COMPLEET BOOK 2014

Transcription

COMPLEET BOOK 2014

A-PDF MERGER DEMO
De Triggerpoint
De
De--activatie cursus
13/14 juni 2014
Vianen
Gepresenteerd door
Ietje van Stolk
Kontakt: course@triggerpoints.co.nz
PROGRAMMA VOOR TRIGGERPOINT DE-ACTIVATIE CURSUS
DAG 1
9.45-10.00
10.00-11.15
11.15-12.00
12.00-12.45
12.45-1.45
1.45-2.15
2.15-2.45
2.45-3.00
3.00-3.15
3.15-3.45
3.45-4.00
4.00-4.45
4.45-5.30
Welkom, koffie en thee
TP theorie en de laatste onderzoeks ontwikkelingen
TP theorie in relatie tot de onderarm spieren
Palpatie en TP-deactivatie van de onderarm spieren in praktijk
LUNCH
TP theorie in relatie tot de spieren van de schouder en achterste
deel van de nek
Palpatie en TP-deactivatie van de spieren van de schouder en achtserste deel van de nek in praktijk
Onderscheid tussen spier stijfheid, fibromyalgie and myofascial
pijn
Plaats van TP-deactivatie in relatie tot manuele therapie van de
gewrichten, zenuw mobilisatie, spier balans & stabiliteit en
ontspanningstherapie
TP theorie in relatie tot de spieren van het centeribre deel van de
nek en de borst
koffie en thee
Palpatie en TP-deactivatie van de spieren van het anteriose deel
van de nek en borst in praktijk
Theorie en praktijk van “spray and stretch”
DAG 2
8.30-9.30
9.30-11.00
11.00.11.15
11.15-12.30
12.30-1.15
1.15-2.45
2.45-3.00
3.00-3.45
3.45-4.30
4.30-5.00
5.00-5.30
Praktijk voorbeelden
Theorie en praktijk in relatie tot de spieren van de rug en buik
koffie en thee
Theorie en praktijk in relatie tot de spieren van de heup-dij en knie
LUNCH
Theorie en praktijk in relatie tot TP`s in de enkel en voet
Koffie en thee
Voorbeeld van behandelings plan in in relatie tot veel voorkomende
pijn klachten
Praktijk voorbeelden
Assessment
Antwoorden en conclusie
Evaluatieformulier voor deelnemers t.b.v. de
accreditatie van bij- en nascholingsactiviteiten
Ietje van Stolk
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januari 2013
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Inhoud
Onderwerp
Slide
Blz.
Theorie & recentelijk onderzoek in relatie tot myofascial triggerpoints
1-25
1-12
Triggerpoints in onder arm, biceps, brachialis
26-36
13-18
Triggerpoints in schouders en achterste deel van de nek
37-52
18-26
Onderscheid tussen spier stijfheid, fibromyalgia and myofascial pijn
53-55
26-28
De plaats van triggerpoint de-activation in relatie tot manuele
therapie van de gewrichten, zenuw mobilisatie, spierbalans en
stabiliteit en ontspannings therapie
56-59
28-30
Triggerpoints in voorzijde van nek & borst gebied
60-69
30-34
Theorie & praktijk van spray and stretch
70-78
35-39
Triggerpoints in rug en buik
79-100
39-50
Triggerpoints in heup, dij en knie
101-121
51-61
Triggerpoints in enkel en voet
122-141
61-71
Voorbeeld van behandelplan in relatie tot veel voorkomende
pijnklachten
142-143
71-72
Triggerpoint de-activatie in relatie tot ademhalings stoornissen
144
72-73
Myofascial Trigger Points An Evidence-Informed review, Jan
Dommerholt, Carol Bron, Jo Franssen, The Journal of Manual
& Manipulative Therapy Volume 14, Number 4, 2006
74-93
Myofascial Pain Syndrome– Trigger Points, David G.Simons,
Jan Dommerholt, Journal of Musculoskeletal Pain, volume
15, Number 1, 2007
94-110
Myofascial Pain Syndrome– Trigger Points, David G.Simons,
Jan Dommerholt, Journal of Musculoskeletal Pain, volume
16, Number 3, 2008
111-128
Myofascial Pain Syndrome– Trigger Points, Jan Dommerholt,
Journal of Musculoskeletal Pain, volume 17, Number 1, 2009
129-134
Jan Dommerholt, Peter Huijbregts: Myofascial Trigger points.
Pathophysiology and Evidence-Informed Diagnosis and Management. Jones and Bartlett Publishers, Sudbury, Massachusetts, USA, 2011
135-156
Literatuur verwijzingen:
1) Simons DG, Travell JG, Simons LS: Myofascial Pain and Dysfunction. The Trigger
Point manual. Vol. 1 second edition Williams & Wilkins1999.
2) Simons DG, Travell JG: Myofascial Pain and Dysfunction. The triggerpoint manual,
the lower extremities. Vol2 Williams & Wilkins1992.
