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  IN THIS Article
 :: Introduction
 ::  Current Evidence...
 :: DN Versus USGDN
 ::  Ultrasound Obser...
 ::  Potential of USG...
 :: Conclusion
 ::  References
 ::  Article Figures
 ::  Article Tables

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EDITORIAL
Year : 2022  |  Volume : 68  |  Issue : 1  |  Page : 1-9

Ultrasound guided dry needling: Relevance in chronic pain


Ashirvad Institute for Pain Management and Research, Mumbai, Maharashtra, India

Date of Submission20-Jul-2021
Date of Decision18-Nov-2021
Date of Acceptance25-Nov-2021
Date of Web Publication19-Jan-2022

Correspondence Address:
L C Vas
Ashirvad Institute for Pain Management and Research, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpgm.jpgm_710_21

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How to cite this article:
Vas L C. Ultrasound guided dry needling: Relevance in chronic pain. J Postgrad Med 2022;68:1-9

How to cite this URL:
Vas L C. Ultrasound guided dry needling: Relevance in chronic pain. J Postgrad Med [serial online] 2022 [cited 2022 Oct 4];68:1-9. Available from: https://www.jpgmonline.com/text.asp?2022/68/1/1/336289





 :: Introduction Top


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]].
Table 1: Salient differences between acupuncture, ultrasound guided dry needling (USGDN), and conventional blindly performed dry needling (DN)

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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.


 :: Current Evidence: MTrPs Top


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]


 :: DN Versus USGDN Top


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]
Table 2: Effectiveness of USGDN in 220 patients of complex regional pain syndrome (CRPS)

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Table 3: A snapshot of the results in a few subsets of chronic pains treated from 2004 to 2019 out of 12,000 patients

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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]
Figure 1: Advantages of ultrasound visualization and the necessity for ultrasound visualization during dry needling-Ultrasound images showing needling of abdominal wall muscles (top left and right), chest wall muscles (bottom left), and intercostal muscles (bottom middle and right). Ultrasonography allows direct visualization of pleura, peritoneum, pericardium, and neurovascular structures so that needles can be steered into muscles while safeguarding these vital structures. EO, external oblique; IO, internal oblique; TR, transversus abdominis; DN, Dry needling, RA- rectus abdominis; PMAJ, Pectoralis major; P MI, Pectoralis minor; V, subclavian vein; A, subclavian artery; PHN, post-herpetic neuralgia; EIC, external intercostal muscle and the muscle superficial to it is the serratus anterior; IIC, internal intercostal muscles; PL, pleura, ICM-intercostal muscle

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Figure 2: Muscle ultrasonography as a diagnostic and prognostic tool in CRPS. Ultrasound images before and after USGDN of the CRPS-affected hand. Ultrasound images of the flexor muscles of forearm just below the elbow before USGDN showing a complete loss of normal outlines and individual muscles cannot be distinguished 1st image. Loss of normal muscle structure is a consistent diagnostic feature of CRPS. The 2nd image after USGDN shows the return of normal outlines as well as return of hypoechoic muscle fibers in the muscles. The bony outlines of radius and ulna obscured by the hyperechoic echoes pre-USGDN become clearer after treatment. There is also an increase in muscle bulk, compared with 1st image. 3rd image shows the tenosynovial effusion around the extensor tendons presumably due to tenosynovial friction from the pull on the tendons by cocontracted digital extensor and the flexor muscles. 4th image shows no effusion post-USGDN. USGDN routinely relaxes agonist/antagonist muscle groups, relieves the effusion, resolves the hallmark stiffness and immobilization of CRPS, and restores the normal reciprocal inhibition between agonist/antagonist muscle groups essential for coordination of movements. MC, metacarpal bone; T, tendons

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 :: Ultrasound Observation of the Sequence of Events in Muscles and Their Clinical Correlation during USGDN (Videos 1-14) Top


  1. The sudden sharp LTR visualized on needle introduction is associated with a sense of heaviness/sharp pain. Patients with moderate-to-severe pain may show additionally sustained twitches that follow LTR. After needle removal, the original pain and stiffness show perceptible reduction.
  2. Physicians down the ages could never objectively confirm the presence of pain. However, severe pain can be seen as constant shimmers (twitches) in painful muscles at rest, whereas its normal counterpart has none. Shocks in trigeminal neuralgia coincide with sudden muscle twitches, which subside 5–15 min after LTR. The resolution of twitches corresponds to perceptible pain relief after needle removal. This makes ultrasound the first investigative modality to objectively “demonstrate” pain and its relief by USGDN.
  3. The post-USGDN pain relief is reflected as muscle quiescence in the next session. Patients report stiffness reduction as well. Cumulative reduction of pain, stiffness, and weakness over successive USGDN sessions translates into a complete reversal of pain and disability in a variety of neuropathic conditions [Figure 3].[5],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27]
Figure 3: Cumulative result of serial ultrasound guided dry needling (USGDN) of agonist and antagonist muscles (digital flexors and extensors) with sequential improvement of pain stiffness and weakness in patients of complex regional pain syndrome. Top row: Appearance of the hand on day 3 (left) with the fingers fixed in minimal flexion with inability to further flex the fingers, day 7 (middle) where she is able to flex the fingers. She is squeezing the ball on day 10 (right) after USGDN was initiated on day 1 carried out thrice weekly. Bottom row: Appearance of the hand on day 12 (left) showing a gradual increase in the flexion at the metacarpophalangeal and interphalangeal joints to enable the formation of a fist to hold a dynamometer on day 17 (middle) and with gradual increase in grip strength from 0 pounds per square inch to 4 pounds per square inch by day 22 (right)

