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Ultrasound guided dry needling: Relevance in chronic pain LC VasAshirvad Institute for Pain Management and Research, Mumbai, Maharashtra, India
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/jpgm.jpgm_710_21
Dry needling (DN) is a specific treatment for myofascial pain syndromes (MPS) wherein a needle is inserted into a painful site in the muscle called myofascial trigger point (MTrP). An MTrP is defined as “a hyperirritable spot” within a painful taut band in a skeletal muscle associated with motor dysfunction, autonomic phenomena, and characteristic referral of pain.[1] MTrPs exhibit a unique local twitch response (LTR) on needle insertion mediated by a spinal reflex. LTR can be seen/felt/recorded electromyographically and visualized with ultrasound. Active MTrPs are spontaneously painful and refer pain and paresthesia to distal sites. Latent MTrPs are painful only on palpation. Importantly, both active and latent MTrPs stimulate muscle nociceptors, disturb motor function by causing muscle stiffness and weakness, and restrict the range of motion (ROM).[2],[3] DN causes immediate, complete analgesia by a physical “needle effect” without any injection.[4] Ultrasound visualization of DN provides novel insights into muscle function and emphasizes that muscles seldom act in isolation. LTRs that are pathognomonic of MTrPs are routinely visualized in coworking muscles indicating that there is a much wider distribution of MTrPs than is currently assumed. For example, MTrPs in agonist muscles (flexors) apparently cause strain leading to reactive MTrPs in coworking muscles like antagonists (extensors), other agonists (synergists), and fixators.[5] Presumably, the MTrP numbers are insufficient to produce pain or tenderness above the perceptible threshold in these muscles. Routine confirmation of LTRs in coworking muscles has led to our hypothesis that pain and tenderness form just the tip of the iceberg, whereas the actual pain pathology lies in the whole muscle and its functional counterparts. Most of the LTRs seen during USGDN would neither be visible nor sought by the present DN practitioners who do not use ultrasound. Thus, ultrasound visualization revolutionizes DN into a more extensive as well as comprehensive version called USGDN, which addresses the interrelated functioning of the various structures in the body that work as parts of the whole: when one part suffers, it appears to involve all the others. Therefore, MPS becomes a neuromuscular problem and neuropathies become neuromyopathies manifesting with MPS. Both DN and USGDN use acupuncture needles because they are the thinnest available in the market (30–34 gauge), but the similarity ends there [see [Table 1]].
Furthermore, USGDN targets not only the pain but also the disability resulting from the structural impairment caused by a taut band that mechanically alters the function in all coworking muscles. This makes USGDN a specific treatment option for all chronic pains such as neuropathic pains, cancer pains, back pains, and arthritic pains, all of which manifest with MPS.[5] This editorial discusses the latest findings on MTrPs and MPS and will put together the various jigsaw pieces scattered across pain literature to present a radically different understanding of chronic pain. We have assembled personal observations and the ultrasound evidence gathered over our experience of 16 years, to hypothesize that motor neuropathy is responsible for the ubiquitous prevalence of MPS seen in chronic pain conditions. As a specific treatment of MPS, USGDN has the potential to revolutionize the current practice of pain management.
Electromyography of normal human neuromuscular endplate demonstrates discrete, random, positive miniature end-plate potentials (MEPPs) at approximately 6/s. The MTrP region is characterized by a barrage of potentials (110/s) called end-plate noise (EPN) due to the grossly (3×) increased release of acetylcholine from the nerve terminal.[1] This crescendo of EPN leads to muscle contracture associated with deep squeezing pain and autonomic manifestations of lightheadedness, diaphoresis, or nausea. Integrated hypothesis and its later modification propose that the relative lack of ATP (and perhaps oxygen), which is required to break the cross-bridges between actin and myosin filaments leads myosin filaments getting stuck at the Z band to form an MTrP.[1] Increased metabolic stress from sustained muscle contraction combined with a relative reduction of blood flow probably triggers increased release of inflammatory mediators (IM) and neurotransmitters, which ensure the generation and persistence of MTrPs in MPS. Abnormally contracted sarcomeres seen to be arranged unevenly on histopathology of human MTrPs corroborates this.[6] Microdialysis by Shah et al.[7] demonstrated significantly higher IM levels, comprising protons, bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor, interleukin-1, serotonin, and norepinephrine in the local milieu of active MTrPs compared with latent MTrPs, which, in turn, is higher than that in normal muscle. Samples obtained before and after DN showed lower IM in the MTrP after DN, presumed to be due to increased local blood flow washing out the IM, which reduces pain and tenderness. These authors described MPS as a complex form of neuromuscular dysfunction: the neurogenic inflammation and IM in the tissue milieu of the MTrP stimulate muscle nociceptors and sensitize the afferent nociceptive nerves. This peripheral sensitization of muscle nociception progresses to central sensitization, and later limbic system dysfunction with ongoing initiation, sustenance, amplification, and perpetuation of MPS.[8] Magnetic resonance elastography and 3D ultrasound can reliably assess and quantify the mechanical characteristics of the MTrP, such as localized areas of increased muscle stiffness at the taut band and the disordered recruitment of muscle fibers that results in weaker, painful, and incoordinate movements.[9],[10]
