Muscle pain in the head: overlap between temporomandibular
disorders and tension-type headaches
Peter Svenssona,b,c
Purpose of review
A variety of painful problems can affect the muscles in the
head and face. Both temporomandibular disorders and
tension-type headaches are believed to have a significant
contribution from the skeletal muscles and have several
clinical features in common. It still unclear, however, to what
extent these two prevalent disorders are separate entities or
have similar pathophysiological background.
Recent findings
There is now reasonably good evidence that myofascial
temporomandibular disorder patients are more likely to have
a tension-type headache problem and vice versa, but the
overlap is not complete. Studies have documented
similarities regarding sensitization of the nociceptive
pathways, dysfunction of the endogenous pain modulatory
systems as well as contributing genetic factors, but there
are also a number of distinct differences between
temporomandibular disorders and tension-type headaches
that need to be considered.
Summary
Using the current classification systems, myofascial
temporomandibular disorder pain and tension-type
headache disorders do overlap and appear to share many of
the same pathophysiological mechanisms, but it would be
premature to consider them as identical entities since the
importance of, for example, the affected muscles and
associated function and genetic background needs to be
established. Orofacial pain and headache specialists
should collaborate to further develop diagnostic
procedures and management strategies of
temporomandibular disorders and tension-type headaches.
Keywords
genetics, myofascial pain, pain mechanisms,
temporomandibular disorders, tension-type headaches
Curr Opin Neurol 20:320–325. ß 2007 Lippincott Williams & Wilkins.
a
Department of Clinical Oral Physiology, School of Dentistry, University of Aarhus,
b
Department of Oral and Maxillofacial Surgery, Aarhus University Hospital, Aarhus
and cOrofacial Pain Laboratory, Center for Sensory-Motor Interaction, Aalborg
University, Aalborg, Denmark
Correspondence to Peter Svensson, Department of Clinical Oral Physiology,
School of Dentistry, University of Aarhus, Aarhus, Denmark
Tel: +45 8942 4191; e-mail: psvensson@odont.au.dk
Current Opinion in Neurology 2007, 20:320–325
320
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Abbreviations
ADRB2 adrenergic receptor b2
COMT catechol O-methyltransferase
DNIC diffuse noxious inhibitory control
ICHD International Classification of Headache Disorders
RDC Research Diagnostic Criteria
TMD temporomandibular disorder
TTH tension-type headache
ß 2007 Lippincott Williams & Wilkins
1350-7540
Introduction
Currently, there are two internationally accepted classi-
fications of temporomandibular disorder (TMD) and
tension-type headache (TTH): the Research Diagnostic
Criteria (RDC) for TMD [1] and the International Classi-
fication of Headache Disorders (ICHD)-II [2]. Both
are based on the consensus of leading researchers and
clinicians and include operationalized diagnostic criteria
and have been subject to extensive testing in terms of
reproducibility [3,4]. TMD and TTH, however, are
mainly based on a combination of well defined signs
and symptoms in the head and face rather than an exact
understanding of the underlying pathophysiology, that is,
it has not been possible to make a mechanism-based
classification because essential information is still
missing. The aim of this review is to compare clinical
features, epidemiological findings, pathophysiological
mechanisms and genetic factors related to myofascial
TMD pain and TTH.
Clinical features
The typical clinical findings in TMD and TTH disorders
have been reviewed recently [5–7] so only a few issues
will be considered here.
The temporal characteristics are given higher priority in
the TTH classification than in the TMD classification
where there is no distinction between infrequent, fre-
quent episodic or chronic disorders. It should be empha-
sized that TMD is not a single entity but rather a cluster
of related pain conditions in the masticatory muscles,
temporomandibular joint (TMJ) and associated struc-
tures. The focus of this review is on myofascial TMD
pain which according to the RDC/TMD criteria requires
both a report of ongoing pain from the masticatory
muscles, that at least three muscle sites out of 20 possible
are painful on standardized palpation and finally that at
least one of these three sites are located on the same side

as the chief pain complaint. If all these criteria are not
met, the patient will not be given a myofascial TMD pain
diagnosis in contrast to many other TMD classification
systems. In particular it is important that the amount of
pressure used for palpation is standardized in the RDC/
TMD.
