CHRONIC MYOFASCIAL PAIN
by Devin J. Starlanyl
Chronic myofascial pain (CMP) due to myofascial trigger points (TrPs) has not previously been adequately defined. We distinguish two stages. Although chronic pain is usually defined as beginning after 6 months (24), using a time parameter for CMP is unrealistic. One patient may have had chronic pain from other sources for years yet only recently have developed TrPs. Another patient may have multiple latent TrPs develop and become latent singly, only to have CMP become evident with the occurrence of an initiating factor such as trauma or infection.
Adding to diagnostic confusion is the common practice of substituting descriptions for diagnoses. Terms such as "atypical facial neuralgia," "chronic low back pain" and "tension headache" are descriptions. Many descriptions have been given diagnostic codes for insurance purposes, and clinicians use them as diagnoses without concern for the cause of pain and dysfunction, treating only symptoms As symptoms are often caused at least in part by TrPs, clinicians need to know to screen for them, and how to diagnose and treat them while still acute, simple, and most responsive to treatment. Patients with TrPs in multiple quadrants are often given the diagnosis of fibromyalgia (FM) without the understanding that the TrPs are the cause of the symptoms, and the FM is the amplifier. Patients and care providers need to understand the cause of their symptoms and the basics of self-treatment to prevent chronicity.
A. Stage 1 Chronic Myofascial Pain (CMP)
Stage 1 CMP consists of simple TrPs that persist due to lack of adequate treatment and control of perpetuating factors. When Stage 1 CMP is inadequately addressed it tends to develop into Stage 2 CMP. A case may initially appear to be Stage 1 CMP, but unsuspected CNS sensitization, co-existing conditions and other complications may be revealed during the history, examination and treatment, indicating that it actually is already Stage 2 CMP.
B. Stage 2 Chronic Myofascial Pain
Stage 2 CMP includes sensitization of the CNS due to persistent pain. These CNS changes tend to enhance and prolong pain experiences. Complex overlapping referral patterns may develop, with enhanced spillover pain. Stage 2 CMP may persist in spite of appropriate treatment and control of all known perpetuating factors, but can be improved by appropriate treatment. It may develop rapidly in patients with potential perpetuating factors who have activators of multiple TrPs such as systemic infection or trauma.
C. Interactive Diagnoses
The term "interactive diagnoses," as opposed to "differential diagnoses," implies bidirectional interaction among co-existing conditions. This concept is a new paradigm to the mainstream practice of differential diagnosis; identifying one specific diagnosis. The importance of interactive diagnoses has been documented in chronic illness by Institute for Functional Medicine that promotes this new way of diagnostic thinking. (28) Common interactive conditions include FM, osteoarthritis (OA), gastroesophageal reflux (GERD), insulin resistance (IR), obstructive sleep apnea (OSA), and congestive obstructive pulmonary disease (COPD.) These conditions contribute to oxygen deprivation or directly irritate susceptible tissues, worsening TrPs. TrPs can aggravate those conditions as well. For examples, specific TrPs can add to congestion as well as restrict respiratory muscle ROM, affecting COPD or OSA. Reflux causes acid fumes that activate throat and nasal TrPs, as well as promoting secretion of excess mucus protecting the upper airway, adding to congestion and OSA and affecting COPD.
III. CHRONIC MYOFASCIAL PAIN
A. Stage 1 Chronic Myofascial Pain
Stage 1 CMP patients are managed by identifying and treating individual TrPs. If they persist by perpetuating factors must be identified and brought under control. Important common factors are listed in Boxes 5.3 and 5.4, and discussed more fully in chapter 4. Therefore, this section simply presents two case reports that illustrate the basic principles of Stage 1 CMP.
1. Case Report 1 (From Garren P. Gebhardt DO)
JP was a 42 year-old female competitive weight lifter who developed severe low back pain several years ago after lifting. A self-therapy regimen of ice application and ibuprofen enabled her to continue to lift weights. Bending forward when she walked completely relieved the pain. After twisting while lifting a heavy object at work, the patient experienced acute left low back pain accompanied by right buttock pain radiating into the posterior right thigh. The pain was worst when arising from bed in the morning. She again used the ibuprofen and ice, but the new pain persisted in addition to the previous chronic pain. She was seen by an orthopedic surgeon who ordered X-rays and an MRI, which were negative. She was referred to physical therapy, which exacerbated her symptoms. On examination JG is well-muscled, walking with hips flexed. The back pain increased with left leg extension, and she had a positive Thomas test on the left. TrPs in taut bands were found on palpation in both the distal left quadratus lumborum and left gluteus medius. These were both injected with 1% procaine, followed by myofascial release. The patient was instructed in a regimen of stretching exercises and safe weight lifting techniques.
On return, the patient had less pain, but against PT advice had resumed lifting. She presented with what appeared to be latent TrPs that had been activated in her left gluteus medius and maximus. These were treated with TrP injection as above. JP returned a final time with all symptoms resolved except for continuing right lower extremity pain. Palpation uncovered a TrP within her right piriformis, which was treated with the above technique. The patient's symptoms resolved and she returned to her job in housing construction.
Comments: The patient may have other undisclosed latent TrPs, especially in deep muscles and ligaments. She must be diligent in stretching. Repetitive stressful motions such as weight lifting can be a perpetuating factor in patients predisposed to the development of TrPs.
2. Case Report 2 (From Garren P. Gebhardt DO)
Case Report 2: JB presented as a 65 year-old female avid tennis player with a history of spinal stenosis and lumbar disk protrusion causing bilateral sciatica that completely resolved with a combination of epidural steroid injections and physical therapy. She also has a history of vulvodynia that responded well to amitriptyline 100 mg. qd. She recently tried to stop the amitriptyline but vulvar pain recurred. She resumed 100 mg. qd.
