Other Common Pain Problems: Fibromyalgia, Myofascial Pain Syndrome and Complex Regional Pain Syndromes

(1)

Wisconsin Rehabilitation Medicine Professionals, Milwaukee, WI, USA

In the previous chapter we addressed low back pain (LBP or back pain) which is responsible for the majority of visits to a physician by pain patients.

In this chapter, we will address complex regional pain syndrome (CRPS), fibromyalgia syndrome (FM), and myofascial pain syndrome (MPS) which are less common than LBP but are also challenging to understand and treat. Like all chapters in this book, the concepts are presented only as a broad overview of common chronic pain conditions and not a comprehensive discussion of the nuances of the conditions and their treatment. I recommend that you explore these topics further, as they relate to your practice, using the materials suggested in the references section of this book.

Pain Syndromes

Unlike a disease with a clear cause and treatment, syndromes like CRPS, fibromyalgia syndrome (FM) and MPS are a collection of symptoms that form a distinct pattern and suggest a certain condition. These are not diseases with a clear or consensus-based cause, a typical course and a set of specific treatments with resolution or control of the disease and associated symptoms. Bacterial pneumonia, meningitis, rheumatoid arthritis, and multiple sclerosis are clearly diseases in which the exact cause and treatment are known. It is ironic that when a disease and its treatment are well known, there are fewer books written about it than vague conditions and syndromes. There is certainly not an entire shelf at the bookstore about bacterial pneumonia as there is, for example, for low back pain or migraine!

A syndrome lacks clear laboratory, X-ray and other consistent clinical findings and its symptoms can be vague and do not all have to be present in a patient for a differential diagnosis, though a number of the symptoms do need to be present. For example depression is a syndrome which, in its mild forms, may be referred to as dysthymia which is Greek for “bad state of mind.” While dysthymia may be characterized by a sad mood, eating and sleep disturbances, and other symptoms, when it becomes severe or long-lasting it is considered the syndrome of depression and may be treated by counseling and/or medication.

Pain syndromes are a difficult area of pain medicine because they are often judgment calls which benefit from clinicians’ experience. For example, I have seen and treated CRPS for years so have little trouble recognizing what is and is not the condition. Those who see CRPS rarely will have more questions.

Both CRPS and FM are simultaneously over- and underdiagnosed in our current healthcare system. Twenty or more years ago, there was a lack of clinician awareness about the syndromes and patients were treated symptomatically with unimodal care instead of holistically with a multidisciplinary approach. While patients with both syndromes might have accompanying depression or anxiety or other psychological symptoms, the conditions are definitely not “in their mind.” Anyone who has seen an edematous and discolored limb affected by CRPS, for example, does not doubt the condition’s physical basis.

While better awareness of the conditions can be valuable, there is a downside. As reimbursement patterns shift and medications become more aggressively marketed, the syndromes can be overdiagnosed. We need to be careful with such diagnoses, especially when a patient is in the Workers’ Compensation or other disability system in which there might be dueling parties and financial judgments at stake. We explored the requirements of many US disability systems in Chap. 7, Evaluation of Disability in Patients with Chronic Pain. We also must be careful to not needlessly alarm patients by giving them a serious diagnosis.

Another problem with diagnosing pain syndromes is that they can coexist and overlap with arthritic, rheumatic, autoimmune, inflammatory, and psychological conditions. For example, a patient may have MPS and fibromyalgia concurrently. A limb that exhibits temperature, color, and trophic changes may not be CRPS but disuse from not using a limb for other pain-related reasons. As with most chronic pain conditions, pain syndromes can be accompanied by anxiety, depression, disuse and self-neglect which can create additional symptoms.

Fibromyalgia and Myofascial Pain

When it comes to FM and MPS, there are two medical misconceptions which complicate diagnosis and treatment. The first is that they are the same condition which they are indubitably not, as you will see in Table 10.1. Dunteman calls the frequent confusion a “tragedy” since “myofascial pain may be effectively treated, while fibromyalgia ‘cures’ are unlikely” (Dunteman 2004).

Table 10.1

Is it fibromyalgia or myofascial pain?

Fibromyalgia	Myofascial Pain
Central nervous system involvement with both peripheral and central sensitization	A peripheral localized muscle problem
Tender points diagnosis	Trigger point diagnosis
Widespread pain	Regional pain in specific muscles
11 of 18 tender points respond	Trigger points—taut palpable bands of muscles
Stiffness especially on wakening	ROM, posture, and pain
May or may not follow illness—usually no specific cause or association with injury	May follow injury but mostly spontaneous
Fatigue	Not usually linked to fatigue
Sleep problems	Not usually linked to sleep problems
Cognition/memory problems	Not linked to cognition/memory problems
Centralized “pain magnification”	Does not usually centralize
Treated with drugs and counseling	Treated with stretching/mechanics/education
Usually does not fully resolve/controllable	Usually resolves with time, education, and treatment
Female predominance, 7 to 1	Female predominance, 3 to 1

The second misconception is that fibromyalgia is an “exclusion diagnosis” after other conditions are ruled out. While it is true that FM can mimic other conditions, and there are disagreements about criteria for a FM diagnosis and objective lab/diagnostic tests are lacking, a clinical diagnosis of fibromyalgia is possible as we will see in this chapter.