Spontaneous pain or pain on jaw movement is a character-
istic and necessary feature for the diagnosis of myofascial
TMD pain. Patient-based drawings of their typical pain
patterns demonstrate a concentration around the masseter
muscle and spreading towards the anterior part of the
temporalis muscle (Fig. 1a). When patients with episodic
or chronic TTH draw the location of their typical pain, the
lower part of the face including the masseter muscle is
usually spared whereas there is a significant occurrence of
pain in the neck and pericranial regions (Fig. 1b). These
findings imply that different muscles and structures are
involved in myofascial TMD pain and TTH.
Interestingly, a recent experimental study using painful
injections of hypertonic saline into various jaw and neck
Figure 1 Patient and subject-based pain drawings
(a) Thirteen patients with myofascial temporomandibular disorder (TMD)
pain. (b) Twenty-two patients with chronic tension-type headache (TTH).
(c) Twenty healthy control subjects exposed to injection of hypertonic
saline into the masseter muscle. (d) Twenty healthy control subjects
exposed to injection of hypertonic saline into the splenius muscle.
Adapted with permission [8,44].
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Muscle pain in the head Svensson 321
muscles reproduced these typical pain patterns [8]. A
visual comparison suggests that myofascial TMD pain is
more similar to the pain patterns produced by injections
into the masseter muscle (Fig. 1c) and that TTH pain is
more similar to the pain patterns evoked by painful
stimulation of the neck muscles, for example, the
splenius muscle (Fig. 1d). These findings support the
notion that different muscles may be involved in
the pathophysiology of TMD and TTH.
Another typical feature of both myofascial TMD and
TTH is the tenderness or pain on palpation. It has been
suggested that the tender sites in the myofascial tissue
represent trigger points, characterized by tenderness to
palpation, taut bands, a local twitch response and referral
of pain recognized as familiar (active trigger points) [9].
Recent studies have emphasized the finding of presumed
active trigger points in both episodic and chronic
TTH [10,11]. For myofascial TMD pain relatively little
information on trigger points is available [12]. The key
concept in trigger point pathophysiology is assumed to
be a localized energy crisis due to excessive release of
acetylcholine leading to tissue distress and release of
algogenic and neuroactive substances [9]. A recent
study [13] described significant changes in the local
micro-environment around active trigger points in the
trapezius muscle with the presence of neuroactive sub-
stances such as bradykinin, substance P, tumor necrosis
factor a and interleukin-1-b. Other microdialysis studies,
however, have failed to detect significant alterations in
inflammatory mediators in patients with chronic TTH
[14]. On a related point, attempts to inactivate trigger
points, for example using botulinum toxin, have not been
particularly promising in myofascial pain [15]. The
importance of trigger points for myofascial TMD pain
and TTH appears to be controversial and further studies
will be needed.
Epidemiology
Descriptive epidemiology has indicated that between 3
and 15% of the Western population will suffer from TMD
pain [16,17]. Few studies have tried to separate TMJ pain
from myofascial TMD pain but the latter appears to
be less prevalent than the former [17]. Most studies have,
however, found that TMD pain is 1.5–2 times more
prevalent in women but it is critical to distinguish
between the number of TMD cases presenting in the
clinic and the number of TMD cases in the community
because treatment seeking patterns and use of health
services may bias a biological sex difference [18]. The
prevalence of TMD across the lifetime is still debated
but there seems to be a peak around 20–45 years for
women although elderly people may also suffer from
TMD pain [19]. There are few good studies on the
incidence of TMD pain but the available estimates are
in the range of 2–4% with the persistent types being
 322 Headache
around 0.1% [17]. Some longitudinal studies have shown
substantial variations in the time course of myofascial
TMD [20] with 31% being persistent over a 5-year
period, 33% being remittent and 36% recurring.
