Myofascial trigger points therapy increases neck mobility and reduces headache pain in migraine patients – pilot study

Abstract

Background

This study aimed to evaluate the effects of Ischemic Compression Myofascial Trigger Points (IC-MTrPs) therapy, applied mainly to the upper trapezius muscle (UTM), on: [1] cervical spine range of motion (CS-ROM), and [2] headache characteristics in migraine patients. Reduced CS-ROM can further contribute to musculoskeletal strain and neurological discomfort in migraine sufferers. The application of IC-MTrPs therapy is of particular interest because it targets these trigger points, potentially normalizing muscle tone and improving local blood flow, which may alleviate pain and restore mobility.

Design

A case series employing a repeated-measures design; pilot study.

Methods

Fifty-three adult female migraine patients were classified into three groups: episodic migraine without aura (MO, n = 31), episodic migraine with aura (MA, n = 15), and chronic migraine (CM, n = 7). Patients underwent seven sessions of IC-MTrPs therapy targeting the shoulder and neck muscles. Assessments were conducted across five sessions: pre-therapy (baseline), post-1st therapy, post-4th therapy, post-7th therapy, and at a 1-month follow-up. Outcome measures included: CS-ROM (assessed using an accelerometer system), subjective headache pain intensity (evaluated via the Visual Analog Scale (VAS)), and calcitonin gene-related peptide (CGRP) concentrations.

Results

CS-ROM for horizontal rotation and forward flexion improved significantly at the 1-month follow-up compared to pre-therapy (baseline) (P < 0.05). Headache intensity during a migraine attacks, as well as headache frequency and duration, significantly decreased at post-7th therapy compared to baseline across all patients (P < 0.05). The highest CGRP concentrations were recorded in CM patients (240.73 ± 79.51 ng/ml). While no significant changes in CGRP levels were observed in patients with MO, CGRP concentration in patients with MA increased significantly at the 1-month follow-up compared to baseline, rising from 151.70 ± 50.85 ng/ml to 176.17 ± 77.21 ng/ml. In patients with CM, the therapy did not result in statistically significant changes in CGRP levels, although reductions in headache frequency and intensity were noted.

Conclusions

IC-MTrPs therapy proved effective in increasing CS-ROM and alleviating headache characteristics in all migraine subtypes. However, no significant changes in CGRP levels were observed. Distinct characteristics and responses among different migraine subtypes highlight the need for tailored therapeutic approaches.

Trial registration

The study protocol was retrospectively registered on December 2, 2022, as a clinical trial in the international clinical trial database ClinicalTrials.gov (identifier: NCT05646160). Clinical trial number: not applicable.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12891-025-08360-1.

Introduction

Migraine is a neurological disorder with debilitating symptoms that significantly affect quality of life. The International Headache Society (IHS) distinguishes three types: chronic migraine (CM), migraine without aura (MO), and migraine with aura (MA) [1]. CM involves headaches on at least 15 days per month for three months, with eight days meeting migraine-specific symptoms. MO is marked by unilateral, pulsating headaches aggravated by physical activity, often accompanied by nausea and light sensitivity. MA includes transient neurological symptoms, such as visual disturbances, accompanying or preceding headache pain [2, 3].

Although migraines are primarily neurological, they are commonly associated with musculoskeletal disturbances, with 70–76% of migraine patients reporting neck pain [4, 5]. Hypertonic muscle bands in the shoulder girdle and neck muscles, including the upper trapezius muscle (UTM), are often observed to contribute to chronic tension and migraine [6–9]. The UTM plays a key role in cervical spine movement, shoulder girdle control, and muscle coordination [10].

Research shows that 93% of migraine patients have active myofascial trigger points (MTrPs), particularly in the temporal, suboccipital, and shoulder regions [11–13]. MTrPs alter the bioelectric and mechanical properties of muscles, potentially reducing cervical spine mobility [15–18]. Ischemic compression (IC) therapy has been proposed to deactivate MTrPs and improve muscle function [19]. Manual therapies, including IC, have shown positive effects in managing migraine pain [20, 21].

To date, there have been no studies investigating the effects of IC-MTrPs therapy on cervical spine range of motion (CS-ROM) in the context of migraine patients [22–26]. Migraine pathophysiology is influenced by both central and peripheral mechanisms, including neurovascular and myofascial components [27]. MTrPs, particularly in the UTM, might contribute to restricted CS-ROM and exacerbation of migraine symptoms [28]. CGRP, a neuropeptide critically involved in migraine pathogenesis, is released during attacks, contributing to both pain and vasodilation [29, 30]. It is also secreted in response to MTrPs, suggesting a potential link between MTrPs therapy and CGRP levels [31].

This study aims to assess both the immediate and long-term effects of IC-MTrPs therapy on CS-ROM, headache features, and CGRP concentrations. CS-ROM will be assessed using accelerometer sensors, headache characteristics through self-reported metrics, and CGRP levels to evaluate therapeutic efficacy.

1. Null hypotheses (H₀):

   • IC-MTrPs therapy does no effect CS-ROM.
   • IC-MTrPs therapy does not reduce headache intensity.
   • IC-MTrPs therapy does not reduce headache frequency.
   • IC-MTrPs therapy does not reduce headache duration.
   • IC-MTrPs therapy does not alter CGRP concentrations in the blood.

