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Fibromyalgia Syndrome (FMS)

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Author:    Julia Tortorice (RN, MBA, MSN, NEA-BC, CPHQ)

History

Fibromyalgia is a syndrome many medical professionals may not have heard of until a few years ago. In fact, it was first described in medical literature in the 1940s by Doctor Hencha in a rheumatology textbook (Fibromyalgia.com 2009). Later, the term was used by Mohammed Yunus in1981 in a presentation to a scientific seminar on arthritis and rheumatism. Muscular rheumatism and fiobrositis were early names given to similar sets of symptoms. The American College of Rheumatology developed diagnostic criteria in 1990 (Dellwo About.com 2009).

Fibromyalgia syndrome (FMS) was long ignored and misunderstood by medical personnel and the public. Even though fibromyalgia is a relatively new term, the symptoms existed long before it was recognized as a syndrome; perhaps thousands of years ago (Fibromyalgia.com 2009).

“Is there nothing to you all that pass by behold and see is there any pain likened to my pain which is done unto me wherewith the Lord has afflicted me in the day of his fierce anger? From above, he set fire to my bones…and I am weary and faint all day” Lamentations 11:12-13.

“…And whereas the nights are appointed to me when I lie down I say ‘When shall I arise and the night be gone’ and am I full of tossing to and fro unto the dawning of the day…and the days of affliction have taken a hold upon me. My bones are pierced in me in the night season, and my sinews take no rest” Job 7:3-4, 30:16-17.

Fibromyalgia literally means pain in muscle fibers. There is chronic, sometimes debilitating fatigue associated with the pain. The syndrome is invisible yet real and affects the quality of life. Many patients cannot maintain their jobs due to pain and chronic fatigue (Dellwo about.com 2009). It is a biopsychosocial syndrome. It affects all three aspects of human life; biological, psychological, and social. The brain cannot separate the three and neither can the patient. The medical team should treat all three areas as well (Winfield 2009).

 

Diagnosis

There is no definitive diagnosis for fibromyalgia, X-rays and lab values are all normal and for many years sufferers were told, “It is all in your head”. The first step in the diagnosis of FMS is to rule out other similar diseases such as rheumatoid arthritis, lupus, osteoarthritis or TMJ. These diseases, if present, must be treated. Many of them may occur concurrently with FMS. The inability to diagnose fibromyalgia has been a problem for patients and physicians. Patients spend thousands of dollars seeking a diagnosis and are frustrated by continuing symptoms and lack of compassion from physicians and their families. Family members are frustrated because the patient does not “look sick”. One patient described it this way, “It was the ‘not knowing’ what was wrong with me that was difficult. I know people did not believe I was sick. It was so frustrating to be sick and in pain all the time and get no relief. I actually thought I’d be better off dead” Often, the patient is first met with skepticism and doubt by health care professionals and families. Diagnosis may take months or years and many visits to different health care providers seeking relief of symptoms and a diagnosis.
Fibromyalgia is diagnosed on the basis of widespread pain and increased pain in 11 of the 18 tender points when pressure is applied in these areas. Pressure should be applied in other random points. The patient with fibromyalgia can tell the difference in pain and will respond differently (Schultz 2004, Winfield, 2009).

The Antipolymer Antibody Assay (APA) is a new potential diagnostic test for FMS. It can detect changes in the immune system of FMS patients not found in others. The level of antibody titers seems to relate directly to severity of symptoms such as fatigue, depression, anxiety, and muscle stiffness. Changes in ASA may be the first evidence of a physiological abnormality rather than simply a psychological basis of the syndrome. The APA Assay is not approved for diagnostic use in the United States at this time but FDA clinical trials are promising (Wilson www.autoimmune.com 2007).

Fibromyalgia may exist in children. What once was considered to be growing pains may be FMS, especially when accompanied with sleep disorders (Neurology channel 2009).

