Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over...
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REVIEW ARTICLE Open Access
Myofascial trigger points in migraine andtension-type headacheThien Phu Do, Gerda Ferja Heldarskard, Lærke Tørring Kolding, Jeppe Hvedstrup and Henrik Winther Schytz*
Abstract
Background: A myofascial trigger point is defined as a hyperirritable spot in skeletal muscle that is associated witha hypersensitive palpable nodule in a taut band. It has been suggested that myofascial trigger points take part inchronic pain conditions including primary headache disorders. The aim of this narrative review is to present anoverview of the current imaging modalities used for the detection of myofascial trigger points and to reviewstudies of myofascial trigger points in migraine and tension-type headache.
Findings: Different modalities have been used to assess myofascial trigger points including ultrasound, microdialysis,electromyography, infrared thermography, and magnetic resonance imaging. Ultrasound is the most promising ofthese modalities and may be used to identify MTrPs if specific methods are used, but there is no precise description ofa gold standard using these techniques, and they have yet to be evaluated in headache patients.Active myofascial trigger points are prevalent in migraine patients. Manual palpation can trigger migraine attacks. Allintervention studies aiming at trigger points are positive, but this needs to be further verified in placebo-controlledenvironments. These findings may imply a causal bottom-up association, but studies of migraine patients withcomorbid fibromyalgia syndrome suggest otherwise. Whether myofascial trigger points contribute to an increasedmigraine burden in terms of frequency and intensity is unclear.Active myofascial trigger points are prevalent in tension-type headache coherent with the hypothesis that peripheralmechanisms are involved in the pathophysiology of this headache disorder. Active myofascial trigger points in pericranialmuscles in tension-type headache patients are correlated with generalized lower pain pressure thresholds indicating theymay contribute to a central sensitization. However, the number of active myofascial trigger points is higher in adultscompared with adolescents regardless of no significant association with headache parameters. This suggests myofascialtrigger points are accumulated over time as a consequence of TTH rather than contributing to the pathophysiology.
Conclusions: Myofascial trigger points are prevalent in both migraine and tension-type headache, but the role they playin the pathophysiology of each disorder and to which degree is unclarified. In the future, ultrasound elastography may bean acceptable diagnostic test.
Keywords: Headache, Myofascial trigger point, Muscle, Treatment, Trigemino-cervical-complex, Migraine, Tension-typeheadache, Diagnostic test
BackgroundMigraine affects 16% of the population in Europe [1]with high individual and socioeconomic costs [2, 3]. Sev-eral mechanisms have been proposed to be involved inits pathophysiology including vascular, peripheral andcentral mechanisms [4–9]. Jes Olesen systematically de-scribed pericranial tenderness in migraine patients, both
during and outside of migraine attacks [10, 11], leadingto speculations that myofascial mechanisms may be in-volved in migraine [12].Tension-type headache (TTH) is the most prevalent
primary headache disorder worldwide [13]. Tendernessin pericranial myofascial tissue is correlated with the in-tensity and frequency of headache in TTH [14–16], andstudies show increased muscle stiffness in TTH patients[17, 18]. Thus, myofascial structures may be associatedwith TTH pathophysiology.
* Correspondence: [email protected] Diagnostic Laboratory, Danish Headache Center and Departmentof Neurology, Rigshospitalet Glostrup, Faculty of Health Sciences, Universityof Copenhagen, Glostrup, Denmark
The Journal of Headache and Pain
© The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made.
Do et al. The Journal of Headache and Pain (2018) 19:84 https://doi.org/10.1186/s10194-018-0913-8
The term myofascial trigger point (MTrP) was popu-larized in the 1950s and is defined as a hyperirritablespot in skeletal muscle that is associated with a hyper-sensitive palpable nodule in a taut band [19, 20]. Thespot is painful on compression and can cause referredpain, referred tenderness, motor dysfunction and auto-nomic phenomena. The interest in myofascial symptomshas been ongoing for centuries with similar descriptionsof localized thickenings of muscles with regional pain[21]. There have been inconsistencies and controversiesin the literature on the underlying pathology, and eventhe existence of MTrPs [22]. While attempts have beenmade to visualize MTrPs [22], the gold standard for de-tection of MTrPs has been unchanged since the 1950s[22] and remains to be by way of palpation of theaffected muscles. However, this technique proves to bepoorly reproducible as practitioners disagree on thelocation of MTrPs when blindly examining different pa-tient groups [23]. Nevertheless, MTrPs have come toplay a central role in the diagnosis and treatment ofmyofascial pain syndrome [19]. Furthermore, MTrPshave been proposed to take part in primary headachedisorders and other chronic pain conditions [12]. Theaim of this narrative review is to present an up-to-dateoverview on MTrPs in general and then in migraine andTTH, respectively.
ReviewMyofascial trigger pointsIn the comprehensive trigger point manual by Travell andSimons [19], MTrPs are subclassified into different types,e.g., active and latent amongst others. An active MTrPproduces a constant pain complaint while a latent onlyproduces pain during manual palpation [19]. It washypothesized that a sustained muscle contraction inMTrPs promotes hypoxia and ischemia with a followingincrease in concentrations of substances such as calcitoningene-related peptide (CGRP) and substance P (SP) [24].Consequently, this would lead to increased peripheralnociceptive transmission [24]. This hypothesis is only sup-ported in active MTrPs, as they have been shown to be as-sociated with higher levels of these substances in the localmilieu compared to latent MTrPs [25, 26]. Other proper-ties such as the consistency of the tissue have also beensuggested to play a key role in MTrPs [27].
Investigations of myofascial trigger pointsUltrasound imagingDifferent ultrasound modalities in ultrasound imaginghave visualized MTrPs. Lewis et al. [28] conducted a pilotstudy to assess the use of ultrasound in determining softtissue changes in the region of active MTrPs in 11 sub-jects. They found no correlation between clinical identifiedactive MTrPs and ultrasound. In contrast, Turo et al. [29]
were able to differentiate between symptomatic MTrPsand asymptomatic muscle tissue with texture-based ana-lysis. Sikdar et al. investigated the stiffness of active and la-tent MTrPs, using ultrasound elastography by Dopplervariance imaging in nine subjects while inducingvibrations with an external handheld massage vibrator[27]. MTrPs appeared as focal, hypoechoic regions ontwo-dimensional ultrasound images and with reduced vi-bration amplitude, indicating increased stiffness. Further-more, they describe hypoechoic regions that were notidentified during palpation prior to ultrasound. In anotherstudy by the same group, MTrPs showed reduced vibra-tion amplitude on elastography indicating increased stiff-ness and distinct blood flow waveform patterns [30].Ballyns et al. [31] used elastography to investigate MTrPsin 44 subjects with acute cervical pain. They were able tomeasure the size and distinguish type (active, latent) ofMTrPs with elastography. In addition, Doppler waveformsof blood flow showed different characteristics in activesites compared to normal tissue. Takla et al. [32] comparedelastography with two-dimensional grayscale ultrasound inidentifying MTrPs. They found that MTrPs had an accur-acy of 100% for both active and latent MTrPs whiletwo-dimensional grayscale ultrasound could only identify33 and 35%, respectively.
MicrodialysisMicrodialysis has been used to measure endogenous andexogenous molecules in the local milieu of MTrPs. Shahet al. [25] used microdialysis to investigate subjects withactive or latent MTrP, and controls without MTrP weredetected by manual palpation by two experienced clini-cians. The authors measured selected substances (pH,bradykinin (BK), CGRP, SP, tumor necrosis factor alpha(TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6),interleukin 8 (IL-8), serotonin, and norepinephrine (NE))in standardized locations of the trapezius muscle andgastrocnemius muscle. Subjects with active MTrPs inthe trapezius muscle showed increased concentrations ofall substances compared to the other groups. Shah et al.[26] found similar results in the trapezius muscle of sub-jects with neck pain and active MTrP compared to agroup with neck pain and no MTrP present and healthycontrols. The results showed that the active MTrP grouphad higher concentrations of BK, CGRP, SP, TNF-α,IL-1β, serotonin, NE.
