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FIBROMYALGIA (FM)

FM-CFS Canada

FIBROMYALGIA

FOR

PHARMACISTS

Janice Sumpton BSc.Phm


TABLE OF CONTENTS
fm-cfs.ca

Table of contents . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .2


1. What is Fibromyalgia? . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .3
1.1 Introduction . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .3
1.2 Epidemiology . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .3
1.3 Etiology . . . . . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .3
1.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .3
1.5 Symptoms . . . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .4
1.6 Pathogenesis of FM . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .4
1.6.1 Pain . . . . . . . . . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .4
1.6.1.1 Central Sensitization Theory . .... ........ . . . . . . . . . . . . . . . . .5
1.6.1.2 Dopamine Theory A Limbic Pain Disorder . . . . . . . . . . . . . . . . .5
1.7 Sleep Deprivation . . . . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .5
1.8 Cognitive Dysfunction . . . . . . . . . . . .... ........ . . . . . . . . . . . . . . . . .5
1.9 Diagnostic Imaging Findings . . . . . .... ........ . . . . . . . . . . . . . . . . .6

2 Management of Fibromyalgia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
2.1 Non-Pharmacological Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
2.1.1 Cognitive Behaviour Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
2.1.2 Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
2.1.3 Other . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
2.2 Pharmacological Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8
2.2.1 Pain Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8
2.2.1.1 Tricyclic Antidepressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8
2.2.1.2 Selective-Serotonin-Reuptake Inhibitors . . . . . . . . . . . . . . . . . . .9
2.2.1.3 Selective-Serotonin-Norepinephrine-Reuptake-Inhibitors . . . . . .9
2.2.1.4 Dopamine Agonists . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11
2.2.1.5 Pregabalin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11
2.2.1.6 Tramadol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12
2.2.1.7 NMDA-Antagonists . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12
2.2.1.8 Opioids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12
2.2.2 Fatigue Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13
2.3 Herbals and Supplements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13

3 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14

4 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14

Acknowledgements:

FM-CFS Canada thanks Janice Sumpton, BSc.Phm for volunteering to research


and write this guide for Fibromyalgia and for giving the copyright to FM-CFS
Canada. See page 6 for FM-CFS Canada contact information.

Fibromyalgia for Pharmacists 2


What is Fibromyalgia? fm-cfs.ca

1 What is Fibromyalgia?

1.1 Introduction

Fibromyalgia (fi-bro-my-AL-ja) is a chronic condition which causes wide-


spread pain as it's primary feature, and fatigue in addition to many other
symptoms.1 It is not an inflammatory joint disorder.2 It is an "invisible dis-
ability" since very little is visible to the public. The word fibromyalgia is
derived from "fibro" (fibrous tissues including tendons and ligaments), "my"
(muscles), and "algia" (pain).1

Fibromyalgia (FM) is not a waste paper basket disease. Its symptoms are very
real. Ongoing research is close to procuring diagnostic tools and a better
understanding of the underlying cause. Once defined, one will be closer to
more specific drug therapy for FM.

1.2 Epidemiology

FM affects over 6 million Americans, predominantly women between 20 and


55 years of age. It also affects men and children.3 Three studies show that
2-10% of the population have FM. This co-relates to 600,000 - 3 million
Canadians.4 The London, Ontario Epidemiology study indicates that 3.3% of
non-institutionalized adults have FM.5

1.3 Etiology

The precise cause of FM is unknown,1,6 and likely multifactorial. FM can be


triggered by a physical trauma (whiplash, spinal injury, surgery, viral ill-
ness)1,4 Some studies have shown a genetic component with a strong famil-
ial pattern.1,4 In some patients there is no obvious trigger, or sudden onset,
but a slow gradual onset of symptoms.4

1.4 Diagnosis

In 1990 An Expert Consensus Panel devised diagnostic criteria that was


adopted by the American College of Rheumatology.1,4,6 Criteria for FM diag-
nosis are:
a) compulsary history of widespread pain for at least three months. Pain on
both sides of the body, above and below the waist, and axial pain.
b) compulsary pain on palpation of at least 11 out of 18 defined tender point
sites when digitally palpated with a 4kg pressure.1,4,6

