Curr Pain Headache RepDOI 10.1007/s11916-011-0205-3
Effects of Treatment of Myofascial Trigger Pointson the Pain of Fibromyalgia
Maria Adele Giamberardino & Giannapia Affaitati &Alessandra Fabrizio & Raffaele Costantini
# Springer Science+Business Media, LLC 2011
Abstract Myofascial pain syndromes (MPSs) from trigger
points (TrPs) and fibromyalgia syndrome (FMS) are commonmusculoskeletal pain conditions that frequently coexist in the
Myofascial pain syndromes (MPSs) from trigger points
same patients. In recent decades, it has become evident that
(TrPs) and fibromyalgia syndrome (FMS) are common
these entities greatly influence each other’s clinical expres-
forms of musculoskeletal pain. Though distinct in diagnos-
sion. FMS is mainly rooted in the central nervous system,
tic criteria and clinical features in typical cases (with
while TrPs have a peripheral origin. However, the nociceptive
regional pain in MPSs and generalized pain in FMS), these
impulses from TrPs may have significant impact on symp-
two entities very often can be confused with each other in
toms of FMS, probably by enhancing the level of central
clinical practice, mostly because of their frequent coexis-
sensitization typical of this condition. Several attempts have
tence in the same patient. This can pose problems of
been made to assess the effects of treatment of co-occurring
differential diagnosis and treatment ].
TrPs in FMS. We report the outcomes of these studies
In recent decades, it has become increasingly evident
showing that local extinction of TrPs in patients with
that this coexistence is not a merely by-chance association,
fibromyalgia produces significant relief of FMS pain. Though
but rather reflects a cause–effect relationship. On one hand,
further studies are needed, these findings suggest that
in fact, TrPs are more frequent in FMS due to a higher
assessment and treatment of concurrent TrPs in FMS should
susceptibility in FMS to microtraumatic events that are
be systematically performed before any specific fibromyalgia
recognized causative factors for TrP formation On the
other hand, muscle TrPs in any individual represent apowerful peripheral source of nociceptive impulses; in time,
Keywords Myofascial trigger points . Local injection .
these are likely to favor the development of central
Fibromyalgia . Fibromyalgia syndrome . Pain syndrome .
sensitization phenomena that can promote the clinical
Peripheral pain generators . Myofascial pain . Pressure pain
manifestation of FMS in predisposed individuals [].
threshold . Musculoskeletal pain . Central sensitization .
These findings have raised the question as to whether
Comorbidity . Taut band . Anesthetic . Management .
treatment of TrPs in patients with the two conditions may have
Pathophysiology . Tender point . Antidepressants . Local
a significant impact on the pain of the more severe of the two:
fibromyalgia. Though not yet very numerous, recent clinicalstudies have addressed this issue and found a significantbenefit of local TrP extinction for the generalized FMS pain.
M. A. Giamberardino (*) : G. Affaitati : A. Fabrizio
This article provides updated information on this complex
Pathophysiology of Pain Laboratory, Ce.S.I., “G. D’Annunzio”
issue, summarizing the current knowledge about clinical
Foundation, University of Chieti,Chieti 66100, Italy
features, pathophysiology, and classic treatment of MPSs/
TrPs and FMS separately; discussing the critical elements indifferentiating the two in routine medical practice; and
reporting the results of the studies showing the impact of
Institute of Surgical Pathology, University of Chieti,Chieti 66100, Italy
MPS treatment on FMS symptomatology.