While the conditions have different etiologies, diagnostic methods and treatments—fibromyalgia is often categorized under the emerging umbrella terms “central sensitivity/sensory amplification syndromes” and myofascial pain is a local muscle problem—both are soft tissue pain syndromes. Notably, both are also well treated with multidisciplinary care.

Myofascial Pain Syndrome and Its Diagnosis

Myofascial pain is a musculoskeletal disorder that accounts for 85–93 % of pain clinic visits, 30 % of general medical visits, and 21 % of orthopedic visits (Chowdhury and Goldstein 2014). Clinically, MPS is characterized by aching or pain in the soft tissues—muscles, ligaments, and tendons—tightness, stiffness, and occasional neurological symptoms like tingling, numbness, or other strange sensations. It is caused by myofascial “trigger points.” Patients may also complain about dizziness, swelling, and feelings of warmth or coldness in the affected areas, sometimes affected by weather.

MPS generally presents as regional pain, which may involve the trapezius, scalene, and sternocleidomastoid muscles and pelvic girdle. It is usually triggered after a muscle injury when it is referred to as posttraumatic MPS, though it can frequently occur without a precipitating event or develop gradually. Sometimes microtrauma, vitamin deficiencies, chronic stress, chronic infection, hypothyroidism, hypoglycemia, hypouricemia, radiculopathy, and depression can contribute to the development of MPS (Chowdhury and Goldstein 2014).

When you examine a MPS patient, you will usually find muscles have become shortened and tight with a palpable taut band within the muscle belly, attributed to increased acetylcholine, ACh receptor activity, and/or changes in hydrolysis. Muscle hyperactivity is seen which, because it increases muscle demand, can lead to hypoperfusion, ischemia, hypoxia, and a cascade of pain-producing neurovasoreactive substances (Chowdhury and Goldstein 2014). The hyperactive muscle(s) produces limited ROM, reduced function, disuse syndromes and, sometimes fatigue and difficulty with sleep.

While this chapter is not intended to provide a complete clinical guideline, MPS is diagnosed on the basis of an assessment of regional pain, taut muscles, trigger points, and positive twitch responses as shown in Table 10.2. Trigger points, when compressed, produce pain both locally and at referred locations; for example, a trigger point in the scalene muscles of the neck may produce pain in the hand when compressed. The unique distribution of pain in MPS trigger points assists the diagnosis. If a trigger point does not cause myotomal radiation it is not diagnostic for MPS or useful in MPS treatment.

Table 10.2

Diagnostic criteria for myofascial pain syndrome

Trigger points	Elicits radiating pain when tight tender muscle is palpated
Local twitch responses (LTR)	Contractions of and around taut band
Regional pain	Remains localized in a muscle or region
Taut band in muscle	Exhibits tenderness, “ropey” consistency of muscle palpated
Trigger point treatments relieve pain	Injections, “spray and stretch,” proper posture, conditioning exercises, PT, relieve or eliminate pain

Physiologically, Chowdhury and Goldstein suggest that MPS trigger points “contain areas of sensitized, low-threshold nociceptors (free nerve endings) with dysfunctional motor end plates” (2014). “These motor plates connect to an end group of sensitized sensory motor neurons in charge of transmitting pain information from the spinal cord to the brain.” Not surprisingly, inactivation of trigger points is the primary treatment for MPS and will reduce pain. However, patients should be cautioned that overuse, overstretching, and psychological distress or anxiety can reactivate trigger points after they have healed.

There are many individuals who may continue to complain of pain after a muscle strain which is sometimes termed posttraumatic MPS. In the medicolegal context such as in work injuries and car accidents that may have initiated the muscle strain, the presence of pain and stiffness, with mild diffuse pain on touching, does not constitute posttraumatic MPS even though it is soft tissue pain. When physicians and healthcare providers label such patients as having posttraumatic MPS and provide ongoing physical or chiropractic therapy or medications and injection of tender areas (calling them “trigger point injections”) they not only do a disservice to the patient, they add to the medical and legal and societal costs of health care. Clearly, MPS should not be a catch-all diagnosis.

