Diagnosing fibromyalgia: Moving away from tender points

By ATUL KHASNIS, MD, WILLIAM S. WILKE, MD | April 11, 2010

Dr Khasnis is a fellow and Dr Wilke is a staff member in the department of rheumatic and immunologic disease at the Cleveland Clinic in Ohio.

ABSTRACT: Since the American College of Rheumatology definition of fibromyalgia syndrome (FMS) was set in 1990, multiple studies have lent support to relying less heavily on tender points. Patients may indicate “areas of pain,” and the diagnostic process includes other common symptoms. The Symptom Intensity Scale provides an objective measure of pain and fatigue. Recognition of FMS may be aided by the presence of other conditions. FMS should be a diagnosis of inclusion rather than exclusion. Multimodal management of FMS starts with patient education, and exercise is a keystone of treatment. Sleep optimization is an important issue. Depression deserves investigation, recognition, and optimal management. Pain management in patients with FMS often is challenging. A combination of patient education and nonpharmacological and pharmacological measures is key to management. (J Musculoskel Med. 2010;27:155-162)

Fibromyalgia syndrome (FMS) is not a novel entity—there has been interest in unexplained pain syndromes since antiquity (Figure 1). The earliest research focused on the symptom of “muscle hardenings,” which may be the equivalent of musculoskeletal symptoms that patients with FMS describe today. More recently, the concept of FMS diagnosis has undergone several changes, including a shift in focus from tender point evaluation to identifying “areas of pain” and from assessment of specific symptoms to looking at the “whole patient.”

As in all other illnesses, clinicians should actively seek a diagnosis of recognition to facili- tate better overall management. A multimodal approach to therapy should be executed in parallel rather than in tandem to achieve optimal benefit.

In this article, we review early and recent developments in the diagnosis of FMS. We also discuss key treatment issues: the importance of patient education, the role of aerobic exercise, and the use of therapeutic agents in optimizing sleep and in managing depression and pain.

EVOLUTION OF THE DIAGNOSTIC CONCEPT

Initial criteria

In 1976, Hench¹ clinically defined FMS on the basis of 2 criteria, pain and no physiological explanation for pain. Since this initial description, FMS has evolved into a diagnosis of inclusion rather than exclusion. In other words, physicians should make a diagnosis of FMS on the basis of its clinical presentation rather than on a battery of tests that are not useful in the diagnosis of this condition and may be potentially misleading because of the detection of incidental findings. Because FMS does not offer immunity to other diseases, however, a reasonable clinically indicated workup is not unjustified.

In 1979, Smythe² proposed diagnostic criteria for FMS as 12 of 14 tender anatomical points (tender with application of 4 kg of pressure), diffuse pain of at least 3 months’ duration, disturbed sleep, skin roll tenderness at the upper trapezius border, and normal laboratory test results. In 1981, Yunus and associates³ included diffuse pain of 3 months’ duration, lack of other obvious causes, and 5 of 40 tender points along with 10 other minor criteria. These criteria gave tender points and other FMS symptoms and signs equal weight.

In 1990, the American College of Rheumatology (ACR) set criteria for FMS on the basis of a study of 293 patients deemed to have FMS compared with 265 control patients matched for age, sex, and rheumatologic diagnoses.⁴ The combination of criteria of widespread pain of at least 3 months’ duration with 11 of 18 tender points provided a sensitivity of 88% and specificity of 81%. On the basis of the ACR criteria, 19% of patients with 11 tender points did not have FMS. This criteria set ignored the myriad other symptoms and signs that are part of FMS, including fatigue; cognitive problems; sleep difficulties; feeling unrefreshed in the morning; hypersensitivity to light, odor, and sound; and generalized weakness.

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by Marly Silverman | June 08, 2011 10:46 AM EDT

It is refreshing to see continued acknowledgement of the science by noting this [FM] is a diagnosis of inclusion. The Proposed criteria do look at inclusion versus exclusion by noting the comorbid conditions with FM and the centralization of pain. My beef and the beef of others is that they are not including the assessment of myofascial trigger points. If we know this is the main complaint in FM, and science shows repeatedly that MTrPs are peripheral pain generators to the centralization of FM, why wouldn't we acknowledge their presence so they can be appropriately treated?

Exercising a muscle with active or latent trigger points (TrPs) will lead to further dysfunction and shortening [of muscle] and development of TrPs in compensating muscles unless the TrPs are treated prior to exercise. It is one of those double edged swords.

Exercise, stretching and aerobic (there is believed to be a cellular hypoxia related to TrPs) conditions muscles and helps prevent TrPs. The problem is, with FM, TrPs are not the same as in the average person who sustains an injury. It appears that the injury occurs at a very basic cellular and metabolic level, hence the release of pro-inflammatory cytokines in the absence of injury and no inflammation measured in FM, and the presence of elevated sensory preceptors. (Light, et al., 2011.)

To me and to others who have studied this extensively this all seems pretty basic, but continues to be overlooked.

The article will help raise awareness to the centralization of FM. It does take a multimodal approach, but part of that is myofascial therapy, which again, has been omitted.

This was the most important bullet of the entire article.
•We refer the patient for sleep study, if indicated; physical therapy; or aquatic therapy. Most patients can motivate themselves for pool therapy. Refer the patient for sleep medicine if that is indicated by the results of the sleep questionnaire.

These days if the doctor asks for a myofascial assessment, the physical therapist will be specialized in this and be able to report back to the physician on the presence of myofascial trigger points, about dysfunction, range of motion of the muscles involved, etc. When this starts to happen, doctors will set up and take note.

TY for allowing me to comment.
Celeste Cooper, RN, author, patient, advocate
"Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome and Myofascial Pain (Co-author, Jeff Miller, PhD)
www.thesethree.com

Light AR, Bateman L, Jo D, Hughen RW, VanHaitsma TA, White AL, Light KC. Gene expression alterations at baseline following moderate exercise in patients with chronic fatigue syndrome and fibromyalgia syndrome. Journal of Internal Medicine.2011 May 26. doi: 10.1111/j.1365-2796.2011.02405.x.

by Paul Little | June 07, 2011 12:57 PM EDT

I am a 52 year old health care professional. I was diagnosed with fibromyalgia in my late 30's after having my second child. I had never experienced any severe joint or muscle pain prior to this time. My father has degenerative osteoarthristis and "connective tissue disease". My father's sister was diagnosed with fibromyalgia. Her daughter was diagnosed with lupus. My deceased grandfather constantly complained of aches in his legs. I believe that whatever the cause, it is genetic in my case. My gynecologist believes that estrogen has a role in fibromyalgia for women. I believe I also have irritable bowen syndome which is accompanied by the fibromyalgia pain. I have never had a problem with depression, but I do feel anxious at times. In my experience, my symptoms suggest that my connective tissue is sometimes hardening--even in my GI tract. I try to take nutritional supplements that would promote elasticity in my tissues, but I do not take anything for the pain because my pain in cyclical The endocrinologist that diagnosed me believes fibromyalgia is caused by the kidneys inablity to rid the body of some of the waste products of metabolism--specifically inorganic phosphate. THerefore, fibromyalgia could be caused by an inborn error of metabolism.

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Diagnosing fibromyalgia: Moving away from tender points

EVOLUTION OF THE DIAGNOSTIC CONCEPT

Initial criteria

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