Myofascial Pain Syndromes from Trigger Points
snapping or pincer techniques (muscle accessible from oneor two directions, respectively) [Both potentially elicit the
“local twitch response” (LTR), a brief local contraction ofmuscle fibers. The TrP is identified as the point within the
MPSs are acute, recurrent, or chronic forms of regional
band of maximal tenderness upon firm digital pressure; this
musculoskeletal pain whose mean prevalences among
elicits pain locally and in the target if the TrP is sufficiently
middle-aged (30–60 years) men and women are 37% and
hyperirritable, and provokes a painful reaction by the patient,
65%, respectively, and 85% in elderly (> 65 years) adults
An MPS is a “complex of sensory, motor and autonomic
symptoms caused by myofascial trigger points”, where TrPsare “spots of exquisite tenderness and hyperirritability in
Hyperalgesia has been shown by decreased pain thresholds
muscles or their fascia, localised in taut, palpable bands,
(pressure, electrical stimuli) at TrP level (in muscle, subcutis,
which mediate a local twitch response (LTR) of muscle
and skin) and at target level (always in muscle, with extension
fibres under snapping palpation and, if sufficiently hyper-
to subcutis and/or skin only in high TrP hyperirritability)
irritable, give rise to pain, tenderness and autonomic
TrP treatment by injection (see below) produces desen-
phenomena as well as dysfunction in areas usually remote
sitization not only locally but also in the target (thresholds
from their site, called targets” []. Active TrPs provoke
significantly increased in skin, subcutis, and muscle),
spontaneous pain, and thus, an MPS; latent TrPs are
confirming the interdependence of the sensory changes at
clinically silent but frequently evolve into active TrPs in
target level and the trigger activity [, ]. Areas outside
time. A primary TrP is located in a muscle directly
the TrPs and targets show sensory normality in patients
subjected to overload/repetitive overuse; a secondary TrP
with MPS who have no concurrent pain conditions
is induced in a muscle, neurogenically or mechanically, by
potentially affecting general pain sensitivity ].
the activity of a nociceptive focus in a different structure(deep somatic or visceral) ].
Routine Laboratory and Instrumental Tests
Diagnostic criteria for MPS derived from international
multicentric studies or expert consensus meetings still are
Specific tests for MPS identification still are needed,
lacking. At present, the most clinically relevant features for
though some findings can be confirmatory of the clinical
diagnosing an MPS in current practice include identifica-
diagnosis (eg, spontaneous electromyography (EMG) ac-
tion of the taut band and reproduction of the spontaneous
tivity at TrP, visualization of an LTR at ultrasounds)
pain complaint by exquisite pressure on a point of
Microdialysis provides very interesting results (ie, high
levels of pronociceptive substances in active TrPs), but the
Essential steps in the approach to patients with suspected
technique is not suitable for routine application in medical
MPSs are clinical history collection and physical examina-
tion TrPs most often result from muscle traumas/microtraumas; thus, patients should be questioned about
any event, activity, or habit potentially causing muscleoverload, overuse, or disuse. Possible secondary TrPs also
A TrP would be a dysfunctional site where an abnormal
should be explored by asking questions about any previous
increase is present in the production and release of acetylcho-
painful visceral disease or other deep somatic pain sources
line packets from the motor nerve terminal under resting
within the neuromeric field of the involved muscles [, ].
conditions (dysfunctional endplate). This mechanism would
MPS pain, at rest and/or on movement, is tensive,
be enhanced by an initiating traumatic/microtraumatic event
constrictive, or cramplike and of variable intensity and
(primary TrPs) or referral process (secondary TrPs), with
duration, with sudden or gradual onset. It rarely is located in
increased motor endplate activity, persistent release of
the TrP zone, but most often occurs in a distant area (target),
acetylcholine, and sustained depolarization of the postjunc-
typical of each muscle/TrP. Accompanying symptoms are
tional membrane of the muscle fiber. This could, in turn, cause
altered muscle motor function, cooling, sweating, and
a continuous release and inadequate uptake of calcium ions
pilomotor activation, or even lacrimation, imbalance, dizzi-
from the local sarcoplasmic reticulum (SR), producing
ness, and tinnitus for MPSs in the head/neck region [
sustained shortening of sarcomeres. A vicious circle of
At inspection during physical examination, the physician
hypoxia (with release of vasoactive/algogenic substances,
