SPECIAL TOPIC SERIES
Muscle Pain: Sensory Implications and Interaction
With Motor Control
Lars Arendt-Nielsen, PhD, Dr Med Sci and Thomas Graven-Nielsen, PhD, Dr Med Sci
Abstract: Muscle hyperalgesia and referred pain plays an
important role in chronic musculoskeletal pain. New knowledge
on the involved basic mechanisms and better methods to assess
muscle pain in the clinic are needed to revise and optimize the
treatment regimes. Increased muscle sensitivity is manifested
as (1) pain evoked by a normally non-nociceptive stimulus
(allodynia), (2) increased pain intensity evoked by nociceptive
stimuli (hyperalgesia), or (3) increased referred pain areas with
associated somatosensory changes. Quantitative sensory testing
provides the possibility to evaluate these manifestations in a
standardized way in patients suffering from musculoskeletal
pain or in healthy volunteers. Some manifestations of sensitisation, such as expanded referred muscle pain areas in chronic
musculoskeletal pain patients, can be explained from animal
experiments showing extrasegmental spread of sensitisation. An
important part of the pain manifestations (eg, tenderness and
referred pain) related to chronic musculoskeletal disorders may
be due to peripheral and central sensitization, which play a role
in the transition from acute to chronic pain. In recent years, it
has become evident that muscle pain can interfere with motor
control strategies and different patters of interaction are seen
during rest, static contractions, and dynamic conditions.
Key Words: muscle pain, experimental pain, hyperalgesia,
referred pain, temporal summation, sensory-motor interaction,
motor control
(Clin J Pain 2008;24:291–298)
M
usculoskeletal pain is a major clinical problem and
often insufficiently treated.1,2 The neurobiologic
mechanisms involved in muscle pain are often difficult
to resolve from clinical studies owing to high variability
between patients, which may be caused by different pain
intensities and duration of their pain condition. Human
experimental pain models applied to healthy volunteers
are a potential strategy to investigate aspects of the
mechanisms involved in muscle pain. Experimental
Received for publication September 12, 2007; accepted September 13,
2007.
From the Laboratory for Experimental Pain Research, Center for
Sensory-Motor Interaction, Aalborg University, Denmark.
Reprints: Prof Lars Arendt-Nielsen, PhD, Dr Med Sci, Laboratory for
Experimental Pain Research, Center for Sensory-Motor Interaction
(SMI), Aalborg University, Fredrik Bajers Vej 7, D-3, DK-9220
Aalborg E, Denmark (e-mail: [email protected]).
Copyright r 2008 by Lippincott Williams & Wilkins
Clin J Pain
Volume 24, Number 4, May 2008
muscle pain research involves 2 separate topics: (1)
standardized activation of the nociceptive system
and (2) quantitative assessment of the evoked sensory
and motor responses. One important advantage with
experimental muscle pain studies is that the cause-effect
relationship is known. In this situation, healthy volunteers transiently become patients with a well-defined
muscle pain where the sensory manifestations and
sensory-motor interaction can be assessed. Moreover,
experimental techniques may be used in clinical studies to
quantify the sensitivity of the nociceptive system in pain
patients and in pharmacologic studies.
CHARACTERISTICS OF MUSCLE PAIN
Sensory manifestations of muscle pain are seen as a
cramplike, diffuse-aching pain in the muscle, pain referred
to distant somatic structures, and modifications in the
superficial and deep sensitivity in the painful areas. These
manifestations are different from cutaneous pain, which
normally is superficial and localized around the injury
with a burning and sharp quality. The sensation of acute
muscle pain is the result of activation of group III and
group IV muscle receptors (nociceptors) responding to
strong (noxious) mechanical or chemical stimulation.3
The nociceptors can be sensitized by release of substances
from the nerve endings. This may eventually lead to
hyperalgesia and central sensitization of dorsal horn
neurones manifested as prolonged neuronal discharges,
increased responses to defined noxious stimuli, pain
response to non-noxious stimuli, and expansion of the
receptive field.3 In humans, limited information is available
on the peripheral neuronal correlate of muscle nociceptor
activation, and only few microneurographic studies have
been published; the main reasons being difficulties in
recording and direct activation of the muscle nociceptors.
