Myofascial pain syndromes from trigger points

Myofascial pain syndrome (MPS) is a common cause of acute and chronic pain that can complicate other medical illnesses and injuries. It is both defined by and diagnosed by the presence of the myofascial trigger point. Current studies indicate that the trigger point is a dysfunctional motor end plate whose abnormal activity is modulated in some way by the sympathetic nervous system. Pain syndromes arise from trigger points as causes of local pain and of referred pain. Referred pain from a few or from many muscle trigger points produces regional or generalized pain. Treatment requires the elimination of the trigger point by manual therapy or by trigger point injection and correction of the mechanical and medical factors that initiate and perpetuate it.     

Myofascial trigger points in early life

OBJECTIVE: To determine whether latent myofascial trigger points (MTPs) can be identified in healthy infants and in healthy adult subjects. DESIGN: Blind comparison. SETTING: Ambulatory. PARTICIPANTS: A convenience sample of 60 healthy adults and 60 infants (age range, 0-12mo). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: An algometer was used to measure the pressure pain threshold (PPT) on 3 different sites, including a midpoint (assumed to be the MTP site) in the brachioradialis muscle. RESULTS: The mean PPT values at the MTP site were significantly lower than the other sites in the adult muscles. However, no significant differences in PPT values among these 3 sites were found in the infants. Taut bands were found in all the adult muscles but none in the infants. CONCLUSIONS: In the adult subjects, the midpoint of brachioradialis muscle was significantly more irritable than other sites and the midpoint was probably a latent MTP. However, in the infants younger than 1 year old, such a phenomenon could not be observed in this study. It is very likely that the latent MTPs might not exist in early life, but develop in later life.     

Myofascial trigger points in persistent posttraumatic shoulder pain

Persistent pain and disability after injuries to the shoulder sometimes create a difficult diagnostic and therapeutic problem. In many such cases, myofascial trigger points seem to cause symptoms. Three cases in which pain had persisted for eight to 33 months after injury illustrate the manifestations of posttraumatic myofascial trigger point disorders. Trigger points are located by finding discrete foci of tenderness in muscles. Trigger points may be palpably firmer than surrounding muscle, forming nodules; they may twitch in response to palpation and may refer pain to a specific area when stimulated. Failure to recognize the myofascial source of pain can lead to erroneous diagnoses of articular, neurologic, or emotional disorder. Current pathophysiologic theories about trigger points may explain the persistence and topographic spreading of pain after muscular injuries. Appropriate treatment of myofascial trigger points can relieve chronic pain and disability.     

Myofascial trigger points in the suboccipital muscles in episodic tension-type headache

Referred pain evoked by suboccipital muscle trigger points (TrPs) spreads to the side of the head over the occipital and temporal bones and is usually perceived as bilateral headache. This paper describes the presence of referred pain from suboccipital muscle TrPs in subjects with episodic tension-type headache (ETTH) and in healthy controls. Ten patients presenting with ETTH and 10 matched controls without headache were examined by a blinded assessor for the presence of suboccipital muscle TrPs. Diagnostic criteria described by Simons and Gerwin were adapted to diagnose TrPs, i.e. presence of tenderness in the suboccipital region, referred pain evoked by maintained pressure for 10 s, and increased referred pain on muscle contraction. Six ETTH patients (60%) had active TrPs and 4 had latent TrPs (40%). On the other hand, 2 control subjects also had latent TrPs. Differences in the presence of suboccipital muscle TrPs between both groups were significant for active TrPs (P<0.001), but not for latent TrPs. Active TrPs were only present in ETTH patients, although TrP activity was not related to any clinical variable concerning the intensity and the temporal profile of headache. Myofascial TrPs in the suboccipital muscles might contribute to the origin and/or maintenance of headache, but a comprehensive knowledge of the role of these muscles in tension-type headache awaits further research.     

Myofascial trigger points, neck mobility and forward head posture in unilateral migraine

This paper describes the differences in the presence of myofascial trigger points (TrPs) in the upper trapezius, sternocleidomastoid, temporalis and suboccipital muscles between unilateral migraine subjects and healthy controls, and the differences in the presence of TrPs between the symptomatic side and the non-symptomatic side in migraine subjects. In addition, we assess the differences in the presence of both forward head posture (FHP) and active neck mobility between migraine subjects and healthy controls and the relationship between FHP and neck mobility. Twenty subjects with unilateral migraine without side-shift and 20 matched controls participated. TrPs were identified when there was a hypersensible tender spot in a palpable taut band, local twitch response elicited by the snapping palpation of the taut band and reproduction of the referred pain typical of each TrP. Side-view pictures were taken in both sitting and standing positions to measure the cranio-vertebral angle. A cervical goniometer was employed to measure neck mobility. Migraine subjects showed a significantly greater number of active TrPs (P<0.001), but not latent TrPs, than healthy controls. Active TrPs were mostly located ipsilateral to migraine headaches (P<0.01). Migraine subjects showed a smaller cranio-vertebral angle than controls (P<0.001), thus presenting a greater FHP. Neck mobility in migraine subjects was less than in controls only for extension (P=0.02) and the total range of motion in flexion/extension (P=0.01). However, there was a positive correlation between the cranio-vertebral angle and neck mobility. Nociceptive inputs from TrPs in head and neck muscles may produce continuous afferent bombardment of the trigeminal nerve nucleus caudalis and, thence, activation of the trigeminovascular system. Active TrPs located ipsilateral to migraine headaches might be a contributing factor in the initiation or perpetuation of migraine.     

