Australian Dental Journal 2008; 53: 201–207

REVIEW
doi: 10.1111/j.1834-7819.2008.00050.x

How does pain affect jaw muscle activity? The Integrated

Pain Adaptation Model
CC Peck,* GM Murray,* TM Gerzina*
*Faculty of Dentistry, The University of Sydney, New South Wales.

ABSTRACT
Pain and limitation of movement are two cardinal symptoms of temporomandibular disorders but it is unclear how one
influences the other. The relationship between pain and movement is clinically significant but controversial with two major
theories having been proposed: the Vicious Cycle Theory and the Pain Adaptation Model. The Vicious Cycle Theory
proposes a vicious cycle between pain and muscle activity. This theory has little scientific basis but underpins many
management strategies. The Pain Adaptation Model is more evidence-based and proposes that pain causes changes in muscle
activity to limit movement and protect the sensory-motor system from further injury. The Pain Adaptation Model has many
positive features but does not appear to explain the relation between pain and muscle activity in all situations. We propose
that the relationship is influenced by the functional complexity of the sensory-motor system and the multidimensional nature
of pain. This new Integrated Pain Adaptation Model states that pain results in a new recruitment strategy of motor units that
is influenced by the multidimensional (i.e., biological and psychosocial) components of the pain experience. This new
recruitment strategy aims to minimize pain and maintain homeostasis. This model emphasizes the individual reaction to
pain and suggests a tailored approach towards management.
Key words: Jaw muscle activity, jaw movement, Vicious Cycle Theory, experimental pain, Pain Adaptation Model, knowledge translation.
Abbreviations and acronyms: EMG = electromyographic; IPAM = Integrated Pain Adaptation Model; TMD = temporomandibular
disorders.
(Accepted for publication 1 May 2008.)