should look for any biomechanical discrepancy and asymme-
responsible for local nociceptor sensitization, and thus,
try that may have caused muscle overload ]. Palpation of
hyperalgesia), failed Ca++ reuptake from the SR (due to
muscles is first aimed at identifying the taut band through
energy impairment), and perpetuation of the contracture
(“integrated hypothesis” of the original “energy crisis”
symptoms. Should they became unanimously recognized,
we probably would witness a change in the profile of thetypical fibromyalgia patient, with an expansion of the
population receiving this diagnosis in the future [
The onset of FMS symptoms can be either gradual or
Deactivation of TrPs must be combined with removal of
post-traumatic (physical injury/psychological stress). The
perpetuating factors (eg, microtraumas, chronic infection,
typical spontaneous pain is a persistent, diffuse, deep, and
stress/mood disorders, poor sleep, and nutritional/metabolic
aching sensation in muscles, most often continuous with
periodic exacerbations of high intensity (flares). Associated
The most frequently applied techniques for TrP deacti-
symptoms (eg, affective dysfunction, cognitive deficits,
vation are spray and stretch, TrP pressure release, and local
short-term memory loss, dizziness, syncope, nonrestorative
injection (see [, ] for a more detailed description of
sleep, daytime fatigue, prolonged morning stiffness, numb-
these and other techniques). The latter represents the gold
ness, tingling, and dysesthesias) are present in various
standard; it can consist of “dry needling” or injection of
combinations. Comorbidity frequently occurs with depres-
active substances, particularly local anesthetics. The effec-
sion, anxiety, irritable bowel syndrome, dysmenorrhea,
tiveness of dry needling probably lies in the mechanical
interstitial cystitis, other rheumatic conditions, chronic
disruption of the integrity of dysfunctional endplates.
fatigue syndrome, myofascial pain syndrome, low back
However, injection of an analgesic markedly reduces the
pain, temporomandibular joint disorder, and headache.
patient’s discomfort during and after the procedure, and
Patients with FMS report even light stimuli applied to their
thus, enhances the global outcome of the therapy. Injection
somatic structures as painful. As documented by many
of any solution in general, including saline, may relieve
experimental studies, this is due to a generalized increased
symptoms temporarily by diluting and dissipating sensitiz-
sensitivity to pain in terms of lowered pain thresholds of
ing substances in the region of the energy crisis ].
skin, subcutis, and muscle to a variety of stimuli (eg,
Injection of botulinum toxin also is effective, but its
mechanical, thermal, electrical, chemical) in both painful
efficacy is no greater than that of the local anesthetic; the
latter, being much less expensive, is thus preferred ].
Though the origin of the syndrome has not been completelyclarified yet, there is a general consensus that the main
disturbance behind FMS is an altered processing of the painsignal. On the whole, a number of neuroendocrine (ie,
FMS is a chronic condition of widespread musculoskeletal
dysfunction of the hypothalamic-pituitary-adrenal axis),
pain and tenderness accompanied by numerous aspecific
neurotransmitter (ie, altered metabolism of serotonin,
symptoms, among which sleep disturbance and affective
norepinephrine, and dopamine, as well as substance P, and
dysfunction are particularly frequent. It affects about 4% of
nerve growth factor) and neurosensory (ie, central sensiti-
the general population; its sex distribution, nearly equal in
zation, abnormalities of descending inhibitory pain path-
childhood, is up to sevenfold more common in women than
ways) disturbances have been implicated in the generation
of the syndrome. Patients with FMS have aberrant
Criteria for FMS diagnosis still remain those established
responses to pain on functional brain neuroimaging and
by the American College of Rheumatology Committee in
also show an accelerated loss of brain grey matter,
1990 [1) a history of widespread pain (involving all
interpreted by some as a sign of premature aging of the
limbs and the trunk) of at least 3-months duration; and, 2)
brain ]. A genetic predisposition would be essential for a
tenderness to digital palpation (with a pressure of 4 kg) in at
variety of environmental stressors to lead to the clinical
least 11 of 18 (9 symmetrical) predetermined body sites
called tender points (TePs). A TeP is a site of exquisitetenderness in soft tissues that, in contrast to the TrP of
MPS, is not included in a taut band of muscle fibers, doesnot evoke LTR under snapping palpation, and, especially,
Though not threatening the patients’ life, FMS severely
does not refer pain at a distance when stimulated [••].