Other quantitative techniques are therefore needed, and
quantitative sensory testing may help to assess muscle pain,
muscle hyperalgesia, and referred pain.
QUANTITATIVE ASSESSMENT OF MUSCLE PAIN
The assessment methods of muscle pain are based
on psychophysical, electrophysiologic, and imaging techniques. Only psychophysical methods will be described
here. Psychophysical determinations can be divided into
response-dependent and stimulus-dependent methods.
The response-dependent methods are constructed by a
series of fixed stimulus intensities and a score to each
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Arendt-Nielsen and Graven-Nielsen
stimulus. The score can be a visual analog scale (VAS),
verbal descriptor scale, magnitude estimation, or crossmodality match. VAS, verbal descriptor scales, McGill
Pain Questionnaire, and similar scales and questionnaires
may be very helpful for the assessment of perceived
intensity and quality.4 One important advantages of the
VAS compared with ordinal scales (eg, numerical scales 0
to 10) is that the VAS have ratio scale properties,5 that is,
for 2 different stimuli intensities, where one of them is
perceived as twice the amount of the other, the high VAS
score should be twice the low VAS score.
The stimulus-dependent methods are based on adjustment of the stimulus intensity until a predefined response,
typically a threshold (eg, detection, pain, or tolerance) is
reached. Therefore the uses of scales are avoided. In general,
2 methods to adjust the stimulus intensity exist. In the
‘‘Methods of Limits,’’ the stimulus intensity is gradually
increased until the threshold is reached, and then decreased
again until the stimulus intensity is just below the threshold.
The threshold is defined as the mean of the 2 limits.
Ascending and descending trials can be repeated to improve
reliability. In the ‘‘Method of Constant Stimuli,’’ the stimulus
intensity is incremented in fixed steps and presented for the
patient several times in contrast to the gradual increase as
in the Methods of Limits. The threshold is defined as the
stimulus intensity that is just above the threshold in 50% of
the stimuli.
Stimulus-response functions are more informative
than a threshold determination as suprathreshold
response characteristics can be derived from the data.
For example, the differentiation between low and high
intensity stimuli is clearly evaluated by stimulus-response
functions. Nevertheless, the stimulus-response function
might often be established with stimuli intensities around
the pain threshold and therefore both assessment
methods are needed. Assessments of the sensory aspects
involve both the evaluations of the muscle pain (local
pain) and of the somatic structures related to the referred
pain area, that is, the ongoing pain intensity and the
sensitivity must be described for both areas.
Verbal assessments of the experienced muscle pain
intensity and other subjective characteristics of the muscle
pain are obviously needed in any clinical and experimental
muscle pain studies. The pain intensity is usually scored in
a continuous mode on an electronic VAS to characterize
the time profile of experimental muscle pain. Experimental
muscle pain studies have found that the most frequently used
word descriptors to characterize muscle pain are ‘‘drilling,’’
‘‘aching,’’ ‘‘boring,’’ and ‘‘taut.’’ The intensity of muscle pain
is easily measured using VAS. However, this is only
1-dimensional aspect of the experienced pain, and additional
VAS could be applied to monitor, for example, unpleasantness and soreness.
EXPERIMENTAL MUSCLE PAIN
A number of procedures can induce muscle pain,
and they can be divided into endogenous and exogenous
techniques.6 The endogenous techniques are methods that
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Volume 24, Number 4, May 2008
induce muscle pain by natural stimuli, for example, by
ischemia or by exercise. The exogenous techniques are
external interventions, for example, electrical stimulation
of muscle afferents or injection of pain-producing
substances. In general, the endogenous experimental
techniques induce a widespread deep pain in muscles
and other somatic structures, which may be used in
studies that require a tissue-unspecific deep pain assessment.
Ischemia
Lewis7 proposed induction of muscle pain by
ischemia. A tourniquet is applied, and after a period of
voluntary muscle contractions, a very unpleasant tonic
pain sensation develops. The level of force, the number of
contractions, and the duration are important determinants for the evoked pain. The involved mechanisms
of deep pain after ischemic contractions are not fully
understood. Accumulation of various substances
(ie, potassium, adenosine, lactate) has been suggested to
excite muscle nociceptors or sensitize nociceptors to
respond to muscle contractions that are normally nonpainful.8 This method induces a widespread pain in the
entire occluded limb (skin, periosteum, muscle, etc).