JB continued to play tennis, developing non-radicular upper and lower back pain. She has used NSAIDS, acetaminophen, and ice to relieve the pain with only minimal response. Massage and physical therapy enabled her to continue tennis, but the pain did not resolve. The pain is generally worse after playing tennis, and is specifically brought on by twisting and forcefully hitting the ball. When she plays doubles (less twisting) the pain is less than when she plays singles.
JB appeared well nourished, well hydrated and in no apparent distress on examination. She was tender to palpation in the area of the right upper back and left thoraco/lumbar fascia. Central active TrPs were palpated in the right trapezius, an attachment trigger point in the right levator scapulae, and bilateral central active TrPs in the quadratus lumborum. The TrPs were injected with 0.25 cc of 1% procaine. With the deactivation of active TrPs, apparently latent ones in the trapezius and longissimus muscle had become activated and were injected with procaine.
The patient was then pain free and resumed vigorous tennis. It wasn't until 6 months later when she deleted the amitriptyline again that she returned to my office with the same TrP pain referral patterns. We addressed her TrPs with procaine injection. At this time there was only moderate relief of her tennis-induced pain and moderate relief of her vulvar pain when she resumed amitriptyline.
Comments: Uncontrolled pain may be a perpetuating factor for activation of this patient's TrPs, and the reason for recurrence of pain. The relief of vulvodynia by amitriptyline is surprising, so identification of the causes of vulvodynia should be helpful. This information might clarify why some TRP symptoms and vulvodynia returned with cessation of amitriptyline. The patient will have to be diligent in avoidance of perpetuating factors to prevent further chronicity.
B. Stage 2 Chronic Myofascial Pain
1. Chronic Myofascial Pain and Interactive Diagnoses
There are many potential interactive diagnoses. It is beyond our scope to explore them in depth. Interactions of diagnoses in common CMP conditions are briefly described here.
a. Chronic Myofascial Pain with Fibromyalgia
Thus far, most books on myofascial medicine have focused primarily on single TrPs. This depiction is necessary to teach individual TrP referral patterns, but TrPs rarely occur alone. Most patients with central sensitization states such as FM also have peripheral nociceptive generators such as TrPs or OA, and there are indications that these generators may be sufficient to initiate or maintain diffuse, widespread pain. (62) Body-wide diffuse FM pain can be reproduced by activating TrPs. (18)
When one considers terms such as "agonizing" and "incapacitating," used to describe pain from some single muscle TrPs, the severe impact of Stage 2 CMP plus FM amplification should be obvious. Patients with FM may need special treatment modifications and higher dose medications to avoid further central sensitization. Once pain has persisted for some time, some neurological and peripheral tissue changes may become irreversible. Biochemical imbalances of FM may themselves be or contribute to perpetuating factors of TrPs.
Patients with FM have global muscle impairment, (40) use fewer energy-rich phosphorus metabolites during high energy expenditure and reach anaerobic threshold earlier than controls. (37) They have a higher rate of DNA fragmentation and lower number of mitochondria (57) coupled with lack of restorative sleep. (13) Add to this mix TrP-laden muscles that start out fatigued, fatigue more rapidly, and become exhausted sooner and there can be difficulty finding an exercise program suitable for the patient.
Stage 2 CMP patients with FM may experience pain in response to some normally non-painful therapies such as electrical stimulation, heat, cold and manual pressure. (31) Biochemicals, such as bradykinin and histamine, released during a TrP local twitch response, (54) are often already imbalanced in FM and may add to interactions among co-existing conditions. For example, histamine can increase congestion and irritation, worsening other conditions such as allergy or COPD, and complicating CPAP treatment for OSA. Pain from TrPs amplified by FM can provoke IR, (22), as can sleep disorders. (51) Insulin resistance is associated with abdominal obesity, which can perpetuate abdominal and thigh TrPs, and with metabolic imbalances, which can worsen FM. Research indicates "…assessment and treatment of concurrent TrPs in FMS should be systematically performed before any specific fibromyalgia therapy is undertaken." (20) Clinicians who treat chronic pain must be able to diagnose and treat TrPs, or at the least be able to diagnose TrPs and refer patients to someone who can treat them. To do otherwise is doing harm. CMP is a rabid dog in the living room of chronic pain. It cannot safely be ignored.
b. Chronic Myofascial Pain with Arthritis or Disc Involvement
Mechanical stress to the joint area can initiate OA. (56). Arthritis treatment and prevention must include treatment of any co-existing TrPs. (11) OA may be prevented or slowed by improving neuromuscular function, (35) such as treating the TrPs. Uneven contracture, such as can be caused by TrPs in the surrounding muscles, can cause TMD and may cause bone misalignment. (29) This may be sufficient to cause erosion of the articular disc. (34) Active TrPs are also associated with cervical disc lesions. (26) As tissues are unevenly contractured, vertebrae may shift out of alignment, irritating the discs. Intervertebral disc dysfunction and associated ligamentous attachment compensations change the angular motion of the body, causing additional stresses on the inferior and superior intervertebral discs of the cervical spine. (30) Disc deterioration may lead to alterations of motion and muscle compensation that can contribute to further pathologies in the facet joints, muscles and ligaments that may result in chronic pain. (7) Patients with pain and dysfunction at insertion sites, osteotendinous or osteoligamentous junctions are often considered to be surgical candidates. Spinal pain from TrPs may be erroneously assumed to be caused by a disc deformity showing on an X-ray. Surgery may be performed without soft tissue evaluations, resulting in "failed" surgery. (14) The surgical scars and resultant tightening of soft tissue from fused vertebrae can then promote additional stress on nearby vertebrae, leading to a cascade of surgeries. Research is needed on the interactions of arthritis, disc dysfunction and TrPs.
