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220 Hau Yan KWOK, Kenneth M.C. CHEUNG
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Introduction
is chapter will address pain perceived to be in “muscular” or
“soft” tissues. e phrase “perceived to be in” has been used,
as not only is there an intimate connection with such pain
and that perceived to be in joints or in bones (see Chapter
16) but also such attributions are made by patients on the
basis of common-sense knowledge rather than biological
insight. Certainly “musculoskeletal” pain is ubiquitous in the
community and is by far the main contributor to the point
prevalence of persistent pain, defined as pain present daily for
at least 3 months, of around 20% [9]. It is highly unlikely
that anyone will get through life without experiencing one
episode of such pain. is set of clinical problems challenges
the biomedical model of disease, especially in light of new
knowledge of the neurobiology of pain and nociception
and the sociocultural contributions to the experience and
expression of pain.
e biomedical or disease-based model of illness — in this
case pain — not only is embedded in our culture but also
is plausible to the sufferer. If pain is felt in, say, the arm or
the low back, it may be common sense to assume that that
pain is coming from the arm or the low back. It follows that a
pathoanatomical “cause” — a structural abnormality — should
be there to be found and treated. Indeed, a glance at most
contemporary textbooks that address “musculoskeletal pain”
will reveal an approach based on structural pathology, often as
“revealed” by imaging. However, it cannot be overemphasised
that the mere presence of pathoanatomy (of bones, of joints
or of “soft tissues”) neither predicts the development of pain
nor indicates the origin of pain when it is present. is raises
a challenge to conventional thinking, namely to assert that
ascertaining the mechanism of production of “muscular” pain
should take primacy over identifying its origin.
Muscular Pain Conditions
14
Milton L. COHEN
INTRODUCTION
Problems with nomenclature
Functional taxonomy
NEUROBIOLOGY OF MUSCLE
NOCICEPTION AND
P
AIN
Muscle nociception
Sensitisation and hyperalgesia
EXPERIMENTAL MUSCLE PAIN IN
HUMANS
Experimental models
Somatic referred pain
CLINICAL ASSESSMENT
Implications from neurobiology
Clinical approach
Diagnostic tests
Diagnosis
Problems with the constructs
of “fibrom
yalgia” and
“myofascial pain syndrome”
PRINCIPLES OF MANAGEMENT
OF MUSCULAR
AND REGION
AL
MUSCULOSKELETAL PAIN
Implications from neurobiology
Rational therapy
Evidence base
Summary
REFERENCES
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222 Milton L. COHEN
Problems with nomenclature
e dominance of the biomedical model has
had several consequences which confound a
rational approach to the clinical assessment and
management of muscular pain. Paramount among
these is the problem of nomenclature. As the
diagnostic labelling of a clinical problem implies
both understanding of its biological nature and the
therapeutic pathway to be followed, the profusion of
labels used by the different practitioner groups that
attend to “muscular” or “soft-tissue” problems has
rendered standardisation of names, sharing of the
knowledge base and interpretation of therapeutic
studies very difficult. For example, what is to be
understood by the labels “frozen shoulder” or
“tennis elbow”; are “adhesive capsulitis” and “lateral
epicondylitis” respectively preferred terms? If so,
what is the evidence that such entities ending in “-
itis” are truly inflammatory in pathogenesis? Given
that true muscle inflammation is rare, how are we
to determine the pathogenesis of pain apparently
originating in muscles?
