Diagnosis and Treatment of Myofascial Pain Syndromes

Treating Myofascial Pain and Impingement Syndromes

Since each striated muscle in the body may be affected by strain, either overuse or traumatic, and may generate a pattern of referred pain and associated symptoms, the subject of diagnosis and treatment of myofascial pain syndromes can be overly complex. It is therefore necessary to focus on the most pathological muscles and fascia. These are generally deep muscles that attach to important bones and joints, which may easily impinge the circulation of blood or nerve conduction, and which are often key stabilizers in postural mechanics. Since the myofascial syndrome is essentially a neuromuscular pathology, attention to the stabilizing and impinging muscles will also significantly resolve chronic problems of joint instability and nerve conduction that contribute to all of the myofascial trigger points.

Clinically, occupational injury and trauma often present with syndromes that are derived from the same type of injury and affect the same muscles. Motor vehicle accidents typically present with whiplash and lumbar destabilization. Office workers present with keyboard derived repetitive and postural stress injuries, coupled with postural strain of the low back stabilizers. Manual labor often presents with shoulder and upper extremity injuries with underlying degenerative conditions from heavy repetitive lifting, or low back injuries with underlying degenerative lumbar pathology. Just as most whiplash injuries predominantly affect the splenii and scalenes, most keyboard derived repetitive postural stress injuries have these muscle syndromes underlying complex regional pain syndromes with tendinosis, carpal tunnel and lateral epicondylitis occuring because of impingement of nutrients (dystrophy) or weakness caused by chronic impingement of the nerve conduction. Dystrophy and motor weakness occur with episodic postural contracture in these cases and are often overlooked in clinical exam.

By focusing on a relatively small number of myofascial syndromes the clinical therapist is able to effectively treat a large percentage of patients efficiently. When patients present unusual patterns of symptoms, reference texts may need to be addressed. This is not unlike any other diagnosis and treatment.

This introduction to treatment of myofascial pain syndromes will focus on these key muscles. The basic list will include splenii, levator scapula, scalenes, pectoral minor, latissimus dorsi, teres major, subscapularis, teres minor, infraspinatus, quadratus lumborum, psoas, tensor fascial latae, gluteal muscles, and the piriformis. After this, key muscles of the limbs will be addressed. Superficial muscles, such as the trapezius, may need to be addressed routinely in therapy as contributors, but are not key to the serious symptoms in most cases.

Etiology and Causes of the Myofascial Pain Syndrome

Dr. Janet Travell, and David and Lois Simons first published a comprehensive study of myofascial pain syndrome in 1983. Dr. Simons was a professor of rehabilitative medicine at the University of California, Irvine, which now produces much essential scientific study of the physiological effects of acupuncture, as well as the integration of Traditional Chinese Medicine into our standard medical protocol via the Susan Samueli Center for Integrative Medicine. He was also the clinical chief of the Electromyography and Electrodiagnosis Section of the Long Beach Veteran Affairs Medical Center. His work was inspired by the lifelong efforts and experience of Dr. Janet Travell, who was President John F. Kennedy's personal physician and friend, and who passed away in 1997. Dr. Travell attempted to persuade the medical community from the 1950s onward that the primary cause and contributor to musculoskeletal pain was a neuromuscular pathology called myofascial syndrome, and which was best treated not by surgery or pharmaceutical medicine, but by manual therapies, especially the needle stimulation at the loci of the problem, the neuromuscular junction, or motor endplate. The text, Myofascial Pain and Dysfunction, the Trigger Point Manual, was expanded to a definitive third edition in 1999, after Dr. Travell's death, and is still the most authoritative and clear clinical guide for understanding and treatment.

Drs. Travell and Simon state that the myofascial pain and dysfunction syndrome is a diffuse neurological pathology with the critical trigger point abnormality being the neuromuscular dysfunction at the motor endplate, or point of innervation, of extrafusal skeletal muscle. Extrafusal meaning situated outside of the striated muscle motor spindle. They found nearly a 90 percent correlation between common acupuncture points and myofascial trigger points, and also found that dry needle stimulation at the trigger points worked better than injection of pharmaceuticals into the points. It was recommended that the focus of therapy in myofascial dysfunction be a comprehensive package of manual release techniques, dry trigger point needling, and neuromuscular reeducation. They classified the myofascial syndrome as a neuromuscular disease.

Modern research has led to an elucidation of the myofascial injury beyond the great work of Dr. Janet Travell in the period from 1950 to 1970. Tearing of the motor endplate tissues with leakage of calcium, as well as a denervation supersensitivity, have both been implicated in the exact physiological etiology of the syndrome. Long term studies have linked development of latent to active trigger points in muscles to peripheral nerve lesions such as radiculopathies, but the totality of evidence indicates that there are multiple causes and perpetuating factors, both local to the trigger point and distally in the nervous system. Ischemia, poor nerve conduction, and poor supply of nutrient chemicals to local tissues, called dystrophy, are all implicated, along with acute tissue injuries and gradual degenerative tissue injuries. In Traditional Chinese Medicine, these are called by various names, such as blood stasis, qi stagnation, damp obstructing the channels, qi congestion, cold obstructing the channels, bi syndrome, wei syndrome, etc. The challenge is for the holistic physician to understand exactly what is going on, and for the allopathic physician to open up to the multifactorial etiology.

Either acute muscle injury, or chronic strain from frequent repetitive and postural stress may cause tearing of the muscle fibers and/or inflammatory degeneration that leads to the dysfunction at the nerve innervation, or motor endplate. Muscle firing is primarily performed when calcium ions and the enzyme adenosine triphosphate (ATP) activate the myosin and actin cross bridges that power contactile motion of the myofibrils. The adenosine triphosphate becomes adenosine diphosphate (ADP) and phosphate in the tissue allows it to recycle, providing energy for futher muscle contraction. The free calcium ions supply electrons to trigger the contracture. The presence of calcium ions that are unspent will immediately trigger another contractile cycle, and so accumulation of calcium at the motor endplate will maintain muscle contraction, and perpetuate strain. The persistent contractile bridging of actin and myosin cannot occur when the fibers fully relax and lengthen (until again fired), and the body has a mechanism for this relaxation and resetting. Unfortunately, when excess calcium accumulation continues to trigger contracture, the muscle fails to release and continuous nerve firing and energy consumption start to weaken the muscle and create neural sensitivity. Normally, the calcium ions are quickly pumped back into the sarcoplastic reticulum, or membrane around the myofibril, in the relax phase of muscle firing. In myofascial pain syndromes, calcium both fails to be recycled efficiently, and also eventually may escape as the membrane degenerates and tears, accumulating around the trigger point. Contributing to this are other mechanisms of tissue calcification, such as poor hormonal regulation and excess consumption of poor quality forms of conjugated calcium supplement without efficient means to assimilate the supplement, and chronic inflammation. Calcification of tissues contributes to free calcium affecting the motor endplate, perpetuating the chronic muscle firing.

Over time, this continuous firing of the strained muscle, compounded by the contributing problems of calcium accumulation, result in a weakened muscle with poor circulation that it unable to produce sufficient ATP. In the abscence of ATP the myosin heads fail to release or recycle, and remains firmly attached to the actin heads, causing a stiffness, or cramp. In the more acute phase, individual motor endplates create taut bands of fibers that are palpable, as well as knots (satellite trigger points). In chronic cases, the lesions at the motor units can be felt as soft focal areas, or hollow at times. Trigger points develop at these loci of motor innervation and eventually create a tissue lesion that results in denervation supersensitivity and various degrees of triggered pain responses. The sensitization of the pain receptors around the trigger point may eventually lead to chronic pain signals, and chronic pain may be adapted to and perceived in various ways by the peripheral and central nervous system.

