Myofacial+Referred+Pain

Myofascial trigger points (TrPs) are taut bands of muscle that can cause local and/or referred pain. Latent TrPs are points where pain is only elicited by direct pressure, while active TrPs cause constant local and referred pain symptoms and can be reduced to the latent classification with treatment. 4 One study has shown that TrPs are reliably close to the muscle innervation zone (IZ) 2, and characteristic of TrPs is an increased endplate potential, and least in mid-fiber TrPs. 11 There are many causes of trigger points: viscerosomatic reflex, lack of exercise, poor posture, vitamin deficiency, repetitive stress on a specific muscle (overuse injury), acute injury, surgical damage, and tissues under constant tension. 1 Emotional stress has been shown to worsen myofascial pain; at least one study showed that emotional stress triggers an increase in EMG activity in trigger points, while surrounding tissue remained silent. 11
 * Introduction**[[image:http://www.easyvigour.net.nz/trigger_points/ptriggerpointdiagram.gif width="342" height="140" align="right" caption="(http://www.easyvigour.net.nz/trigger_points/ptriggerpointdiagram.gif )"]]



Referred pain patterns resulting from TrPs have been extensively mapped by Travell & Simons’ //Myofascial Pain and Dysfunction//. This pain often presents itself in nearby joints and limbs. There are multiple theories to explain the pathways of referred pain, spanning from central sensitization to tension across the fascia. In one study on neck and shoulder trigger points, referred pain was defined as “pain located at least 1 cm outside the local pain area evoked by TrP palpation”. 4

Myofascial referred pain involves the spinal cord, motor and sensory neurons, and muscle. Each should first be understood independently.
 * Functional Anatomy**



Muscle contraction is triggered by acetylcholine (Ach) release in the neuromuscular junction. ACh binds to receptors on the muscle membrane and the resulting potential triggers calcium release. The calcium binds to troponin, which slides tropomyosin off the actin binding sites. It is important to note that ATP is not required for the myosin power stroke, but to break the actin-myosin bond. Once the neural command has ended, acetylcholinesterase (AChE) enters the synaptic cleft and breaks down ACh.

There are a number of factors believed to be involved in the formation of TrPs; these are all covered in the integrated trigger point hypothesis. At the synaptic cleft, three things may happen: excessive ACh, decreased AChE, or increased ACh receptor sensitivity. Any combination of these result in muscle contraction, and because of the intensity of trigger point contractions, there may be structural damage that occurs. TrPs have been widely associated with Type 1 oxidative muscle fibers and this would make sense in the context of Henemann’s size principle. It has been suggested that in addition to motor neuron irritability, during contraction myosin filaments get stuck in the gel-like substance titin in the Z-band, preventing the sarcomere from returning to resting length. Constant shortening of the muscle results in muscle tissue ischemia. Without oxidative ability, there is a shortage in ATP. The shortage of ATP in TrPs also contributes to the sustained tautness—the muscle is not able to break down actin-myosin bonds—an “energy crisis.” This energy crisis releases sensitizing substances which cause pain and send autonomic stimulation back to the neuromuscular junction to restart the cycle and further aggravate the problem. 3



Muscle nociceptors are mostly acid-sensitizing and P2X3 (ATP binding) receptors. Other sensory fibers include thermoreceptors and mechanoreceptors. Fiber types include slow conducting myelinated group III (A-δ) and unmyelinated group IV (C), and cell bodies exist in the dorsal root ganglion (DRG). These fibers are primary afferents, so they enter the central nervous system (CNS) through the dorsal root. 9 From the dorsal root, nociceptors/thermoreceptors and mechanoreceptors follow separate pathways to the brain. Nociceptors and thermoreceptors follow the spinothalamic pathway: First order neurons enter into the dorsolateral tract of Lissauer and travel one or two levels in the spinal cord before entering the dorsal horn gray matter. They synapse mostly via interneuron to the second order neuron which crosses over at the spinal cord level and travels through the spinothalamic tract to the VPL of the thalamus. From here, a third order neuron reaches the somatosensory cortex. Mechanoreceptors follow the dorsal column medial lemniscus (DCML or PCML) pathway: First order neurons travel ipsilaterally to the medulla where they synapse in the dorsal column nuclei (gracilis from lower body and cuneate from upper body). From here they decussate and travel to the VPL of the thalamus where they synapse to the third order neuron and decussate again, terminating in the somatosensory cortex.

