The interest in dry needling as a treatment option for myofascial pain has flourished for the last decades and will probably continue to do so, because multiple clinical effects can be attributed to this technique. However, evidence about the underlying physiological mechanisms of its effects is still underrepresented in scientific research and caution must be taken in generalizing results from acupuncture or animal research. This review offers an overview of the possible mechanisms involved in the pathophysiology of myofascial trigger points, that is, the formation of the taut band, the presence of local pain and inflammation, and the occurrence of referred pain. Subsequently, the effect of dry needling on these same aspects will be discussed. The goal of this article is to provide clinicians with the most up to date insights in the underlying (neuro)physiological mechanisms of trigger point dry needling and to identify the opportunities for further research on this topic.

ABSTRACT:The interest in dry needling as a treatment option for myofascial pain has flourished for the last decades and will probably continue to do so, because multiple clinical effects can be attributed to this technique. However, evidence about the underlying physiological mechanisms of its effects is still underrepresented in scientific research and caution must be taken in generalizing results from acupuncture or animal research. This review offers an overview of the possible mechanisms involved in the pathophysiology of myofascial trigger points, that is, the formation of the taut band, the presence of local pain and inflammation, and the occurrence of referred pain. Subsequently, the effect of dry needling on these same aspects will be discussed. The goal of this article is to provide clinicians with the most up to date insights in the underlying (neuro)physiological mechanisms of trigger point dry needling and to identify the opportunities for further research on this topic.

The International Symposium on Myofascial Pain, Fibromyalgia, and Fascial Pain Disorders was held at the University of Padua, Padua, Italy in June of 2023. This report presents a summary of the presentations from scientists and clinicians from around the world who presented to the symposium. The purpose of this symposium and resultant paper is improve health professional’s recognition and understanding of the clinical characteristics, co-morbidities, mechanisms, and treatment strategies for these common conditions to better understand and manage their pain, dysfunction, and quality life.

The origin of the myofascial trigger point (TrP), an anomalous locus in muscle, has never been well-described. A new trigger point hypothesis (the new hypothesis) presented here addresses this lack. The new hypothesis is based on the concept that existing myoprotective feedback mechanisms that respond to muscle overactivity, low levels of adenosine triphosphate, (ATP) or a low pH, fail to protect muscle in certain circumstances, such as intense muscle activity, resulting in an abnormal accumulation of intracellular Ca2+, persistent actin-myosin cross bridging, and then activation of the nociceptive system, resulting in the formation of a trigger point. The relevant protective feedback mechanisms include pre- and postsynaptic sympathetic nervous system modulation, modulators of acetylcholine release at the neuromuscular junction, and mutations/variants or post-translational functional alterations in either of two ion channelopathies, the ryanodine receptor and the potassium-ATP ion channel, both of which exist in multiple mutation states that up- or downregulate ion channel function. The concepts that are central to the origin of at least some TrPs are the failure of protective feedback mechanisms and/or of certain ion channelopathies that are new concepts in relation to myofascial trigger points.

Myofascial pain syndrome is featured by the presence of myofascial trigger points (TrPs). Whether TrPs are primary or secondary phenomena or if they relate to central or peripheral nervous system disorders is controversial. Referred pain, a cardinal sign of TrPs, is a central phenomenon driven by peripheral input. In 2021, the International Association for the Study of Pain (IASP) proposed a clinical criteria and grading system for classifying patients with pain on nociceptive, neuropathic, or nociplastic phenotypes. Myofascial TrP pain has been traditionally categorized as a nociceptive phenotype; however, increasing evidence supports that this condition could be present in patients with predominantly nociplastic pain, particularly when it is associated with an underlying medical condition. The clinical response of some therapeutic approaches for managing TrPs remains unclear. Accordingly, the ability to classify myofascial TrP pain into one of these phenotypes would likely be critical for producing more successful clinical treatment outcomes by a precision medicine approach. This consensus paper presents evidence supporting the possibility of subgrouping individuals with myofascial TrP pain into nociceptive, nociplastic, or mixed-type phenotype. It is concluded that myofascial pain caused by TrPs is primarily a nociceptive pain condition, is unlikely to be classified as neuropathic or nociplastic, but can be present in patients with predominantly neuropathic or nociplastic pain. In the latter cases, management of the predominant central pain problem should be a major treatment goal, but the peripheral drive from TrPs should not be ignored, since TrP treatment has been shown to reduce sensitization-associated symptomatology in nociplastic pain conditions, e.g., fibromyalgia.