In treatment of the trigger point lesions, classic acupuncture needling and palpation utilizes different techniques with the needles related to the palpation of hardness, called excess, or softness, called deficiency. These techniques can also be applied appropriately in trigger point needling. The acute lesion will often have a different pathophysiology than the chronic tissue lesion, and may need different types of stimulation to resolve. Special acupuncture techniques, classically called a shi needling (literally that's it, identifying the trigger point), are used to perform myofascial trigger point needling in Traditional Chinese Medicine. As with dry needling technique, or modern trigger point needling, it is important to isolate the muscle with palpation, identify the main or satellite trigger point with palpation, and needle with the appropriate technique. Since the Licensed Acupuncturist is very well trained in needle techniques, and performs this type of physiotherapy routinely, this type of physician is well suited to perform trigger point needling.

Understanding and diagnosis are very important in the treatment of myofascial syndromes

Since 1978 the medical field has gone from a frequent denial of peripheral neuropathic pain to acceptance of a broad array of neuropathic pain scenarios. Sensitization of nerve receptors and their relationship to hyperactive motor innervation due to myofascial dysfunction is now generally recognized, but only in recent years. Many of the hallmarks of neuropathic pain may develop with the myofascial syndrome, including diffuse nonlocalized sensation of pain, referred pain patterns, dysesthesias such as burning sensation, pain felt in an area of paresthesia, paroxysmal pain, hyperalgesia, allodynia, and pronounced summation of pain signals after repetitive stimuli. Many of these painful sensations occur with sensitization following tissue inflammation and degenerative changes at the myofascial trigger points, and satellite trigger points at the myotendinous junction. Radiculopathy itself can be caused by chronic myofascial contracture of the deep stabilizing muscles, which cause both subluxation impingement at the vertebrae, as well as inhibited circulation and accumulation of inflammatory mediators well known to incite neuropathy at the nerve roots, foramen, and the overlying facet joint tissues. Supersensitivity occurs when atrophy of a series of efferent neurons results in increased irritability to chemical agents that accumulate. This can eventually result in some denervation. Denervated structures all develop supersensitivity. Hyperalgesia and allodynia result.

In the past, this denervation supersensitivity was too often treated as a mental disorder, and prescription of antidepressants for chronic myofascial pain became common. Eventually, one type of selective serotonin reuptake inhibitor actually proved somewhat effective for this pain by affecting 5HTP metabolism and firing and release of substance P at the spinal cord. Tricyclic antidepressants and antipsychotic and antiseizure medications are also prescribed, and are mildly effective because they inhibit sodium channels that are overactive with denervation supersensitization of the whole neurons. Unfortunately,the activity of this sodium channel inhibition is not selective, and CNS and cardiovascular side effects are often alarming. More often than not, the patient finds these drugs ineffective. A more direct approach to resolving the physiological causes of myofascial pain with a conservative care approach and holistic protocol is much more desirable.

Treatment must focus physiologically on a number of goals. One goal is to cause full release, or relaxation of the muscle to allow recycling of the calcium ions and ATP. Another goal is to clear the calcium accumulation, and perhaps the bits of dysfunctional protein enzyme that may result from the dysfunctional recycling of ATP. A third principle goal is to flush the tissue surrounding the trigger points to allow the clearing of excess calcium and protein fragments, as well as inflammatory mediators that may have accumulated. Myofascial release techniques are combined with needle stimulation, electrical stimulation, diathermy, or focused deep heat, tissue mobilization, and use of antioxidants and proteolytic enzymes. Of course, various topical and internal herbal formulas may also help achieve these goals. Only when these principle goals are met concurrently will sufficient progress be made in many cases. Of course, stopping the continuing sources of strain, especially in repetitive postural stress syndromes, is also sometimes necessary and has to be achieved concurrently also. The Licensed Acupuncturist is thus well equipped, with a broad scope of practice that includes all of these therapies, to deliver a therapeutic protocol that is most effective.

Motor endplates are located in the middle of each muscle fiber, and each neuron may service up to 1500 fibers, with contractile firing going both ways out of the endplate. The motor unit in most muscles, which tend to be comprised of a parallel set of fibers, is located in the center of the muscle belly. More complicated muscles are comprised of sets of fibers that run in different directions, and these have more than one main trigger point. Certain muscles are actually sets of fibrous bundles in parallel, and these too have multiple trigger points. The trigger point can be objectively identified by a twitch response that may be visible or palpable when a minimal surface electrical stimulation is applied. Sometimes the palpation of the trigger point itself is enough to elicit the localized twitch response, which may be subtle, and sometimes unseen but felt by the experienced physician. In almost all muscles, there is one endplate zone, some with parallel motor endplates close together. One motor unit of a typical muscle spans 5-10mm, and the diameter of the motor unit may be wider than 15mm (one inch equals 25mm). Effective treatment involves experience in palpating these motor units and acquiring the ability to find the trigger points accurately. A combination of anatomical visualization, palpation of the edges of the muscle fibers, location of the muscle belly, palpation that searches for the trigger point, and a palpable sense of the trigger point by identification of knots, ropy bundles, twitch response, and of course the eliciting of trigger point symptoms, all come into play to build experience for the practitioner. The muscle usually must be held in some tension with stretch and position to accomodate these manual palpations. In time, the practitioner easily senses the locations and goes right to the trigger point in the same way that a violinist eventually applies just the right force at the right point on a string to elicit the perfect note.

Understanding the Myofascial Pain and Impingement Syndromes

The term myofascial refers to both the muscle and a broad sheet of fascia, or connective tissue under the skin, that includes nerve, blood vessels, binding of tendon and joint capsules, ligamentous tissues and sheaths around bones. Because of this, most myofascial pain is referred, patterned and impinging. The pain syndrome is more than an acute muscle strain. It is usually a chronic syndrome, or an acute syndrome with underlying subclinical problems, that involves sensory, motor and autonomic symptoms caused by tissue lesions, which are electrically active loci, or trigger points. The main trigger point of a muscle is located at the point or points of innervation, causing a constant firing at the sarcolemma instead of a contract and release mechanism. This constant neural firing weakens the muscle and eventually may cause autonomic dysfunction, or overload stress of the sympathetic and parasympathetic system. Satellite trigger points are often active, especially at the musculotendonous junction, causing enthesopathy and referred pain around the joint. The precise physiology of referred pain patterns associated with myofascial trigger points and endplate dysfunction is still unclear, but it is generally agreed that it is a multifactorial pathological process. Referred pain may be due to a combination of nerve irritation, projecting along dermatomes or myotomes, and connective tissue disorder extending along fascia, as well as indirect causes related to expansion of the syndrome to other myofascial foci, or muscles.

Trigger points (TrP) involve dysfunction of motor endplates, which are the endings of motor nerve fibers in relation to skeletal muscle fiber. Focal ischemia is also found in an area of knotted or contracted muscle fiber around this point of muscle innervation, contributing to the dysfunction. This endplate dysfunction causes a constant neural firing, creating a problem with recycling the calcium and ATP that are used in muscle firing, and which chemically recycle during the rest phase of muscle contraction. This constant firing and contraction causes accumulation of these chemicals in the surrounding tissues that also increases pathology, with inflammatory reactions and hardening, or calcification, of the local tissues. Inflammatory mediators, as well as calcium and other chemicals, stimulate sensory pain response. Chemicals known to stimulate pain receptors, or nociceptors, in concentration, include prostaglandins, bradykinin, 5HTP, hydrogen ions, and substance P. Certain prostaglandins, PGE2, are the focus of aspirin and nonsteroidal anti-inflammatory drugs in pain relief by blocking production. COX-2 inhibitors, such as Vioxx, more specifically block production of prostaglandin-endoperoxide synthase, but these drugs are also linked to serious cardiovascular pathologies, including atherosclerosis. Myofascial release is a method of ending the motor endplate dysfunction without side effects, and combined with localized soft tissue mobilization effectively clears the tissues of accumulations of all chemicals that trigger pain. A number of treatment strategies can be combined with direct myofascial release to increase the effectiveness of therapy. This includes increasing the production of the prostaglandins PGE1 and PGE3 with nutrient medicine, which limits the production of PGE2, as well as providing healthier anti-inflammatory action and improved tissue healing. Herbs that contain linoleic and linolenic acids, and essential fatty acid supplements, such as krill oil, with concentrated EPA and DHA, help achieve this metabolic goal. A number of therapeutic principles ultimately may be combined to achieve therapeutic goals in myofascial release, including antioxidant supplementation, neuromuscular reeducation, diathermy with far infrared and electric acupuncture, etc.

