Editorial

Received: May 11, 2004

Eur Neurol 2004;52:67–72
Accepted: May 14, 2004
DOI: 10.1159/000079748 Published online: July 13, 2004

Myofascial Pain, Fibromyalgia or

Fibrositis?
J.M.S. Pearce
Emeritus Consultant Neurologist, Department of Neurology, Hull Royal Infirmary, Hull, UK

Key Words utility of these terms. The only claimed physical sign is
Myofascial pain W Fibromyalgia W Fibrositis W Nociceptor W the presence of tender trigger points over muscles or
Central pain muscle attachments. Research suggests that tender
points are a measure of general distress related to pain
complaints but separately associated with fatigue and
Abstract depression. They are present in some normal subjects
The terms myofascial pain, fibromyalgia and fibrositis and are variable in occurrence in time in the same indi-
are critically examined. They constitute diagnostic labels vidual. They reflect no demonstrable pathology. It is
for non-specific musculoskeletal aches and pains. Analy- therefore argued that none of these commonly used
sis of the evidence shows that none of these labels is diagnoses represent distinct disease entities. A possible
substantiated by hard physical signs or by laboratory but unproven alternative hypothesis is that such symp-
evidence of consistent pathological or biochemical ab- toms relate to neural pain with both peripheral and cen-
normality. What is the objective evidence for disorder(s) tral components, and in some instances psychological or
of muscle, fascia or fibrous tissues, so clearly indicated wilful embellishment.
by these diagnostic names? Alternative terms such as Copyright © 2004 S. Karger AG, Basel

‘regional pain syndrome’ or ‘chronic pain syndrome’

merely redefine the clinical problem without providing a
mechanism or basis for diagnosis. Despite different diag- ‘Belief like any other moving body
follows the path of least resistance.’
nostic criteria, these conditions, along with chronic fa-
tigue syndrome, have many demographic and clinical Samuel Butler (1612–1680)
similarities, most notably tender trigger points. Indeed,
the terms are often used interchangeably. There are few A wide variety of painful syndromes has for many
differences in the symptoms, physical findings, laborato- years been attributed to a disorder of muscles, tendons,
ry tests, functional status, psychosocial features and psy- ligaments and fascia. Chronic backache, neck ache, tem-
chiatric disorders. This paper seeks not to deny the exis- poromandibular joint syndrome and a variety of pelvic,
tence of aches and pains, but to critically examine the limb and chest wall pains have been explained on this

