CLINICAL SIGNIFICANCE OF MYOFASCIAL TRIGGER POINTS IN CERVICOGENIC HEADACHE: FROM PHENOTYPING TO TARGETED BOTULINUM TOXIN TYPE A THERAPY

Abstract

Cervicogenic headache (CGH) is a secondary headache attributed to cervical structures and soft tissues, with a clinical phenotype that may partially overlap with migraine and tension-type headache. Active myofascial trigger points can reproduce a patient’s familiar headache, increase local pressure sensitivity, and amplify symptoms provoked by cervical movement or sustained posture. These observations support a view of CGH as a heterogeneous clinical syndrome in which articular, muscular, myofascial, and nociceptive mechanisms contribute in different proportions. This narrative review analyzes the clinical and pathophysiological significance of myofascial trigger points in CGH and examines the value of pressure pain threshold assessment, cervical range of motion, the Cervical Flexion-Rotation Test, the Neck Disability Index, and the Headache Impact Test-6 for phenotyping patients. The biological rationale for botulinum toxin type A (BoNT-A) is considered beyond muscle relaxation, including its capacity to interfere with the release of nociceptive mediators from peripheral sensory terminals. Current clinical evidence for BoNT-A in CGH is inconsistent: some controlled studies report reductions in headache intensity and frequency, whereas a methodologically rigorous crossover trial found no significant advantage over placebo. Recent reviews emphasize substantial heterogeneity in diagnostic criteria, toxin formulation, dose, injection sites, and outcome measures. We therefore propose a hypothesis-generating clinical framework that integrates the number and distribution of active trigger points, reproduction of the habitual headache on palpation, pressure pain thresholds, cervical mobility, functional disability, headache burden, and analgesic use. Such multidimensional phenotyping may provide a more rational basis for future prospective studies designed to identify patients who are more likely to respond to trigger point-targeted BoNT-A therapy.