Etiology

The pain and fatigue can make performance of everyday tasks difficult to almost impossible. Many patients are unable to continue working. They may lose their job related to absences or poor performance. With treatment, many patients can successfully continue working and perform activities of daily living. While the cause of this syndrome is unknown, several contributing factors such as sleep disorders, history of depression, and physical or psychological trauma at an early age have been recognized as potential contributing factors. Depression can be a causative factor in the development of fibromyalgia and fibromyalgia can lead to or worsen depression. Other causes that have been suggested are muscle hypoxia related to a functional inability of the muscles to use oxygen effectively. Abnormal deep phases of sleep has also been implicated

Due to the lack of evidence of a particular etiology, several areas have been studied. These areas of study include: Autoimmunity, since many sufferers also have forms of arthritis or lupus. Sex hormones, since FMS is much more common in women than in men, genetics since there is a familial connection. The best evidence at this time indicates that there may be alterations in perfusion to the brain as well as hormonal alterations (Eustice 2006) (Winfield 2009).

Winfield refers to this as “a self sustaining neuroendocrine cascade”. He continues, “In addition to strictly sensory-discriminative elements of nociception and afferent input from somatic reflexes, major contributions from pathways and regions of the brain that are associated with emotional, motivational, and cognitive aspects of pain are evident and help determine the subjective intensity of pain. The two principal effectors of the stress response, the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathetic nervous system (SNS), are also activated”.

FMS sufferers show altered blood flow in areas that recognize pain intensity and produce our emotional response to pain (Winfield 2006) (Verbunt et al 2009). In patients with fibromyalgia, there are deficiencies in substance P and serotonin. Substance P is a neurotransmitter that initiates pain signals following tissue injury and the process of pain perception. Serotonin is an important hormone known to reduce the perception of pain intensity and it also plays a role in regulation of sleep (Eustice 2006). In other words, the brain cannot control some impulses and frequently, ordinary sensations are felt as painful ones (Winfield, 2009). There are times of flare-ups and remission. Flare-ups may occur with stress, cold, damp weather, or over activity. There is no cure and treatment is directed toward symptom control (Winfield, 2009).

Symptoms

Symptoms of fibromyalgia are broad and variable. The main symptom is diffuse pain bilaterally over the entire body; above and below the waist. Pain has been described as a constant aching, burning pain all over the body. Since it involves muscles and joints, the pain is usually worse at attachment sites (Bierms and Helmuth 2009). The pain is severe and debilitating. In the words of one patient with fibromyalgia, “It hurts to wear clothes…I can’t even stand for the wind to blow on me.” There are tender points that elicit increased pain when pressure is applied to these areas. Tender points of fibromyalgia exist at these nine bilateral muscle locations:

  • Low Cervical Region: (front neck area) at anterior aspect of the interspaces between the transverse processes of C5-C7.
  • Second Rib: (front chest area) at second costochondral tender junctions.
  • Occiput: (back of the neck) at suboccipital muscle insertions.
  • Trapezius Muscle: (back shoulder area) at midpoint of the upper border.
  • Supraspinatus Muscle: (shoulder blade area) above the medial border of the scapular spine.
  • Lateral Epicondyle: (elbow area) 2 cm distal to the lateral epicondyle.
  • Gluteal: (rear end) at upper outer quadrant of the buttocks.
  • Greater Trochanter: (rear hip) posterior to the greater trochanteric prominence.
  • Knee: (knee area) at the medial fat pad proximal to the joint line.

Fibromyalgia is not an inflammatory disease. There are no lumps or nodes and there is no permanent damage to other body systems. The syndrome is not progressive, nor is it fatal (Robertson, 1999). Although the fibromyalgia patient may suffer from arthritis, chronic fatigue syndrome, and/or lupus, the diseases are distinctly different. Autoimmune disorders may be a contributing factor in development of FMS (Dewello, about.com 2009) (Winfield, 2009).

Fatigue, depression, joint stiffness, sleep problems, there is a disturbance in stage 4 or deep sleep and the patient awakens tired, sleepy, and unrefreshed (Robertson 1999). Headaches, cognitive disturbances, (confusion, disorientation, and forgetfulness; often called fibro fog) catastrophizing, dysmenorrhea, endometriosis, and irritable bowel syndrome (IBS) are frequently reported. In fact, the cognitive disturbances may cause impairments in working, episodic, and semantic memory that are equivalent to 20 years of aging (Winfield 2009). Symptoms may be different in different patients. They also vary at different times in the same patient. Fibromyalgia takes its own direction (Fibromyalgia.com).