The foundational work on MTrPs and DN was carried out by eminent physicians, yet the current practice and formal teaching of DN are carried out by physiotherapists. Needles are inserted by anatomical guesswork which can miss low-intensity LTRs, MTrPs in deeper muscles, and those in obese patients [Table 1]. There is no way to identify evolving, yet-to-become-painful MTrPs, nor the presence of taut bands, which are still too fine to be felt by gross clinical examination. MTrPs in coworking muscle groups are neither acknowledged nor elicited. These might well be the reasons for the findings of a 2017 systematic review and meta-analysis on DN effectiveness performed by physical therapists. The authors concluded that that the efficacy of DN in reducing pain in short-term follow-up had low-to-moderate quality evidence compared with no treatment. Evidence for the long-term benefit of DN is currently lacking.[11] These results are very markedly different from the effectiveness of USGDN at our center, in a variety of pain conditions [Table 2] and [Table 3].[5],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27]
USGDN requires a thorough knowledge of sonoanatomy and the ability to steer needles under ultrasound visualization, which ensures accurate needle placement [Figure 1] while avoiding visceral, pleural, and neurovascular injury, all of which have been reported with blindly performed DN.[1] But we believe that by far the most significant lacuna of blind DN is that it confines the practitioner's understanding of MPS to a few detectable MTrPs. In contrast, USGDN emphasizes the actual enormity of the MPS problem by demonstrating LTRs in coworking muscles as the needle passes through various muscle layers, particularly in the deepest muscles closest to ribs, pleura, and peritoneum. Furthermore, observation of structural disruption of muscle in complex regional pain syndrome (CRPS) and its reversal by USGDN has led to a novel understanding of CRPS pathophysiology [Figure 2], [Table 2].[12],[13],[14],[15],[16],[17]
The videos can be accessed using below links: Video 1 - [Additional file 1] Video 2 - [Additional file 2] Video 3 - [Additional file 3] Video 4 - [Additional file 4] Video 5 - [Additional file 5] Video 6 - [Additional file 6] Video 7 - [Additional file 7] Video 8 - [Additional file 8] Video 9 - [Additional file 9] Video 10 - [Additional file 10] Video 11 - [Additional file 11] Video 12 - [Additional file 12] Video 13 - [Additional file 13] Video 14 - [Additional file 14]
Neuropathic pains that form the majority of chronic pains are defined as “pains arising as a direct consequence of a lesion or disease affecting the somatosensory system.”[28] Hence, current treatments target the different components of the somatosensory pain pathway, including:
However, the above interventions leave behind significant residual pains for which opioids are routinely prescribed, in both cancer and noncancer pains. Unfortunately, neuropathic pains are notoriously resistant to opioids leading to drug-seeking behavior, a major contributor to the present opioid crisis in the west. [Figure 4] shows the diagrammatic representation of a working hypothesis, which links the robust evidence for MTrP genesis to motor neuropathy,[1],[2],[3],[4],[5],[6],[7],[8],[9],[10] to explain the staggering prevalence of MPS (70%–95%) in chronic pains.[29],[30],[31],[32] Instead of dismissing this MPS as “secondary” to pain and disuse,[28] this hypothesis emphasizes that muscles are not just passive expressors of neuropathy/neuromyopathy but are its dynamic perpetrators, facilitators, sustainers, and amplifiers. The sheer interdependent complexity of muscle function ensures the production of myriad bizarre symptoms, which are the hallmark of neuropathic pain syndromes. These pains from MPS persist despite surgery, opioid administration, and current pain management interventions, including spinal cord stimulation.
These recalcitrant pains from MPS are comprehensively addressed by systematic USGDN and USGDN-guided botulinum toxin injection, with a dramatic and lasting reversal of many chronic pain conditions [Table 2] and [Table 3], including the residual pains that persist after current neural interventions. USGDN is unique in providing not just pain relief but lasting disability relief, which all the other current interventions fail to achieve. Routine and predictable relief of “sensory neuropathic symptoms” such as burning, allodynia, hyperalgesia, and hyperaesthesia (in postherpetic neuralgia, postsurgical neuropathy, postlaminectomy syndrome, cancer pains, brachial plexus injuries, CRPS, etc.) by USGDN suggests an interesting possibility that these “sensory” symptoms might actually be manifestations of intense spasm of underlying muscles and/or dermal motor elements and erector pili muscles.[16]
A paradigm change of the current understanding of neuropathy that includes the motor as much as the somatosensory system not only explains the ubiquitous presence of MPS in chronic pains but also opens up new exciting possibilities in pain management. Effective treatments such as USGDN alone or in combination with neural interventions could significantly reduce the biological contribution to the biopsychosocial model of chronic pain. Further research is required to unequivocally prove the concept of neuromyopathy and the efficacy of USGDN over opioids through well-designed clinical trials.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]
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