ElectromyographyElectromyography (EMG) can be used to measure theelectrical activity of skeletal muscles. Simons et al. com-pared the prevalence of motor endplate potentials in ac-tive MTrPs, endplate zones, and taut bands of skeletalmuscles in subjects with palpable MTrPs [33]. The au-thors found that endplate noise was more common in
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 2 of 17
MTrPs than in sites outside of the trigger point, evenwithin the same endplate zone. Ge et al. evaluated intra-muscular muscle activity in a synergistic muscle duringisometric contraction in 15 subjects with latent MTrPs[34]. The needle was inserted into a latent MTrP or anon-MTrP in the upper trapezius at rest and duringcontraction. The EMG activities were recorded from themiddle deltoid muscle and the upper, middle, and lowerparts of the trapezius muscle. The intramuscular EMGactivity in the upper trapezius muscle was significantlyhigher at rest and during contraction at latent MTrPscompared with non-MTrPs. Yu et al. measured max-imum voluntary isometric contraction, endurance, me-dian frequency, and muscle fatigue index in three groupsof participants: an active MTrP group, a latent MTrPgroup, and a control group [35]. The active MTrP grouphad a higher median frequency and muscle fatigue indexthan the control group. Wytrążek et al. compared theEMG activity of muscle motor units at rest and maximalcontraction with surface EMG recordings [36]. The re-sults showed MTrPs correlated with an increase in EMGamplitude at rest.
Infrared thermographyInfrared thermography can be used to measure the skintemperature. Dibai-Filho et al. [37] have reviewed the lit-erature on infrared thermography investigations ofMTrPs. The authors included three comparative studies[38–40] and one accuracy study [41]. The conclusion ofthe review is that the included studies do not agree onskin temperature patterns in the presence of MTrPs.The included studies of the review are briefly presentedin the following. Merla et al. [38] found that individualswith myofascial pain had a greater difference betweenthe right and left side in skin temperature over the mas-seter and sternocleidomastoid muscles before and aftermaximal voluntary clenching compared to healthy vol-unteers. They also found that the myofascial pain grouphad a greater temperature change over the measuredmuscles after maximum voluntary clenching. Kimura etal. [39] evaluated the vasoconstrictor response after pro-voking pain in MTrPs with an intramuscular glutamateinjection. Furthermore, they activated the sympatheticoutflow by using a breath-holding maneuver. Theyfound a decrease in skin temperature over time in latentMTrPs. In contrast, Zhang et al. [40] did not find thatthe skin temperature was affected following an intra-muscular glutamate injection into latent MTrPs. Haddadet al. [41] compared infrared thermography and alg-ometer measurements of MTrPs in the masticatory mus-cles. The authors found a positive correlation betweenskin surface temperature and pressure pain threshold.Regarding diagnosing MTrPs, infrared thermography
had an accuracy of 0.564 to 0.609 (area under the re-ceiver operating characteristic curve).
Magnetic resonance imagingChen et al. [42] examined 65 patients with myofascialpain-associated taut bands using magnetic resonanceelastography. They found that agreement between physi-cians and imaging raters were relatively poor (63%; 95%CI, 50%–75%), but that these bands could be assessedquantitatively using magnetic resonance elastography.The authors suggest that clinicians might overestimatewhile magnetic resonance elastography may underesti-mate MTrPs.
Migraine and myofascial trigger pointsPericranial tenderness in migraine patients was system-atically described by Jes Olesen in 1978, both during andoutside of attacks [10, 11] leading to speculations thatmyofascial mechanisms may be involved in migraine[12]. The bottom-up model states that increased periph-eral nociceptive transmission sensitizes the central nervoussystem to lower the threshold for perceiving pain while thetop-down model suggests these changes are alreadypresent in the central nervous system [43]. While it can beargued that pericranial tenderness in migraine may becaused by a top-down central sensitization, a bottom-upassociation was implied in 1981 when Tfelt-Hansen et al.[44] demonstrated that injections of lidocaine and salineinto tender trigger points could relieve migraine attacks.They infiltrated the most tender spots of 26 cranial andneck muscles and tendon insertions in 50 migrainepatients. The most frequent sites of tenderness weresternocleidomastoid, anterior temporal, neck and shouldermuscles, the coronoid process and occipital insertions. Thetender points in the mentioned study do not necessarilyoverlap with Travell and Simons’ definition of MTrPs, butthe implication stands that peripheral myofascial mecha-nisms may be involved in migraine pathophysiology. Con-sequently, there has been an interest in exploring MTrPsin migraine (Table 1) [45–58].
The occurrence of myofascial trigger points in migraineSeveral studies have demonstrated a high occurrence ofactive and latent MTrPs in migraine patients [45–49].Studies show that there is a significantly higher preva-lence of active MTrPs in migraine patients compared tohealthy controls [45, 46, 58]. There are conflicting re-sults in which muscles are the most affected [47, 48].Fernández-de-Las-Peñas et al. [46] observed that activeMTrPs were most prevalent ipsilateral to the migraineheadaches. More unclear is whether the amount ofMTrPs is correlated with the frequency and intensity ofheadache attacks. Calandre et al. [45] found a positivecorrelation between the number of MTrPs and
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 3 of 17
Table
1Migraineandmyofascialtrig
gerpo
ints
Firstauthor
(year)
Blinding
Participants
Meanage(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Calandre(2006)
[45]
Non
e8EM
A55
EMO
35CMO
32CTRLs
(18(56%
)ofthese
repo
rted
infre
quen
tTTH)
38.5±13.5(15–75)
41.4±16.8(21–83)
9M,
79F
13M,
19F
Interictally
MTrPdiagno
sisby
manualp
alpatio
nwith
apressure
byno
morethan
4kg.
Thenu
mbe
randlocatio
nof
trigge
rpo
intsin
each
patient
were
recorded
.
Fron
tal,tempo
ral,
andsupe
rior
trapeziusmuscles
andsubo
ccipitaland
occipitalarea
•93.9%
migrainepatientsrepo
rted
referred
pain.
•Thenu
mbe
rof
MTrPs
correlated
with
frequ
ency
anddu
ratio
nof
migraineattacks.
Fernánde
z-de
-Las-Peñas
(2006)
[46]
Exam
iner
blinde
dto
diagno
sis
5EM
A15
EMO
20CTRLs
33±10
(17–57)
30±8(19–55)
7M,
13F
8M,
12F
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
FHPwas
documen
tedin
relaxed
standing
positio
nandrelaxed
sittingpo
sitio
n.Neckmob
ility
was
assessed
.
Upp
ertrapezius,
sterno
cleido
mastoid,
tempo
ralis,and
subo
cciptalm
uscles
•ActiveMTrPs
wereon
lyfoun
din
themigrainepatients.
•ActiveMTrPs
wereprim
arily
locatedipsilateraltothemigraine
headache
sexcept
forthe
subo
ccipitalreg
ion.
•Migrainepatientshave
agreater
FHPandless
neck
motility
inextensionandflexion
-exten
sion
comparedto
controls.
Ferracini(2017)
[47]
Exam
iner
blinde
dto
diagno
sis
98EM
45CM
With
orwith
outaura
notrepo
rted
.
37±12
(18–60)
38±12
(18–60)
143F
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
TheMigraineDisability
Assessm
ent
Scale(M
IDAS)
questio
nnaire
was
used
.
Tempo
ralis,m
asseter,
subo
ccipital,
sterno
cleido
mastoid,
uppe
rtrapeziusand
splenius
capitis
•Nosign
ificant
differencewas
inthetotaln
umbe
rof
MTrPs
betw
eenthetw
ogrou
ps.
•ActiveMTrPs
inthetempo
ralis
andmassetermuscleweremost
prevalen
tin
both
grou
ps.