Treatment

Treatment is a multidisciplinary effort and should include a rheumatologist, medical psychologist, physical therapist, exercise physiologist as well as a massage therapist (Dellwo, about.com). The goal is to relieve pain, improve sleep and relieve or reduce associated symptoms (Neurology channel 2009).

Treatment involves lifestyle changes such as changes in sleep routines for those experiencing sleep disturbances, stretching exercises and swimming in a warm pool, counseling, stress reduction, patient education, support groups, nutritious diet, complementary therapies; acupuncture, behavioral therapy, massage, and relaxation techniques along with prescribed medications (Winfield, 2009). The syndrome is managed, not cured.

There are several classes of medications prescribed to manage FMS symptoms. They include: anticonvulsants, analgesics, antidepressants, sleep medications, and muscle relaxants.

Anticonvulsants

Pregabalin (Lyrica) binds to voltage-gated calcium channels in central nervous system tissues. Pregabalin is an anti-epileptic. It affects the chemical messenger gamma aminobutyric acid (GABA), which helps prevent nerve cells from over-firing.

Side effects include peripheral edema, weight gain, dizziness, sleepiness, suicidal thoughts or actions, mood changes, dry mouth, blurred vision, hypersensitivity and possible angioedema.
Pregabalin is approved for treatment of

  • Fibromyalgia
  • Neuropathic pain associated with diabetic peripheral neuropathy
  • Postherpetic neuralgia

Gabapentin (Neutrontin) has been used as well.

Analgesics

Tramadol (Ultram) is commonly prescribed. The most common side effects are drowsiness, dizziness, constipation, and nausea. Tramadol should not be used in combination with tricyclic antidepressants. It may be given in combination with acetaminophen for increased pain relief. Side effects include nausea, vomiting, constipation, dizziness, and headache.

Opiods are commonly given for pain of FMS although they should be used with caution due to potential for dependency and potentiating effects on other medications. Opiods should be reserved for times relief cannot be obtained with other medications. When used, the patient should be evaluated frequently for degree of pain relief, and signs of dependency.

Antidepressants

Tricyclics are prescribed to aid sleep and reduce pain. They are normally prescribed in smaller doses than when used to treat depression. Tricyclics reduce alpha waves during stage 4 sleep, promoting restful sleep (Schultz et al 2004). They increase levels or serotonin and nor-epinephrine in nerve cells. Side effects include sedation, drowsiness, blurred vision, dry mouth urinary retention, constipation, weight gain, anorexia, sexual dysfunction. Adverse reactions include orthostatic hypotension, cardiac dysrhythmias, and extrapyramidal syndrome. Life threatening reactions include thrombocytopenia, leucopenia, seizures, and agranulocytosis. Tricyclics are contraindicated in acute myocardial infarction (AMI), narrow angle glaucoma, and prostate disease. Tricyclics should use with caution in liver or kidney disease (Kee 2006).

Selective Serotonin reuptake Inhibitors (SSRIs) SSRIs increase serotonin in nerve cells which reduces pain and increases sleep. SSRIs are contraindicated in acute myocardial infarction (AMI), taking in conjunction with MAOIs and should be used with caution in severe kidney or liver disease. Side effects include headache, insomnia, restlessness, GI problems, and sexual dysfunction. Adverse reaction to SSRIs may include seizures.

Serotonin-norepinephrine Reuptake Inhibitors (SNRIs) are used for depression, and anxiety. SNRIs increase the amounts of nor-epinephrine and serotonin available to the brain. They do not cause cardiovascular problems or sedation. Drugs in this category include duloxetene (Cymbalta) and venlafaxine (Effexor). Duloxetene is FDA approved for treating FMS. It has been shown to reduce pain by 30%. Side effects include GI distress: (nausea, dry mouth, constipation, decreased appetite), sleepiness, increased sweating, and agitation. It may also increase the risk of hemorrhage in patients taking NSAIDs, aspirin, or blood thinners (Winfield).