I would label a patient as having MPS when he meets these criteria:

The pain is a muscle or regional muscle group

There is a palpable taut band of muscle (ropey consistency of muscle)

There is a trigger point characterized by a twitch response

Palpation of the trigger point leads to reproduction of the patient’s pain and the pain radiates in a myotomal not nerve pattern

The trigger point can be inactivated with physical therapy (stretch, myofascial release, and injections)

A useful resource for helping you assess and treat trigger points is Myofascial Pain and Dysfunction: The Trigger Point Manual Volumes 1 and 2 (Simons and Travell 1998).

Treating Myofascial Pain Syndrome

Both the treatment of myofascial pain syndrome and fibromyalgia start with reassurance—letting the patient know that he does not have a progressive or crippling disease. While MPS can rarely become or coexist with fibromyalgia, MPS of a specific muscle in a regional distribution is usually a time-limited condition with healing seen in between 2 and 12 weeks. MPS does not require or respond to surgery or require ongoing medication.

MPS can be treated invasively with injections of trigger points with a combination of local anesthetic and steroid. It can also be treated manually by dry needling, although there are no long-term evidence-based studies, despite the modality’s theoretical rationale. These trigger point injections should be a mutual decision reached with the patient and always part of multimodal treatment that includes stretching, posture, relaxation, and empowerment through education, stressing self-efficacy. Patients should be educated to exercise after the acute phase and to recognize, accept, and incorporate their awareness of the difference between “hurt” (which implies pain) and “harm” (which implies damage/reinjury) in their rehabilitation.

Interestingly, this is how many athletic injuries are treated in sports medicine, including those of quarterbacks and other football players. The injured athlete is moved from injury to healing with a graded exercise program that gradually progresses to higher levels of activity. It is ironic that even though multidisciplinary care and physical therapy are the basis of sports medicine, our healthcare system is phasing them out in favor of unimodal treatment.

Manual methods and/or physical therapy should be used for patients presenting with new, acute trigger points or trigger points not easily accessible by injection such as psoas muscles (Chowdhury and Goldstein 2014). If you and the patient decide to employ injections, local anesthetics such as lidocaine are usually introduced into the trigger points, with or without cortisone. The very insertion of needles can sometimes modify pain sensations and some studies have found that needles with no medication at all—called dry needling—can be effective, though more research into its effectiveness is required.

Dunteman cautions that injections should not be regarded as a “cure” but rather as an “adjunct” to help a patient address dysfunctional postures and movements (2004). Anti-inflammatory drugs can be useful for short periods of time but opioids are to be avoided as they are in most chronic pain conditions. While for a time, opioids were increasingly used in minor pain conditions in the United States, the pendulum has definitely swung back to avoiding opioids beyond the first 2–4 weeks, only to assist in increasing activity and function. The risks of dependence and addiction outweigh their use and, on a long-term basis, they are ineffective and may even worsen pain symptoms.

Dysfunctional postures such as a forwardly displaced shoulder girdle or forward rotation of the pelvis and abdominal muscle weakness and hip flexor tightness are frequently behind MPS. In my clinical experience, the most effective physical treatment for MPS is stretching followed by vigorous aerobic exercise and conditioning with a cool down period. The patient should commit to a regular home program of the above to keep functional levels and trigger points inactive. Common MPS treatments are seen in Table 10.3.

Table 10.3

Treatments for myofascial pain syndrome

Trigger point injections	Lidocaine, cortisone; “dry needling”; part of multidisciplinary care
Physical/mechanical treatments	Heat, stretching, exercise, aerobic conditioning, rarely temporary TENS
Physical therapy	Address dysfunctional posture, weak muscles, increase muscle length and range of motion
“Spray and stretch”	Stretching with fluoromethane, ethyl chloride sprays (Stretch is action; spray is distraction) works well with localized pain
Medication	Anti-inflammatory, NSAIDs, sleep medication (for brief period only to increase function)
Psychological treatment	Cognitive Behavioral, relaxation therapy when chronic MPS exceeds 6 months
Education	Assurance: not progressive or crippling condition; “hurt” versus “harm” education
Self-efficacy	Commitment to home program and self-care; self-responsibility, avoiding dependence on medical, chiropractic and passive therapies

Because of its postural components, MPS is ideally treated with multidisciplinary care and especially responsive to physical therapy, myofascial release and educating patients about the condition so they are motivated to maintain a home program of exercise and stretching.

Fibromyalgia and Its Diagnosis

As we have noted, fibromyalgia is often confused with MPS. MPS and FM are separate conditions with different etiologies, treatments, and prognoses. Both, however, respond well to multidisciplinary care as opposed to uncoordinated, unimodal care (Masters 2014).

The first modern description of fibromyalgia emerged in 1972 when Hugh Smythe first described criteria for the diagnosis of “fibrositis” (a term coined by Gowers in early 1900s), which included the presence of widespread pain and tenderness at many of the points that were eventually incorporated in the 1990 American College of Rheumatology (ACR) criteria (Harden et al. 2014). The term fibromyalgia comes from the Latin word fibra for fibrous tissue and the Greek words myos and algos for muscle and pain respectively and was adopted in 1976 and eventually, as noted incorporated by the ACR in 1990.