3) Myofascial Trigger Points An Evidence-Informed review, Jan Dommerholt, Carol
Bron, Jo Franssen, The Journal of Manual & Manipulative Therapy Volume 14, Number
4, 2006
4) Myofascial Pain Syndrome– Trigger Points, David G.Simons, Jan Dommerholt, Journal of Musculoskeletal Pain, volume 15, Number 1, 2007
5) Myofascial Pain Syndrome– Trigger Points, Jan Dommerholt, Journal of Musculoskeletal Pain, volume 17, Number 1, 2009
6) Myofascial Pain Syndrome– Trigger Points, David G.Simons, Jan Dommerholt, Journal of Musculoskeletal Pain, volume 16, Number 3, 2008
7) Jan Dommerholt, Peter Huijbregts: Myofascial Trigger points. Pathophysiology and
Evidence-Informed Diagnosis and Management. Jones and Bartlett Publishers, Sudbury,
Massachusetts, USA, 2011
8) Myofascial trigger points: spontaneous electrical activity and its consequences for pain
induction and propagation, Hong-You Ge, Cesar Fernandez-de-las-Penas, Shou-Wei Yue
Aanbevolen boeken:
Claire Davies (2003, 1e druk) – Handboek Triggerpoint-therapie, verminder zelf
pijnklachten, Altema-Brecht BV, Haarlem, Nederland.
Peter Jonckheere (1993, 1e druk) – Spieren en Dysfuncties, Trigger punten, Basisprinciples van de Myofasciale therapie, Satas n.v., Brussel, Begie.
Wat is een triggerpoint?
Thanks to Mr. David Simons and
Travell & Simons, Williams &
Williams Baltimore/London
Triggerpoints
Abnormale verkorting en abnormale verlenging van
de sarcomeren van de spiervezel die de “contractieknoop” heeft (in het midden van de tekening)
Thanks to Mr. David Simons and Travell & Simons, Williams & Williams Baltimore/London
Hypothese
Triggerpoints
Actieve Triggerpoints.
– lokatie van toegenomen irritatie in spier of fascia,
resulterend in pijn. Het pijnpatroon is specifiek
voor de betreffende spier. Pijn is aanwezig in rust
en in beweging.
– Symptomen
Gevoelig
Volledige spier verlenging niet mogelijk.
Spier verzwakking
Gerefereerde pijn bij directe compressie op de
triggerpoint
Triggerpoints
Latente Triggerpoints
– lokatie van toegenomen irritatie in spier of
fascia, dit veroorzaakt:
Geen spontane pijn
Alleen pijnlijk bij palpatie
Kan spier stijfheid, –verkorting, -zwakte
veroorzaken
LATENTE TRIGGERPOINTS KOMEN VEEL
MEER VOOR DAN ACTIEVE TRIGGERPOINTS.
Triggerpoints
Een latent triggerpoint kan jaren aanwezig zijn, zonder problemen te
veroorzaken, maar het kan (acuut) pijn veroorzaken door verrekking,
overbelasting en kou op de spier
Zowel latente als actieve triggerpoints veroorzaken dysfunctie
(verkorting, verzwakking) alleen actieve triggerpoints veroorzaken pijn.
Spieren hebben normaal
•Geen trigger points.
•Geen strakke banden
•Geen pijn bij palpatie
•Geen “twitch” reactie
•Geen referentie pijn bij directe compressie
Triggerpoints
L A T E N T
T .P .
A C T IV E
P e r p e t u a ti n g
T .P.
F a c to r s
R e s t
N O
P e r p e tu a tin g
fa c to r s
B o d y le a r n s h o w to
lim it m o v e m e n ts o f
th a t m u s c le ( G u a r d in g )
C h r o n ic m u s c le
S tiffn e s s
D y s fu n c tio n
T h is
c a n
c o n t in u e
fo r
p a in
y e a r s :
M u s c le g o e s fr o m
n e u r o m u s c u la r d y s fu n c tio n a l
to d y s tr o p h ic p h a s e
Triggerpoints
Wat betekent het hebben van een aktief
of latent trigger point?
Triggerpoints
Primaire Trigger Points,
Door faktoren van buitenaf zoals herhaling van
contractie of een statische contractie
Secondaire Trigger Points,
Door compensatie van de synergist en antagonist
Satelliet Trigger Points,
In het gerefereerde pijn gebied
Triggerpoints
Een patiënt presenteert met pijn in een specifiek
gebied en met veel triggerpoints.
Normaal gesproken komt de pijn van het
triggerpoint dat het laatst geactiveerd is
De pijn verschuift naar een eerder triggerpoint na
behandeling. Maar als het eerste (primaire) TP
eenmaal behandelt is, dan is er een goede kans
dat de patient volledig herstelt zonder verdere
interventie
Hoe vindt je een primair
triggerpoint
Iemand moet dit de therapeut vertellen
Primair Triggerpoint?