c. Chronic Myofascial Pain with Interactive Spirals
Multiple diagnoses including TrPs can be simple and bidirectional. They can also develop into complex reciprocal interactive nonlinear physiological feedback spirals. LA was an elder but spry woman with OA and chronic pain, with loss of upper body strength due to latent TrPs in her scalene muscles. They primary TrP was from an ankle skiing injury sustained in her youth, but most of her TrPs were latent although restriction of ROM was apparent. As TrPs developed satellites, she became unable to provide adequate nutrition for herself. Nausea, gastrointestinal irritation and intestinal permeability caused by medications taken on an empty stomach result in further food restriction. She developed IBS, GERD and IR. When the weakness was not recognized as due to TrPs, prescribed upper body strengthening exercises activated latent TrPs, causing pain and more weakness, so medication dosages were raised. Her diet worsened due to further irritation from the medications, resulting in a lack nutrients needed to provide rate-limiting steps for a variety of metabolic functions. The IBS and GERD activated TrPs in the upper abdominal obliques and diaphragm, contributing to IBS symptoms and paradoxical breathing, further worsening the TrPs. Activity lessened due to increased pain, worsening the OA. The GERD irritated primary TrPs in her scalene muscles, which developed satellites in her arms, further worsening upper body weakness. Increased mucus formed to protect the nasopharyngeal area from acid fume irritation, causing difficulty swallowing and adding to eating difficulties. She was prescribed antacids and proton-pump-inhibitors, further adding to intestinal permeability and digestion dysfunction. Pain flared, and care providers had no idea what was causing the pain intensity, although others vainly tried to educate the care providers about TrPs. The patient had worked as assistant on a myofascial TrP book. She was able to describe pain referral patterns until she lost consciousness, but was unable to convince her care providers concerning the cause of the pain. This woman developed pneumonia and died. This type of worsening symptom spiral is common, but usually unrecognized in chronic illness and the elderly. It is often aggravated by the conventional single-minded medical approach of drug solutions to a diagnosis. To treat these interactive diagnoses successfully, the cycle must be broken, but first it must be recognized and causes identified.
(1.) Case Report 1 (Walter P. Sy MD and Devin J. Starlanyl)
JM is a 56 year-old woman with a long history of chronic pain, including childhood growing pain, and sinus surgery resulting in a 3 month hospital stay before the age of 10. Frequent infections occurred throughout life, and she developed depression, GERD, IBS, FM, and TMD. She worked as a secretary before disability. She reported bruxism, morning stiffness, post nasal drip, lack of restorative sleep, and fatigue. She is in counseling. She recently developed a gruff voice with coughing. Direct laryngoscopy showed no lesions or abnormalities. She had been treated for recurrent bilateral upper body TrPs but recently developed leg pain. She had been troubled by leg weakness, including buckling knees. She is constantly fatigued, with dysphagia, headaches, memory impairment, trouble concentrating, and tinnitus. She tries to keep going in spite of pain, but this often produces increased hand, arm and thumb pain.
Examination revealed TrPs in 4 quadrants, myalgia paresthetica, moderate external throat swelling, motor coordination dysfunction including ataxia, and dermographia. Injections of TrPs bioccipital, bitrapezius, left rhomboid, and bilateral inner gluteal muscles were performed. A total of 12 cc 1% plain Xylocaine was injected in the most troubling TrPs. Referral for gastric and thyroid evaluation and a follow-up appointment were made.
Perpetuating factors include interactive diagnoses, poor diet, and lack of specific exercise program, poor body mechanics, previous surgeries, inappropriate footwear, unrestorative sleep and pain. Attention to perpetuating factors, nutrition and body mechanics was suggested. Appropriate medications were prescribed. Specific TrP bodywork was suggested, with nonrepetitive exercise and continuing TrP injections. The addition of an antihistamine was considered. During later visits the patient showed some continuing improvement.
Comments: There may be multiple contributors to the gruff voice, including TrPs. GERD episodes that occur while sleeping on the back can trigger jaw muscle activities, including bruxism. (47) GERD can contribute to chronic cough, excessive throat phlegm, and unrestorative sleep. This pattern of symptoms warrants polysomnography for OSA, as well as a check for TrPs and other perpetuating factors that may contribute to post nasal drip.
(2.) Case Report 2 (Walter P. Sy MD and Devin J. Starlanyl)
BLM is a 60-year old woman with long-standing depression. She was a bookkeeper and real estate agent before disability. She sustained previous injuries including a fractured pelvis, and has had multiple surgeries, falls and infections. She has also been diagnosed with FM, IBS, cervical OA, migraines, hypercholesteremia, and hypertension. She is chief care giver for her disabled husband, and under considerable stress. A year ago she began having debilitating general neck, shoulder, arm and back pain. A variety of therapies, including physical therapy, have been of limited help. She uses a treadmill 10 minutes a day. History includes hypoglycemic symptoms such as sweats, episodic rapid and fluttering heartbeat, bloating, nausea, carbohydrate cravings and yeast sensitivity. She reports low back pain, irritable bladder, shortness of breath, confusional states, arch cramps, sciatic pain, buckling knees and ankles, tight hamstrings, and balance problems. She has TrPs in all 4 quadrants. The patient has joined a positive, information-oriented support group for FM and CMP.
A focused examination revealed the most troublesome bilateral TrPs in her pectorals, many areas of her trapezius, and bilateral rhomboids. These TrPs were injected using a total of 8 cc's 1% plain Xylocaine and 5 mg. Depo-Medrol. The injections were well-tolerated. The patient was encouraged to return for periodic TrP injections. A future appointment was made. There was a discussion that raising the narcotic dose would not allow a pain-free existence, but that the goal was to minimize pain and maximize function, and the patient seemed to understand this and was encouraged that this is a process. Suggestions for pain control included very gentle and brief self-therapy in the form of TrP tennis ball work on the sofa to start as the TrPs were very sensitive, with the addition of craniosacral release and gentle, nonrepetitive stretching. The patient was instructed in the use of a footstool and arm supports and the use of a rolled up blanket under her feet at night, and asked to find an enjoyable nonrepetitive exercise alternative to the treadmill. Medications were adjusted to her needs. Confusion was minimized by giving written instructions.