Exercise
Exercise-induced muscle pain by concentric muscle
work is normally short-lasting and a result of impaired
blood flow during work. It may, therefore, resemble the
condition of ischemic muscle pain. As an example, muscle
pain was induced during cycle ergometry of various
loads.9 Eccentric muscle work may cause delayed onset of
muscle soreness with peak soreness after 24 to 48 hours.
Delayed onset muscle soreness has been widely used to
explore pathophysiologic components of the musculoskeletal system. A model of deep tissue hyperalgesia in wrist
extensors with characteristics similar to tennis elbow pain
has recently been described.10 The mechanism underlying
delayed onset muscle soreness is probably related to
ultrastructural damage, resulting in the release of painrelated substances.11 This may produce an inflammatory
reaction, as an anti-inflammatory drug (nonsteroidal antiinflammatory drugs) seems to have an effect on this type
of jaw muscle soreness.12 Howell et al13 were, however,
unable to demonstrate an nonsteroidal anti-inflammatory
drugs effect on delayed soreness in limb muscles. Another
feature of delayed onset of muscle soreness is the fact that
there is no pain at rest, but pain is evoked by muscle
function and during palpation. This is in contrast to
spontaneous pain induced by the exogenous experimental
techniques.
Electrical
In human studies, intramuscular (IM) electrical
stimulation (Fig. 1A) can be used to assess the sensitivity
of muscles, to study basic aspects of deep pain, and to
investigate electrophysiologic properties of muscle afferents by microneurography. IM electrical stimulation is a
tissue-specific (although receptor unspecific) and reliable
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Volume 24, Number 4, May 2008
Muscle Pain
A
B
10
VAS (cm)
Clin J Pain
5
Pain tolerance
threshold
0
0
500
1000
1500
Pressure intensity (kPa)
FIGURE 2. In the automated version of pressure algometry,
the increment rate and intensity of pressure is computercontrolled ensuring a high degree of standardization (A). The
patient scores the pressure sensation on a VAS and stops the
stimulation at pressure pain tolerance (B).
model to study sensory manifestations of muscle pain
such as referred pain and temporal summation, but is
confounded by concurrent activated muscle twitches.
Electrical stimulation offers a unique possibility to
compare both muscle and cutaneous tissues with the
same stimulus modality; for example, a systemic given
anesthetic drug (remifentanil) caused a higher increase in
the pain threshold to IM electrical stimulation compared
with the relative increase in pain thresholds induced by
cutaneous stimulation.14 This indicates that remifentanil
inhibits muscle pain more effectively than cutaneous pain.
Electrical stimulation has also been extensively used to
explore mechanisms of referred pain.
Mechanical
Mechanical painful stimulation can be achieved
with pressure algometers (Fig. 1B). The most widely used
technique is manual pressure algometry. It is important to
recognize that pressure stimulates both the skin and
muscle. Anesthetizing the skin can, however, reduce the
skin pain contribution during pressure stimulation.15
Pressure algometry is actually recommended as one of
the diagnostic procedures for evaluation of patients with
tension-type headache, but so far not for examination
of other musculoskeletal pain conditions. Methodologic
concerns like short-term and long-term reproducibility,
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influence of pressure rates and muscle contraction levels,
and examiner expectancy have all been addressed carefully (for references, see Graven-Nielsen et al15).
