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7 Articles in Volume 14, Issue #7
Fibromyalgia: What Clinicians Need to Know
Interactions Between Pain Medications and Illicit Street Drugs
Arachnoiditis Part 1: Clinical Description
Meralgia Paresthetica—A Common Cause of Thigh Pain
Editor's Memo: Real Progress—Non-Opioid Advances in Pain Management
Ask the Expert: Dependence vs. Addiction
Letters to the Editor August 2014

Fibromyalgia: What Clinicians Need to Know

The most successful medical treatment of fibromyalgia is a interdisciplinary approach.

Fibromyalgia (FM) is a syndrome manifested by widespread pain, stiffness, fatigue, cognitive difficulties (“fibrofog”), and non-refreshing sleep. Despite numerous articles, revised diagnostic guidelines, and FDA-approved medications, there are still physicians who believe that the disorder is not real and consider it a “wastebasket” diagnosis—given when no other pathological entity is found.

In ICD-9, there is no specific diagnosis for FM (or myofascial pain syndrome; both would fall under myositis). For many clinicians in the field, this represents a lack of “respect” for the diagnosis.

Much has changed about our understanding of the etiology of FM since the beginning of this millenium. The disorder now is considered a central sensitivity syndrome (CSS) because of its basic neurophysiological etiology. This makes FM a neurosensory disorder associated with difficulties with pain processing by the central nervous system (CNS).1,2

This also ties FM, which is estimated to effect 2% to 5% of the population, to other similar, if not overlapping, conditions, including chronic fatigue syndrome, interstitial cystitis, irritable bowel syndrome, vulvodynia, post-traumatic stress disorder, and others.3 Some groups also classify migraine as a CSS. However, migraine has an apparent physiologic basis (with a possible generator in the trigeminal nucleus caudalis) and is relieved by medications (triptans), which work via specific serotonergic receptor agonists (5-HT1BDF); this does not occur in a true CSS.

FM also may overlap with other regional pain syndromes, as well as anxiety and mood disorders, which may lead to incorrect primary diagnoses. FM may be considered primary or secondary to an associated disorder, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and chronic hepatitis C infection. It is important to identify the primary and the secondary clinical issue. For example, the treatment for the primary cause (SLE or RA) also will enable appropriate treatment of FM.

Still, FM may be a diagnosis of exclusion, and entities that can cause similar symptoms must be looked for and/or ruled out. This article will review the recent research into the diagnosis and etiology of FM, as well as updated treatment guidelines.

Diagnosing FM

The diagnosis of FM is made both by the art and science of medicine. The basic signs and symptoms of FM include persistent (≥3 months) widespread pain (tenderness/pain on both sides of the body, above and below the waist, including the axial skeletal spine), along with stiffness, fatigue, non-refreshing sleep, cognitive difficulties, and many other unexplained symptoms, including anxiety and/or depression as well as loss of the ability to perform activities of daily living (ADL). Table 1 reviews the evolution of FM diagnosis.

Diagnostic Criteria

In 1990, the American College of Rheumatology (ACR) endorsed a set of diagnostic criteria for FM developed by a group of researchers led by Frederick Wolfe, MD.4 The criteria originally were developed for recruiting patients for clinical studies and included a physical examination as well as tender point testing (typically 11/18 active symmetrical tender points was considered “positive”). Critics noted that the ACR 1990 criteria made it more difficult to accurately diagnose patients with FM.5

Objections to the physical examination led the ACR to revise its diagnostic criteria in 2010.6 The goal of the new criteria was to create a simple, practical guide for the clinical diagnosis of FM that could be used in a community setting. It included 2 scales, the widespread pain index (WPI), which allowed patients to describe where in the body it hurt, and the symptom severity scale (SSS), which measured fatigue, daytime sleepiness, somatic symptoms, and cognitive problems.

The 2010 ACR guidelines were further modified in 2011 (2011ModCr), at which time the physician estimate of somatic symptoms was eliminated and the WPI and SSS were expanded.7 The new 0-31 FM symptom scale (FS) included 19 pain locations and 6 self-reported symptoms, including difficulty sleeping, fatigue, poor cognition, headache, depression, and abdominal pain.6

To evaluate the validity of the new scale, Wolfe et al administered a questionnaire to 729 patient previously diagnosed with FM, 845 with osteoarthritis (OA) or with other noninflammatory rheumatic conditions, 439 with SLE, and 5,210 with RA. The authors found a score ≥13 correctly classified 93% of patients (sensitivity, 96.6%; specificity, 91.8%).

