Myofascial Trigger Points: Pathophysiology And ...
Questions from patients about pain conditions and analgesic pharmacotherapy and responses from authors are presented to help educate patients and make them more effective self-advocates. Trigger point pathophysiology in myofascial pain syndrome, which involves muscle stiffness, tenderness, and pain that radiates to other areas of the body, is considered. The causes of trigger points and several theories about how they develop are reviewed, and treatment approaches, including stretching, physical therapy, dry needling, and injections, are offered.
Myofascial Trigger Points: Pathophysiology and ...
Myofascial trigger points (MTrPs), also known as trigger points, are described as hyperirritable spots in the skeletal muscle. They are associated with palpable nodules in taut bands of muscle fibers.[1] They are a topic of ongoing controversy, as there is limited data to inform a scientific understanding of the phenomenon. Accordingly, a formal acceptance of myofascial "knots" as an identifiable source of pain is more common among bodyworkers, physical therapists, chiropractors, and osteopathic practitioners. Nonetheless, the concept of trigger points provides a framework which may be used to help address certain musculoskeletal pain.
Since the early 2000s several research studies have been conducted to determine if there was a way to visualize myofascial trigger points using tools such as ultrasound imaging and magnetic resonance elastography.[7][8][9][10] Several of these studies have been dismissed under meta-analysis.[11] Another synthetic literature review expressed more optimism about the validity of imaging for myofascial trigger points, but admitted small sample sizes of the reviewed studies.[12]
The misdiagnosis of pain is the most important issue taken up by Travell and Simons. Referred pain from trigger points mimics the symptoms of a very long list of common maladies, but physicians, in weighing all the possible causes for a given condition, rarely consider a myofascial source. The study of trigger points has not historically been part of medical education. Travell and Simons hold that most of the common everyday pain is caused by myofascial trigger points and that ignorance of that basic concept could inevitably lead to false diagnoses and the ultimate failure to deal effectively with pain.[14]
Studies have shown a moderate level of evidence for manual therapy for short-term relief in the treatment of myofascial trigger points. Dry needling and dry cupping have not shown evidence of efficacy greater than a placebo. There have not been enough in-depth studies to be conclusive about the latter treatment modalities, however.[25]
In the 19th century, British physician George William Balfour, German anatomist Robert Froriep, and the German physician Strauss described pressure-sensitive, painful knots in muscles, sometimes called myofascial trigger points through retrospective diagnosis.[31][32]
A review from 2015 in the journal Rheumatology, official journal of the British Society for Rheumatology, came to the conclusion that the concept of myofascial pain caused by trigger points was nothing but an invention without any scientific basis.[33] A rejection of this criticism appeared in the Journal of Bodywork & Movement Therapies, the official journal of several therapeutic societies, including The National Association of Myofascial Trigger Point Therapists USA.[34][35]
Active myofascial trigger points are one of the major peripheral pain generators for regional and generalized musculoskeletal pain conditions. Myofascial trigger points are also the targets for acupuncture and/or dry needling therapies. Recent evidence in the understanding of the pathophysiology of myofascial trigger points supports The Integrated Hypothesis for the trigger point formation; however unanswered questions remain. Current evidence shows that spontaneous electrical activity at myofascial trigger point originates from the extrafusal motor endplate. The spontaneous electrical activity represents focal muscle fiber contraction and/or muscle cramp potentials depending on trigger point sensitivity. Local pain and tenderness at myofascial trigger points are largely due to nociceptor sensitization with a lesser contribution from non-nociceptor sensitization. Nociceptor and non-nociceptor sensitization at myofascial trigger points may be part of the process of muscle ischemia associated with sustained focal muscle contraction and/or muscle cramps. Referred pain is dependent on the sensitivity of myofascial trigger points. Active myofascial trigger points may play an important role in the transition from localized pain to generalized pain conditions via the enhanced central sensitization, decreased descending inhibition and dysfunctional motor control strategy.
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 how active MTPs are involved in the transition from the localized pain to generalized pain conditions.
An example of motor behavior of spontaneous electrical activity (SEA) of a myofascial trigger point (MTP) during trapezius muscle contraction. The electromyographic (EMG) activity of the SEA of an MTP is similar to the surface EMG over an MTP on one side of the upper trapezius and to both the surface and intramuscular EMG activity of a normal muscle point on the other side of the upper trapezius. Note: following needle insertion into a MTP, surface EMG recording shows low amplitude activities.
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.
Migraine affects 16% of the population in Europe [1] with high individual and socioeconomic costs [2, 3]. Several mechanisms have been proposed to be involved in its pathophysiology including vascular, peripheral and central mechanisms [4,5,6,7,8,9]. Jes Olesen systematically described pericranial tenderness in migraine patients, both during and outside of migraine attacks [10, 11], leading to speculations that myofascial mechanisms may be involved in migraine [12]. 041b061a72