Myofascial trigger points in migraine and tension-type headache

Different ultrasound modalities in ultrasound imaging have visualized MTrPs. Lewis et al. [28] conducted a pilot study to assess the use of ultrasound in determining soft tissue changes in the region of active MTrPs in 11 subjects. They found no correlation between clinical identified active MTrPs and ultrasound. In contrast, Turo et al. [29] were able to differentiate between symptomatic MTrPs and asymptomatic muscle tissue with texture-based analysis. Sikdar et al. investigated the stiffness of active and latent MTrPs, using ultrasound elastography by Doppler variance imaging in nine subjects while inducing vibrations with an external handheld massage vibrator [27]. MTrPs appeared as focal, hypoechoic regions on two-dimensional ultrasound images and with reduced vibration amplitude, indicating increased stiffness. Furthermore, they describe hypoechoic regions that were not identified during palpation prior to ultrasound. In another study by the same group, MTrPs showed reduced vibration amplitude on elastography indicating increased stiffness and distinct blood flow waveform patterns [30]. Ballyns et al. [31] used elastography to investigate MTrPs in 44 subjects with acute cervical pain. They were able to measure the size and distinguish type (active, latent) of MTrPs with elastography. In addition, Doppler waveforms of blood flow showed different characteristics in active sites compared to normal tissue. Takla et al. [32] compared elastography with two-dimensional grayscale ultrasound in identifying MTrPs. They found that MTrPs had an accuracy of 100% for both active and latent MTrPs while two-dimensional grayscale ultrasound could only identify 33 and 35%, respectively.

Microdialysis has been used to measure endogenous and exogenous molecules in the local milieu of MTrPs. Shah et al. [25] used microdialysis to investigate subjects with active or latent MTrP, and controls without MTrP were detected by manual palpation by two experienced clinicians. The authors measured selected substances (pH, bradykinin (BK), CGRP, SP, tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), interleukin 8 (IL-8), serotonin, and norepinephrine (NE)) in standardized locations of the trapezius muscle and gastrocnemius muscle. Subjects with active MTrPs in the trapezius muscle showed increased concentrations of all substances compared to the other groups. Shah et al. [26] found similar results in the trapezius muscle of subjects with neck pain and active MTrP compared to a group with neck pain and no MTrP present and healthy controls. The results showed that the active MTrP group had higher concentrations of BK, CGRP, SP, TNF-α, IL-1β, serotonin, NE.

Electromyography (EMG) can be used to measure the electrical activity of skeletal muscles. Simons et al. compared the prevalence of motor endplate potentials in active MTrPs, endplate zones, and taut bands of skeletal muscles in subjects with palpable MTrPs [33]. The authors found that endplate noise was more common in MTrPs than in sites outside of the trigger point, even within the same endplate zone. Ge et al. evaluated intramuscular muscle activity in a synergistic muscle during isometric contraction in 15 subjects with latent MTrPs [34]. The needle was inserted into a latent MTrP or a non-MTrP in the upper trapezius at rest and during contraction. The EMG activities were recorded from the middle deltoid muscle and the upper, middle, and lower parts of the trapezius muscle. The intramuscular EMG activity in the upper trapezius muscle was significantly higher at rest and during contraction at latent MTrPs compared with non-MTrPs. Yu et al. measured maximum voluntary isometric contraction, endurance, median frequency, and muscle fatigue index in three groups of participants: an active MTrP group, a latent MTrP group, and a control group [35]. The active MTrP group had a higher median frequency and muscle fatigue index than the control group. Wytrążek et al. compared the EMG activity of muscle motor units at rest and maximal contraction with surface EMG recordings [36]. The results showed MTrPs correlated with an increase in EMG amplitude at rest.