It follows that a rational somatically based
nomenclature should attempt to combine
an anatomical descriptor with a mechanistic
descriptor. To determine the mechanism of
pain production is the first step in formulating
a rational approach to therapy. The allocation
of an anatomical descriptor in a diagnostic
label allows a choice between site of perceived
pain and site of origin of pain. In the case
of an inflamed joint, those two are likely to
correspond. But what of more diffuse pain in
a regional distribution? This raises the related
issues of somatic referred pain [31] and of central
sensitisation of nociception [10]. Each of these
inferences are commonly made after clinical
assessment of pain in a regional distribution
discloses no evidence of a local tissue nociceptive
process (such as inflammation) but does identify
mechanical allodynia or hyperalgesia in the
area of pain. Such a situation, by definition,
is pain of neuropathic pathogenesis occurring
in a regional musculoskeletal distribution. For
example, pain experienced in the arm, for which
no local nociceptive process can be identified
confidently but which may be associated with
neck dysfunction, might be labelled as “regional
neuropathic arm pain” (i.e. site of perceived pain
plus inferred mechanism) or “referred arm pain
from the cervical spine” (i.e. anatomical origin
of pain with inference of why it is felt in the arm
but no inference of mechanism in the neck).
Functional taxonomy for
muscular (or non-articular or
“soft-tissue” or “regional”) pain
is example illustrates the challenge to
nomenclature now faced by pain clinicians arising
out of better understanding of mechanisms of
production of pain and associated hyperaesthetic
phenomena. Keeping this in mind, a functional
taxonomy for non-articular musculoskeletal
pain can be devised. is taxonomy turns on the
pathophysiological phenomenon of tenderness
— technically, hyperalgesia or allodynia — and a
clinical dichotomy which distinguishes between
primary hyperalgesia which tends to characterise
nociceptive pain and secondary hyperalgesia which
suggests that the pain may be neuropathic [38] or
neuroplastic [32] in pathogenesis.
is addresses the somatic contribution to the
biopsychosocial matrix that characterises the current
understanding of and clinical approach to pain in
general [17, 53]. Musculoskeletal pain problems
in particular are characterised by high prevalence,
major impact in terms of personal disability,
largely empirical management programmes, and
by socioeconomic cost to individuals and to the
community [54].
is issue will be addressed again in Diagnosis
below.
Neurobiology of Muscle
Nociception and Pain
Muscle nociception
Receptors and primary aerents
Specific nociceptors are present in skeletal muscle,
of which the majority may be free nerve endings,
subserved by group III (A-delta) and group IV (C)
afferents [37]. Typical muscle nociceptors respond
to noxious local pressure and to local application of
bradykinin. ere are also receptors which respond to
only chemical or mechanical stimulation, suggesting
heterogeneity of nociceptor types, not unlike
cutaneous nociceptors. e degree of specificity of
muscle nociceptors has been difficult to assess.
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Muscular Pain Conditions 223
A relatively high proportion of slowly conducting
muscle afferents is non-nociceptive, responding
to low threshold mechanical stimuli including
muscle contractions. Similar endings are present in
tendons. ese receptors may signal pressure, force
or movement.
In microneurographic studies in humans, afferents
subserving muscle nociceptors have been found
in the A-delta and C range, with response profiles
to local pressure and to algesic substances similar
to those in the cat and rat. Repetitive electrical
stimulation of these muscle afferent units was
associated with cramp-like sensations. Arising out
of the difficulties inherent in recording and directly
activating muscle nociceptors, it remains difficult to
assess whether different qualities of muscle pain are
mediated by different types of muscle nociceptors
and what are their peripheral neuronal correlates
[36, 50].
Spinal and supraspinal connections
At the spinal cord level, nociceptive-specific
and wide-dynamic-range neurons in the dorsal
horn receive convergent inputs from cutaneous,
muscle, joint and visceral afferents. Dorsal horn
neurons responding exclusively to activation
of muscle nociceptors are very rare. In the cat,
the pattern of intraspinal afferents from joints,
muscles and viscera are similar, mainly to laminae
I and V, in contrast to cutaneous afferents. No
studies to date have correlated spinal termination
site with electrophysiologically identified types
of joint afferents, while differential termination
of presumably nociceptive and non-nociceptive
muscle afferent units has been reported [50].
e degree of convergence of deep afferents at the
spinal level provides an anatomical basis for the poor
localisation and discrimination which may attend
joint and muscle pain but also raises the problem
of discrimination between joint and muscle as the
origin of pain in clinical conditions.