Conclusie
Kennis en interdisciplinaire
samenwerking in relatie tot TP’s is
een cruciaal deel van de
behandeling van KANS
Veroorzakende faktoren
Mechanische faktoren
– Assymetrie (scoliose, korte bovenarm,
etc)
– Verkeerd ontworpen meubels
– Slechte houding
– Overbelasting van de spieren
– Langdurige immobilisatie
Triggerpoints
Veroorzakende faktoren
Psychologische faktoren
– Depressie
– Spanning door angst
– ‘Good sport” syndroom
– Secundaire voordelen
– “Ziekte gedrag”
Triggerpoints
Andere veroorzakende faktoren
Onvolledige voeding
Metabole en endocriene stoornissen
Chronische ontstekingen
Allergieën
Verstoorde slaap
Radiculopathie
Chronische viscerale stoornissen
Screening laboratory tests
Serum vitamin levels
Blood chemistry profile
Complete blood-count with indices
Erythrocyte sedimentation rate
Thyroid hormone levels (T3-T4 by radio
immuno assay)
Tiggerpoints
Janet Travell
Patiënten met klachten van het
bewegingsapparaat hebben normaal
gesproken veel oorzakelijke faktoren die
verantwoordelijk zijn voor het totale
klachten beeld
OOS, CTD, RSI, KANS,
waar praten we over?
OOS CTD RSI KANS
myofasciale pijn door Trigger
Points?
Is myofasciale pijn een betere
term?
Het refereert naar wat er gebeurt in
de spier
Het refereert naar alle oorzakelijke
faktoren (niet alleen faktoren die te
doen hebben met werk)
Triggerpoints
Spierzwakte veroorzaakt door T.P.
– Spierkracht wordt onvoorspelbaar, voorwerpen vallen
plotseling uit de hand van de patient
– Kracht test is negatief
Spierzwakte blijkt voort te komen uit centrale
inhibitie, dat zich ontwikkeld heeft om de
spieren te beschermen van een pijnlijke spier
contractie. De spierzwakte is aanwezig zonder
atrofie.
Triggerpoints
Rekken
Als er een actieve T.P. is --- veroorzaakt passief of
aktief rekken pijn.
Als de pijn begint, veroorzaakt dat een beschermend
spier spasme.
actief T.P.
Passief of aktief rekken
geeft pijn
Verminderende mobiliteit
Beschermend spier
spasme
Maar als het ons lukt om tot totale spierverlenging te komen
(seperatie van “myosin-heads and actin filaments”) dan deactiveren
we het triggerpoint
Triggerpoints Behandeling
Spray and stretch
– Correct gebruik van “koel-spray” of van een scherp object (scratch
& stretch) faciliteert het rekken. (te veel gebruik van de spray,
onderkoelt de spier en verergert de T.P.)
Ischemiche compressie
– Vibratie
– Andere massage vormen
Gebruik van naalden
– “Dry needling” (acupunctuur naald)
– Injectie met saline of locale anaesthesie
U.G
– Aanhoudend gebruik van ultrageluid (lage intensiteit) de-activeert
T.P.s
Triggerpoints
Behandeling
Gebruik van warmte (hotpacks) direct na de
therapie, helpt met verdere spierverlenging. De
verbetering zal meer duurzaam zijn als de patient
de behandelde spieren een aantal keren door het
totale bewegings-bereik beweegt aan het einde
van de therapie (na warmte).
Als de patient doorgaat met het beperken van de
beweging van de spier en het beschermen van de
spier, na de behandeling, dan zal de TP activiteit
terug komen.
Triggerpoints
Pain Guide
Travell & Simons, Williams & Williams Baltimore/London
Thanks to Mr. David Simons
Travell & Simons, Williams & Williams Baltimore/London
Email: and
muisarm@oos.co.nz
260
Hand muscles
Aanhoudend of repeterende
“pincer grip”
Behandeling van de
interosseus TP’s kan de
ontwikkeling van
osteoarthritis vertragen
(Heberden's nodes).
Abductor & opponens pollicis
Tuinierders duim,
gebruik van penceel,
naaien, schrijven
Na een breuk
Finger-extensors
Krachtige herhaalde vinger
bewegingen: pianisten,
timmermannen, monteurs.
Pees subluxatie in
metacarpo-phalangeaal
gewricht veroorzaakt
intense spier overbelasting
en operatie zal
noodzakelijk zijn.
Extensor carpi ulnaris, radialis
brevis, radialis longus
Hoe groter het voorwerp,
hoe erger de ulnaire
deviatie, hoe erger de
TP’s
Tuinieren
Handen schudden
Strijken
Stabilisatie van intens duim
gebruik (fysio’s!)
Brachioradialis m.
Schrijverskramp heeft
meer te maken met
brachioradialis en
onderarm extensoren
dan de antagonische
flexoren.
Palmaris longus m.
TP’s zijn meestal
satellieten van de
Triceps Brachii
•Veroorzaakt door het
vasthouden van
gereedschap
•Vaak is alleen de druk
van het gereedschap
in de palm al genoeg
irritatie
Supinator m.
Tenniselleboog symptomen,
als de speler de bal half mist
(“off-centre”)
Het draaien van het racket
met gestrekte elleboog (nu
kan de biceps niet assisteren)
Tenniselleboog is vaak een
aktetas elleboog, hond
uitlaten elleboog, of is
veroorzaakt door de was
uitwringen, de jam pot open
draaien, of handen schudden
forearm flexors
TP's in deze hand en
vinger flexoren worden
niet door fijne hand
bewegingen verergerd,
maar door grote
grijpende hand
bewegingen.
Hard vastgrijpen van
ski stokken of
gereedschap
Flexor pollicis longus &
pronator teres
•Tuinier duim
•Draaien en
trekken
•Breuk in pols of
elleboog
Biceps Brachii m.