OBJECTIVES:To develop evidence-based expert recommendations for non-pharmacological treatments for pain, fatigue, sleep problems, and depression in fibromyalgia.METHODS:An international, multidisciplinary Delphi exercise was conducted. Authors of EULAR and the Canadian Fibromyalgia Guidelines Group, members of the American Pain Society and clinicians with expertise in fibromyalgia were invited. Participants were asked to select non-pharmacological interventions that could be offered for specific fibromyalgia symptoms and to classify them as either core or adjunctive treatments. An evidence summary was provided to aid the decision making. Items receiving >70% votes were accepted, those receiving <30% votes were rejected and those obtaining 30-70% votes were recirculated for up to two additional rounds.RESULTS:Seventeen experts participated (Europe (n = 10), North America (n = 6), and Israel (n = 1)) in the Delphi exercise and completed all three rounds. Aerobic exercise, education, sleep hygiene and cognitive behavioural therapy were recommended as core treatments for all symptoms. Mind-body exercises were recommended as core interventions for pain, fatigue and sleep problems. Mindfulness was voted core treatment for depression, and adjunctive treatment for other symptoms. Other interventions, namely music, relaxation, hot bath, and local heat were voted as adjunctive treatments, varying between symptoms.CONCLUSIONS:This study provided evidence-based expert consensus recommendations on non-pharmacological treatments for fibromyalgia that may be used to individualise treatments in clinical practice targeting the diverse symptoms associated with fibromyalgia.

OBJECTIVEThe myofascial trigger point hypothesis postulates that there are small foci of contracted sarcomeres in resting skeletal muscle. Only one example, in canine muscle, has been published previously. This study evaluated human muscle biopsies for foci of contracted sarcomeres.SETTINGThe Departments of Rehabilitation Sciences and Physiotherapy at Ghent University, Ghent, Belgium.SUBJECTSBiopsies from 28 women with or without trapezius myalgia were evaluated, 14 in each group.METHODSMuscle biopsies were obtained from regions of taut bands in the trapezius muscle and processed for light and electron microscopy and for histochemical analysis. Examination of the biopsies was blinded as to group.RESULTSA small number of foci of segmentally contracted sarcomeres were identified. One fusiform segmental locus involved the entire muscle fiber in tissue from a myalgic subject. Several transition zones from normal to contracted sarcomeres were found in both myalgic and nonmyalgic subjects. The distance between Z-lines in contracted sarcomeres was about 25-45% of the same distance in normal sarcomeres. Z-lines were disrupted and smeared in the contracted sarcomeres.CONCLUSIONSA small number of foci of segmentally contracted sarcomeres were found in relaxed trapezius muscle in human subjects, a confirmation of the only other example of spontaneous segmental contraction of sarcomeres (in a canine muscle specimen), consistent with the hypothesis of trigger point formation and with the presence of trigger point end plate noise.

Trigeminal neuralgia (TN), the most common form of severe facial pain, may be confused with an ill-defined persistent idiopathic facial pain (PIFP). Facial pain is reviewed and a detailed discussion of TN and PIFP is presented. A possible cause for PIFP is proposed. (1) Methods: Databases were searched for articles related to facial pain, TN, and PIFP. Relevant articles were selected, and all systematic reviews and meta-analyses were included. (2) Discussion: The lifetime prevalence for TN is approximately 0.3% and for PIFP approximately 0.03%. TN is 15–20 times more common in persons with multiple sclerosis. Most cases of TN are caused by neurovascular compression, but a significant number are secondary to inflammation, tumor or trauma. The cause of PIFP remains unknown. Well-established TN treatment protocols include pharmacotherapy, neurotoxin denervation, peripheral nerve ablation, focused radiation, and microvascular decompression, with high rates of relief and varying degrees of adverse outcomes. No such protocols exist for PIFP. (3) Conclusion: PIFP may be confused with TN, but treatment possibilities differ greatly. Head and neck muscle myofascial pain syndrome is suggested as a possible cause of PIFP, a consideration that could open new approaches to treatment.

The diagnosis of myofascial pain syndrome (MPS) is made by physical examination and history; the physical examination is the palpation of muscle, and the history is that of the nature of the pain. There is as yet no laboratory test that allows a clinical diagnosis to be made. The diagnosis is currently made by identifying a myofascial trigger point (TrP) in a person whose pain is consistent with the pain of a TrP and whose pain is reproduced in part by activation of the TrP. However, even this statement is contentious because there has been no consensus on how to identify the TrP or how to diagnose MPS. Fern andez-de-las-Pe~ nas and Dommerholt in this issue [1] have provided us with such a consensus, that will be useful in guiding further studies.