An alternative to pressure algometry, and to the
inherent variability related to manual application, is
computer-controlled pressure algometry where the rate
and peak pressure can be predefined and automatically
controlled (Fig. 2). This method allows estimation of
the stimulus-response function between pressure and pain
intensities.15 The facilitated pain response to sequential
stimuli of equal strength is defined as temporal summation. The facilitated degree of temporal summation
indicates an enhanced central integrative mechanism
(central sensitization). Repeated tapping on muscle by
a pressure probe has recently been used to assess the
efficacy of temporal summation.16 Pressure algometry
assesses a relatively small volume of tissue. Instead a
larger volume can be assessed by computer-controlled
cuff-algometry technique. In short, the pain intensity
related to inflation of a tourniquet applied around an
extremity can be used to establish stimulus-response
A
VAS (cm)
FIGURE 1. The muscle pain sensitivity can be assessed by
electrical, chemical, and mechanical stimulation of muscle
nociceptors. A, Needle electrodes inserted into the tibialis
anterior muscle. The tip of the electrodes is uninsulated and
the muscle nociceptors can be excited by constant current
stimulation at stepwise increasing intensities until the pain
threshold is reached. Various algesic substances can also
be infused into the muscle and thereby excite the muscle
nociceptors. In this situation, the pain intensity to a specific
infusion paradigm is scored on a VAS where the end points
indicate no pain and maximal pain. B, With the handheld
pressure algometer, the pressure intensity is manually
increased until the patient presses a button when the pressure
becomes painful. The actual pressure intensity where the
stimulation was stopped defines the pressure pain threshold.
B
7
6
5
4
3
2
1
0
Local pain
Referred pain
0
1
2
3
4
5
6
8
Time (min)
Saline infusion
FIGURE 3. A typical VAS-time
0.5 mL (6%) saline into the
Typically, the patient feels pain
often referred pain to the ankle
profile after IM injection of
tibialis anterior muscle (A).
around the injection site and
area (B).
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Arendt-Nielsen and Graven-Nielsen
curves assessing the deep tissue sensitivity. After IM
injections of anesthetics (lidocaine), the stimulus-response
curve between the tourniquet pressure and pain intensity
was right-shifted, indicating the ability to assess the
sensitivity of muscles.17 A left-shifted stimulus-response
curve between the tourniquet pressure and pain intensity
illustrates deep tissue hyperalgesia.
Chemical
IM injections of pain-producing substances (ie,
glutamate, capsaicin, hypertonic saline) have been used
to induce human muscle pain (see Graven-Nielsen et al18).
The experimental method that has been used extensively
is IM injection of hypertonic saline, as the quality of the
induced pain is comparable with acute clinical muscle
pain with localized and referred pain (Fig. 3). The work of
Kellgren19 in the late 1930s initiated the method of salineinduced muscle pain, and the safety of the technique is
illustrated by no reports of side effects after more than
1000 IM infusions. Recent animal studies have shown
that the method does not cause muscle toxicity and
therefore it is adequate for human experimentation. A
major advantage of the hypertonic saline model is that a
detailed description of sensory and motor effects can be
obtained as the pain lasts for minutes (Fig. 3). Furthermore, the model is reliable for studying referred pain from
musculoskeletal structures owing to the longer lasting
pain. In most of the earlier studies, manual bolus
infusions of hypertonic saline have been used. However,
standardization of the infusion of small volumes is easier
to accomplish by computer-controlled infusion pumps. A
systematic evaluation of the infusion parameters (infusion
concentration, volume, rate, and tissue) has been studied
on pain intensity, quality, and also on local and referred
pain patterns.20
The sensitization of muscle nociceptors is the bestestablished peripheral mechanism for the subjective
tenderness and pain during movement of a damaged
muscle. The sensitized nociceptors not only have a
lowered mechanical excitation threshold, but also exhibit
larger responses to noxious stimuli. If the muscle lesion is
extensive, high amounts of endogenous pain-producing
agents will be released, which could lead to direct
excitation of nociceptors resulting in spontaneous pain.
In humans, this has been reported as decreased pressure
pain thresholds after IM injections of capsaicin.21 Intraarterial injections of serotonin, bradykinin, and prostaglandin have been found effective in sensitizing animal
nociceptors.3 In humans, a decrease in the pressure pain
threshold after combined IM injections of serotonin and
bradykinin was found.22
IM injections of glutamate produce pain and muscle
hyperalgesia to pressure stimuli in humans.23 Interestingly, injections of glutamate in women induced significantly more muscle pain than similar injections in men.24
This might be explained by a greater glutamate-evoked
afferent fiber activity in female compared with male
rats.24 This sex difference is particularly important in
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Volume 24, Number 4, May 2008
relation to the high dominance of women with musculoskeletal pain syndromes.
REFERRED PAIN
Pain perceived at a site adjacent to or at a distance
from the site of origin is defined as referred pain (Fig. 3).