Tillen van zware voorwerpen
me de hand in supinatie
Plotseling optillen met
gestrekte elleboog
Aanhoudende elleboog flexie
(gitaar)
Ongewoon krachtige
supinatie
Teveel elleboog extensie
(tennis)
Plotselinge verrekking (val)
Brachialis m.
Zwaar tillen met gebogen
onderarm (hand in pronatie)
Strijken
Electrisch gereedschap
vasthouden
Gebruik van krukken
Tennis elleboog, eerst
supinator, dan biceps en
brachialis samen.
Deltoideus m.
Voorste deel
Krachtig contact letsel (“recoil
of gun”)
Plotseling opvang van val
Constant tillen
Achterste deel
Injecties
Overmatig gebruik van ski
stokken
Zelden alleen in de problemen
Triceps brachii m.
Gebruik van krukken
Kruk of stok te lang
Backhand mis-hit tennis
Lange kop van de biceps door arm
ongesteund voor je te houden zoals
bij autorijden
Herstellende acties
Houdt de arm verticaal met de
elleboog ACHTER het borst vlak en
NIET naar voren geprojekteerd als je
typt of schrijft.
Medial deephead of triceps
muscle
Anconeus m.
Levator scapulae m.
“Levator scapulae achtige stijve neck”
door stress op het werk.
Typen met gedraaid hoofd (om tekst te
lezen). Alle langdurige nek rotatie
Gespannen houding
Arm leuning te hoog
Stok/kruk te hoog
Voor en na verkoudheid.
Trapezius m.
Voorover gebogen
houding en reiken met
de armen
Trapezius m.
Overbelast terwijl arm
aanhoudend in “reikende
positie” is
Latente T.P’s in pec major
trekken de schouders naar
voren, trap. transversa moet
dat voortdurend
tegenwerken.
Handen boven aan het stuur
met “ronde-schouder”
positie.
Trapezius m.
Trap. descendens werkt
aanhoudend om nek en hoofd
verticaal te houden en de ogen op
gelijk niveau te houden.
Trap. desendens werkt tegen de
zwaartekracht als de arm niet
ondersteund is.
Microtrauma door BH bandjes
Gewoonte van schouder
optrekken (stress)
Rhomboideus m.
Langdurig voorover
leunen met ronde
schouders
Scoliose
Langdurige positie met
arm in abductie
Overbelasting door
tegenwerking van de TP’s
in pec.major
Infraspinatus m.
Naar achter reiken
(retroflexie)
Iemand rond de
ijsbaan trekken
Supraspinatus m.
Zware voorwerpen
tillen, zoals koffers,
met de arm naar
beneden hangend.
Regelmatig trekken
van hond aan riem
Tillen met gestrekte
arm tot, of boven,
schouderhoogte
Teres major m.
Krachtige endorotatie
Zwemmen (Crawl)
Boven het hoofd tillen met
gelijktijdige adductie
Arm achterwaarts uitstrekken om
een val op te vangen
Dislokatie schouder gewricht
Breuk prox. humerus/ kapsel
scheur
Langdurige immobilisatie van
schouder gewricht
Teres minor m.
Zelfde factoren als
voor de infraspinatus
Zelden alleen in de
problemen
Serratus anterior m.
Heel snel of
langdurig rennen
Zware gewichten
tillen
Zwaar hoesten
Push ups
Latissimus dorsi m.
Herhaaldelijk naar voren
en naar boven reiken
Een grote stoel tillen
Aan een touw of
schommel zwaaien
Tuinieren
Seratus posterior superior m.
Overbelasting door
thoracaal ademen.
Schrijven op een te
hoog bureau (forceert
de scapula tegen de
serr. post.).
Protrusie van de thorax
tegen de scapula door
scoliosis.
Spier Stijfheid
Toename van Titin (verbindt Myosin aan
de Z-band)
Er is meer Titin (en meer sarcomeren
parallel) als er hypertrophie is
De spier is stijf maar kan volledig
verlengen
Triggerpoints
De gespannen spiervezels resulteren in
verminderde spierlengte
Je kan de contractie knopen voelen als
je aan het rekken bent
Fibromyalgie
Er zijn “tenderpoints” in plaats van
“triggerpoints”
Deze tenderpoints overlappen de lokaties van
de triggerpoints gedeeltelijk, maar niet
volledig
Ze zijn aanwezig in het hele lijf en niet alleen
in het deel met de klachten
Ze reageren negatief op vele soorten
stimulatie, zelfs warmte
Het onderscheid tussen de twee fenomenen
zit op een doorlopende lijn
Manueel therapie versus
triggerpoint de-activatie
Kan jij je een schouder gewricht voorstellen met een volledig
stijf kapsel, en daarom heen ontspannen lange spieren, fascia
en zenuwen?
Kan jij je voorstellen dat een schouder slecht kan bewegen door
verkorte spieren, terwijl het kapsel soepel en ruim is?
Wat was er eerst, de kip of het ei?
Conclusie: Het combineren van manuele
therapie en triggerpoint de-activatie is het
meest effectief
Spierbalans versus
TP de-activatie
TP de-activatie herstelt lengte en kracht
Wat heb je nodig voor spierbalans?