Perpetuating factors include interactive diagnoses, unrestorative sleep, paradoxical breathing, pain, repetitive exercise, previous traumas including surgeries, poor diet, adhesions, yeast sensitivity, good sport syndrome, poor posture, poor body mechanics, life style habits including alcohol consumption (she has quit smoking), chronic infection, job stress, proportionally short upper arms and short lower legs.
TrP injections and other therapy have revealed increasing numbers of TrPs, creating additional symptoms including chest wall pain with esophageal spasm. The patient came in distressed that she was undergoing a relapse. Previous TrP injections of the upper back activated or revealed more TrPs in the rhomboids and subscapularis. The latter were anticipated by history, but had been latent. As tissue changed in response to therapies, tenderness along the posterior iliac ridge with lumpy fatty degenerative tissue changes were revealed. Exquisite tenderness over the left trochanteric bursa appears to be true bursitis rather than TrPs. The patient was encouraged in a lessened reliance on increasing narcotics. She began decreasing other medications including nightly Trazadone. Discussion resulted in the patient understanding that she will not be pain-free, but that quality of life includes function, and that coping abilities could improve considerably as she continues to help bring perpetuating factors under control. She was encouraged and left understanding that she will weather this process.
Comments: Long-term activation of the stress-response system, such as is associated with FM, may cause IR (53), as can pain (22) and sleep dysfunction (27). Women with FM have increased risk of developing insulin resistance. (36) Further evaluation may disclose this perpetuating factor, opening new avenues for symptom control. At the time this patient was seen, it was Dr. Sy's practice to use steroids for selected patients with inflammatory conditions. The use of steroids is not recommended for TrP injection.
Note: the patients in these case reports are by no means worst-case CMP scenarios. Patients
with unsuspected CMP may be utilizing substantial resources and still living in preventable misery, often due to lack of training on the part of their care providers.
2. Stage 2 CMP History
Many 3rd party payers may balk at reimbursement for adequate patient evaluation yet pay for needless surgeries the lack of this preventative care causes. They need education concerning cost-effectiveness of a thorough history and exam. Chronic myofascial pain patients often come with a bewildering stack of files. Scan raw data with new eyes and an open mind. For example, a meaningful TSH result requires a functioning HPA-axis, and this is often imbalanced in FM patients. Even NSAIDs affect thyroid hormone test results. (5) You may find a series of "low-normal" worsening test results that may indicate a developing metabolic problem. Insulin resistance and thyroid resistance often occur in the same patient. (17)
Some previous conclusions may be misleading. Kinesiophobia Index results may indicate a psychological problem, yet avoidance of extending ROM when there is pain at the end of ROM due to CMP is a healthy, normal response. If patients drop out of therapy programs with repetitive or too vigorous exercise that cause increasing pain and dysfunction due to CMP they are using common sense, but are likely to be labeled 'noncompliant" by 3rd party payers refusing reimbursement. Any chronic pain state may also include secondary depression from unrelieved symptoms, plus feelings of isolation, frustration and hopelessness, especially if the CMP component has not been recognized. Once it is recognized and treated appropriately, some of the emotional burden on the patient is lifted. Currently, patients are paying for others' lack of training.
Be alert to life patterns. There may be migrating pains due to recurrent TrP activations. Ask about frequent school or work absences as the patient struggled to fulfill commitments in spite of TrPs and chronic pain, only to be exhausted by them. Listen for a pattern of one or more TrP cascades. These occur when one TrP generates one or more satellites and those generate still more. With each observation or symptom, ask yourself, why? Tight muscles: is there interstitial edema, fibrosis, taut bands or increased viscoelasticity? IBS: when did each symptom develop, and what else was happening at that time or just previous? Was there trauma: repetitive, surgical, biochemical? Even minor trauma can cause postural dysfunction (16) leading to TrPs. What happened immediately after the trauma? Six months after? Why? There could be delayed pain response due to neural plasticity (4), or masking of symptoms due to extra support, medications and therapies used for the initial trauma. Explain to your patient that discovering additional co-existing conditions has not changed his or her health status, but has revealed more avenues to control existing symptoms.
History taking may continue during the exam and treatment as more questions arise as other connections become suspected. The history is a written record of onset of pain related to activities. For example, long-standing loss of ROM in one arm requires that the other side compensate. All dysfunctions have consequences. During the history, your patient describes dysfunctions, or potential causes, of TrPs. During the examination, you look for their consequences.
3. Stage 2 CMP Physical Examination
Mapping TrPs is important, but the initial pain chart may seem unhelpful if totally colored in. It may also be misleading if there are multiple latent TrPs, or if unsuspected TrPs lurk in areas that have become fibrotic or calcified. Surface EMG may help determine and document dysfunctional muscle recruitment and compensation. Using restricted ROM to locate TrPs may be unreliable in patients with hypermobility, which may not become apparent until the TrPs are successfully treated. The activation of TrPs may in some cases be the body's attempt to compensate for hypermobility.
The CMP exam is different than that for single TrPs. It may not be possible to determine all predisposing, initiating, or aggravating factors during the first exam. Ensure that the patient is aware of the process and knows that his or her input is important and critical for success. If there is pain involving the spine, torso, or TrPs in multiple quadrants, you may need to perform the exam in multiple sessions. The patient may require extra support in the form of medication and therapies before and after exam sessions to avoid further central sensitization. In attachment areas, cellular tissues are folded and convoluted, giving them greater flexibility but allowing more chance of tearing, scaring and other tissue changes. (8). Examination of these areas should not be rushed. Let the patient know there may be pain or other sensation if a TrP is activated, and that you will use the lightest touch possible. Strumming taut bands or using snapping palpation is neither necessary nor advisable, causing needless TrP activation. Develop a light touch. Encourage feedback. If the pain level becomes too high, the balance of the exam needs to be postponed.