Sensitisation and hyperalgesia
e cardinal clinical sign of muscle pain is
hyperalgesia, more familiarly known as tenderness.
Hyperalgesia is defined as increased pain in
response to a noxious stimulus [38]. In the current
state of usage of pain terms, the clinical concept
of hyperalgesia includes the phenomenon of
allodynia, pain in response to a non-noxious
stimulus [38]. In clinical assessment, non-noxious
(mechanical) stimuli such as touch, pressure and
passive movement are usually employed, so that
* Including myophosphorylase deficiency, phosphofructokinase deficiency, glycolytic disorders, carnitine
palmityltransferase deficiency and mitochondrial disorders; not discussed here.
** See Chapter 16.
*** Not discussed here.
Table 14.01 Functional taxonomy for muscular pain
ASSOCIATED WITH NOCICEPTION WITHIN
MUSCLE
ASSOCIATED WITH NOCICEPTION OUTSIDE
MUSCLE
Characterised by primary hyperalgesia Characterised by secondary hyperalgesia
Trauma
Exercise-induced
ischaemia
delayed-onset
impaired energy metabolism*
Inflammation**
polymyositis/dermatomyositis
other vasculitides
“polymyalgia rheumatica”
Primary infection***
viral
Somatic referred pain
Neural impingement
radiculopathy
entrapment neuropathy
Polyneuropathy
Spinal cord disease or damage
Putative syndromes of unknown mechanism
fibromyalgia
myofascial pain
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224 Milton L. COHEN
sensitivity to those stimuli is, strictly, allodynia.
However, in view of the fluid debate regarding these
terms, hyperalgesia will be used here to denote the
phenomenon of tenderness.
Primary and secondary hyperalgesia
e clinical characteristics of hyperalgesia are
spontaneous pain, decreased threshold to noxious
stimuli, increased pain from suprathreshold
stimuli; the neurophysiological correlates of these
phenomena at the receptor/afferent fibre level are
decreased threshold to response, increased response
to suprathreshold stimuli and spontaneous activity
respectively.
In the context of cutaneous injury, the most
extensively studied model, two types of hyperalgesia
have been described [27, 34]. Primary hyperalgesia
occurs in an area of injury, while secondary
hyperalgesia may be found in the undamaged
tissue surrounding the injury. e characteristics
and mechanisms of these two types are distinct
[47, 58, 59]. Regions of primary cutaneous
hyperalgesia are characterised psychophysically
by reduced pain threshold and pain tolerance to
both thermal and mechanical stimuli; regions of
secondary cutaneous hyperalgesia are identified
by normal pain threshold to these stimuli and
reduced pain tolerance to mechanical but not to
thermal stimuli.
e main mechanism of primary cutaneous
hyperalgesia to thermal stimuli is sensitisation of A-
delta and C fibre afferents [47]. Primary mechanical
hyperalgesia may be attributable to sensitisation of
some nociceptors to mechanical stimuli [15] or to
enlargement of the mechanical receptive field of the
primary afferent nociceptor (spatial summation),
although sensitisation of central nociceptive
pathways may also be relevant.
Activation and sensitisation of muscle
nociceptors
e experience of acute muscle pain is the result
of activation of group III (A-delta fibre) and group
IV (C fibre) polymodal muscle nociceptors [37].
In the experimental situation, these nociceptors are
activated particularly by mechanical stimulation and
by bradykinin. ey can be sensitised by increase
in temperature, increase in acidity and exposure
to substances such as bradykinin, serotonin and
prostaglandin E2. Once irritated by a noxious
mechanical stimulus, muscle nociceptors develop
sensitivity to adrenaline.
Inflammatory pain, produced by carrageenan-
induced myositis in the cat or rat, is associated
with increase in resting discharge in both
presumed nociceptors and receptors responding
to weak mechanical stimuli and with an increase
in proportion of the latter. is is attributed to
release of neuropeptides and vasoactive agents
from the inflamed tissue. e role of ischaemia in
activation and sensitisation of muscle nociceptors
remains controversial. It has been proposed that
that tissue hypoxia or acidosis releases bradykinin
or prostaglandin E2, which are then responsible for
sensitisation to mechanical stimuli [37].