Milnacipran (Savalla), approved by the FDA in 2009, is a newer SNRI similar to Cymbalta but it increases norepinephrine levels more than serotonin levels. Side effects are said to be mild to moderate (Dellwo about.com). Side effects include excessive drowsiness, mood changes, and thoughts of suicide. Patients taking milnacipran should not drink alcohol and the drug should not be prescribed for patients on MAOIs.
Teach patients that compliance with medication regimen is important when taking anti depressants. Alcohol use should be avoided due to potential for addiction.

Antidepressants may be taken with food if GI disturbances occur. Advise patient to check weight at least weekly and rise slowly due to potential for orthostatic hypotension. The patient should know that herbal medications may interfere with antidepressants and should inform the health care provider of any herbal use.

Sleep medications

Zolpidem (Ambien), a CNS depressant and neurotransmitter inhibitor is frequently prescribed for FMS patients. It should be used with caution in patients with kidney or liver disease, the elderly or children. Side effects include drowsiness, lethargy, residual sedation, anxiety, confusion and disorientation. Patients may develop tolerance or dependence. It works rapidly; patients should be instructed to be ready for sleep when the drug is taken. Food decreases absorption (Kee 2006).

Eszopiclone (Lunesta) Lunesta is a non-benzodiazepam hypnotic drug used as a sleep aid. Side effects include chest pain, drowsiness, dry mouth, nausea and vomiting, decreased libido, puritis. It should be taken immediately before going to bed to prevent falls and should not be taken in close proximity to a high fat meal as this decreases absorption (Kee, 2006).

Muscle relaxants

Skeletal muscle relaxants (diazepam, meprobamate) are used to reduce muscle spasms and pain of fibromyalgia resulting from excitable neurons (Kee 2006). Centrally acting muscle relaxants (SOMA, Flexeril, Parafon Forte) depress the CNS. Most muscle relaxants should be taken with food to prevent GI upsets. Monitor liver function when the patient is taking carisoprodol (SOMA) or dantrolene (Dantrium) (Kee 2006). Side effects include dizziness, nausea and vomiting, headache and diplopia (Kee 2006).

Patient Education

FMS is real. Most individuals do not understand what they cannot see. Pain is invisible. The pain of fibromyalgia is real even though unseen. There is no bleeding, swelling, discoloration, or other visible abnormalities. Families and the public may have difficulty accepting the biophysical aspects of the disease. The FMS patient is encouraged to avoid withdrawal from favorite activities when possible. These activities provide pleasure and help the FMS patient avoid depression (Robertson 1999) (Schultz, 2004).

Exercises recommended for FMS should be gentle to prevent muscle damage. They should include stretching, and should be conducted on the floor or in a stable position because patients with FMs are prone to dizziness and falls should be avoided. The types of exercise should focus on aerobics, strength training and flexibility exercises. Recommended exercises are Tai Chi, pilates, yoga, or exercises in a warm pool (Robertson 1999) (Schultz 2004).

Bicycling and walking are other exercises that are beneficial. When riding a bike or if walking near the street, remember safety precautions. Monitor symptoms during and after exercising. Increased pain should be avoided. Take breaks and do not exercise on days when activity is high such as running errands, house work, etc. Start slowly and increase exercise times or levels as tolerated (Robertson 1999) (Schultz 2004).

Avoid “triggers” (activities or situations that cause increases in symptoms) as much as possible. Triggers may be different for different individuals. Common triggers are fatigue, lack of sleep, damp or cold weather, stress and overexertion.

Sleeping problems may cause changes in the immune system that cause pain, inflammation, fatigue, and decreased pain tolerance. Sleeplessness can be avoided by listening to soft music, consuming a warm non-alcoholic beverage, and relaxation techniques practiced before bed time. Avoid caffeine, exercise, and large meals 4-6 hours before bed time. Develop a routine for sleep and awakening and maintain the routine. If unable to fall asleep in 15-20 minutes, go to another room and perform a relaxing activity such as reading. When sleepy, return to bed. The bed should be used for sleep and sexual activity only.

Dressing appropriately for weather extremes and learning to deal with stress (biofeedback, hypnosis guided imagery, meditation) can also reduce triggers. Many sources question the helpfulness of bio feedback in FMS. The patient should select whatever therapy works.

