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What is Fibromyalgia??
Background: Fibromyalgia is a complex disorder defined only recently, but it is not a recently discovered disorder. Descriptions have been found in the medical literature as far back as the early 17th century. Many physicians prefer not to deal with patients who have this complicated disorder and question the actual existence of the disorder. In the past, poor recognition and lack of treatment for this disorder could be explained by a lack of meaningful research. Today evidence supports the diagnosis of fibromyalgia, as well as the accepted treatments.
Some experts propose that physicians should make a paradigm shift in their approach to patient care to treat patients with fibromyalgia successfully. Since no widely available laboratory tests confirm diagnosis of fibromyalgia, a physician skilled in taking a careful history, listening to the patient's concerns, and performing a thorough examination remains the foundation for diagnosis and treatment of fibromyalgia.
This article reviews synonyms and clinical features of fibromyalgia, as well as an approach to obtaining a medical history, physical examination, and recommended treatment. Treatment suggestions are meant to be a resource for developing a creative treatment program, not a cookbook approach to all patients with fibromyalgia.
A definition of fibromyalgia
Fibromyalgia, a common disorder, is a syndrome composed of a specific set of signs and symptoms. Fibromyalgia long has been considered a "wastebasket" diagnosis, but, in 1987, the American Medical Association (AMA) acknowledged fibromyalgia as a true illness and a potential cause of disability. Fibromyalgia is accepted as a legitimate clinical entity by many well-respected organizations, such as the AMA, National Institutes of Health (NIH), and the World Health Organization (WHO) (Starlanyl, 1996).
Patients with fibromyalgia generally see many physicians before receiving a correct diagnosis. Some report that patients seek medical advice for more than 5 years before a correct diagnosis is made, and over 50% of patients are misdiagnosed and undergo unnecessary surgery.
Although the syndrome has been known by other names, the word fibromyalgia was first introduced in 1976. This word is derived from the Latin roots "fibro" (fibrous tissue), "my" (muscles), "al" (pain), and "gia" (condition of). Fibromyalgia was known most commonly by the misnomer fibrositis, the "itis" implying an inflammatory component. Chaitrow asserts that no inflammatory process ever has been found to be part of this disease.
Pathophysiology: Although the sequence of events that cause fibromyalgia remains unknown, recent advances and discoveries may help to unravel the mysteries of this disease. Recent research shows biochemical, metabolic, and immunoregulatory abnormalities associated with fibromyalgia. Clinicians' approach to diagnosis and treatment may be enhanced by broadening their knowledge of these biochemical and immunoregulatory abnormalities, which may be involved in the way patients interpret the nociceptive signals to the central nervous system (CNS) and how they respond physiologically to stress. Current understanding of the pathophysiology of fibromyalgia describes the disease as a central pain processing disorder.
The most widely acknowledged biochemical abnormality associated with fibromyalgia is abnormally low serotonin levels. Many studies by researchers have linked serotonin, a neurotransmitter, to sleep, pain perception, headaches, and mood disorders. Lower than normal levels of serotonin have been observed in fibromyalgia patients. Low platelet serotonin is believed to be the cause of the low serum levels. Studies show low serum levels correlate with painful symptoms. Serotonin levels in the CNS are thought to be low due to both low tryptophan (the amino acid precursor to serotonin) and 5-hydroxyindole acetic acid (a metabolic by-product) in spinal fluid. Investigators have proposed a link between low serotonin levels and fibromyalgia symptoms. Moreover, many investigators propose that low serotonin levels may cause fibromyalgia totally or in part.
In support of the idea of a systemic biochemical abnormality in fibromyalgia, 4 independent studies reported elevation by 2-3 times of substance P, the neuropeptide in spinal fluid. Substance P is a neurotransmitter 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 cause fairly normal stimuli to result in exaggerated nociception. Some authors believe that neither elevated substance P nor low serotonin alone can be primary causative agents but that the dual dysfunction may be responsible for fibromyalgia.
Researchers also have found the existence of low levels of adenosine triphosphate (ATP) in red blood cells of patients with fibromyalgia. Although the significance is unknown, some suggest low platelet serotonin levels could be explained if platelet ATP levels are also low. ATP is necessary to move and then hold serotonin in platelets. More investigation into ATP and the link to serotonin is needed.