• 2.First-level alternative hypotheses (H₁):
  • IC-MTrPs therapy increases CS-ROM.
  • IC-MTrPs therapy reduces headache intensity.
  • IC-MTrPs therapy reduces headache frequency.
  • IC-MTrPs therapy reduces headache duration.
  • IC-MTrPs therapy improves CGRP concentrations in blood.

• 3.Second-level alternative hypotheses (H₂):
  • IC-MTrPs therapy improves CS-ROM by reducing myofascial tension and enhancing cervical muscle coordination.
  • IC-MTrPs therapy reduces headache intensity through normalization of neural drive and inhibition of nociceptive pathways.
  • IC-MTrPs therapy reduces headache frequency by decreasing muscle hypertonicity and improving local blood flow.
  • IC-MTrPs therapy reduces headache duration by restoring musculoskeletal balance and alleviating sustained trigger point activation.
  • IC-MTrPs therapy alters CGRP concentrations by modulating neurochemical pathways involved in pain regulation.

By integrating data from accelerometer-based CS-ROM assessments, self-reported headache metrics, and CGRP levels, this study aims to evaluate the analgesic and functional effects of IC-MTrPs therapy. The pivotal role of CGRP in migraine pathophysiology has been well-established. Over the past decade, clinical trials have demonstrated the efficacy of CGRP-receptor antagonists, further indicating them as a therapeutic target in migraine management [32].

Materials and methods

Subjects

The study included 83 participants (81 women and 2 men) with various headache types. A neurologist diagnosed migraine in 74 women based on ICHD-3 criteria [1, 33], including predefined inclusion and exclusion criteria. Patients were recruited between January and May 2021.

In the first stage of participant recruitment, a confidence level of 0.05 and a population size of 83 (survey participants) were assumed, with an expected margin of error of 5%. This yielded a required sample size of 68 participants. A total of 74 participants were qualified for further studies, indicating that the sample size for this stage was adequate.

Using the effect sizes observed in this study, the calculated power (1 − β) of the primary outcomes (e.g., cervical spine range of motion, headache intensity, frequency, and duration) exceeded 75%, demonstrating that the sample size of 57 participants was sufficient to detect meaningful effects. The post-hoc power analysis, assuming a medium effect size (Cohen’s d = 0.5) and a significance level of 0.05, yielded an estimated power of approximately 0.75, indicating a 75% probability of correctly rejecting the null hypothesis if the alternative hypothesis were true—a value close to the desired threshold of 0.80.

For the 53 participants who completed the study, the calculated power was approximately 72%, assuming the same medium effect size and a stringent 5% margin of error. While slightly below the desired 80% threshold, this level of power suggests the sample size was sufficient to detect significant effects. However, the reduced power may have limited the detection of smaller effect sizes.

A neurologist and a physiotherapist conducted detailed interview with the subjects, and respondents completed an original questionnaire. In total of 57 out of the 74 women, aged 18–65 years and with a history of migraines lasting at least 12 months, were qualified for the study based on the inclusion and exclusion criteria. Ultimately, 53 patients completed the study (Table 1).

Table 1.

Anthropometric and clinical data of subjects with migraine patients

Anthropometric and clinical parameters (migraine patiens, N)	MO, N = 31	MA, N = 15	CM, N = 7
Age [years]	40,1 ± 10,5	44,2 ± 9,0	53,9 ± 7,5*
Duration of migraine [years]	17,1 ± 10,3	20,6 ± 14,9	34,0 ± 20,8*
Body Mass [kg]	70,0 ± 21,6	66,7 ± 12,8	65,9 ± 5,0
Height [cm]	163,0 ± 3,9	163,5 ± 6,2	161,1 ± 5,9
Body Mass Index [kg/m2]	26,4 ± 8,2	25,1 ± 3,7	25,5 ± 3,0

Data are expressed as mean (SD)

* - statistically significant difference (p ≤ 0.05)

The study was conducted at the Council of the Regional Center for Research and Development located at the university, where patient recruitment, measurements and analyses, were performed.

The inclusion criteria were: adult age, female sex, a history of migraine persisting for at least 12 months confirmed by a neurologist, absence of metabolic or cardiovascular disorders, no neurological or orthopedic conditions affecting the shoulder girdle or cervical spine, written informed consent for participation, and a diagnosis aligning with ICHD-3 criteria for migraine classification.

The exclusion criteria included: age under 18 years, male sex, participants on essential pharmacological treatments that could not be paused, presence of other headache types, potential medication-overuse headache (MOH), prior injuries affecting the cervical spine or shoulder region, dermatological conditions, and other health issues such as deep vein thrombosis.

The study complied with the Declaration of Helsinki (86/609/ECC) and was approved by the Senate Research Ethics Committee at the Jozef Pilsudski Academy of Physical Education in Warsaw, Poland (approval number: SKE 01–52/2017), as well as by the Council of the Regional Center for Research and Development (RCRD) in Biala Podlaska (approval number: 14/21//10/11/2017). Additionally, the research protocol was retrospectively registered as a clinical trial on December 2, 2022, in the international database ClinicalTrials.gov (identifier: NCT05646160). Note: Clinical trial number is not applicable.