OBJECTIVE:To improve the understanding of chronic pelvic pain (CPP) and to provide evidence-based guidelines of value to primary care health professionals, general obstetricians and gynaecologists, and those who specialize in chronic pain.BURDEN OF SUFFERING:CPP is a common, debilitating condition affecting women. It accounts for substantial personal suffering and health care expenditure for interventions, including multiple consultations and medical and surgical therapies. Because the underlying pathophysiology of this complex condition is poorly understood, these treatments have met with variable success rates.OUTCOMES:Effectiveness of diagnostic and therapeutic options, including assessment of myofascial dysfunction, multidisciplinary care, a rehabilitation model that emphasizes achieving higher function with some pain rather than a cure, and appropriate use of opiates for the chronic pain state.EVIDENCE:Medline and the Cochrane Database from 1982 to 2004 were searched for articles in English on subjects related to CPP, including acute care management, myofascial dysfunction, and medical and surgical therapeutic options. The committee reviewed the literature and available data from a needs assessment of subjects with CPP, using a consensus approach to develop recommendations.VALUES:The quality of the evidence was rated using the criteria described in the Report of the Canadian Task Force on the Periodic Health Examination. Recommendations for practice were ranked according to the method described in that report (Table 1).RECOMMENDATIONS:The recommendations are directed to the following areas: (a) an understanding of the needs of women with CPP; (b) general clinical assessment; (c) practical assessment of pain levels; (d) myofascial pain; (e) medications and surgical procedures; (d) principles of opiate management; (f) increased use of magnetic resonance imaging (MRI); (g) documentation of the surgically observed extent of disease; (h) alternative therapies; (i) access to multidisciplinary care models that have components of physical therapy (such as exercise and posture) and psychology (such as cognitive-behavioural therapy), along with other medical disciplines, such as gynaecology and anesthesia; G) increased attention to CPP in the training of health care professionals; and (k) increased attention to CPP in formal, high-calibre research. The committee recommends that provincial ministries of health pursue the creation of multidisciplinary teams to manage the condition.

Post-dry needling soreness is a common complication of myofascial trigger point (MTrP) dry needling treatment. The prevention, management and relevance of this complication remain uncertain. This paper examines the current state of knowledge and suggests directions for further studies in this area. MTrPs are hypersensitive nodules in skeletal muscles' taut bands, present in several pain conditions. Dry needling has been recommended for relieving MTrP pain. MTrP dry needling procedures have shown to be associated with post-needling soreness, which is thought to be a consequence of the neuromuscular damage, and hemorrhagic and inflammatory reaction generated by the needle. Postneedling soreness is a very frequent effect after deep dry needling, usually lasting less than 72 h. It may not be especially distressing for most patients. However, patients presenting with higher levels of post-needling soreness, not perceiving dry needling effectiveness in the first session, or not having high myofascial pain intensity before treatment, could be the most likely to find post-needling soreness more distressing, functionally limiting and to abandon treatment. Future research should assess the clinical relevance of post-needling soreness. Post-needling soreness should be considered when investigating dry needling effectiveness since it could overlie the original myofascial pain and influence the patients' pain ratings.

The longus colli muscle is a neck flexor believed to play an important role in pain originating in the neck region, including pain resulting from whiplash injuries. Despite the clinical importance attributed to it, the pain referral pattern of the longus colli has previously been described only in a small cohort of subjects. Here, we aim to delineate the pain referral pattern of the longus colli muscle. Thirty-five healthy volunteers underwent deep massage of the longus colli followed by dry needling of the muscle. The subjects depicted the distribution of the pain they experienced on a blank manikin. Their drawings were digitized and used to produce pain pattern histogram maps. The pain referral pattern during deep massage and needling of the longus colli was primarily local, with referral to the ipsilateral ear and lateral to the ipsilateral eye. Some subjects reported pain on the contralateral side of the neck.

This issue of WJMP contains two articles (1,2) that address the problem of hypermobility syndrome (1,2): one article, Inter- and Intra-rater Reliability of the Beighton Score Compared to the Contom...

Dear Editor, I thank Drs. Quintner and Cohen for their interest in my editorial [1] about the study by Albrect et al. [2]. Drs. Quintner and Cohen have raised several concerns about my discussion of the implications of that study, especially of the concept that peripheral nociception by myofascial trigger points initiates central sensitization. They object to the idea that peripheral nerve sensitization is the fundamental “driver” of, as they put it, all possible somatic mechanisms of pain in fibromyalgia, which they claim is found in the editorial. I agree that this idea is extreme and is incorrect. However, my editorial states only that “peripheral nociceptive sites play an important role in initiating and maintaining pain … Pain is the outcome of a complex interplay between … central modulation and peripheral input.” However, Albrecht et al. [2] in their article do discuss in detail the implications of their work on some of the many manifestations of fibromyalgia, specifically fatigue, sleep, and cognition, through the potential of reduced blood flow to skeletal muscle caused by shunting blood from muscle to glaborous skin during exercise. The central issue raised by Quintner and Cohen is the role that active peripheral nociception plays in chronic widespread pain. This is a role that they doubt exists. Quintner and Cohen question the evidence that I presented in the editorial that demonstrates that trigger points are a peripheral nociceptive input leading to central sensitization. They believe that it is a …