Myofascial trigger points and sensitization: an updated pain model for tension-type headache

Present pain models for tension-type headache suggest that nociceptive inputs from peripheral tender muscles can lead to central sensitization and chronic tension-type headache (CTTH) conditions. Such models support that possible peripheral mechanisms leading to pericranial tenderness include activation or sensitization of nociceptive nerve endings by liberation of chemical mediators (bradikinin, serotonin, substance P). However, a study has found that non-specific tender points in CTTH subjects were not responsible for liberation of algogenic substances in the periphery. Assuming that liberation of algogenic substances is important, the question arising is: if tender muscle points are not the primary sites of on-going neurogenic inflammation, which structure can be responsible for liberation of chemical mediators in the periphery? A recent study has found higher levels of algogenic substances, and lower pH levels, in active myofascial trigger point (TrPs) compared with control tender points. Clinical studies have demonstrated that referred pain elicited by head and neck muscles contribute to head pain patterns in CTTH. Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles. In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH.     

Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache

OBJECTIVE: To assess the presence of trigger points (TrPs) in several head and neck muscles in subjects with chronic tension-type headache (CTTH) and in healthy subjects; and to evaluate the relationship of these TrPs with forward head posture (FHP), headache intensity, duration, and frequency. BACKGROUND: Tension-type headache (TTH) is a headache in which myofascial TrPs in head and neck muscles might play an important etiologic role. DESIGN: A blinded, controlled, pilot study. METHODS: Twenty-five CTTH subjects and 25 matched controls without headache were studied. TrPs in bilateral upper trapezius, sternocleidomastoids, and temporalis muscles were identified according to Simons et al's diagnostic criteria: tenderness in a hyperirritable spot within a palpable taut band, local twitch response elicited by snapping palpation, and elicited referred pain with palpation. A TrP was considered active if the subject recognized the evoked referred pain as familiar headache. If the evoked referred pain was not recognized as familiar headache, the TrP was considered as latent. Side-view pictures of each subject were taken in both sitting and standing positions in order to assess FHP by measuring the cranio-vertebral angle. Both measurements were made by a blinded assessor. A headache diary was kept for 4 weeks in order to assess headache intensity, frequency, and duration. RESULTS: The mean number of TrPs on each CTTH subject was 3.9 (SD: 1.2), of which 1.9 (SD: 1.2) were active TrPs and 1.9 (SD: 0.8) were latent TrPs. Control subjects only exhibited latent TrPs (mean: 1.4; SD: 0.8). There was a significant difference between the CTTH group and the controls for active TrPs (P < .001), but not for latent TrPs (P > .05). Differences in the distribution of active and latent TrPs within each muscle were also significant for all the analyzed muscles (P < .01). CTTH subjects with active TrPs in the right upper trapezius muscle or left sternocleidomastoid muscle showed a greater headache intensity and duration, but not headache frequency, compared to those with latent TrPs (P < .05). Active TrPs in the right temporalis muscle were associated with longer headache duration (P < .01), whereas active TrPs in the left temporalis muscle were associated with greater headache intensity (P < .05). CTTH subjects with active TrPs in the analyzed muscles had a greater FHP than those with latent TrPs in both sitting and standing positions. Differences were only significant for TrPs in the left sternocleidomastoid and FHP in the sitting position (P < .01). CONCLUSIONS: Active TrPs in upper trapezius, sternocleidomastoid, and temporalis muscles were associated with CTTH. CTTH subjects with active TrPs usually reported a greater headache intensity and longer headache duration than those with latent TrPs. CTTH subjects with active TrPs tended to have a greater FHP than CTTH subjects with latent TrPs.     