De correcte spierbalans en stabiliteit staat
ontspanning van de spieren toe die anders
overbelast zijn
Conclusie: Een combinatie therapie van
zowel spierbalans correctie en TP de-activatie
is het meest effectief
Zenuw mobilisatie versus TP deactivatie
Butler heeft het over de “interphase”
Voor goede therapie behandelen we zowel zenuwen
als de “interphases”. Voorbeelden zijn:
Supinator – nervus radialis
Pronator teres – nervus medianus
Triceps caput med.& flexor carpi ulnaris – nervus
ulnaris
Conclusie; Een combinatie therapie van zowel
zenuw mobilisatie als TP de-activatie is meest
effectief
Ontspanningstherapie versus
T.P. de-activatie
Ontspannings therapie stopt de aanhoudende
overbelasting van vele spieren
Het is een belangrijke faktor in het ontstaan
van T.P.s
S p ie r
s p a n n in g
fig u r e
1
P ijn
A
Spier spanning
B
G e s p a n n
e n B a s e
lijn
Noodzakelijk
Voor werk
O n ts p a n n e n b a s e
l i Travell
j n & Simons, Williams & Williams Baltimore/London
Thanks to Mr. David Simons and
Subclavius m.
Langdurige protractie
positie
Verminderde kracht in
trapezius descendens
Sternocleido mastoideus m.
Het slapen op twee kussens verkort de
sternocleidomastoideus (alternatief:
plaats houten blokken onder de bed
poten)
Protractie samen met nek extensie
(schilderen van plafond)
Op hoofd vallen
Whiplash
SCM zorgt dat de ogen op gelijk
niveau zijn
Paradoxaal ademen/hoesten
Kater hoofdpijn kan verlicht worden
door rekken van SCM
Scaleni m.
Wordt geactiveerd door trekken en
tillen
Paarden rond leiden
Onhandige grote voorwerpen tillen
Paradoxaal ademen of hoesten
Scoliose
Voorover leunen door te korte
bovenarmen
Een ernstige stijve nek met een
gespannen lev.scap. heeft vaak
ook scaleni T.P.’s
Pectorlis minor m.
Door hartinfarct
Satelliet T.P.’s van
scaleni
Fractuur van de rib
Overbelasting door
inspiratie
Slechte houding
(chronische verkorting)
Pectoralis major m.
Zwaar tillen
Overbelasting arm
Aanhoudend tillen in gefixeerde
positie (gebruik van kettingzaag)
Immobilisatie van arm in adductie
(mitella)
Aanhoudende mentale spanning
Ronde-schouder houding , speciaal
tijdens lang schrijven, lezen etc.
Na een hart-infarct kunnen de T.P.’s
lang aanhouden
Subscapularis m.
Krachtige endorotatie
Zwemmen (Crawl)
Boven het hoofd tillen samen
met adductie
Naar achter reiken om een
val op te vangen
Dislokatie van schouder
gewricht
Fractuur prox
humerus/kapsel scheur
Langdurige immobilisatie van
schouder gewricht
Sternalis m.
Hartinfarct
Satellieten van de
SCM
Multifidus & semispinalis
Kopiehouder of muziekstandaard
niet in het midden geplaatst
Reflectie van bril
Pec major triggerpoints
Licht niet direct op boek
Slecht hoofd kussen
Splenius capitis and cervicis
Gelijktijdige T.P activiteit in
zowel de lev.scap als splenius,
kan alle rotatie blokkeren
Zitten in thoracale flexie samen
met nek extensie (zoals bij
kijken door een verrekijker)
Met een gedraaid en naar voren
geprojekteerd hoofd aan buro
werken
Bril, whiplash
In slaap vallen in slechte
houding
Suboccipitalis m.
Stabilisatie van flexie
positie
Het vasthouden van nek
extensie
Het “spiegelen
voorkomen”
Typen met bladzijdes
plat naast de computer
Suboccipital T.P.’s zijn
vaak de reden voor
hoofdpijn na trauma
Spray & stretch
S&S gevolgd door warmte kan pas begonnen
worden 5 dagen na acuut trauma (gebruik ijs
ter vermindering van zwelling)
Patiënt moet warm en ontspannen zijn voor
het gebruik van S&S.
Combineer S&S met isometrische
ontspanning gecoördineerde ademhaling en
reciprocale inhibitie
Na Spray & Stretch
Warmte (bijvoorbeeld hotpack) voor 10
minuten
Beweeg de spier door het hele
bewegingstraject.
Vermijdt overbelasting
Beweeg de spier door het hele
bewegingstraject elke 2 uur
Stretch & spray technique for
triggerpoints in levator
scapulae m.
pectoralis minor m.
extensor digitorum m.
scaleni muscle
triceps brachii muscles
biceps brachii m.
Specific biceps stretch
Iliocostalis & longissimus
Functie
– Dubbelzijdige
extensie van rug
– Enkelzijdige rotatie
en lateroflexie
– ademhaling
Iliocostalis & longissimus
activatie
– Satellieten van latissimus
T.P.