Neuroinflammation and interstitial swelling can be integral parts of CMP. The composition of each TrP contraction nodule depends on variables including the number of loci and the amount and nature of fluid infiltration. These variables affect not only the feel of the nodule, but also its accessibility to treatment. Are the nodules large and swollen, or like ball bearings or marbles? Do motor nerve endings feel calcified, like tough little seeds? The increased muscle tension itself may be painful. Note rolling veins, varicosities, and other abnormalities. Check for TrPs proximal and distal to varicosities. Note restricted joints including fascial restrictions such as scars that can be sources of pain. Restriction of one major leg joint can increase the energy up to 40% needed to walk; for two major joints in the same leg, up to 300%. (21) This may add significantly to patient fatigue.
Even a small scar may affect large muscle patterns and create unpredictable dysfunction. (33) Map each one and ask about its origin. Fibrotic changes can extend over tissue not directly subjected to trauma, as sensitizing substances produced by traumatized tissue infiltrate the surrounding tissue. (8) The muscle may feel homogeneously hard, hiding multiple TrPs and taut bands. An active TrP produces low pH as well the release of neurotoxic substances that are greatly enhanced by an LTR. (54) A low pH can sensitize receptors and be part of the neuroplastic changes, causing spontaneous pain, hyperalgesia and allodynia. (46) Even a light touch may evoke an LTR, each TrP may produce more than one LTR, and a muscle may have multiple TrPs. A Stage 2 CMP patient may have hundreds of TrPs. A CMP exam, however gentle, may activate many of them and release significant amounts of noxious substances. It's not uncommon for patients to experience nausea, headaches, cognitive dysfunction, severe pain exacerbation and/or extreme exhaustion after exam, bodywork or TrP injections. This response may be delayed for 24 to 48 hours, but may last for weeks or more.
Skin rolling may be too painful for CMP patients. Tissue may be adherent from skin to underlying bone. Avoid fascial tearing during exam, as this is exceedingly painful, especially if central sensitization is present. Boundaries of adherence between areas can often be mapped by moving one finger horizontally across the surface of the skin with very gentle pressure. You may be able to feel the tug of underlying tissue resisting the movement. In addition, you may find geloid clearly definable, measurable masses that overlie areas of resistant TrPs. (61) A geloid mass may be extremely sore and intolerant to touch. Approach its boundaries carefully from the side, using flat palpation, to detect firm borders that resemble the texture of silicon implants. These geloid masses may be accompanied by areas of dense tissue, with palpable multiple taut bands in adjacent areas leading to TrPs underneath the geloid masses.
Be attentive to clues that may help avoid unnecessary palpation. Do the patient's eyes follow a moving object in a smooth circle, or are corners being cut? Are eye muscles painful when they are stretched, or does eye muscle stretching cause dizziness or headache? Sitting or standing, is any part of the face or body asymmetrical? Inspect the bite for symmetrical active centered opening and compare it to dental history. Does the jaw click or crackle when it moves? Are there spontaneous stretching movements? Is there stiffness or instability? Are muscle antagonists being recruited to maintain postural function? Note gait dysfunctions such as foot clearance. Proprioceptor dysfunction is associated with TrPs. Proprioceptive feedback is necessary for basic motor coordination, and deficiency in this area is an often overlooked contributor to disability. (26)
Pain itself can affect muscle activation and recruitment patterns, affecting muscle ability to perform synergistically. (63) Look for patterns contributing to compensatory scoliosis, rotoscoliosis, rotated pelvis, or other dysfunction. Note areas of dermographia, goose bumps, or histamine reaction after palpation. Histamine is one of the substances released during an LTR. Remind your patients that it has taken time to develop Stage 2 CMP, and it will take time and effort to unravel stuck and twisted tissues. After the exam, supportive therapy may be required, including craniosacral release, rest, hot or cold packs, and extra medication. In a few days, make a follow-up call to discover any additional pain or dysfunction and its extent subsequent to the exam to guide future exams and assess symptom support level.
4. Stage 2 CMP Treatment
a. Patient Education
Patient education is a large part of the management of stage 2 CMP. Empower your patient with the knowledge that you are working as partners to discover what is contributing the symptoms and what can help to relieve them. Practice preventative medicine. For example, a handout explaining the difference between necessary positive feedback and a negative repetitive complaint may be useful. The patient is a member of the pain management team, and as such has responsibilities too. The principle that identification and control of perpetuating factors as the key to selecting the most efficient therapeutic regimens is as valid for Stage 2 CMP and interactive conditions as for individual TrPs. Many medications and procedures may also have unforeseen interactions, and the risk/benefit ratios of any treatment must be considered. The patient must be involved in this process and understand the ramifications.
It is vital to ensure that adequate communications occur between medical team members so that therapeutic effects can be followed. A function-oriented support group that both informs and promotes positive attitude is a valuable resource, (64) as are patient organizations with those goals. (68) The support of a significant other can significantly improve pain processing on multiple levels. (48) Conversely, the lack of family understanding or support may have a disastrous impact. This is frequently the case with "invisible" and/or poorly understood conditions such as TrPs. It is difficult to keep a positive attitude in a negative environment. There may be denial of the reality of CMP and rejection from multiple family members, adding to stress and pain. Then, family or marriage counseling may be a critical part of CMP treatment.