Routine laboratory and X-Ray testing is usually normal.1

Fibromyalgia for Pharmacists 3


What is Fibromyalgia? fm-cfs.ca

1.5 Symptoms

FM patients with pain and fatigue may also experience one or more of the fol-
lowing; body stiffness, increased frequency of headaches or facial pain, sleep
disturbances, digestive complaints (including Irritable Bowel Syndrome
(IBS)), genito-urinary problems, paresthesias especially in the hands and
feet, highly sensitive to cold ambient temperatures, skin complaints including
dry skin , eyes and mouth, and a sensation of swelling of the extremities,
chest muscle pain and shortness of breath, light-headedness and balance
problems, cognitive disorders termed "fibro-fog", memory lapses and "spaci-
ness", Restless Legs Syndrome (RLS), hypersensitivity to the environment
including noise, odours, light and weather patterns, and anxiety and
depression. 1,4,6 Patients may also suffer from Chronic Fatigue Syndrome
(CFS).6

1.6 Pathogenesis of FM

The exact cause of fibromyalgia is not known at this time.1 Increased evi-
dence is pointing to a number of pathophysiologic differences. FM patients
have a decreased amount of neurotransmitters that amplify and distort pain
signals.4 Low serotonin levels,1,2,4 lead to anxiety, depression, pain, sleep
disorders and smooth muscle dysfunction.2

Other hormones and neurotransmitters that are low include cortisol, thy-
rotropin-releasing hormone (TRH), growth hormone, dopamine, epinephrine
and norepinephrine.2,6 Growth hormone is required for muscle repair and
metabolism. Epinephrine and norepinephrine levels lead to erratic elevations
in heart rate and blood pressure. Orthostatic hypotension (lightheadedness),
constricted blood vessels and Raynaud's phenomenon may be present.2

1.6.1 Pain

The neurotransmitter substance P is elevated,1,4,6 up to three times normal


in the cerebral spinal fluid (CSF). 2,4,5 Substance P is responsible for the
transmission of pain.2 This likely explains the increased pain sensations
(hyperalgesia) by increasing pain perception, and possibly increasing inflam-
matory cytokines production.6 Neurokinin A (also transmits pain), N-methyl-
D-asparate (NMDA) and the excitatory amino acids (aspartate and glutamate)
also increase the responsiveness of the central nervous system (CNS) to pain.
Nerve growth factor (NGF) is essential for the survival of sympathetic neu-
rons and sensory neurons NGF is four times higher in the CSF of primary FM
patients compared to controls.7

Fibromyalgia for Pharmacists 4


What is Fibromyalgia? fm-cfs.ca

1.6.1.1 Central Sensitization Theory

The abnormal levels of these neurotransmitters and neurochemicals increase


the responsiveness of the CNS neurons, thus becoming more sensitive to
stimuli and the response to these stimuli is amplified. This process is termed
"Central Sensitization", defined as "an exaggerated response of the CNS
(spinal cord and brain) to noxious and non-noxious stimuli"8 Central sensiti-
zation results in a stimulus that causes hyperalgesia (painful stimulus causes
an exaggerated painful response), allodynia, (normally non-painful stimulus
(gentle touch) becomes painful). The pain spreads to areas of the body
beyond the area of stimulation, and is more sustained than normal.8 The
pain may be burning, sharp, stabbing, shooting, throbbing, deep aching, tin-
gling, a bruised feeling, widespread and exhausting.4

1.6.1.2 Dopamine Theory A Limbic Pain Disorder

The hippocampus is important in FM and the deficiency of dopamine (espe-


cially D3 ) is key.9 Chronic pain alters the Hypothalamic-Pituitary-Adrenal
(HPA) axis leading to atrophy of the hippocampus. This impairs the modula-
tion of adrenergic arousal10 Mesolimbic dopamine is the main pain fighter.
Decreased dopamine causes the stimulus (pain, noise, sensations) to be more
intense. FM patients show atrophic changes in their brain in areas involved
with pain processing.11

1.7 Sleep Deprivation

Up to 90% of FM patients have a decrease in restorative restful sleep.2 In


light sleep (stages 1 and 2) the brain waves are mixed alpha waves (type
when awake) and delta waves. Deepest sleep (stage 4) is 100% delta waves.
FM patients continue with alpha waves throughout sleep, therefore experienc-
ing little deep sleep. Chronic sleep deprivation causes extreme fatigue,2 and
exacerbates pain.