The pain signal in myofascial syndrome is transmitted on both slow and fast nerve fibers, with chronic pain signals on slow nerve fibers affecting not only the spinal cord and cortex, but also the hypothalamus and forebrain, creating a complex pain syndrome with autonomic dysfunction. Pain is thus often non-localized, deep, aching, regional and patterned in the chronic myofascial syndrome, and diverse related autonomic symptoms may also arise. Autonomic symptoms vary widely from patient to patient, but often complaints are made of insomnia, abnormal sweating or dryness, increased nasal congestion, dizziness, tinnitus, imbalance, and distorted weight perception of lifted objects causing dropping of implements at work (dropsy). If impingement occurs, symptoms of paresthesia, such as numbness and tingling, heavy sensation, and episodic weakness occur, as well as dysethesia, such as pins and needles, burning sensation, or crawling sensations. These neuropathic symptoms are usually episodic, and often antalgic, or related to postural positions that the patient acquires to avoid pain. Unfortunately, the postural distortions often perpetuate the myofascial strain and cause impingement of nerves and blood circulation, either directly or indirectly. To achieve both temporary cure and long lasting effect, neuromuscular reeducation, such as instruction in correct postural mechanics, or ergonomics, as well as targeted stretch and exercise, and various proactive therapeutic techniques, must also be included in the therapeutic protocol.

Neuromuscular reeducation (NMR), or retraining, is a "Mind-Body" medical specialty increasingly used and supported by modern musculoskeletal medicine. A number of techniques are utilized, and with a modest education in anatomy and physiology, are easy to utilize in physical medicine. The creation of schools of thought, or labeling of NMR techniques, is probably counterproductive to the encouragement of all physicians in musculoskeletal practice from utilizing these techniques. The essential techniques are well described in Travell and Simon's text, as well as Warren Hammer's Functional Soft Tissue Examination and Treatment. Proactive therapeutic techniques work best when the breathing reflex is utilized, with the patient deeply inhaling during contraction, and deeply exhaling with a sigh during relaxation. Active release technique (ART) utilizes patient focus and targeted primary movement as the physician treats satellite trigger points, mainly in the myotendinous portion, with cross-fiber friction. This is especially useful in treating enthesopathies. Contract-release and reciprical inhibition are easy to learn and incorporate into therapy. These are now called muscle energy technique (MET), and include postfacilitation stretch and proprioceptive neuromuscular facilitation (PNF). These creations of anacronyms and complex names to simple techniques, though, may be creating a mindset of specialization that is unnecessary. Frequent use of NMR is most beneficial, and even an orthopeadic specialist or physiatrist could easily learn and use a few minutes of these NMR techniques during patient exams and assessment. Certified massage therapists, Licensed Acupuncturists, Osteopaths, Chiropractors, and even trainers could utilize NMR to benefit the treatment protocol.

The neuropathic symptoms mentioned in relation to impingement must be seen with a broad and knowledgable diagnostic perspective in the myofascial pain syndrome. Neuropathic symptoms may have two distinct causes, the direct impingment of nerves, and the denervation supersensitivity seen in the chronic syndrome. Approach to treatment of these symptoms must address both of these potential causes in chronic cases. Sometimes the release of impinging muscles doesn't provide complete relief, and a more comprehensive approach to resolving the dysfunction of the whole nerve pathway must be utilized, which would take a little longer to effect.

Satellite trigger points may also occur in the muscle tissues, usually at lesions felt as knots, or ropy tissues. These satellite trigger points may contribute to the pathology at the main trigger point of endplate dysfunction, but are usually not significant in and of themselves. Massage therapy often targets these superficial knots, bringing temporary relief, but not an end to the myofascial syndrome. The satellite trigger points may also be active and trigger referred pain, usually localized, and respond to needling, but ultimately, focus on these satellite TrPs diverts the physician from the more important therapeutic goals. Soft tissue mobilization will often eliminate satellite TrPs, and it is helpful to start the treatment session with various Tui na, or soft tissue mobilization, techniques, both to resolve these superficial TrPs and to increase circulation and relaxation of the patient.

Diagnosis of Myofascial Syndromes

Myofascial syndromes are objectively diagnosed by physical exam alone. Surface EMG may show accelerated fatiquability, and thermography and skin-resistance point finders may identify the trigger points, but these tests are rarely performed. Simple postural, range of motion and strength exams allow the physician to accumulate data on muscle length and strength, and affects on the joint mobility, and this pattern of data, coupled with palpation of trigger points, is a simple and definite means of specific diagnosis. Trigger point palpation and needling will trigger patient symptom complainst, identifying causal muscles. Not only complaints of symptoms from trigger point stimulation, but also localized twitch responses may be noted. Sensitivity to and recreation of TrP symptoms will vary greatly between patients. Pain is usually marked when the patient suddenly contracts against resistance with the muscle in a shortened position, and this resisted isometric exam may be used at the end of exam to further clarify specific muscle pathology.

Each muscle has a pattern of symptoms and referred pain. The main trigger point, or point of innervation, is located in the center of the belly of the nmuscle, although some large muscles have multiple points of innervation. Tendinous insertions may be palpated for trigger points, and the muscle fibers may be palpated along the fibers horizontally to find knots or hard wiry areas that identify more satellite trigger points. The location of trigger points and the patterns of symptoms and dysfunction is outlined clearly in Dr. Janet Travell and Peter Simon's two volume Myofascial Pain and Dysfunction, The Trigger Point Manual. Videotape of Dr. Travell performing exams on key muscles is also available. This book also outlines the most suspect of muscles for all regions of the body, in a descending order of most frequent involvement in studies, at the beginning of each part in the book. It also gives frequent associated muscle patholgies and specific tests, and describes the needling approach to most trigger points. These books are thus essential to the clinician.

Another essential diagnostic text when considering musculoskeletal pathologies of the extremities is Warren Hammer's text Functional Soft Tissue Examination and Treatment. Differential diagnosis is clear in this text, and a description of active release technique, usually used on the enthesopathy, or trigger points of the myotendinous junction, is clear. Of course, clinical experience is the only real way to accumulate an expertise in trigger point palpation, manual release, needling and active release techniques. Instruction is very important for efficacy in treatment.

Methods of Achieving Myofascial Release and Neuromuscular Reeducation

CPT 97140, manual therapy, was devised to describe the combination of various manual therapies recommended in the treatment of myofascial pathologies, and incorporated three previously used procedural codes. It is thus a hybrid code encompassing myofascial release, joint mobilization, soft-tissue manipulation, manual traction, and is appropriate for trigger-point therapy, deep tissue therapy, proprioceptive neurofacilitation, and post-isometric relaxation. These treatment skills define the practice of Tui na in Chinese medical practice, and distinctly describe the type of combination of skills and therapies that I am presenting in this article. In fact, the formation of my therapeutic practice, involving three distinct therapies bundled within a one hour treatment session, was guided by this international description, and approximately fifteen minutes are spent each session with patient/provider contact utilizing myofascial release, neuromuscular reeducation, and acupuncture.

Chronic myofascial syndromes demand a thorough therapeutic package of both restoring proper firing and function of the muscle and correcting dysfunction of body mechanics and postural problems that are often key contributors to the etiology of the muscle strain. Neuromuscular reeducation is often a key component to not only successful myofascial release, but also to restoring a healthy neuromuscular function, dealing with learned pain and hyperalgesia, and teaching the body proper body mechanics and postural habits. First and foremost, patient focus and active participation is a key to myofascial release. A reflex breathing routine of release during a relaxing exhalation, such as a sigh, is a great facilitator to a complete manual release. The patient should also be focused on the particular muscle that is being released. This focus will carry through to successful therapeutic stretch at home as well as focused strengthening and use in postural mechanics.