Secondary hyperalgesia and central
sensitisation
e comments above apply to the process of
peripheral sensitisation of nociceptors occurring in
the area of induced muscle damage or nociception.
However, the phenomenon of tenderness, as defined
above, can also be elicited in clinically normal
tissue, related to an area of nociception. Arising
out of work mainly with cutaneous nociception
models, this hyperalgesia in undamaged tissue was
labelled “secondary” hyperalgesia. An extensive
literature now attributes this phenomenon to
changed function of nociceptive neurons in the
dorsal horn of the spinal cord, a process labelled as
central sensitisation. is process is a manifestation
of central nervous system plasticity at the level of
the spinal cord: in response to persistent nociceptive
input — injury, noxious stimulation or C fibre
afferent electrical stimulation — dorsal horn cells
show increased activity, enhanced responsiveness to
peripheral stimuli and enlarged receptive field size
[9, 10, 49, 58]. e clinical correlates of this are
spontaneous pain, painful response to non-noxious
stimuli and increased pain in response to noxious
stimuli (allodynia/hyperalgesia) and an increase
in the area of the body from which pain can be
elicited.
Experimental Muscle Pain in
Humans
is discussion has suggested that dissection of the
phenomenon of tenderness is critical in assessing pain
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Muscular Pain Conditions 225
perceived in muscular or soft tissues. e challenge
is to distinguish whether the clinically elicited
hyperalgesia/allodynia is “primary”, occurring in an
area of disease, damage or discernable nociception,
or “secondary”, occurring in normal tissue. e
implications are profound, as the identification of
an area of secondary hyperalgesia/allodynia leads to
an inference that central sensitisation of nociception
may have occurred.
e burgeoning experimental muscle pain literature
has afforded some insight into this conundrum.
In contrast to cutaneous pain, which is normally
felt superficially, localised around the injury and
described as having a burning and sharp quality,
experimental muscle pain is experienced as cramp-
like, aching or boring, felt deeply and diffusely,
and accompanied by alteration in sensitivity to
mechanical stimuli in deep and superficial tissues.
Furthermore experimental muscle pain is often
experienced in somatic structures distal to the
initiating stimulus, again accompanied by altered
sensitivity in the painful areas [1, 24, 31, 55].
Experimental models for muscle
pain in humans
Information regarding muscle nociception and
pain has been obtained through endogenous
techniques simulating natural stimuli, such as
ischaemia or exercise, or through exogenous
techniques employing electrical, mechanical or
chemical stimuli [1, 55]. Voluntary limb muscle
contraction under tourniquet-induced ischaemia
is associated with the development of acute deep,
tonic pain in many tissues. Although commonly
attributed to accumulation of algogenic substances
such as potassium, adenosine and lactate [25],
extrapolation of this explanation to conditions
not characterised by circulatory arrest is difficult.
Exercise-induced muscle pain and delayed-onset
muscle soreness are two related endogenous models.
e former is normally brief in duration and
attributed to impaired blood flow to the muscle(s).
Delayed onset muscle soreness is characterised
by pain in response to palpation or usage of the
muscle but absence of pain at rest. is may be
related to ultrastructural damage with local release
of algogenic substances [39, 42]. e allodynic
nature of this soreness suggests that sensitisation of
muscle nociceptors has occurred.
Intramuscular electrical stimulation has been
used as a tool to investigate the sensory qualities
of induced muscle pain and to infer nociceptive
sensitivity of muscles in clinical situations [2, 33].