•Thenu
mbe
rof
MTrPs
didno
tcorrelatewith
migrainerelated
disabilityno
rmigrainefeatures.
Ferracini(2016)
[48]
Non
e50
EMWith
orwith
outaura
notrepo
rted
.
34.1(18–55)
5M,
45F
Interictally:
46%
Ictally:54%
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
Eigh
tmeasuresof
head
andne
ckpo
sturewereob
tained
byradiog
raph
anddifferent
angles
werede
fined
.
Tempo
ralis,m
asseter,
subo
ccipital,
sterno
cleido
mastoid,,
uppe
rtrapezius,and
splenius
capitis
•Individu
alswith
migraineshow
edMTrPs
inallthe
muscles.
•ActiveMTrPs
was
positively
associated
with
aredu
ctionin
cervicallordosisandhead
extensionof
thehead
ontheneck.
•Noassociationbe
tweenthe
numbe
rof
activeMTrPs
and
clinicalfeatures
ofmigrainewas
observed
.
Floren
cio
(2017)
[49]
Non
e70
EMO
42±12
(39–45)
70F
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]and
byGerwin
etal.[89]
Surface
EMGwas
recorded
from
supe
rficialflexorandextensor
muscles
bilaterally
assubjects
perfo
rmed
astaged
task
ofcranio-
cervicalflexion
.The
averageRo
otMeanSquare
(RMS)
was
calculated
from
each
10scontraction.
Sterno
cleido
mastoid,
uppe
rtrapeziusand
splenius
capitis
•AllpatientsexhibitedactiveMTrPs
intheircervicalmuscles
•Participantswith
activeMTrPs
intheinclud
edmuscles
hadlower
norm
alized
RMSin
theirsupe
rficial
neck
flexors
•Subjectswith
activeMTrPs
inthe
splenius
capitis
andup
per
trapeziushadhigh
erno
rmalized
RMSvalues
inthesplenius
capitis.
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 4 of 17
Table
1Migraineandmyofascialtrig
gerpo
ints(Con
tinued)
Firstauthor
(year)
Blinding
Participants
Meanage(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Gando
lfi(2017)
[50]
Sing
le-blind
22CM
patients
receiving
onabotulinum
toxinA
treatm
ent
Patientswere
divide
dinto
two
grou
ps:
12individu
als
receiving
manipulative
treatm
ent
10individu
als
receivingelectrical
stim
ulation(placebo
grou
p)With
orwith
outaura
notrepo
rted
.
45.8±14.1
(18–66)
50.2±6.2
(40–61)
3M,
19F
2M,
10F
1M,
9F
Not
repo
rted
Patientswererand
omlyassign
edto
receiveeither
manipulativetreatm
ent
(treatmen
taimed
atim
proving
mob
ility
andredu
cing
stiffne
ssin
the
cervicotho
racicspine)
ortranscutaneo
uselectricalne
rve
stim
ulationin
theup
pertrapezius.
Treatm
entconsistedof
4sessions
(30min
once
aweekin
4weeks)
Patientswereaskedto
keep
ahe
adache
diary:ou
tcom
eswere
evaluatedbe
fore
treatm
ent,du
ring
treatm
ent,and1mon
thafterthe
endof
treatm
ent.
Cervicalactiverang
eof
motionand
trigge
rpo
intsensitivity
were
measuredpre-
andpo
sttreatm
ent.
MTrPsensitivity
was
assessed
bymeasurin
gPPTusingan
algo
meter.
Fron
talis,tem
poralis,
occipital,and
trapezius
•Thetotalcon
sumptionof
analge
sics
andNSA
IDswas
sign
ificantlylower
inthepatients
treatedwith
manipulative
treatm
entthan
inthosetreated
with
electricalstim
ulation.
•ThePPTs
attheMTrPs
inthe
uppe
rtrapezius,occipitaland
tempo
ralm
uscles
were
sign
ificantlylower
inthepatients
treatedwith
manipulative
treatm
entthan
inthosetreated
with
electricalstim
ulation.
•Afte
rtrialp
atientswho
received
manipulativetreatm
enthada
sign
ificantlylower
consum
ptionof
NSA
IDs,analge
sics
andtriptans.
Ghanb
ari
(2015)
[51]
Non
e44
migrainepatients
Whe
ther
patients
hadchronicor
episod
icmigraine
with
orwith
outaura
was
notrepo
rted
.
37.25
38.63
35.86
Rang
eno
trepo
rted
20M,
24F
9M,
13F
11M,
11F
Not
repo
rted
MTrPs
wereconsidered
tobe
active
if1)
referred
pain
dueto
palpation
reprod
uced
thesubjects’headache.
2)Therewas
ajumpsign
that
was
thecharacteristic
behavioralrespon
seto
pressure
onatrigge
rpo
int.All
subjectsinclud
edhadactivetrigge
rpo
ints.
Subjects(alw
ererand
omlyassign
edto
oneof
twogrou
ps:
1)Med
icationon
ly2)
Med
ication+po
sitio
nalrelease
therapy
Thetreatm
entph
aselasted
2weeks
andmed
icationinclud
edNSA
IDs,
nortrip
tyline,prop
rano
loland
depakine
.Subjectscompleted
adaily
headache
diarythroug
hout
thestud
yand
tablet
coun
twas
recorded
.Afte
rabaselinepe
riodof
2weeks
thesensitivity
oftrigge
rpo
ints(using
adigitalforce
gaug
e)andcervical
rang
eof
motionwereassessed
.Thiswas
repe
ated
afterthe
treatm
entph
aseandas
afollow
upafter1,2and4mon
ths(cou
nting
from
startof
treatm
ent)
Subo
ccipital,
sterno
cleido
mastoid,
uppe
rtrapezius,
cervicalmultifidus,
rotatorsand
interspinales
•Bo
thgrou
psshow
edsign
ificant
redu
ctionin
headache
intensity,
frequ
ency,d
urationandtablet
coun
tafter4mon
thsfollow
up.
•Thesensitivity
oftrigge
rpo
ints
was
sign
ificantlyredu
cedin
the
med
icationpo
sitio
nalrelease
therapygrou
p,whileitremaine
dun
change
din
themed
icineon
lygrou
p.
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 5 of 17
Table
1Migraineandmyofascialtrig
gerpo
ints(Con
tinued)
Firstauthor
(year)
Blinding
Participants
Meanage(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Giambe
rardino
(2007)
[52]
Exam
iner
blinde
dto
diagno
sis
Prim
aryexpe
rimen
t78
MO
(7also
diagno
sed
with
TTH)
20he
althyCTRLs
Second
ary
expe
rimen
t12
MO(2
also
diagno
sedwith
TTH)
31.4±5.8(23–46)
33.3±7(18–46)
29.3±4(24–35)
32.33±6.44
(24–
44)
11M,
43F
5M,
19F
5M,
15F
3M,
9F
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]A
MTrPwas
considered
activeifpalpationindu
ced
both
localand
referred
pain.
Pain
thresholdwas
assessed
byelectricalstim
ulation.
Subseq
uent
tothreshold
measuremen
tsgrou
p1also
received
0,5mLbu
pivacaine(5
mg/mL).The
infiltrationandpain
threshold
measuremen
tswererepe
ated
onthe
3.,10.,30.,and
60.d
ay.
PPTin
healthycontrolswas
assessed
with
thesamefre
quen
cy.
Migraines
(num
berandintensity
ofattacks)wereassessed
60days
prior
tothestud
yand60
days
afterthe
stud
ystarted.
Thiswas
done
usinga
headache
diary.
Thesecond
stud
yisa30
days
“placebo
-like
stud
y”whe
resalinewas
injected
near
theMTrPs.