1.8 Cognitive Dysfunction

Impaired cognitive function and memory problems are referred to as "fibro


fog" by FM patients. The cognitive problems increase during times of a flare-
up in symptoms. A decrease in neurotransmitters and deficient neurophysiol-
ogy of the CNS may contribute to cognitive dysfunction and memory difficul-
ties.2 Increased pain and decreased sleep during a "fibro-flare" also con-
tribute.2 Park et al studied FM patients for the presence of cognitive deficits
compared to controls. FM patients functioned similar to matched controls
that were 20 years their senior.12

Fibromyalgia for Pharmacists 5


What is Fibromyalgia? fm-cfs.ca

1.9 Diagnostic Imaging Findings

Single-Photon-Emission-Computed-Tomography (SPECT) scans show


decreased cerebral blood flow in areas of the brain that modulate pain per-
ception.8 Functional-Magnetic-Resonance-Imaging (fMRI) shows very quick
changes in the brain. Gracely found using fMRI and increasing pain stimulus
to FM patients and controls, that FM patients showed changes in regional
cerebral blood flow in structures involved in pain processing. These changes
on fMRI were seen at a lower pain stimulus than the pain stimulus necessary
in the patients without FM.13

With thanks once again to Janice Sumpton, BCSPhm, FM-CFS Canada


seeks to freely distribute this guide to health practitioners, and most
of all, pharmacists.

This up-to-date guide was completed in January 2007, and will be


regularly updated when new developments warrant change.

Visit fm-cfs.ca to find this and other guides for health professionals.

For more information:

FM-CFS Canada
99 Fifth Avenue
Suite 412
Ottawa ON
Canada K1S 5P5
fm-cfs.ca

Charity #: 89241 7742 RR0001

Fibromyalgia for Pharmacists 6


MANAGEMENT OF FIBROMYALGIA fm-cfs.ca

MANAGEMENT OF FIBROMYALGIA
There is no "magic bullet" to treat FM. Control of symptoms is currently the
focus of treatment. Goals include improving deep sleep and establishing a
regular exercise program.2

2.1 Non-Pharmacological Treatment

Cognitive Behaviour Therapy (CBT), and exercise are the best studied non-
pharmacological therapies and have shown efficacy in the treatment of FM.14

2.1.1 Cognitive Behaviour Therapy

Nielson reports benefits of a cognitive behaviour approach to FM treatment.15


In 198 FM patients the largest belief changes were patients belief in
increased control over pain, a decreased belief that hurt necessarily equals
harm, and a decreased belief in avoidance of activity is a good approach. The
coping strategies with the largest changes were the use of increased relax-
ation and frequency of exercise.15

2.1.2 Exercise

FM patients benefit from exercise which must be introduced very slowly.


Stretching and strengthening exercises are important to condition the mus-
cles.16 Cardio-vascular exercise is very important. The patient must "go-
slow" and progress at their own pace.2

2.1.3 Other

Improved sleep hygiene to maximize sleep,4,16 eating a healthy diet, pacing


activities and education about FM are also beneficial.4

One out of three controlled studies on acupuncture in FM showed significant


benefit compared to placebo.17 Massage, mineral baths, and ultrasound may
provide pain relief but sustained improvement is unusual.17

Fibromyalgia for Pharmacists 7


PHARMACOLOGICAL TREATMENT fm-cfs.ca

2.2 Pharmacological Treatment

At present there is no cure or "magic pill" to treat fibromyalgia.1 One is left


with symptom management that targets chronic pain and fatigue which are
often intertwined.

2.2.1 Pain Treatments

Patients with fibromyalgia have many pain features that are seen in neuro-
pathic pain syndromes,(eg. Diabetic peripheral neuropathy and Herpes Zoster
(shingles)). All of these pain syndromes are chronic in nature. There is a
stimulus-dependent pain sensation accompanied by hyperalgesia/allodynia
and parasthesias.18 These similarities in syndromes have led to the use of
drugs to treat FM pain that have been used in shingles and diabetic pain syn-
dromes.

The target of pain control is centrally-mediated in the brain and spinal


cord.18 Drugs that affect neurotransmitters, specifically serotonin and norep-
inephrine have been studied.