To distinguish between ‘‘referred pain’’ and ‘‘spread of
pain,’’ referred pain is typically restricted to areas outside
the local pain area. Referred pain has been known and
described for more than a century and has been used
extensively as a diagnostic tool in the clinic. Originally the
term referred tenderness and pain was used. Mainly
musculoskeletal and visceral pain conditions are accompanied by local or referred pain.
Kellgren19 was one of the pioneers to study
experimentally the characteristics of muscle pain and
the actual locations of referred pain to selective stimulation of specific muscle groups. Several theories regarding
the appearance of referred pain have been suggested, but
no firm neurophysiologic-based explanations for referred
pain exist. It has been shown that wide dynamic range
neurones and nociceptive-specific neurones in the spinal
cord and in the brain stem receive convergent afferent
input from the skin, muscles, joints, and viscera. This may
cause misinterpretation of the afferent information
coming from muscle afferents when reaching higher levels
in the central nervous system, and hence be one reason for
the diffused and referred characteristics.
Referred pain is probably a combination of central
processing and peripheral input, as it is possible to induce
referred pain to limbs with complete sensory loss owing to
an anesthetic block. However, the involvement of
peripheral input from the referred pain area is not clear
as anesthetizing this area shows inhibitory or no effects on
the referred pain intensity. Central sensitization may be
involved in the mechanism of referred pain. A complex
network of extensive collateral synaptic connections for
each muscle afferent fiber onto multiple dorsal horn
neurones is assumed.3 Under normal conditions, afferent
fibers have fully functional synaptic connections with
dorsal horn neurones and latent synaptic connections to
other neurones within the same region of the spinal cord.
After ongoing strong noxious input, latent synaptic
connections become operational thereby allowing for
convergence of input from more than one source. Animal
studies show a development of new or expansion of
existing receptive fields by a noxious muscle stimulus.
Recordings from a dorsal horn neurone with a receptive
field located in the biceps femoris muscle show new
receptive fields in the tibialis anterior muscle and at the
foot after noxious stimulation of the tibialis anterior
muscle.25 In the context of referred pain, the unmasking
of new receptive fields owing to central sensitization could
mediate referred pain. The area of the referred pain is
correlated with the intensity of the muscle pain and the
appearance of referred pain is delayed (20 to 40 s)
compared with the local muscle pain, indicating that a
time-dependent process, like the unmasking of new
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Volume 24, Number 4, May 2008
SENSORY-MOTOR INTERACTION
IN MUSCLE PAIN
It is well accepted from daily life activities that
muscle pain interacts with the movement performance.
This section illustrates how muscle pain affects the muscle
control in different ways depending on the specific motor
task (Fig. 4).
Resting Muscle Activity and Muscle Pain
Increased resting muscle activity after salineinduced muscle pain is found compared with baseline
recordings, but not compared with a sham pain condition
where patients recalled a painful condition without
having the actual pain stimulation.29 This indicates that
hyperactivity is not present owing to the muscle pain per
se. In another study, a transient increase in the resting
electromyographic (EMG) activity during infusion of
hypertonic saline was recorded in contrast with infusion
of isotonic saline.30 Importantly, on-going muscle pain
did not produce sustained increased EMG activity.
Moreover, experimental muscle pain does not cause any
changes in resting EMG activity between repeated,
maximal voluntary contractions (MVC).31 In contrast to
the experimental studies, both increased and unchanged
resting EMG activity have been reported in musculoskeletal pain patients.
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No muscle pain
Muscle activity
synaptic connections (see above), is involved in the neural
mediation of referred pain.
Substantial clinical knowledge exists on the patterns
of referred muscle pain from various skeletal muscles and
after activation of trigger points in myofascial pain
patients. Referral of muscle pain is typically described
as a sensation from deep structures in contrast to visceral
referred pain that is both superficially and deeply located.
