Yes, my daughter had her Vit level checked and it was low. After a week or two of high dose Vit D...she is on a daily dose now, as am I. But it has made NO difference in her fibro pain. You must be one of the lucky ones to find that you really don't have Fibro, but a lack of vit D which is an easy fix. Unfortunately, that alone won't work for a lot of people with true Fibromyalgia.

Wishing they would find a miracle drug for all who suffer from it.
Hugs...Grammyx3

I also had extremely low Vitamin D - supposedly it's an epidemic in this country now that we're all worried about skin cancer. The supplementation has helped my energy levels, but not resolved any of my other symptoms including the pain. Even my energy level isn't "resolved"... it's just slightly better than "absolutely none". So I agree that if taking Vitamin D supplements solves all your problems, you probably didn't have Fibro in the first place.

My pcp caught the low vitamin D when he first had my blood tested for RA and ANA. I've been taking Vit D for a full year now and the newest blood test showed my Vit D level to be within the normal range now. That has not done anything at all to help with my fatigue, pain, etc. Those symptoms continue to this day. Dumped Tramadol for gabapentin, now I have insomnia laced with full-body restlessness, which is a symptom of an allergic reaction according to the gabapentin script insert. So back to Tramadol just until the 23rd when I see my neurologist again.

I'll tell you, finding the right drug combo for pain, sleep and neuropathy has been really difficult so far.

i agree with the others run dont walk to the next doc. He stinks.

BuffyS when did you stop Tramadol? Insomnia and restlessness are withdrawal symptoms. Had them both even though I weaned off over several weeks. Just wondering if you stopped it recently and maybe that's what is causing your symptoms.

I say shame on him! The first they teach in the medical field is " pain is what the patient says it is, where the patient says it is and how bad the patient says it is.". To disregard your pain is a failure to improve your quality of life. Not a good doctor, glad you got a new one. I agree with the arrogant a** comments.

In no way am I mocking anyone here as I have gunfire too.I just wanted to say fibromyalgia is actually looked at as a Psychiatric illness how do I know this well in order for me to get any kind of help I had to go to mental health .I have seen many Drs 2 of them told me eyesight out that I was mentally ill and a rheumy tell me that there is no thing called fm.The rheumy I see now has actually taken my fm dx away and has told me I have arthritis with out doing tests.I'm waiting to see a different rheumy as I know I have it as I have all the sx and I have more than 18 trigger points.I hope your app goes better with the neurologist than it went with the rheumy and good luck.

I really hate spell check where it says gunfire its suppose to be fibromyalgia sorry

I have a friend who is a PCP. He sent me this information from his online up to date doctor book. The medical profession does recognize fibromyalgia as a valid condition so your rheumy's opinion is nothing more than his egotistical opinion. (sorry for the doctor language)

INTRODUCTION Fibromyalgia is a chronic pain disorder that is difficult to treat. It is most important to educate the patient and family regarding the uncertainty involved in pathogenesis, diagnosis, and treatment [1]. There is no test that confirms this diagnosis, which is currently based upon the following clinical criterion [1]:



Widespread musculoskeletal pain
Excess tenderness in at least 11 of 18 predefined anatomic sites (figure 1)


The treatment of fibromyalgia will be reviewed here. Patients with fibromyalgia generally respond best to a multidisciplinary, individualized treatment program that incorporates physician as well as non-physician providers [2]. This includes a team of physical medicine, rehabilitation, and mental health specialists.

Other issues related to fibromyalgia, including clinical manifestations, diagnosis, the differential diagnosis of widespread pain, pathogenesis, and fibromyalgia in children, are discussed separately. (See "Clinical manifestations and diagnosis of fibromyalgia in adults" and "Differential diagnosis of fibromyalgia" and "Pathogenesis of fibromyalgia" and "Clinical manifestations and diagnosis of fibromyalgia in children and adolescents".)

PATIENT EDUCATION Patients with fibromyalgia (as well as those with the myofascial pain syndrome and the chronic fatigue syndrome) need to understand their illness before any medications are prescribed [2,3] (see 'Information for patients' below).



