Fibromyalgia

Documentation & Treatment   (PDF Format)

By Russell Rothenberg, M.D.

Rheumatologist in Private Practice &

Assoc. Professor, George Washington 

University Medical Cente

FM is not a new medical problem, it is just better understood recently. It used to be called by different names. There are medical articles on "neurasthenia" and "muscular rheumatism" which date back to the mid-1800’s that describe illnesses similar to FM. Dr. Gowers created the term "fibrositis" in 1904, but it wasn’t until 1978 that Drs. Smythe and Moldofsky published research on the associated sleep pathology and the peripheral and central nervous system (CNS) pain sensitization that appears to be essential to the development of FM.¹

Rheumatologists have taken the lead in diagnosing and treating FM, which makes sense since rheumatology was the medical specialty that defined the syndrome. In addition, many fibromyalgia patients have joint pain and other forms of musculoskeletal pain in addition to their FM, as well as elevated levels of inflammatory chemicals that cause pain called cytokines (anti-TNF and Il6) in their central nervous systems—abnormalities shared by many other rheumatology patients. There is also a strong association between FM and many of the diseases rheumatologists treat (rheumatoid arthritis, Sjögren’s syndrome and systemic lupus). It has been estimated that 10-20% of patients in a rheumatologist’s office practice have FM.²

Despite all of the recent advances in the understanding of FM, the problem many FM patients still experience is a long, time delay between the onset of their symptoms and the diagnosis of FM. Since FM patients often have multiple symptoms, and there are no objective lab tests or imaging studies that are readily available to make the diagnosis, they often face years of multiple medical evaluations, multiple specialists, a lot of frustration and suffering, and no answers. It would benefit the FM patient if more primary care doctors considered FM in their differential diagnosis when a patient presented with chronic pain and fatigue since FM is a relatively common illness estimated to affect 4-10 million Americans. Demographic studies show that FM has a prevalence in the U.S. of 3½ % of all women and ½ % of all men over the age of 18 years. These figures are similar to the prevalence of FM in other countries.³ Many of my patients have reported having symptoms for over five years and consulting more than five doctors before being referred to me for diagnosis.

The definition of FM includes identification of at least 11 of a possible 18 tender points and widespread pain for at least three months duration as described in the 1990 ACR definition of FM. These tender points can be assessed by pressing on specific locations of the body with a pressure of 4 kg/m2 (enough pressure to blanch the skin under the thumb nail). Pressing on these painful points usually creates an involuntary painful response, and the doctor usually doesn’t have to ask if it hurts. The tender points exam includes good diagnostic criteria (82% sensitive and 87% specific to FM), but tender points are not the only tender areas FM patients have. They also demonstrate generalized hyperalgesia that gets better and worse consistent with other FM symptoms.⁴ It is important to note that successfully treated FM patients may have fewer than 11 positive of the 18 tender points, and this just means they are doing well.

Other doctors have shown in studies that the tender point exam is reproducible in FM patients. Dr. Bradley has demonstrated that lower pain threshold responses to thermal stimuli consistently are present in FM patients compared to normal controls, and this scientific finding has been reproduced by Dr. Geisser. Drs. Gracely and Clauw have demonstrated on functional brain MRI’s that FM patients’ response to pressure stimuli consistently activates the areas of the brain associated with pain at a lower pressure threshold than in normal controls.⁵

The sleep abnormalities in FM are reproducible on overnight sleep EEG studies (this test may be ordered but is not necessary for the diagnosis of FM). One sees alpha wave intrusion in delta sleep and a decrease in delta (stage 3 and 4) sleep in many FM patients (though these findings may not be present in treated patients). Such findings are sensitive indicators of the classical non-restorative sleep often described in FM patients, but they can also be seen in patients with rheumatoid arthritis, osteoarthritis, and Sjögren’s syndrome as well as other illnesses.⁶

There is scientific evidence that a subset of fibromyalgia patients have genetic factors that predispose them to vulnerability to FM. These patients tend to have primary FM. Primary FM usually has been present since childhood though the symptoms may not be clinically apparent until the patient is exposed to a significant physical or emotional stressor. Secondary FM is usually secondary to an overwhelming infection, injury, or a predisposing rheumatic disease. Genetic abnormalities in the functional polymorphism in the promoter region of the serotonin transporter gene have been noted in FM.⁷  Patients with adequate serotonin promoter genes seem to be less susceptible to the adverse effects of chronic stress and depressive events. Another gene, catecholamine-O-methyltransferase (COMT) has been shown to be associated with pain regulation and myofascial pain of the jaw, and there is an increased association of COMT in FM patients.⁸