Others have studied the neuroendocrine aspects of fibromyalgia and found hypothalamic-pituitary-adrenal (HPA) axis dysfunction in these patients. The HPA is a critical component of the stress-adaptation response. In a normally functioning system, the anterior pituitary is stimulated by corticotropin-releasing hormone (CRH) to release adrenocorticotropic hormone (ACTH). The adrenal cortex then is stimulated by ACTH to produce glucocorticoids, which are powerful mediators of the stress-adaptation response. Circadian regulation and the stress-induced stimulation of the HPA axis are, in part, regulated by serotonin. Serotonin metabolism perturbations (as well as premorbid HPA-axis abnormalities) may explain HPA-axis abnormalities in fibromyalgia.
The effects of abnormal serotonin metabolism may be exaggerated by HPA-axis dysfunction. Low central serotonin actually may be caused by HPA-axis hypoactivity. Some authors have noted the following 5 main measurable neuroendocrine abnormalities associated with HPA-axis dysfunction:
Growth hormone, produced during delta sleep, is involved in tissue repair. The low levels of growth hormone may be explained by disrupted stage 4 (delta) sleep associated with fibromyalgia. Growth hormone stimulates liver production of insulinlike growth factor I (IGF-I). Some authors have found that low levels of IGF-I are present in most patients with fibromyalgia and that low levels are both specific and sensitive in fibromyalgia.
Some studies have found that nerve growth factor was 4 times higher in the spinal fluid of patients with fibromyalgia. This factor is important to the pathophysiology of fibromyalgia, since the process enhances substance P production in the afferent neurons, thereby increasing the sensitivity or awareness to pain. Nerve growth factor also may play a role in spreading or redistributing perceived pain signals.
Increasing evidence suggests the existence of a genetic predisposition for developing fibromyalgia. The inheritance pattern is autosomal-dominant. Some investigators propose that the genetic predisposition requires either reaching a critical age or sustaining an external insult such as trauma or illness.
Although the pathogenesis of fibromyalgia is not understood completely, the currently known abnormalities substantiate the proposal that fibromyalgia can no longer be considered a subjective pain condition. Many research groups suggest that fibromyalgia may be a condition of abnormal central processing of nociceptive pain input.
Mortality/Morbidity: The social, emotional, economic, and functional impact of fibromyalgia on an individual's life have been compared, by some authors, to the effects of rheumatoid arthritis. Approximately one third of patients with fibromyalgia have reportedly modified their work to keep their jobs. Some patients have shortened their workdays, their workweeks, or both. Many patients with fibromyalgia have changed to less physically and mentally taxing jobs. Often, this type of job change leads to decreased income and increased financial burdens. One figure suggests that approximately 15% of the people diagnosed with fibromyalgia currently are receiving disability benefits. An estimate of the overall annual cost of this disease to the American economy is over $9 billion.
Race: No racial predilection exists in fibromyalgia. Researchers have reported the condition in all ethnic groups and cultures.
Sex: Studies have shown that fibromyalgia is 4-7 times more common in females. No universally accepted explanation exists for this predilection for females, as there is hardly any difference in incidence among males and females in childhood.
Age: Fibromyalgia may be diagnosed in individuals of all ages. Symptoms usually arise between the ages of 20-55 years, but the condition also may be diagnosed in childhood.
History: Although it may take a little more time to gather a thorough and detailed initial history, the author finds that a good history saves time in the long run, reduces potential for litigation, helps prevent incorrect diagnosis, and eliminates inappropriate or unnecessary treatments.
Start the evaluation with identifying the chief complaint, which usually is related to pain. Although the initial interview starts with the chief complaint, avoid treating patients based on the chief complaint alone. Premature treatment may lead to symptom chasing and ineffective treatment. Patients with fibromyalgia experience a change in symptoms from day to day, which may not reflect the global nature of their disorder.
Next, expand on the chief complaint with specific questions about the pain. Question the patient about the distribution of the pain (eg, ask whether the pain is regional or generalized). Ask about the duration and onset of the pain. Patients usually can remember sudden onset of pain; if there was a gradual onset, determining the exact time of onset is difficult. Inquire about pain aggravating and alleviating factors. Record the description or characteristics of their pain (eg, ask whether the pain is migratory, burning, tender, sore, aching, sharp, radiating).