A number of techniques have been found to be effective in myofascial release, and combination of these various techniques assures a quicker and greater success. Quick rhythmic rocking of the spinous process at the appropriate nerve root, deep focal heating of tissues, or diathermy, and increasing circulation to ischemic areas with mobilization, are all important. Manual release is perhaps still the most direct and effective method of myofascial release, although it often involves triggering of painful symptoms for about 20 seconds. Manual release may be synonymous with the Japanese techniques of Shiatsu in part, since Dr. Janet Travell noted a greater than 90% correlation with myofascial trigger points and common acupuncture points, and the technique of slow deep steady pressure at these points is common in Shiatsu. In fact, we might surmise that the use of pressure release and needling was integral to the discovery and use of acupuncture and tuina historically. Needle stimulation of the trigger point, with proper technique, may also be a direct and highly effective means of therapy. While the purpose of manual release is to deny the ability of the muscle to continuously fire, thus causing a relaxation phase, needle release seeks to alter the dysfunction of continuous firing and contraction by altering the membrane ion exchange with manipulation of a fine metal needle point. Medical doctors have also used hypodermic insertion of chemical agents into the points to alter dysfunctional myofascial firing, but Travell states that dry needle technique is usually found to be more effective. In fact, Travell & Simon recommend techniques of a skilled acupunturist with fine needles.

A number of additional techniques are helpful, such as reciprocal inhibition, and contract and release techniques, such as post-isometric relaxation. This group of therapies is useful under the umbrella of neuromuscular reeducation techniques because it requires the focus and participation of the patient and succeeds in retraining their proprioreceptive mechanisms while achieving myofascial release. Another popular and useful technique is called active release technique, or A.R.T. This technique is helful primarily for setellite trigger points in the tendons, or myotendinous junctions, of muscles that are prime movers of the joints. The technique, which requires skill and expertise, works by applying manual pressure across the myotendinous trigger point, identified by palpation, while the patient isolates and uses the particular muscle. Repeated flexion while applying a steady manual pressure across the trigger point lesion will result in less active triggered symptoms and greater function. Use of reflexive breathing during ART is also helpful. This pathology is call an enthesopathy, or pathology of the myotendinous portion of the muscle attachment.

Contract and release and reciprocal inhibition may be performed together, usually after the manual release, needling, or ART, but sometimes may be useful preceding these techniques, if the pathology is so bad that the patient has trouble tolerating these other techniques and needs some mild gentle release first. When used after the more aggressive techniques, these therapies are useful to also reeducate the muscle and finish or smooth the therapy. Contract and release is performed with the muscle isolated into a cardinal position of targeted stretch and uses some mild resistance applied by the physician. The patient repeats a contracting and then uses a relaxing outbreath, or sigh, to facilitate a mild increase of extension or lengthening. Post-isometric relaxation describes this process, where the muscle start in a lengthened cardinal position, is contracted slowly against minimal resistance with a slow inhalation, then released and stretched with a relaxing exhalation. Reciprocal inhibition uses targeted contraction of the opposing muscle with mild resistance applied and then a relaxation with outbreath of the muscle being worked. Both techniques use a mild force of contraction, instructing the patient to contract slowly and use about one fourth of the their strength. For tendon pathologies, eccentric strengthening will also facilitate correct healing and stretch. This neuromuscular reeducation technique starts with the muscle in a cardinal contracted position, with the patient exerting mild isometric active flexion as the physician exerts a stronger force to achieve extension, with slow and gentle stretch of the fibers against active contracture. Of course, this eccentric loading requires some patient instruction and awareness to correctly balance these forces. Mobilization after eccentric loading and stretch facilitates the whole process of healing, and these various neuromuscular reeducation and active release techniques (ART) should be combined to achieve a holistic array of goals to improve tissue remodeling and release.

Trigger point needling takes great skill and care, although ultimately this is a simple technique. It is very important to isolate the muscle between the fingers, locate the trigger point lesion, and not needle past the trigger point in the muscle. In certain deep muscles, the direction of needling also needs to be correct in order to minimize the danger of needling into adjacent tissue structures, especially the lung. A stretch of the muscle is important during release to facilitate a release from contracture. Myofascial release of a muscle not held in stretch is much more difficult. Dry needling involves a quick insertion, slow penetration until symptoms are excited, and then reducing techniques applied as tolerated. Usually the needle is quickly removed from the tissue within about 30 to 60 seconds. In traditional texts from China, this is called A shi needling, which means 'that's it', referrring to the acknowledgement of the trigger point symptoms by the patient. Repeated needling, and sometimes 'trail needling', where needling is applied to satellite trigger points revealed by the needling reactions of the first trigger point, were often utilized. Both the main meridian acupuncture points, and A shi points can be used in trigger point needling, but the technique is important with both types of points, palpating, isolating the muscle fibers between fingers, holding the muscle fibers in mild stretch while needling, and needling the actual trigger point, not just the point on the skin. Positioning the body with trigger point needling requires different techniques than standard acupuncture point selection and needling.

The Important and Most Pathological Muscles in Myofascial Pain Syndromes

It is important to understand that most myofascial syndromes involve more than one muscle, since problems with one muscle causes added strain on others, and overstrain is the etiology of the myofascial syndrome. The reason that fascia is included in the name of these syndromes is to stress that muscle tissues are interconnected and not isolated. Fascial tissues connect not only to adjacent muscle tissues but also to the joint tissues, resulting in both subluxation and capsular tissue pathologies. Over time, as calcification of tissues progress, ischemia prevents clearing of tissues, and other metabolites such as protein fragments accumulate in the tissues. Chronic inflammatory degeneration progresses. Neuropathies may be caused by both mechanical impingement of the nerve or nerve root, and by chronic inflammatory irritation of the nerves. If the pathology is an acute simple traumatic overstrain, an isolated muscle may be seen. If the pathology is chronic, usually the myofascial syndrome involves more and more muscles, as the body adapts to favored use and weakness of the pathological muscles, causing a broader pathology of increased strain on surrounding muscles and sometimes, eventually, opposite sides of the body and contralateral deep muscles. Exam and treatment usually includes the related muscles as well as the primary pathology. It is important to become familiar with the patterns of pathology as well as the location of trigger points with each important muscle.

The first group of muscles we need to become familiar with are the prime movers and stabilizers of the neck. This is an interconnected group of adjacent muscles that includes the main extensors, splenii cervicis and capitis, the main rotators, the levator scapulae, and the main lateral flexors and stabilizers, the set of scalenes. In whiplash injuries, the splenii and scalenes take the brunt of the sudden strain, and these are the muscles that are involved in the more chronic syndromes that result. Also in repetitive postural strain with forward head and neck postures resulting from continuous computer use, most of the strain is on the extensors and scalenes, and if the patient frequently holds the head in rotation to read documents, the levator scapulae. The splenius origins are on the upper thoracic and lower cervical vertebrae spinous processes, and the attachments are on the mid cervical vertebrae and the base of the skull at the mastoid. Most stress headaches are due to myofascial syndromes of the splenii. The splenius capitus headache usually is felt at the occiput and vertex, while the splenius cervicis is felt along the side of the head, parietal temporal, to the posterior orbit. A painful stiff neck is the common complaint, and active range of motion is inhibited by pain. Usually, restriction of active rotation to the same side, and restriction of passive rotation to the opposite side, is seen. The manual release of these muscles is performed prone. The captitis overlies the cervicis and the trigger point is found by palpating under the edge of the trapezius and rotating the neck toward you while searching the belly of the muscle at about the level of C3-4. After this muscle is released, the thumb may palpate inferiorly while the neck is rotated away to find the cervicis trigger point. Trigger point needling is not as obvious with these muscles as with others. It may be performed prone or side-lying (which Travell diagrams).

Underlying muscles, especially the semispinalis cervicis and capitis, are often implicated in occipital nerve entrapment and torticollis, as well as temporoparietal headaches, but direct manual release and needling are difficult with these deep muscle groups. Usually, release of the overlying splenii, and mobilization of the spine will result in relief. The trigger points are located under the splenii trigger points, and so release of these muscles will result in some myofascial release of the semispinalis muscles. Needling should be performed with caution, and Travell recommends insertion at about the C5 level.