To further study the new questionnaire, Bennett et al performed a study to help validate the 2011ModCr.8 The research team studied chronic pain and psychiatric patients from various sites in the US. The study of the 2011ModCr found diagnostic sensitivity of 83.5% and specificity of 67.2%; and correctly classified 73.8% of patients with FM compared with the 1990 criteria. An alternate criteria (2013MedCr) was less sensitive (80.7%) but had higher specificity (79.6%); it classified 80.1% of patients correctly.8

Both the 2011ModCr and 2013ModCr found an increased prevalence of FM in men (16% for 2011ModCr and 14% for the 2013AltCr), as compared with that found with the ACR 1990 criteria (6%).8 An example of the current diagnostic questions/criteria taken from the Fibromyalgia Network.9

Other Exams

Although the new ACR criteria do not specify the need for a physical examination in the diagnosis of FM, it is appropriate. It also would be appropriate to assess tenderness, but a formal tender point examination is not required, nor “counted” in the diagnostic criteria.

There are no specific lab markers available to diagnose FM. When a clinician obtains a history that gives a possible indication of specific problems, that information should be explored using further tests. Table 2 lists the blood tests typically ordered by the author. In addition to the tests listed, the author orders rheumatoid factor, depending on any leading history or signs/symptoms. Although not totally verified, genetic markers (HLA-B27, HLA-B51, and FMF) may be considered based on clinical suspicion, but they should not be used to “rule-out” the diagnosis if the 2011ModCr indicate it. Epigenetics developed a blood test to diagnosis FM (FM/a test), but questions have been raised about inconclusive test results and undue influence by the manufactuerer.10 Experts such as Wolfe do not consider the test to be diagnostic of FM.11

Central Sensitivity Syndromes

As noted, it is now thought that FM is a problem with central pain processing: a CSS. It has been described as a problem with “volume control”—FM patients have a lower threshold for responding to pain, as well as other stimuli, such as heat, noise, and even strong odors. Patients with FM also may have developed such hypersensitivities secondary to neurobiologic changes that may affect their perception of pain or because of hypervigilance, or heightened expectancy, both of which may be secondary to psychological factors.12

There is a long list of metabolic, biochemical, hormonal, immunoregulatory, and CNS abnormalities that could contribute to the development of FM that have been described in great detail in a previous publication.13 Predispositions include genetics, as well as early childhood issues/trauma, and learned behavior.

There are overlaps between pathophysiological mechanisms that are acknowledged to be associated with FM and other CSS disorders. This would involve how the CNS processes pain, and may involve abnormalities in this intrinsic function that may essentially be sensory amplification. Many patients with CSS have apparent hyperalgesia and/or allodynia (pain associated with stimulus that normally provokes no pain).

Moreover, this increasing sensitivity appears to be found with visual and auditory stimuli. This may indicate a fundamental CNS problem with intrinsic pain or sensory amplification but not a structural or specific inflammatory condition in a specific body part and/or region. This would lead to the conclusion that all individuals (with and without pain/FM/CSS) have different “volume control settings” controlling their pain and sensory processing.14

If a patient’s pain and sensory sensitivity were illustrated as a bell-shaped curve over the course of his/her lifetime, genetics, early childhood issues/trauma, and learned behavior would illustrate the wind-up phase. Along with pain and sensory amplification, FM patients may experience an epiphenomena, such neurogenic inflammation of the mucosal surfaces, which may lead to increased mast cells and the appearance of a mild neuroinflammatory process, autonomic nervous system (ANS) dysfunction, and endocrinopathy—including a hypothalamic pituitary dysfunction.13

Similar types of therapies are efficacious for many or most of the CSS conditions, including pharmacological (using tricyclic antidepressants [TCAs], for example) as well as non-pharmacological treatments (exercise and cognitive behavioral therapy [CBT]). Patients with these conditions who have pain do not respond to therapies that would be helpful if they were due to damage or tissue inflammation, such as opioids, non-steroidal anti-inflammatory drugs, local injections, and surgery.13


We know that the pain threshold is lower in FM patients than in controls. Patients with FM have tenderness, not limited to the tender points but throughout the body. A number of studies have shown that this is not secondary to hypervigilance.14-21 Rather, when random pressure was applied, the pain experience was not influenced by levels of distress. The investigators concluded that FM patients were no more hypervigilant than controls.

