PERSPECTIVE
Headache: muscle tension, trigger points and referred
pain
Scientific interest in the pathogenesis of tension-type head-
ache (TTH) has lagged behind that of migraine, although
TTH is the most common headache disorder and consid-
ered the most important in terms of socioeconomic
impact (1). As a result, understanding of the underlying
mechanisms of TTH has remained relatively incomplete.
Tension type
In recent years, research into the pathogenesis of
headache is a TTH has focused on the role of muscles and pain
very common processing defects. It is becoming increasingly clear
condition and that the pain in TTH is of muscular origin and that
we need more peripheral, as well as central, nervous system factors
play a crucial role in its development (2,3).
research to
explore the
Muscle pain: peripheral and central
underlying sensitisation
mechanisms
Studies point towards a muscular origin for headache
pain. Muscle pain is caused by the excitation of mus-
cle nociceptors. These are free nerve endings that
respond to external mechanical, thermal or chemical
stimuli, as well as to direct stimulation by endoge-
nous algogenic substances, for example bradykinin,
serotonin and prostaglandin E2.
Under normal circumstances, the threshold for
activating nociceptive signals is high so that a pain
response in the brain is only triggered by stimuli that
are potentially or actually damaging to body tissues.
However, the algogenic substances mentioned above
can also act as sensitising agents that increase the
excitability of nociceptors (2). As a result, low-inten-
sity stimuli that are not normally perceived as pain-
ful can trigger an electrical signal that results in the
sensation of pain. This peripheral sensitisation might
be one of the mechanisms that contribute to the
development of TTH (2).
Peripheral nociceptive afferents from several differ-
ent areas converge onto the same second-order neu-
rons in the spinal cord and brainstem. If the input
from muscle nociceptors is strong and long-lasting,
this can also lead to changes in the way pain is pro-
cessed in these higher structures. Evidence indicates
that this might be the case in TTH.
Studies in patients with frequent episodic or
chronic TTH have revealed decreased pain detection
thresholds in response to various types of experimen-
tal stimuli, including pressure, thermal and electrical
triggers and intramuscular infusion of algogenic sub-
ª 2015 John Wiley & Sons Ltd Int J Clin Pract, May 2015, 69 (Suppl. 182), 8–12
8 doi: 10.1111/ijcp.12651
stances. Notably, sensitivity was
increased both in the head area and
at other locations, for example, the
Achilles tendon (2,4).
The widespread and non-specific
nature of the hypersensitivity in
these patients points towards an
increased excitability of dorsal horn
and supraspinal neurons (2). It has also been sug-
gested that there might be decreased descending inhi-
bition of nociceptive transmission in the dorsal horn
(2,5).
These central processes appear to play an impor-
tant role in patients with frequent or chronic TTH,
whereas there is no evidence of central sensitisation
in patients with infrequent episodic TTH.
Referred muscle pain
Another phenomenon thought to be involved in the
development of TTH is the referral of muscle pain to
distant sites. As a result of the fact that peripheral sen-
sory afferents from several different areas converge
onto the same nerves in the spinal cord, messages to
supraspinal neurons could be misinterpreted as origi-
nating from structures that are distant from the actual
site of the painful stimulus (5). In addition, dorsal
horn neurons often receive input from other bodily
regions, not just the muscles. This could explain the
features of TTH headaches – dull and tight heaviness,
diffuse pressure and general soreness (5).
The concept that TTH headaches may represent
referred pain from neck and shoulder muscles is un-
derpinned by a study in which hypertonic saline (an
algogenic substance) was injected into the anterior or
posterior temporalis muscles to induce experimental
pain in healthy individuals (6). The participants per-
ceived these stimuli as head pain. Similar evidence
has been obtained for the upper trapezius muscle
(5).
Myofascial trigger points
Assuming that release of endogenous algogenic sub-
stances provokes the sensitisation of muscle nocicep-
tors and the resulting processes lead to central
sensitisation, the question then arises: which struc-
tures and mechanisms cause the initial liberation of
the pain-causing chemicals?
 Perspective 9