Experimental procedures

Patients diagnosed with migraines participated in a series of seven therapeutic sessions (labeled as 1–7; see Fig. 1; Tables 2, 3, 4, 5 and 6) involving ischemic compression of myofascial trigger points (IC-MTrPs) therapy, conducted with three-day intervals between sessions (Fig. 1). The complete treatment cycle spanned approximately 25 days, covering the period from the 1st to the 7th IC-MTrPs therapy session (Fig. 1).

Fig. 1.

Graphic time schedule of therapeutic and testing sessions with an indication of types of measurements collected during particular testing sessions

ROM – range of motion; CS – cervical spine, CGRP – calcitonin gene-related peptide

Table 2.

Cervical spine range of motion in various planes in migraine without aura [MO, n = 31]

Measurement session name (No.)	Cervical spine range of motion (CS-ROM) [°] in various planes (mean (SD))
	Horizontal rotation	Side bend (lateral flexion)	Forward bend (flexion)
Pre-1’st therapy (I)	126,9 ± 26,5	75,13 ± 15,5	39,6 ± 12,3
Post-1’st therapy (II)	128,8 ± 20,8	72,41 ± 13,8	39,3 ± 9,1
Post-4’th therapy (III)	132,2 ± 20,5	74,10 ± 13,5	41,3 ± 8,9
Post-7’th therapy (IV)	135,0 ± 21,6	74,85 ± 13,5	44,2 ± 10,1
1-month follow up (V)	140,3 ± 19,0*	78,33 ± 15,6	47,9 ± 8,3*
ANOVA Friedman:	F = 19,10; p = 0,0008 ‡	F = 6,78; p = 0,1478	F = 21,18; p = 0,0003 ‡
Post Hoc For Friedman (differences between measurement sessions)	I vs. V; p = 0,001*	all no significant p > 0,005	I vs. V; p = 0,001*

‡ - statistically significant effect of measurement session based on ANOVA Friedman;

* - statistically significant difference (p ≤ 0.05) compared to the pre-1’st therapy measurement session value in the post hoc analysis

Table 3.

Cervical spine range of motion in various planes in migraine with aura [MA, n = 15]

Measurement session name (No.)	Cervical spine range of motion (CS-ROM) [°] in various planes (mean (SD))
	Horizontal rotation	Side bend (lateral flexion)	Forward bend (flexion)
Pre-1’st therapy (I)	125,29 ± 17,97	71,95 ± 12,83	34,45 ± 8,04
Post-1’st therapy (II)	125,49 ± 19,25	70,74 ± 12,45	35,85 ± 8,12
Post-4’th therapy (III)	124,31 ± 19,56	71,79 ± 13,08	36,09 ± 11,79
Post-7’th therapy (IV)	130,90 ± 21,52	75,26 ± 11,69	39,65 ± 8,10
1-month follow up (V)	136,71 ± 14,59	77,29 ± 13,71	45,45 ± 8,17*
ANOVA Friedman:	F = 8,44; p = 0,0767;	F = 4,45; p = 0,3479;	F = 21,20; p = 0,0003; ‡
Post Hoc For Friedman (differences between measurement sessions)	all no significant p > 0,005	all no significant p > 0,005	I vs. V; p = 0,001*

‡ - statistically significant effect of measurement session based on ANOVA Friedman;

* - statistically significant difference (p ≤ 0.05) compared with the pre-1’st therapy measurement value in the post hoc analysis

Table 4.

Cervical spine range of motion in various planes in chronic migraine [CM, n = 7]

Measurement session name (No.)	Cervical spine range of motion (CS-ROM) [°] in various planes (mean (SD))
	Horizontal rotation	Side bend (lateral flexion)	Forward bend (flexion)
Pre-1’st therapy (I)	114,26 ± 21,13	66,37 ± 15,25	32,53 ± 4,36
Post-1’st therapy (II)	119,20 ± 33,00	63,04 ± 17,65	34,00 ± 9,89
Post-4’th therapy (III)	117,10 ± 21,79	85,36 ± 9,25	35,10 ± 7,69
Post-7’th therapy (IV)	134,83 ± 25,10	86,26 ± 7,92 #	44,99 ± 10,38*
1-month follow up (V)	118,99 ± 21,81	79,44 ± 17,89	41,40 ± 6,57*
ANOVA Friedman:	F = 6,86; p = 0,1436;	F = 10,63; p = 0,0311; ‡	F = 10,86; p = 0,0282; ‡
Post Hoc For Friedman (differences between measurement sessions)	all no significant p > 0,05	I vs. IV p = 0,001*	I vs. IV, V; p = 0,001*

‡ - statistically significant effect of measurement session based on ANOVA Friedman;

* - statistically significant difference (p ≤ 0.05) compared with the pre-1’st therapy measurement value in the post hoc analysis

Table 5.