The levator scapula is a muscle often implicated in cases where the patient wakes with a severe wry neck, or inability to turn the head due to painful spasm. This results because the muscle was already strained and the patient slept in a position that required use of the muscle for a prolonged period of time. The muscles origins are on the C1-4 transverse processes and the attachment is to the superior medial scapula border. Common symptom complaints are tight pain to the lower neck and upper back, sometimes radiating deep along the medical scapula or to the posterior shoulder, as well as spasmodic pain with rotation, and sometimes extreme restriction of active rotation to the same side and mild restriction of rotation to the opposite side. To find the trigger point the muscle must be stretched by same side rotation of the head and neck in the prone position. The physician palpates under the edge of the trapezius in the belly of the levator scapula. Needling is problematic because of the position requirements for stretch, but Travell recommends a side-lying posture with the trapezius pulled down and the fingers of the left hand outlining the borders of the belly of the muscle.

Perhaps the most pathological muscle group in the body is the scalenes, a set of 3 or 4 muscles in the lateral neck that are prime lateral flexors and stabilizers of the cervical spine, and assist in rotation, flexion, deep breathing and mastication. The scalenes attach to the third to sixth cervical vertebrae typically, and also to the first to third ribs, as well as the clavicle. The anterior muscle attaches to the vertebral bodies, and the larger medius attaches to the facets and transverse processes of the cervical spine. Between these muscles the brachial plexus and subclavian artery flow. Contracture impinges both the blood and nerve circulation. Tests for thoracic outlet syndrome (Adson, Allen) as well as a brachial Tinel's sign are important to confirm these impingement pathologies. Symptoms are numerous for the scalenes. The most typical symptoms are associated with the anterior and medial scalenes. Anterior scalene pathology usually produces neck pain, lateral shoulder pain, radial forearm pain, pain around the wrist, radial hand pain, and numbness and tingling predominantly on the ulnar hand and fingers. Medial scalene pathology usually produces medial scapular pain, neck pain, posterolateral shoulder pain, and also numbness and tingling to the wrist and hand. Some or all of these symptoms may be seen, depending on the severity of the pathology, and other symptoms are sometimes produced. The muscles are palpated with the patient supine, the neck relaxed and the sternocleidomastoid muscle pulled medially with the right hand while the fingers of the left hand are placed on either side of the belly of the scalene muscle. The main trigger point is in the belly of the muscle, and may be palpated with the thumb of the right hand released from holding the SCM, and when found, steady pressure applied to release the muscle. The patient's symptoms are reproduced by the pressure on the trigger point, or with needling. The medial scalene is found just posterior to the anterior scalene. The levator scapula borders this muscle. The other scalenes, posterior and minimus, are smaller, and located beneath the lower portion of the medius. Treatment of these smaller muscles is usually not necessary.

The first cervical rib syndrome is often part of the chronic scalene pathology. This term is sometimes used to denote the elevated first rib at the cervical spine from chronic contracture, and sometimes to denote the rare abnormality of an anatomical variation of an extra small rib or a deformed first rib joint. Clinically, since these latter abnormalites occur in less than .1 percent of the population, we look to the elevated first rib and cervical joint. This condition stiffens the spinal movement, may impinge the vertebral vessels, irritate the nerve root, and cause further pain with rotation. A number of structures compose the thoracic inlet, and first cervical rib syndromes, together with the anterior scalene syndrome, may affect the subclavian artery, vertebral artery, carotid artery, vagus nerve, and phrenic nerve, contributing to a variety of confusing symptom. After the scalenes are released, a mild repetitive pressure on the first cervical rib at the joint, with the scalenes in stretch, will facilitate more correct position of the rib. A more thorough treatment of this condition may be performed with the patient seated, the head rotated away and cradled with the physician's other arm, and a combination of release techniques used, included mild contract and release, and breathing reflex, with inbreath and upward gaze contracting the scalenes, and outbreath sigh and downward gaze relaxing so that the placement of the rib in the joint may be fully facilitated.

Costoclavicular Syndrome is a term used to denote the impingement of the brachial plexus between the clavicle and an elevated first rib. Chronic contracture of the scalenes, which attach to both the clavicle and the first rib, is the primary cause of this neuropathic syndrome, but carrying a heavy back pack, or holding the shoulders back in a military posture are also usual causes of the pathology. Pectoralis minor contracture could also contribute to the first rib elevation indirectly by pulling the third to fifth ribs upward. The forward shoulder posture, and the forward head and neck posture, frequently seen in patients with prolonged keyboard and computer use, indicate contracture of the pectoral minor and scalenes, and this is the most frequently seen workplace injury in occupational medicine.

Scalene syndrome is grossly underdiagnosed. It is a primary cause of symptoms in many cases, and an important secondary cause in many diagnoses of carpal tunnel, lateral epicondylitis, forearm tendinitis and even the C6 radiculopathy. Cervicobracial syndrome of impingement or inflammatory irritation, thoracic outlet syndrome, or a myofascial origin to loss of normal cervical lordosis, usually diagnosed as degnerative arthritis, is finally being included in specialists assessments when radiological evidence does not show a clear disc pathology to explain cervical neuropathy. Even in cases where the patient has developed carpal tunnel, forearm tendinosis and lateral epicondalgia, impingement of motor nerve and blood circulation, producing dystrophy, is often the origin of the problems, especially with insidious and gradual onset. Thoracic outlet syndrome, which describes this impingement of blood circulation to the extremities, is often seen in these various pathologies and is easily tested with a variety of tests, including Adson's, Allen's, Wright's hyperabduction and Roos' tests. Acquaintance of these tests is essential to the diagnostic workup, and David Magee's Orthopedic Physical Assessment is an essential reference text for clinical use.

Thoracic outlet syndrome (TOS) is primarily caused by the chronic scalene and/or pectoralis minor contracture, but a number of other muscles can also produce symptoms that indirectly impinge the thoracic outlet or cause referred pain that mimics TOS symptoms. The internal rotators of the shoulder, a group of three muscles that include the latissimus dorsi (LD), the teres major (TM), and the subscapularis (SbS), are the main contributors to what is called Pseudothoracic Outlet Syndrome. A First Cervical Rib anomaly may also contribute. TOS not only indicates impingement of blood circulation, with episodic positional dystrophy to the tissues of the limb, but indicates a probable nerve impingement also, as the brachial plexus lies alongside the subclavian artery or thoracic outlet. This neuropathy is often traced to tissue lesions around the cervical and brachial plexus, and is diagnosed by Tinel's sign around the scalenes, or by reproducing symptoms with manual palpation or needling of the trigger points in the scalenes. After the syndrome was discovered and elucidated, standard medicine tried various surgical decompressions to relieve symptoms, without addressing the root cause, or myofascial syndromes with impingement. This, unfortunately, resulted in a majority of cases with worse chronic symptoms and debility than what were seen prior to the surgeries. These surgeries were then discontinued, or no longer authorized. After this dramatic failure, decades of orthopedic specialists' denials that the syndrome actually even existed occurred. In 2014, a meta-review of current studies of revisions of these surgical solutions, by the London Hand Clinic at London Bridge Hospital (see link to the review in Additional Information) concluded that, while "thoracic outlet syndrome is one of the most controversial diagnoses in clinical medicine" and "rigorous scientific investigation of this syndrome leading to evidence-based management is lacking", in 2014, "there was very low quality evidence that transaxillary first rib resection decreased pain more than supraclavicular neuroplasty, but no randomized evidence that either is better than no treatment. There is moderate evidence to suggest that treatment with BTX (botox) injections yielded no greater improvements over placebo injections of saline. There is no evidence from RCTs (randomized controlled clinical trials) for the use of other currently used treatments." This meta-review of all published studies was conducted by 3 independent experts with the highest quality of study determinations. In other words, standard treatment is still a complete failure in treating TOS in 2014. On the other hand, a well designed combination of modalities as presented here, with myofascial release, trigger point needling, neuromuscular reeducation, joint tissue mobilization, and instruction in targeted therapeutic stretch and correction of postural mechanics, perhaps combined with herbal and nutrient medicines to facilitate tissue healing and relief of muscle spasm, is very effective. There has been no studies of this protocol, and there will not be, with randomized controlled human clinical trials that are designed to test only one modality at a time, and are not designed to test manual therapies, where the physical acts cannot be blinded regarding a fake or placebo sticking with a needle or manual technique on the soft tissue. The very nature of these TCTs cancels even an attempt at such a study design in reality. This does not mean that this protocol does not work, though. For instance, no surgical treatment has ever been subjected to RCTs to prove that they work. Believe me, this holistic treatment protocol works for TOS.

