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17 Articles in Volume 19, Issue #4
Analgesics of the Future: Inside the Potential of Nerve Growth Factor Antagonists
Best Practices Are Still Largely Undefined in Task Force Report
Brief Behavioral Interventions for Chronic Pain
Cervicogenic Headache: Diagnosis and Management
Chronic Headache and Central Pain Conditions
Considering Comorbidities When Selecting Medications for Pain (Part 4)
For APPs: How to Contribute to Clinical Research
Gabapentin and Suicidal Ideation: Is There a Link?
Intranasal Ketamine for the Relief of Cluster Headache
Letters: Slipping Rib Syndrome; Burning Leg Pain; CGRP Complications
Pain Assessment Tools for Malingering in Patients with Chronic Pain
Refractory Chronic Migraine: Mild, Moderate, or Severe
Should Probuphine be considered for MAT?
Special Report: The Abuse Potential of Gabapentin & Pregabalin
Tension-Type Headache: Evidence for Trigger Points
Treatment Alternatives for Migraine
Trigeminal Neuralgia: Current Diagnosis and Treatment Options

Tension-Type Headache: Evidence for Trigger Points

Tracking the pathogenesis of this often-debated aspect of the chronic headache.
Pages 42-45

The mysteries of muscle pain or myalgia, including headache pain, continue to perplex clinicians. A tendency to want to diagnose or identify the causative agent has led to much speculation. In musculoskeletal medicine, the putative role of trigger points (TrPs) in myofascial pain spurs much divisiveness. Headache and trigger points, it seems, are interconnected, especially when treating tension-type headaches (TTH). These TrPs, also called contraction knots, have been characterized as discrete, hard, irritable nodules found in taut bands of muscle and associated with pain, tenderness, and subsequent restrictions in muscle strength and joint mobility.1,2

For many years, the diagnostic process for differentially diagnosing TrPs has relied upon careful clinical examination, which has caused many to doubt their existence. Research over the past several years, however, has added substantial scientific evidence in the form of histochemistry, imaging, electro-diagnostic, and echo-diagnostic methods. This report focuses on the role of TrPs in TTH as they are understood today, how they are implicated, and their various treatment strategies (see "Interventions and Instrumentation Used in the Treatment of Trigger Points").

The author provides scientific evidence to the presence of trigger points in tension headaches. (Source: 123RF)

Current Theories On the Mechanism of Trigger Points

That the presence of TrPs is associated with TTH has already been established; whether they cause, or are a manifestation of, the headache, however, is not clear, since not every patient with TTH has active TrPs.3 There is evidence to suggest that TrPs may initiate a peripheral nociceptive mechanism which contributes to changes in the central nervous system (CNS). Sensitization of nociceptive pain pathways secondary to persistent nociceptive activity from active TrPs may then contribute to the progression from acute to more chronic tension headache attacks.4

According to classic TrP doctrine described by Simons and Travell,5 an active TrP has the following characteristics:

  • is tender
  • is located in a firm or taut band of muscle
  • refers pain on deep palpationdisplays a “twitch” response under the palpating fingers.

In the author’s clinical experience, TrP assessment in patients does not always meet all the aforementioned criteria. It is difficult to determine, therefore, whether the presence of trigger points is the primary cause of TTH, or whether chronic tension in the suboccipital and paraspinal muscles may be causing the problem.

Interventions and Instrumentation Used in the Treatment of Trigger Points (TrPs)

Figure A. Infrared thermography.

The author has used infrared thermography to provide temperature readings over dysfunctional tissue, including active trigger points. Temperature variations can often alert the practitioner of underlying metabolic dysfunction in tissue as observed in musculoskeletal injury and subsequent inflammation.

Figure B. Pressure Algometry (PA).

Tenderness may be the best surrogate measure for pain through the quantification of the pain threshold, which can be measured using pressure algometry (PA). The use of PA as an outcome measure is indicative of injury or pathology status (as injuries or pathologies heal, they become less tender). The use of PA in evaluating the presence/absence and resolution of TrPs in myofascial dysfunction is a crucial outcome measure from a clinical perspective.

Figure C. Dry needling.

Dry needling involves inserting needles into a known TrP, which is active (symptomatic) and lies in the causal pathway of a patient’s pain response. Physical therapists use dry needling to stimulate intramuscular knots or TrPs with the goal of providing pain relief.

Figure D. Ischemic compression or acupressure.

One of the most cost-effective methods of treating active TrPs is by using an inexpensive cryocompression tool (such as CryoProbe) that can be applied firmly over the suspected TrP. The use of musculoskeletal diagnostic ultrasound to guide TrP treatment is highly recommended to ensure precise targeting.

Figure E. Class III cold laser system.

Figure E shows a class III cold laser system being used over a sonographically-confirmed TrP with pain and tenderness reduction resolution experienced by the patient post-treatment. This is just one example of an emissive modality used for TrP treatment, which could also include ultrasound, pulsed electromagnetic fields, and electrical muscle stimulation. The author is unaware of any comparative effectiveness studies that demonstrate which energy modality may be superior for quiescing a symptomatic muscular knot.

Figure F. Vibration-induced pain relief.

The application of focal vibration devices (such as VibraCool) can also be effective at restoring more normal tissue tension levels when applied over an active TrP.

 

Under routine circumstances, there is a rather high resting activation threshold for the free nerve endings that form muscle nociceptors, meaning it takes a rather significant stimulus to trigger a response. It is thought that the presence of algogenic substances such as substance P, glutamate, bradykinin, and serotonin all act as sensitizing agents which may increase the excitability of nociceptors.6 Studies have consistently linked the presence of TrPs to higher than normal levels of these algogenic substances.7 As a result, low intensity stimuli may become problematic as they trigger electrical activity and lead to deep-aching pain.