– Gecombineerd buigen en
draaien
– Aanhoudende
immobilisatie (in de
meest ontspannen
zithouding wordt binnen
30 minuten de spanning
opgebouwd)
Multifidi & rotatores
Functie
Dubbelzijdige
extensie
Enkelzijdig contralaterale rotatie
Bijstellen van fijne
bewegingen
Meer een stabilisatie
dan bewegings
functie
Multifidi & rotatores
Activering
– Satellieten van latissimus
T.P.s
– Gecombineerd buigen
met rotatie
– Aanhoudende
immobiliteit
– (in de meest ontspannen
zithouding wordt
spanning binnen 30
minuten weer
opgebouwd)
Rectus abdominus m.
Door spanning
Voorover leunen
(spier verkorting)
“Visceral” ziektes
Post operatief
External oblique
Zit aan een buro
met lateroflexie
(b.v. door lichtval).
Quadratus Lumborum
♦ Functie
– Verlengende
contractie om
heterolaterale
latero-flexie tegen
te gaan
– Homolaterale
lateroflexie
– Gelijktijdige
contractie geeft
extensie
Quadratus Lumborum
Activering & in stand
houden van T.P’s
– Been lengte verschil
– Flexie met gelijktijdige
lateroflexie
– Tillen van te zwaar
voorwerp
– Rennen op zijwaarts
aflopend terrein
– zwakke transversus
abdominis
Quadratus Lumborum
Welk been is korter?
Spray & Stretch positie
Morton Foot Structure
Iliopsoas Muscle
♦ Functie
– Contractie van psoas
maj. vermeerdert de
belasting van de discus
– extensie van de rug als
we een normale lordose
hebben
– Flexie als we voorover
buigen
– Belangrijkste functie is
flexie van de heup
Iliopsoas Muscle
houden van T.P’s
– T.P’s zijn vaak secundair
– Val
– Zitten met de knieën hoger dan
de heupen
– Slapen in foetus positie
– Rectus femoris te kort (ilio
psoas kan nu niet tot volle
lengte komen)
– Beenlengte verschil
– T10 – L1 disfunctie
– Gehurkt zitten
Thomas Test
Wat gebeurt er als we heup abductie doen?
Gluteus Maximus Muscle
♦Functie
Als de voet gefixeerd is, heeft de glut.max een verlengende functie om beweging te
controleren (bijv. bij voorover buigen)
Tijdens lopen is de spier functioneel kort na hielplaatsing
De heup extensie en exorotatie functie gebeurt tijdens activiteiten zoals rennen en
springen
Er is minimale actie tijdens lopen en gebalanceerd staan.
Afwezigheid van glut max (door trauma of operatie) maakt ons niet mank
Glut max stabiliseert de knie via de iliotibiale band.
Gluteus Maximus Muscle
Activering & in stand houden T.P`s
–
–
–
–
–
Een korte metatarsale I leidt tot endorotatie in heup en overbelasting glut max
Een val op de billen, of een “bijna val”
Langdurig naar voren leunen als er omhoog gelopen wordt (in de bergen)
Slapen in stabiele zijligging
Zwemmen (crawl)
Gluteus Medius Muscle
♦ Functie
– Stabiliseren om op één
been te staan
– Tijdens lopen zorgen glut
med. en andere
abductoren ervoor dat het
bekken op gelijk niveau
blijft
– Glut med is de sterkste
abductor van de heup
Gluteus Medius Muscle
houden T.P`s
– SIG stoornis
– Langdurig heupflexie >
900
– Morton’s voet.
Geproneerde voet
– Langdurig tennis spel
– Val
– Op portemonnee zitten
Gluteus Minimus Muscle
♦ Functie
– Assisteert glut.
med in het
stabiliseren van
het bekken
– Abductie; voorste
deel endorotatie
– Abductie;
achterste deel
exorotatie
Gluteus Minimus Muscle
houden T.P`s
– SIG dysfunctie
– Zenuwwortel irritatie
– Na succesvolle
operatie, kan
dezelfde pijn
veroorzaakt worden
door glut. min T.P’s
– Langdurige
immobilisatie
– Instabiel tijdens lopen
of zitten
Piriformis
♦ Functie
– Piriformis controleert
endorotatie heup, bijv. tijdens
snel lopen.
– Assisteert bij het stabiliseren
van de femur in het
acetabulum
– In neutrale positie; exorotatie
heup
– Heup in 900 flexie; abductor
– Heup in max flexie;
endorotator
Piriformis
houden T.P`s
– Morton’s foot.
– Langdurige verkorting
(bijv. gynacologische
procedures)
– Opvangen van een val,
slippen, opzij buigen
tijdens tillen
Piriformis
Spray & Stretch positie piriformis
Tensor fasciae latae
♦ Functie
– Tijdens stand fase
assisteert glut. min met
het stabiliseren van het
bekken.
– Achterste laterale vezels
stabiliseren de knie
– Actie; flexie, abductie,
endorotatie van heup.
Tensor fasciae latae
houden T.P`s
– De heuvel op rennen met
geproneerde voeten (o.a
Morton’s voet)
– Regelmatig lopen of
rennen op aflopend
terrein
– Landurig immobilisatie in
een verkorte positie (o.a.
zitten)
Pectineus Muscle
♦ Functie
– Voornamelijk een
gecombineerde
beweging van flexi en
adductie
– Endo- of exo rotatie?