2.2.1.1 Tricyclic Antidepressants

Amitriptyline, and the biologically similar cyclobenzaprine, and dox-


epin are the most commonly used in FM (USA data). A meta-analysis
of nine controlled trials of tricyclic antidepressants (TCAs) in FM pro-
duced significantly greater effects versus placebo when assessed by
patients and their physicians. Improvements were seen in pain, stiff-
ness, fatigue and quality of sleep.16

The biggest drawback of the TCAs is side-effects, especially sedation


and anti-cholinergic effects. These may be minimized by starting at a
very low dose a few hours before bed, and increasing the dose as tol-
erated. In some cases switching TCAs eg. amitriptyline changed to a
morning dose of desipramine with decreased anticholinergic side-
effects. Some patients may require a further change to imipramine
at night (mid-anticholinergic effects) to eliminate daytime dizziness
and nightmares that may occur with desipramine.19

Fibromyalgia for Pharmacists 8


PHARMACOLOGICAL TREATMENT fm-cfs.ca

2.2.1.2 Selective-Serotonin-Reuptake Inhibitors

Patients unable to tolerate TCAs may be treated with Selective-Serotonin-


Reuptake-Inhibitors (SSRIs). Fluoxetine, paroxetine and citalopram have
been studied in FM as randomized placebo-controlled trials.14 The results
have been mixed. Fluoxetine and paroxetine have fared better in FM relief
than citalopram.14,16,20 Citalopram has greater effects on serotonin reup-
take than the older SSRIs that have some affect on norepinephrine reup-
take.20

This observation has led to the study of Selective-Serotonin and


Norepinephrine Reuptake Inhibitors (SNRIs).

2.2.1.3 Selective-Serotonin-Norepinephrine-Reuptake-Inhibitors

Serotonin and norepinephrine are key players in descending pain pathways.


SNRIs are tolerated better than TCAs because they do not interact with
cholinergic, adrenergic, histaminergic receptors, or sodium channels that are
responsible for most of the TCA side-effects. 20 Venlafaxine, duloxetine ( on
USA market as Cymbalta®), and milnacipran (not available on the Canadian
or USA market) have shown positive results in the treatment of FM.

A 12-week study in 15 patients with FM were assessed before and after treat-
ment with 75mg venlafaxine daily. The primary outcome was the
Fibromyalgia Impact Questionaire (FIQ) and pain score. Depression and anxi-
ety were measured using the Hamilton Depression and Beck Depression
scales, and Beck Anxiety and Hamilton Anxiety scales respectively.
Venlafaxine significantly reduced pain ( F=14.3; p=0.0001) and disability
caused by FM ( F=42.7; p=0.0001). Patient and physician rated anxiety and
depression were reduced significantly.21

Duloxetine is a potent SNRI anti-depressant that has also been studied in


pain syndromes. It is currently indicated by the FDA in the USA for the treat-
ment of adults with major depressive disorder and adults with diabetic
peripheral neuropathic pain.20

Fibromyalgia for Pharmacists 9


PHARMACOLOGICAL TREATMENT fm-cfs.ca

The first duloxetine study in FM patients was randomized, double-blind, place-


bo-controlled, parallel group 12 week study of duloxetine titrated to 60mg po
BID in 207 patients with or without a current major depressive disorder. In
the first two weeks the dose was increased from 20mg once daily to 60mg
BID. The slow titration decreased nausea and insomnia. Duloxetine patients
significantly improved on the total FIQ score ( p=0.027 ), but not significantly
on the pain FIQ score ( p=0.13 ). Duloxetine was significantly better in the
Brief Pain Inventory average pain severity score ( p=0.008 ) and Brief Pain
Inventory average interference from pain score ( p=0.004 ), number of ten-
der points ( p=0.002 ) and FIQ stiffness score ( p=0.048 ) than placebo.
Improvement was seen in patients with or without a major depressive disor-
der. Duloxetine was well tolerated; Some duloxetine treated patients had
insomnia, dry mouth and constipation more often than the placebo treated
patients ( not significantly different ). Adverse effects were described as mild
or moderate in severity.22

The second duloxetine study was randomized, placebo-controlled, double-


blind parallel group 12 week study in 354 women with or without current
major depressive disorder. It compared placebo to duloxetine 60mg daily
versus 60mg BID. A significantly greater number of patients on duloxetine
60mg daily (41%) and 60mg BID (41%) had a = 50% reduction in the Brief
Pain Inventory average pain severity score compared with placebo (23%).
Overall, 60mg daily and BID had no significant difference in efficacy outcomes
measured. But, only the higher duloxetine dose significantly improved tender
point assessments. Higher doses may be needed to improve pressure pain
thresholds.23 In conclusion, duloxetine 60mg daily or BID is effective in the
treatment of FM with or without a major depressive disorder.

