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BackgroundResearch in migraine points towards central-peripheral complexity with a widespread pattern of structures involved. Migraine-associated neck and shoulder muscle pain has clinically been conceptualized as myofascial trigger points (mTrPs). However, concepts remain controversial, and the identification of mTrPs is mostly restricted to manual palpation in clinical routine. This study investigates a more objective, quantitative assessment of mTrPs by means of magnetic resonance imaging (MRI) with T2 mapping.MethodsTen subjects (nine females, 25.6 ± 5.2 years) with a diagnosis of migraine according to ICHD-3 underwent bilateral manual palpation of the upper trapezius muscles to localize mTrPs. Capsules were attached to the skin adjacent to the palpated mTrPs for marking. MRI of the neck and shoulder region was performed at 3 T, including a T2-prepared, three-dimensional (3D) turbo spin echo (TSE) sequence. The T2-prepared 3D TSE sequence was used to generate T2 maps, followed by manual placement of regions of interest (ROIs) covering the trapezius muscles of both sides and signal alterations attributable to mTrPs.ResultsThe trapezius muscles showed an average T2 value of 27.7 ± 1.4 ms for the right and an average T2 value of 28.7 ± 1.0 ms for the left side (p = 0.1055). Concerning signal alterations in T2 maps attributed to mTrPs, nine values were obtained for the right (32.3 ± 2.5 ms) and left side (33.0 ± 1.5 ms), respectively (p = 0.0781). When comparing the T2 values of the trapezius muscles to the T2 values extracted from the signal alterations attributed to the mTrPs of the ipsilateral side, we observed a statistically significant difference (p = 0.0039). T2 hyperintensities according to visual image inspection were only reported in four subjects for the right and in two subjects for the left side.ConclusionsOur approach enables the identification of mTrPs and their quantification in terms of T2 mapping even in the absence of qualitative signal alterations. Thus, it (1) might potentially challenge the current gold-standard method of physical examination of mTrPs, (2) could allow for more targeted and objectively verifiable interventions, and (3) could add valuable models to understand better central-peripheral mechanisms in migraine.

Pathogenic variants in PRRT2, encoding the proline-rich transmembrane protein 2, have been associated with an evolving spectrum of paroxysmal neurologic disorders. Based on a cohort of children with PRRT2-related infantile epilepsy, this study aimed at delineating the broad clinical spectrum of PRRT2-associated phenotypes in these children and their relatives. Only a few recent larger cohort studies are on record and findings from single reports were not confirmed so far. We collected detailed genetic and phenotypic data of 40 previously unreported patients from 36 families. All patients had benign infantile epilepsy and harbored pathogenic variants in PRRT2 (core cohort). Clinical data of 62 family members were included, comprising a cohort of 102 individuals (extended cohort) with PRRT2-associated neurological disease. Additional phenotypes in the cohort of patients with benign sporadic and familial infantile epilepsy consist of movement disorders with paroxysmal kinesigenic dyskinesia in six patients, infantile-onset movement disorders in 2 of 40 individuals, and episodic ataxia after mild head trauma in one girl with bi-allelic variants in PRRT2. The same girl displayed a focal cortical dysplasia upon brain imaging. Familial hemiplegic migraine and migraine with aura were reported in nine families. A single individual developed epilepsy with continuous spikes and waves during sleep. In addition to known variants, we report the novel variant c.843G>T, p.(Trp281Cys) that co-segregated with benign infantile epilepsy and migraine in one family. Our study highlights the variability of clinical presentations of patients harboring pathogenic PRRT2 variants and expands the associated phenotypic spectrum.

Purpose: Repetitive peripheral magnetic stimulation (rPMS) has been successfully applied recently in migraineurs to alleviate migraine symptoms. Symptom relief has been achieved by stimulating myofascial trigger points (mTrPs) of the trapezius muscles, which are considered part of the trigemino-cervical complex (TCC). However, effects on musculature have not been assessed in detail, and the specificity of effects to muscles considered part of the TCC yet has to be elucidated. Against this background, this study presents the setup of rPMS in migraine and evaluates effects on skeletal musculature. Materials and Methods: Thirty-seven adults (mean age: 25.0 ± 4.1 years, 36 females) suffering from migraine and presenting mTrPs according to physical examination underwent rPMS either to mTrPs in the trapezius muscles (considered part of the TCC; n = 19) or deltoid muscles (considered not part of the TCC; n = 18) during six sessions over the course of 2 weeks. Standardized questionnaires were filled in to assess any adverse events and experience with rPMS as well as satisfaction and benefits from stimulation. Algometry was performed to evaluate changes in pressure pain thresholds (PPTs). Results: All stimulation sessions were successfully performed without adverse events, with 84.2% of subjects of the trapezius group and 94.4% of subjects of the deltoid group describing rPMS as comfortable ( p = 0.736). Muscular pain or tension improved in 73.7% of subjects of the trapezius group and in 61.1% of subjects of the deltoid group ( p = 0.077). PPTs of the trapezius muscles clearly increased from the first to the last stimulation sessions—regardless of the stimulated muscle (rPMS to the trapezius or deltoid muscles). However, depending on the examined muscles the increase of PPTs differed significantly (subjects with stimulation of trapezius muscles: p = 0.021; subjects with stimulation of deltoid muscles: p = 0.080). Conclusion: rPMS is a comfortable method in migraineurs that can improve local muscular pain or tension. Furthermore, it is able to increase directly and indirectly the PPTs of the trapezius muscles (considered part of the TCC) when applied over mTrPs, supporting the role of the TCC in migraineurs.