– Hangt af van
anatomische variaties
Pectineus Muscle
houden T.P`s
– Door struikelen of vallen
– Paardrijden met knellen
van de benen i.p.v de
voeten
– Secundair na heup
athrose
– Kleermakers zit
Sartoris Muscle
♦ Functie
– Assisteert iliacus and TFL
met heup flexie tijdens de
zwaaifase.
– Assisteert het korte deel
van de biceps femoris
met knie flexie
– Actie (net als TFL);
abductie en exorotatie
Sartoris Muscle
houden T.P`s
– Hoofdzakelijk secondaire
T.P’s
– Acute verrekking tijdens
val
– Te veel voet pronatie
Quadriceps femoris Group
Rectus Femoris
Vastus Medialis
Vastus Intermedius
Vastus Lateralis
♦ Functie
–
–
–
–
–
–
–
–
Belangrijke knie extensoren
Rec fem; flexie van femur naar bekken
Rec fem; flexie van bekken naar femur
Gebalanceerde spanning van de patella tussen vastus medialis &
lateralis resulteert in gebalanceerd sporen van de patella
Quadriceps is aktief na de hielplaatsing en voorkomt knie flexie
Niet aktief in de extensie fase van de zwaai
Aktief aan het einde van de zwaai in voorbereiding voor het dragen
van het lichaamsgewicht
In het tekstboek; belangrijkste functie van vastus medialis is de
laatste 150 van de extensie, maar het controleren van de patella
(schuine vezels) is belangrijker
Activering & in stand houden T.P`s
• Overbelasting quadriceps door verrekking (in een
gat stappen, struikelen)
• Quadriceps T.P.’s vaak aktief door hamstrings en
soleus T.P.’s
• Immobilisatie (gips, operatie)
• Rectus femorus T.P’s zijn vaak langdurig omdat de
spier over twee gewrichten loopt, en we het daarom
in het dagelijkse leven, nooit rekken.
• Vastus med.: kniebuiging
• Rec. fem, verkort in “lazy-boy” positie
Onderzoek
patella
mobiliteit
Spray & Stretch
positie
Adductor Muscles of the hip
♦ Functie
– Tijdens lopen controleert het de
flexie (magnus)
– Tijdens lopen controleert het de
abductie
– Magnus aktief als we de trap
afdalen
– Add longus aktief tijdens
hiellanding
– Als er slechte stabiliteit is, en het
bovenlichaam schommelt naar
opzij, (relatief is dat abductie van
het been) dan moeten de
adductoren hard werken om te
stabiliseren.
houden T.P`s
– Plotselinge overbelasting ,
met name uitglijden op het
ijs, tegengaan van spagaat.
– Osteoarthritis heup
– heupoperatie
– Autorijden, met gestrekte
benen zitten
– Skiën
Spray& stretch adductor
Longus & Brevis
Spray& stretch adductor
Magnus
Hamstring muscles
♦
Functie
♦
Tijdens standfase, rechthouden van
het lichaam
♦
Het vertragen van het zwaaiende
been aan het eind van de zwaai
fase.
♦
Als we stil staan zou de hamstrings
niet aktief moeten zijn, maar als we
ook maar iets voor over buigen, of
zelfs alleen maar een arm optillen, is
de spier aktief!
♦
Heup extensie
♦
Korte deel biceps femoris: knie flexie
♦
Als de heup in extensie is;
Geven semitendinosus en
semimembranosus endorotatie
en het lange deel van de
biceps femoris exorotatie
Hamstring muscles
houden T.P`s
– Druk van de stoel onder
het dijbeen
verkort ilium
– Zwakke glut max
Spray& stretch hamstrings
Popliteus Muscle
♦ Functie
♦ Als het been gefixeerd is;
exorotatie bovenbeen zo dat
de knie vrijkomt (“unlock”)
♦ Als het been vrij kan bewegen
(bijv. zitten) endorotatie tibia
♦ De popliteus werkt hard
wanneer het het afglijden van
het bovenbeen van de tibia
tegen gaat (zoals bij gehurkt
zitten)
Popliteus Muscle
houden T.P`s
– Overbelasting door bovenbeen
beweging af te remmen (over
de tibia). Zoals bij de berg
aflopen
– Trauma van de achterste
kruisband
– Voet pronatie
– De heuvel afrennen
Tibialis Anterior Muscle
♦ Functie
♦ Het stabiliseert het lichaam als
♦
♦
♦
♦
het naar achteren uit balans
raakt
Verkorting om lichaam en
benen naar voren te trekken
over de enkel
Optillen van de voet
gedurende de zwaaifase
Dorsiflexie en supinatie van de
voet
Optillen van metatarsale I
Tibialis Anterior Muscle
houden T.P`s
– Verlengende belasting tijdens
struikelen
– Zelfde bewegingen die een
verstuikte enkel veroorzaken
– Zelfde krachten die “voorste
compartiment syndroom”
veroorzaken
– Gespannen kuitspieren
Peroneal Muscles
♦ Functie
♦ Peroneus long + brevis samen
♦
♦
♦
♦
met tib post & soleus
controleren de tibia beweging
over de enkel
Med/lat balans van voet tijdens
lopen
Peroneus long.brev/tert geven
alle drie voet eversie
Peroneus long.brev; plantar
flexie
Peroneus tert; dorsiflexie
Peroneal Muscles
houden T.P`s
– Vallen met enkel rotatie en
eversie
– Verzwakking (na gips)
– Satellieten van T.P’s van het
voorste deel glut min
Gastrocnemius Muscle
♦ Functie
– Tijdens de standfase: helpt met
knie en enkel stabiliteit
– Het gaat verticaal oscilleren van
het lichaam tegen
– Tijdens lopen, houdt tibia rotatie
naar voren (op de talus) tegen
– Gastrocnemius helpt nauwelijks
bij de afzet tijdens rennen.