The myofascial pain syndrome may be a localized form of fibromyalgia. Patients with this disorder complain of pain in one anatomic region, such as the right side of the neck and shoulder, and tenderness is confined to that area [4]. (See "Overview of soft tissue rheumatic disorders", section on 'Regional myofascial pain'.)
There also appears to be a close relationship between the chronic fatigue syndrome and fibromyalgia. Diagnostic criteria for the classification of chronic fatigue syndrome (CFS) are similar to those for fibromyalgia, and the majority of patients with CFS meet tender point criteria for fibromyalgia [5]; similarly, approximately 70 percent of patients with fibromyalgia meet the criteria for CFS [6]. (See "Clinical features and diagnosis of chronic fatigue syndrome".)


Discussing the diagnosis of fibromyalgia Most patients have had fibromyalgia for years before the diagnosis is finally made. They often have undergone multiple diagnostic evaluations and have consulted with many different specialists. Some patients may feel rejected by the medical profession, while others may fear that a life-threatening illness will eventually be found.

There is emerging evidence that a diagnosis of fibromyalgia is helpful to patients as well as society.



One report from the United Kingdom found that there were fewer referrals and less diagnostic testing after a fibromyalgia diagnosis was made [7].
Another report found that following a diagnosis of fibromyalgia, patients underwent less diagnostic testing and imaging, there were fewer specialty referrals, fewer primary care visits, and fewer drug prescriptions [8].


Thus, the patient must be reassured that fibromyalgia is a real illness, and not imagined or "in your head." The benign nature of the disorder should also be emphasized. As an example, patients must be told that this is not a deforming or deteriorating condition, and that it is neither life threatening nor a cosmetic problem. The relationship of neurohormones to pain perception, fatigue, abnormal sleep, and mood disturbances should be discussed; this will help the patient to understand the rationale of therapy with medications such as tricyclic antidepressants and serotonin reuptake inhibitors.

Some patients with fibromyalgia, particularly those who also meet the criteria for chronic fatigue syndrome (table 1) may believe that their illness is caused by an undiagnosed infection. Although infections may be important precipitating factors, there is no evidence that these syndromes are related to persistent infection. Patients generally have a better response to treatment when they understand that they are not harboring some infectious agent over which they have no control. (See "Clinical features and diagnosis of chronic fatigue syndrome".)

It has been suggested that blood flow to muscle and skin may be sluggish in fibromyalgia. A discussion of the role of muscle 'spasm' and deficient muscle blood flow are useful when prescribing exercise and physical therapy.

Physical or emotional stress may precipitate or aggravate fibromyalgia. Approximately 30 percent of patients with fibromyalgia have major depression at the time of diagnosis; the lifetime prevalence of depression is 74 percent and that of an anxiety disorder is 60 percent [2,9,10]. In addition, a review of the role of stress and mood disturbances in fibromyalgia will encourage the patient to learn simple relaxation techniques and to consider formal stress-reduction programs. The patient must be taught to recognize the role of sleep disturbances and methods to correct them.

Finally, patients need to appreciate that their symptoms will wax and wane but that the pain and fatigue generally persist. Despite the presence of these chronic symptoms, it is reassuring to emphasize that the great majority of patients live normal and active lives.

Effectiveness of patient education Patient education has a therapeutic effect. A 2004 systematic review of treatment of fibromyalgia assessed the reported effectiveness of educational interventions when compared to controls who were waiting for care or receiving training in gentle stretching exercises [11]. The studies reviewed were typically unblinded. Small group sessions, printed materials, lectures, and demonstrations were used to inform patients of the nature of fibromyalgia. Numbers of sessions ranged from 6 to 17. Those receiving the educational intervention had significantly more improvement than the controls, and beneficial effects lasted from three to 12 months after the sessions ended.

A single intensive educational intervention may also be beneficial, as was the case in a study in which patients received education from a multidisciplinary team over 1.5 days [12]. A month afterward there was significantly less pain and more improvement in self-reported function, fatigue, stiffness, anxiety, and depressed mood in those who received the educational intervention.