Milnacaprin is currently marketed in Asia and Europe for the treatment of


depression.16 It is a SNRI with mild inhibition of N-methyl-D-aspartate
(NMDA). NMDA antagonists may inhibit or attenuate central sensitization,
potentially decreasing pain in FM.20

A phase-II trial studied milnacaprin in 125 FM patients.. It was a three-month


study, randomized, double-blind, placebo-controlled study. Patients were
randomized to 3:3:2 to daily:BID:placebo respectively. Active doses started
at 25mg daily versus 12.5mg BID and doses could be escalated up to 200mg
daily. The primary end-point was pain reduction. Twice daily dosing was
more effective, and patients experienced less side-effects compared to the
same total daily dose given once daily. Significant decreases in pain, fatigue
and morning stiffness were reported. Nausea was the most common side
effect. 24

Fibromyalgia for Pharmacists 10


PHARMACOLOGICAL TREATMENT fm-cfs.ca

2.2.1.4 Dopamine Agonists

Dopamine agonists are approved for the treatment of Parkinson's disease.


Dopamine agonists are effective in the treatment of RLS which occurs 10X
more frequently in FM patients compared to normal controls (31% versus
3%). RLS symptoms have been further shown to inhibit deep sleep and lead
to non-restorative sleep as experienced by many FM patients.17 Ropinirole
(Requip®) has specificity to the D2 and D3 subreceptors.

An open-label, four-month trial with a mean dose of 4mg QHS in 17 FM


patients reported a 64% decrease in tender-point score. A second trial was
randomized, placebo-controlled in 30 FM patients with doses gradually
increased over 14 weeks to 8mg QHS. It showed non-statistically significant
improvement in pain, tenderness, fatigue and function compared to place-
bo.17

Pramipexole (Mirapex®) has a stronger effect on the D3 receptor than ropini-


role. Pramipexole was studied in 60 FM patients. It was a randomized, dou-
ble-blind, placebo-controlled, study with every 2:1 patients receiving 4.5mg
QHS pramipexole: placebo, respectively. Pramipexole patients experienced
gradual and more significant improvement in measures of pain, fatigue, func-
tion, and global status at 14 weeks. The most common side-effects were
transient anxiety and weight loss. No patients withdrew from the study
because of inefficacy or side-effects.10

In conclusion, dopamine agonists are effective in FM since chronic pain states


alter the HPA axis which impairs the modulation of adrenergic arousal.
Dopamine inhibits adrenergic arousal by its affects on the hippocampus that
mitigates memory, learning, stress-modulation and nociception.10

2.2.1.5 Pregabalin

Antiepileptic drugs are used widely in the treatment of chronic pain condi-
tions. Pregabalin (Lyrica®) is a gamma-amino-butyric-acid (GABA) analog.14
In Canada it is approved for neuropathic pain associated with diabetic periph-
eral neuropathy and post-herpetic neuralgia.25

Pregabalin works by decreasing the release of glutamate, norepinephrine and


substance P. Decreases in these neurotransmitters are greatest when they
are already activated, as found in FM patients. Crofford et al, studied prega-
balin in doses of 150mg, 300mg, and 450mg per day in a multi-centre, dou-
ble-blind, randomized, placebo-controlled eight-week trial. The group receiv

Fibromyalgia for Pharmacists 11


PHARMACOLOGICAL TREATMENT fm-cfs.ca

2.2.1.5 Pregabalin (continued)

ing 450mg per day significantly decreased average severity of pain compared
with placebo ( p = 0.001). Significantly more in the 450mg group had = 50%
improvement in pain than placebo (29% versus 13%, p=0.003). Both the
300mg and 450mg doses per day groups showed significant improvements in
sleep quality and fatigue. Quality of Life measures improved in those on
450mg per day. The most frequent side-effects were dizziness (usually disap-
peared over time), and somnolence.26