impacts on the quality of life and physical function [
A critical revision of the above criteria is currently
Complete resolution of symptoms is rarely achieved, but a
underway. The newly proposed criteria no longer consider
significant improvement is obtained with an adequate
the presence of TePs, but only assess clusters of clinical
After a comprehensive evaluation of pain, function, and
activating/precipitating factors of conditions other than
psychosocial context of the patient, a multidisciplinary
treatment approach should systematically be taken, includ-
As stated above, the coexistence of TrPs and FMS is
ing a combination of pharmacologic and nonpharmacologic
very common epidemiologically, TrPs being significantly
interventions. Options for pain treatment include para-
more frequent in patients with FMS than in the general
cetamol or weak opioids, such as tramadol, while NSAIDs
population []. This probably happens because FMS
or corticosteroids are not recommended unless a coexisting
patients, due to their chronic pain and disability and
inflammatory/autoimmune disorder is present.
consequent poor posture/antalgic attitudes, are more prone
Antidepressants are recommended for long-term treat-
to muscle microtraumas, well-known promoting factors for
ment (cycles of several months) because they decrease pain
TrP formation. Once developed, TrPs can, in turn, enhance
and often improve function. Particularly employed are
FMS symptoms through their input to the central nervous
tricyclics (especially amitriptyline), but also selective
system [Several authors have thus evaluated the
serotonin reuptake inhibitors (eg, fluoxetine) or dual
possible contribution of TrPs to fibromyalgia symptoms,
(serotonin and noradrenalin)-reuptake inhibitors (eg, ven-
though with some methodological differences among
lafaxine, duloxetine, and milnacipran). Antiepileptics, es-
pecially pregabalin, also are recommended for pain
Alonso-Blanco et al. [] systematically explored the
treatment in FMS [While the U. S. Food and Drug
presence of TrPs in multiple muscles in 44 patients with
Administration has officially approved the use of three
FMS versus 50 control subjects and determined whether the
compounds, duloxetine, milnacipran, and pregabalin, for
local and referred pain from active TrPs reproduced the
FMS, no official drug specific for the syndrome has been
overall spontaneous fibromyalgia pain pattern and whether
approved in Europe, where these compounds are currently
widespread hypersensitivity (pressure pain thresholds
used off-label for the syndrome, by the European Medicines
[PPTs] at TePs sites) was related to the presence of
widespread active TrPs. FMS patients had a mean of 11
Nonpharmacologic management includes heated-pool
TrPs (10 active, 1 latent) in contrast to control subjects only
treatment, individually tailored exercise programs (eg,
showing latent TrPs (mean: 2). The combination of the
aerobic exercise, strength training), and cognitive-
referred pain patterns from active TrPs fully reproduced the
behavioral therapy. Relaxation, rehabilitation, physiothera-
overall spontaneous pain area of FMS. Patients with FMS
py, and psychological support also can be of help in many
had significantly lower PPTs than control subjects and a
significant positive correlation between the number of
One approach gaining progressively more importance
active TrPs and spontaneous pain intensity. The authors
in FMS management is treatment of the so-called
interpreted these results as an indication of the contribution
“peripheral pain generators.” It had been noted for quite
of nociceptive inputs from active TrPs to central sensitiza-
some time in clinics that FMS patients with concurrent
sources of nociceptive pain in their somatic periphery,
According to several authors, in addition to having
such as an MPS from TrPs or a painful joint (a very
more frequent TrPs than the normal population at all
frequent situation, given the high comorbidity level in
muscle levels, patients with FMS would commonly
FMS) [], have exacerbation of their typical fibromyalgia
harbor TrPs at the very site of their TePs, with a
pain [This has suggested that, after appropriate
significant overlap between TePs and TrPs [, ]. In
identification, local suppression of these peripheral sour-
2010, Ge et al. ] indeed tested the hypothesis that the
ces of nociceptive inputs may be beneficial not only for
18 predetermined sites of TePs in fibromyalgia frequently
the local pain but also for the widespread symptoms of
are associated with myofascial TrPs and that the induced
FMS []. An account of the recent studies specifically
pain from active TrPs at TeP sites may mimic fibromyalgia
addressing this issue in the case of myofascial TrPs in
pain. In their study of 30 patients with FMS, the TeP sites
were specifically tested for trigger characteristics, bothmanually and at EMG recording of spontaneous activity,and the features of the spontaneous FMS pain were
Effects of Treatment of Myofascial Trigger Points
compared with those of the pain evoked by TrP stimula-
tion. The authors found that most of the TeP sites wereTrPs, with local and referred pain from active triggers
TrPs in muscles are recognized powerful sources of
partly reproducing the overall spontaneous pain pattern.