The pattern and size of referral seem to be changed in
other chronic musculoskeletal pain conditions; for
example, fibromyalgia patients experience stronger pain
and larger referred areas after exogenous muscle pain
(hypertonic saline) compared with matched controls.26
Interestingly, these manifestations were present in lower
limb muscles where the patients typically do not
experience ongoing pain. Normally pain from the tibialis
anterior is projected distally to the ankle and only rarely
proximally (Fig. 3). In fibromyalgia patients, substantial
proximal spread of the experimentally induced referred
pain areas was found. Enlarged referred pain areas in
pain patients suggest that the efficacy of central processing is increased (central sensitization). Moreover, the
expanded referred pain areas in fibromyalgia patients
were partly inhibited by ketamine (an N-methylD-aspartate receptor antagonist) targeting central sensitization.27 Extended referred pain areas from the tibialis
anterior muscle, indicating central sensitization, have also
been shown in patients suffering from other chronic
musculoskeletal pain conditions.28
Muscle Pain
Muscle pain
Resting condition
Muscle activity
Static contraction
Muscle activity
Clin J Pain
Agonist
contraction
Antagonist
contraction
FIGURE 4. Summary of findings on the interaction between
muscle pain and motor control. In resting conditions, there is
no effect of muscle pain on the muscle activity of the painful
muscle. In static contractions, the muscle activity is decreased
both in the painful muscle and in other synergistic muscles.
The synergistic muscles are not painful, but involved in the
force generation together with the painful muscle. In dynamic
contractions, the general finding is decreased agonistic muscle
activity and in some situation also increased antagonistic
muscle activity independently of which muscle is painful.
Static Muscle Activity and Muscle Pain
The maximal voluntary contraction during salineinduced muscle pain is significantly lower than in the
control condition.32 Attenuation of MVC force during
experimental muscle pain was not associated with the
changes in contractile properties of muscle fibers, but to a
pure central effect; that is, a motor control modulation. A
clinical demonstration of the observed decrease in muscle
strength during voluntary isometric contractions of a
painful muscle has also been made in musculoskeletal
pain patients. In fibromyalgia patients, the reduction in
strength is suggested to be due to a deficient central
activation of motor units because supramaximal stimulation of the ulnar nerve shows no difference in the strength
of the adductor pollicis muscle between patients and a
control group.33 The modulating effect of muscle pain on
motor control is highlighted by a correlation between
pain intensity and EMG changes34 or motor unit firing
inhibition35 in static contractions.
During a static contraction (ie, 80% of the
MVC before pain), experimental muscle pain causes a
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Arendt-Nielsen and Graven-Nielsen
significant reduction in endurance time.36 The different
findings between submaximal and maximal contractions
may be explained by changes in the descending neural
drive to motorneurones. The descending neural drive
cannot be voluntarily increased during MVC, and an
inhibitory mechanism controlling the motorneurones
might therefore explain the decreases in MVC. When
submaximal contractions are performed, the voluntary
neural drive may be increased and thus compensate for
potential inhibitory mechanisms. An interesting observation is that the muscle pain during static contractions not
only decreases the muscle activity of the painful muscle,
but also attenuates synergistic muscles.36 To produce the
required force, the generalized inhibition calls for a
changed muscle coordination and eventual overload of
otherwise nonpainful muscles. In accordance with experimental findings, a decreased endurance time is reported in
musculoskeletal pain patients performing a submaximal
contraction compared with age-matched and sex-matched
control patients. If submaximal contractions during
muscle pain are obtained by increased voluntary neural
drive, the decreased endurance time may alternatively be
due to a more pronounced central fatigue.37 In clinical
studies, various physiologic factors within the muscle
(eg, microcirculation) could influence endurance time, but
this is not likely to occur in healthy volunteers exposed to
acute muscle pain.