Gracely et al evaluated the brains of patients with FM and controls during stimuli and responses using magnetic resonance imaging (MRI).22 They found that similar pain intensities, produced by significantly less pressure in FM patients, resulted in overlapping or adjacent activations in the contralateral primary somatosensory cortex (SI), inferior parietal lobule (IPL), secondary somatosensory cortex (SII), superior temporal gyrus (STG), insula, and putamen, as well as in the ipsilateral cerebellum. In the FM group, a relatively low stimulus pressure (2.4 kg/cm2) produced a high pain level. In the stimulus pressure control group, administration of a similar stimulus pressure (2.33 kg/cm2) produced a very low level of rated pain. In the subjective pain control group, administration of significantly greater stimulus pressures (4.16 kg/cm2) produced levels of pain similar to those produced in patients by lower stimulus pressures.

FM patients show a low noxious threshold to auditory tones, implicating a more global problem in sensory processing, in at least some patients. The idea that FM and related CSSs may represent biological amplification of all sensory stimuli has strong support from functional imaging studies (fMRI) that suggest that the insula is the most consistently hyperactive region.23

Insula Cortex

The insula (or insular cortex) plays a role in survival needs, including visceral sensation and autonomic functions. Damasio and Damasio proposed that the insula consists of somatic markers and hypothesized that this part of the cortex maps the bodily states associated with our emotional experiences, thus giving rise to conscious feelings and “embodied cognition,” or conscious rational thought that cannot be separated from emotions.24

The insula provides the emotional context suitable for a given sensory experience. It integrates information about the state of the body, making it available to higher-order cognitive and emotional processes; it receives homeostatic sensory inputs via the thalamus and sends outputs to the limbic system structures, including the amygdala, the ventral striatum, and the orbitofrontal cortex.

The insula has been shown to be associated with pain processes, as well as basic emotions, such as anger, fear, disgust, joy, and sadness. These emotions may be combined with the nociceptive feelings of pain, and may, thereby, change the context of the pain. The most anterior part of the insula is regarded as part of the limbic system because it is deeply involved in conscious desires (ie, the active search for food or drugs). Looked at another way, the anterior part of the insula in the right hemisphere may enable more precise decoding of bodily states, for example, the capability of translating a bad odor to feelings of disgust.

Pathoetiology of FM

There are 3 hypotheses that the author believes may play a part in the pathoetiology of FM. FM is:

  • Central sensitization secondary to constant peripheral nociception (pain amplification)
  • A failure of the descending pain pathway (antinociceptive)
  • A dysfunction of m-opioid receptors, possibly contributing to the failure of the descending pain pathway.

To begin to understand FM, the clinician has to understand the nociceptive and antinociceptive systems, as well as the neurochemistry involved. For more information on this, see Practical Guide to Chronic Pain Syndromes.13

Patients with FM exhibit hyperalgesia to mechanical, thermal, and electrical stimulation. The mechanisms of hyperalgesia include sensitization of vanilloid receptors, acid-sensing ion channel receptors, and purino-receptors.25 Tissue modulators of inflammation and nerve growth factor can excite these receptors, leading to changes in pain sensitivity.

Clinically, first pain is described as sharp/lancinating, whereas second pain (associated with chronic pain) is dull, aching, or burning. Both enhanced temporal summation of second pain (windup) and central sensitization has been described in FM. They occur after prolonged C-fiber nociceptive input and depend on activation of specific nociceptive neurons and wide dynamic range neurons in the dorsal horn of the spinal cord. They also rely on both spinal cord and supraspinal mechanisms that facilitate and inhibit pain.13,26

Brain imaging studies provide evidence of abnormal central pain mechanisms in FM. Corroboration of augmented pain experienced by FM patients is seen, as well as thalamic activity that is decreased in FM patients (the thalamus, of course, contributes to pain processing).13,26

Changes in the autonomic nervous system and in the hypothalamic-pituitary-adrenal axis also are seen in patients with FM. There is reduced reactivity in the central pain processing in FM, leading to hyperalgesia, allodynia, and abnormal temporal summation of second pain. All muscle studies to date have been negative.27-30