One theory of referred pain is derived from the recent research by Barker and Briggs that showed a continuous fascia from the lower extremities to the skull. As Werenski explains, “anatomical studies have demonstrated the continuity, provided by muscular insertions onto fascia.” Studies have shown that tension on muscles can stretch specific portions of this fascia. This new knowledge has given way to the theory that fascia—which has pain fibers and can transmit tension—can refer pain across the tissue. 12 TrPs are taut bands of muscle, so there is a possibility that this tension stretches the fascia and activates pain receptors in other areas of the fasica. Strengthening this view is the research finding that release of TrPs resulted in the immediate increase in corresponding joint flexibility. 6
 * Theories of Referred Pain**

The most common theory explaining referred pain is the convergence projection theory. This states that nociceptive afferents from various parts of the body converge onto the same dorsal horn neuron, and noxious stimulus (such as the noxious “substance P”) from one of these body parts is believed to diffuse through a few spinal levels and sensitize nociceptor neurons from other bodily regions. 7 Multiple active TrPs in a given region may have a spatial summation of nociceptive information effect on the trigemino-cervical nucleus caudalis. 4,5,10



A relatively new (2006) theory accredits referred pain to higher brain centers, such as the thalamus and the somatosensory cortex. Using fMRI information, researchers were able to demonstrate that there is some level of somatotopic organization in the primary somatosensory cortex (S1) for deep pain. In addition, referred pain was reflected in increased neural activity in the S1, cerebellar cortices, and other discrete cerebral areas. The right anterior insula was shown to display a somatotopic organization of signals during noxious stimulus. More importantly, signals in this region were shown to mirror the perceived intensity of the referred pain, while subjects with no referred pain had no change in this region. Perceived intensity of pain and the extent of muscle pain referral have been shown to be positively correlated. Macefield et al. suggest that the right anterior insula integrates information from muscle nociceptors with the “personal relevance” of this pain. They suggest that the location of the pain may be helpful in deciding on the correct behavioral response. 8 This may be further explained by the location of referred pain; Travell & Simons’ mappings demonstrate a large number of pain patterns that act on the joint affected by the injured muscle. It is possible that referred pain is a protective mechanism used by the body to immobilize limbs/segments when further use could result in further injury.

Myofascial TrPs are caused by both acute and chronic injury. There is no conclusive evidence as to how they form, but the integrated trigger point hypothesis is currently the best attempt to explain these common and painful occurrences. Referred pain is a product of trigger points, and there is currently even less research on this topic. Most scientists believe that nociceptor sensitization is the mechanism behind this pain, but new research has suggested higher level sources. TrPs and referred pain have not been widely studied, and continued research will help scientists reach more evidence-based conclusions.
 * Summary**

Acetylcholinesterase: A hydrolase that hydrolizes acetylcholine
 * Glossary**

Henemann's Size Principle: States that motor units are recruited from small to large

Ischemia: Restriction of blood supply to tissue, resulting in oxygen and glucose shortages

Fascia: A layer of fibrous connective tissue

Trigemino-Cervical Nucleus Caudalis: A region of the upper cervical spinal cord where sensory nerve fibers in the descending tract of the trigeminal nerve (trigeminal nucleus caudalis) are believed to interact with sensory fibers from the upper cervical roots 13

Right Anterior Insula: Area of the insular cortex where the intensity of pain is perceived


 * Quiz**

1. Trigger points are mostly muscle spindle fibers. T / F 2. Referred pain is defined as pain located a. 1 cm from the trigger point location b. 1 inch from the local trigger point pain area c. 10 cm from the trigger point location d. 1 cm from the local trigger point pain area 3. Pain pathways generally consist of large-diameter myelinated axons. T / F 4. The DCML and the spinothalamic pathways are both pain pathways. T / F 5. Trigger point release results in an immediate increase in joint tension. T / F 6. Fascia contains no pain fibers, and rarely transmits tension. T / F 7. Convergence projection theory states that a. Noxious stimulus diffuses across multiple spinal levels b. Noxious stimulus is carried via the bloodstream to the brainstem c. Noxious stimulus can only effect its target neuron 8. Active trigger points may have a temporal summation effect on the trigemino-cervical nucleus. T / F 9. There is new evidence that deep pain is somatotopically organized in the primary somatosensory cortex. T / F 10. The right anterior insula is responsible for integrating the pain information with personal relevance of the pain. T / F 11. Briefly explain the three ways muscle contraction occurs according to the integrated trigger point hypothesis. 12. Describe the pathways of the DCML and the spinothalamic tract. 13. Explain why the integration of pain and perception may be important in referred pain.

Trigger Points: Diagnosis and Management- http://www.aafp.org/afp/2002/0215/p653.html
 * Further Reading**
 * This article provides an overview of trigger points and injection treatment.

Myofascial Trigger Points: An Evidence-Informed Review- http://www.dgs.eu.com/uploads/media/MTrP_an_evidence_informed_review.pdf
 * This article provides a detailed and technical overview of current theories and studies on trigger points.

Discrete Changes in Cortical Activation during Experimentally Induced Referred Muscle Pain- http://cercor.oxfordjournals.org/content/17/9/2050.long
 * This article provides a new and developing theory of referred pain.