Parameters assessing headache characteristics in migraine patients (MO, MA, CM)

Measurement session name (No.)	Average headache level (VAS score) while migraine attack [cm]	Frequency of migraine attack [no. of days / month]	Duration of a single migraine attack [no.of days]
Pre-1’st therapy (I) MO	7,55 ± 1,53	6,29 ± 4,95	2,83 ± 2,05
Post-7’th therapy (IV) MO	5,71 ± 2,01*	4,00 ± 3,91*	1,18 ± 1,11*
Wilcoxon signed - rank test	Z = 3,78; p = 0,0002 *	Z = 3,08; p = 0,002 *	Z = 3,19; p = 0,0001 *
Pre-1’st therapy (I) MA	7,53 ± 2,14	5,33 ± 3,59	2,06 ± 1,57
Post-7’th therapy (IV) MA	4,54 ± 2,73*	2,42 ± 1,82*	0,71 ± 2,12*
Wilcoxon signed - rank test	Z = 2,80; p = 0,0051 *	Z = 3,05; p = 0,002 *	Z = 2,41; p = 0,015 *
Pre-1’st therapy (I) CM	8,71 ± 1,25	15,71 ± 4,27	5,00 ± 3,10
Post-7’th therapy (IV) CM	6,29 ± 1,98*	7,14 ± 3,67*	0,85 ± 0,89*
Wilcoxon signed - rank test	Z = 1,99; p = 0,0464 *	Z = 2,36; p = 0,017 *	Z = 2,36; p = 0,017 *

* - statistically significant difference (p ≤ 0.05) compared with the pre-1’st therapy measurement session

Table 6.

CGRP concentration [ng/ml] in migraine patients

Measurement session name (No.)	CGRP concentration MO, (n = 31) [ng/ml]	CGRP concentration MA, (n = 15) [ng/ml]	CGRP concentration CM, (n = 7) [ng/ml]
Pre-1’st therapy (I)	195,61 ± 130,28	151,70 ± 50,85	240,73 ± 79,51
Post-1’st therapy (II)	185,51 ± 120,03	174,54 ± 73,76	206,84 ± 105,10
Pre-7’th therapy (IV)	200,13 ± 118,87	176,17 ± 77,21	222,80 ± 91,46
Wilcoxon signed - rank test	F = 1,49; p = 0,4752;	F = 1,20; p = 0,5488;	F = 0,29; p = 0,8669;

Assessments were performed at five specific time points (designated as I-V; refer to Fig. 1; Tables 2, 3, 4, 5 and 6): I– pre-1’st therapy; II – post-1’st therapy; III – post-4’th therapy; IV – post-7’th therapy; V – one month after the 7’th therapy (1 month follow up) (Fig. 1).

Primary outcomes, specifically cervical spine range of motion (CS-ROM), were evaluated at all five testing sessions: pre- and post-1st therapy, post-4th therapy, post-7th therapy, and at a 1-month follow-up (i.e., during testing sessions I–V; Fig. 1). Secondary outcomes included headache characteristics, assessed twice: pre-1st therapy and post-7th therapy (i.e., during testing sessions I and IV; Fig. 1), and calcitonin gene-related peptide (CGRP) levels, measured in blood samples during three testing sessions: pre-1st therapy, post-1st therapy, and pre-7th therapy (i.e., before testing sessions I, II, and IV; Fig. 1).

Therapeutic intervention - IC-MTrPs

The therapeutic intervention aimed to deactivate myofascial trigger points (MTrPs) using the ischemic compression (IC) method, defined by Travell and Simons (2018) [10]. IC-MTrPs therapy was applied bilaterally to the shoulder girdle and neck regions, targeting the upper trapezius, sternocleidomastoid, temporalis, levator scapulae, supraspinatus, and suboccipital muscles [7, 8, 10]. Each session commenced with treatment on the right side, followed by the left, maintaining this order for all patients. MTrPs were identified through palpation and pinch pressure while patients reclined on the treatment couch [26].

The physiotherapist positioned themselves behind the patient’s head, applying sustained pressure for approximately 10–15 s, with 2–3 s pauses. Each session lasted 15 min and was conducted in the morning of the same designated measurement day. Patients were informed that mild pain or discomfort during pressure application would typically subside as therapy progressed. Pressure was maintained until a significant relaxation was noted, coupled with the patient reporting reduced pain [14]. If no improvement was observed within two minutes, the procedure was halted, and it was immediately stopped if pain intensified [34]. The pressure induced local ischemia, indicated by skin paleness, followed by improved blood flow upon release [19]. Each patient completed seven IC-MTrPs sessions over approximately 25 days (Fig. 1).

Measurements of cervical spine range of motion (CS-ROM)

The CS-ROM was assessed using the Noraxon Myo Motion system (Noraxon, Scottsdale, AZ, USA), a validated method for recording and analyzing human movement in 3D space, using wireless, self-calibrating accelerometer sensors. Calibration involved sitting straight with a neutral head position and arms by the side to establish a 0° baseline for cervical joint measurements.

Two accelerometer sensors were placed: (i) one on the skin above the spinous process of the first thoracic vertebra (Th₁) and (ii) another attached to the occipital center (C₀) using an elastic belt. CS-ROM measurements included left and right horizontal rotation, side bending (lateral flexion), and forward bending (flexion), recorded in degrees (°). Sampling frequency was 100 Hz, with an accuracy of ± 1^o in the sagittal and frontal planes, and ± 2^o in the transverse plane [35].

The Noraxon MyoMotion system has demonstrated strong validity and reliability in kinematic assessments, supporting its use in clinical and research settings for populations with movement limitations or musculoskeletal conditions [36, 37].

Evaluation of headache characteristics

Research has highlighted the VAS as being particularly suited for clinical trials where detecting fine variations in pain is crucial [38, 39] The Visual Analogue Scale (VAS) is widely regarded as the gold standard in migraine and pain research due to its sensitivity and validity. It has been extensively used in studies examining headache and migraine, ensuring consistency and comparability with other work in this field [40].

