Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over...

17
REVIEW ARTICLE Open Access Myofascial trigger points in migraine and tension-type headache Thien 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 with a hypersensitive palpable nodule in a taut band. It has been suggested that myofascial trigger points take part in chronic pain conditions including primary headache disorders. The aim of this narrative review is to present an overview of the current imaging modalities used for the detection of myofascial trigger points and to review studies 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 of these modalities and may be used to identify MTrPs if specific methods are used, but there is no precise description of a 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. All intervention studies aiming at trigger points are positive, but this needs to be further verified in placebo-controlled environments. These findings may imply a causal bottom-up association, but studies of migraine patients with comorbid fibromyalgia syndrome suggest otherwise. Whether myofascial trigger points contribute to an increased migraine burden in terms of frequency and intensity is unclear. Active myofascial trigger points are prevalent in tension-type headache coherent with the hypothesis that peripheral mechanisms are involved in the pathophysiology of this headache disorder. Active myofascial trigger points in pericranial muscles in tension-type headache patients are correlated with generalized lower pain pressure thresholds indicating they may contribute to a central sensitization. However, the number of active myofascial trigger points is higher in adults compared with adolescents regardless of no significant association with headache parameters. This suggests myofascial trigger 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 play in the pathophysiology of each disorder and to which degree is unclarified. In the future, ultrasound elastography may be an acceptable diagnostic test. Keywords: Headache, Myofascial trigger point, Muscle, Treatment, Trigemino-cervical-complex, Migraine, Tension-type headache, Diagnostic test Background Migraine 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 in its pathophysiology including vascular, peripheral and central mechanisms [49]. Jes Olesen systematically de- scribed pericranial tenderness in migraine patients, both during and outside of migraine attacks [10, 11], leading to speculations that myofascial mechanisms may be in- volved in migraine [12]. Tension-type headache (TTH) is the most prevalent primary headache disorder worldwide [13]. Tenderness in pericranial myofascial tissue is correlated with the in- tensity and frequency of headache in TTH [1416], and studies show increased muscle stiffness in TTH patients [17, 18]. Thus, myofascial structures may be associated with TTH pathophysiology. * Correspondence: [email protected] Headache Diagnostic Laboratory, Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health Sciences, University of 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 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the 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

Transcript of Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over...

Page 1: Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over time as a consequence o f TTH rather than contributing to the pathophysiology. Conclusions:

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

Page 2: Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over time as a consequence o f TTH rather than contributing to the pathophysiology. Conclusions:

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

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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

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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.

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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

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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

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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

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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

Page 9: Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over time as a consequence o f TTH rather than contributing to the pathophysiology. Conclusions:

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

Page 10: Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over time as a consequence o f TTH rather than contributing to the pathophysiology. Conclusions:

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

Page 11: Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over time as a consequence o f TTH rather than contributing to the pathophysiology. Conclusions:

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

Page 12: Myofascial trigger points in migraine and tension-type ... · trigger points are accumulated over time as a consequence o f TTH rather than contributing to the pathophysiology. Conclusions:

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

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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

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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

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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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