Further study of myofascial syndromes on this site will involve the most pathological shoulder muscles, the internal rotators, teres major, latissimus dorsi and subscapularis, the pectoral minor, and the external rotators, the teres minor and infraspinatus. The low back pathologies will be examined with attention to the main stabilizers, the quadratus lumborum, the iliopsoas, and the gluteals, along with the tensor fascial latae and piriformis. The piriformis, a hip adductor and stabilizer, is oftent the source of sciatic impingement.

Small workshops to review myofascial pathologies and treatments may soon be possible in San Francisco, at Spring Wind Dispensary. These workshops and classes will be geared for the professionals to review myofascial musculoskeletal pathophysiology and to address manual release, trigger point needling and other therapies in a targeted and economical way. You may contact me to inquire on these workshops. They will be small in size and a few treatment tables will be available for small groups to receive direct instruction. While I don't pretend to be the world expert on this subject, my extensive study, teaching experience at ACTCM, and long clinical practice provides a wealth of usable clinical knowledge that can be easily applied to your practice.

Headache and neck pain, the essential myofascial causes

The tension headache is primarily caused by chronic myofascial dysfunction of the primary neck extensors, the splenii muscles. The more superficial muscles, the sternocleinomastoids and trapezii, are not the primary cause of concern. The SCM (sternocleinomastoid) holds much tension but is not the cause of neck pain whatsoever. The more sternal division refers pain to the face, around the eye, and to the occipital-parietal area of the skull, usually felt as superficial pain. The deeper clavicular part of the muscle refers pain to the ear and forehead. Sometimes, vertigo and nausea are related to the TrPs of the SCM, and thus these may be components of what is diagnosed as Meniere's syndrome. Targeted stretch should be taught to the patient to alleviate the SCM symptoms. TrP needling is usually ineffective and often leaves the patient with soreness and headache. Dr. Travell recommends avoiding SCM needling, or at least performing the trigger point needling as a last resort, and on one side only. The local superficial muscle, the temporalis, is also implicated in common tension headaches, but should be treated by various myofascial or soft tissue techniques preferrably over TrP needling. TuiNa techniques that are useful include stretch, skin rocking and tapping. Release of the pterygoids manually may also be important if TMJ syndrome is present.

The trapezius is a broad three part muscle, with the key characteristic being frequent tension and contracture in the upper part and weakness with lack of stabilization of posture in the lower trapezius. This feature is very important to the typical repetitive postural stress syndromes, and the patient must learn to use the lower trapezius and serratus as girdling muscles while relaxing the upper trapezius and the shoulders. Jutting out of the sternum will initiate engagement of these girdling muscles and allow relaxation of the shoulders. The Trapezius is easily contracted with stress and posture, but is also easily relaxed with rest or massage. The key pattern of pain associated with the trapezius is lateral neck pain behind the mastoid and forward temporal pain, but release of the trapezius trigger points alone will rarely cure these complaints. The trapezius is always released in therapy with temporal headache and neck pain, but lack of investigation of the deeper causes of the syndromes is a classic mistake in differential diagnosis. Articular dysfunctions of the cervical and upper thoracic vertebrae, and the key stabilizers of these vertebrae, the splenii and scalenes, as well as the levator scapulae, are the main causes of concern. Common acupuncture therapy utilizing GB21, LI16, UB17 and SI15 usually relieve the trapezius symptoms, as do the kneading and manual releases, and the classic trapezius stretch that should be taught to the patient.

The splenii, both cervicis and capitum, are the main causes of tension headache. The Splenius capitis lies over the splenius cervicis and is released first in manual relase. These muscles attach to the mastoid process and originate at the spinous processes of C3 through T3. The splenius cervicis attach to the transverse processes of the upper cervical vertebrae, and originate at the spinous processes of the T1 through T6. The semispinalis muscles lie deep to the the splenii, are difficult to treat with myofascial needling or manual release directly, and are less of a concern clinically. A two inch needle will not reach the semispinalis TrPs, located at about the level of C5, on most people. Release of the splenii will often result in a concurrent release of the semispinalis TrPs, which are located almost directly below the splenii TrPs. Contracture of the splenii will cause a pulling down on the occipital skull and upper cervical vertebrae, and range of motion exam will show loss of lordosis and decreased flexion of the upper cervicals in initial dropping of the chin, as well as some loss of rotation bilaterally, with active head and neck rotation to the same side perhaps restricted by pain at the extreme range. The levator scapulae (LS) are the main restrictors of head and neck rotation, and also attach to the transverse processes of the upper cervical vertebrae. Thus, splenii and LS can often be seen as a conjoined set of tissues in myofascial syndromes related to neck and upper back pain, but not to tension headache. The levator scapulae will often be strained with sleep postural strain (waking with a wry neck), especially if subjected to cold temperature change, or if the patient holds the shoulders elevated at work with stress and poor postural habits.

The splenii are often a key pathological components in repetitive postural strain, as well as in whiplash, and palpation of the key trigger points will often elicit marked pain, even if the patient does not complain of local splenii pain at all as part of the normal symptom syndrome. The key trigger points of the splenii lie lateral to the mid cervical vertebrae, and can be released manually face down, by first rotating the head to the same side, feeling the muscle tighten over the thumb, under the trapezius, and after releasing this splenius capitits, rotating the head away and feeling the underlying splenius cervicis trigger point appear under the thumb. A lower trigger point can be sometimes palpated and released lateral to C7. Needling of the trigger points is difficult, but if normal acupuncture technique face down does not release the muscles sufficiently, needling the TrPs side lying is recommended, with angle of the needles caudally, or towards the lower body, and the muscle bellies and trigger points located by placing the thumb and forefinger of the assisting hand on either side of the belly of the muscle, while the needling hand first palpates to locate the triggering part of the muscle, and then needles this point. Targeted stretch of the muscles is essential to therapy.

The levator scapuli are sets of thin muscles with much stretch, that attach to the upper cervical transverse processes, and originate at the upper medial scapula. Contracture of these muscles will cause much pain with head and neck rotation actively, as well as passive restriction. While the levaotor scapulae are not directly implicated in headaches, contracture and irritation contribute much to chronic aggravation of the splenii and scalenes. The LS TrPs are palpated with the patient face down, the head rotated to stretch the muscles, and then the key TrP found under the trapezius as it crooks lateral to the cervical thoracic joint. A second trigger point is often active at the origin, with an enthesopathy causing much of the upper back pain. This second TrP is most effectively released with active release technique, laying the thumb across the myotendonous tissue and having the patient take a deep breath, raise and rotate the head to the opposite side, and relax with an outbreath or sigh. The SI acupuncture points reflect the normal TrPs of this muscle, and should be needled through the trapezius until the symptoms trigger. If these points do not fully release the LS, side lying again is recommended for the TrP needling, with the trapezius pulled back and the muscle belly palpated with the assisting hand, the forefinger and midfinger straddling the muscle belly near the crook of the trapezius. Often, the LS has multiple taut bands and satellite TrPs that may need to be needled, with needle direction, of course, always toward the spine if the lower part of the muscle is needled, to avoid the upper lung. Postural mechanics at work and during sleep are very important in the treatment protocol. Use of the chair to turn at work, instead of repetitive overuse of these muscles turning the head, and use of a telephone headset are important. Proper height support of the neck during sleep, with avoidance of tucking the arm under the body are most important at night. The levator scapulae are often strained during sleep, resulting in waking with a painful stiff neck. Targeted stretch is also very effective therapeutically, especially when combined with heat in the shower or with a heating pad.