Patients reported the intensity of their last migraine attack using 10 cm (100 mm long) paper scale, with endpoints labeled ‘no pain at all’ (number “0”) and ‘pain as bad as it could be’ (number “10”). Each patient was asked: “What was the intensity of the last migraine attack?“.

Participants also documented the frequency of migraine attacks (number of attacks per month) and the duration of each migraine attack (in days) through a custom-designed questionnaire administered before therapy and at a 1-month follow-up.

Biochemical determinations

Peripheral blood was collected from the cubital vein of the subjects between 6:00 am and 9:00 am before and after the first therapy session and 24 h after the sixth session. The samples were transferred into tubes without serum anticoagulants. Sterile blood (8 ml) was left to stand for 30 min at room temperature, then centrifuged at 1500 rpm for 10 min. The serum was transferred to new 300 µl tubes and stored at -70 °C until biochemical assays were performed. The serum concentration of CGRP was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) kit (R&D Systems, Minneapolis, MN, USA) following the manufacturer’s instructions and a previously published protocol [41]. The CGRP concentration was reported in ng of protein per ml of serum, with a limit of detection set at 20 pg/ml. Each measurement was repeated twice, ensuring a mean inter-assay precision, expressed as the coefficient of variation, of approximately 8%.

Statistical analysis

The results are presented as mean values with standard deviation (mean ± SD) for the entire tested group. Statistical differences between the testing sessions were analyzed using the Friedman analysis of variance (ANOVA) due to the absence of normal distribution. When a significant effect of the measurement session was detected, post hoc analysis for Friedman’s test was conducted. For intersession comparisons involving parameters measured during only two testing sessions (as with headache parameters), a nonparametric test for two dependent samples, specifically the Wilcoxon signed-rank test, was employed.

Results were considered statistically significant at a p-value of ≤ 0.05. All statistical analyses were performed using Statistica v.10 software (StatSoft, Inc., 2001, Kraków, Poland).

Results

Intersession comparisons of measurements of the CS-ROM

The CS-ROM for horizontal rotation, forward bending, and lateral flexion clearly tended to increase value ​​for most patients after therapy and after the 1-month follow-up measurement session, compared to the recorded values ​​before the first therapy (Tables 2, 3 and 4) in all migraine groups.

However, the statistical analysis revealed that, compared to pre-1’st therapy measurements, ROM values for horizontal rotation and forward bend were significantly higher (P < 0.05) only during the 1-month follow up measurements (Table 2) in the MO group. Forward bend (flexion) tended to improve after 1 month of therapy in the MA group (Table 3). In contrast, statistical analysis showed significant improvement in the CM group, with a statistically significant increase in lateral flexion mobility observed at the end of the therapy and a continued tendency for improvement 1-month after therapy (Table 4).

Intersession comparisons of headache characteristics

Compared to the first therapy session, all assessed headache characteristics demonstrated significant improvement after the post-7th therapy session, including the average headache intensity during a migraine attack, the frequency of headache, and the duration of migraine attack (P < 0.05; Table 5).

Intersession comparisons of CGRP concentrations

The highest concentration was observed in the CM group. No changes in CGRP concentration were noted in patients with MO, but an increase was observed in patients with MA following the first IC-MTrPs session (Table 6). Statistical analysis revealed no significant changes in serum CGRP levels in patients with migraine after intervention.

Discussion

Therapeutic effects of IC-MTrPs on migraine outcomes

The results of our study showed that in all migraine patients, IC-MTrPs therapy caused: (i) increased CS-ROM, (ii) reduced headache intensity, frequency, and duration, and (iii) modest changes in CGRP levels, observed primarily in episodic migraine patients. No significant changes in CGRP levels were noted in chronic migraine patients. These findings highlight the potential efficacy of IC-MTrPs therapy as a non-pharmacological treatment for improving both musculoskeletal function and headache characteristics.

Demographic characteristics and sample size adequacy in the study population

The demographic profile of our participants aligns with established epidemiological trends, including a predominance of women (81 out of 83 participants), a mean disease duration of 23.9 ± 15.3 years, and migraine subtype distributions consistent with prior studies [42–45]. Specifically, 58.5% of patients had migraine without aura, 28.3% had migraine with aura, and 13.2% had chronic migraine. These findings corroborate reports indicating a higher prevalence of episodic migraine compared to chronic migraine and a greater proportion of migraine with aura in middle-aged individuals. Notably, the observation that patients with chronic migraine (CM) were older and had a longer history of migraine aligns with literature suggesting that CM often develops from episodic migraine as the condition progresses, influenced by age and other factors.

Analysis of CS-ROM by migraine subtype

The rationale behind analyzing CS-ROM by migraine subtype was based on previous literature suggesting that chronic migraines (CM) might lead to more significant musculoskeletal dysfunctions compared to episodic migraine types (MO and MA) due to the higher frequency and longer duration of attacks.

To explore whether the presence of aura in migraines impacts cervical ROM, we distinguished MA from MO. We hypothesized that the neurological symptoms associated with aura could influence cervical spine mobility. MO and MA were not combined for analysis, as differences in aura-related mechanisms warranted separate evaluation.