MEDICATIONS The medications that have been most consistently effective in the treatment of fibromyalgia are antidepressants. From 2008 to 2009, two antidepressants, duloxetine and milnacipran, and one anti-seizure medication, pregabalin, were approved for the treatment of fibromyalgia by the FDA in the United States.

Choice of medications We use the following general guidelines for pharmacologic management:



In general, drugs should be started at low doses and built up slowly (see discussion of each medication and class below).
A low dose of a tricyclic medication at nighttime should be considered as initial therapy, especially since it is far less costly than some of the newer agents. The dose may be limited by adverse side effects, especially in the elderly.
In patients with more problems with sleep, as an alternative to amitriptyline, we start with pregabalin at night. Gabapentin is an acceptable alternative that may cost less for some patients.
In patients who have more exhaustion, we prefer to initiate therapy with duloxetine or milnacipran at breakfast.
Some patients do better with polypharmacy, such as a low dose of an SNRI in the morning with a low dose of an anticonvulsant in the evening, although there are no published studies using combinations of the newer agents.


The medications differ from one another in efficacy for given symptoms and in their side-effect profiles. A meta-analysis of the relative efficacy of the three FDA-approved drugs, involving 7739 patients in 17 studies, found that all three were superior to placebo for pain relief, although duloxetine (DLX) and pregabalin (PGB) were superior tomilnacipran (MLN) [13]. The drugs also differed in their effects on sleep disturbance, depression, and in alleviating fatigue. Headaches and nausea were more likely with DLX and MLN; diarrhea with DLX and MLN; and cognitive defects and weight gain with PGB.

Amitriptyline and the several medications approved by the FDA for use in fibromyalgia have not been compared directly; however, a 2010 systematic review and meta-analysis has provided an indirect comparison demonstrating greater efficacy of amitriptyline (AMT) compared with DLX and MLN in reducing pain, sleep disturbance, and fatigue, without differences in acceptability [14]. The strength of the conclusions is limited to some degree by the lower methodologic quality of the AMT trials.

Antidepressants Antidepressants, including tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), and dual serotonin and norepinephrine reuptake inhibitors (dual reuptake inhibitors, SNRIs) are helpful in relieving many symptoms of fibromyalgia. A 2009 meta-analysis included 18 randomized, placebo-controlled studies of a variety of antidepressants and concluded that there was strong evidence for efficacy of antidepressants for pain relief, fatigue, depressed mood, sleep disturbance, and in improving health-related quality of life [15]. Although the effect sizes for tricyclic antidepressants were larger than those for SSRIs and SNRIs, the authors of the meta-analysis concluded that it did not allow for "a definitive conclusion regarding the superiority of one class of antidepressants over another". Also notable is that this meta-analysis did not include two pivotal trials of the SNRI milnacipran that are discussed below.

Tricyclic antidepressants Tricyclic antidepressants and related agents are often used as initial treatment for patients with fibromyalgia. Individual randomized trials have demonstrated that clinically important improvement occurs in 25 to 45 percent of patients treated with these medications [16-22]. However, their use is limited by a lack of uniform effectiveness and relatively high frequency of side effects. In addition, the efficacy of the tricyclic drugs may decrease over time in some patients [20,23].

The doses of amitriptyline studied have been 25 to 50 mg, usually given as a single bedtime dose. These doses are usually lower than those required to treat depression. Nevertheless, even at low doses, dry mouth, constipation, fluid retention, weight gain, grogginess, and difficulty concentrating are common. Such side effects and possible cardiotoxicity limit use in elderly patients.

Desipramine is a tricyclic antidepressant that has been less well studied for fibromyalgia but remains a possible alternative because it generally has fewer anticholinergic side effects.

Regardless of the agent chosen, patients with fibromyalgia should be started on very low doses; a typical starting dose of amitriptyline or desipramine is 5 to 10 mg one to three hours before bedtime. The dose may be increased by 5 mg at two-week intervals. The final dose should be set by the patient, based upon efficacy and side effects, always keeping the dose as low as possible.