Intramuscular injection of algogenic substances,
such as hypertonic saline, glutamate and capsaicin,
may induce muscle pain [23, 31] with localised
and remote components. ese two techniques,
by definition, induce local nociception in muscle
tissue. Application of pressure, usually to a small
volume of tissue [26], may if sufficient also induce
tissue damage, but commonly is used to reveal
locally altered (mechanical) sensitivity.
ese exogenous techniques have led to the
inference that the pain on movement or on
palpation of a damaged muscle is due to sensitisation
of muscle nocieptors in the periphery. Clearly this
concept is important when there is evidence of
muscle damage: the question arises, to what extent
does this apply in apparently spontaneous muscle
pain?
Somatic referred pain
Experimental muscle nociception is characterised
by the development of referred pain, that is, pain
experienced remotely from its origin. is critically
important phenomenon is well recognised to
depend on neural mechanisms [27, 31, 34, 35],
neuroanatomical convergence at a spinal level and
perceptual divergence at thalamic and cortical
levels. Regions of experimentally induced referred
pain are typically hyperalgesic to mechanical
stimuli. e psychophysical characteristics in those
regions are those of secondary hyperalgesia [3, 7,
10, 59], implying that central sensitisation is the
mechanism responsible.
Referred pain is recognised in chronic arthropathy
(for example, pain from an osteoarthrotic hip felt in
the knee). In patients with osteoarthrosis, enhanced
psychophysical responses to mechanical stimuli
applied to normal muscle tissue remote from the
involved joints were consistent with secondary
hyperalgesia, implying a central mechanism; in
patients with rheumatoid arthritis, regions of
increased cutaneous hypersensitivity remote from
joints have been demonstrated [7, 41].
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226 Milton L. COHEN
Clinical Assessment
Implications from neurobiology
of muscle nociception and pain
e presentation of regional musculoskeletal
problems is characterised by pain in and difficulty
moving the affected part, resulting in compromised
function. e clinical challenge is to determine
whether this myalgia is due to a pathological
process in the muscle(s) (myopathy) or otherwise.
e taxonomy suggests that not only is myopathy
relatively uncommon but also such muscle disease
is inflammatory in pathogenesis, either infective
(viral myositis, pyomyositis) or auto-immune
(polymyositis) in aetiology. However, the main
clinical feature of myopathy, inflammatory or
otherwise, is weakness. In the presence of pain,
especially related to muscle or joint movement, the
distinction between antalgic weakness and that due
to disease can be difficult.
Inflammatory muscle disease is an example
of nociceptive pain, characterised clinically
by primary hyperalgesia. By contrast, in the
absence of tissue disease or damage (peripheral
nociception), the hyperalgesia elicitable in
clinical myalgia should be secondary. It follows,
as sensitisation of central nociceptive processes
may reasonably be inferred, that these situations
may be examples of somatic referred pain. is
inference moves the framework of assessment
proximally to central nociceptive pathways and to
a search for neuroanatomically related potential
nociceptive generator(s). For example, pain and
soft-tissue hyperalgesia in the suprascapular
region may be associated with painful limited
movement of the cervical spine and with
mechanical sensitivity over the (anatomically
related) C4/5 level, suggesting that the latter may
be the origin of nociception and the former an
area of referred pain and its intimately associated
psychophysical phenomenon of tenderness.
is discussion implies that alteration in function
may be more relevant than alteration in structure
in this clinical context. e inferential sequence
is: allodynia in painful normal tissue defines
secondary hyperalgesia from which is inferred
central sensitisation of nociception which implies
both the possibility of other nociceptive drivers and
modulation by “higher” centres.
ese comments apply to assessment of the somatic
contribution. Interacting with this in determining
the clinical presentation of myalgia will be the
affective, behavioural and cognitive dimensions,
consequent on the experience of pain, assessment
of which may be more important than the somatic
in determining management programmes.
In summary, the implications from the
neurobiology of muscle pain and nociception for
clinical assessment are:
• Distinction between primary and secondary
hyperalgesia
• Identification of possible nociceptive
“drivers”
• Place in biopsychosocial framework.