Functional Anatomy of Muscle: Muscle, Nociceptors and Afferent Fibers __ [] __
 * This is a helpful chapter from Mense's textbook, //Muscle Pain: Understanding the Mechanisms//


 * References**
 * 1) Alvarez, D., & Rockwell, P. (2002, February 15). Trigger Points: Diagnosis and Management. //American Family Physician//, //65//(4), 653-661.
 * 2) Barbero, M., Cescon, C., Tettamanti, A., Leggero, V., Macmillan, F., Coutts, F., & Gatti, R. (2013, June 8). Myofascial trigger points and innervation zone locations in upper trapezius muscles. //BMC Musculoskeletal Disorders//, //14//, 179.
 * 3) Dommerholt, J., Bron, C., & Franssen, J. (2006). Myofascial Trigger Points: An Evidence-Informed Review. //The Journal of Manual & Manipulative Therapy//, //14//(4), 203-221.
 * 4) Fernández-de-las-Peñas, C., & Fernández-Mayoralas, D, Ambite-Quesada, S., Palacios- Ceña, D., & Pareja, J. (2011, February). Referred pain from myofascial trigger points in head and neck–shoulder muscles reproduces head pain features in children with chronic tension type headache. //Journal of Headache and Pain//, //12//(1), 35-43.
 * 5) Giamberardino, Maria A., Giannapi Affaitati, Rosanna Lerza, and Leonardo Vecchiet. (2004). Referred Muscle Pain and Hyperalgesia from Viscera: Clinical and Pathophysiological Aspects. //Basic and Applied Myology////, 14//(1), 23-28.
 * 6) Grieve, R., Cranston, A., Henderson, A., John, R., Malone, G., & Mayall, C. (2013, October). The immediate effect of triceps surae myofascial trigger point therapy on restricted active ankle joint dorsiflexion in recreational runners: a crossover randomised controlled trial. //Journal of Bodywork and Movement Therapies//, //17//(4), 453-461.
 * 7) Huguenin, L. (2004). Myofascial trigger points: the current evidence. //Physical Therapy in Sport//, //5//, 2-12.
 * 8) Macefield, V., Gandevia, S. C., & Henderson, L. A. (2007, September). Discrete Changes in Cortical Activation during Experimentally Induced Referred Muscle Pain: A Single-Trial fMRI Study. //Cerebral Cortex//, //17//, 2050-2059.
 * 9) Mense, S., & Gerwin, R. D. (2010). //Muscle Pain: Understanding the Mechanisms// (pp. 17-45). Berlin: Springer.
 * 10) Mense, S. (2003). The Pathogenesis of Muscle Pain. //Current Pain and Headache Reports//, //7//, 419-425.
 * 11) Resteghini, P. (n.d.) Myofascial Trigger Points : Pathophysiology and Treatment with Dry Needling. In //Homerton University Hospital//. Retrieved December 13, 2013, from http://www.homerton.nhs.uk/uploaded_files/Our_services/Sports%20clinic/myofascial_trigger_points_pathophysiology_and_treatment_with_dry_needling.pdf
 * 12) Werenski, J. (2011, June 17). //The Effectiveness of Myofascial Release Techniques in the Treatm ent of Myofascial Pain : A Literature Review// (Doctor of Chiropractic thesis).
 * 13) Biondi, D. (2005, April 1). Cervicogenic Headache: A Review of Diagnostic and Treatment Strategies. //Journal of the American Osteopathic Association//, //105//(4).

 a. 1 cm from the trigger point location b. 1 inch from the local trigger point pain c. 1cm from the local trigger point pain d. 10 inches from the local trigger point pain
 * Answers**
 * 1) **False**: Trigger points are mostly Type 1 oxidative muscle fibers.
 * 2) **C**: 1 cm from the local trigger point pain area
 * 3) **False**: Pain pathways consist of small-diameter axons. Myelination depends on the type of neuron.
 * 4) **True**
 * 5) **False**: Trigger point release results in an immediate in joint flexibility
 * 6) **False**: Fascia does contain pain fibers, and transmits tension in all movements.
 * 7) **A**: Noxious stimulus diffuses across multiple spinal levels
 * 8) **False**: Active trigger points may have a spatial summation effect on the trigemino-cervical nucleus.
 * 9) **True**
 * 10) **True**
 * 11) Through excess ACh, deficient AChE, increased ACh receptor sensitivity
 * 12) Spinothalamic: First order neurons enter the dorsolateral tract of Lissauer and travel one or two levels in the spinal cord before entering the dorsal horn gray matter. They synapse via interneuron to the second order neuron which crosses over at the spinal cord level and travels through the spinothalamic tract to the VPL of the thalamus, and a third order neuron reaches the somatosensory cortex. DCML: First order neurons travel ipsilaterally to the medulla where they synapse in the dorsal column nuclei (gracilis from lower body and cuneate from upper body). From here they decussate and travel to the VPL of the thalamus where they synapse to the third order neuron and decussate again, terminating in the somatosensory cortex.
 * 13) It is possible that referred pain is a protective mechanism used by the body to immobilize limbs/segments when further use could result in further injury.