Infrared thermography can be used to measure the skin temperature. Dibai-Filho et al. [37] have reviewed the literature on infrared thermography investigations of MTrPs. The authors included three comparative studies [38‐40] and one accuracy study [41]. The conclusion of the review is that the included studies do not agree on skin temperature patterns in the presence of MTrPs. The included studies of the review are briefly presented in the following. Merla et al. [38] found that individuals with myofascial pain had a greater difference between the right and left side in skin temperature over the masseter and sternocleidomastoid muscles before and after maximal voluntary clenching compared to healthy volunteers. They also found that the myofascial pain group had a greater temperature change over the measured muscles after maximum voluntary clenching. Kimura et al. [39] evaluated the vasoconstrictor response after provoking pain in MTrPs with an intramuscular glutamate injection. Furthermore, they activated the sympathetic outflow by using a breath-holding maneuver. They found a decrease in skin temperature over time in latent MTrPs. In contrast, Zhang et al. [40] did not find that the skin temperature was affected following an intramuscular glutamate injection into latent MTrPs. Haddad et al. [41] compared infrared thermography and algometer measurements of MTrPs in the masticatory muscles. The authors found a positive correlation between skin surface temperature and pressure pain threshold. Regarding diagnosing MTrPs, infrared thermography had an accuracy of 0.564 to 0.609 (area under the receiver operating characteristic curve).

Chen et al. [42] examined 65 patients with myofascial pain-associated taut bands using magnetic resonance elastography. They found that agreement between physicians and imaging raters were relatively poor (63%; 95% CI, 50%–75%), but that these bands could be assessed quantitatively using magnetic resonance elastography. The authors suggest that clinicians might overestimate while magnetic resonance elastography may underestimate MTrPs.

Several studies have demonstrated a high occurrence of active and latent MTrPs in migraine patients [45‐49]. Studies show that there is a significantly higher prevalence of active MTrPs in migraine patients compared to healthy controls [45, 46, 58]. There are conflicting results in which muscles are the most affected [47, 48]. Fernández-de-Las-Peñas et al. [46] observed that active MTrPs were most prevalent ipsilateral to the migraine headaches. More unclear is whether the amount of MTrPs is correlated with the frequency and intensity of headache attacks. Calandre et al. [45] found a positive correlation between the number of MTrPs and frequency and duration of migraine attacks, whereas two studies by Ferracini et al. [47, 48] found no such correlation. Interestingly, Landgraf et al. [54] could visualize MTrPs on MR imaging as focal signal alterations in a small pilot study.

There appears to be an association between neck mobility and MTrPs [46, 48, 49, 58]. Ferracini et al. [48] found that a higher number of active MTrPs was positively correlated with a reduction in cervical lordosis and head extension of the head on the neck. In addition, that lower cervical angles were correlated higher then the number of active MTrPs. Florencio et al. [49] hypothesized that active MTrPs in the cervical musculature alters the activity of the related muscles and that this would be reflected in EMG readings. They observed that the presence of active MTrPs in the cervical musculature had different activation in the neck flexor muscles compared to those without active MTrPs in the same muscles regardless of the presence of pain. Palacios-Ceña et al. [55] found that the number of active MTrPs in head, neck and shoulder muscles were associated with widespread pressure hypersensitivity in a migraine population.

Two unblinded studies show that manual palpation of MTrPs can provoke a migraine attack [45, 53]. Calandre et al. provoked a migraine attack in one-third of a migraine population by palpating MTrPs [45]. Landgraf et al. provoked migraine headache by inducing pressure to MTrPs and could not replicate this by pressure to non-trigger points in the trapezius in an adolescent migraine population [53].

Interventions targeted at MTrPs show promising results [50‐52, 56, 57], but the quality of studies varies greatly and lack placebo-control. Giambierardino et al. demonstrated that local anesthetic infiltration of MTrPs resulted in a reduction of migraine symptomatology in terms of frequency and intensity [52]. Furthermore, there was a reduction of hyperalgesia, not only at the injection site but also in referred areas overlapping with migraine pain sites. Similar, Ranoux et al. injected botulinum toxin in MTrPs with similar results in terms of reduction in headache days [56]. Gandolfi et al. improved the outcome of prophylactic botulinum toxin treatment in chronic migraine patients with manipulative treatment of MTrPs [50]. The outcome was a lower consumption of analgesics, improvement in pressure pain threshold and increased cervical range of motion. Likewise, Ghanbari et al. reported that combined positional release therapy targeted at MTrPs with medical therapy is more effective than the sole pharmacological treatment [51]. Interestingly, sessions of magnetic stimulation of active MTrPs reduced headache frequency and intensity in adolescent migraineurs [57]. Though these findings need to be verified in a placebo-controlled study. There has not been any studies on the effect of systemic musculoskeletal analgesics on MTrPs [59], which would be of interest for future studies.