PPT,injections
andtheheadache
diary
werefulfilledsim
ilarly
tothetheprior
experim
ent.(onlyup
till30days)
Sterno
cleido
mastoid,
semispinalis
cervicis,
splenius
cervicis
•Group
1and2painthresholds
weresig
nificantly
lower
than
incontrolsatbaseline.Ingrou
pon
epainthresholdincreased
significantly
durin
gtreatm
ent.In
grou
ptwotherewas
nosig
nificant
change.Inthecontrolgroup
there
was
nosig
nificantvariatio
n.•In
grou
p1maxim
alintensity
and
numbe
rof
migraineattacks
decreasedsign
ificantly.Ingrou
p2
thechange
was
notsign
ificant.
•Themeannu
mbe
rof
rescue
med
icationtakenfellsign
ificantly
ingrou
p1,bu
tno
tin
grou
p2.
•Thegrou
pthat
participated
inthe
second
expe
rimen
talso
hada
pain
thresholdlower
than
norm
al.
Land
graf
(2017)
[53]
Non
e26
adolescent
migrainepatients
(chron
ic/episodicno
trepo
rted
)17
MO
5MA
4with
vestibular
migraine
14.5(6.3–17.8)
13M,
13F
Not
specified
MTrPs
wereiden
tifiedby
palpation
andthePPTon
thesepo
intswas
measuredusingan
algo
meter.
Manualp
ressurewas
appliedto
the
trigge
rpo
ints,and
theoccurren
ceanddu
ratio
nof
indu
cedhe
adache
wererecorded
.Atasecond
consultatio
n(4
weeks
afterthefirst),manualp
ressurewith
thede
tected
pressure
thresholdwas
appliedto
non-trigge
rpo
intswith
inthesametrapeziusmuscle(con
trol).
Trapeziusmuscle
•Manualp
ressureto
MTrPs
inthe
trapeziusmuscleledto
lasting
headache
afterterm
inationof
the
manualp
ressurein
13(50%
)patients(from
5sto
over
30min).
•Nopatient
expe
rienced
headache
whe
nmanualp
ressurewas
appliedto
non-trigge
rpo
intsat
thecontrolvisit.
•Headachewas
indu
ced
sign
ificantlymoreoftenin
children≥12
yearsandthosewith
internalizingbe
havioraldisorder.
Land
graf
(2015)
[54]
Non
e3migrainepatients
Whe
ther
patients
hadchronicor
episod
icmigraine
with
orwith
outaura
was
notrepo
rted
.
23.67(23–24)
1M,
2FInterictally
MTrPdiagnosis
was
perform
edfollowing
thecriteria
described
bySimonsetal.[19]
andby
Gerwinetal.[89]
Theseareasweremarkedby
nitrog
lycerin
capsules
onthe
adjacent
skin
surface.
High-resolutio
nMRim
agingof
the
posteriorcervico-cranialm
uscles
was
perfo
rmed
ona3TMRscanne
rwith
Trapezius
•MRim
agingde
mon
stratedfocal,
partlyT2
hype
rintensesign
alalteratio
nswith
inthetrapezius
muscles
inallthree
stud
yparticipants.A
llof
theob
served
sign
alalteratio
nswerein
close
proxim
ityto
thefid
ucialm
arkers
tape
don
theskin.
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 6 of 17
Table
1Migraineandmyofascialtrig
gerpo
ints(Con
tinued)
Firstauthor
(year)
Blinding
Participants
Meanage(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
aspinearrayas
wellassurface
coils.
Highresolutio
nT2
weigh
tedandT1-
weigh
tedsequ
encesas
wellasshort
tauinversionrecovery
(STIR)
sequ
ences
wereacqu
iredin
acoronaland
axialsliceorientation.
Palacios-Ceñ
a(2017)
[55]
Non
e95
EMWith
orwith
outaura
notrepo
rted
.
40(37–43)
0M,
95F
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19].
PPTwas
assessed
usingan
algo
meter.in
thefollowingregion
s:•Overthetempo
ralis
muscle.
•C5/C6zygapo
physealjoint.
•Tibialisanterio
rmuscle(a
pain-free
distantcontrolsite)
Tempo
ralis,m
asseter,
subo
ccipital,
sterno
cleido
mastoid,
uppe
rtrapezius,and
splenius
capitis
•Thehigh
ertheintensity
ofmigrainepain,the
lower
thePPTs
over
thecervicalspine.
•Thenu
mbero
factiveMTrPs
was
significantly
andnegatively
associated
with
PPTinallthe
points.
Rano
ux(2017)
[56]
Non
e7CMA
50CMO
57chronicmigraine
patients(re
fractory
toconven
tional
treatm
ent)
44.3(17–85)
14M,
43F
Not
specified
Observatio
nal,op
enlabe
l,real-life,
coho
rtstud
y.Thepatientswere
injected
with
Onabo
tulinum
toxinA
usinga“fo
llow-the
-pain”
patternin
MTrPs.
Corrugatorsupe
rcilii,
tempo
ralis
and
trapeziusmuscles
•65.1%
respon
dedto
treatm
ent.
•Theassociated
cervicalpain
and
muscletend
erne
ss,p
resent
in33
patients,was
redu
cedby
≥50%
in31
patients(94%
).•Triptanconsum
ptionde
creased
(81%
)inrespon
ders.
Sollm
ann
(2016)
[57]
Non
e6MO
14MA
(50%
also
hadsome
degree
ofTTH)
chronic/ep
isod
icno
trepo
rted
23±1.8(19–27)
1M,
19F
Interictally
rPMS(repetitiveperipheralm
agnetic
stimulation)
was
used
tostimulate
activeMTrPs
oftheuppertrapeziu
smuscles.Thiswas
done
in6stimulation
sessions
over2consecutiveweeks.
PPTwas
assessed
usingan
algo
meter.
Participantscompleted
astandardized
headache
questio
nnaire
includ
ingoccurren
ce,
duratio
nandintensity
ofhe
adache
s.Thiswas
repe
ated
over
3mon
ths.
Trapeziusandde
ltoid
(asacontrol)
•In19
subjectsMTrPalgo
metryvalues
weresig
nificantly
high
erimmediately
afterm
agnetic
stimulation.
•PPTincreaseddu
ringthetrial.
Tali(2014)
[58]
Exam
iner
blinde
dto
diagno
sis
durin
gup
per
cervicalfact
jointmob
ility/
stiffne
ssMTrP
evaluatio
nno
tblinde
d
20EM
20CTRLs
Distributionof
with
/with
outaura
not
repo
rted
.
24.95±1.79
(20–
27)
25.65±1.42
(23–
28)
2M,
18F
3M,
17F
Interictally
MTrPdiagno
sis
was
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]and
Gerwin
etal.[89]
Neckrang
eofmotionwas
assessed
using
acervicalrang
eofmotioninstrument.
FHPwas
notedin
aseated
positio
n.Upp
ercervicalfacetjointmob
ility/
stiffne
sswas
evaluatedusinga
motionpalpationtechniqu
e.
Sterno
cleido
mastoid
andup
pertrapezius
muscle
•ActiveMTrPs
wereon
lyfoun
din
themigrainegrou
p.•Sign
ificant
differences
werefoun
din
neck
rang
eof
motion
measuremen
tsandFH
Pbe
tween
themigraineandcontrolg
roup
s.
C*chronic,E*
episod
ic,M
Amigrainewith
aura,M
Omigrainewith
outau
ra,C
TRLs
healthycontrols,F
female,
Mmale,
MTrPmyo
fascialtrig
gerpo
int,EM
Gelectrom
yograp
hy,P
PTpressure
pain
threshold,
FHPforw
ard
head
posture,
VASvisual
analog
scale,
NRS
numericratin
gscale
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 7 of 17
frequency and duration of migraine attacks, whereas twostudies by Ferracini et al. [47, 48] found no such correl-ation. Interestingly, Landgraf et al. [54] could visualizeMTrPs on MR imaging as focal signal alterations in asmall pilot study.
