Myofascial trigger points are a well-documented source of back, head, neck and face pain.  Travell and Simons have mapped myofascial trigger points in the muscles of the low back, skull, jaw, and cervical spine that refer pain in characteristic patterns.¹  Myofascial pain can cause sever and even debilitating pain as well as restrictions in the normal biomechanical function of the joints.  It can also cause impairment of normal neurological fuction, circulation and lymphatic flow resulting in a variety of symptoms such as lymphatic congestion, vasomotor rhinitis, sinus congestion, difficulty swallowing, ear pain, dizziness, tinnitus, dry cough, blood pressure fluctuations, paresthesias in the face, itchy ears, toothaches, eye pain, blurred or double vision, migraines, tension headaches, bladder irritation, and restrictions in cervical, lumbar and thoracic motion.^{1, 2}  In general, the patient perceives the pain and paresthesia as emanating from the referral area and is unaware of the location of the trigger point causing the pain.¹

When a muscle sustains trauma or when the body is exposed to repeated stressors, the muscle responds with spasm or, more commonly, contracture.  Contracture is a chemical rather than action potential mediated shortening of the muscle.¹  Dr. Hans Selye observed that patients responded to repeated stressors with something that he called "calciphylaxis".  He defined calciphylaxis as "an induced hypersensitivity in which tissues respond to various challenging agents with a sudden calcification".⁴  It didn't matter whether the stressor was chronic illness, severe emotional trauma, multiple or severe injuries to the tissue.  Repeated experience of a sympathetic stress response caused predictable tissue changes.^{4, 2}  These tissue changes caused tightening of the myofascia and muscle contracture promoting formation of a trigger point.²  Travell proposes a more mechanical model in which a traumatic, rapid over-stretching of the muscle or crush injury can rupture the myofibrils causing leakage of calcium from the sarcomere and subsequent contracture.¹  Whatever the proposed mechanism, mineral deposits in the myofascia set the stage for contracture and trigger point formation.

Both spasm and contracture cause a reduction in the blood supply to the areas decreasing oxygen transport and waste removal, and causing the myofascia to tighten.  Dysfunction in this delicate fascial membrane, which encases each myofibril, disrupts the flow of neurotransmitters.  Ground substance within the myofascia changes from a liquid to a gel to a solid further tightening the myofascial tissue.^{3, 1} The local ischemia in the muscles containing myofascial trigger points decreases ATP production, disrupts the sodium pump and normal membrane conductance, and increases metabolic wastes creating a self sustaining cycle of dysfunction which perpetuates trigger point formation.

Treatment of these trigger points has been difficult due to the delicate nature of the structures underlying the cervical and abdominal muscles containing the trigger points.  In some muscles, such as the psoas, the pterygoids, and the suboccipitals, the location of the muscle has made access difficult.¹  A series of coincidences has resulted in a very promising new treatment for trigger points using microcurrent applied with graphite/vinyl gloves.