Chronicwhiplashandcentralsensitization;anevaluationoftheroleofamyofascialtriggerpointsinpainmodulation

Chronic neck pain following whiplash injury is a debilitating condition that affects many people long after their initial trauma. One of the key phenomena associated with this persistent pain is called central sensitization, where the central nervous system becomes hypersensitive to pain signals. In this condition, not only does the injured area hurt, but even uninjured parts of the body can become more sensitive to pain. Researchers have long debated what keeps this heightened sensitivity going, with some suggesting that ongoing signals from peripheral sources—such as painful muscles—might continuously feed into and maintain this central hypersensitivity.

Myofascial trigger points, which are hyperirritable spots in skeletal muscle associated with palpable nodules in taut bands, have been proposed as one such peripheral source. However, previous research has yielded conflicting results about whether treating these trigger points can actually change the signs of central sensitization. This study aimed to test whether carefully identified myofascial trigger points in the upper trapezius muscles could modulate central sensitization in patients with chronic, intractable neck pain.

The researchers conducted a controlled case series at an outpatient chronic pain clinic. They recruited 17 patients who had been suffering from intrusive daily neck pain for at least 12 months, all of whom had failed conservative treatments like physical therapy, chiropractic manipulation, or acupuncture. These patients were being evaluated for possible surgical intervention due to the refractory nature of their pain. The study also included 10 healthy volunteers without neck pain complaints as a control group.

For the symptomatic patients, the researchers first conducted thorough pre-intervention evaluations. They measured cervical range of motion using inclinometry, assessed pressure pain thresholds at three distant body sites (infraspinatus, wrist extensors, and tibialis anterior) using a calibrated algometer, tested for photophobia by shining light from an ophthalmoscope into the eye, and recorded subjective neck pain on a 0-10 visual analog scale. The control group only had pressure pain thresholds measured.

The intervention involved identifying myofascial trigger points in the upper trapezius muscles through careful palpation, then pinpointing the exact pain generator within each trigger point using a 25-gauge needle to elicit a twitch response—a characteristic reaction that distinguishes true trigger points from simple tender points. Each identified trigger point was then injected with 1-2 cc of 1% lidocaine. Patients received an average of 3.8 injections, ranging from 1 to 8 trigger points, until they reported significant relief of neck pain. The control group received 6 cc of 1% lidocaine injected into the thigh.

Post-intervention evaluations were completed rapidly—all within 7 minutes of the final injection, with pressure pain thresholds measured within 60 seconds. This quick turnaround was crucial for capturing immediate effects before the anesthetic wore off.

The results were striking and immediate. In the symptomatic group, cervical range of motion improved dramatically across all directions: 49% increase in flexion (p = 0.000), 44% in extension (p = 0.001), 47% in right lateral flexion (p = 0.000), 28% in left lateral flexion (p = 0.016), 27% in right rotation (p = 0.002), and 45% in left rotation (p = 0.000).

Pressure pain thresholds at distant, uninjured sites increased substantially: 68% at the infraspinatus (p = 0.000), 78% at the wrist extensors (p = 0.000), and 64% at the tibialis anterior (p = 0.002). These improvements at sites far from the injection location strongly suggested a central rather than purely local effect.

Among 11 subjects who had photophobia before treatment, only 2 remained sensitive to light after the trigger point injections (p = 0.033)—a particularly intriguing finding given that light sensitivity would seem unrelated to neck muscle pathology.

Subjective pain levels dropped by 57%, from a mean of 6.1 to 2.6 on the visual analog scale (p = 0.000).

Importantly, the control group showed no significant changes in pressure pain thresholds after receiving thigh injections of lidocaine, ruling out a simple systemic effect of the anesthetic as the explanation for the improvements.

The researchers noted that as the anesthetic wore off, all pre-injection symptoms returned to baseline over hours to several days, indicating that the effects, while dramatic, were temporary.

This study provides compelling evidence that myofascial trigger points can serve as modulators—or even perpetuators—of central sensitization in chronic whiplash patients. The rapid, widespread improvements in pain thresholds at uninjured body sites, along with the resolution of photophobia in most affected patients, suggest that peripheral nociceptive input from trigger points continuously drives central hypersensitivity. When that peripheral input is temporarily blocked, the central nervous system quickly normalizes its pain processing.

For clinicians, this finding supports the importance of carefully identifying true myofascial trigger points—using the twitch response as a confirmatory sign—rather than simply injecting tender areas. The distinction between trigger points and tender points may explain why some previous studies found no effect of injections on central sensitization.

For patients with chronic whiplash-associated pain, this research offers hope that their condition may not represent permanent, irreversible changes in the nervous system. Instead, central sensitization may be more "neuroelastic" than "neuroplastic"—capable of rapid change when the peripheral driver is addressed. However, since lidocaine effects are temporary, the challenge remains finding longer-lasting solutions. The authors speculate that surgical excision or ablation of trigger points might offer more permanent relief, though this approach requires much more study.

The findings also argue against attributing chronic whiplash pain primarily to psychological or litigation-related factors, as these patients showed objective, immediate physiological changes with a purely physical intervention.