Myofascial trigger points, neck mobility, and forward head posture in episodic tension-type headache

OBJECTIVE: To assess the differences in the presence of trigger points (TrPs) in head and neck muscles, forward head posture (FHP) and neck mobility between episodic tension-type headache (ETTH) subjects and healthy controls. In addition, we assess the relationship between these muscle TrPs, FHP, neck mobility, and several clinical variables concerning the intensity and the temporal profile of headache. BACKGROUND: TTH is a headache in which musculoskeletal disorders of the craniocervical region might play an important role in its pathogenesis. Design.-A blinded, controlled pilot study. METHODS: Fifteen ETTH subjects and 15 matched controls without headache were studied. TrPs in both upper trapezius, both sternocleidomastoids, and both temporalis muscles were identified according to Simons and Gerwin diagnostic criteria (tenderness in a hypersensible spot within a palpable taut band, local twitch response elicited by snapping palpation, and elicited referred pain with palpation). Side-view pictures of each subject were taken in both sitting and standing positions, in order to assess FHP by measuring the craniovertebral angle. A cervical goniometer was employed to measure neck mobility. All measures were taken by a blinded assessor. A headache diary was kept for 4 weeks in order to assess headache intensity, frequency, and duration. RESULTS: The mean number of TrPs for each ETTH subject was 3.7 (SD: 1.3), of which 1.9 (SD: 0.9) were active, and 1.8 (SD: 0.9) were latent. Control subjects only had latent TrPs (mean: 1.5; SD: 1). TrP occurrence between the 2 groups was significantly different for active TrPs (P < .001), but not for latent TrPs (P > .05). Differences in the distribution of TrPs were significant for the right upper trapezius muscles (P= .04), the left sternocleidomastoid (P= .03), and both temporalis muscles (P < .001). Within the ETTH group, headache intensity, frequency, and duration outcomes did not differ depending on TrP activity, whether the TrP was active or latent. The craniovertebral angle was smaller, ie, there was a greater FHP, in ETTH patients than in healthy controls for both sitting and standing positions (P < .05). ETTH subjects with active TrPs in the analyzed muscles had a greater FHP than those with latent TrPs in both sitting and standing positions, though differences were only significant for certain muscles. Finally, ETTH patients also showed lesser neck mobility than healthy controls in the total range of motion as well as in half-cycles (except for cervical extension), although neck mobility did not seem to influence headache parameters. CONCLUSIONS: Active TrPs in the upper trapezius, sternocleidomastoid, and temporalis muscles were more common in ETTH subjects than in healthy controls, although TrP activity was not related to any clinical variable concerning the intensity and the temporal profile of headache. ETTH patients showed greater FHP and lesser neck mobility than healthy controls, although both disorders were not correlated with headache parameters.     

Myofascial trigger points in subjects presenting with mechanical neck pain: a blinded, controlled study

The aim of this study was to describe the differences in the presence of myofascial trigger points (TrPs) in the upper trapezius,sternocleidomastoid, levator scapulae and suboccipital muscles between patients presenting with mechanical neck pain and control healthy subjects. Twenty subjects with mechanical neck pain and 20 matched healthy controls participated in this study. TrPs were identified, by an assessor blinded to the subjects' condition, when there was a hypersensible tender spot in a palpable taut band, local twitch response elicited by the snapping palpation of the taut band, and reproduction of the referred pain typical of each TrP. The mean number of TrPs present on each neck pain patient was 4.3 (SD: 0.9), of which 2.5 (SD: 1.3) were latent and 1.8 (SD: 0.8) were active TrPs. Control subjects also exhibited TrPs (mean: 2; SD: 0.8). All were latent TrPs. Differences in the number of TrPs between both study groups were significant for active TrPs (P < 0.001), but not for latent TrPs (P > 0.5). Moreover, differences in the distribution of TrPs within the analysed cervical muscles were also significant (P < 0.01) for all muscles except for both levators capulae. All the examined muscles evoked referred pain patterns contributing to patients' symptoms. Active TrPs were more frequent in patients presenting with mechanical neck pain than in healthy subjects.     

Myofascial trigger points are very prevalent in patients with chronic tension-type headache: a double-blinded controlled study

OBJECTIVES: Myofascial pain syndromes due to trigger points (TrPs) are clinical entities, but more evidence is needed to evaluate TrP palpation. Chronic tension-type headache (CTTH) is the most prevalent chronic headache with high socioeconomic costs. The primary aim was to study whether TrP palpation can distinguish patients with headache patients from healthy controls. DESIGN: Double-blinded, controlled design. PATIENTS: Twenty patients with the diagnosis of CTTH, and 20 healthy age-matched and sex-matched control participants. RESULTS: TrP palpation revealed more TrPs in patients (N=17) versus controls (N=6) (P=0.0005). Referred pain was also more frequent in patients (N=17) versus controls (N=9) (P=0.04). Further, TrP palpation also identified a higher pain intensity than at a control point (CtP) in both groups (P=0.0001). Pain intensity at TrPs in patients was higher than in controls (P=0.0010), and CtPs were also more tender in patients than in controls (P=0.0167). For spontaneous electromyographic activity no difference between TrPs versus CtPs within or between groups could be detected. CONCLUSIONS: These findings suggest that active TrPs are much more frequent in CTTH than in controls and the number and pain intensity of TrPs may be used to distinguish between the 2 groups. Spontaneous electromyographic activity could not be demonstrated, and the underlying biology of TrPs is still unclear.     