New research points towards myofascial trigger Table 1 Myofascial abnormalities in patients with TTH
points. These are palpable nodules within a taut (8)
band of skeletal muscle that are hypersensitive to
compression, responding with a local twitch Controls
response or a familiar referred pain pattern distant Myofascial trigger points (n = 24) TTH (n = 24)
...........................
from the spot (7). Trigger points can be formed
as a result of various factors, including muscle No trigger points 11 (45.8) 5 (20.8)
Latent trigger points 12 (50) 17 (70.8)
overuse, psychological stress, accidents and poor
Active trigger points 1 (4.2) 2 (8.3)
posture (5). ...........................
Myofascial trigger points can be active (generating Values are given as number (%).
spontaneous pain or pain in response to movement)
or latent (not producing pain unless they are com-
pressed). In patients with TTH, the referred pain
evoked by active trigger points in the cervicocranial promoting the cycle of peripheral sensitisation that
region reproduces at least part of the pain pattern leads to the development of TTH.
experienced during headache attacks (5). By contrast, Figure 1 gives an overview of common TTH trig-
the referred pain evoked by mechanical stimulation ger points and their referred pain patterns (10).
of latent trigger points does not reflect a usual or
familiar headache pattern.
Diagnostic comparisons
Patients with TTH are more likely to have active
and latent myofascial trigger points than controls (8) Like TTH, cervicogenic headaches also originate
(Table 1). Similarly, TTH patients with active trigger from muscles in the neck. However, accurate diag-
points have greater headache intensity and frequency, nostic comparison can help differentiate TTH from
and longer headache duration, than those with latent this type of headache – and other common headache
trigger points (5). disorders like migraine (see Figures 2–4 for a com-
At the molecular level, active trigger points are parison of the pathophysiological changes in TTH
associated with higher levels of bradykinin and other with other types of headache).
chemical mediators both near the trigger points and Distinguishing TTH from cervicogenic headache
also in distant, uninvolved regions (9). Bradykinin is can prove challenging – particularly as TTH pain
a potent stimulator of prostaglandin synthesis. may also be felt in the neck (11). The ICDH-3
Release of these two algogenic substances therefore describes cervicogenic headache as headache caused
contributes to a decrease in the pain threshold, by a disorder of the cervical spine and its component

Figure 1 Referred pain from active trigger points in pericranial muscles. Adapted from Fern

andez-de-las-Pe~
nas et al. (10)

ª 2015 John Wiley & Sons Ltd Int J Clin Pract, May 2015, 69 (Suppl. 182), 8–12
10 Perspective

Figure 2 The pathophysiology of TTH. When activated,

trigger points in the head (marked as X) neck and shoulder
muscles release pain-causing mediators such as
prostaglandins and bradykinin. Peripheral nerves become
sensitised resulting in a pain signal being referred from
the muscles to the brain (marked in block colour) –
which is felt as TTH. Adapted from Fern
andez-de-las-Pe~ nas
et al. (5)

bony, disc and/or soft tissue elements, usually (but
not always) associated with neck pain (3). Features
that can help distinguish cervicogenic headache from
TTH include side-locked pain, headache pain that is
provoked by pressing the fingers into neck muscles
or by moving the head, and pain that radiates from
the back to the front of the head (3). However, these
features are not unique to cervicogenic headache and
any headache associated with trigger points in the
neck may still be coded as TTH if it meets other key
diagnostic criteria (3).
Most of the characteristics of a typical migraine
attack clearly set this type of headache apart from
TTH, and therefore aid in accurate diagnosis. Like
episodic TTH, migraine is a recurrent headache
which can last from a few hours to several days (11).
However, while TTH is usually generalised, migraine
pain is unilateral; and where TTH presents as a
mild-to-moderate tight or pressing pain affecting the
whole head, migraine pain has a pulsating quality
and is moderate-to-severe in intensity (3,11). TTH
does not usually affect patients’ ability to carry on
with their daily duties but migraine can be aggra-
Figure 4 The pathophysiology of cervicogenic headache.
Originates from disorder of the bone, disc and soft tissues
regions in the cervical spine region of the head. Adapted
from IHS (3)
vated by routine physical activity, forcing sufferers to
seek bed rest and dark/quiet surroundings (3,11).
Migraine can also be associated with accessory symp-
toms such as aura, nausea, vomiting, photophobia
and/or phonophobia which are not found in TTH
(3,11).
TTH in specific patient populations
The population of patients affected by TTH is
diverse. Adults, adolescents and children can all
experience episodic TTH, which is more common
than migraine across each major age group (1). TTH
is extremely common in teenagers and working
adults – supporting the link to muscular trigger
points and contributory factors such as psychological
stress, muscle overuse and poor posture (12,13).
Notably, the prevalence of TTH tends to decrease

