CompressionatMyofascialTriggerPointonChronicNeckPainProvidesPainReliefthroughthePrefrontalCortexandAutonomicNervousSystem:APilotStudy

Chronic neck pain is a widespread problem, particularly among women, and myofascial trigger points (MTrPs) in neck and shoulder muscles are a key contributor. Abnormal autonomic nervous system activity, especially excessive sympathetic activity, is thought to worsen chronic pain. The prefrontal cortex, particularly the dorsomedial prefrontal cortex (DMPFC), has been implicated in both pain processing and autonomic regulation. While compression at MTrPs (ischemic compression) is a well-known manual therapy technique that provides immediate pain relief, the underlying neural mechanisms—especially whether the prefrontal cortex plays a role—remained unclear.

This pilot study aimed to investigate whether MTrP compression affects prefrontal cortical activity and whether this relates to changes in autonomic function and pain perception.

The researchers recruited 21 women with chronic neck pain lasting more than 3 months, all diagnosed with myofascial pain syndrome by a licensed acupuncturist with over 6 years of experience. Participants were randomly assigned to two groups: MTrP compression (n = 11) or Non-MTrP compression (n = 10). MTrPs were identified in the upper trapezius muscle using established diagnostic criteria, while Non-MTrP control points were located 2 cm away where no taut band or referred pain existed. Compression was applied at an intensity midway between each participant's pressure pain threshold and maximally tolerable pain, maintained for 30 seconds and repeated 4 times with 120-second rest intervals.

During the procedure, prefrontal hemodynamic activity was measured using near-infrared spectroscopy (NIRS), and autonomic activity was assessed via heart rate variability (HRV) from electrocardiography. Subjective pain was rated on a 100-mm visual analog scale (VAS) before and after the experiment.

MTrP compression significantly reduced subjective pain scores compared with Non-MTrP compression (P < 0.01). Autonomic measures showed that the high-frequency (HF) component of HRV, reflecting parasympathetic activity, was significantly increased during MTrP compression compared with Non-MTrP compression (P < 0.01). Conversely, the low-frequency (LF) component and LF/HF ratio, indicators of sympathetic activity, were significantly decreased during MTrP compression (P < 0.01 for both). Prefrontal hemodynamic activity, measured as oxy-hemoglobin (Oxy-Hb) concentration, was significantly decreased in the DMPFC during MTrP compression compared with Non-MTrP compression, where Oxy-Hb actually increased.

A repeated-measures two-way ANOVA showed a significant main effect of treatment [F(1,19) = 6.624, P < 0.05]. Critically, changes in autonomic parameters were significantly correlated with both changes in subjective pain and changes in DMPFC hemodynamic activity. Specifically, HF% changes were negatively correlated with pain score changes (r² = 0.272, F(1,20) = 7.092, P < 0.05) and with DMPFC hemodynamic responses (r² = 0.235, F(1,20) = 5.830, P < 0.05), while LF/HF ratio changes were positively correlated with both pain changes (r² = 0.285, F(1,20) = 7.573, P < 0.05) and DMPFC activity changes (r² = 0.192, F(1,20) = 4.514, P < 0.05).

This pilot study provides novel evidence that MTrP compression may relieve chronic neck pain through a central mechanism involving the prefrontal cortex and autonomic nervous system. The findings suggest that compression at MTrPs suppresses DMPFC activity, which in turn reduces sympathetic tone and enhances parasympathetic activity, ultimately leading to pain reduction. This supports the hypothesis that hyperactivity in the medial prefrontal cortex contributes to chronic pain maintenance through abnormal autonomic regulation. For clinicians, this reinforces the value of ischemic compression as more than just a local tissue technique—it appears to engage central pain-modulatory and autonomic regulatory pathways.

For patients, it means that manual pressure on trigger points may help not only by directly affecting muscle tissue but also by calming the nervous system's stress response. However, as a pilot study with only 21 participants, larger randomized trials are needed to confirm these mechanisms and establish optimal treatment protocols. The authors also note that further research using techniques like transcranial direct current stimulation (tDCS) could help clarify causal relationships between DMPFC activity, autonomic function, and pain.