Neck mobility and specific musclesThere appears to be an association between neck mobilityand MTrPs [46, 48, 49, 58]. Ferracini et al. [48] found thata higher number of active MTrPs was positively correlatedwith a reduction in cervical lordosis and head extension ofthe head on the neck. In addition, that lower cervical an-gles were correlated higher then the number of activeMTrPs. Florencio et al. [49] hypothesized that activeMTrPs in the cervical musculature alters the activity ofthe related muscles and that this would be reflected inEMG readings. They observed that the presence of activeMTrPs in the cervical musculature had different activationin the neck flexor muscles compared to those without ac-tive MTrPs in the same muscles regardless of the presenceof pain. Palacios-Ceña et al. [55] found that the number ofactive MTrPs in head, neck and shoulder muscles were as-sociated with widespread pressure hypersensitivity in amigraine population.
Provocation and intervention studiesTwo unblinded studies show that manual palpation ofMTrPs can provoke a migraine attack [45, 53]. Calandreet al. provoked a migraine attack in one-third of a mi-graine population by palpating MTrPs [45]. Landgraf etal. provoked migraine headache by inducing pressure toMTrPs and could not replicate this by pressure tonon-trigger points in the trapezius in an adolescent mi-graine population [53].Interventions targeted at MTrPs show promising re-
sults [50–52, 56, 57], but the quality of studies variesgreatly and lack placebo-control. Giambierardino et al.demonstrated that local anesthetic infiltration of MTrPsresulted in a reduction of migraine symptomatology interms of frequency and intensity [52]. Furthermore,there was a reduction of hyperalgesia, not only at the in-jection site but also in referred areas overlapping withmigraine pain sites. Similar, Ranoux et al. injected botu-linum toxin in MTrPs with similar results in terms of re-duction in headache days [56]. Gandolfi et al. improvedthe outcome of prophylactic botulinum toxin treatmentin chronic migraine patients with manipulative treat-ment of MTrPs [50]. The outcome was a lower con-sumption of analgesics, improvement in pressure painthreshold and increased cervical range of motion. Like-wise, Ghanbari et al. reported that combined positionalrelease therapy targeted at MTrPs with medical therapyis more effective than the sole pharmacological treat-ment [51]. Interestingly, sessions of magnetic stimulation
of active MTrPs reduced headache frequency and inten-sity in adolescent migraineurs [57]. Though these find-ings need to be verified in a placebo-controlled study.There has not been any studies on the effect of systemicmusculoskeletal analgesics on MTrPs [59], which wouldbe of interest for future studies.
Tension-type headache and myofascial trigger pointsBoth peripheral and central mechanisms have been sug-gested as important components of TTH [14–16, 60]. Ten-derness in pericranial myofascial tissue is correlated withthe intensity and frequency of headache [14–16]. Further-more, there has been demonstrated increased muscle stiff-ness in the trapezius muscle in TTH patients [17, 18] notdiffering between headache and non-headache days [18].Although a recent study found no increased muscle stiff-ness in TTH patients, this may be due to the method used[61]. Studies show that the referred pain elicited by activeMTrPs reproduce the headache pattern in TTH patients[62–66]. Accordingly, there has been an interest in investi-gating the occurrence of MTrPs in TTH (Table 2) [62–80].
The occurrence of myofascial trigger points in tension-typeheadacheThere is a high occurrence of active and latent MTrPs inpatients with TTH [63–67, 69–72, 79] Active MTrPs arefound almost only in TTH patients compared to con-trols [63, 65, 69, 72, 80]. MTrPs are more prevalent onthe dominant side of the patients [66]. The number ofactive MTrPs is higher in adults in comparison to ado-lescents regardless of no significant association betweenthe number of active MTrPs and headache frequency,duration and intensity [62]. Other studies have foundthat active MTrPs are correlated with the severity ofTTH [65, 67, 78, 80] with a greater occurrence of MTrPsin chronic TTH in comparison to episodic TTH [80].Furthermore, studies show that active MTrPs are corre-lated with the intensity, duration and frequency of head-ache episodes in TTH [65, 80]. In contrast, other studiesfailed to show a correlation between MTrPs and chronicand frequent episodic TTH [78] and showed no correl-ation between MTrPs and headache parameters either inepisodic TTH patients [69].
Neck mobility and specific musclesEpisodic TTH patients had less neck mobility comparedto controls [69]. Patients with active MTrPs had a greaterforward head position than subjects only with latentMTrPs [69]. However, neither forward head position orneck mobility was correlated with headache parameters[69]. In a different study, active MTrPs in the right uppertrapezius muscle and left sternocleidomastoid muscle wascorrelated with a greater headache intensity and duration[72]. Furthermore, active MTrPs in the right and left
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 8 of 17
Table
2Tension-type
headache
andmyofascialtrig
gerpo
ints
First
author
(year)
Blinding
Participants
Meanage
(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Alonso-
Blanco
(2011)
[62]
Non
e20
CTTHadult
patients
20CTTH
adolescent
patients
41(18–47)
8(6–12)
10M,10F
10M,10F
Interictally
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19]
Tempo
ralis,sub
occipital,
sterno
cleido
mastoid,and
uppe
rtrapezius
•Thenu
mbero
factiveMTrPs
were
high
erinadultsversus
children.
•Referred
painelicitedfro
mactive
MTrPs
shared
similarp
ainpatterns
asspon
taneou
sCTTH
inbo
thgrou
ps.
Nosig
nificantassociationbetween
thenu
mbero
factiveMTrPs
and
headache
parameters.
Cou
ppé
(2007)
[67]
Dou
ble-
blinde
d20
CTTH
patients
20CTRLs
37.5(33.3–41.6)
Not
repo
rted
Ictally
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19]
EMGexam
inationat
aMTrPanda
controlp
oint
inthesamesubject.
Upp
ertrapezius
•Thenu
mbero
factiveMTrPs
were
high
erinpatientsversus
controls
•Nodifferenceinelectro
myographic
activity
betweenMTrPs
versus
control
points.
Fernánde
z-de
-las-
Peñas
(2011)
[63]
Exam
iner
blinde
dto diagno
sis
50CTTH
patients
50CTRLs
8(6–12)
14M,36F
Interictally
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19].
Tempo
ralis,sup
eriorob
lique,
masseter,subo
ccipital,
sterno
cleido
mastoid,levator
scapulae,and
uppe
rtrapezius
•ActiveMTrPs
wereon
lyfoun
din
patients.
•IntheCTTH
patients,thenu
mbero
factiveTrPs
correlated
with
the
duratio
nof
aheadache
attack.
•Thelocaland
referred
painselicited
from
activeMTrPs
shared
similar
pain
patternas
spon
tane
ousCTTH.
Fernánde
z-de
-las-
Peñas
(2009)
[68]
Non
e40
CTTH
40(20–57)
40F
Interictally
<4on
a11
NRS
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]and
Gerwin
etal.[89]
PPTwas
assessed
usingan
algo
meter.
Tempo
ralis
(9land
marks
total,3each
respectivelyin
theanterio
r,med
ialand
posteriorpart)
•Theanalysisof
variancedidno
tdetectsig
nificantd
ifferencesinthe
referredpainpatte
rnbetweenactive
MTrPs.
•Thetopo
graphicalpressurepain
sensitivitymapsshow
edthedistinct
distributionoftheMTrPs
indicatedby
locations
with
lowPPTs.
Fernánde
z-de
-las-
Peñas
(2007)
[69]
Exam
iner
blinde
dto diagno
sis
15ETTH
15CTRLs
39±17
(20–70)
37±12
(21–70)
3M,12F
4M,11F
Interictally
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19]andGerwin
etal.[89]
FHPwas
notedbo
thseated
and
standing
.
Tempo
ralis,sternocleidom
astoid,
andup
pertrapezius
•ActiveMTrPs
intheaffected
muscles
wereon
lyfoun
dwith
intheETTH
grou
p.•MTrPs
wereno
trelatedto
any
clinicalvariableconcerning
the
intensity
andthetempo
ralp
rofile
ofhe
adache
.