Life style changes may be among the most affordable yet difficult perpetuating factors. Almost everything will be complicated in CMP. For example, changes in diet are not sufficient to enact changes in healthy nutrition. You are what you absorb, not what you eat. Gastrointestinal irritants must be removed, deficient digestive factors must be replaced, healthy intestinal flora must be restored, and the intestinal mucosa must be healed. Fortunately, clear and concise guidelines are available to help the care provider and the patient with these steps. (28) Even restoration of healthy breathing requires release of all respiratory muscles with TrPs, a written handout and demonstration of belly breathing, plus a firm commitment on the part of the patient to refrain from paradoxical respiration. Ingrained habits change only with dogged persistence. Healthy behavior modification rewards are much more effective than criticism.
Assess the patient for ability to perform potential self-therapy, providing the tools he or she needs to be an effective working partner. For example, this author has found the Empi 300 PV NMES unit helpful to manage TrP tightness. Frequency Specific Microcurrent can help manage multiple conditions, providing that there is a practitioner nearby to provide direction and oversight. Some of this work must be tailored to the individual. Much help can be provided in the form of resources including books, referenced web sites, and handouts. Handouts for CMP patients are available ( ), as are forms such as those for office visits and phone calls. (59) Modify them to fit personal needs as you develop understanding of what information is most useful to you and your patients. For example, the book "Migraine Brains and Bodies" (55) contains useful information, including relevant TrPs, that can empower and educate patients who have this co-existing condition. Know your resources. There may be limits to what can be achieved. You can't always modify for multiple structural defects such as short upper arms, proportionally short lower legs or a proportionally long torso, especially when all of them occur in one patient. If multiple foot abnormalities occur, even finding comfortable, supporting shoes may be a formidable quest. The patient may require services of a variety of therapists to aid them in such tasks, but all medical team members must understand TrPs and that each mechanical adjustment requires body compensations that can have repercussions. Improving cognitive dysfunction may be necessary to allow the patient to understand what is required for the treatment process, and to implement those changes effectively. Control of pain, identifying and removing impediments to restorative sleep, improving diet, breathing and exercise may restore some cognitive clarity.
Unraveling the symptoms takes teamwork and communication among team members. Primary care physicians assure me that one problem with these patients is the overwhelming paperwork required to integrate the health care team. The educated patient or care provider can assist in the smooth flow of information. The patient must be an active team member, and most patient groups and recent research advocate shared responsibilities including management of the health care team and shared decision-making.
Patient must change life as they know it, but life as they know it includes pain and other symptoms and their life will improve as these fade. These patients may come to you physically, mentally, emotionally, spiritually and financially exhausted, and many of their support networks may be exhausted as well. The choice for them is either to focus on pain or focus on regaining function and a higher quality of life. Adequate pain control may allow the patient to initiate and maintain needed lifestyle changes. CMP patients must believe that pain control and other symptom relief is possible, and that you will work with them to help find options that will work Give your patient the greatest gift, that of hope. With patience and care, these patients can become your most rewarding success stories.
Any trauma sustained throughout life tends to cause cells and tissues to accumulate substances in abnormal quantities. Most commonly, such accumulations include triglycerides, glycogen, calcium, uric acid, melanin, and bilirubin. (32) Even a healthy liver and kidneys may not be able to immediately metabolize all the biochemical by-products released during a bodywork session, and your patient may have dysfunctional detoxification mechanisms. The Stage 2 CMP manual treatment process may be the reverse of many illnesses, with the initial phase having less therapy less frequently, allowing time to recover and detoxify between treatments as biochemicals trapped within the myofascia are released and processed.
Some perpetuating factors and TrPs may not be evident until treatment progresses. Myofascial TrP activation by some treatments may spread as chains or cascades along one side, across or diagonally. Respect for the inter-relationship of muscles and muscle function groups are vital to successful treatment. Releasing piriformis TrPs may further stress an already overstressed, tender sacrotuberal ligament, the contralateral piriformis, the iliopsoas, pelvic floor or other muscles. Treating the knee while leaving the hip and ankle tight may result in an unstable gait and further tightening of other muscles as they try to compensate. The order of unraveling myofascial TrPs is explained in detail elsewhere. (15) Fibrotic and calcified tissue may sometimes, at least partially, be reversed, but this can be painful and slow. Frequency Specific Microcurrent therapy characteristically speeds the process and minimizes the pain of tissue transformation. (www.frequencyspecific.com )
Each patient needs assessment as to what constitutes strenuous activity or appropriate therapies at any given time. Patient needs and tolerances will change as healing progresses. It is helpful for the patient to keep a symptom diary including specific motions that cause or intensify pain, dysfunction, and other symptoms. Integrative exercise such as t'ai chi chuan can be helpful to monitor coordination and can also be used as a gauge of treatment effectiveness and TrP activation, but may require modification by a teacher who is aware of CMP limitations. (58) Stretching and then soaking in a tub of hot water with Epsom salts and ground ginger may minimize post-treatment soreness. Therapies such as craniosacral release may help integrate other therapies, and gentle massage may reduce pain and muscle tension.
After successful treatment the patient may notice loosening of tissue layers. Deeper TrPs may cause pain to shifts to other areas, as tissues that formerly guarded them return to a healthier state. This is often part of the process of unwinding tissues, but the patient may believe their health is worsening and stop treatment unless they understand what is happening. Books are available to explain TrPs and teach self-therapy techniques to patients (60; 6; 25), including coping methods and self-treatment strategies. Body workers who understand CMP can be great assets. Tolerance to therapy can vary considerably in one patient. During times of high stress such as travel or heavier workload, a longer recovery period may be needed between therapy sessions. Using therapies that benefit more than one condition can be extremely helpful. For example, Frequency Specific Microcurrent may benefit both FM (43) and TrPs, (42) shows promise for other conditions, and is extremely gentle. Interactive diagnoses can be used to advantage when it comes to treatment. For example, successful CPAP treatment for OSA may improve unsuspected GERD. (49)
With the repeated injections are needed in Stage 2 CMP, use the least myotoxic agent, because the "C" in CMP stands for "chronic." An arbitrary cut-off limiting the amount of reimbursement for TrP injections or other therapies in chronic pain conditions has no logic and no reason other than the short-term bottom line of the 3rd party payer. The injections help restore function and relieve long- term pain (although the injections themselves may be painful) but they will not cure the coexisting conditions that reactivate TrPs. If 3rd party payers ask you "how many TrP injections will it take," or "how many therapy sessions will it take" to treat a specific patient, ask them in writing to specify in writing, "Will it take to do what?" and say "It takes what it takes as long as we are making progress." Insurance companies must be warned that if these patients aren't adequately treated they are likely to worsen and require additional medical resources and expense to them.