The scalenes are major contributors to headache and neck pain, but mainly via indirect cause or contribution to pathology. The scalenes are covered extensively in the article above, but it should be noted that these muscles are involved in mastication and deep breathing as well as head and neck stabilization and movement, and all of these aspects could contribute to perpetuation of headache and neck pain. In addition, the attachments to the vertebrae and fascial attachments to the splenii and levator scapulae allow for fairly direct contribution to spinal subluxation and typical stress contracture that causes tension headaches, impingement to the key muscles of healthy nerve flow, and impingement of the vertebral arteries as well as the carotid arteries. The complex of muscles and myofascial problems at the neck not only causes superficial headaches with referred myofascial pain patterns, but causes deep headaches, and contributes to migraines and other vascular headaches by impinging health blood circulation. In addition, the scalene contracture could put extra stess upon the masticatory muscles, especially the pterygoids, which cause TMJ syndrome as well as put direct mechanical stress upon the local termporalis muscles. The scalenes are easily released manually and needled to resolve TrP pathology, but care must be taken in technique to avoid irritation of the numerous nerves and vessels that overlie the scalenes. The assisting hand and thumb pulls aside these vessels and nerves, along with the SCM to expose the TrPs and avoid irritation of other structures. You should seek proper instruction to learn how to do these simple therapies properly.

TMJ, or temporalmandibular joint syndrome, is primarily caused by strain and contracture of the pterygoids, which lie posterior to the teeth and mandible. To release these muscles fully, one must get at the TrPs by reaching into the patient's mouth, although needling the belly of the main muscle at the surface is also somewhat effective. The release of the pterygoids in TMJ is very uncomfortable and triggers much pain usually, although typically one or two sessions of release will do wonders, along with instruction in targeted stretch, and release of the scalenes in addition to the pterygoids. TMJ has been found to be a multifactorial syndrome, with a number of potential contributing factors. Since the scalenes are both masticatory muscles and muscles of deep inspiration, chronic cough could be a significant cause of TMJ, as well as the various pathologies of the scalenes. The splenii cause tension headache, which affect the temporalis muscle, and chronic tension from repetitive stress syndromes must often be addressed to prevent the episodic return of TMJ. Recent research has found that the often recommended oral surgery and dental corrections have had little benefit in TMJ. To see an overview of these findings in a New York Times article, click here: http://www.nytimes.com/2009/02/03/health/03brod.html?_r=1&ref=health

The importance of neuromuscular reeducation and targeted stretch and exercise in the treatment protocol for myofascial pain syndromes

Often, instruction given to the patient that is targeted, succinct and to the point is crucial in the overall treatment success. One example is in the treatment of degenerative knee disorders. Myofascial release of the muscles that stabilize, as well as the muscles below the knee that wrap around the joint and frequently are the main cause of pathology, such as the gastrocnemius and tibialis posterior and anterior, are important to the success of treatment of the complex joint of the knee. Other key contributors that wrap the knee include the TFL and hamstrings. Stress imbalances of the pelvic girdle, low back, hip and foot can also be significant contributors to pathology. But if the targeted strengthening and toning of the stabilizing quads is not taught to the patient, success may never be realized. Even modern medicine has now come to realize the importance of these strategies, as evidenced from this article in the New York Time, Health: http://www.nytimes.com/2009/02/03/health/nutrition/03exer.html. Targeted strengthening of the quads involves isolating each of the vastus muscles with leg position, and strengthening each individually according to the need of the muscle. The number of repetitions is determined by the patient and should not exceed the limits of the muscles. When sufficient tone is achieved in all of these muscles, especially the vastus medius, the knee is supported in activity and repeated strain does not set back the course of rehabilitation.

This same principle is applied to all treatment protocols in myofascial pathology. Without a simplified and direct instruction in postural mechanics, targeted stretch and exercise, your success in treatment may be eliminated by the strain injuries that the patient continues to experience in activities of daily living. Seminars in these neuromuscular reeducation techniques will hopefully be the subject of future CEU seminars.

What is neuromuscular reeducation (NMR) exactly? CPT 97112 is defined as "Therapeutic procedure, one or more areas, each 15 minutes; neuromuscular re-education of movement; balance; coordination; kinesthetic sense; posture; and proprioception." When the physician instructs the patient in the kinesthetically correct methods of postural mechanics, targeted stretch and targeted exercise, with correct postural balance, coordination, proprioception and kinesthetic sense, this is neuromuscular reeducation. When the physician uses this time to merely assist or direct the patient performance of therapeutic exercise, range of motion, or flexibility, it is described differently, and is coded as CPT 97110, Therapeutic Exercise. Neuromuscular re-education is thus concerned with the correct instruction of the patient in body mechanics and focus of attention onto the targeted muscle, or other tissue, as well as the focus of the patient in the reflex of breathing technique concerning muscle relaxation, postural stresses, and a holistic approach to using self-administered therapies to achieve cessation of repetitive postural stress injury at work or during activities of daily living. Myofascial release techniques of focused contract and release and reciprocal inhibition also are considered re-education, as is active release technique (ART). Myofascial release is thus integrally tied to neuromuscular re-education, and is most successful when coupled in every treatment session. CPT 97112 should use the -59 modifier to signify use of a mutually exclusive procedure such as chiropractic manipulative treatment, CPT 98942, in the same treatment session, but not when performing myofascial release and soft tissue manipulation, CPT 97140. Various NMR techniques may be easily incorporated into the active physician therapy. Contract-release and reciprical inibition techniques of myofascial release, followed by mild proprioceptive facilitation and postfacilitation stretch is common. Sherrington's concepts are utilized, with isometric contraction for 7 seconds followed by 12 seconds of assisted stretch.

Information Resources

1. A pretty complete explanation of myofascial syndrome and pathophysiology that relates the trigger point pathology to acupuncture is available here in a research article from the University of California Irvine: http://www.acupunctureinmedicine.org.uk/servearticle.php?artid=382
2. A comprehensive paper on supersensitivity denervation and the neuropathic aspects of myofascial pain syndrome is presented here: http://www.www.northwestims.com/Bonica-Chapter.pdf This was published in Bonica's Management of Pain, Third Edition, John D. Loeser, MD, et al, Lippincot and Wilkens.
3. A 2014 meta-review of standard therapy to treat thoracic outlet syndrome (TOS), by the London Hand Clinic, at London Bridge Hospital, determined that the standard revised procedures, with supraclavicular neuroplasty, transaxilary first rib resection, and botox injections still did not show any evidence at all of benefit over placebo - myofascial release and trigger point needling is still not even mentioned, although the documented evidence of its efficacy by Drs. Janet Travell and Simons has been standard reference in medicine for decades: http://www.ncbi.nlm.nih.gov/pubmed/25427003

Anatomical drawings should always be considered in context. Actual anatomy varies from body to body, and the anatomical drawings approximate the midrange of anatomical variance. The physician must rely on physical exam and palpation to be accurate in therapy, and must consider the anatomical variations when using a sense of anatomy in analysis of diagnosis. Modern diagnosis in musculoskeletal medicine is primarily application of one's knowledge of anatomy and physiology, and one's analytical skills must not be overlooked when utilizing standards of differential diagnosis.