Fernánde
z-de
-las-
Peñas
(2007)
[70]
Exam
iner
blinde
dto diagno
sis
20CTTH
20CTRLs
36(18–56)
35(20–56)
11M,9F
13M,7F
<4cm
ona10
cmVA
S
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
PPTwas
assessed
usingan
algo
meter.
Upp
ertrapezius
•CTTHsubjectswith
activeMTrPs
show
edgreaterhe
adache
intensity,
anddu
ratio
nthan
thosewith
latent
TrPs.
•Patientswith
bilateralM
TrPs
repo
rted
agreaterhe
adache
intensity
anddu
ratio
nthan
those
with
unilateralTrPs.
•CC
THsubjectsshow
edadecreased
PPTcomparedto
controls.
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 9 of 17
Table
2Tension-type
headache
andmyofascialtrig
gerpo
ints(Con
tinued)
First
author
(year)
Blinding
Participants
Meanage
(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Fernánde
z-de
-las-
Peñas
(2007)
[66]
Exam
iner
blinde
dto diagno
sis
30CTTH
30CTRLs
39±16
(18–65)
39±12
(19–65)
9M,21F
9M,21F
<4cm
ona10
cmVA
S
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
Tempo
ralis
•Referredpainwas
evoked
in87
and
54%on
thedo
minantand
non-
dominantsides
inCTTH
patients,
which
was
significantly
high
erthan
incontrols(10%
vs.17%
,respectively).
•CTTHpatientswith
activeMTrPs
ineither
right
orlefttempo
ralis
muscleshow
edlong
erhe
adache
duratio
nthan
thosewith
latent
MTrPs.
•CTTHpatientsshow
edsign
ificantly
lower
pressure
pain
threshold
whe
ncomparedwith
controls.
Fernánde
z-de
-las-
Peñas
(2006)
[71]
Exam
iner
blinde
dto diagno
sis
10ETTH
10CTRLs
35±15
(18–66)
34±13
(18–66)
2M,8F
3M,7F
Interictally
MTrPdiagno
sisas
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
Subo
ccipital
•In
theETTH
grou
p,60%
show
edactiveMTrPs;40%
show
edlatent
trigge
rpo
ints.IntheETTH
grou
p,he
adache
intensity,frequ
ency
and
duratio
ndidno
tdifferde
pend
ing
onwhe
ther
theMTrPs
wereactive
orlatent.
Fernánde
z-de
-las-
Peñas
(2006)
[72]
Exam
iner
blinde
dto diagno
sis
25CTTH
25CTRLs
40±16
(18–72)
38±9(18–73)
8M,17F
9M,16F
<4cm
ona10
cmVA
S
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
FHPwas
notedbo
thseated
and
standing
.
Tempo
ralis,
sterno
cleido
mastoid,and
uppe
rtrapezius
•ActiveMTrPs
wereon
lyfoun
din
CTTHpatients.
•Therewas
significantassociation
betweenthepresence
ofactiveMTrPs
andheadache
intensity
andduration.
Fernánde
z-de
-las-
Peñas
(2006)
[65]
Exam
iner
blinde
dto diagno
sis
20CTTH
20CTRLs
38±18
(18–70)
35±10
(20–68)
9M,11F
12M,8F
Pain
intensity
<4on
a10
cmVA
S
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
FHPwas
notedbo
thseated
and
standing
.
Subo
ccipital
•ActiveMTrPs
wereon
lyfoun
din
CTTHpatients.
•CTTHpatientswith
activeMTrPs
repo
rted
greaterhe
adache
intensity
andfre
quen
cythan
those
with
latent.
•Acranioverteb
ralsmalleranglewas
positivelycorrelated
with
increased
headache
frequ
ency
andne
gatively
correlated
with
headache
duratio
n.
Fernánde
z-de
-las-
Peñas
(2005)
[64]
Exam
iner
blinde
dto diagno
sis
15CCTH
15ETTH
15CTRLs
37±16
38±14
38±14
Rang
eno
trepo
rted
5M,10F
4M,11F
5M,10F
CTTH:Pain
intensity
<4cm
ona10
cmVA
STTH:
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
Supe
riorob
lique
•86%
CTTHpatientsand60%
ETTH
patientsrepo
rted
referred
pain
from
MTrPs.
•Thepain
was
perceivedas
ade
epache
locatedat
theretro-orbitalre-
gion
–sometim
esextend
ingto
the
supraorbitalreg
ionor
theho
mo-
lateralforeh
ead.
•Pain
intensity
was
greaterin
CTTH
patientsthan
inETTH
patients.
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 10 of 17
Table
2Tension-type
headache
andmyofascialtrig
gerpo
ints(Con
tinued)
First
author
(year)
Blinding
Participants
Meanage
(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Harde
n(2009)
[73]
Dou
ble-
blinde
d23
CTTHwith
activecervical
MTrPs
(12in
activegrou
p,11
inplaceb
ogrou
p)
49.6in
active
grou
p40.8in
placeb
ogrou
pRang
eno
trepo
rted
7M,5F
7M,4F
Not
repo
rted
Patientsreceived
i.m.injectio
nsof
botulinum
toxinAor
isoton
icsaline
(placebo
)in
MTrPs.25un
itsdo
sepr.
MTrP,bu
tno
morethan
100un
itsin
totalp
r.patient
(maxim
umfour
trigge
rpo
intstreatedpr.p
atient).
Sterno
cleido
mastoid,trape
zius,
andsplenius
capitis
(which
overliesinvolved
cervical
musclegrou
ps:sem
ispinalis
capitis,lon
gissim
uscapitis,recti
capitis
posteriorandob
liquu
scapitis
supe
rior)
•Patientsin
theactivegrou
prepo
rted
greaterredu
ctions
inhe
adache
frequ
ency
durin
gthe
firstpartof
thestud
y,bu
tthese
effectsdissipated
byweek12.
Karadas
(2013)
[74]
Dou
ble-
blinde
d48
CTTHwith
activeMTrPs
(24in
active
grou
p,24
inplaceb
ogrou
p).
40.4±12
inactivegrou
p40.7±13.2in
placeb
ogrou
pRang
eno
trepo
rted
4M,20F
5M,19F
Not
repo
rted
Patientsreceived
i.m.injectio
nswith
0.5%
lidocaine
or0.9%
NaC
l(placeb
o)to
thetrigge
rpo
intsof
themuscles
inne
rvated
byC1-C3andthetrigem
inaln
erve,exitpo
intof
thefifth
cranialn
erve
andarou
ndthesupe
rior
cervicalgang
lion.
Muscles
inne
rvated
byC1-C3
andthetrigem
inalne
rve,exit
pointof
thefifth
cranialn
erve
andarou
ndthesupe
riorcervical
gang
lion
•Patientsin
theactivegrou
prepo
rted
sign
ificantlygreater
redu
ctions
inhe
adache
frequ
ency
andintensity.
Lattes
(2009)
[75]
Non
e27
CTTH
App
roximately
46(18–80)
7M,20F
Not
repo
rted
I.m.injectio
nswith
gonyautoxinin
10land
marks
considered
asMTrPs.
EMGexam
inationbe
fore
andafter
injections.
Occipitalis
andtrapezius
•Respon
ders(70%
)had
anaverage
of8,1weeks
freeof
pain
following
treatm
ent.
•TheEM
Grecorded
immed
iately
afterinjectionin
allcases
show
edthat
thehype
ractivity
inthe
trapeziusmusclewas
completely
abolishe
d.