The epidemiology of TTH is well described [21]. The
prevalence of infrequent episodic TTH is in the range
51–58%, frequent episodic TTH 24–43% and chronic
TTH between 1 and 5.6%. The female : male ratio of
5 : 4 in TTH is somewhat lower than in TMD but a
similar peak in prevalence between 20 and 39 years
followed by a decline is similar to the epidemiology of
TMD. Thus, both conditions are prevalent and have a
female predominance.
Several epidemiological studies point towards a sig-
nificant overlap between myofascial TMD and TTH
(e.g. [22–26]), and there is good evidence that several
persistent musculoskeletal pain conditions such as fibro-
myalgia, chronic fatigue syndrome, TMD and TTH
overlap [27] and that widespread pain is a significant risk
factor for TMD pain [28]. Furthermore, a recent study
[29] suggested that the development of TMD pain in
adolescence may reflect an underlying vulnerability to
musculoskeletal pain that is not unique to the orofacial
region. Using stringent RDC/TMD and ICHD criteria it
has been shown that 59% and 32% of patients with a
myofascial TMD diagnosis also fulfil the criteria for an
episodic TTH or a chronic TTH [30]. A recent study has
shown that about 40% of patients including a TTH
diagnosis will also have a myofascial TMD diagnosis
(V.C.D. Ballegaard et al., in preparation).
Taken together these findings clearly demonstrate a
substantial, but not complete overlap between myofascial
TMD and TTH. A temporal or causal relationship cannot
be inferred from cross-sectional studies, however, and,
indeed, a partial overlap would be expected even if the
two conditions represented completely separate entities
and pain mechanisms simply due to the high prevalence.
It is therefore imperative to consider other clinical mani-
festations and knowledge related to the pathophysiolo-
gical mechanisms.
Peripheral and central sensitization
Both peripheral and central sensitization processes have
been implicated in the pathophysiology of myofascial
TMD and TTH [31,32,33,34,35,36]. It should be
pointed out that currently there is no accurate electro-
physiological or imaging test of either peripheral or
central sensitization of the nociceptive pathways in the
human trigeminal system but rather a number of clinical
‘proxies’ of these mechanisms such as quantitative
sensory testing (standardized application of thermal,
mechanical, chemical or electrical stimuli and recording
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
of patient-based responses or evoked physiological
measures).
Patients with myofascial TMD pain have generally lower
thresholds to mechanical stimuli applied to the painful
area when compared to control subjects [30,37,38]. It has
also been shown, however, that myofascial TMD patients
have decreased pain thresholds outside the painful area
and have a greater temporal summation of nociceptive
cutaneous input [39]. These latter observations are
difficult to explain with peripheral sensitization and
clearly implicate the central nociceptive pathways. A
generalized hyperexcitability of central nociceptive pro-
cessing in TMD patients has recently been indicated by
the finding of more pronounced temporal summation of
pain and greater after-sensations following repetitive
painful mechanical stimulation of the fingers versus con-
trol subjects [40]. It seems that the central changes not
only are restricted to the second order neuron in the
trigeminal sensory nucleus complex, although neuronal
hyperexcitability has clearly been demonstrated in
animal models of noxious inputs to the subnucleus inter-
polaris and subnucleus caudalis [41,42].
Intramuscular injection of hypertonic saline into the
masseter muscles causes localized pain around the injec-
tion site and a spread and referral of pain to the temple,
teeth and ear in healthy control subjects, but when
patients with myofascial TMD pain are provoked with
this type of longer-lasting painful input, they experience
significantly more pain and pain in a larger area than
control subjects [30]. The same technique has now been
used in frequent episodic and chronic TTH patients and
both groups have significantly more pain and significantly
larger pain areas than healthy controls [43]. An intri-
guing difference between myofascial TMD patients and
TTH patients is that TMD patients do not report sig-
nificantly higher pain scores when the nonpainful leg
muscle is stimulated whereas patients with TTH also
have higher pain scores on the nonpainful leg. This is in
line with another recent study [44] on chronic TTH
patients showing a generalized hyperalgesia to single and
repetitive electrical stimuli. An important finding is also
that there were no major differences between patients
with frequent episodic TTH and chronic TTH and there
was no significant influence of actual headache status,
that is, whether TTH patients were examined with or
without headache did not have any significant effect on
the pain responses to injection of hypertonic saline [43].