Thirdly, question the patient about his/her sleep habits and environment. If possible, ask the sleep partner if the patient snores or kicks while asleep. The clinician needs to know how long it takes for the patient to fall asleep and how many times he or she awakens. Ask patients how they feel in the morning.
Pellegrino and the author suggest that physicians obtain information about the patient's diet, particularly caffeine and carbohydrate intake. The history should include any symptoms that may indicate the presence of one or more of the coexisting conditions. Information on medications, exercise, and fatigue also is important. List any allergies and perpetuating factors.
Unfortunately, no medical test or x-ray can help provide definitive diagnosis of fibromyalgia, although these tests can help evaluate suspected coexisting conditions or rule out other possible diseases. Prior to 1990, there were no guidelines for evaluating and diagnosing fibromyalgia.
To reduce misdiagnosis and confusion, the American College of Rheumatology (ACR) recognized the need to establish a clear definition and guidelines. They sponsored a multicenter study to develop these criteria. In 1992, at the Second World Congress on Myofascial Pain and Fibromyalgia, the diagnostic criteria were expanded and refined.
The diagnostic criteria include 2 basic requirements. The first is the presence of pain in all 4 quadrants of the body, as well as in the axial skeleton on a more or less continuous basis for at least 3 months. The pain often is described as widespread or global. The second criterion is the presence of at least 11 of 18 anatomically specific tender points. A tender point hurts only at the area where pressure (enough to cause the examiner's nail bed to blanch, or about 4 kg) is applied, and there is no referred pain. An instrument known as a dolorimeter can be used to apply exactly 4 kg of pressure over the tender points during the examination. The 18 possible tender points exist as 9 pairs. Tender points may be found in any palpable muscle, but there are 18 sites that have been found to be present consistently in patients with fibromyalgia and are used for diagnosis. The ACR criteria describe 4 pairs of tender points on the anterior of the body and 5 pairs on the posterior of the body.
Some authors have noted that the typical patient has seen an average of 15 physicians and has been affected for approximately 5 years prior to being diagnosed correctly with fibromyalgia. Many patients are misdiagnosed and endure costly treatments that provide little benefit. At some point, most patients have been told that nothing is medically wrong and that the condition is all in their heads. Many patients are frustrated and skeptical. Although most are relieved when a correct diagnosis finally is made, some patients affirm that the clinician may need to convince the patient that he or she actually knows what is wrong and that there is a treatment plan.
Most patients with fibromyalgia are female and do not appear chronically ill. They may look fatigued or agitated. Their chief complaint is often "I hurt all over all the time." The quality of their constant pain is described as burning, aching, and soreness. They may feel as if they are bruised all over but without visible signs. Although the pain is constant, the location migrates and the intensity varies. Many patients may complain of only a single painful area, such as the low back or neck. A careful history reveals that their pain is not focal in its distribution but global. Initially, they may complain of pain at one site because they tend to be concerned primarily with their worst pain. Since many patients do not understand that the symptoms are connected, they give a fragmented history. The physician must ask the right questions to develop a complete understanding of the patient's pain distribution.
Patients generally do not tell the physician that they have a sleeping disorder. Again, a carefully taken history reveals unrefreshing sleep in about 65% of patients and morning fatigue in about 80% according to recent studies. Patients awaken as tired as they were before sleeping. Most patients awaken frequently throughout the night, and some have difficulty falling asleep. Generally, they finally fall asleep in the early morning hours, describing this as their best sleep. Many patients fall asleep immediately, deny sleep onset problems, and report only infrequent awakenings. Sleep onset this rapid is abnormal and should not be overlooked. Most patients complain of morning stiffness of variable duration. Question the sleeping partner about lower extremity movements. Approximately 20% of fibromyalgia patients have concomitant restless legs syndrome, the presence of which may lead the physician to choose or add medications other than antidepressants to the treatment.
The patients report their fatigue is second only to pain. The fatigue is worse in the morning and early evening. By ten or eleven o'clock in the morning, the fatigue subsides somewhat. Several investigators, including this author, have found patients' fatigue is worsened by poor sleep, physical activity, and diet.