2.2.1.6 Tramadol

Tramadol is a novel analgesic with weak mu-opiod receptor agonist activity


and inhibition of the reuptake of norepinephrine and serotonin.16,20 These
effects may exert anti-nociceptive properties that affect ascending and
descending pain pathways.20 Tramadol has been studied in 315 FM patients
in a 91 day, double-blinded, placebo-controlled trial of tramadol 37.5mg with
acetaminophen 325mg (Tramacet®). Patients taking 4 ± 1.8 tablets per day
active drug were significantly more likely to continue therapy and have
improved pain and physical function, than those taking placebo. The most
common side-effects in the tramadol group were nausea, dizziness, somno-
lence and constipation.27 Caution in starting tramadol needs to be exercised
in patients already taking SSRIs or SNRIs due to the potential of Serotonin
Syndrome and reduced seizure threshold with combined therapy.

2.2.1.7 NMDA-Antagonists

The N-methyl-D-aspartate (NMDA) receptor plays a role in chronic pain.


Blockade of this receptor can relieve pain in FM patients.16 Amantadine, dex-
tromethorphan and ketamine are all NMDA-antagonists.

2.2.1.8 Opioids

Opioids have been used in some FM patients. They have been used with
mixed results. One theory to explain their ineffectiveness in FM may be that
FM patients already have increased endorphin release. Their receptors are
already full.28

Fibromyalgia for Pharmacists 12


PHARMACOLOGICAL TREATMENT fm-cfs.ca

2.2.2 Fatigue Treatments

Disrupted and non-restorative sleep is common in FM patients. The non-ben-


zodiazepine sedatives zopiclone and zolpidem (USA product, not currently
available in Canada) have been used and may improve sleep and decrease
fatigue.16,20 In patients suffering with RLS clonazepam at night can be of
benefit.1 Other drug alternatives for insomnia are low-dose tricyclics, prega-
balin or gabapentin which have sedative effects.20

2.3 Herbals and Supplements

Very little research study of herbs and supplements in FM has been done.4
The internet is abound with therapy "cures" for FM which are very expensive
and not cures.

Ko GD et al, studied a topical herbal agent in FM patients. This was a one-


month, randomized, placebo-controlled pilot study. The over-the-counter
product tested was 024 Fibromyalgia™ consisting of six herbal oils. These are
rosemary, peppermint, camphor, eucalyptus, aloe vera, and lemon/orange.
The placebo oils (peppermint oil) was identical in appearance and smell to the
test product. A blinded consultant (a RN.) supplied one-half of the 153 par-
ticipants with active product, the remaining with placebo. Patients were to
apply Q4H PRN for pain. Statistically significant improvement in the 024
Fibromyalgia™ group was seen in the Visual Analog Scale (VAS) Worst pain,
active tender points, average pain threshold, average Jamar left and right grip
strength.29

024 Fibromyalgia™ works as a counter-irritant. It inhibits pain fibers at the


dorsal horn of the spinal cord. Locally it inhibits the pain transmitters
bradykinin, histamine and prostaglandins. 024 Fibromyalgia™ is dosed up to
three sprays massaged into painful muscle areas, initially best applied at
night, then applied Q8H as needed for breakthrough pain.29

024 Fibromyalgia™ is available in a 30ml spray bottle, or pre-moistened tow-


elettes. For more wide-spread pain relief two sprays or two towelettes can
be added to bath water and the patient soaks in the tub for at least 20 min-
utes. 024 Fibromyalgia™ is absorbed into the skin quickly. If the patient
finds the scent unpleasant the product can be washed off after 20 minutes
without decreasing it's effectiveness. This product is supported by FM-CFS
Canada and the National Fibromyalgia Association Seal of Approval in the
United States.30

Fibromyalgia for Pharmacists 13


SUMMARY fm-cfs.ca

3 Summary

Exciting research is in progress that is leading us to firm data as to the under-


lying cause of FM. This is likely to be multifactorial based on findings thus
far, and the different classes of drugs that have provided symptom relief.

Once the cause/s are confirmed, then more specific drug treatment can be
studied and available to patients suffering from this disabling, chronic pain
condition.

REFERENCES

1. FMS Monograph from http://www.fmpartnership.org/engmonog.htm

2. Peterson J. Understanding fibromyalgia and its treatment options. The


Nurse Practitioner 2005;30(1):48-57.

3. National Fibromyalgia Research Association. USA. Awareness Pin Card.

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