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December 2002


Finding Clues to Pain

By Jeffrey R. Cram, PhD



Muscles serve three masters: emotions, posture, and movement. When it comes to assessing and treating musculoskeletal injuries of 6 months’ duration or longer, each of these three elements needs to be considered. From an interdisciplinary perspective, understanding how each of these aspects of muscle function is out of balance helps the team members decide how to approach the healing process. Surface electromyography (sEMG) can provide some clues on how to proceed in the most effective and efficient manner.

Consider a patient who presents with persistent neck and shoulder pain 6 months after falling down stairs. Given the length of time since the initial injury, the natural healing process should have run its course. Unfortunately, the pain and dysfunction are still present, and this patient would be considered to have some type of chronic pain syndrome. Such patients can be among the most difficult to treat, since something is obviously maintaining the pain. Trying to figure out how a self-perpetuating faulty motor schema is maintaining the pain may be the key to success.

When muscles are involved in persistent pain, sEMG monitoring can help provide some clues (see Table 1). Obviously, none of these elements are necessarily mutually exclusive, and can easily coexist within the patient, but sEMG monitoring can be used to help discover which aspect needs to be treated. To study the concepts presented here in greater depth, please refer to Clinical Applications in sEMG by Kasman, Cram, and Wolf.1


Table 1. Possible reasons for persistent neck and shoulder pain associated with a fall down stairs.

STRESS AND MUSCLE HYPERACTIVITY

Muscle hyperactivity, due to generalized central nervous system arousal or a conditioned emotional response to a traumatic event, can elevate sEMG activity at rest or during movement. In a patient who has fallen down stairs, we can monitor sEMG while the patient engages his or her imagination to assess the emotional triggers. This is called a “stress profiling” procedure. Here, the offending muscle is monitored during a baseline recording, followed by a period of time in which the patient recalls the fall in detail, followed by a “recovery” period. Increases in sEMG recruitment during an imaginal recall of the fall down the stairs provide evidence as to this emotional component, possibly a post-traumatic stress disorder (PTSD).

Once identified, this post-traumatic response would need to be treated in order for the persistent pain disorder to go and stay away. A somatically oriented PT might utilize “somato-emotional release” techniques2 to approach this problem. A somatically oriented psychotherapist might utilize Peter Levine’s methods,3 or Pat Ogden’s “sensorimotor psychotherapy,”4 to help the body release these muscle memories. And the traditional behaviorally oriented psychologist might utilize sEMG biofeedback to “downtrain” the faulty motor schema,5 or blend in some systematic desensitization6 or eye movement desensitization,7 to help alter the negative cognitive engrams leading up to the emotional response.

The bottom line is that unless the emotional component is adequately addressed, no physical restorative care procedure will show long-term gains, since the emotional network will continue to be triggered by daily life, thus activating and perpetuating a faulty motor schema.

SIMPLE POSTURAL DYSFUNCTION

With simple postural dysfunction, aberrant motor activity is shown to be a direct function of posture. The increased paraspinal muscle activity seen in this tracing is reduced as the head is moved from a forward position, to one in which the head is well positioned over its center of gravity. The initial sEMG elevation is likely due to the increased load from the head being forward of its center of gravity. This increased load would also place untoward loading of the articular structures and chronically stretch the ligaments.

According to McKenzie,8 this chronic physical stress on the soft tissue creates the foundations for pain. In addition, muscle-length-tension relationships become inefficient. As the load movements are increased by lengthening the lever arm through which gravity acts, the normal force couples are disrupted and some muscles may recruit at an increased level, while the antagonists take on a lesser role.

Whether this head posture was present before the fall, or resulted from muscle disuse following the fall down the stairs, it will need to be treated in order to eliminate yet another perpetuating factor.