Evaluation and treatment of MTrPs in migraine

The gold standard for the detection of MTrPs is still manual palpation of muscles, a technique that has remained largely unchanged for decades [10, 46]. Although widely used, manual palpation is limited by subjective variability, and examiners often lack reproducibility and reliability [10, 47]. Alternative methods, including infrared thermography (IT), needle electromyography (EMG), ultrasound (US), and MRI, have been explored [46, 48, 49]. However, these techniques are often limited by cost, availability, and interpretative challenges, restricting their widespread adoption.

Previous studies have indicated that MTrPs influence pain mechanisms, serving as additional stimuli that may contribute to the onset of a migraine attack [46, 50, 51]. Our observation is in agreement with other studies that reported that the inhibition of MTrPs by neck muscle relaxation techniques including EMG biofeedback and dry needling technique, led to a decrease in the frequency and severity of migraine attacks [47, 52]. Neck muscle relaxation techniques and other techniques are frequently used as nonpharmacological additions to reduce migraine attacks. The mechanisms of the influence of these therapies, which have the same effects as pharmacological therapies on pain, still need to be elucidated. Studies have shown that patients with migraine have a greater number of MTrPs than healthy subjects, and a higher number of MTrPs in the neck and shoulder areas correlates with muscular pain severity and the duration of migraine attacks. Studies have repeatedly demonstrated that a high occurrence of MTrPs associated with such points, neck mobility, and migraine attack in individuals with migraine [10, 47].

Biomechanical analysis of CS-ROM in relation to IC-MTrPs therapy

Various methods and devices are used to test spine mobility. Most often, these methods include visual assessment, goniometers, inclinometers, various types of photos and complex three-dimensional (3D) analysis [53]. Cervical spine mobility was assessed using the MyoMotion 3D motion analysis system (Noraxon Inc., Scottsdale, AZ, USA). Inertial measurement units (IMU) are increasingly used to collect objective data for clinical analyses [54]. These sensors include a gyroscope, a magnetometer, and an accelerometer, and the combination of the data they record provides a three-dimensional analysis of the rotational movement of each body segment. The obtained results can be used directly in traditional algorithms for kinematic calculations. These devices are relatively cheap and easy to use, which makes them attractive options for tasks related to traffic analysis. Additionally, the test preparation and calibration times are significantly shorter than those of other forms of motion capture. Small sensors of the IMU placed on the appropriate body segment can track the angular orientation in 3D and do not cause discomfort to the subject. Motion analysis performed using a 3D IMU is considered acceptable in terms of the quality and reliability of measurements [55].

Our findings demonstrated that IC-MTrPs therapy significantly improved CS-ROM, particularly for horizontal rotation and forward bending, as confirmed during the 1-month follow-up period. These improvements correlate with reduction in muscle tone and hypertonia in the UTM, as revealed by myotonometry [26, 56]. Neck pain can increase tone and a decrease elasticity of posterior cervical muscles, and modify ROMs in flexion and rotation, highlighting the importance of assessing these features for treating spinal pain syndrome in clinical settings [57]. Another study revealed that, compared with symptomatic individuals, patients with neck pain displayed reduced variability in trunk rotation (p = 0.021) [58].

These improvements in CS-ROM align with research indicating that neck pain, muscle tone changes, and reduced cervical mobility can contribute to migraine pathology by increasing tension in the cervical muscles and affecting spinal pain pathways. Moreover, our use of the MyoMotion 3D motion analysis system was instrumental in providing objective, reliable, and non-invasive measurements of neck movement, underscoring the importance of incorporating advanced technology in clinical assessments for its accuracy and ease of use [37, 38].

Effects of IC-MTrPs therapy on the headache characteristics

We assessed headache characteristics before and after the 3-week period of IC-MTrPs therapy and reported a significant decrease in (i) the average headache intensity during migraine attacks, (ii) the frequency of headache pain, and (iii) the duration of a migraine attack. Our findings of a positive effect of IC-MTrPs therapy on headache characteristics might be caused by changes in cervical spine biomechanics (associated with changes in shoulder girdle and neck muscle tone and CS-ROM), which might contribute to a reduction in adverse tension in the spinal dura. This tension reduction is assumed to be one of the neurophysiological mechanisms underlying headache.

This assumption is in accordance with studies by Crooks et al. (2018) [59] and Espi-López et al. (2018) [60], who reported that soft tissue techniques and mobilization techniques might reduce headache frequency in migraine patients. However, the precise neurophysiological mechanisms underlying this effect require further investigation. It is plausible that IC-MTrPs therapy influences pain modulation through the activation of mechanoreceptors and decreased muscle hypertonia, thereby contributing to improved pain management.

Effects IC-MTrPs therapy on CGRP level

Previous studies have shown that MTrPs increase pain levels through elevated concentrations of CGRP, S100 and substance P (SP) in the blood, which many researchers associate with the development of pain [10, 34]. MTrPs and muscle tone induced by physical activity cause increased release of neuropeptides such as CGRP. People often experience neck pain as a symptom of migraine attack. The abovementioned biomechanical and biochemical factors play important roles in migraine pathomechanisms [9, 61].

