Physical Medicine and Rehabilitation for Fibromyalgia

Optimal rehabilitation outcomes in a fibromyalgia patient require that the treatment be tailored to the individual patient's symptoms, examination findings and subject to periodic testing to allow for adjustment.
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Fibromyalgia is not only a difficult illness for patients who are forced to live with chronic pain and other co-morbid conditions, it is also perplexing to physicians who often do not have the tools necessary to feel comfortable in making an accurate diagnosis or to prescribe a successful treatment regimen. In his discussion of the pathophysiology of fibromyalgia, medications, and rehabilitation strategies, Dr. Stoney highlights the usefulness of the Fibromyalgia Oswestry Pain Questionnaire as a tool to measure pain management efficacy in this patient population.

“The days of affliction have taken hold of me. My bones are pierced in the night and my sinews take no rest." —Job 30:16-17

Physical medicine and rehabilitation (PM&R), also known as physiatry, is a branch of medicine that aims to enhance and restore functional ability and quality of life to those with physical impairments or disabilities. Physical medicine and rehabilitation involves the management of disorders that alter the function and performance of the patient. Emphasis is placed on the optimization of function through the combined use of medications, physical modalities, physical training with therapeutic exercise, movement and activities modification, adaptive equipments and assistive device, orthotics (braces), prosthesis, and experiential training approaches. The major concern of the field is the ability of the person to function optimally within the limitations placed upon them by a disease process for which there is no known cure. The emphasis is not on the full restoration to the pre-morbid level of function, but rather the optimization of the quality of life for those who may not be able to achieve full restoration. A team approach to chronic conditions is emphasized to coordinate care of the patients.

Figure 1. Pain Sensing System Malfunction in Chronic Pain

Normal Pain
Pain-sensing signals are initiated in response to a stimulus
They elicit a pain-relieving response

Chronic Pain
Pain signals are generated for no reason and may be intensified
Pain-relieving mechanisms may be defective or deactivated

Pathophysiology of Fibromyalgia

Fibromyalgia has been acknowledged as a disease state by the AMA, the NIH, Social Security Administration, and the American College of Rheumatology. There is a wealth of biochemical data that both substantiates this disorder and helps providers understand its pathophysiology.

The patient with fibromyalgia has demonstrated gray matter loss, with one year of fibromyalgia pain equivalent to nine years of brain aging.1 Fibromyalgia is a chronic pain disorder affecting 2-4% of the population.2 Biological and neuroimaging studies support the hypothesis that aberrant pain processing in the central nervous system (CNS) of fibromyalgia patients may represent an important underlying defect.3

A CNS mechanism may explain generalized heightened pain sensitivity of FM patients; increased levels of excitatory neurotransmitters (glutamate, substance P); may contribute to neuronal hyperactivity and central sensitization; and decreased activity of inhibitory signaling mediated through noradrenergic and serotonergic descending pathways. Biologic and genetic influences, environmental triggers, and abnormalities in neuroendocrine and autonomic nervous systems also contribute to the pathophysiology of FM (see Figure 1).

Neuroendocrine4 and neurotransmitter abnormalities, autonomic dysfunction, shared biological and genetic factors,5 psychiatric/ psychological6 and social distress are present in patients with fibromyalgia. The peripheral mechanism is also impaired in patients with fibromyalgia as these patients have hypersensitivity or widespread pain.

The biochemical changes seen in the CNS—the low levels of serotonin, the four-fold increase in nerve growth factor, and the elevated levels of substance P—all lead to a whole-body hypersensitivity to pain and suggest that fibromyalgia may be a condition of central sensitization or of abnormal central processing of nociceptive pain input.7 Evidence has suggested that suppression of the normal activity of dopamine-releasing neurons in the limbic system is the primary pathology in fibromyalgia. Increasing evidence indicates that fibromyalgia may represent a dysregulation of dopaminergic neurotransmission. Researchers have found low levels of adenosine triphosphate (ATP) in red blood cells of patients with fibromyalgia but the most widely acknowledged biochemical abnormality associated with fibromyalgia is abnormally low serotonin levels which have been correlated with painful symptoms. Many studies have linked serotonin, a neurotransmitter, to sleep, pain perception, headaches, and mood disorders.

Serotonin levels in the CNS are thought to be low due to low levels of tryptophan (amino acid precursor to serotonin) and 5-hydroxyindole acetic acid (metabolic by-product) in the spinal fluid. Investigators have proposed a link between low serotonin levels and symptoms of fibromyalgia.8 Moreover, many propose that low serotonin levels may cause fibromyalgia in whole or in part.

Investigators have studied the neuroendocrine aspects of fibromyalgia and have found dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis.9 The HPA axis is a critical component of the stress-adaptation response. In a normally functioning system, corticotropin-releasing hormone (CRH) stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal cortex to produce glucocorticoids, which are powerful mediators of the stress-adaptation response.

In support of the idea of a systemic biochemical abnormality in fibromyalgia, investigators from four independent studies reported levels of substance P that were two to three times higher than normal.10

Substance P, the neuropeptide in spinal fluid, is a neurotransmitter that is released when axons are stimulated. Increased levels of substance P increase the sensitivity of nerves to pain or heighten awareness of pain. The elevated levels in the spinal cord of fibromyalgia patients cause fairly normal stimuli to result in exaggerated nociception. This results in an impairment in the normal regulation of muscle tone within the spinal cord, contributing to increased muscle tone and focal muscle spasm (see Figure 2).

Figure 2. Regulation of muscle tone. Loss of descending controls (MS/SCI) leads to excitatory imbalance = spasticity

Some authors have also found that most patients with fibromyalgia have low levels of IGF-I and that low levels are specific and sensitive for fibromyalgia.11

Disability

It wasn’t until 1987 that the American Medical Association (AMA) acknowledged fibromyalgia as a true illness. Since the diagnosis is relatively new in the western medical medical community, many patients see multiple physicians before being diagnosed—with a resulting delay, or even lack, of treatment.

The average woman with FM has been reported as having less functional ability related to ADLs (activities of daily living) than the average community-dwelling woman in her 80s.12 In 1998 a multi-center study published in the June issue of Journal of Rheumatology revealed that 26% of the fibromyalgia patients surveyed were receiving some form of disability payment. 57.1% of those with FM left the workforce because of their symptoms of FM. Among those who continued in their jobs, the majority (59.4%) had reduced the time they spent working.

Rehabilitation

According to Regina P. Gilliland, MD, Department of Internal Medicine and of the Division of Rehab Medicine at the Mobile Infirmary Medical Center, investigators believe that a successful fibromyalgia rehabilitation program involves a multidisciplinary team of professionals and various modalities individualized for each patient.13 The team should include a physician, a medical psychologist, physical and massage therapists, and an exercise physiologist. The team members should have expertise in the treatment of soft-tissue disorders.

First published on: April 1, 2010