ACUTE REFLEXIVE SPASM

Spasm is defined as an involuntary hypertonicity induced by the spinal reflex system, and is commonly triggered by noxious mechanical or chemical stimulation of the pain receptors within the muscle or the associated joint. In the neck shoulder pain example, let us say that the patient herniated the right aspect of the cervical disks at C4 as a result of the fall. This will cause elevated sEMG activity in the right cervical and upper trapezius. This increased sEMG activity could be seen at rest or during movements that further irritate the nerve in the affected area. The thing to remember is that the increased sEMG activity would be on the same side as the pain. This differs from the learned guarding described below. As manual therapy techniques are applied and spasm ceases, the sEMG activity would subside.

LEARNED GUARDING OR BRACING

This pattern of neuromuscular activity differs from the reflex spasm model, in that the pattern of muscle activity is “learned” or operantly conditioned, rather than being strictly mandated by a reflex. The heightened muscle activity usually occurs upon movement or postural loading and is done in an attempt to avoid pain and the possibility of further injury. The activation pattern is always seen on the opposite (contralateral) side of the pain as the patient exhibits a “learned disuse” and inhibition of the painful side, and a hyperactivity of the non-painful side. This is one of the features that differentiates “protective guarding” from “splinting” or reflex spasm.

Consider the pattern of muscle activity for a patient with neck and shoulder pain. sEMG data was collected using the muscle scanning procedure,9 in which the right and left aspects of multiple muscle groups were quickly sampled in the seated and standing postures. The patient has right-sided neck and shoulder pain, which can radiate down into the right hand. Disc herniation is known not to exist. The pattern of activity shows increased sEMG activation on the side opposite the pain, suggesting a protective guarding pattern. Here the patient has “learned disuse” of the right shoulder, along with an elevated right shoulder, or an antalgic posture.

DIRECT COMPENSATION FOR JOINT HYPERMOBILITY OR HYPOMOBILITY

In this syndrome, the neuromuscular system compensates by attempting to stabilize lax joint structures, by affecting movement against joint stiffness, or by subserving linked compensatory movements over kinetic chains.11

Although sEMG activity would be aberrant, the primary problem is a biomechanical articular fault. The articular fault causes a compensatory motor control pattern, which may spontaneously resolve upon improvement in joint mechanics. Chronic joint dysfunction may lead to motor control problems that contribute to deterioration of the kinetic segment and persist even after joint mobility improves. The distinction is made because if aberrant motor activity is believed to be directly compensatory to articular dysfunction, then biofeedback is not a first choice of treatment. The joint dysfunction should be addressed and then sEMG activity reassessed. To facilitate a more permanent change in musculoskeletal relationships, sEMG-guided exercises could be used to retrain the new motor schema.

This could be done if the patient who slipped and fell down the stairs also affected his or her temporomandibular joint (TMJ) and thus also has jaw pain, as well as neck shoulder pain. Physical examination shows hypomobility at the left TMJ. There is a deviation of the midline of the jaw during opening and closing, and a palpable difference between the motions of the left and right mandibular condyles. As opening is initiated, or closing completed, the condyles spin in place. The condyles then translate forward as opening continues. This rolling/gliding relationship is necessary for normal jaw range of motion and is expected to be symmetrical at the left and right TMJs. In our case example, sEMG activity shows greater recruitment at the right masseter during jaw opening/closing range of motion. In this case, the right mandibular condyle translates a greater distance along the articular surface of the zygomatic process. The right masseter is activated to a greater degree to subserve the greater range of movement than the right TMJ. The fundamental problem, however, is not one of the right having greater masseter sEMG activity than the left, but one of the left having less joint mobility than the right. The sEMG spontaneously becomes symmetrical once the left TMJ is mobilized with manual techniques or exercises. Retraining would be instituted at this point.

CHRONIC FAULTY MOTOR PROGRAMS

The final syndrome is an amalgamation and perpetuation of all of the above syndromes. Here, we assume that the central nervous system learns to cope with pain, muscle weakness, joint instabilities, trigger points, myofascial extensibility issues, and other problems. As a result, there is a learned disruption of the normal agonist-antagonist-synergist relationships.12,13 The assessment (and treatment) of this broad syndrome requires sEMG monitoring, along with assessment of coincident joint segment dysfunction, soft tissue dysfunction, and behavioral analysis.