Russo and others postulate that FM may be secondary to a clinical endocannabinoid deficiency.31-35 This would explain the therapeutic benefit from exogenous and possible endogenous cannabinoids. In one randomized clinical trial, nabilone (Cesamet) showed promise in the treatment of FM.34 Mu receptors are close to, and may interact with, the cannabinoid receptors in the CNS.31-35 FM may be characterized by cortical or subcortical augmentation of pain processing or centrally mediated abnormal pain sensitivity (pain amplification).36-38

Changes in Gray Matter

Voxel-based morphometric studies have shown that compared with controls, patients with FM have decreases in gray matter in the prefrontal, cingulate, and insular cortex, which are significant regions of the pain pathways.39 Similar gray matter changes have been seen in patients with chronic low back pain, migraine, and many other chronic pain diatheses.40

A study by Kuchinad et al found that FM patients had significantly less total gray matter volume, and 33 times greater age-associated decreases in gray matter compared with controls.41 These changes were most notably seen in the cingulate and insular cortex, the medial frontal cortices, and the parahippocampal gyri. Decreases in gray matter also were seen in the right superior temporal gyrus and left posterior thalamus, and increased gray matter was noted in the left orbitofrontal cortex, the left cerebellum, and the bilateral striatum—all parts of the somatosensory system and the motor system.

The syndrome also is associated with significant changes in the cerebral microstructure of brain areas known to be functionally associated with core symptoms of FM.39-42

Central Sensitization

Central sensitization involves enhanced spinal cord and dorsal horn neuronal excitability associated with spontaneous neuronal activity; enlarged receptive fields in the spinal cord and augmentation of stimuli transmitted by both large and small diameter primary afferent fibers.43 Central sensitization may be secondary to activation of glial cells by neurotransmitters, cytokines, or chemokines. This may contribute to the neurophysiological enhancement of CNS mechanisms that lead to central sensitization.25

Repetitive stimulation of C-fibers will increase the discharges from second order neurons in the spinal cord. This will induce pain amplification related to the temporal summation of second pain (wind-up); N-methyl-D-aspartate (NDMA) receptors mediate wind-up, which is also inhibited by NMDA receptor antagonists.44,45

Central sensitization may be relevant to FM pain because it is frequently associated with extensive secondary hyperalgesia and allodynia. Psychophysiological studies show that input to central nociceptive pathways is abnormally processed in FM.46

Failure of Descending Pain Pathway

Yunus and Inanici, however, raised the possibility of an “intrinsic” central sensitization in susceptible FM patients.47 This would be a central sensitivity rather than a central sensitization and would occur, possibly, with a peripheral nociceptive stimulus. The authors note that this may occur secondary to defective inhibitory systems or a “hyperstimulated facilitatory pathway and/or generalized hyperexcitement of peripheral nociceptors.”48

Mu-Receptor Dysfunction

The final hypothesis states that FM patients appear to have impaired functioning of the mu-opioid receptor, diminishing the brain’s ability to process and respond to pain stimuli. Abnormal pain signal processing is associated with reduced opioid receptor binding. Staud et al have suggested that the brain’s normal pain-inhibiting processes malfunction in FM patients.49 This certainly may be the reason that opioids don’t typically help pain in FM patients.13

Staud et al found that opioid receptor binding was reduced in certain brain regions, such as the right posterior insula, left medial insula, left orbital frontal cortex, and right amygdala. When the binding of opioid receptors was reduced, the evoked brain analgesic response went up in key brain regions involved in pain processing; either the receptors were down-regulated, or when activated, the receptors induced pain.49

In another study, it was found that an opioid peptide was elevated in patients with FM and in chronic low back pain patients.50 Levels of nociceptin, a neurotransmitter that helps to modulate pain, were not elevated. Patients with FM had higher levels of MEAP (methionine-enkephalin[Met-Enk]-Arg6-Phe7), an antinociceptive opioid peptide in the CSF, and lower pain thresholds than controls or patients with chronic low back pain.50 Because MEAP has an antinociceptive effect, it would be expected that the levels would have been reduced as the peptide was used. The FM group had systemic hyperalgesia. It was suggested that antinociceptive pathways may be elevated to compensate for increased sensitivity to pain.50

As noted above, FM may be secondary to primary disturbances in central pain processing. This hypothesis is supported by several studies that explored central pain processes. If pain can be evoked at a stimulus intensity that is painless in a control group of healthy volunteers, hypersensitivity is likely due to a central process, since no pathology is present at the stimulated tissue. Several studies have consistently showed enhanced pain responses in FM, which is suggestive of central hypersensitivity.