© 2004 S. Karger AG, Basel J.M.S. Pearce

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basis. Yet such attribution is at best conjectural since tance when stimulated’ [6], but it fell from favour because
there is a striking dearth of physical signs or investiga- nobody could show a pathology [7]. Some still speculated
tions, which would serve to validate myofascial pain, without proof on regional pain syndromes caused by a
fibromyalgia (FM) or fibrositis as explanations, or to pro- pathology so subtle that it could not be demonstrated;
vide a convincing objective basis for the symptoms. they called this myofascial pain syndrome (MPS).
Painful muscles, tendons and ligaments are common,
but usually symptoms are short-lived and pose no lasting
medical problems. For over 100 years they were called Fibromyalgia
muscular rheumatism, rheumatic neuralgia (Gowers) or
fibrositis to distinguish them from arthritis, a condition FM has more recently been invoked to account for
with pathology demonstrable within joints [1]. Rheuma- chronic and widespread musculoskeletal pains [8]. Ac-
tism was ascribed to inflammation of fibrous tissues in cording to the diagnostic criteria for FM syndrome pub-
bursae, tendons, ligaments, fascia, muscles and nerve lished by the 1990 American College of Rheumatology,
sheaths [2]. More often rheumatism was used to imply an FM patients must have: (1) widespread pain in all four
undefined, but essentially transient benign non-specific quadrants of their body for a minimum of 3 months; (2) at
inflammation [1]. least 11 of the 18 specific tender points. Commonly asso-
Ten years ago Henriksson noted: ‘The conclusion is ciated symptoms include: fatigue, sleep disorder, tempo-
that no one single mechanism can explain FMS and is romandibular joint dysfunction, postexertion malaise and
thus in that sense a compromise. FMS [fibromyalgia syn- muscle pain, numbness and tingling, skin sensitivities,
drome] in some patients may start in the muscle, in other morning stiffness, irritable bowel, chronic headaches (ten-
patients in the brain. The combination of peripheral and sion type or migraines), cognitive or memory impairment,
central factors is the key to the pathogenesis of FMS as menstrual cramping and premenstrual syndrome, dizzi-
long as FMS is defined as a pain syndrome’ [3]. This paper ness or impaired coordination.
aims not to deny the existence of aches and pains, but to FM shares many similarities with myofascial pain,
critically examine (like Henriksson) the utility of the chronic fatigue syndrome and fibrositis [9, 10]. The nota-
terms myofascial pain, FM and fibrositis. ble authorities, Cohen and Quintner [9], state:
‘Its pathophysiology, physical and psychological, is un-
known, and the nature of the allegedly mandatory TPs
Fibrositis [trigger points] remains obscure. Diagnostic criteria
convey no pathophysiological insight and they have
Sir William Gowers in 1904 [4] invented the term: been ‘validated’ via a circular argument in which the
‘I think we need a designation for inflammation of evidence on which the construct is based is taken as
the fibrous tissue which has not such results [sc. the proof of its veracity. The concept of fibromyalgia syn-
production of induration or suppuration] ... We may drome is valid only in the sense that it includes all pos-
conveniently follow the analogy of cellulitis and term sibilities. An alternative approach is to consider sec-
it fibrositis.’ ondary hyperalgesia.’
Fibrositis could spread to the fascial investments of
adjacent tendons, joints and nerve sheaths, thus explain-
ing for example some instances of ‘interstitial sciatic neu- Tender Trigger Points
ritis’. A British Medical Association committee in 1933
recognized subgroups of fibrositis [5]: intramuscular and Trigger points (TPs) are allegedly an important sign of
fascial; periarticular; bursal and tenosynovial; subcuta- MPS and FM. A classic TP is defined as the presence of
neous (panniculitis), and perineuritic. ‘Perineuritis’ could discrete focal tenderness located in a palpable taut band
cause radiating pain, paraesthesiae, cutaneous hyperaes- of skeletal muscle, which produces both referred regional
thesia, tenderness in muscles and joints within the sensory pain (zone of reference) and a local twitch response. TPs
innervation and local nerve tenderness attributed to the are used to define MPSs. Tender points, by comparison,
involvement of the nervi nervorum. are associated with ‘pain at the site of palpation only, are
Slowly the concept of the fibrositic nodule arose, ‘an not associated with referred pain and occur in the inser-
area in the substance of a muscle or its tendinous sheath tion zone of muscles, not in taut bands in the muscle belly’
which gives rise to localized pain or referred pain at a dis- [11]. By definition [12], patients with FM have tender