Cyclobenzaprine Although cyclobenzaprine is not marketed as an antidepressant, its chemical structure and mode of action is very similar to the tricyclic antidepressants. Various doses of cyclobenzaprine have been used in placebo-controlled trials, including 10 mg in the morning and 20 mg at night [19], 10 mg three times daily [24], 10 mg in the morning and 30 mg in the evening [25], and 10 to 40 mg daily as needed [18]. Doses are typically begun at 10 mg near bedtime and increased as tolerated to the larger doses.

The best evidence of the efficacy of cyclobenzaprine was provided by a 2004 meta-analysis of five placebo-controlled trials that included 312 patients [20]. Self-reported 'improvement' (measured in three studies) was more likely in subjects receiving cyclobenzaprine than placebo (odds ratio 3.0, 95% CI 1.6-5.6), the absolute difference in the rate of improvement was 21 percent, suggesting that approximately five patients would need to be treated with cyclobenzaprine for one to improve. The effect size was similar to that of two meta-analyses of the effectiveness of amitriptyline in this disorder [21,22].

This meta-analysis also found that pain decreased more in those who received cyclobenzaprine than placebo for four weeks, but the change in pain was not significantly different in active or placebo groups after eight or 12 weeks. Changes in pain and the number of tender points were not significantly different between the groups at any time.

A randomized eight-week trial involving 36 patients demonstrated that very low-dose cyclobenzaprine (1 to 4 mg at bedtime), improved the symptoms of fibromyalgia, including pain, fatigue, and depression, compared with use of placebo, which did not result in significant improvement [26]. Significantly more patients who received the low dose cyclobenzaprine had improved restorative sleep, based upon analysis of cyclic alternating pattern sleep by electroencephalography; the increase in nights with improved sleep by this measure correlated with improvements in fatigue and depression. The authors proposed that improvement in cyclic alternating sleep may be a biomarker for treatment efficacy.

Dual reuptake inhibitors Duloxetine, milnacipran, and venlafaxine inhibit both norepinephrine and serotonin reuptake and have been studied in patients with fibromyalgia.

Duloxetine Duloxetine is approved by the FDA for treatment of fibromyalgia, and it is also approved for the treatment of depression and diabetic neuropathy. The efficacy of duloxetine in patients with fibromyalgia was initially demonstrated in two multicenter trials of 12 weeks duration [27,28]. A longer term benefit was demonstrated in a subsequent six month multicenter, randomized, double-blind placebo-controlled trial of 520 patients who were assigned to single daily dose of either 60 mg or 120 mg of duloxetine or to placebo [29].

Duloxetine significantly reduced pain severity and improved global assessments at three and six months. The reductions in pain were seen in the first week of therapy and occurred in patients with and without major depression. Mental fatigue improved, but general fatigue did not. The most common side effects were nausea, headache, and dry mouth. They usually occurred within the first three months of therapy.

When duloxetine is used, it is best tolerated in the morning. The usual starting dose in patients with fibromyalgia is 20 to 30 mg/day, which is gradually increased to the recommended dose of 60 mg/day.

Milnacipran Milnacipran has been approved for use for patients with fibromyalgia by the FDA. In clinical trials it improved pain and global well being more than placebo [30-35]. As an example, in one pivotal trial 1196 patients were randomly assigned to treatment with one of two doses of milnacipran or placebo [32]. Primary outcomes were improvement in a composite of pain, patient-reported global status, and self-reported physical function after 15 weeks of treatment.

A greater than 30 percent improvement in the composite was achieved by a significantly larger proportion of those receiving milnacipran at either dose (100 mg/day or 200 mg/day) than the placebo group. Greater improvements in individual component scores (ie, pain, global status, and physical function) were also noted in the milnacipran-treated patients versus the placebo group.

Adverse effects leading to discontinuation of study drug were more common in the milnacipran-treated subjects than the placebo group (19 to 24 percent versus 9.5 percent, respectively). Commonly reported adverse effects were nausea, headache, and constipation.

The other pivotal trial randomly assigned 888 patients, followed similar efficacy measures, and also noted greater efficacy for milnacipran than placebo for pain relief, improvement in global well being, and physical function [33]. Nausea and headache were the most frequent adverse effects.

Venlafaxine There are fewer data on the efficacy of venlafaxine for fibromyalgia. A small study using a flexible dose design in which the final mean dose of venlafaxine was 167 mg per day, suggested that this dual uptake inhibitor may be effective [36].