During a pain attack, neurovascular disorders occur as a result of the release of various endogenous substances, such as CGRP, SP, and cyclic guanosine monophosphate (cGMP) into the space surrounding the arachnoid vessels. CGRP, a peptide released during migraine attacks, plays an important role in the pathogenesis but is also secreted in skeletal muscles as a result of the MTrPs formation [62, 63].

Within the trigeminal system, fibers dominate whose stimulation causes the release of the CGRP, leading to vasodilation and intensified pain, which are hallmark symptoms of migraine. During migraine attacks, serum CGRP concentration increases but tends to decrease following migraine treatment with triptans [32].

Our studies revealed significantly increased serum CGRP concentrations in patients with CM and episodic migraine compared with healthy controls [62]. In addition, the most significant increase in CGRP concentration was observed in patients with CM [41]. Additionally, in our research similar results were observed: the highest serum CGRP concentration was found in CM, whereas the concentration was greater in patients with MO/MA. During migraine attacks, the concentration of CGRP increases significantly, which is why it may play an important role in the pathomechanism of migraine [41]. Over the last decade, a key treatment for migraine has been reducing CGRP concentrations through pharmacological agents. Recently, research has focused on use of CGRP-receptor antagonists to treat migraine pain [61].

This is particularly significant, given that CGRP is a well-established biomarker linked to migraine pathophysiology and the onset of pain attacks. Elevated serum CGRP concentrations in CM, MO and MA patients compared with healthy controls further reinforce its role in migraine. Previous literature has demonstrated that MTrPs can increase the release of neuropeptides, including CGRP, thereby exacerbating pain. However, IC-MTrPs therapy’s limited effect on CGRP levels suggests that this therapy primarily modifies mechanical muscle properties rather than directly altering inflammatory pathways. This finding contrasts with pharmacological strategies targeting CGRP reduction, such as receptor antagonists, which show more direct effects on migraine relief.

During pain attacks, there is a significant increase in the release of proinflammatory factors and CGRP. Migraine induces the formation of MTrPs in neck muscles, which results in the release of proinflammatory factors and CGRP. IC-MTrPs therapy improves the mechanical properties of muscles with MTrPs in migraine pain patients. This may be one of the reasons for the lack of effects of the IC-MTrPs on reducing levels of inflammatory substances observed by other researchers. In addition, the respondents could not take painkillers during the study [41].

Discussion of findings

This study primarily focused on mechanical (CS-ROM) and behavioral (headache features) assessments, providing indirect insights into the biochemical and neural mechanisms involved in pain relief. Migraine often involves musculoskeletal and functional dysfunctions of the cervical spine [64–68], which we excluded based on specific criteria.

Although there is extensive research on the long-term effects of MTrPs therapy for conditions such as musculoskeletal pain and tension-type headache, research specifically related to migraine remains limited. Fernández-de-Las-Peñas et al. [69] showed that MTrPs treatment led to sustained improvements in pain and range of motion up to 3 months after treatment in chronic myofascial pain syndrome. Similarly, Simons et al. [70] highlighted the potential of MTrPs therapy to provide long-term relief from musculoskeletal pain, although more research is needed, especially for migraine.

In migraine, research on the long-term effects of MTrPs therapy is sparse. Ueda et al. [71] found significant improvement after intervention for chronic migraines, but the benefits were unclear after 1 month.

Our results provide preliminary evidence that IC-MTrPs therapy effectively reduces migraine pain, offering new insights into clinical practice and scientific understanding [26]. We acknowledge the limitations of our study, which we describe in detail in the section below.

Implications and limitations of our findings, and perspectives for future research

Implications of our findings

Our study provides preliminary evidence suggesting that IC-MTrPs therapy may be an effective treatment for migraine. Specifically, the therapy appears to lead to (i) an increased cervical spine range of motion (CS-ROM), (ii) a reduction in headache intensity, frequency, and duration, and (iii) a decrease in CGRP concentrations in individuals with episodic migraine. These results offer new insights into the potential of IC-MTrPs therapy to reduce migraine pain and improve patient quality of life.

Limitations of our study

Several limitations were identified that could have influenced the results and the interpretation of the findings:

1. Sample size and power analysis: One significant limitation of our study was the lack of a priori sample size calculation. Although the post-hoc power analysis suggested that the sample size was adequate to detect significant effects, future studies should perform a priori power calculations to optimize sample size for the specific outcomes being measured. This would increase the robustness of the findings and reduce the risk of Type II errors.

2. Questionnaire validity: The custom-made questionnaire used for participant recruitment was not validated, nor were its sensitivity and specificity assessed. This lack of validation could potentially impact the reliability of the data collected. Future studies should consider using standardized, validated tools for assessing migraine severity and associated symptoms.

3. Granularity of pain assessment: Pain duration was measured in days rather than hours, which limited the granularity of pain assessment. More precise measurement tools, such as hourly logs of migraine attacks, could provide more detailed information on the timing and intensity of headache episodes, potentially revealing additional insights into the effects of IC-MTrPs therapy.

4. Absence of objective measures: The study lacked objective tools such as electromyography (EMG), magnetic resonance imaging (MRI), or ultrasonography to assess changes in muscle and tissue structure. Future research should incorporate these objective measures to better understand the underlying physiological changes that accompany IC-MTrPs therapy and confirm the results of subjective assessments.