We know that prolonged nociceptive inputs from the periphery may lead to CNS alterations, and evidence suggests that deep nociceptive inputs (ie, joints/muscles) may adversely affect dorsal horn neurons more so than with superficial structure inputs (ie, skin).8 Furthermore, during the sensitization process, the neurons contained in the dorsal horn become hyper-excitable, leading to an increase in the dorsal horn receptive field which may allow a greater number of stimuli to be captured and responsive.9 There are a number of other hypothesis suggesting that TrPs evolve as a function of muscular overload and strain.10

Another theory, referred to as the Cinderella hypothesis, describes muscle recruitment patterns during submaximal muscle actions using low to moderate physical loads. These types of exertion patterns may often be observed in patients whose occupations involve repeated tasks (eg, assembly lines or clerical work). Due to the prolonged submaximal nature of the muscle activity, the same muscle fibers may be “activated” and thus become fatigued and metabolically overloaded. This reaction may then lead to damage and calcium dysregulation, both implicated in the formation of TrPs.11 A similar hypothesis promulgated by Shah, et al,2 suggested that sustained submaximal muscle contractions, including resting tensions, may contribute to postural dysfunctions which, when sustained over time, lead to areas of lowered perfusion.

The Evidence for TrP

As noted, assessment of trigger points has relied primarily on manual techniques (ie, palpation), which were notoriously unreliable and subject to debate and discord.12 In the past 10 years, however, diagnostic techniques have advanced whereby some of these subtle musculoskeletal lesions may now be identified and characterized with more precision and reliability. Electromyography studies, for example, have identified spontaneous electrical activity (SEA) at active TrP locations and not seen in surrounding tissue.13 With regard to latent or non-active TrPs that are asymptomatic until provoked, there is evidence to suggest that even these lesions behave in a similar manner as active TrPs such that there is a more rapid development of fatigue during a sustained isometric contraction,14 synergistic muscle activation,15 as well as increased antagonist muscle activity during agonist activation.16 Further verification lies in diagnostic ultrasonic evidence provided by high-resolution imaging that, when combined with palpation, provide compelling evidence for the presence of TrPs.17,18,19 These findings are in stark contrast to a report by Lewis and Tehan20 which found limited value in using ultrasound imaging in identification of TrPs.

Another unclear aspect of ultrasound imaging is whether TrP scans as hyperechoic (white appearance) or hypoechoic (dark appearance), and because they have been reported as both, detractors continue to deny their existence. Work at the author’s practice confirms and concurs with the work of Turo, et al.21 Turo has shown that patterns of the greatest preponderance of TrPs appear as hypoechoic, especially fresher or more recent TrPs that may otherwise be associated with a more acute process, including edema.

On occasion, the author’s clinic has identified what appears to be a hyperechoic TrP in patients with more chronic and longer-lasting symptoms (see Figure 1). It is difficult to know whether these entities are actually a different manifestation (phenotype) of the same entity, or something different altogether. There does not appear to be a difference in how a patient reports symptoms from a hypoechoic (dark) versus a hyperechoic (white) trigger point. From a sonographic perspective, they definitely have distinct acoustic properties, hence the different echogenicity.

Figure 1. Pre- and post-treatment ultrasound scans of an active levator scapula trigger point (TrP), which shows a marked difference in the echogenicity of the area where the TrP was located pre-ischemic compression as compared to that same area post-ischemic compression treatment. The TrP identified in this sonogram was hypoechoic in appearance (darkened area).

Since soundwaves are propagated at different velocities depending on tissue composition, the relative hardness of a TrP is reliably detected by elastography, which has a high sensitivity for tissue density. Sonoelastography has been used successfully to characterize and validate the presence of TrPs.22 It is now known that TrPs, whether acute or chronic, are firmer or harder than surrounding muscle and fascial tissue, so their detection would lend itself well to elastographic analysis.

The histochemical analysis of the TrP environment for relevant biomarkers is another distinguishing feature that helps to confirm the existence of trigger points. The work of Zhang, et al,23 demonstrates that artificially-induced TrPs have characteristic features in both early and later stages of evolution. The early TrP has inflammatory infiltrate as a defining characteristic while, months later, the TrP milieu tends to change to include small amounts of inflammatory infiltrate along with greater SEA and contraction knots. The sonographic appearance of the TrP is related to its age and stage, with more acute lesions appearing hypoechoic and the more chronic lesions appearing hyperechoic. It has been argued that the number of contraction knots may be the determining factor which differentiates the active from the latent trigger point.21 Further investigations carried out by Shah, et al,24 has identified several biomarker substances that are elevated in the TrP environment, including interleukins (IL-1b, IL-6, IL-8), tumor necrosis factor, calcitonin gene-related peptide, contraction knots, and substance P.

Conclusion

There is a high prevalence of active trigger points in individuals with chronic tension-type headaches, more so than in persons without TTH and especially, but not exclusively, in the suboccipital muscles.25 Some investigators have even identified a minimal clinically important difference between pressure pain threshold in the trapezius muscle between those persons having tension-type headache versus those who do not.26,27

When reviewing the evidence for TTH, it becomes increasingly clear that TrPs are a crucial element to address in a treatment plan. The clinical management of TTH may depend to a large degree on the clinician’s ability to identify and quiesce the active trigger point component in the patient’s symptom presentation.

Last updated on: June 21, 2019
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