Clinical approach
When evaluating a complaint of pain perceived in
musculoskeletal structures, the principles of clinical
evaluation are:
1. What is the anatomical origin(s) of the pain
and what is the mechanism of the pain
(nociceptive or neuropathic/neuroplastic)?
2. Are there clues to an associated disease
process?
3. What are the functional consequences of the
pain? (Disability)
4. What are the cognitive and affective
components of the presentation? (Beliefs
regarding diagnosis and prognosis,
compromised performance of activities of
daily living, mood)
Traditional teaching includes the following steps in
bedside assessment:
• Inspection (“look”)
• Palpation (“feel”) for temperature, tenderness
(allodynia/hyperalgesia) and swelling
• Assessment of movement (“move”):
• passive movement of muscles and
peripheral joints
• active movement of spinal segments
• specific stressing (resisted movement) of
muscle groups
to which can be added
• Signs of neurological dysfunction
• Evoked hyperaesthetic signs (see Table 14.02)
• Tests of function, e.g. hand grip,
Trendelenburg’s test, gait assessment.
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Muscular Pain Conditions 227
ese techniques of clinical assessment, in pursuit
of principles 1, 2 and 3 above, may have variable
reliability, reasonable face validity and construct
validity in terms of identifying underlying pathology
(even if a gold standard for the last of these existed),
but they can help the clinician formulate the “bio-”
component of the diagnostic assessment, tailored
to that patient.
Diagnostic tests
Laboratory investigations are of very limited
value in the assessment of muscular or regional
musculoskeletal pain and are largely directed towards
making the distinction between inflammatory and
non-inflammatory processes.
Blood tests
• e peripheral blood white cell count is a poor
reflector of musculoskeletal inflammation.
A normal count does not exclude acute
inflammation, especially infection.
• Mild normochromic normocytic anaemia
(secondary anaemia) may reflect chronic
inflammation.
• Mild thrombocytosis may also reflect
inflammation.
• e erythrocyte sedimentation rate (ESR)
is a time-honoured but very non-specific
indirect indicator of inflammation. e main
determinants of this in vitro phenomenon are
the haematocrit of the sample of anticoagulated
blood and the presence of proteins, the so-
called acute-phase reactants, which promote
red blood cells to form rouleaux. Foremost
among the acute phase reactants is fibrinogen,
levels of which increase with age, which may
account for the higher reference range for
ESR in the elderly. Reliance on this test to
determine inflammation, especially in the
presence of anaemia, is discouraged.
• C-reactive protein is an alpha-2 globulin,
elaborated as an acute-phase reactant. Its
measurement and interpretation are not
influenced by the haematocrit of the blood
sample.
• Creatine kinase is a marker for muscle damage
and may be elevated in inflammatory myopathy
Table 14.02 Clinical elicitation of hyperaesthetic phenomena
FEATURE BEDSIDE EXAMINATION MECHANISM
Static mechanical allodynia Gentle pressure Sensitisation of C-afferents
Mechanical (pinprick)
hyperalgesia
Pin-prick Sensitisation of C-afferents
Punctate mechanical allodynia Toothpick Transmitted by A-delta: impinging
on sensitised second-order
neurons
Dynamic mechanical allodynia
Brush allodynia
Touch evoked allodynia
Brush Transmitted by A-beta: impinging
on sensitised second-order
neurons
Deep somatic mechanical
allodynia
Deep pressure
Passive movement
Unknown
Warm allodynia
Heat hyperalgesia
Metal roller or tube at 45°C Sensitisation of C-afferents
Cold allodynia
Cold hyperalgesia
Metal roller or tube at 20°C Transmitted by A-delta:
Central sensitisation
Central disinhibition
Temporal summation (wind-up)
After-sensation
Repeated stimuli 2/sec for 30 sec, Central sensitisation; A-delta input
Source: Cohen ML. Possibilities and problems of a mechanism-based approach to the diagnosis and management of
musculoskeletal pain. In Justin DM, ed. Pain2005 – An Updated Review: Refresher Course Syllabus. IASP Press,
Seattle, 2005
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228 Milton L. COHEN
(Chapter 16) or metabolic myopathy [19].