68 Eur Neurol 2004;52:67–72 Pearce

points, but patients with MPS may also have TPs; these muscle, and antagonists are overloaded when they coun-
two pain syndromes may therefore overlap and be diffi- ter its tautness. The chronicity of pain that follows stimu-
cult to differentiate. lation by palpation or electrical stimulus of a myofascial
The mechanism of myofascial pain with characteristic TP is explained by a feedback cycle maintained by the
TPs and taut bands is said to be a spinal reflex disorder central nervous system (CNS) receiving impulses arising
caused by a reverberating circuit of sustained neural in the TPs. But since the painful muscles in MPS are elec-
activity in a specific spinal cord segment. However, this is trically silent, the suggestion of myofibrillar or myofas-
conjecture unsubstantiated by experimental data. When cicular contraction is highly improbable [15]. Further-
blinded to the diagnosis, experts in MPS found TPs in more, the efferent Á-motoneuron activity was diminished
only 18% of subjects with a diagnosis of MPS [13]. In the rather than increased in muscles with carrageenan-in-
same study, assessments for taut bands and muscle twitch duced injury [16]; thus, these authors concluded that
responses were also found to be ‘unreliable’. these models ‘have to be considered as working hypothe-
How useful are TPs? Unfortunately there is a dearth of ses rather than explanations of known mechanisms’.
large series and no independent hallmark by which the They later showed that at all central nervous levels the
diagnoses can be validated. One study reported [14] 250 connections and processing of nociceptive information
subjects selected from participants in a chronic pain sur- from muscle and skin are different. They deduced that a
vey who had a TP examination. Of these, 100 had chronic dysfunction of descending pain-modulating pathways
widespread pain, 100 regional pain and 50 no chronic could lead to chronic deep pain as in fibromyalgia. This
pain. On the day of examination, pain in many patients remains hypothetical since the data were partly from
had shifted. For instance 3/74 with stated chronic wide- anaesthetized rats, and partly from healthy subjects or
spread pain now had no pain, and 7/39 with no chronic FM patients [17].
pain now had chronic widespread pain. According to their Chronic fatigue syndrome and FM [18] are clinical
status on the day of examination, the criterion of 11 of 18 conditions both characterized by a variety of non-specific
painful TPs was found in 40% of patients with chronic symptoms including prominent pain near muscles, fa-
widespread pain, 20% of those with regional pain and 5% tigue and sleep disturbances. ‘Many researchers now be-
of those with no pain. Overall 20 of 132 patients without lieve patients with the chronic fatigue syndrome have
one of the two criteria of FM had at least 11 painful TPs. many similarities with FM patients [19, 20], and about
By contrast, 29% of patients with chronic widespread 75% of patients meeting the diagnostic criteria of chronic
pain had only 0–4 painful points. In this study, Croft et al. fatigue syndrome also meet the criteria for a diagnosis of
[14] observed that similar sites are common in asymp- FM.
tomatic individuals: There are no diagnostic investigations or widely ac-
‘The distinctive sign is tenderness to pressure at spe- cepted pathogenic mechanisms for either illness. Despite
cific sites over muscles or muscle attachments. Tender different diagnostic criteria, chronic fatigue syndrome,
points are a measure of general distress. They are relat- MPS and FM have many demographic and clinical simi-
ed to pain complaints but are separately associated larities including TPs. The terms are often (mis)used
with fatigue and depression ... Fibromyalgia does not interchangeably. There are few differences in the symp-
seem to be a distinct disease entity.’ toms, physical findings, laboratory tests, functional sta-
The criterion of 11 painful TPs thus appears unreli- tus, psychosocial features and psychiatric disorders [21].
able: a poor diagnostic test. There is no gold standard Myofascial TPs may be initiated by many diverse pre-
against which they can be measured. Experts elicit differ- cipitants: trauma, muscular strains, chilling of fatigued
ent numbers in the same patients [13, 14]. muscle or nerve root injury [22]. These same factors are
These findings cast serious doubt on the internal valid- also said to be capable of activating latent TPs [23]. These
ity of the concept. The TPs vary from person to person injuries are thought to release neurokinins, histamine,
and from hour to hour. Proponents consider TPs as latent serotonin and prostaglandins, which stimulate nocicep-
or dormant if not causing referred pain. Latent TPs are tors and cause reflex muscle contraction. But the evidence
thought to increase with age. Satellite TPs are in muscles does not support this concept. Muscle pain and damage
within the pain reference zone of another TP. Secondary following eccentric contractions have been studied [24].
TPs develop in muscles that are either synergists or antag- In normal subjects, unless there are muscle tears or deep
onists of the muscle primarily affected. Synergists are said haematomata, recovery from injury is complete. Electro-
to be overloaded when they substitute for the affected myography of painful muscles [15] and thermographic