These patients may not admit to feeling depressed or anxious; therefore, the physician must inquire. The source of their emotional stress may be multifactorial.
Several studies show approximately 50% of patients present with complaints of tissues feeling swollen and numbness and tingling in the extremities. These symptoms generally are more common in the upper extremities than in the lower extremities. Objective swelling, sensory changes, and other neurologic findings usually are absent.
Some investigators list many other common complaints, including chronic headaches and tenderness of the scalp to the touch. Complaints of chest pain, shortness of breath, and palpitations are common. Serious cardiac problems should be considered and may require extensive evaluation. Many of these patients' symptoms are related to mitral valve prolapse syndrome. Approximately 40% of patients with fibromyalgia describe symptoms of alternating diarrhea and constipation, bloating, cramping, and an increased urge to defecate. These symptoms most likely are related to irritable bowel syndrome. Some patients also may complain of symptoms that include urgency, frequency, and a sense of incomplete voiding. Pelvic pain and dysmenorrhea may be present as well.
Several medical conditions and diseases are thought to coexist frequently with fibromyalgia. These coexisting conditions can aggravate and perpetuate symptoms. Left unrecognized, the physician inadvertently might prescribe an ineffective or even harmful treatment regimen, leading to costly and unnecessary testing. Several of the most common conditions are discussed briefly. The most common associated conditions include the following:
Sleep is not a state of massive system shutdown, but quite the contrary. During sleep, the brain is very active, constantly communicating with the body. Many neurohormones, antibodies, and other molecules also are synthesized during sleep; therefore, when sleep is disrupted, biochemical abnormalities can occur, leading to multisystem disturbances.
Sleep studies have shown that patients with fibromyalgia have disordered sleep physiology. Most of these patients experience unrefreshing sleep with morning fatigue.
To understand abnormal sleep architecture, it is essential to know the basics of normal sleep. Sleep can be divided into 2 main parts, nonrapid eye movement (NREM) and rapid eye movement (REM) sleep, which alternate cyclically through the night, always starting with NREM sleep. In each successive NREM and REM cycle through the night, the amount of NREM sleep decreases and the amount of REM sleep progressively increases. Each cycle, NREM plus REM, lasts about 90 minutes. NREM is divided even further into 4 stages: stage 1 is initial drowsiness; stage 2 is light sleep; and stages 3 and 4 are progressively deeper levels of sleep.
In stages 3 and 4 of NREM sleep, the electroencephalogram (EEG) shows a pattern called delta waves, which are high-amplitude waves (greater than 75 mV) that move slowly (0.5-2 Hz). Much of the body's regulatory work, as well as synthesis of many substances (eg, antibodies, growth hormone, other neurochemicals), occurs during NREM sleep.
REM sleep has a low-voltage mixed-frequency pattern on EEG and is considered dream sleep. In this stage, the body has a complete loss of muscle tone, known as flaccid paralysis, and cannot move. During this part of sleep, consolidation of memories may occur, but there is still disagreement over exactly what occurs with memory during REM sleep. Some investigators found that during waking hours, the brain generates alpha waves with a frequency of 7.5-11 Hz.
Sleep dysfunction is considered an integral feature of fibromyalgia syndrome. Seventy percent of patients with fibromyalgia recognize a connection with poor sleep and an increased pain, along with feeling unrefreshed, fatigued, and emotionally distressed. Several studies have linked abnormal sleep with these symptoms.
Some researchers have studied fibromyalgia and sleep, confirming the disordered sleep physiology in fibromyalgia. This abnormality has been identified as an alpha-wave intrusion sleep anomaly, which occurs during NREM stage-4 sleep. This intrusion into deep sleep causes the patient to awaken or to be aroused into a lighter level of sleep.