Myofascial trigger point syndromes: an approach to management

The treatment of myofascial trigger point (TP) pain syndromes is not difficult once the source of the problem has been determined. Whereas many modalities may be used, two of the most effective are spray-and-stretch and TP injection. These can be followed by deep massage, specific, manual resistive exercises, and an exercise program which the patient can follow at home. The goal of management is to inactivate the TPs and to restore shortened and stretch resistant muscles to their full range of motion. A number of such syndromes are discussed in terms of recognition and management.     

Differences between myofascial trigger points and tender points

The article describes and compares the characteristics of myofascial trigger points (MTrPs) of the myofascial pain syndrome and the tender points (TePs) of the fibromyalgia syndrome. Many statements are hypothetical, because not all aspects of the disorders have been clarified in solid studies. Signs and symptoms of MTrPs: (1) palpable nodule, often located close to the muscle belly, (2) often single, (3) allodynia and hyperalgesia at the MTrP, (4) referral of the MTrP pain, (5) normal pain sensitivity outside the MTrPs, (6) local twitch response, (7) local contracture in biopsy material, (8) peripheral mechanism probable. Signs and symptoms of TePs: (1) no palpable nodule, (2) location often close to the muscle attachments, (3) multiple by definition, (4) allodynia and hyperalgesia also outside the TePs, (5) enhanced pain under psychic stress, (6) unspecific histological changes in biopsy material, (7) central nervous mechanism probable. The multitude of differences speak against a common aetiology and pathophysiology.     

Documentation of myofascial trigger points

Two basic diagnostic features of myofascial trigger points (TPs), namely, local tenderness and alteration of tissue consistency (such as in taut bands, muscle spasm), can be documented quantitatively by simple hand-held instruments. A pressure threshold meter (algometer) assists in location of TPs and their relative sensitivity. A side-to-side difference exceeding 2kg in comparison with normal values indicates pathologic tenderness. The effect of treatment can be quantified. Pressure tolerance, measured over normal muscles and shin bones, expresses pain sensitivity. Myopathy is suspected if muscle tolerance drops below bone tolerance. Tissue compliance measurement documents objectively and quantitatively alteration in soft tissue consistency. Muscle spasm, tension, spasticity, taut bands, scar tissues, or fibrositic nodules can be documented. The universal clinical dynamometer is used as part of a physical examination to quantify weakness. Thermography (heat imaging) demonstrates discoid shaped hot spots over TPs. Muscle activity, spasm, or contraction is visualized as increased heat emission in the shape of the active muscle.     

Thermographic imaging of myofascial trigger points

Thermographic findings in two patients suffering from myofascial trigger points are presented. These are shown as discrete foci of increased thermal emission, with corresponding areas of diffuse hyperthermia. These thermal findings correlate highly with the classic locations of specific trigger points and their areas of pain referral, respectively, as described in literature. Not only do these cases describe a thermal pattern that varies somewhat from previous reports, but they also illustrate the previously unreported imaging of areas of pain referral from specific trigger points.     

Understanding effective treatments of myofascial trigger points

This article considers specific treatment approaches and the role of etiological mechanisms in terms of clinical feature characteristics of MTrPs: increased muscle tension, pain and tenderness, painful stretch range of motion, initiating causes of MTrPs. Final sections note additional treatments that are currently used, and summarize the etiological and clinical distinctions between MTrPs and fibromyalgia.     

Effect of helium-neon laser on musculoskeletal trigger points

Cold lasers have been proposed recently as a therapeutic tool for treating a wide variety of pathological conditions, including wounds, arthritis, orthopedic problems, and pain. These proposed therapeutic effects largely have been unsubstantiated by research. A randomized, double blind study was undertaken to ascertain the effect of a helium-neon (He-Ne) laser on the resistance of areas of skin overlying musculoskeletal trigger points. These areas usually demonstrate decreased skin resistance when compared with the surrounding tissue. Thirty patients with musculoskeletal trigger points were assigned randomly to either an experimental or a placebo group. In addition to standard physical therapy, each patient received three 15-second applications of a He-Ne laser or placebo "stimulation" from an identical unit that did not emit a laser. The results of a two-way analysis of covariance with one repeated measure showed a statistically significant increase (p less than .007) in skin resistance. This increase in an abnormal skin resistance pattern may accompany the resolution of pathological conditions.