Myofascial Pain, Fibromyalgia or Eur Neurol 2004;52:67–72 69

Fibrositis?
studies [25] have not shown diagnostic abnormalities in factors is vast and includes the full spectrum of supposed
TPs. Muscle biopsies of TPs have shown no consistent aetiologies of MPS and the related ‘syndromes’ men-
muscle inflammation or damage. tioned [10, 16, 23, 24]. This reiterates the circular reason-
ing. Trying to provide external confirmation of their
notion, researchers say that TPs arise from muscle dam-
Myofascial Pain Syndrome age, despite electrical silence and the lack of histological
or biochemical abnormality. But, there is neither support
The term myofascial pain [26] was introduced in 1952 from an animal experimental model nor from studies of
and developed by Travell and co-workers [22, 27]. It has human muscle damage or injury [24]. Spread of pain is
been defined as a regional pain syndrome with: (1) the TP, attributed to the activation of latent TPs or to the ‘metas-
a localized area of deep muscle tenderness or hyperirrita- tasis’ of TPs. This teleological argument is physiologically
bility, and (2) a predictable, discrete reference zone of unsound. Taken together, the evidence on which MPS is
deep aching pain, which may be located in the immediate founded arises from an illogical definition.
region of or remote from the TP, may be quite extensive
and is worsened by palpation of the TP.
TPs have been described in the skin, joint capsules, Possible Basis of Soft Tissue Pain
ligaments and periosteum as well as in muscles and their
fasciae. The clinical and epidemiological features overlap The pain in question has the features of deep somatic
impressively with FM, fibrositis and chronic fatigue. On pain. By the 1930s, the experiments of Sir Thomas Lewis
‘snapping’, palpation or needling of a myofascial TP, a [30] and Kellgren [31] convincingly demonstrated distant
local twitch response can be elicited. This is accompanied referral of somatic pain, such as originates in muscles, ten-
by an irritable electromyographic response. A muscle con- dons and bone. Kellgren [31] noted:
taining a TP is said to exhibit antalgic inhibition when ‘The diffuse pain from a given muscle is always distrib-
tested for strength and is intolerant to stretch. Inactiva- uted within certain regions, though the distribution
tion of the relevant TPs by physical or chemical means is within these limits varies from individual to individual,
needed to relieve pain. The specific muscle or muscle and according to the part of the muscle stimulated’ and
group that causes the symptoms should be identified. TPs ‘pain from muscle may be confused with pain arising
are nonetheless said to be maintained via the CNS, not from other deep structures such as joints and testis.’
only by their own activity but also by many processes It is prudent to be cautious in diagnosing the precise
associated with afferent neural input. Central sensitiza- origin of such pain. The roles of psychogenic, central and
tion is claimed to involve ‘wind-up phenomena’ due to peripheral neural mechanisms may each be relevant. Af-
activation of N-methyl-D-aspartate receptors on second- ferents from sites of referred muscle pain are the same as
order neurons in the brainstem. Derangements in de- those that act centrally on the spinal neurons that process
scending endogenous pain-modulating systems due to ‘pain information’ from deep structures, thus leading to
central serotonin deficiency may explain the disordered central summation [32] and probable enhancement. Pal-
antinociception. Simons and Travell [23] have somewhat lor, cyanosis, hypo-aesthesia and abnormal sweating are
vaguely defined MPS as ‘primarily a dysfunction of one or commonly seen in the skin overlying a source of deep
more specific muscles’. Myofascial TPs have no gold stan- somatic pain. These phenomena occur commonly and
dard diagnostic criterion [28]. normally in a limb immobilized after fracture, the immo-
It is difficult to ignore the fact that the proponents of bility being an important causal feature (invariably
MPS [22; for extensive literature, see ref. 29] have present in reflex sympathetic dystrophy). These signs may
included their conclusions and beliefs within their defin- be explained as somatic referred pain [33]. Since human
ing, diagnostic criteria. Unfortunately this elementary peripheral nerves are well innervated by nervi nervorum
error in logic and reasoning largely invalidates any consid- [34], peripheral neural pain may also be important. Nerve
eration of other possible explanations of the symptoms – trunk pain may simulate myofascial pain. Such pain has
as they define them. been attributed to increased activity in mechanoceptors
The definition of MPS is fallacious since its definition and nociceptors, within the neural sheath. Pain with the
incorporates the very hypothesis it seeks to prove: an characteristics of ‘nerve trunk pain’ is recognized in
example of circular reasoning. The permitted number and patients with irritative cervical and lumbar radiculopathy
nature of predisposing, precipitating and perpetuating [35] and with peripheral nerve injury [36].

70 Eur Neurol 2004;52:67–72 Pearce

 Hyperalgesia in muscles that are structurally and elec- aetiology and, as the explanation of chronic, deep, aching,
trically normal suggests that the hyperalgesia [37] is poorly localized pain, lack both internal and external va-
referred owing to peripheral antidromic activation or sen- lidity.
sitization [38] of nociceptive afferents or results from cen- Fallacies in this concept include a logically implausi-
tral sensitization of nociceptive dorsal horn neurons [39]. ble, circular definition of MPS that incorporates a theory
Radiation of pain and tenderness may depend on altered of its cause. TPs, commonly used in diagnosis, are non-
central processing held responsible for secondary hyperal- specific and clinically unreliable. Both predisposing and
gesia maintained by nociception arising in peripheral precipitating factors are numerous and occur in many
nerves. But these factors still leave us without any good other pain syndromes. Histological, biochemical and elec-
explanation of a mechanism to account for the persistence trical evidence of causal pathology is lacking, and experi-
of aches and pains after a self-limited or unknown prima- mental human models of muscle injuries yield no consis-
ry ‘illness or injury’. tent pathogenetic findings. A neural basis, involving cen-
tral pain and/or peripheral hyperalgesia though equally
unproven, is a more attractive hypothesis. Psychogenic
Conclusion factors and motives, outside the scope of this study, are
important, particularly in persistent pain.
A painful condition of soft tissues is undoubtedly a
genuine entity, though as a consequence of sprain or trau-
ma it is usually short-lived. Persistent or recurrent soft Acknowledgement
tissue pain is commonly ascribed to MPS or FM, and cri-
This review was stimulated by the writings of many authors, par-
teria have been generally accepted. It is suggested that
ticularly M.L. Cohen, J.L. Quintner, R.M. Bennett and F. Wolfe.
MPS, fibrositis and FM simply redefine the problem of

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