Experimental procedures exploring endogenous inhibition have found alteration in FM patients compared to healthy controls. These studies show pain hypersensitivity that likely is due to central processes primarily because pain is evoked after stimulation of healthy tissue, endogenous inhibition is impaired, spinal cord nociceptive processes are enhanced, and pain-related brain areas are hyperactivated.20, 51-53

If impaired descending inhibition is involved, what is the cause? Is opioid receptor inhibition enough? Looked at another way, a brain imaging study examining regions involved in inhibitory processes were further activated by painful stimuli after drug treatment with milnacipran (Savella), compared to baseline.54 This indirectly suggests that endogenous inhibition is impaired in patients with FM and that antidepressants may work by restoring it.


The typical patient with FM has a great many side effects to almost every drug. FM patients tend to cycle through their drugs, taking one drug for 3 to 4 months, if that, then switching to another, and eventually returning to use the initial drug. Brand name medications appear to work better than generic medications for FM patients. Some dietary supplements may be helpful; for example, some studies show that deficiencies of magnesium are found in FM patients, so a magnesium supplement may be helpful.

One of the first classes of medications used to treat FM was antidepressants, particularly TCAs such as amitriptyline, which fixes sleep architecture, including the alpha intrusion into stage IV sleep associated with FM. Doxepin and nortriptyline also can be used. In 2 meta-analyses, doxepin and nortriptyline were considered to be beneficial.13

Both 5-HT (serotonin) and norepinephrine can be associated with antinociception in chronic pain states. Selective serotonin reuptake inhibitors (SSRIs), including fluoxetine, paroxetine, citalopram (citalopram is the most 5-HT selective), are not very helpful by themselves. Selective norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine, showed benefit in one trial.13 The combination of positive results for TCAs and poor results for SSRIs suggest that serotonin may play a secondary role to norepinephrine for analgesia in chronic pain. A combination of 5-HT and norepinephrine is synergistic and probably optimal for FM treatment. Duloxetine and milnacipran, both SSRI/SNRIs, have been approved for the treatment of FM by the FDA.

Pregabalin (Lyrica), a gabapentenoid, also has been approved by the FDA as a treatment for FM. The trick with this agent is to start with very low dosages and increase very slowly.

Anxiolytics including clonazepam, an antiepileptic and anxiolytic, may help by increasing gamma-aminobutyric acid (GABA) via internuncial neurons in the spinal cord.

Melatonin has no effect on the level of pain or fatigue, but it may help sleep.

Tizanidine, an alpha-2 noradrenergic agonist, decreases muscle spasm by increasing presynaptic inhibition of motor neurons. Multiple sites of alpha-2 adrenergic receptors are found in both ascending and descending pathways. alpha-2 stimulation decreases the activation of primary afferent fibers terminals and decreases substance P (SP) release.

SP has been found to be 2 to 3 times higher in the CSF of FM patients compared to healthy controls.12 Russell et al presented a study during the American College of Rheumatology annual meeting in October 2002 that showed that tizanidine reduced CSF SP levels at doses of 12 mg/d.55 However, this didn’t correlate with clinically improved sleep, pain, or depression.

There are no clinical data in reference to FM and baclofen.

Serotonin (5-HT3) antagonists, including ondansetron and tropisetron, are antiemetics that have some analgesic effects. There have been positive studies with tropisetron in Europe.

NMDA receptor antagonists (including ketamine, dextromethorphan, amantadine, and methadone) are used, but they may have significant dose-limiting side effects.56,57

SP or neurokinin 1 (NK1) receptor antagonists have had disappointing results in human trials.58

Other trials have been done with intermuscular growth hormone, which did show promise after 8 to 9 months, but it was prohibitively expensive.

The antinociceptive effects at various locations in the ascending and descending pain pathways would be involved in opioid usage. But as noted earlier, no study showing the efficacy of opioids in FM has been published. Thus, it probably is not a coincidence that low-dose naltrexone can decrease pain from FM.13, 59

A partial m agonist such as tramadol, a 5-HT1A receptor agonist that also enables monoamine reuptake inhibition, has been shown to be helpful.13 Tramadol has now been categorized as a Schedule IV agent.