5. Medication adherence and Medication-Overuse Headache: The study did not assess medication adherence or investigate the presence of medication-overuse headache (MOH), which could have influenced the results. Future research should control for these variables to ensure that the observed therapeutic effects are solely attributable to IC-MTrPs therapy, rather than confounding factors.

6. Short follow-up period: Another important limitation is the short follow-up period. Most studies on IC-MTrPs therapy and MTrPs treatment in general have focused on short-term outcomes (e.g., within a month of treatment). Our study was similarly limited by a one-month follow-up, which prevents us from fully understanding the long-term effects of the therapy. Research incorporating follow-up periods of three to six months could provide valuable insights into the sustainability of the therapeutic effects.

Future research directions

Future studies should address these limitations and build on our findings in several key areas:

1. Larger and more diverse sample: To improve generalizability and statistical power, future studies should include a larger and more diverse sample of migraine patients, including individuals with both episodic and chronic migraines. Stratifying participants by migraine subtype could provide more nuanced insights into how IC-MTrPs therapy affects different patient populations.

2. A priori power analysis: To ensure sufficient sample sizes, future studies should conduct a priori power analyses tailored to the specific outcomes being measured. This will help to optimize the power of the study and minimize the risk of Type I and Type II errors.

3. Longer follow-up periods: Given the absence of long-term follow-up data in our study, future research should include follow-up periods beyond one month to assess the durability of the treatment effects. A follow-up period of three to six months would provide valuable data on whether the benefits of IC-MTrPs therapy persist over time.

4. Controlled, randomized study design: A randomized controlled trial (RCT) design would help to reduce potential confounding variables and increase the reliability of the findings. Randomization would allow for a more robust evaluation of the efficacy of IC-MTrPs therapy compared to other treatment options, such as pharmacological interventions or other physical therapies.

5. Biochemical and neurophysiological assessments: Future research should integrate biochemical (e.g., SP100, BDNF, SP, cGMP) and neurophysiological assessments to explore the mechanisms underlying IC-MTrPs therapy. Detailed biomarkers and neurophysiological measures could offer deeper insights into the neural processes and pain pathways affected by the therapy, providing a more comprehensive understanding of its effects.

6. Long-term effects: Given that long-term follow-up studies are scarce in the context of migraine treatment, further research should investigate the long-term sustainability of IC-MTrPs therapy. This includes evaluating whether the positive effects on pain reduction and cervical spine mobility last beyond the initial treatment period and whether maintenance treatments might be necessary.

Conclusions

Our study demonstrated that IC-MTrPs therapy may offer effective relief for patients with episodic migraine by targeting myofascial trigger points. Specifically, IC-MTrPs therapy was associated with (i) az increased cervical spine range of motion, (ii) a reduced headache intensity, frequency, and duration, and (iii) a decreased CGRP concentrations.

Our findings suggest that regular IC-MTrPs therapy may provide preventive benefits for certain migraine sufferers by targeting the trigger points that contribute to headache symptoms. However, significant distinctions between episodic and chronic migraines were observed, emphasizing the need for further research to better understand these patient subgroups and refine treatment approaches accordingly.

Future studies should aim to address the limitations outlined above and explore the long-term effects, optimal dosage, and potential mechanisms of IC-MTrPs therapy. A more detailed and comprehensive understanding of this intervention could lead to more effective, tailored treatments for migraine patients.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Abbreviations

BDNF

Brain-derived neurotropic factor

cGMP

Cyclic guanosine monophosphate

CGRP

Calcitonin gene-related peptide

CM

Chronic migraine

CS-ROM

Cervical spine range of motion

EMG

Electromyography

IC-MTrPs

Ischemic compression myofascial trigger points

IMU

Inertial measurement units

IT

Infrared thermography

MA

Episodic migraine with aura

MO

Episodic migraine without aura

MOH

Medication-overuse headache

MRI

Magnetic resonance imaging

MTrPs

Myofascial trigger points

SP

Substance P

US

Ultrasound

UTM

Upper trapezius muscle

VAS

Visual analogue scale

Author contributions

M. Olesiejuk and M. Chalimoniuk wrote the main manuscritpt text. M. Olesiejuk was responsible for recruting and screening the subjects. He was responsible for the intervention and management of the subjects too. M. Chalimoniuk evaluating and directing the program of the study. T. Sacewicz was responsible for mobilizing intervention sites. M. Olesiejuk prepered Fig. 1. T. Sacewicz prepered Tables 1, 2, 3 and 4, M. Chalimoniuk Table 5, and 6. All authors reviewed the manuscript.

Funding

This study is not funded.

Data availability

The data is included in the manuscript and as a file with supplementary information. The data that support the findings of this study are available from the corresponding author, upon reasonable request.

Declarations

Ethics approval and consent to participate

The research was carried out in accordance with the Helsinki Declaration (86/609/ECC) and the research protocol was approved by the Senate Research Ethics Committee at Jozef Pilsudski Academy of Physical Education in Warsaw, Poland (consent number: SKE 01–52/2017) and the Council of the Regional Center for Research and Development (RCRD) in Biala Podlaska (consent number: 14/21//10/11/2017). Written informed consent was obtained from individual.

Clinical trial

The study protocol has been retrospectively registered 2022-12-02 as a clinical trial in the international clinical trial database ClinicalTrials.gov (identifier: NCT05646160). Clinical trial number: not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.