(A) (B) (C)

Figure 3 The three hypotheses for the pathophysiology of migraine. Theory A – widening of blood vessels in the meninges
activate pain signals. Theory B – waves of activity in the cortex (cortical spreading depression) cause aura and activate
pain signals. Theory C – dysfunctional areas in the brain stem cause cascades of neurological events that cause migraine
symptoms. Adapted from Harvard Health Letter (16)

ª 2015 John Wiley & Sons Ltd Int J Clin Pract, May 2015, 69 (Suppl. 182), 8–12
 Perspective 11

from 40 years of age onwards, probably because of
differences in stress levels as the population gets
older (12,13). Overall, this type of headache affects
slightly more women than men (1). TTH is also the
most common headache disorder experienced by
children from age 7 upwards (14).
Current therapeutic strategies for TTH
Current therapeutic strategies for treating TTH
include both non-drug management and pharmaco-
therapy (15). Information, reassurance and identifi-
cation of headache trigger factors such as poor
posture or stress can be particularly rewarding for
patients (15). Other effective non-drug approaches
include electromyography biofeedback, cognitive-
behavioural therapy and relaxation training (15).
Despite a lack of robust scientific evidence support-
ing their efficacy, physical therapy and acupuncture
can also prove useful options for patients with fre-
quent bouts of TTH (15). For the drug treatment of
episodic TTH, simple analgesics and NSAIDs are rec-
ommended in European guidelines as first-line ther-
apy (15). Combination analgesics containing caffeine
are positioned as drugs of second choice, while
experts caution against the use or triptans, muscle
relaxants or opioids (15).
In time, greater understanding of the underlying
pathophysiology of TTH may lead to more targeted
treatment approaches that exploit new knowledge of
muscular trigger points and referred pain pathways
associated with this type of headache.
Conclusion: a pain model for TTH
Tension-type headache has its origins in muscular
pain. Patients with TTH have an increased number
of myofascial trigger points in muscles of the head,
neck and shoulders. These trigger points can release
inflammatory mediators, such as prostaglandins,
which stimulate and sensitise nociceptive nerve end-
ings, causing referred pain that is perceived as head-
ache. The sensitisation of muscle nociceptors is
thought to be the main peripheral mechanism lead-
ing to episodic TTH.
Under some circumstances, the peripheral noci-
ceptive inputs may be more prolonged and/or
intense, producing continuous afferent stimulation.
In predisposed individuals, this may lead to sensiti-
sation of the central nervous system, which may in
turn contribute to the persistence, amplification and
spread of pain and the conversion from episodic to
chronic TTH.
Interventions should take these aspects into con-
sideration. Based on the understanding that periph-
eral and central sensitisation mechanisms have a key
role in the development and chronification of TTH,
it seems particularly pertinent to choose interven-
tions with the potential to reduce sensitisation and
reset the patient’s pain threshold.
Disclosure
LAN has consulted and lectured for a number of
pharmaceutical companies (including Reckitt Benck-
iser) for activities related to sensory-motor interac-
tion, and received research support from charities,
government and industry sources at various times.
L. Arendt-Nielsen
Center for Sensory-Motor Interaction, Department of
Health Science and Technology, Faculty of Medicine,
Aalborg University, Aalborg, Denmark
Correspondence to:
Lars Arendt-Nielsen, Center for Sensory-Motor
Interaction, Department of Health Science and
Technology, Faculty of Medicine, Aalborg University,
Fredrik Bajers Vej 7, Bld. D3, DK-9220 Aalborg E,
Denmark
Tel.: + 45 9940 8830
Fax: + 45 9815 4008
Email: lan@hst.aau.dk

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