Approximately five million adults in the United States have fibromyalgia syndrome which strikes patients at an average age of 30 and 50 years, The largest demographic for FM is women aged 55–64 report White et al. (Karvelas and Vasudevan 2011). Because of the lack of objective imagery or laboratory findings to confirm FM, it has erroneously been cast as a psychogenic disorder or even a result of industrialized culture. Russell, however, reports that FM is also seen in nonindustrialized countries. Certainly emotional and cognitive symptoms are part of the syndrome by they do not explain its pathogenesis.

Perhaps no chronic pain condition is so complicated or paradoxical in its diagnosis: A FM designation requires that other conditions be ruled out but is not merely an exclusionary diagnosis. A FM designation is based on the subjective and clinical findings but it is not just a symptom–based diagnosis.

It is not the purpose of this chapter to provide complete treatment guidelines for FM but a basic familiarity with this condition will help you better serve your patients. While widespread pain above and below the waist lasting for more than 3 months is the primary FM symptom, Table 10.4 shows the breadth of symptoms that may be present in a patient.

Table 10.4

Possible presenting symptoms of fibromyalgia

Widespread pain

Joint pain tenderness

Muscle tenderness

Fatigue

Morning stiffness

Anxiety

Paresthesia

Depression

Headache

Sleep disturbances

Feeling cold

Non restful sleep

Dry itchy eyes/blurred vision

Changes in bowel habits/abdominal pain, irritable bowel

Bladder symptoms

Jaw pain

Memory/cognitive problems (“fibro fog”)

Rash, hives, sun sensitivity

Ringing in ears/hearing difficulty

Changes in appetite and food taste

In 1990, the ACR introduced criteria for a fibromyalgia diagnosis which were based on the presence of widespread pain and tenderness in 11 areas of 18 possible “tender points” as shown in Table 10.5.

Table 10.5

Tender points to consider in a fibromyalgia diagnosis

Occiput	Bilateral, at suboccipital muscle insertions
Low cervical	Bilateral, at anterior aspects of intertransverse spaces at C5–C7
Trapezius	Bilateral, at midpoint of upper border
Supraspinatus	Bilateral, at origins above scapula spine near medial border
Second rib	Bilateral, at second costochondral junctions just lateral to junctions on upper surfaces
Lateral epicondyle	Bilateral, 2 cm distal to epicondyles
Gluteal	Bilateral, in upper outer quadrants of buttocks in the anterior fold of muscle
Greater trochanter	Bilateral, posterior to trochanteric prominence
Knee	Bilateral, at medial fat pad proximal to joint line

Since the introduction of ACR criteria for fibromyalgia in 1990, there have been objections and calls for clarification. First, it was found that medical professionals rarely actually conducted tender point counts in clinical settings and that they sometimes did not know how, reducing the condition to a symptom-based diagnosis (Wolfe et al. 2010). Secondly, some felt the 1990 criteria overlooked the important cognitive and somatic symptoms that patients often report with FM like memory problems and fatigue. Thirdly, some medical professionals regard FM as a spectrum disorder and worried that a tender point orientation could preclude a spectrum diagnosis or incorrectly link fibromyalgia to peripheral muscle abnormality conditions.

There was even another problem: if a patient improved or his tender points decreased, he could fail to meet FM criteria yet still clearly have the condition.

In 2010, the ACR introduced new criteria acknowledging cognitive and affective symptoms and somatic symptoms like sleep problems, chest pain, fatigue, irritable bowel syndrome, bladder irritability, and headache (Russell 2011). Like the 1990 diagnostic criteria, the 2010 included a Widespread Pain Index and a Symptom Severity Scale for additional accuracy.

What Causes Fibromyalgia?

Like related pain syndromes, fibromyalgia is believed to be a disorder of increased central sensitization and decreased function of the descending pain inhibition systems (Clauw 2013). These disruptions, called descending inhibitory controls, which are part of decreased descending systems, result in abnormal temporal summation and sensory amplification (Karvelas and Vasudevan 2011). Even the perception of sound can be amplified in fibromyalgia patients reports Gary Jay, MD.

Fibromyalgia seems linked to genetic polymorphisms relating to serotoninergic, dopaminergic, and catecholaminergic systems but also no doubt has environmental factors which can include physical, sexual or emotional trauma, chronic stress or the aftermath of an acute illness. Abeles et al. state “fibromyalgia seems to be a final common pathway for a myriad of conditions, or combinations thereof, ranging from the psychosocial to the mechanical to the biological.”

Only gold members can continue reading. Log In or Register to continue