Why go deeper?
After a motor vehicle accident (MVA) or other injury, pain patterns often blur together. Muscle-based (myofascial) referral can mimic nerve pain, and central sensitization can broaden pain beyond anatomy. This deeper dive explains how I use sensory mapping alongside electrodiagnostics (EMG/NCV) to clarify mechanisms, calm the system, and guide a paced, effective plan.
Mechanisms that matter
- Myofascial referral: Trigger points in tense, ischemic muscle send pain to predictable remote zones that rarely match a single dermatome or nerve territory.
- Neuropathic pain: Symptoms follow dermatomes/peripheral nerves (e.g., C6 to the thumb; median nerve in the palm) and can be confirmed with exam and EMG/NCV when indicated.
- Central sensitization: Limbic and spinal circuits (including amygdala-related pathways) amplify signals, creating widespread, shifting tenderness and sensory hypersensitivity.
Pathophysiology: how myofascial pain persists after trauma
1. Peripheral mechanisms
Myofascial trigger points are hyperirritable foci within taut muscle bands. They involve sensitized nociceptors, dysfunctional motor endplates, and local biochemical changes (excess acetylcholine and inflammatory mediators) that lower pain thresholds and perpetuate contraction and ischemia. These mechanisms produce reproducible, non-dermatomal referral patterns and tenderness on palpation.
2. Central & amygdala-driven mechanisms
After trauma, nociceptive input from trigger points can drive central sensitization via limbic circuits (e.g., parabrachial to central amygdala), reinforcing negative emotional associations and avoidance behaviors. The loop is bidirectional: peripheral trigger points sensitize the CNS, and central mechanisms sustain peripheral trigger point activity.
Takeaway: persistent post-traumatic myofascial pain is both muscular and neuro-emotional; effective care addresses both levels.
Recognizing myofascial referral patterns
- Neck/shoulder: Upper trapezius or levator scapulae can refer to the temple, neck, or scapular border.
- Back/hip: Paraspinals and gluteals may refer around the ribs or down the leg, sometimes "sciatica-like".
- Forearm/hand: Wrist-extensor or pronator teres trigger points can mimic carpal tunnel sensations without median conduction slowing.
Distinguishing muscle-based maps from nerve distributions prevents over-treatment and points to the right therapies sooner.
How I perform sensory mapping (step-by-step)
Adapted from methods I learned during a Mayo Clinic rotation with a neurologist who used (and taught) this approach.
- Identify the target area: The patient points to regions with altered sensation (tingling, numbness, "different" touch).
- Eyes closed, compare points: Using a light sharp stimulus (e.g., toothpick), I touch the symptomatic area and a distant control site: "Same or different?"
- Distal to proximal mapping sweep: In the upper limb I start distally at the pinky and sweep across the hand toward the thumb. The patient tells me where sensation changes.
- Mark the transition: I place a tiny ink dot at the change point. I then move slightly closer to the wrist and repeat: adding dots wherever sensation shifts.
- Create a visual map: Proceeding from fingertips toward forearm (and proximal if needed) draws a dotted border outlining the altered field.
- Interpret the pattern: Neat dermatome/nerve indicates neuropathic; patchy multi-dermatomal indicates myofascial; broad shifting field indicates central sensitization.
- Confirm when needed: If nerve involvement is suspected or imaging is equivocal, I use EMG/NCV. A normal EMG with a non-anatomic map supports myofascial/central drivers.
- Show-and-tell: We review the dot-map together: seeing what is and what is not wrong reduces fear and supports a paced plan.
This process converts subjective sensation into a shared, visual aid that guides whether we calm first, reactivate, or investigate nerves with EMG/NCV.
EMG correlation (and why I always "show the screen")
During EMG, healthy muscle is quiet at rest; trigger zones can reveal fasciculations or spontaneous activity. I often show these differences in real time: turning a diagnostic test into a teaching moment that reduces fear and reinforces safety. The fine needle also provides precise dry needling of referral sites, which may relieve local tension while we evaluate.
What EMG/NCV can and can't do: electrodiagnostics are essential to confirm/exclude neuropathic involvement (radiculopathy, entrapment). EMG may show activity in painful muscles but is not specific for myofascial pain: results must be interpreted with the map and exam.
Treatment: multimodal and paced
- Early (calm first): Education and reassurance, breath-based regulation, gentle myofascial release/massage. Avoid over-stimulation that can reinforce limbic alarm.
- Intermediate: Stretching, posture retraining, cognition-targeted exercise; correct ergonomics/overuse drivers.
- Later: Progressive strengthening and task-specific reloading; consider TPI/IMS if conservative progress stalls.
Medication evidence is limited (brief NSAIDs or muscle relaxants when appropriate). Avoid opioids for MPS. Dry needling, acupuncture, and manual therapy are reasonable adjuncts with evolving evidence.
References
- Steen JP, Jaiswal KS, Kumbhare D. Myofascial Pain Syndrome: Update. Muscle & Nerve. 2025;71(5):889–910.
- Lam C, Francio VT, Gustafson K, et al. Myofascial Pain: A Major Player. Best Pract Res Clin Rheumatol. 2024;38(1):101944.
- Weller JL, Comeau D, Otis JAD. Myofascial Pain. Semin Neurol. 2018;38(6):640–643.