However, there is a high prevalence of false-
positive creatine kinase levels which may
be found in normal people or those taking
cholesterol-lowering medication [16].
Imaging studies
Imaging studies are of limited utility in the context
of muscular or regional musculoskeletal pain. e
mere presence of an anatomical abnormality does
not establish either the anatomical origin of pain
or its mechanism. Furthermore, the prevalence
of anatomical “abnormality” in asymptomatic
populations is dependent upon age and needs to be
taken into account before inferences are made.
Muscle biopsy
Muscle biopsy has a very limited role in the investigation
of isolated muscle pain. e probability of finding
definite muscle pathology in the context of muscle pain
and a normal examination is very low [19].
Local diagnostic tests
Infiltration of local anaesthetic into soft tissues
(“focal local”) is popular as a diagnostico-therapeutic
manoeuvre, the argument being that the anatomical
origin of the pain is determined instantly and relief
follows. While this may work in some instances, it
gives no insight into the mechanism of production
of the pain and quite overlooks the contextual
(placebo) component of an invasive procedure. Such
tests have not been subjected to systematic review.
Diagnosis
Diagnostic labelling of muscular or regional
musculoskeletal pain problems is necessarily
confined to the somatic component and depends
upon the conceptual framework of assessment. A
nociceptive orientation may seek to label problems
conveniently as “myositis”, “tendonitis”, “bursitis”,
etc. (implying local inflammation) or to identify
putative local structural pathology (such as
“myofascial trigger points”; see below). A broader,
neurobiologically based approach might infer
that central sensitisation of nociception may have
occurred, but is then frustrated by the inability to
determine what process(es) may have initiated or
may be maintaining the clinical problem and by
the lack of consensus regarding terminology, as
discussed above. In the current state of knowledge
and opinion, these difficulties are circumvented by
the construction [anatomical part in which pain is
perceived] + [“pain syndrome”], as, for example,
“carpal tunnel syndrome”, “cervicobrachial pain
syndrome”, “piriformis (pain) syndrome”. Such
labelling conveys no insight into the mechanism
responsible for clinical presentation, spuriously
invokes the concept of syndrome (which refers
to the concurrence of apparently diverse clinical
features) and elevates the presenting problem —
“pain” — to the level of diagnosis.
An alternative, suggested by the author, would
be to use the term “impairment” to denote
abnormal function of the painful bodily part and
to suggest a mechanism of pain production such as
“nociceptive” or “neuropathic/neuroplastic”. us,
a patient with pain experienced diffusely in an upper
limb, characterised clinically as being an area of
secondary hyperalgesia, with no features to suggest
local nociception or neural impingement, might be
labelled as having “neuropathic (cervico-)brachial
impairment in the absence of cervical radiculopathy”.
A person with widespread musculoskeletal pain
and associated tenderness (who might attract
the label “fibromyalgia” — see below) might be
labelled as having “diffuse (presumed neuroplastic)
musculoskeletal impairment”. However, such an
alternative does not address the other dimensions
of the biopsychosocial framework which would
characterise the clinical presentation.
Although this vexed question of diagnostic
nomenclature for muscular or regional
musculoskeletal pain problems is far from resolution,
the implication that alteration of nociceptive
function is more relevant than structural pathology
may form the basis for a rational approach.
Problems with the constructs of
bromyalgia” and “myofascial
pain syndrome”
Over the last decade or two, the field of “soft
tissue rheumatism” or regional musculoskeletal
pain has become dominated by two competing
constructs, fibromyalgia syndrome [61] and
myofascial pain syndrome [57]. ese constructs
are examples of the circular argument that ensues
when clinical phenomenology (in these cases,
“tender points” or “trigger points”) leads directly
to syndromic labelling (fibromyalgia syndrome or
myofascial pain syndrome), without being linked
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Muscular Pain Conditions 229
to pathophysiology. Furthermore, both constructs
have fallen foul of the fallacy of reasoning which
occurs when the evidence on which a proposition is
based is taken as proof of its validity [45, 46]. us
they have become tautologies, as their diagnostic
criteria can be violated so easily as to include all
possibilities [11].
