Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation

Myofascial trigger points (MTPs) are hyperirritable spots in skeletal muscle associated with palpable nodules in the taut bands of muscle fibers. When these palpable nodules are stimulated mechanically, local pain and referred pain can be induced together with visible local twitch response [1,2]. MTPs can be either active or latent. An active MTP is one that refers pain either locally to a large area and/or to another remote location, the local and referred pain can be spontaneous or reproduced by mechanical stimulation which elicits a patient-recognized pain. A latent MTP does not reproduce the clinical pain complaint but may exhibit all of the features of an active MTP to a minor degree. Myofascial pain syndrome due to MTPs can be acute or chronic, regional or generalized; it can also be a primary disorder leading to local or regional pain syndromes or a secondary disorder as a consequence of other conditions [3]. Active MTPs contribute significantly to the regional acute and chronic myofascial pain syndrome [2,3], such as lateral epicondylalgia [4], headache and mechanical neck pain [5] and temporomandibular pain disorders [6]. Active MTPs are also the main peripheral pain generator in generalized musculoskeletal pain disorders [3], such as fibromyalgia and whiplash syndrome [7,8]. MTPs are the targets for acupuncture and/or dry needling [9] and other pain therapies. Indeed, MTP anesthetization decreases both pain intensity and central sensitization in local pain and generalized pain conditions [8,10,11]. Two reviews have been published recently focusing on the current state of knowledge of myofascial pain syndrome associated with MTPs [12,13]. New evidence has emerged suggesting an important role of spontaneous electrical activity (SEA) at MTPs in the induction of muscle pain and central sensitization. This article reviews the literatures in the last decade about the SEA at MTPs; in particular, how SEA contributes to the induction of local and referred pain and