peripheral nociceptive impulses that can have profound
The total number of active TrPs was positively correlated
influences on the sensory processing of painful messages at
with the spontaneous FMS pain intensity. This study
central level [In this view, they can be potential
provided evidence in FMS patients of the importance of
active TrPs, which may serve as peripheral generators of
The study protocol was double-blind, with neither
fibromyalgia pain, and the authors suggested that inacti-
patients nor clinicians collecting data and sensory evalua-
vation of active TrPs may be an alternative for the
tion being aware of the patients’ group. Only the clinician
treatment of FMS. Indeed, the year before (2009), a paper
performing therapy was unblinded. After treatment, in the
by Staud et al. [•], in which the role of peripheral
active-treatment group but not placebo-treated group,
muscle input was explored in the initiation and mainte-
number and intensity of myofascial episodes and para-
nance of FMS, was published. In a randomized, double-
cetamol consumption decreased while PPTs at TrP site
blind, placebo-controlled trial of 22 female control sub-
increased, with all changes being significant. In parallel,
jects and 28 female patients with FMS, the authors tested
FMS symptoms also significantly improved; pain intensity
the effects of trapezius muscle TeP injections with 1%
decreased and all thresholds increased progressively in the
lidocaine on local pain thresholds and remote heat hyper-
TePs and nonpainful site. At day 8, all placebo-treated
algesia in the forearm. Before muscle injections, shoulder
patients requested active local therapy, which was delivered
pain was standardized by tonic mechanical muscle stimu-
on days 8 and 11, while none of the patients under active
lation, resulting in local pain ratings of 4.0 ± 0.5 visual
treatment requested additional therapy. At a 3-week follow-
analogue scale (VAS) units. This stimulation was interrupted
up (days 30 or 37), FMS pain still was lower than the
for the injections but continued afterwards at the same
initial, pre-study pain in patients not undergoing further
level. Both control subjects and patients showed signif-
therapy and had decreased in those receiving active therapy
icantly increased PPTs at the trapezius after lidocaine
injections, but not placebo. Heat hyperalgesia in the
The results of this study thus showed that in fibromy-
remote site also was significantly reduced by lidocaine,
algia patients with concurrent MPSs due to TrPs not
but not placebo, in patients with FMS. Neither lidocaine
coincident with TePs sites, local treatment of the peripheral
nor saline injections significantly affected clinical FMS
muscle sources not only relieves regional symptoms but
pain ratings, probably due to the very low dose of lidocaine
also produces a significant improvement of the widespread
employed (50 mg). These results confirm the important role of
FMS symptoms (ie, lesser spontaneous pain and TePs
peripheral inputs in maintaining central sensitization in
hypersensitivity as well as reduced generalized hyper-
fibromyalgia. In this study, the injection site was apparently
algesia). The authors claimed that the diffuse tissue
not specifically tested for TrP characteristics. However, given
desensitization observed is not attributable to a systemic
the high frequency of coincidence of the trapezius TeP
action of the drugs delivered locally to TrPs because TrP
with a TrP area, it is highly probable that the beneficial
anesthetic infiltration previously had been shown to not
effects of treatment in these patients were indeed due to
produce any significant change in pain thresholds in a
nonpainful area in patients without fibromyalgia ]. The
A recent paper by Affaitati et al. ••] specifically
decreased level of generalized hyperalgesia, as well as of
evaluated the effects on fibromyalgia pain of treatment of
spontaneous diffuse pain, must thus reflect other mecha-
concomitant TrPs that were not coincident with the TeP
nisms related to the hypothesized pathophysiology of FMS
sites. They studied 68 female FMS patients with coexisting
(ie, a reduction of the degree of central sensitization). The
unilateral MPSs of the upper body, manifesting as accesses
extent of symptom decrease obtained in this study is not
of regional pain from active TrPs in the trapezius (1 trigger
such to allow suspension of specific FMS treatments, but is
in the medial third of the upper border, clearly distinct from
sufficiently marked (22%–30%) to hypothesize either a
the fibromyalgia TeP in the same muscle; n = 20) or
possible dose reduction of chronically administered drugs
infraspinatus muscle (1 or 2 triggers; n = 48).
