain elicited by stimulation of the TrP. Additional helpful signs for the diagnosis include muscle weakness, pain on contraction, pain on stretching, a jump sign, autonomic phenomena or motor disturbances (Simons et al. 1999). Although Gerwin et al. (1997) concluded that some muscles are more reliably examined than others, there is no general consensus on the reliability of TrP diagnosis.

TrPs are mainly identified through manual palpation. Clinicians can use either a flat palpation where the finger or thumb presses the muscle against underlying bone tissue, or a pincer palpation in which a particular muscle is palpated between the clinician’s fingers. Taut band can be identified by palpating perpendicular to the fiber direction, which can elicit a local twitch response (strumming palpation). Once the taut band is located, the clinician moves along the taut band to find a discrete area of intense pain and, sometimes, hardness, which will elicit referred pain.

Once the clinician has localized the TrP, the intervention will depend on the irritability of the tissue, the accessibility of the muscle, and the symptoms. For instance, in patients with higher levels of pain and irritability, the clinician can choose indirect release methods targeting the taut band (e.g. longitudinal strokes or myofascial induction) or pain-free compression methods (e.g. TrP pressure release or strain–counterstrain). In such a patient, the application of TrP-DN may not be the first choice because of the DN-related pain. On the contrary, in patients with lower irritability of the CNS, TrP-DN can be the first therapeutic option, or compression interventions at the pain threshold level applied over the TrP. Nevertheless, clinicians should use a biopsychosocial clinical reasoning to determine which TrP release method is the most suitable for a particular patient.

Any therapeutic intervention should be evidence-informed and based on scientific evidence, clinicians’ judgments, expertise and clinical decision-making (Dommerholt 2012). It is difficult to determine the exact therapeutic mechanism involved in TrP release methods since mechanical and neurophysiological mechanisms are involved at the same time. In fact, TrP release methods are complementary since they can act at different tissue levels including taut band, TrP region, muscle tissue, and surrounding fascia. The therapeutic aim of TrP release methods is to stop the vicious cycle of the evidence-informed integrated TrP hypothesis (Simons et al. 1999). The updated version of this etiological hypothesis is the most comprehensive framework currently available to explain the TrP formation and to guide the therapeutic management (Gerwin et al. 2004). According to this hypothesis, any TrP release method should focus on decreasing TrP-related symptoms by reversing the observed hypoxia and low pH, and by decreasing the excitability of the muscle nociceptors.

• From a mechanical viewpoint, it has been proposed that TrP release methods that compress the muscle in a vertical or perpendicular manner equalize the length of the muscle sarcomeres. This effect would be increased if the muscle contracts at the same time (Fernández-de-las-Peñas et al. 2011). Either TrP release intervention can be applied along or across the TrP taut band. By applying these interventions, clinicians will exert transverse or longitudinal mobilization to the taut band and surrounding fascia.

• The activation of the gate control is elicited by stimulation of αδ-sensory afferent fibers by the nociceptive mechanical stimulation induced by the TrP release intervention. This activation provokes segmental nociceptive effects over the TrP (Fernández-de-las-Peñas et al. 2011). In fact, current evidence supports that TrP release methods show a localized hypoalgesic effect, by increasing pressure pain thresholds, when compared with no-treatment and sham/inert groups, and their effects are comparable with those of other active treatments (Gay et al. 2013).

• The segmental anti-nociceptive effect is based on the premise that active TrPs are a source of peripheral nociception since the concentrations of bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor-α, interleukins 1β, IL-6 and IL-8, serotonin and norepinephrine were significantly higher near active TrPs than near latent TrP or non-TrP points (Shah et al. 2008). It is not known whether the therapeutic effects of all the TrP release methods, particularly the reduction in referred pain, are related to a reduction of nociceptive afferences to the dorsal horn neurons.

• It is known that TrP-DN reduces segmental nociceptive input (Srbely et al. 2010). In fact, although no study has investigated the effect of TrP-DN in activation of cortical areas, there is evidence suggesting that the insertion of a needle into acupuncture and non-acupuncture points involves the activation of the limbic system and the descending inhibitory pathways (Dommerholt & Fernández-de-las-Peñas 2013). This hypothesis is partly supported by a study where a single application of TrP-DN decreased widespread pressure pain sensitivity, a clinical manifestation of central sensitization, in patients with acute neck pain (Mejuto-Váquez et al. 2014).