Some authors describe the altered sleep physiology and somatic symptoms as a nonrestorative sleep syndrome. This sleep dysfunction is believed to be linked to the numerous metabolic disturbances associated with fibromyalgia, including abnormal levels of neurotransmitters (serotonin, substance P) and neuroendocrine and immune substances (growth hormone, cortisol, and interleukin-1). These authors propose that these metabolic imbalances are responsible for the increase in symptoms associated with this alpha-wave intrusion sleep disorder by impairing tissue repair and disturbing the immunoregulatory role of sleep. Studies show that the greatest amount of alpha-wave intrusions occur during the first few hours of sleep, decreasing throughout the night to normal levels by early morning. Some researchers note that this hypothesis correlates well with patients' frequent reporting that their best sleep is obtained in the early morning hours just prior to arising.
Depression in fibromyalgia is a controversial topic. In support of the contention that fibromyalgia is not a psychiatric illness, some authors believe that no correlation exists between fibromyalgia symptoms and psychological factors; others have determined that fibromyalgia is not a psychiatric disorder. The depression associated with fibromyalgia is believed to result from the pain, sleep deprivation, and dysfunction.
Depression in fibromyalgia may be treated with a regimen that includes nonpharmaceuticals. Antidepressants may help, but the clinician also should address other symptoms, such as fatigue or pain. Modifying diet and practicing good sleep hygiene are crucial. Starting a rehabilitation exercise program also is important. Some authors suggest that behavioral modification techniques and stress management also should be employed.
Myofascial pain syndrome
Fibromyalgia and myofascial pain syndrome may coexist, presenting a complex clinical picture; however, fibromyalgia and myofascial pain syndrome are not one and the same condition. As stated, fibromyalgia is a generalized amplification of pain or hypersensitivity condition and is associated with tender points in the muscles. Tender points are focal areas of muscle tissue that are exquisitely tender to compression. The tender points of fibromyalgia are painful locally at the site where the pressure is applied, without referred pain to distant areas.
By contrast, myofascial pain syndrome is considered in the narrow definition to be a disorder of trigger points. Similar to tender points, trigger points also are discreet areas in muscle tissue and/or its associated fascia that are exquisitely tender to compression; however, unlike tender points, when pressure is applied to the trigger point, pain occurs not only at the site of the applied pressure, but also at a distant site (zone of pain referral). Trigger points are found in taut bands (firm elongated bands) within the muscle fibers and are associated with the local twitch response. This local twitch response is an involuntary transient contraction of the taut band muscle fibers and can be elicited by snapping or pinching the taut band. Some authors assert that both disorders (fibromyalgia and myofascial pain syndrome) can magnify and perpetuate the symptoms of the other.
Several differences have been noted between fibromyalgia and myofascial pain syndrome, and a few mentioned by some investigators are listed below. A more detailed review of the similarities and differences in these 2 syndromes is found in Acupuncture: Trigger Points and Musculoskeletal Pain (1993) by a leading British physician and acupuncturist, DP Baldry.
Central nervous system imbalances have been linked to cognitive dysfunction or "fibrofog." This condition may cause some patients the most disability. According to some investigators, such symptoms include confusion and forgetfulness, inability to concentrate and recall simple words and numbers, and transposing words and numbers. Often, their cognitive functions are so impaired that they are unable to perform their usual activities of daily living (ADL), and the patient may get lost in familiar places or not be able to communicate effectively. Those patients who work face the fear of losing their jobs. Some school-aged patients drop out because of their inability to complete schoolwork.
Advances in noninvasive technology have made it possible to visualize the brain. New methods such as single photon emission computed tomography (SPECT) scanning have helped define some of the abnormalities linked to the cognitive dysfunction. Studies involving SPECT scanning show decreased blood flow in the area of the right and left caudate nuclei and thalami in fibromyalgia patients. Cognitive dysfunction may be caused by abnormal levels of neurotransmitters such as substance P, serotonin, dopamine, norepinephrine, and epinephrine. Some investigators claim that neuroendocrine imbalance of the HPA axis also may play a role in fibrofog. Others studies have implicated yeast overload, water retention, and glial cell abnormalities as causes of cognitive dysfunction in fibromyalgia.
Physical: The goal of the physical examination is to confirm the diagnosis, rule out concomitant systemic diseases, and recognize the presence of common coexisting conditions. The examination should include neurologic, joint, and musculoskeletal evaluations. Note the presence of swelling, deformities, and erythema. Examine the patient's gait, joint range of motion (ROM), and posture for structural asymmetry and skeletal deficiencies. Palpate the soft issues for tone, spasm, and tender points. Also check for taut bands, twitch responses, and trigger points; their presence signals the coexistence of a myofascial pain syndrome.