Non-Medication Treatments

These treatments are very helpful, but many patients may not want to stick to them, and generally, only a small number of FM patients improve significantly over a 10-year period.13

Aerobic exercise has been shown to be very helpful. Hauser et al found that an aerobic exercise program for FM patients should consist of land- or water-based exercises with slight to moderate intensity 2 or 3 times per week for at least 4 weeks, leaving the patient motivated to continue to exercise.60 A Cochrane review showed that there was “gold level evidence” that supervised aerobic exercise training is beneficial to the physical capacity of FM patients and their symptoms. Strength training also may be beneficial to helping some FM symptoms.61

Relaxation training is used to good effect in the FM patients, particularly if done in combination with physical therapy.62 Acupuncture treatment has been shown to be effective, with significant reductions in FM symptoms after 8 weeks of treatment.63 Massage therapy, postural corrections, and other non-medication therapy has been found to have some benefit for some patients.

Psychological care—particularly cognitive behavioral therapy (CBT)—also has been found to be very helpful for FM patients. Individual as well as group therapy, via extended as well as brief CBT, has been shown to be effective in decreasing emotional distress in female patients with long standing FM.64

Interdisciplinary Pain Treatment

The most successful medical treatment of FM is a interdisciplinary approach that coordinates care from a physician, a nurse, a physical therapist, a psychotherapist, a relaxation therapist (biofeedback), and as needed, an occupational therapist. Unfortunately, here is where there is obtuse mural dyslexia—the inability to read the hand-writing on the wall.65 Despite all of the positive studies, improved quality of life, and decreased medical costs, generally speaking, insurers have mural dyslexia. In 1996, Bennett wrote about the appropriateness of multidisciplinary group treatment programs being “especially suited to treating FM patients,” in such multidisciplinary group therapy and individualized clinician-based treatment.66

Dennis Turk, who first introduced the author to the concept of mural dyslexia, wrote of the differential responses by psychosocial subgroups of FM patients to an interdisciplinary treatment. Basically, the result of his study gave support for the hypothesis customizing treatment based on patients’ psychosocial needs will lead to enhanced treatment efficacy.67

Since then, the evidence has grown to support this avenue of treatment. In 2009, Lera et al showed that multidisciplinary treatment of FM, including CBT, increases the response to treatment, improves functional capability, and reduces the symptom impact.68 Martin et al looked at both 6- and 12-month followups of an interdisciplinary FM treatment program and found that such a program was associated with improvements in quality of life (QOL), pain, physical function, anxiety and depression, as well as pain coping strategies up to 12 months after the program.69 They followed up a year later and found that the interdisciplinary intervention demonstrated effectiveness in improving the health-related QOL of 153 patients with FM for an extended period.70

In 2014, Martin et al looked at a 6-week interdisciplinary treatment program that combined coordinated psychological, medical, educational, and physiotherapeutic interventions and compared it with the standard of pharmacologic care.71 They found that the beneficial effects of an 6-week interdisciplinary treatment program for FM showed significant improvement in key domains of FM, including QOL, pain, fatigue, and anxiety at 12 months.

Earlier this year, a study by Vij presented at the American Academy of Pain Medicine 2014 annual meeting evaluated clinical outcomes for 366 patients with FM who received treatment through the interdisciplinary program at the Cleveland Clinic’s Neurologic Center for Pain.72 This treatment included pain physicians, pain psychologists, physical and occupational therapists, group therapy, individual therapy, biofeedback, and other disciplines. It was reported that FM patients treated in such an intensive program (Monday through Fridays from 7:30 am to about 5 pm for 3-4 weeks), maintained clinically significant improvements for as long as 12 months after discharge from this program.71 Vincent et al reported that they had a similar program at the Mayo Clinic, in which patients received 3 weeks of interdisciplinary therapy dealing with physical and cognitive reconditioning, and that the patients maintained their gains for 12 months after the interdisciplinary therapy.72

It is hard to ignore this wealth of evidence. It is not typically ignorance that causes mural dyslexia, but motives not quite so pure.


The FM population is difficult to diagnose and treat. The data shows that appropriate treatment is possible and does occur, with improvement lasting for at least a year. That’s probably the best reason in the world to have insurers recognize the value of such multidisciplinary programs for this difficult to treat patient population.



Last updated on: January 4, 2016
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