These findings imply that frequent episodic TTH and
chronic TTH are part of a continuum and not separate
entities.
In summary, both myofascial TMD and TTH patients
have several clinical features that are compatible with
both a peripheral and central sensitization of the

nociceptive pathways but also endogenous pain modu-
latory systems could play a role.
Endogenous pain modulatory systems
Indeed, one intriguing concept related to TMD and
many other chronic pain conditions is that they may
reflect a dysfunctional state of endogenous pain modu-
latory systems. A dysfunction reflecting less efficient
diffuse noxious inhibitory control (DNIC) mechanisms
has been reported, using different experimental para-
digms, in patients with myofascial TMD [37,45]. Also in
patients with migraine and chronic TTH deficiencies in
DNIC-like mechanisms have been described [46,47],
and it has been suggested that patients with chronic
TTH suffer from a dysfunctional pain modulatory system
in a similar manner as do patients with anatomically
generalized chronic pain like fibromyalgia [46]. It can
be speculated that impairment or imbalances of such
endogenous pain modulatory systems may contribute
to the development or maintenance of central sensitiza-
tion in primary headaches [47], but it is not known if
changes in DNIC-like mechanisms are a cause of, for
example, myofascial TMD pain and TTH or if such
changes could occur in response to a persistent pain
problem.
Genetics
In the field of TMD one of the most exciting new avenues
towards a better understanding of the pathophysiology
comes from genetics and in particular the importance of
variation in the coding of catechol O-methyltransferase
(COMT), an enzyme that metabolizes catecholamines and
is critically involved in pain perception, cognitive function
and affective mood [48]. An association between COMT
haplotypes and sensitivity to experimental painful stimuli
has been established [49,50] and, importantly, carriers
of the low-pain sensitivity haplotype appear to have
2.3 times less risk of developing a myofascial TMD
[49]. The influence of COMT activity on pain sensitivity
is, in part, mediated through the adrenergic receptor b2
(ADRB2) [51], and individuals who carry one haplotype
coding for high and one coding for low ADRB2 expression
have been shown to display high positive psychological
traits, have higher levels of resting arterial pressure, and to
be about 10 times less likely to develop TMD [52].
Numerous other genes coding for neurotransmitters and
neuromodulators, however, may also have implications for
pain sensitivity [53]. Nevertheless, these studies imply the
need for individually tailored treatment of myofascial
TMD pain for example by pharmacological agents that
block ADRB2 function.
For headaches, the genetic contribution to familial
hemiplegic migraine (FHM) is well established [54]. Also
for TTH, however, a genetic factor has been implicated,
for example, the 5-HTT-gene-linked polymorphic
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Muscle pain in the head Svensson 323
region (5-HTTLPR) genotypes. Thus, a recent study
[55] suggested that serotonergic activity could be involved
in the development of chronic TTH and that 5-HTTLPR
might be one of the genetically contributing factors.
Another recent study [56] on twins concluded that genetic
factors play a role in frequent episodic tension-type head-
ache, while infrequent episodic tension-type headache
appears to be caused primarily by environmental factors.
In summary, there is emerging evidence to support the
notion of a genetic component involved in both myo-
fascial TMD and TTH and further studies may help
to further identify vulnerable genes that interact with
environmental factors such as physical and emotional
stress to produce pain prone phenotypes at risk for
development of myofascial TMD pain or TTH.
Conclusion
Using the current classification systems, TMD and TTH
disorders do overlap and appear to share many of the
same pathophysiological mechanisms. It would be pre-
mature, however, to consider them as identical entities
since the importance of for example the affected muscles
and associated function in addition to genetic background
factors need to be further examined. Orofacial pain and
headache specialists should collaborate to improve diag-
nostic techniques and management strategies of TMD
and TTH.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
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