Myofascial pain is a big problem for many FM patients. Patients with this condition get palpable "knots" in their muscles and soft tissues that look and feel like painful muscle spasms. Doctors of physical medicine and rehabilitation often describe myofascial pain as originating in painful tissue which contains nodules associated with "trigger points"(not to be confused with the diagnostic "tender points" of fibromyalgia) in palpable, tense, or taut bands that may produce a twitch response upon palpation. These trigger points are often so painful that the patient is very uncomfortable. There can also be latent trigger points that are only painful upon palpation. Trigger points are typically associated with a referred pain pattern, sometimes at distant sites in the body. All trigger points are responsible for musculoskeletal stiffness, weakness, and limitation of motion.

There is scientific evidence that myofascial tissue on muscle biopsy has reduced blood flow, reduced oxygen receptors,⁹ increased levels of the pain neurotransmitter substance P,¹⁰ and reduced ATP receptors.¹¹ Muscle biopsies are not necessary for the diagnosis of myofascial pain, but they may be ordered if there is an abnormal EMG-nerve conduction study, and neuromuscular disease is suspected. Sympathetic nerve blockade reverses many of the abnormal findings in the muscle which accompanies myofascial tissue pain, and these findings appear to confirm a neuromuscular link and evidence of sympathetic nervous system dys-function in myofascial pain.¹²

Drs. Price and Staud have demonstrated that with increasing nociceptive input there is an increased temporal summation of CNS pain discharges or "windup." Windup of the nociceptive neurons in the dorsal horn of the spinal cord involves increased NMDA receptor activity and neural plasticity of nociceptive spinal cord pathways, and it is an important factor in central sensitization.¹³ The increased brain activity in response to painful stimuli appears to be related to the increased pain processing in FM. This helps to explain why non-steroidal anti-inflammatory pain medications (NSAID’s) are not that effective in FM since they help reduce peripheral pain and not the CNS pain present in FM patients.

FM patients commonly have autonomic nervous system abnormalities that make them vulnerable to coexistent conditions such as neurally-mediated hypotension, irritable bowel and bladder syndromes, vascular headaches, and reduced heart rate variability. These medical problems are partially due to neuroendocrine abnormalities including alterations in the hypothalamic-pituitary-adrenal (HPA) axis. There are a number of studies showing dysregulation of the HPA in FM. Documented abnormalities include low AM cortisol and 24-hour urinary cortisol levels, inappropriately high levels of adrenocortical trophic hormones (ACTH), and failure to suppress normally with dexamethasone.¹⁴ The physician needs to be aware of the need to treat neurally-mediated hypotension in FM patients with adequate salt and fluids as well as stressing conservation of energy. If the hypotension is more severe, cardiac consultation and tilt table testing can be ordered.

Important non-pain symptoms associated with FM usually include fatigue, nonrestorative sleep disturbances, cognitive dysfunction, increased anxiety, and reactive depression (which is clearly distinguished from major depressive disorder).¹⁵ In my clinical experience as a rheumatologist who has treated FM patients for over 20 years, successful treatment of these other concurrent FM problems is essential to a good clinical outcome.

1. Antidepressants: These drugs block the biogenic amines that are abnormal in the CNS in FM.

2. Anti-Epileptic Drugs: These drugs have been shown to be effective in the treatment of various neuropathic pain disorders and are widely used as analgesics.

1. Education: When a FM diagnosis is made, and the condition is properly explained to the patient and family, the intensity of symptoms will often be reduced by one-third due to reductions in anxiety and abnormal pain processing. An essential goal of treatment is to empower the patient to understand his or her illness and learn how to best manage FM.

2. Physical therapy: Proper posture, balance, muscle tone, and exercise conditioning are important needs to correct in many FM patients. It is often necessary to prescribe physical therapy before the patient can successfully progress to an appropriate exercise program.

3. Exercise: Low impact, aerobic exercises are an important treatment for most FM patients to improve their pain, mood, and functional status. It is important to combine exercise with adequate stretching as well as energy conservation to prevent injury or FM flare. I find core exercises to be very important for many of my FM patients.

4. Cognitive behavioral therapy as well as psychological and behavioral therapies are being used in FM with increasing frequency and success. Energy conservation and reduced anxiety over chronic pain are important goals in the management of FM.