Moraska
(2017)
[76]
Sing
le-
blind
34CTTH
28ETTH
Massage
:13
CTTH
7ETTH
Placeb
o:11
CTTH
10ETTH
Wait-list
10CTTH
11ETTH
31.2±11.3
34.4±10.7
33.0±9.0
7M,55F
1M,19F
2M,19F
4M,17F
Not
repo
rted
Individu
alswith
ETTH
orCTTHwere
rand
omized
toreceive12
twice-
weekly45-m
inmassage
orsham
ultrasou
ndsessions
orwait-list
control.Massage
focusedon
MTrPs.
PPTwas
assessed
usingan
algo
meter.
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]
Subo
ccipitaland
uppe
rtrapezius
•PPTincreasedacross
thestud
ytim
eframein
allfou
rmusclesites
tested
formassage
,but
notsham
ultrasou
ndor
wait-listgrou
ps.
Moraska
(2015)
[77]
Sing
le-
blind
30CTTH
26ETTH
32.1±12
inactivegrou
p34.7±11
inplaceb
ogrou
pRang
eno
trepo
rted
8M,48F
(2M,
15Fin
active
grou
p;2M,17F
inplaceb
ogrou
p;4M,16F
inwait-list
grou
p)
Not
repo
rted
56patientswith
TTHwererand
omized
toreceive12
massage
orplacebo
(detun
edultrasou
nd)sessio
nsover
6weeks,ortowait-list.
Massage
focusedon
MTrPs
incervical
musculature.
PPTwas
assessed
usingan
algo
meter.
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]
Subo
ccipital,
sterno
cleido
mastoid,
andup
pertrapezius
•Headachefre
quen
cyfellin
both
themassage
andtheplaceb
ogrou
p.•PPTim
proved
inthemassage
grou
p.
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 11 of 17
Table
2Tension-type
headache
andmyofascialtrig
gerpo
ints(Con
tinued)
First
author
(year)
Blinding
Participants
Meanage
(rang
e)Gen
der
Timingof
recordings
Metho
dsMuscles
Mainfinding
s
Palacios-
Ceñ
a(2016)
[78]
Exam
iner
blinde
dto diagno
sis
77CTTH
80ETTH
46(42–50)
47(43–51)
46M,111F
Interictally
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]
PPTwas
assessed
over
thetrigem
inal
area,extra-trig
eminalarea
andtw
odistantpain
freepo
intsusingan
algo
meter.
Tempo
ralis,m
asseter,
subo
ccipital,
sterno
cleido
mastoid,splen
ius
capitis,and
uppe
rtrapezius
•Nodifferencein
numbe
rof
MTrPs
andPPTin
thetw
ogrou
ps.
•Therewas
asign
ificant
negative
correlationbe
tweenthenu
mbe
rof
trigge
rpo
ints(activeor
latent)and
PPT.
Romero-
Morales
(2017)
[79]
Non
e60
ETTH
60CTRLs
38,30±10,05
34±8,20
Rang
eno
trepo
rted
24M,32F
27M,33F
Not
repo
rted
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]
PPTwas
assessed
usingan
algo
meter.
Tempo
ralis
andup
pertrapezius
Minim
umclinicaldifferences
inPPT
betw
eenTTHandCTRLs
were
•Righ
tup
pertrapezius;0,85
kg/cm
2
•Leftup
pertrapezius;0;76
kg/cm
2
•Righ
ttempo
ralis;0;16kg/cm
2
•Lefttempo
rals;0,17kg/cm
2
Sohn
(2012)
[80]
Exam
iner
blinde
dto diagno
sis
23CTTH
36ETTH
42CTRLs
53.43±16.97
51.11±14.42
51.69±16.18
Rang
eno
trepo
rted
2M,21F
7M,29F
8M,34F
Headache
intensity
<3on
a10
cmVA
S
MTrPdiagno
siswas
perfo
rmed
followingthecriteria
describ
edby
Simon
set
al.[19]andby
Gerwin
etal.[89]
FHPwas
used
toevaluate
posture
abno
rmalities.
Measuremen
tof
neck
mob
ility
was
used
toevaluate
mechanical
abno
rmalities.
Tempo
ralis,sub
occipital,
sterno
cleido
mastoid,and
uppe
rtrapezius
•Thenu
mbe
rof
activeMTrPs
was
sign
ificantlygreaterin
CTTH
subjectsthan
inETTH
subjects.
•Thenu
mbe
rof
activeMTrPs
were
correlated
with
thefre
quen
cyand
duratio
nof
headache
.•Nocorrelations
wereob
served
for
FHPor
neck
mob
ility.
CTTH
chronictension-type
head
ache
,ETTHep
isod
ictension-type
head
ache
,CTRLs
healthycontrols,F
female,
Mmale,
MTrPmyo
fascialtrig
gerpo
int,EM
Gelectrom
yograp
hy,P
PTpressure
pain
threshold,
FHPfron
tal
head
positio
n,VA
Svisual
analog
scale,
NRS
numericratin
gscale
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 12 of 17
temporalis muscles correlated with longer headache dur-ation and greater headache intensity, respectively [72].Suboccipital active MTrPs correlated with increased in-tensity and frequency of headache [65]. Chronic TTH pa-tients with active MTrPs in the analyzed muscles had agreater forward head position than those subjects onlywith latent MTrPs [65, 72]. Sohn et al. [80] identified agreater occurrence of MTrPs in chronic TTH comparedto episodic TTH and that the number of active MTrPscorrelated with the frequency and duration of headache,although they did not find any correlations for forwardhead posture and neck mobility in contrast to Fernández--de-las-Peñas et al. [65, 72].
Pressure pain thresholdThe number of active and latent MTrPs was signifi-cantly and negatively associated with pressure painthresholds on the temporalis muscle, C5/C6 zygapo-physeal joint, second metacarpal, and tibialis anteriormuscle [78]. Thus, a higher number was associatedwith a more generalized sensitization regardless of thefrequency of headache. Another study observed thatthe location of active MTrPs in the temporalis musclecorresponded to areas with lower pain pressurethresholds which establishes a relationship betweenthe two [68]. The same group found that chronicTTH patients with bilateral active MTrPs in the tra-pezius muscles have a significantly lower pain pres-sure threshold compared to patients with onlyunilateral active MTrPs [70]. Minimum clinical differ-ences in pressure pain thresholds in TTH patientsmay be used to evaluate treatment of MTrPs [79].
Therapeutic studies targeting myofascial trigger pointsKaradas et al. [81] investigated pericranial lidocaineinjections in MTrPs in 108 patients with frequent epi-sodic TTH using a double-blind placebo-controlledrandomized study design. Repeated local lidocaineinjections into the MTrPs in the pericranial musclesreduced both the frequency and intensity of paincompared to placebo. Another placebo-controlled studyfound similar results with lidocaine injections in MTrPs inchronic TTH with a reduction in pain frequency, pain in-tensity, and analgesic use [74]. In addition, there was a sig-nificant effect on anxiety and depression of the subjects. Arandomized, double-blind, placebo-controlled pilot studyof botulinum toxin A injections in MTrPs included 23 pa-tients with chronic TTH [73]. The subjects were assessedat 2 weeks, 1, 2 and 3 months after injection. The botu-linum toxin A group reported a reduction in headache fre-quency that disappeared by week 12. There was nodifference in intensity between the groups. In a random-ized, placebo-controlled clinical trial, Moraska et al. ap-plied massage focused on MTrPs of patients with TTH
[77]. For both active and placebo groups, there was a de-crease in headache frequency, but not for intensity or dur-ation. Thus, there was no difference between massage andplacebo [81].