for FMS or a better symptom control at the same doses,
In basal conditions, patients were assessed for their
with obvious advantages for the patients. The authors thus
myofascial pain symptoms, (ie, number/intensity of pain
proposed that identification and treatment of peripheral pain
episodes, PPTs at trigger site, paracetamol consumption),
generators represent the first approach to FMS before any
and FMS symptoms (ie, spontaneous diffuse pain [VAS]
other therapy is initiated. In this research, only FMS pain
and hypersensitivity [PPTs at TePs sites, PPTs and electrical
symptoms were tested; it will be important in future studies
pain thresholds in skin, subcutis, and muscle in a distant,
using a similar protocol to verify if other typical FMS
nonpainful area at quadriceps level]). They then were
complaints, such as sleep disturbance, fatigue, physical
randomly assigned to two groups of 34 patients each to
impairment, or affective dysfunction, also can actually
receive either active or placebo-like local TrP treatment
benefit from extinction of peripheral nociceptive sources.
(TrP injection with anaesthetic [1 mL of 0.5% bupivacaine
No other controlled study to date appears to have
hydrochloride] or needle penetration in an area near the
addressed the impact of treatment of clearly identified TrPs
trigger) on days 1 and 4. Evaluations were repeated on days
on FMS symptoms. However, a recent study by Castro-
Sánchez et al. ] has shown how local treatment of
muscles, through massage able to release the TeP areas, has
ably forecast a dose reduction of specific drugs for FMS,
a positive impact on FMS symptoms. In view of the
and/or a better symptom control at the same doses. Thus, a
elevated number of TrPs in patients with fibromyalgia, it is
systematic search for TrPs in FMS, at the TePs sites as well
probable that the observed beneficial effects of this
as in other locations, and their extinction is an approach that
treatment are secondary to TrP extinction. In this random-
should systematically be adopted before any other therapy
ized controlled trial, 74 patients with FMS were randomly
is initiated when faced with a patient with fibromyalgia.
assigned to experimental (massage–myofascial releasetherapy) and placebo (sham treatment with disconnectedmagnotherapy device) groups for an intervention period of
No potential conflicts of interest relevant to this article
20 weeks. Pain, anxiety, quality of sleep, depression, and
quality of life were determined at baseline, after the lasttreatment session, and at 1 and 6 months. Immediately aftertreatment and at 1 month, anxiety levels, quality of sleep,
pain, and quality of life were improved in the experimentalgroup over the placebo group. Significant differences
Papers of particular interest, published recently, have been
persisted at 6 months in the quality-of-sleep index.
Myofascial-release techniques thus improved pain and
On the whole, the results of the reported studies indicate
that nociceptive muscle input in FMS, most often originat-
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Best Evidence Summaries of Topics in Mental Healthcare BEST in MH clinical question-answering service www.bestinmh.org.uk Section for Evidence-Based Mental Health P.O. Box 32 Health Services and Population Research Department Institute of Psychiatry De Crespigny Park London SE5 8AF Tel: 020 7848 0498 Email: contact@bestinmh.org.uk Question : In adults with depression, what
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