Cognitive behavioral therapy (CBT) is an important part of the treatment component. It involves changes in attitude and response to negative situations. Participants attend sessions and learn how to view stressors differently. They may be asked to keep a diary of stressors and record any symptom changes during times of stress. They are expected to confront negative thoughts and behaviors, set limits, and prioritize activities. Many FMS patients have personalities that demand perfection and once they fall short of perfection, they believe they are failures. CBT can improve these attitudes and beliefs and help the patient overlook their lack of perfection.

Again, therapy should be selected, in conjunction with the physician, on an individual basis. Not all treatments work equally for all patients. Trial and error should be anticipated.

The nurse can be a patient advocate by acknowledgement of the reality and severity of the patient’s symptoms, encouraging active patient involvement in treatment and care decisions, remind the patient that there are no “instant cures”. The goal of treatment is to alleviate symptoms as much as possible and improve the quality of life. Remind the patient to identify and accept limitations on activity and assist them in making the most of their strengths while minimizing tasks that cannot be accomplished successfully (Robertson, 2006).

Conclusion

The public and many health care professionals have long regarded fibromyalgia as a mental health disease, therefore the symptoms are “made up” and not “real”. Many of the contributing factors may be related to the mind but the symptoms are “real” and debilitating. Fibromyalgia is a biopsychosocial syndrome and all aspects of the disease must be treated to alleviate symptoms and promote quality of life for the patient. Nurses are an important part of the treatment team and can focus advocating for the patient as well as patient and family education. Research is ongoing and can provide answers to the many questions about fibromyalgia.

References

Bierma P, Helmuth L, fibromyalgia: gaining ground on the “invisible disability. Retrieved on 10/27/2009

Dellwo A, (2009) mind body fibromyalgia treatments: biofeedback, hypnotherapy, and cognitive behavioral therapy. Retrieved on 11/21/2009 from http://chronicfatigue.about.com/od/alternativetreatments/a/mindbodyFMS.htm.

Dellwo A, (2009) the broad range of fibromyalgia drugs. Retrieved on 10/20/1009 from http://chronicfatigue.about.com/od/treating MSCFS/a/fibromyalgia.htm.

Eustice C, Eustice R (2006) Part 1 fibromyalgia: researching the cause of fibromyalgia syndrome (the role of sleep, muscles, substance p, and serotonin) .Retrieved on 10/22/2009 from http://arthritis.about.com/cs/a/fmscause.htm.

Eustice C, Eustice R (2006) Part 2 fibromyalgia: researching the cause (the role of hormones, genetics, and autoimmunity) retrieved on 10/22/2009 from http://arthritis.about.com/cs/a/fmscause.htm.

Key J, Hayes E, (2006) Pharmacology: a nursing process approach. Saunders. St Louis.

Pujol J, López-Solà M, Ortiz H, Vilanova JC, Harrison BJ, et al. (2009) Mapping Brain Response to Pain in Fibromyalgia Patients Using Temporal Analysis of MRI. PLoS ONE 4(4): e5224. doi:10.1371/journal.pone.0005224.

Robertson T, (1999) Alberta RN misunderstood illnesses: fibromyalgia and chronic fatigue syndrome. 55(5).

Schultz, M, Hernandez N, Hernandez, J RN Web. Help patients cope with fibromyalgia. Retrieved on 10/23/2009 from http://license.icopyright.net/user/viewFreeuse.act?fuid=NTYzOTQ2Nw==.

Verbunt JA, Pernot DH, Smeets RJ. (2008) Disability and quality of life in patients with fibromyalgia. Health Qual Life Outcomes. 6 (8).

Winfield J, (2009) fibromyalgia. Retrieved on 10/27/2009 from http://emedicine.medscape.com/article/329838

Wilson R, the anti-polymer antibody assay (APA assay) and fibromyalgia syndrome. Retrieved on 11/10/2009from autoimmune.com 2007.

Yunus, M; Masi, A; Calabro, J; Miller, Ka; Feigenbaum, S (Aug 1981). "Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls". Seminars in arthritis and rheumatism 11 (1): 151–71.