movements depend on contractile jaw muscle activity

INTRODUCTION
The following is based on a recent, comprehensive
review of orofacial pain and motor function to which
the reader is referred.1 Temporomandibular disorders
(TMD) are a group of conditions involving pain in or
about the temporomandibular joint and ⁄ or jaw mus-
cles, limitation of jaw movement, and ⁄ or joint sounds
and are the most prevalent non-odontogenic chronic
pain condition in the orofacial area.2–8 TMD are severe
enough to prompt 5–10 per cent of the population to
seek treatment3,9 and can have considerable detrimen-
tal effects on a patient’s work, family life and social
activities.10,11
Pain and motor function are interrelated
While the aetiology of TMD is unclear, patients and
clinicians alike know that pain and jaw motor function
are somehow interrelated. For example, patients with
TMD frequently have restricted mouth opening and
reduced jaw function. It is well to recall that jaw
ª 2008 Australian Dental Association
which can be recorded experimentally as electromyo-
graphic (EMG) activity. There have been several
theories formulated over the years that have a bearing
on the relationship between pain and muscle activity.
The two major theories are the Vicious Cycle Theory
and the Pain Adaptation Model. An understanding of
this pain-muscle activity relationship could help eluci-
date the mechanisms underlying pain and impaired
function in the orofacial region.
The Vicious Cycle Theory essentially proposes that
an initiating factor such as an abnormality in structure,
posture, movement or stress results in pain that
reflexively* leads to ‘‘muscle hyperactivity’’ that in
turn leads to spasm or fatigue and thereby further pain
and dysfunction, thus perpetuating the cycle.9,10,12–15
This theory (which was never much more than an initial
hypothesis16) has become, probably because of its
simplicity,17 the basis of many management strategies
*That is, via sensory inputs to the central nervous system either
exciting or inhibiting motor neurones supplying muscles.
201
CC Peck et al.
that attempt to break this purported vicious cycle in a
variety of pain conditions.10,12,13,15,18–20
The Pain Adaptation Model on the other hand
proposes that the pain does not arise from muscle
hyperactivity but from other causes (which the model
does not presume to explain), and that, via segmental
brainstem or spinal cord motor circuits, the pain leads
to alterations in muscle activity that limit movement
and protect the skeletomotor system from further injury
and thereby promote healing.18–20 Specifically, the
model proposes that for any movement, agonist mus-
cles (i.e., those primarily responsible for the movement)
decrease in activity (e.g., decreases in lateral pterygoid
muscle activity during opening), and antagonist muscles
(i.e., those resisting the movement) increase in activity
(e.g., increases in masseter activity during jaw opening).
The effect of these changes is to make movements
slower and smaller and thereby reduce the chance of
aggravating the injury and thus aid healing. Although it
is generally considered the most appropriate explana-
tion of the relation between pain and muscle activ-
ity,10,21,22 there has been much debate on this relation
in the literature.9,10,12,14,15,17,21–23
Evidence consistent with some aspects of the Vicious
Cycle Theory
In terms of one of the arms of the Vicious Cycle Theory,
namely, that pain induces increases in muscle activity,
there is abundant animal experimental evidence that
noxious stimulation can reflexively evoke short-dura-
tion increases in jaw muscle EMG activity.11,24–27 In
the human, some studies of experimental or clinical
pain do report small increases in jaw muscle EMG
(where jaw muscle activity is recorded) activity during
pain. However, as indicated below, the small increases
in jaw muscle EMG activity identified in these studies
are unlikely to be of any clinical significance. In terms
of the other arm of the Vicious Cycle Theory, namely,
that increases in muscle activity lead to pain, there are
some experimental studies that indeed show that
repeated low level clenching over five days does result
in pain that in some subjects can lead to a diagnosis
of TMD.28,29
Evidence against the Vicious Cycle Theory
Although the Vicious Cycle Theory or its fundamental
premises still forms the basis of some treatments in the
current clinical management of chronic pain, there is
actually no convincing evidence in support of one of its
critical tenets, namely, that pain leads to increased jaw
muscle activity.10,18,20,21,23,30 Thus, many EMG studies
have shown that clinical muscle pain has very little
effect on jaw muscle EMG activity, whereas the Vicious
Cycle Theory would predict increases in jaw muscle
202
activity. Although some studies have reported increases
in EMG activity in association with pain (see above),
the increases are very small (only a few lV) and not to a
level of clinical significance that would allow a muscle
to be classified as ‘‘hyperactive’’ or expected to cause
pain.18,21 Furthermore, there is the very real issue in
many of these studies reporting increases in jaw muscle
EMG activity that the increases were actually increases
in facial muscle activity (e.g., buccinator activity with
grimacing) that is well-known to occur in patients in
pain and which can be picked up by the adjacent jaw
muscle EMG electrodes that are located on the surface
of the skin;18,21,31 note that this contamination issue
does not apply to intramuscular jaw muscle EMG
electrodes.
Supporting evidence for the Pain Adaptation Model
In contrast to the lack of supporting evidence for the
Vicious Cycle Theory, there is much scientific literature
consistent with or supportive of the Pain Adaptation
Model.10,18–23 Numerous experimental pain and clin-
ical pain studies have repeatedly shown that pain results
in smaller and slower movements than pain-free
controls.10,21,23,32–35 Furthermore, controlled studies
have demonstrated changes in muscle activity (e.g.,
decreased agonist EMG activity) that result in these
smaller and slower movements following wisdom tooth
removal or minor oral surgery,36,37 during empty open-
close-clench cycles in the presence of experimental pain
induced by hypertonic saline into the left masseter
muscle,18 and in a variety of other experimental and
clinical pain studies in the jaw, limb, and trunk motor
systems.23,34,38–45 As well, increased activity in the
antagonist muscles (e.g., increased jaw closer activity
during jaw opening) has been demonstrated during
maximum opening under experimental pain in com-
parison with pain-free controls,18 and during the
opening phase of the chewing cycle in TMD
patients.40,46
The Pain Adaptation Model does not appear
to explain all the associations between pain and
motor activity
Despite the supporting literature, there are some
research findings that do not fit closely with the Pain
Adaptation Model. For example, some studies of
experimental and clinical orofacial pain41,46,47 showed
that pain had no effect on jaw movement amplitude
during mastication in comparison with pain-free con-
trols. Some muscle EMG activity changes are also not
completely consistent with the Pain Adaptation Model.
For example, some studies of the effects of human
experimental or clinical pain on jaw muscle EMG
activity do not always find significant decreases in
ª 2008 Australian Dental Association