When adequate measures are available to relieve pain and improve function but insurance companies refuse to cover them, patients suffer needlessly. Physicians take an oath to do no harm. Insurance companies do not. Document treatment progress and possible perpetuating factors and what is being done to help bring symptoms under control, and work to change at least one insurance company in the system by getting them to understand that it is in their best financial interest for these patients to receive competent treatment. Document your track record of reducing the need for expensive medical care.
Ideally, medications should be the lowest dose of the most effective, least expensive agent with the fewest undesirable side effects. Some medications indirectly help TrPs by affecting co-existing conditions. Aspirin, NSAIDS or acetaminophen may often be the first choice for pain relief, but may be insufficient or unsuitable for many Stage 2 CMP patients. Patients faced with increasing pain and difficulty functioning may increase dosage of these analgesics and add whatever else is available over the counter to dull the pain, often without telling their doctors. They may be unaware that these medications may contribute to interacting diagnoses and may interact with other medications. Even acetaminophen can affect lung function (41) and can have serious kidney side-effects.
Develop a relationship with a good compounding pharmacist. Try treating localized symptoms transdermally, with the awareness that insurance companies may require education to understand the need. You may be able to use a smaller dose than offered by a drug company, and it will lessen stress on the liver and gastrointestinal system. For example, I have found small amounts of topical carisoprodol to provide local relief to tight tissues and allow treatment access to dense contraction nodules, or to relax veins directly before otherwise difficult blood draws. Investigate possible deficits in metabolic reactions that may affect rate limiting steps and second messengers. (28) If bodywork causes pronounced histamine reaction, an antihistamine may reduce symptom burden. If general muscle tightness is a problem, muscle relaxants may help. (66)
There is impressive clinical research validating the use of opioids for chronic musculoskeletal pain (39) and other chronic conditions, yet some care providers are unwilling to use them. Lack of training, prejudice, and fear of addiction that is rarely associated with taking them for pain rather than recreation impede optimum prescribing. (44) The International Association for the Study of Pain and the American Pain Society have worked towards this understanding for more than 5 years. Stage 2 CMP patients must be assessed individually for opioid use. When used, opioids must be used wisely and as part of a pain management plan. Co-administration of an NMDA-receptor antagonist may prevent opioid tolerance. (3) Codeine, hydrocodone, and oxycodone require metabolism by CYP2D6, thus patients who lack this enzyme are not good candidates for their use, and patients with impaired enzyme metabolism may require a higher dosage for the same effect. These medications should not be given with drugs that inhibit this enzyme. (9) Benzodiazepines (19) and DL-phenylalanine (52) decrease or block opioid effectiveness. Phenergan, dextromethorphan, and pentoxifylline may potentiate opioids, and may be used in some cases to boost effectiveness without increasing dosage.
In chronic non cancer pain, opioids may:
- be necessary for adequate pain control (Savage 1999),
- ease pain from coexisting conditions, central sensitization, and pain from therapies,
- have higher analgesic potential and wider range of indications than other medications (Pappagallo. 1998),
- have the best side effect profile...."(Horning, 1997), and
- improve cognitive function via adequate pain control, (Tassain, et al. 2003)
d. General Treatment Plan
Due to the complexity and variability of Stage 2 CMP, no time limits are associated with the treatment plan. Different specialists may be involved, and each may take differing amounts of time depending on tests required and test results. Treatment goals should be realistic, with the goal of optimized function and minimized pain. The amount of disability may depend on many variables, including how many co-existing conditions are involved and how severe they are, ability to control perpetuating factors, extent of central sensitization, length of time the conditions have persisted, support system, type of work done, and ability to modify work hours or conditions.
Summary of Plan:
Immediately address any treatable perpetuating factor or life altering symptom.
- Identify and map as many TrPs as possible and rank TrPs and symptoms in order of their impact on quality of life and function.
- Identify all known perpetuating factors and co-existing conditions. Rank them as to impact on the patient. Note those that can be addressed immediately. List potential interactions, suspected perpetuating factors and co-existing conditions, and tests needed.
- Review medications, supplements, exercise, sleep hygiene and diet.
- Confer with the patient about treatment goals. Treatment options must be tailored not only to the needs of the patient but also to the ability to afford them. Chronic pain patients may face a huge gap between resources and needs. Some treatments may not be available.
- Assign patient diaries (pain, food, sleep, etc) and other patient information gathering appropriate to patient's or supporter's ability to monitor.
- Assess the patient's quality and quantity of social support system, and provide or guide the patient to appropriate support groups and educational resources. Encourage patients to bring their support people with them so you can answer their doubts and questions personally.
- Create an initial treatment and medication plan for TrPs and control of co-existing conditions. Some treatment will be delegated to other team members, and the patient will assume responsibilities as health allows.
Frequently reassess changes related to treatment, progress.
When a combination of medications and therapies are found that optimize function while minimizing pain and side-effects and a good self-therapy program is developed, care providers should not seek to "wean" patients off of the very medications and therapies that work. This should be self-evident, but it happens too often. Patients often walk a very fine line to maintain health balance. Anything may upset this; a fall, a loud noise, an infection, etc. When it does, the patient can lose ground fast. Patients and their companions need to be aware of this and know what to do. The "good sport syndrome" may be especially self-destructive to stage 2 CMP patients. They can't expect others to respond to them if they don't pay attention to themselves.
