A myofascial trigger point is defined as a hyperirritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band. It has been suggested that myofascial trigger points take part in chronic pain conditions including primary headache disorders. The aim of this narrative review is to present an overview of the current imaging modalities used for the detection of myofascial trigger points and to review studies of myofascial trigger points in migraine and tension-type headache. Different modalities have been used to assess myofascial trigger points including ultrasound, microdialysis, electromyography, infrared thermography, and magnetic resonance imaging. Ultrasound is the most promising of these modalities and may be used to identify MTrPs if specific methods are used, but there is no precise description of a gold standard using these techniques, and they have yet to be evaluated in headache patients. Active myofascial trigger points are prevalent in migraine patients. Manual palpation can trigger migraine attacks. All intervention studies aiming at trigger points are positive, but this needs to be further verified in placebo-controlled environments. These findings may imply a causal bottom-up association, but studies of migraine patients with comorbid fibromyalgia syndrome suggest otherwise. Whether myofascial trigger points contribute to an increased migraine burden in terms of frequency and intensity is unclear. Active myofascial trigger points are prevalent in tension-type headache coherent with the hypothesis that peripheral mechanisms are involved in the pathophysiology of this headache disorder. Active myofascial trigger points in pericranial muscles in tension-type headache patients are correlated with generalized lower pain pressure thresholds indicating they may contribute to a central sensitization. However, the number of active myofascial trigger points is higher in adults compared with adolescents regardless of no significant association with headache parameters. This suggests myofascial trigger points are accumulated over time as a consequence of TTH rather than contributing to the pathophysiology. Myofascial trigger points are prevalent in both migraine and tension-type headache, but the role they play in the pathophysiology of each disorder and to which degree is unclarified. In the future, ultrasound elastography may be an acceptable diagnostic test.

The current gold-standard method for diagnosing exercise-induced laryngeal obstruction (EILO) is continuous laryngoscopy during exercise (CLE), with severity classified by a visual grade scoring system. We evaluated the precision of this approach, by evaluating test–retest reliability of CLE and both inter- and intra-rater variability.In this prospective case–control study, subjects completed four consecutive treadmill CLE tests under identical conditions. Laryngoscopic video recordings were anonymised and graded by three expert raters. 2 months following initial scoring, videos were re-randomised and rating repeated to assess intra-rater agreement.20 subjects (16 cases and four controls) completed four CLE tests. The time to exhaustion increased by 30 s (95% CI 0.02–57.8, p<0.05) in the second CLE compared with the first test, but remained identical in the subsequent tests. Only one-third of subjects retained their initial diagnosis in the subsequent three tests. Inter-rater agreement on grade scores (weighted Cohen's ϰ) was 0.16–0.45, while intra-rater agreement ranged from 0.30 to 0.67.The CLE test is key in the diagnostic assessment of patients with EILO. However, the widely adopted visual grade scoring system does not appear to be a robust means for reliably classifying severity of EILO.

Ictal neck pain is a frequent symptom reported by half of migraine patients. It is unknown if neck pain is caused by peripheral or central mechanisms. Neck muscle stiffness can be investigated with ultrasound shear wave elastography. To determine if migraine patients with ictal neck pain have stiffer neck muscles interictally compared with patients without ictal neck pain and controls. This was a cross-sectional study investigating neck muscle stiffness, pressure pain thresholds and neck pain symptoms in 100 migraine patients recruited from a tertiary headache center and 46 controls. Patients with ictal neck pain had increased mean neck muscle stiffness interictally compared to both migraine patients without ictal neck pain (p = 0.018) and controls (p = 0.036). Muscle stiffness was negatively correlated with pressure pain thresholds in the neck in migraine patients with ictal neck pain (r = −0.292, p = 0.042). There were no differences in mean pressure pain thresholds between migraine subgroups. Migraine patients with ictal neck pain have stiffer neck muscles interictally compared with migraine patients without ictal neck pain and controls measured with ultrasound shear wave elastography. The increased stiffness could be due to local alterations in the neck muscles. Trial registration: clinical-trials.gov, identifier: NCT03626805

Neck pain is reported in more than 50% of migraine patients during migraine attacks and may be an important source to migraine pain. To investigate phenotypical differences between migraine patients with and without ictal neck pain in the interictal phase. Additionally, to prospectively examine the association between pericranial muscle tenderness and the impending migraine attack. Migraine patients (n = 100) and controls (n = 46) underwent a semi-structured interview and sensory testing interictally. Pericranial muscle tenderness was determined using total tenderness score and local tenderness score. The occurrence of migraine attacks was then prospectively recorded for the following seven days. Patients with ictal neck pain had increased tenderness of pericranial neck muscles compared to migraine patients without (p = 0.023). Ictal neck pain was not associated with migraine localization, tension-type headache, or markers of central sensitization. Prospective data of 84 patients showed that tenderness of trigeminal sensory innervated muscles increased the migraine attack rate (p = 0.035). The distinction of migraine patients based on the occurrence of ictal neck pain could indicate migraine subtypes and possible involvement of peripheral tissue in the pathophysiology. Whether treatment responses differ among these groups would be fascinating. Additionally, we found that cephalic muscle tenderness is a risk factor for an impending migraine attack.

Background: Neck pain in migraine patients is very prevalent between and during migraine attacks, but the underlying mechanism behind neck pain in migraine is unknown. The neck muscle rectus capitis posterior minor muscle (RCPmi) may be important since it is connected to the occipital dura mater. In this study, we examined the RCPmi volume in migraine patients and compared with controls. Methods: We conducted a cross-sectional MRI study examining muscle volume in 40 episodic migraine patients and 40 controls in preexisting images from prior studies. Three-dimensional T1 weighted sequences were collected with a 3.0 T MRI Scanner. The volume of RCPmi was examined by manually tracing the muscle circumference with Horos medical image viewer. The observer was blinded to participant information. No information regarding neck pain status during or between migraine attacks were available. Results: The mean RCPmi volume was 1.22cm³ in migraine patients and 1.17cm³ in controls (p = 0.549). We found no differences in RCPmi volume on the pain side vs. the non-pain side (p = 0.237) in patients with unilateral migraine. There were no association between the muscle volume and years with migraine, headache or migraine frequency, age or BMI. Conclusions: We found no difference in RCPmi volume between migraine patients and controls, suggesting no structural RCPmi pathology in migraine.

Supraglottic EILO could be inherited. Different modes of inheritance can explain the results of this study.http://ow.ly/5XAv30csDRa