There is a high occurrence of active and latent MTrPs in patients with TTH [63‐67, 69‐72, 79] Active MTrPs are found almost only in TTH patients compared to controls [63, 65, 69, 72, 80]. MTrPs are more prevalent on the dominant side of the patients [66]. The number of active MTrPs is higher in adults in comparison to adolescents regardless of no significant association between the number of active MTrPs and headache frequency, duration and intensity [62]. Other studies have found that active MTrPs are correlated with the severity of TTH [65, 67, 78, 80] with a greater occurrence of MTrPs in chronic TTH in comparison to episodic TTH [80]. Furthermore, studies show that active MTrPs are correlated with the intensity, duration and frequency of headache episodes in TTH [65, 80]. In contrast, other studies failed to show a correlation between MTrPs and chronic and frequent episodic TTH [78] and showed no correlation between MTrPs and headache parameters either in episodic TTH patients [69].

Episodic TTH patients had less neck mobility compared to controls [69]. Patients with active MTrPs had a greater forward head position than subjects only with latent MTrPs [69]. However, neither forward head position or neck mobility was correlated with headache parameters [69]. In a different study, active MTrPs in the right upper trapezius muscle and left sternocleidomastoid muscle was correlated with a greater headache intensity and duration [72]. Furthermore, active MTrPs in the right and left temporalis muscles correlated with longer headache duration and greater headache intensity, respectively [72]. Suboccipital active MTrPs correlated with increased intensity and frequency of headache [65]. Chronic TTH patients with active MTrPs in the analyzed muscles had a greater forward head position than those subjects only with latent MTrPs [65, 72]. Sohn et al. [80] identified a greater occurrence of MTrPs in chronic TTH compared to episodic TTH and that the number of active MTrPs correlated with the frequency and duration of headache, although they did not find any correlations for forward head posture and neck mobility in contrast to Fernández-de-las-Peñas et al. [65, 72].

The number of active and latent MTrPs was significantly and negatively associated with pressure pain thresholds on the temporalis muscle, C5/C6 zygapophyseal joint, second metacarpal, and tibialis anterior muscle [78]. Thus, a higher number was associated with a more generalized sensitization regardless of the frequency of headache. Another study observed that the location of active MTrPs in the temporalis muscle corresponded to areas with lower pain pressure thresholds which establishes a relationship between the two [68]. The same group found that chronic TTH patients with bilateral active MTrPs in the trapezius muscles have a significantly lower pain pressure threshold compared to patients with only unilateral active MTrPs [70]. Minimum clinical differences in pressure pain thresholds in TTH patients may be used to evaluate treatment of MTrPs [79].

Karadas et al. [81] investigated pericranial lidocaine injections in MTrPs in 108 patients with frequent episodic TTH using a double-blind placebo-controlled randomized study design. Repeated local lidocaine injections into the MTrPs in the pericranial muscles reduced both the frequency and intensity of pain compared to placebo. Another placebo-controlled study found similar results with lidocaine injections in MTrPs in chronic TTH with a reduction in pain frequency, pain intensity, and analgesic use [74]. In addition, there was a significant effect on anxiety and depression of the subjects. A randomized, double-blind, placebo-controlled pilot study of botulinum toxin A injections in MTrPs included 23 patients with chronic TTH [73]. The subjects were assessed at 2 weeks, 1, 2 and 3 months after injection. The botulinum toxin A group reported a reduction in headache frequency that disappeared by week 12. There was no difference in intensity between the groups. In a randomized, placebo-controlled clinical trial, Moraska et al. applied massage focused on MTrPs of patients with TTH [77]. For both active and placebo groups, there was a decrease in headache frequency, but not for intensity or duration. Thus, there was no difference between massage and placebo [81].