Serotonin reuptake inhibitors Other CNS active medications that have some efficacy in fibromyalgia include the selective serotonin reuptake inhibitors (SSRIs) [37,38].



Fluoxetine While a study that compared a fixed dose of fluoxetine (20 mg/day) found it was not superior to placebo [39], another that allowed dose escalation, from 20 to a maximum of 80 mg/day, found fluoxetine to be significantly more effective than placebo [38]. In this study the effect on pain was independent of change in mood.
Paroxetine In the largest study to date, an escalating dose of a continuous release formulation of paroxetine (12.5 mg/day to 62.5 mg/day) was compared with placebo in a trial that randomly assigned 116 patients and followed their composite scores on the fibromyalgia impact questionnaire (FIQ) from baseline to 12 weeks [40]. Significantly more of those assigned to paroxetine than to placebo achieved a 25 percent improvement in FIQ score (57 versus 33 percent). Among those who completed the assigned treatment, the response rates were higher in those receiving paroxetine than placebo (66 versus 33 percent, respectively).
Fluvoxamine was compared with amitriptyline in a study that randomly assigned 68 patients to one of the two active treatments for four weeks [41]. Withdrawals were more common in the amitriptyline than fluvoxamine groups (40 versus 16 percent). Pain relief was not significantly different in the two groups.
Citalopram Inconsistent results have been noted in small studies using citalopram to treat patients with fibromyalgia [42,43].


Antidepressant combinations Combinations of agents that individually inhibit reuptake of norepinephrine and serotonin or use of single drugs that inhibit reuptake of both neurotransmitters (dual serotonin and norepinephrine reuptake inhibitors or SNRIs) may be more useful than a drug that targets only one or the other. Because tricyclic antidepressants are generally used in low doses that are not likely to be useful for improving mood in depressed patients, the addition of an SSRI to a tricyclic or use of an SNRI is a reasonable option for a patient with fibromyalgia and depressed mood.



Combination of SSRI and tricyclic The combination of 20 mg of fluoxetine in the morning with 25 mg of amitriptyline at bedtime was more effective than either medication used alone in a randomized trial [37].


Antiinflammatory and analgesic drugs Antiinflammatory and analgesic drugs and central nervous system (CNS) active medication other than antidepressants have been used in the treatment of fibromyalgia [11].

Antiinflammatory medications There is no evidence that tissue inflammation is present in patients with fibromyalgia. Thus, it is not surprising that antiinflammatory medications are not an effective form of treatment. As an example, therapeutic doses of naproxen, ibuprofen, and prednisone (20 mg/day) were found to be no better than placebo in clinical trials [11]. However, nonsteroidal antiinflammatory drugs (NSAIDs) may have a synergistic effect when combined with central-nervous system (CNS) active medications such as antidepressants or anticonvulsants. At present, there is no data concerning the efficacy of selective COX-2 inhibitors in this disorder.

Glucocorticoids are also ineffective and also have the potential for serious adverse effects when used chronically [11].

Analgesics Other analgesics, such as acetaminophen-tramadol, alone or in combination, may be helpful [44,45]. They are generally used in combination with CNS active medications when the latter are not effective alone.

The modest clinical efficacy of the fixed combination of these two agents (up to 650 mg acetaminophen and 75 mg tramadol four times daily) in relieving pain was illustrated in a study that randomly assigned 315 predominantly white female patients to active combination therapy or placebo [45]. Discontinuation rates and secondary measures such as pain, pain relief, and self reported health status were assessed over a three-month period. The following results were noted:



A greater proportion of the patients treated with acetaminophen-tramadol had a 50 percent or greater reduction in pain (35 versus 18 percent with placebo)
Those on the active combination had significantly greater overall decrease in pain (19 mm versus 7 mm on a 100 mm scale).
Discontinuation rates were lower with active treatment (48 versus 62 percent). Nausea was more than twice as common among those on the active medication than among those on placebo (9 versus 4 percent).