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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]




 :: Potential of USGDN to Revolutionize Neuropathic Pain Treatment Top


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:

  1. Central nervous system (oral medications, intravenous lignocaine/ketamine infusions)
  2. Spinal cord (epidural injections, neurostimulation, intrathecal drug delivery)
  3. Somatic nervous system (peripheral plexus and nerve blocks, neuropreservative/ablative radiofrequency procedures)
  4. Sympathetic ganglia (stellate/lumbar sympathetic/ganglion impar/coeliac/hypogastric plexus blocks)


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.
Figure 4: A diagrammatic representation of a working hypothesis to explain neuromyopathy; sequence of events leading to MTrP generation, production of inflammatory mediators, consequences of MTrP, and taut bands. The relevance of neural blocks and USGDN in this sequence of events and the significance of USGDN in neuropathic pains are shown

Click here to view


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]


 :: Conclusion Top


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.



 
 :: References Top

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Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Lippincott Williams & Wilkins; 1983.  Back to cited text no. 1
    
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Arendt-Nielsen L, Castaldo M. MTPs are a peripheral source of nociception. Pain Med 2015;16:625-7.  Back to cited text no. 2
    
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Dommerholt J, Huijbregts P, editors. Myofascial Trigger Points: Pathophysiology and Evidence-Informed Diagnosis and Management. Jones & Bartlett Learning; 2010.  Back to cited text no. 3
    
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Vas L. Effectiveness of ultrasound guided dry needling in chronic pain. Pain News 2019;17:202-12.  Back to cited text no. 5
    
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Jin F, Guo Y, Wang Z, Badughaish A, Pan X, Zhang L, et al. The pathophysiological nature of sarcomeres in trigger points in patients with myofascial pain syndrome: A preliminary study. Eur J Pain 2020;24:1968-78.  Back to cited text no. 6
    
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Shah JP, Thaker N, Heimur J, Aredo JV, Sikdar S, Gerber L. Myofascial trigger points then and now: A historical and scientific perspective. PM R 2015;7:746-61.  Back to cited text no. 7
    
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Mense S. The pathogenesis of muscle pain. Curr Pain Headache Rep 2003;7:419-25.  Back to cited text no. 8
    
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Sikdar S, Shah JP, Gebreab T, Yen RH, Gilliams E, Danoff J, et al. Novel applications of ultrasound technology to visualize and characterize myofascial trigger points and surrounding soft tissue. Arch Phys Med Rehabil 2009;90:1829-38.  Back to cited text no. 10
    
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Gattie E, Cleland JA, Snodgrass S. The effectiveness of trigger point dry needling for musculoskeletal conditions by physical therapists: A systematic review and meta-analysis. J Orthop Sports Phys Ther 2017;47:133-49.  Back to cited text no. 11
    
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Vas LC, Pai R, Radhakrishnan M. Ultrasound appearance of forearm muscles in 18 patients with complex regional pain syndrome 1 of the upper extremity. Pain Pract 2013;13:76-88.  Back to cited text no. 12
    
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Vas LC, Pai R, Pattnaik M. Musculoskeletal ultrasonography in CRPS: Assessment of muscles before and after motor function recovery with dry needling as the sole treatment. Pain Phys 2016;19:E163-79.  Back to cited text no. 13
    
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Vas LC, Pai R. Musculoskeletal ultrasonography to distinguish muscle changes in complex regional pain syndrome type 1 from those of neuropathic pain: An observational study. Pain Pract 2016;16:E1-13.  Back to cited text no. 14
    
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Vas L, Pai R. Complex regional pain syndrome-type 1 presenting as deQuervain's stenosing tenosynovitis. Pain Physician 2016;19:E227-34.  Back to cited text no. 15
    
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Vas L, Pai R, Geete D, Verma CV. Improvement in CRPS after deep dry needling suggests a role in myofascial pain. Pain Med 2018;19:208-12.  Back to cited text no. 16
    
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Vas L. Commentary: Selective fiber degeneration in the peripheral nerve of a patient with severe complex regional pain syndrome. Front Neurosci 2019;13:19.   Back to cited text no. 17
    
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Vas L, Pai R, Pawar KS, Pattnaik M. “Piriformis syndrome”: Is it only piriformis? Pain Med 2016;17:1775-9.  Back to cited text no. 18
    
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Vas L, Pai R. Ultrasound-guided dry needling as a treatment for postmastectomy pain syndrome-A case series of twenty patients. Indian J Palliat Care 2019;25:93-102.  Back to cited text no. 19
[PUBMED]  [Full text]  
20.
Vas L, Phanse S, Pai R. A new perspective of neuromyopathy to explain intractable pancreatic cancer pains; Dry needling as an effective adjunct to neurolytic blocks. Indian J Palliat Care 2016;22:85-93.  Back to cited text no. 20
[PUBMED]  [Full text]  
21.
Sharma M, Gupta S, Vas L. Chest wall pain from mesothelioma or lung cancer. In: Sharma M, Simpson KH, Bennett MI, Gupta S, editors. Practical management of complex cancer pain. 2nd ed. Oxford: Oxford University Press; 2022 (in press).  Back to cited text no. 21
    
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[PUBMED]  [Full text]  
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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