In this instance, the patient who had the fall now has chronic cervical paraspinal and suprascapular pain. Motion takes place throughout the shoulder girdle to elevate the arms to the side (abduction). This includes upward rotation of the scapula, achieved by the coordinated actions of the upper trapezius, the lower trapezius, the lower fibers of the serratus anterior, and numerous other muscles with direct and indirect stabilizing roles. A motor program is a planned set of commands from the central nervous system that serves to coordinate the actions of muscles so that a specific goal is achieved, in this case shoulder abduction.

If an inefficient motor program is selected, then one muscle might contract with excessive or reduced tension relative to its synergist, resulting in abnormal loading patterns of both myofascial and articular tissue. With our patient example, it is observed that the sEMG activity of the upper trapezius is considered hyperactive, whereas the activity of the lower trapezius is inhibited. In addition, the patient has a poor ability to recognize these patterns of activation and tension and is unable to voluntarily activate the lower trapezius. sEMG biofeedback may be used to reeducate the patient about his muscle function, and to develop a more appropriate motor program, one that includes the scapular stabilizers (lower trapezius) in arm movement patterns.

SUMMARY

In summary, sEMG is a procedure that can provide beneficial information concerning chronic pain disorders. Disorders that could possibly be assessed and treated using sEMG include: tension headache, temporomandibular dysfunction (TMD) and myofascial pain disorders, post-traumatic stress disorder, cervical dysfunction, shoulder girdle and upper extremity dysfunction, lower back dysfunction, hip dysfunction, knee dysfunction, stroke, and urinary incontinence.

Jeffrey R. Cram, PhD, is clinical director of the Sierra Health Institute, Nevada City, Calif, and serves on the board of directors for the Biofeedback Society of California.

REFERENCES

  1. Kasman G, Cram JR, Wolf S. Clinical Applications in SEMG. Gaithersburg, Md: Aspen Publications; 1998.
  2. Upledger J. Somato Emotional Release. New York: North Atlantic Books; 2002.
  3. Levine P. Waking the Tiger: Healing Trauma. New York: North Atlantic Books; 1997.
  4. Ogden P, Minton K. Sensorimotor psychotherapy: one method for processing traumatic memory. Traumatology. 2000;4(3):1-15.
  5. Cram JR, Kasman G. Introduction to Surface EMG. Gaithersburg, Md: Aspen Publications; 1998.
  6. Wolpe J. Life Without Fear: Anxiety and Its Cure. Boston: New Harbanger; 1988.
  7. Shapiro F. Eye Movement Desensitization and Reprocessing. New York: Guilford Press; 2001.
  8. McKenzie R. The Cervical and Thoracic Spine: Mechanical Diagnosis and Therapy. Minneapolis: Orthopedic Physical Therapy Products; 1990.
  9. Cram JR. EMG muscle scanning and diagnostic manual for surface recordings. In: Cram JR, ed. Clinical EMG for Surface Recordings. Vol 2. Nevada City, Calif: Clinical Resources; 1990:1-142.
  10. Cram JR, Engstrom D. Patterns of neuromuscular activity in pain and non-pain patients. Clinical Biofeedback and Health.1986;9(2):106-116.
  11. Hertling D, Kessler RM. Management of Common Musculoskeletal Disorders. 2nd ed. Philadelphia: JB Lippincott Co; 1990.
  12. Taylor W. Dynamic EMG biofeedback in assessment and treatment using a neuromuscular re-education model. In: Cram JR, ed. Clinical EMG for Surface Recordings. Vol 2. Nevada City, Calif: Clinical Resources; 1990:175-196.
  13. Lewit K. Manipulative Therapy in Rehabilitation of Locomotor System. Boston: Butterworth; 1985.

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