Fibromyalgia syndrome
Fibromyalgia syndrome is said to be diagnosed if,
in a presentation of widespread musculoskeletal
pain of at least 3 months duration, 11 “tender
points” out of 18 defined sites can be identified
by digital palpation [61]. Although this criterion
was published for classification purposes, it has
been abused clinically, both in terms of the “tender
point” count and by the caveat that fibromyalgia
syndrome may coexist with any other painful
condition. No distinctive anatomical, biochemical,
physiological or psychological pathology has been
found to explain the nature of these “tender points”.
It has been asserted that the “tender points” are
central to the diagnosis but epiphenomenal to the
pain; indeed that they may be present in people
not complaining of pain [52]. A study in the
general population did find “tender points” to be
associated with pain complaints but independently
also with depression, fatigue and sleep problems
[14]. No specific therapy other than the use of
tricyclic antidepressant drugs, exercise programmes
and cognitive-behavioural techniques as used in
other examples of chronic pain has been generated
let alone validated [48]. e status of fibromyalgia
syndrome as an externally valid clinical entity
remains controversial [28].
Myofascial pain syndrome
Myofascial pain syndrome is a regional pain
syndrome comprising a discrete zone of deep
aching pain which may be located close to or
distant from a “trigger point”, a localised area of
mechanical allodynia which is assumed to be in
muscle tissue, although they have been described
in other tissues. Such “trigger points” are said to
be located within palpable “taut bands”; their
“inactivation” by physical (needling or stretch) or
chemical (local anaesthetic) means is required for
pain to be relieved. e manual [57], widely held to
be authoritative, documents extensive observations
and proposes a pathophysiology for which evidence
is meagre and treatment regimens which have not
been subjected to testing. “Active” “trigger points”,
responsible for both local and remote pain are said
to occur in multiple locations within a muscle,
with diurnal variation in irritability; “latent”
“trigger points” are said not to cause referred pain
but may be present in asymptomatic subjects;
“satellite” “trigger points” may emerge in the pain
reference zone of another “trigger point” and then
themselves become primary generators of local
and referred pain. is construct incorporates its
hypothesis of causation and invites tautological
reasoning [11, 45]. e assertion that the patient
may only be aware initially of referred pain and not
of its putative “trigger point” source [51] begs the
question. ere are no histological, biochemical or
electrophysiological clues to the nature of “trigger
points”. A recent review concluded that there is still
limited consensus regarding case definition and, as
such, caution needs to be exercised in evaluating
claims about effective interventions [56]. As with
fibromyalgia syndrome, the status of myofascial
pain syndrome as describing an externally valid
entity is suspect.
Relationship between “tender points” and
“trigger points”
ese two sets of phenomena appear to have much
in common. e two studies that compared them
identified fundamental problems with reliability
and validity of trigger points in general and the
concept of “latent” trigger points in particular,
to a greater extent than the proposed criteria for
fibromyalgia [21, 62]. e candidacy of either
type of “point” to be the primary site of origin of
nociception is not supported by the literature.
Clues to the nature of “tender points” and
“trigger points”
e phenomenon of “tender points” is not
disputed, even though most psychophysical studies
have shown that putative fibromyalgia syndrome
patients are more sensitive than controls at non-
tender points as well [11]. Numerous clinical and
psychophysical studies suggest that the clinical
phenomena of fibromyalgia syndrome may be an
expression of secondary hyperalgesia, implying
central nociceptive changes [4, 60]. If so, the
challenge is to find the initiating and/or sustaining
nociceptive driver(s).
Similarly the phenomena of “trigger points”
and of pressure over them being experienced
elsewhere in the body (but constrained by known
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