DiscussionUltrasound and EMG appear to be the most promis-ing modalities to be used as a diagnostic test forMTrPs. While the use of ultrasound in headache dis-orders has primarily been focused on vascularchanges and not on myofascial structures [82], ultra-sound may also be used to identify MTrPs if specificanalysis methods are applied [29] or with the use ofelastography [27, 30, 32]. However, there is no precisedescription of a gold standard using these techniques,and they have yet to be evaluated in headache pa-tients. Active MTrPs affect the electrical activity atrest and during muscle contraction in EMG studies[33–36]. Out of the two modalities, ultrasound is pre-sumably the most viable candidate as a diagnostic testas it has an immediate availability at most treatmentsites, it is time-efficient and is non-invasive. Althoughthere are currently no studies investigating if it ispossible to identify MTrPs with ultrasound withoutprior manual palpation. Future studies should investi-gate if ultrasound is comparable with manual palpa-tion in identifying MTrPs. The other modalities donot appear to be suitable as microdialysis show mixedresults regarding whether the local milieu of MTrPsis changed and needs further exploration before aconclusion can be made [25, 26, 83]. According tothe review by Dibai-Filho et al. [37], infrared therm-ography appears to be a promising non-invasivemethod, but it should still only be used as an auxil-iary tool in the evaluation of MTrPs due to conflict-ing results. Magnetic resonance elastography indiagnosing MTrPs has only been investigated in a fewstudies, and the sensitivity may be too low for suit-able use as a diagnostic test [42].Studies show a high occurrence of active and latent
MTrPs [45–49] and correlation between neck mobilityand MTrPs in migraine patients [46, 48, 49, 58]. How-ever, there are conflicting results in which muscles arethe most affected [47, 48], and it is unclear whetherthere is a positive correlation with the degree of head-ache frequency or intensity due to conflicting results.Palpation of MTrPs may provoke a migraine attack insome patients [45, 53] but needs further confirmationin placebo-controlled studies. Intervention studies tar-geting MTrPs are mostly positive [50–52, 56, 57], butthey lack placebo-control. Thus, a bottom-up associ-ation between MTrPS and migraine [44] cannot be fullysupported based on the evidence (Fig. 1). In addition,in patients with migraine-fibromyalgia comorbidity, it
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 13 of 17
has been shown that migraine attacks exacerbate fibro-myalgia symptoms, suggesting a top-down centralsensitization [84] as fibromyalgia symptoms includespecific tender points [85]. Although a study showedmigraine severity was similar in migraine patients withand without fibromyalgia [86]. One would expect an as-sociation between migraine severity and co-existingfibromyalgia if a top-down central is taking place inpatients with this comorbidity. It is possible thatMTrPs may have an important role in some subpopu-lations of migraine patients. This calls for therapeuticstudies targeting patients with a high degree ofMTrPs, but this is only speculative at this point.The prevalence of active MTrPs in TTH [65–67, 73,
74, 77, 78, 80, 81] is coherent with the hypothesis thatperipheral mechanisms are involved in the pathophysi-ology of TTH [14–16, 60]. It has been speculated thatan increased peripheral nociception increases the
sensitization of central mechanisms resulting in an in-crease in the sensitivity to peripheral pain (Fig. 1). Ac-tive MTrPs may contribute to a central sensitization asthey are correlated with lower pain pressure thresholds[68, 70, 78]. This would also provide an explanationfor the efficacy of injections of lidocaine in MTrPs [74,81] as these would reduce the transmission of periph-eral nociception. However, these assumptions are incontrast with a study showing that the number of ac-tive MTrPs is higher in adults in comparison to adoles-cents, regardless of no significant association withheadache parameters [62]. This suggests that activeMTrPs are accumulated over time as a consequence ofTTH [62] instead of being an integrated part of thepathophysiology of TTH. Previous studies of botu-linum toxin A injections in pericranial muscles havebeen shown to have no effect in TTH [87]. The efficacyof botulinum toxin A in MTrPs [73] might be ex-plained by its possible action of modulating the releaseof nociceptive and inflammatory mediators e.g., CGRPand SP [88]. These inflammatory mediators may be in-creased in the local milieu of MTrPs [25, 26]. Thiswould also account for its poor efficacy in injectionprotocols targeting fixed landmarks in pericranial mus-cles instead of MTrPs [87], as these substances appearto be concentrated at MTrPs [25, 26].There are many overlapping findings in studies of
MTrPs in migraine or TTH. In both disorders, MTrPsare prevalent and may be related to neck mobility. Pal-pation of MTrPs can, in some cases, provoke an attackin migraine patients, while palpation of MTrPs in TTHcan provoke pain resembling the usual headache pat-tern of patients. Intervention studies are promising inboth disorders. The quality of studies in both disordersvaries greatly as many of the reviewed studies lackedblinding (Table 3). Furthermore, true blinding is diffi-cult to achieve as active MTrPs by definition cause re-ferred pain.
ConclusionIn conclusion, ultrasound elastography is the mostpromising tool to assess MTrPs [27, 30, 32], but stillneeds to be performed combined with palpation,which introduces risk of bias and interobserver vari-ation. MTrPs are very frequent in both migraine pa-tients [45–49] and TTH patients [65–67, 73, 74, 77,78, 80, 81] compared to healthy controls. Active
Table 3 An overview on the use of blinding, control groups and placebo
Migraine Tension-type headache Total
Blinding 36% (5/14 relevant studies) 79% (15/19 relevant studies) 61% (19/33 relevant studies)
Control group 44% (4/9 relevant studies) 79% (11/14 relevant studies) 65% (15/23 relevant studies)
Placebo 40% (2/5 relevant studies) 80% (4/5 relevant studies) 60% (6/10 relevant studies)
Fig. 1 The bottom-up model states that increased peripheralnociceptive transmission sensitizes the central nervous system to lowerthe threshold for perceiving pain while the top-down model suggeststhese changes are already present in central nervous system. In relationto myofascial trigger points, a bottom-up model would suggest thatincreased nociceptive transmission from myofascial trigger points lowersthe threshold for perceiving pain (red). A top-down model wouldsuggest that central sensitization may contribute to the occurrence ofmyofascial trigger points rather than the other way around (blue)
Do et al. The Journal of Headache and Pain (2018) 19:84 Page 14 of 17
MTrPs are especially interesting as these are rarelyfound in control groups. However, their role in thepathophysiology of each disorder and to which degreeis still unclear. The results of the provocation andintervention studies support the hypothesis of atrigemino-cervical-complex pathophysiology model inboth migraine [45, 50–53, 56, 57] and TTH [73, 74, 81].Whether MTrPs contribute to an increased disease bur-den in migraine is uncertain [45, 47, 48] and needs furtherexploration [50, 52]. Future research should aim to in-crease the quality of studies before further speculationsare made. To elucidate this, large-scale studies to stratifythe headache populations into more homogenous sub-groups should be conducted.
AbbreviationsBK: Bradykinin; CGRP: Calcitonin gene-related peptide; CTRL: Healthy control;EMG: Electromyography; F: Female; FHP: Forward head posture; IL-1β: Interleukin1 beta; IL-6: Interleukin 6; IL-8: Interleukin 8; M: Male; MA: Migraine with aura;MO: Migraine without aura; MTrP: Myofascial trigger point; NE: Norepinephrine;NRS: Numeric rating scale; PPT: Pressure pain threshold; SP: Substance P;TNF-α: Tumor necrosis factor alpha; TTH: Tension-type headache;VAS: Visual analog scale
FundingTPD and JH were funded by a grant from Candys Foundation. LTK wasfunded by a grant from the Lundbeck Foundation.
Availability of data and materialsData sharing is not applicable to this article as no datasets were generatedor analysed during the current study.
Authors’ contributionsTPD contributed with data interpretation, drafting and revision of themanuscript for intellectual content. GFH, LTK and JH contributed withrevision of the manuscript for intellectual content. HWS contributed withconceptualization, data interpretation and revision of the manuscript forintellectual content. All authors read and approved the final manuscript.
Ethics approval and consent to participateNot applicable.
Consent for publicationNot applicable.
Competing interestsHWS has received travel grants or speaking fees from Pfizer, AutonomicTechnologies and Novartis. TPD, GFH, LTK and JH declare that they have nocompeting interests.
Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims inpublished maps and institutional affiliations.
Received: 21 August 2018 Accepted: 3 September 2018
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