Dynamic Muscle Activity and Muscle Pain
The lumbar muscle EMG activity during a flexionextension exercise is higher in low back pain patients in
full extension than in control patients where it is normally
silent.38 This indicates that the pain modulation of muscle
activity is dependent on the specific muscle function
(agonist/antagonist phases). This has been found in
several previous clinical studies (for review, see Lund et
al39). The lumbar muscle EMG activity in low back pain
patients and during saline-induced lumbar muscle pain is
(1) increased in phases where the EMG activity is
normally silent, and (2) not affected or decreased in the
phases with strong EMG activity in control patients.34
During dynamic contractions, muscle pain causes decreased EMG in the agonistic phase40 and increased
EMG in the antagonistic phase31 of the muscle activity in
painful muscles. Decreased activity in both the agonistic
and antagonistic muscles during muscle pain has been
found without impairing the movement amplitude or
acceleration significantly.41 Especially, the initial (100 ms)
agonistic EMG burst activity was decreased, illustrating
that the motor strategy was affected by muscle pain. This
might be highly important in occupational settings where
such a change may need compensatory actions from other
muscles to fulfill the required movement and thereby
possibly contribute to the development of musculoskeletal pain problems. Increased trapezius activity during
contractions has been found during biceps muscle pain
that might illustrate a compensatory action.41
Reduced movement amplitudes have been reported
in many experimental and clinical musculoskeletal pain
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Volume 24, Number 4, May 2008
conditions such as low back pain. The increased EMG
activity of the muscle (antagonistic phase) opposite to the
painful muscle and the decreased EMG activity of the
painful muscle (agonistic phase) are probably a functional
adaptation of muscle coordination to limit movements.
This adaptation may protect the painful muscle by
reducing the muscle activity and contraction force.
Similar functional protection may account for painful
muscles showing increased muscle activity in the antagonistic phase. In this case, a reduction in the muscle
lengthening (a result of decreased movement amplitude
by increased activity in the antagonistic phase) may
protect the painful muscle.
Experimental models of muscle pain have also been
used in occupational settings (low load, repetitive work)
where saline-induced neck muscle pain was found to
cause changes in motor strategies, for example, a
decreased working rhythm and a muscle coordination
change which may be interpreted as protective.42 Intensive studies of the relationship between work-related
muscle pain and muscle activity have been carried out in
an attempt to find a valid predictor for the development
of neck-shoulder pain. A decreased frequency of unconscious gaps in the low-level EMG activity was found to
predict the patients who developed neck-shoulder pain.43
A higher EMG level during low load repetitive work was
found among the group of workers who developed neckshoulder complaints, highlighting that the level of activity
may have some prognostic relevance for the development
of chronic neck-shoulder pain.44
Neurophysiologic Mechanisms
Muscle hyperactivity initiated by a vicious cycle due
to ischemia was one of the first theories trying to explain
the cause of muscle pain.45 Hyperactivity was also
proposed in the reflex-spasm and stress-causality models,
which are based on either a few experimental observations or literature reviews and thus not systematically
investigated.46 In addition, a physiologic model based on
animal data suggests muscle hyperactivity owing to
facilitation of the muscle-spindle system by muscle pain.47
The evidence for human muscle hyperactivity is, however,
not convincing (Fig. 4).
Lund et al39 suggested the pain-adaptation model to
explain the link between activity in nociceptive afferents, a
central pattern generator, the motor function, and
coordination of muscles. This pain-adaptation model
predicts increased muscle activity in antagonistic phases
and decreased muscle activity in agonistic phases during
muscle pain. Such a coordination may produce a decrease
in movement amplitude and velocity. The pain-adaptation model includes inhibition and excitation of motorneurones according to the functional phases (agonist or
antagonist) of the painful muscle. Findings indicate that
the coordination change owing to muscle pain is not
voluntary, but caused by a reflex mechanism because (1)
muscle pain affects the muscle activity in heteronymous
muscles, and (2) muscle pain differentially modulates the
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Clin J Pain
Volume 24, Number 4, May 2008
muscle activity during one movement-cycle depending on
the specific muscle function.
CONCLUSIONS
A significant part of the manifestations of muscle
and myofascial pain (eg, tenderness and referred pain) in
chronic musculoskeletal disorders may be the results of
peripheral and central sensitization. Reliable methods for
quantitative induction and assessment of muscle sensitization, referred pain, and muscle sensitivity are available.
From a mechanistic point of view, sensory assessment
procedures can provide complementary clinical information and give qualified clues to revise and optimize
treatment regimes.
The interactions between muscle pain and motor
control depend on the specific motor task. Muscle pain
causes no increase in EMG activity at rest and reduces
MVC and endurance time during submaximal contractions. Moreover, muscle pain causes a change in
coordination during dynamic exercises. This is in line
with the pain-adaptation model predicting a decrease in
movement amplitude and velocity when muscle pain is
present. The functional adaptation to muscle pain may
also involve increased muscle activity, reflecting changed
muscle coordination and strategy.
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