A muscular contribution to persistent pain merits examination, including when attention has focused on spinal pathology. The clinical task is to distinguish tissue generating pain from sites of referred tenderness, then evaluate treatment with reproducible methods.
A muscle can be a primary pain generator, as well as a site of pain referred from elsewhere. Distinguishing between the two is central to identifying the tissue responsible.
Structural pathology and nerve compression explain pain in many patients. Others have persistent symptoms despite treatment, or no clear target for an invasive intervention. Systematic examination of muscle and other soft tissues can help identify a potentially treatable contributor to pain. [1][2]
Palpation can identify tenderness, but the tender site may receive referred pain. Overlapping muscle layers and variation in applied pressure also complicate localization and examiner agreement. Identifying a tender point and identifying the muscle generating pain are therefore different clinical tasks. [1][2]
The protocol studied by Dr. Norman Marcus, MD, and colleagues used electrical stimulation to elicit muscle contraction and identify muscles suspected of generating pain. Identifying the specific muscle allows examination to follow its course and include its origin and insertion. In this protocol, that localization guided muscle-tendon injections to the muscle and its attachments, followed by physical therapy and exercise. A tender point alone does not provide the same anatomical specificity. [1]
Electrical localization is a developing approach. Its diagnostic accuracy requires further study.
In a retrospective analysis of 56 patients with chronic low back pain after unsuccessful invasive treatments, mean Brief Pain Inventory (BPI) severity fell from 5.54 to 3.96, a reduction of approximately 29%. Mean interference fell from 6.09 to 3.40, a reduction of approximately 44%. Both changes were statistically significant (P < 0.001). [1]
Follow-up was approximately 18 months. Prior interventions included spine surgery, epidural steroid injections, facet blocks, and/or trigger point injections; this was not an exclusively postsurgical cohort.
A separate presurgical pilot: three of seven patients canceled planned spine surgery after completing a substantial part of the protocol and reported relief at 16–19 months. This small observation cannot estimate the likelihood of avoiding surgery in a broader population. [1]
Study limitations: no randomized comparison group; a selected sample; incomplete follow-up and exclusions; and multiple treatments delivered together. The results support further controlled investigation, but cannot isolate treatment effects or establish comparative efficacy.
The paper discloses that Dr. Marcus invented an electrical muscle stimulation instrument and holds a patent on the evaluation and treatment methodology. Stevens Proof of Concept, Inc. supported his travel and expenses for the San Diego study. Edward Gracely, PhD, was a statistical consultant to Dr. Marcus.
FRAME holds no financial interest in the device. Dr. Marcus is an Emeritus Board Member with no stake or voting rights.
In a clinic organized by Dr. Barbara Stimson in 1944, 17% of more than 3,000 patients with back pain were diagnosed with a structural or organic cause, according to Hansen and Marcus’s 2016 commentary. Many of the remaining patients had deficits in postural muscle strength or flexibility and responded favorably to a muscle-focused program. [2]
The commentary also reports improvement in more than 80% of 11,809 participants who completed the later “Y’s Way to a Healthy Back” exercise course at 900 YMCA facilities.
Historical context and limitations: these are historical observations reported through a commentary. Absence of an identified structural cause does not prove a muscular cause, and course-completer outcomes do not establish efficacy against a control group.
These observations support investigating a muscular contribution to persistent pain in selected patients, including those whose symptoms persist after spine-directed treatment. The diagnostic method and treatment protocol still require validation through prospective controlled studies. [1][2]
Sensitization of nociceptive pathways can alter thresholds and amplify responses, helping explain pain with activity that would ordinarily be tolerated.
Hansen and Marcus’s 2016 commentary discusses experimental work on dorsal horn sensitization, expansion of receptive fields, and muscle-to-muscle referred pain. These mechanisms help explain why the perceived location of pain may differ from its initiating tissue. [2]
The examination of soft tissue pain must also consider fascia. The same commentary describes experimental findings in which inflammation of back muscle alters neuronal responses to input from the thoracolumbar fascia. [2]
The animal-model findings are mechanistic evidence, rather than proof of clinical efficacy.
FRAME advances research and education on the examination and treatment of muscle pain.
Establish inter- and intra-rater reliability, diagnostic accuracy, and clinically useful criteria for identifying a painful muscle. Compare electrical localization with standardized examination methods.
Use prospective controlled studies to distinguish the effects of localization, needling, physical therapy, and exercise. Measure function, durability of benefit, and adverse events alongside pain severity.
Investigate how muscle and fascia contribute individually and interactively to persistent pain, and which measurable findings predict a response to treatment.
We welcome discussion with clinicians, educators, and researchers working on these questions.
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