The standard criterion for diagnosis of fibromyalgia is the presence of 11 of 18 designated tender points. Other tender points may be present and also should be recorded. Some patients may present with less than 11 tender points. Experts contend that fibromyalgia can be diagnosed with as few as 8 or 9 tender points if other symptoms are present, such as sleep problems, fatigue, and any of the characteristic coexisting conditions.
The 1990 ACR criteria for the location of tender points are as follows:
Causes: No cause for fibromyalgia has been accepted universally, although there are many theories. Some authors suggest that there may even be an inheritance factor. Ongoing research may soon elucidate the cause(s).
| Lab Studies:
Other Treatment (injection, manipulation,
Trigger point injection is an important technique to provide mechanical disruption (myolysis) of the trigger point. Disruption leads to reduction of pain and an increase in ROM, exercise tolerance, and circulation; therefore, it is a valuable tool in the treatment of patients with tender points and trigger points. Long-term outcomes improve when trigger point injections are used in conjunction with physical therapy, massage therapy, or home stretching exercises.
Both dry needling and needling with infiltration are effective in eliminating trigger points and tender points. Many authors report that needling with infiltration is most effective. Patients with fibromyalgia who receive trigger point injections have shown significant improvement in pain intensity and pain threshold and improvement of ROM after trigger point injection. These patients may experience a delayed improvement of their pain but an immediate improvement in ROM following injection. They also experience more severe soreness that develops sooner and lasts longer following injection.
A number of both materials and techniques are used for needling with infiltration. Most physicians prefer either 1% lidocaine without epinephrine or 0.5% procaine. Lidocaine often is chosen over procaine because of fewer allergic reactions, more rapid onset of action, and greater potency. Steroids generally are not indicated or recommended for trigger point injections in patients with fibromyalgia. Sterile saline can be used in patients allergic to local anesthetics.
When performing a trigger point injection, use a sufficiently long needle. Usually an extensive area must be infiltrated, so a relatively large volume (2-12 mL) is injected. Before injecting the local anesthetic, make certain that the needle is in the trigger point. Localization of the trigger point is ascertained when the needle either causes a marked increase in pain with referral pain, a fasciculation is seen or felt, or both.
Several contraindications to trigger point injections
must be observed. Avoid trigger point injections in patients with local or systemic
infection. Patients with bleeding disorders or who are taking anticoagulation medication
should not have trigger point injections without proper medical evaluation and only after
the risks and benefits are explained clearly to them.
Fibromyalgia patients have difficulty tolerating regular doses of most medications and supplements; they are very sensitive to medications, and side effects are common. To avoid these problems, use the lowest dose available or perhaps half to a quarter of the lowest recommended dose.
Several medications should be avoided or used very carefully. Most investigators recommend using narcotics sparingly. In fibromyalgia without concomitant rheumatic illnesses, steroids are not helpful and should be avoided.
Avoid complications and confusion by providing written instructions and drug information. These instructions need to be easy to understand. Patients should be instructed to consult their physicians before starting any over-the-counter (OTC) medications or supplements to avoid potentially harmful drug interactions.
Useful medications for treating fibromyalgia
Drug Category: Antidepressants -- These drugs are used not only to treat depression, but also to improve sleep and pain. Antidepressants increase CNS serotonin. Delta-wave sleep also improves. The end result is an improvement of the symptoms experienced by patients with fibromyalgia.
Drug Category: Anticonvulsants -- Clonazepam is a benzodiazepine used to control anxiety and improve sleep. Also used to control seizures.
Drug Category: Nonbenzodiazepine hypnotic -- Used to improve sleep onset and maintenance
Drug Category: Muscle relaxants -- Helpful in short-term management of muscle spasms along with rehabilitation measures.
Drug Category: Narcotic analgesics -- These agents should be used for the short-term relief of pain.
Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDS) -- Used to help control the pain associated with fibromyalgia. Although effects in treatment of pain tend to be patient specific, ibuprofen is usually DOC for initial therapy. Other options include flurbiprofen, ketoprofen, and naproxen.
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