Multidisciplinary pain clinics with a thorough understanding of Stage 2 CMP and interactive conditions could do much to reverse the trend towards disability in chronic pain. They also need to help the patient find a pain management specialist, as research indicates "...establishment of a pain diagnosis and a pain management plan by a pain specialist was not sufficient to enable the referring general practitioner to manage severely chronic pain patients." (2)
e. Common Pitfalls and Their Prevention
- Business as Usual: Treat Stage 2 CMP seriously. It's ok to tell the patient that you don't know the reason for a symptom and will search for an answer. Many medications and therapy trials may be required before the best combination is found for any specific patient. Explain that this is not failure, but part of the learning process. Avoid frustration and a sense of failure. Replace it with realistic hope.
- Lack of Thorough Documentation: Clear, comprehensive and precise documentation is vital. The old saw "meet the patient, greet the patient, treat the patient," is too often followed by the 3rd party payer's "defeat the patient" or "delete the patient." Your notes may make the difference, and may also limit or eliminate your time in court if your patient is involved in litigation.
- Underestimating Potential Treatment Response: Begin every
new therapy with the knowledge that no matter how gentle, it may provoke an extreme response.
Patients with central sensitization may rapidly reach sensory overload during treatment.
Depending on other co-existing conditions, pain could cause FM flare, a post-traumatic episode, a vasovagal or other response. Monitor your patient for signs of impending shock. Be prepared to decrease stimuli immediately. Have a dimmer switch on lights, have blankets close by, and be able to mute sound. Further emergency response may be required.
- Failure to Anticipate CMP Impact: For example, even a blood draw may provoke TrP activation and enhance CNS sensitization. Ask the patient if there has been difficulty drawing blood, and if so, get specifics such as: finding veins, getting blood flow to continue, rolling veins, collapsing veins, or symptom flare after tests. Note problems on the order slip, alerting techs to the presence of pain amplification and extra precautions. The tech should ask the patient which veins work best. The patient should be instructed to keep the blood draw area warm. Topical carisoprodol or diazepam on the vein area 20 minutes beforehand may also help the tissues relax and the veins to be available. If there is a specialist in difficult phlebotomies available, s/he should be contacted and an appointment made.
- Underestimating Interactions from Treatments: What is necessary for one condition may worsen another. For example, automatically adjusting CPAP (AUTOPAP) units are often a better choice for Stage 2 CMP patients with OSA because of varying airway patency due to factors such as TrP contraction and congestion. Order maximum pressure to equal the highest pressure required on polysomnography to avoid subjecting patients to initial pressures that are too high. A printout of the first 3 months of the AUTOPAP SmartCard provides documentation of the need for AUTOPAP, facilitating reimbursement. It is common for the early CPAP user to experience temporary scalene and diaphragm TrPs as the lungs experience healthy expansion. CPAP head and chin straps, mask and outgoing airflow may activate TrPs. Nose tubes instead of a mask can be helpful if the strap arrangement fits well.
- Lack of Adequate Pain Control: "For over 20 years the medical
literature has carefully documented the undertreatment of all types of pain...." (50) Successful pain management includes aggressive identification and management of all perpetuating factors, and bringing them under control using all available means.
- Inadequate Training: A motivated, function-oriented patient with
appropriate resources and a trained care provider can significantly improve patient quality of
life, improve function and decrease pain level. (12)
The much needed effective preventative medicine for CMP is prompt diagnosis and treatment of single TrPs and single conditions by primary care physicians, including soft-tissue injury follow-up on ER and surgical patients, and patient education in TrP recognition and self-treatment.
Prevention of Stage 2 CMP comes with educating primary care clinicians including emergency service physicians, family practice and internal medicine physicians and their physician assistants and nurse practitioners. This also applies to physical therapy training programs. Also important is educating care providers, patients, 3rd party payers, and the legal system about TrPs, the onset of CMP and interactive diagnoses. This includes insurance company recognition and coding for TrPs and CMP. The end result will be more efficient care that will save time and considerable money in the long-term. We must train care providers to treat acute pain appropriately or an increasing number of patients will develop chronic pain. We presently have a cadre of patients who have endured persistent pain, even for decades, and they require comprehensive care. A small number of trained professionals and patients have been attempting to educate 3rd party payers using by meticulous clinical notes and seemingly endless resubmissions for reimbursement or by lawsuit. Both processes wear down the clinicians and the patients. This needs to change.
IV. CONCLUSION: HOPE FOR THE FUTURE
As we develop an understanding of the mechanisms of CMP and interactive diagnoses, we will discover new methods of symptom control. Research abounds on new pain medications and therapies and muscle tension relievers, promising help for CMP and accompanying dysfunctions. Greater understanding of the mechanisms of chronic pain is leading to new avenues for treatment. This includes research on protein kinase C (67), a new class of analgesics that activate nicotinic acetylcholine receptors (38) and modulate CNS sensitizing local pain signaling, and a selective neuronal N-type calcium channel blocker that may be more effective than morphine. Glial cell moderators such as pentoxifylline (45) are under investigation and very promising. Research on ion channel dysfunction (10), excitatory amino acid receptors, (65) cannabinoid receptors (23), and 5-HT receptors (1) offer hope for new treatment options. Therapies such as Frequency Specific Microcurrent and EEG stimulation neurotherapy are available or proving effective. High-powered ultrasound is being developed. Even today, Stage 2 CMP and accompanying interactive diagnoses can be treated successfully once they are recognized.
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Authors' Note: This was written and accepted as the Chronic Myofascial Pain chapter for the 3rd edition of Myofascial Pain and Dysfunction: Travell and Simons' Trigger Point Manual. At the time of Dr. Simons death, it was the only completed chapter, and was released to the author.
The author wishes to thank Nye Ffarrabas for help in preparing this article.
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