agonist EMG activity33,46 or significant increases in
antagonist EMG activity33 in comparison with painless
function. Further, in a well-studied experimental rat
model of TMJ pain (mustard oil or glutamate injected
into the TMJ), short-duration increases in EMG activity
in both jaw opening and jaw closing muscles are
routinely observed.11,24–27 Although the Pain Adapta-
tion Model was developed for human chronic pain, it is
interesting to note that the model would predict
increases in one but not both muscle groups in this
experimental rat model. Furthermore, findings from
human studies of the effects of pain on locomotor,44
trunk,23 or forelimb48,49 muscle activity are also not
always consistent with the Pain Adaptation Model. For
example, many inconsistencies have recently been
identified in the literature on the relation between
chronic low-back pain and muscle activity,23 and
neither the Vicious Cycle Theory nor the Pain Adap-
tation Model adequately predicted the effects of back
pain on trunk muscle activation. It was suggested that
the muscle activity changes tended to depend on the
task and the individual problem and therefore highly
variable between and within individuals (see below).23
These relationships are supported also by our recent
observations where experimental human pain induced
in the masseter muscle did not always result
in antagonist muscle increases and agonist muscle
decreases during movement.30
Why does the Pain Adaptation Model not always
explain the association between pain and motor
activity?
It is proposed that the effect of pain on motor activity
depends on the interaction of the biopsychosocial
variables that make up the complexity of an individ-
ual’s pain experience (i.e., the multidimensional nature
of pain) with the anatomical and functional complexity
of an individual’s sensory-motor system (Fig 1). In
terms of anatomical and functional complexity (i.e.,
jaw muscles, central neural control, specific nature of
the task being performed), it is argued that the jaw’s
complex sensory-motor system and movements influ-
ence the effects that pain has on jaw muscle activity.
For example, the effect of pain on motor activity will
depend on the particular jaw movement that is being
carried out. We have recently shown that human
experimental pain had a different effect on lateral
pterygoid muscle EMG activity during jaw opening in
comparison with jaw protrusion or lateral jaw move-
ment.30 The lateral pterygoid muscle is active as an
agonist in all three of these tasks. These data suggest
that it is not possible to ascribe a uniform effect of pain
on motor activity.
In terms of the multidimensional nature of pain, it is
proposed that the sensory-discriminative (e.g., pain’s
ª 2008 Australian Dental Association
Jaw muscle activity and pain
Fig 1. Diagram outlining essential components of the Integrated Pain
Adaptation Model (IPAM). The effect of pain on motor activity
depends on the interaction of the multidimensional features (biological
and psychosocial) of pain with an individual’s sensory-motor
(i.e., sensorimotor) system. The net result is a new optimized motor
recruitment strategy that results in a unique motor response that aims
to minimize pain. Sometimes, however, the new motor response may
be associated with the development of new pain or worsening
of existing pain. (With permission from Quintessence Publishing
Company.)
location, intensity, duration, quality), motivational-
affective (e.g., unpleasant emotional experience that
motivates avoidance, escape behaviour) and cognitive-
evaluative (e.g., beliefs based on previous experiences)
dimensions that comprise the complex experience of
pain all need to be considered in determining the effects
of pain on motor activity. There is indeed support for
such psychosocial variables as influencing an individ-
ual’s motor behaviour. For example, catastrophizing
(excessive focus on pain, magnification of the threat
associated with pain, feelings of helplessness in con-
trolling pain) has been associated with increased TMD-
related activity interference including limited unassisted
jaw opening, and limited self-reported jaw activities
such as speaking, laughing, yawning and kissing.8 A
patient’s confidence that they can manage pain (self-
efficacy beliefs) predicts avoidance behaviour50 and the
ability to persist with a task.8 This concept that these
multiple dimensions of pain influence the effect that
pain has on motor activity receives some basis from the
recent new view of pain as a homeostatic emotion
reflecting an adverse condition in the body that requires
autonomic and motor behavioural responses, and that
different types of pain engage specific behavioural
responses.51 Therefore, it is proposed that each pain
experience, in terms of its quality, location, intensity
and ⁄ or duration in an individual, may be associated
203
CC Peck et al.
with a particular pattern of change in EMG activity,
and this is in line with the evidence from the trunk
muscle literature.23
The effect of pain on motor activity: the Integrated
Pain Adaptation Model (IPAM)
In the presence of pain, it is suggested that an
individual’s multidimensional pain experience11,52,53
interacts in a unique way with that individual’s
sensory-motor system. A new strategy of muscle
activation is formulated to help maintain homeostasis.
One important aspect in maintaining homeostasis could
be the need to minimize the generation of further pain
at rest or during a subsequent movement. This hypo-
thesis is consistent in general terms with analyses in
chronic low-back pain23 in neck pain patients,54 and in
limb joint pain.37
For example, under this new model, pain in part of
the masseter muscle will lead to the development of a
new ⁄ modified activation of the muscle that may involve
the same and ⁄ or different parts of the muscle and other
muscles. The particular pattern of activation that is
selected in any one individual will be determined by
the anatomical and functional complexity of the jaw
sensory-motor system (e.g., the specific jaw movement
that is being performed) as well as the multidimensional
pain experience (e.g., beliefs based on past experience,
catastrophizing). The multidimensional nature of pain
will influence the sensory-motor system through the
connections that the peripheral and central sensory-
motor systems have with the limbic system, the
hypothalamo-pituitary-adrenal axis and the autonomic
nervous system.51 Muscle strategies will be developed
to maintain homeostasis and minimize pain and ⁄ or
the metabolic cost.55 It is possible, however, in some
individuals, these changes in muscle activity could lead
to further pain, injury and disability for reasons that
have yet to be elucidated.23,35,49,56–62 This raises
the possibility that the Integrated Pain Adaptation
Model reflects, in one sense, a unification of compo-
nents of the Vicious Cycle Theory and the Pain
Adaptation Model.
Clinical implications
The Integrated Pain Adaptation Model suggests that the
interaction of variables that make up the complexity of
the pain experience (e.g., acute ⁄ chronic, muscle ⁄ joint,
prior experience, beliefs, emotional contributions,
motivation, social context, genetic factors) will uniq-
uely affect motor activity. Just as an individual’s
experience of pain varies widely, we propose that so
too will an individual’s motor response to pain. We
suggest that it is inappropriate to manage all chronic
pain patients in exactly the same way, even if the
204
patients have the same physical diagnosis. It may be
necessary to define how each individual’s sensory-
motor system operates under pain to allow a tailoring
of management strategies to that individual. Indeed,
individualizing management based on the multidimen-
sional pain experience with a focus on psychosocial
status rather than the physical pain experience has
demonstrated successful outcomes.63 Since the Inte-
grated Pain Adaptation Model encompasses the overall
pain experience and its relationship to muscle recruit-
ment strategies with the overarching purpose of min-
imizing pain and ⁄ or maintaining homeostasis, further
research is needed to elucidate those pain-related
variables that have important influences on jaw muscle
function. We have recently proposed a number of
hypotheses within an IPAM framework.64
Knowledge translation: the next step
The new model presented here, based on an
organized critical review and fundamental research,1
attempts to advance our understanding of the com-
plex and debilitating human experience of pain with a
focus on how pain and motor function interrelate.
The model encapsulates recent data and considers
pain in a biopsychosocial context to progress earlier
landmark research.18–20 It has stimulated dialogue
within the research community16,17,65 and provides a
number of challenging research opportunities. The
consideration of this research by decision makers
(i.e., clinicians) is an important step in ultimately
advancing the impact of theory on practice and
patient care. This next step, called knowledge trans-
lation, is defined as the exchange, synthesis and
application of research findings with the aim of
accelerating the capture of the benefits of research.66
As more evidence and organized endeavour assesses
the value of the model, it will give rise to new
knowledge. New knowledge impacts practice by
aiding the revision of clinical practice guidelines, by
broadening the suite of knowledge and competencies
expected in continued professional development, and
by increasing the confidence of patients that evidence
supports clinical decisions. The determinants that
should guide knowledge translation of any research
are the following: definition of the core message,
identification of the target audience, the credibility of
the messenger, the process and support of the
knowledge transfer and, finally, the evaluation of
the effect of the translation such as behaviour change,
increased awareness and introduction of debate.67,68
CONCLUSIONS
The model presented points to a change in percep-
tion, to that of a unique or individualized interaction
ª 2008 Australian Dental Association