Various TrP release methods can be used in clinical practice depending on the patient’s features and clinical experience. They differ in the amount of pressure used, presence/absence of pain, duration of the technique, position of the tissues and employment, or not, of active contraction (Fernández-de-las-Peñas et al. 2011, Fernández-de-las-Peñas & Pilat 2011). Several systematic reviews investigating the effectiveness of TrP release methods (Vernon & Schneider 2009, Gay et al. 2013) and DN (Furlan et al. 2005, Gattie et al. 2017) have been published. The conclusion in relation to manual release methods is that there is evidence supporting their use for short-term relief but not for medium- and long-term follow-ups. The effectiveness of TrP-DN is still controversial although one Cochrane Review found evidence for its use in patients with low back pain (Furlan et al. 2005) and a recent review and meta-analysis concluded that TrP-DN performed by physical therapists is more effective than a no-treatment control or sham dry needling for reducing pain (Gattie et al. 2017). Future studies including long-term follow-ups are clearly needed. Nevertheless, it is difficult to draw clinical conclusions from current evidence since most studies investigated TrP release methods or DN as single modalities, whereas multimodal manual therapy approaches are practiced by clinicians. In fact, current research supports that pain is produced by the brain when there is a perception of bodily danger requiring specific action. Therefore, consideration of the patient’s overall situation is critical for a therapeutic approach. The effects of TrP release methods including TrP-DN cannot be considered independently of the biopsychosocial model and must be approached from a pain science perspective, as it is no longer sufficient to consider any TrP release method strictly as a tool to address local muscle pathology (Dommerholt & Fernández-de-las-Peñas 2013).

• In this particular approach, longitudinal strokes (glides, slides) are performed over the taut band containing TrPs. The strokes are generally applied with the thumb ( Fig. 21.1B ), elbows or knuckles. In muscles where taut bands can be grasped with pincer palpation, the strokes can be applied with a pincer grip ( Fig. 21.1C ). Again, the degree of pressure and the speed of gliding will depend on the irritability and tone of the tissue. In the author’s clinical experience the best result comes from repetitive, deep and slow strokes (6–10 times) over the affected tissue.

Figure 21.1

Different trigger point (TrP) release methods. (A) Ischemic compression intervention targeted at infraspinatus TrPs. (B) Longitudinal stroke along the taut band over paraspinal muscle TrPs. (C) Centrifugally longitudinal stroke with a pincer palpation along the taut band on the sternocleidomastoid muscle TrPs. (D) Dynamic intervention: longitudinal stroke along the taut band of extensor wrist muscle TrPs as the patient simultaneously and actively extends the wrist

• MET involve the accurate localization of forces to the muscle barrier (first sign of resistance of the taut band), a sub-maximal isometric contraction of the muscle against an unyielding counterforce supplied by the therapist, followed by patient relaxation and engagement of a new tissue barrier, or stretching past the previous barrier. The force and duration of the isometric contraction will adapt to the irritability of the tissues ranging from 3 to 9 seconds (see Ch. 12 ).

Exercise

The clinician, following a clinical reasoning based on the clinical history of the patient, suspects the presence of a TrP in the right sternocleidomastoid muscle. The patient suffers from unilateral headaches located over the temple and the orbit.

The clinician palpates the right sternocleidomastoid muscle with a pincer palpation all along the muscle searching for the presence of active TrPs. During the examination, the muscle exhibits two painful points in the muscle belly.

One of these points elicits referred pain to the head at 6 seconds on compression by the therapist. This referred pain reproduces the headache of the patient (i.e. it is an active TrP). The other point does not refer pain, there is only local pain and tenderness on palpation.

The clinician decides to treat the active TrP with manual release methods. The first attempt would be the application of an ischemic compression technique. The muscle is grasped with a pincer palpation over the TrP and the clinician compresses the muscle until moderate pain appears. The compression is maintained at this level of pressure.

After 15 seconds of compression the patient comments that the compression elicits referred pain to the head and is highly uncomfortable. The clinician decides to reduce the intensity of the intervention, and to maintain the compression level at the tissue resistance (i.e. TrP pressure release).

Therefore, the compression is maintained at the tissue resistance level, which is mainly asymptomatic for the patient.

After 20 seconds, the tissue resistance eases and the clinician again increases the level of compression until the next tissue barrier is reached. This procedure is repeated 3–4 times.

After the compression intervention, manual palpation of the TrP does not elicit referred pain but the right sternocleidomastoid muscle is still tender and slightly painful because of the TrP taut band. The clinician then decides to apply a longitudinal stroke along the taut band away from the TrP.

The clinician grasps the muscle with a pincer palpation at the TrP area with both hands. The pressure should be applied at the tissue resistance for 5–10 seconds.

At this moment, a longitudinal stroke along the taut band is applied centrifugally away from the TrP. The speed of the stroke is gentle and smooth at the tissue barrier level. This procedure can be repeated 3–4 times.

	Muscle position	Degree of compression	Time of pressure	Duration of the technique
Ischemic compression	Fully lengthened	Sufficient to induce moderate pain between 3 and 6–7 (where 10 is maximum)	Until pain decreases by around 50–75%	Up to 90 seconds
TrP pressure release	Partially lengthened or neutral	Usually pain-free (first perception of tissue barrier)	Until the therapist perceives TrP or taut band release	Up to 90 seconds
Strain– counterstrain	Neurologically silent (usually shortened)	Reduction of pain by around 70–80%	Constant throughout	90 seconds
Pulsed ischemic compression	Neutral or at the ‘first sign of resistance’ barrier, i.e. no lengthening	5 seconds compression to induce pain at level 5–6 followed by 3 seconds no pressure – repeated until local or referred pain change or reduction in tissue resistance	5 seconds pressure, 3 seconds no pressure, repeated	Up to 90 seconds – or until change in pain is reported, or taut band release perceived
NPRS: Numerical Pain Rate Scale (0–10).