While these findings are encouraging, the patients had received little treatment before enrollment, and prior use of tricyclic antidepressants, cyclobenzaprine, and analgesics (including acetaminophen) were criteria for exclusion. How effective the combination of acetaminophen-tramadol would be for patients who had tried and failed other treatments, and how the combination would perform if added to ongoing treatment with one or more of the CNS active medications is unclear.

There is some concern regarding the long-term potential for abuse of tramadol, although the risk is less than with more potent narcotic analgesics that have also been tried in fibromyalgia. Prolonged use of such agents is controversial and should be avoided unless prescribed by a pain management specialist.

Anticonvulsants Pregabalin and gabapentin have similar effects on cellular calcium channels and may exert their analgesic effects by blocking the release of various neurotransmitters. The efficacy of these agents was best described in a meta-analysis of five placebo-controlled randomized trials (four and one with pregabalin and gabapentin, respectively) consisting of 2918 patients with fibromyalgia [46]. Compared with placebo, active therapy significantly reduced pain (standardized mean difference (SMD) of -0.39), improved sleep (SMD -0.12), and improved quality of life (SMD -0.30). The pharmacologic properties of these medications are discussed in detail elsewhere. (See "Pharmacology of antiepileptic drugs", section on 'Drugs with other mechanisms of action'.)

Pregabalin Pregabalin, a second generation anticonvulsant, was the first drug approved by the FDA for the treatment of patients with fibromyalgia. In the pivotal study, 529 patients were randomly assigned to placebo or pregabalin (150 mg, 300 mg, or 450 mg/day) for eight weeks [47]. Pregabalin, 450 mg/day, significantly reduced the average severity of pain compared to placebo (difference in means -0.93 on a 1 to 10 visual analog scale). Among those receiving the highest dose, more pregabalin-treated patients had a >50 percent improvement in pain (29 versus 13 percent). There were also significant improvements in sleep, fatigue, and health-related quality of life among those receiving 300 and 450 mg/day.

In a second 13-week study of 798 patients, 300, 450 and 600 mg doses of pregabalin improved pain and global well being more than placebo [48]. The 450 mg and 600 mg doses had comparable efficacy compared to placebo but there was greater adverse side effects with the higher dose. Dizziness and somnolence were the most common adverse side effects.

The durability of pregabalin was studied in a 6 month trial during which patients initially were treated with increasing doses of pregabalin for 6 weeks [49]. Then, pregabalin responders, those with a 50 percent decrease in pain and a self-rating of "much" or "very much" improved, were randomized to placebo or optimal dose of pregabalin as determined during the dose titration (open label) phase. The primary outcome was time to loss of therapeutic response (LTR), defined as

This is the mail paragraph I wanted you all to see but pasted the whole article for those that were interested.

Thus, the patient must be reassured that fibromyalgia is a real illness, and not imagined or "in your head." The benign nature of the disorder should also be emphasized. As an example, patients must be told that this is not a deforming or deteriorating condition, and that it is neither life threatening nor a cosmetic problem. The relationship of neurohormones to pain perception, fatigue, abnormal sleep, and mood disturbances should be discussed; this will help the patient to understand the rationale of therapy with medications such as tricyclic antidepressants and serotonin reuptake inhibitors.

Interesting article Tammy, thanks for sharing.

SmileThro...I took Tramadol 2X per day for the past 6 months, but the pharmacy people contacted rheumatologist and told him not to prescribe it to me as long as I'm taking Lexapro as the combo can cause seizures. Funny, it's the only time this rheumatologist has spoken to me with any respect and it was just to cover his own ass. He was going to put me on something else but I told him my neurologist had already put me on gabapentin so I wasn't taking the Tramadol anymore anyway. He was downright relieved b/c I guess it could have been a potential lawsuit if I had had a seizure due to his prescribing me Tramadol recently knowing I've been on SSRIs and Lexapro in particular for the past 15 years.

I see the neurologist again on July 23 so for right now, I'll just take the Tramadol, as lame as I find it to be as a pain reliever, until then. Maybe you're right and I was having withdrawal symptoms. I don't know b/c I've been suffering insomnia for at least 3 months now, but the restlessness was a brand new part of the insomnia. I am so damned confused.