between pain and motor function. This individualized
interaction suggests that a clinical approach to the
assessment and management of pain patients that
does not involve interaction with other health pro-
fessionals may at times fall well short of providing
adequate patient care. An interprofessional or multi-
disciplinary approach, in reflection of the complexity
of the patient situation may hold the path to better
patient outcome. The target audience of this article
includes those clinicians who assess and manage
patients presenting with TMD. Graduate and post-
graduate researchers could dissect and digest the
model and subsequent critical reviews. The process
and support of the knowledge transfer lies in the
recruitment of methods that the clinical community
can embrace and these include ensuring individual
understanding of the basic reviews that have sup-
ported the thinking in the model, questioning indi-
vidual current clinical practice and knowledge, engag-
ing clinical study groups in discussion of the new
model and engaging directly with the researchers.
The reader is directed to the valuable websites
of the American Academy of Oro-Facial Pain
(http://www.aaop.org/) and the International Associa-
tion for the Study of Pain (http://www.iasp-pain.org).
ACKNOWLEDGEMENTS
We thank Drs John P Murray and Barry J Sessle for
comments on an earlier draft of the manuscript.
The authors wish to acknowledge the National Health
and Medical Research Council of Australia (grants
#302005; 512309), the Australian Dental Research
Foundation Inc., and the Dental Board of New South
Wales who have financially supported the authors’
research.
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ª 2008 Australian Dental Association
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