1. anatomy of the pterygoid muscles, primary myofascial concern with TMJ: http://www.bartleby.com/107/illus383.html
2. anatomy of the scalenes, levator scaula and splenius cervicis, lateral view, to demonstrate approach to the myofascial TrPs: http://www.bartleby.com/107/illus385.html
3. anatomy of the myofascial complex at the neck, demonstrating the fascial connection between the overlying scalenes, splenii and levator scapula at the level of the 5th to 6th cervical vertebrae, approximately the level of the myofascial TrPs: http://www.bartleby.com/107/illus384.html
4. anatomy of the scalenes attachments to the first rib and transverse processes of the cervical spine, anterior view; note that the TrP of the scalene posterior would lie under the inferior TrP of the scalene medius: http://www.bartleby.com/107/illus387.html
5. anatomy of the scalenes underlying the sternocleidomastoid (SCM) and the numerous superficial nerves that must be pulled anteriorly when exposing the scalene TrPs for manual release or TrP needling: http://www.bartleby.com/107/illus805.html
6. anatomy of the brachial plexus and thoracic outlet of the subclavian artery under and between the scalenes and between the pectoralis major and minor, the areas of direct impingement in thoracic outlet syndrome (TOS): http://www.bartleby.com/107/illus808.html
7. anatomy of the brachial plexus and thoracic outlet of the subclavian artery over the internal rotators, the latissimus dorsi, teres major and subscapularis, and under the corachobrachialis and pectoral minor, which may cause indirect impingement in thoracic outlet syndrome (TOS): http://www.bartleby.com/107/illus809.html
8. anatomy of the splenii and levator scapula, showing the approaches under the trapezius to the myofascial TrPs; the trapezius would be pulled aside at approximately C5-6 to reach to splenii TrPs, and the head would be rotated to stretch the LS and the Trp would be located under the crook of the trapezius to release the LS: http://www.bartleby.com/107/illus409.html
9. anatomy of the internal rotator complex of the shoulder, including the overlying subscapularis, teres major and lattissimus dorsi, which frequently cause the pseudothoracic outlet syndrome; the coracobrachialis is sometimes of concern with lateral deltoid, and dorsal farearm and hand pain, which skips that elbow and wrist, and usually involves an enthesopathy, requiring a tendon approach with acupuncture: http://www.bartleby.com/107/illus411.html
10. anatomy of the teres major (TM) and latissimus dorsi (LD) to help picture the TrP locations in the belly of the muscles, approximately 2 inches apart; the external rotator complex, the teres minor (Tm) and infraspinatus (IS), which primarily results in deep anterior shoulder pain when reaching up and forward, or when reaching behind to fasten a brassiere, is also pictured; IS and Tm pain usually mimics shoulder joint pain, but eventually shoots down the anterolateral aspect of the arm to the radial aspect of the hand; active release technique (ART) is most helpful with the external rotators: http://www.bartleby.com/107/illus412.html
11. anatomy of the teres minor and major, with the infraspinatus, to demonstrate the teres triangle, or typical area of impingement of the axillary nerve plexus, or branch of the brachial plexus in the quadrilateral space; the teres triangle syndrome will typically cause shoulder pain and limitation of abduction with rotation, mimicing subdeltoid bursitis, and radiating to the muscles innervated by the axillary nerve, the teres minor, deltoids: http://www.bartleby.com/107/illus810.html
12. anatomy of the latissimus dorsi, part of the internal rotators complex in pseudothoracic outlet syndrome, and its relationship to lateral low back pathology and stabilization: http://www.bartleby.com/107/illus392.html
13. anatomy of the primary low back muscles of concern in myofascial syndromes, the quadratus lumborum overlying the psoas at the approximate level of L2-3; the psoas minor would be a thin ropy muscle on the anterior belly of the psoas major, on the approximately 80% of individuals with this anatomical feature: http://www.bartleby.com/107/illus388.html
14. anatomy of the low back muscles, the QL, psoas minor, and iliacus, from an anterior view, with the TrPs located in the bellies of the muscles at approximately L1-2: http://www.bartleby.com/107/illus430.html
15. anatomy of the lumbosacral and femoral nerve plexus; to the right, the unmarked psoas and QL are seen to overlie the major nerve plexus as well as to potentially impinge the femoral cutaneous nerve to contribute to neuropathy of the lower extremity, typically referred to with a catch-all term 'sciatica': http://www.bartleby.com/107/illus824.html
16. anatomy of diaphragm and its relationship to the quadratus lumborum and psoas major at the level of L1-3; since the QL and psoas also attach to the 12th rib, chronic postural strain in office work, with loss of correct diaphragmatic breathing, may lead to chronic contracture of the diaphragm affecting low back pathology: http://www.bartleby.com/107/illus391.html
17. anatomy of the piriformis and gluteus minimus underlying the gluteal maximus (cut away); the sciatic nerve may take one of 3 routes through, under, or atop the piriformis, causing various types of sciatic irritation; note the relationship of the greater trochanter anatomically to find the TrPs: http://www.bartleby.com/107/illus434.html
18. anatomy of the inguinal ligament, which overlies the femoral outlet and the psoas hip flexor, and is of concern in Meralgia Paresthetica, or thigh pain with paresthesia, when chronic myofascial syndromes contribute to calcification and inflammatory irritation of the ligament, which chronically irritates the femoral nerve plexus: http://www.bartleby.com/107/illus394.html
19. anatomy of the inguinal ligament again, and its relationship to the tensor fascia lata (TFL) as well as the fossa ovalis under the inguinal ligament, where the femoral outlet and the nerve plexus emerges into the thigh, part of the cause of the Meralgia Paresthetica, along with nerve irritation deep to the anterior superior iliac spine (ASIS): http://www.bartleby.com/107/illus431.html
20. anatomy of the Femoral nerve plexus and cutaneous femoral nerve under the inguinal ligament and through or over the iliopsoas; the pattern of numbness and weakness seen in Meralgia paresthetica is clearly demonstrated: http://www.bartleby.com/107/illus827.html
21. anatomy of the piriformis muscle in relation to the coccygeus, the primary cause of myofascial strain perpetuating coccygodynia, or coccyx pain, in occupational injuries; often the contributing myofascial problems must be treated before progress can be achieved; xie of GB34 and GB35 is also effective: http://www.bartleby.com/107/illus404.html
22. anatomy of the forearm, with the thumb flexor and supinator of the left arm, frequent causes of pain in the thenar, or palmar/volar aspect of the thumb base (called the fish belly in TCM literature): http://www.bartleby.com/107/illus415.html
23. anatomy of the forearm, crossection 2/3 or the way from the wrist to the elbow, shows the complex of the extensors and thumb abductor that lies over the radius; these are the most pathological muscle in forearm pathology, the extensor carpi radialis, extensor digitorum and abductor pollicis, and the TrPs are very close together, with the thumb abductor TrP underlying; chronic contracture of these muscles perpetuates both lateral epicondylitis, and forearm and wrist pain syndromes: http://www.bartleby.com/107/illus417.html
24. anatomy of the forearm, with the TrPs revealed in the belly of the muscles of the left wrist and finger extensors; the wrist and fingers should be flexed when releasing these TrPs manually: http://www.bartleby.com/107/illus418.html
25. anatomy of lateral epicondyle of the elbow and the relationship of the supinator in perpetuating the chronic tissue inflammation at the epicondyle, as well as entrapment irritation of the radial nerve in peripheral neuropathies and poor firing of the thumb abductor, finger extensors, and wrist extensors: http://www.bartleby.com/107/illus420.html
26. anatomy of the wrist and palm, showing both the carpal tunnel under the ligament and flexor tendon sheaths (and aponeuroses tendon not shown), as well as the flexor tendon sheath of the 4th digit, which is the cause of trigger finger syndrome, where inflammatory calcification prevents the sheath from moving smoothly and thus catching the finger in a painful flexed position with use: http://www.bartleby.com/107/illus418.html
27. anatomy of the lower leg, with the key pathological muscles, the tibialis anterior, extensor digitorum, and peroneals forming a complex with TrPs close together: http://www.bartleby.com/107/illus437.html
28. anatomy of the foot, demonstrating how the tibialis anterior will dorsiflex and invert, or supinate the foot, while the adjacent peroneals will plantar flex and evert, or pronate the foot: http://www.bartleby.com/107/illus441.html
29. anatomy of the lower leg, with the soleus underlying the gastrocnemius; the main soleus TrP is located approximately at LV5 on the medial aspect, and can contribute to diverse pathologies, including typical runner's strain or medial tibial sprain, as well as chronic stiffness of the low back and spine: http://www.bartleby.com/107/illus438.html
30. anatomy of the lower leg, with the tibialis posterior and popliteus muscles, frequent contributors to chronic knee pain; the main tibialis posterior TrP is located near SP9 on the medial aspect: http://www.bartleby.com/107/illus439.html
31. Use of the treatment codes for myofascial release and neuromuscular re-education should be bundled, with 15 minutes spent on each aspect of treatment, but use of the -59 is appropriate when combining the 97112 NMR code with the chiropractic manipulation of the spine. Here is the government guideline: http://www.cms.hhs.gov/NationalCorrectCodInitEd/Downloads/modifier59.pdf