– Nauwelijks actief tijdens stilstaan,
tenzij de balans wordt verstoord
– Meer aktief als we vooruit leunen
– Reserve spier voor plantarflexie
(zoals bij stijl omhoog lopen)
Gastrocnemius Muscle
houden T.P`s
– Aanhoudende
verkorting (hoge
hakken)
– Aanhoudende
contractie (als de hiel
de vloer niet haalt)
– Immobiliteit
– Verminderde circulatie
– Afkoeling
Soleus muscle
♦ Functie
– Net als gastrocnemius,
maar geen invloed op de
knie
– Soleus niet snel
vermoeid
– Soleus assisteert inversie
– Soleus belangrijk als
“venous pump” (soldaten)
Soleus muscle
houden
– Langdurige verkorte
positie
– Rennen en skiën
– Voet glijdt weg tijdens
“toe-off”
– Satellieten van
post.glut.min
Lany position for
reflex testing
Position for Spray & stretch
Soleus T.P palpation
Tibialis Posterior Muscle
♦ Functie
♦ Tijdens het dragen van het gewicht zorgt de tib.
♦
♦
♦
♦
♦
posterior er voor dat de krachten gelijk verdeeld zijn
over de middenvoetsbeentjes en het verplaatst het
lichaamsgewicht naar het laterale deel van de voet.
Houdt teveel enkel pronatie tegen
Controleert het naar voren bewegen van de tibia
over de enkel
Met een vrije voet; inversie – adductie en helpt bij
plantair flexie
Houdt de vorm van de voet in stand door cocontractie van tib.post en peroneus
Als de tib.post scheurt; pronatie en pes planus
Tibialis Posterior Muscle
houden T.P`s
– Hyperpronatie
– Rennen op
ongelijk terrein
Long extensors of toes
Extensor digitorum longus, extensor hallucis longus
♦ Functie
– Vertragen van de voet naar de
grond (na hiellanding)
– Preventie “floor slap”
– Optillen van de voet tijdens de
zwaaifase
– Voorkomt het naar achteren
leunen
– Ext.dig longus: dorsaalflexie &
eversie en extensie van de vier
kleinere tenen
– Ext hall long, dorsaalflexie,
inversie en extensie grote teen
Long extensors of toes
Extensor digitorum longus, extensor hallucis longus
houden T.P’s
– Zenuwcompressie L4 - L5
geeft ext.long TP’s
– Struikelen
– Voorste compartiment
syndroom
– Hoge hakken (langdurige
verlengde positie)
– Fractuur tibia of fibula
Long flexor muscles of toes
Flexor digitorum longus, flexor hallucis longus
♦ Functie
– Stabiliseert voet in stand fase
– Med/lat balans
– Assisteert met het verplaatsen van het
gewicht naar de voorvoet
– Assisteert met plant flexie en inversie
– Flex dig longus; flexie dip 4 kleinere
tenen
– Flexor hall. long helpt bij balanceren
tijdens het op tenen lopen
– Belangrijke functie voor
gewichtsverplaatsing naar de voorvoet
Long flexor muscles of toes
Flexor digitorum longus, flexor hallucis longus
houden T.P’s
– Als er zwakte is in de kuit
spieren bij een voet met
hoge wreef
– Ongelijke grond, Morton
voet
– Voet pronatie
– Stijve schoenzool die het
onmogelijk maakt voor de
MP gewrichten om te
buigen
Extensor Hallucis brevis
Extensor digitorum brevis
Abductor hallucis
Abductor digiti minimi
Superficial Intrinsic Foot Muscle
♦ Functie
– Schok absorptie en balans
tijdens lopen
– Zorgt voor stabiliteit tijdens
afzet
– In het algemeen
functioneren deze spieren
als een geheel
Thanks tobrevis
Mr. David Simons and Travell & Simons, Williams & Williams Baltimore/London
Flexor digitorum
Extensor Hallucis brevis
Extensor digitorum brevis
Superficial Intrinsic Foot Muscle
Abductor hallucis
houden T.P`s
– Schoenen die te strak
zitten
– Na fraktuur en of gips
– Hyperpronatie
Abductor digiti minimi
Thanks tobrevis
Mr. David Simons and Travell & Simons, Williams & Williams Baltimore/London
Flexor digitorum
Oefeningen thuis
Spray & Stretch positie
Deep intrinsic footmuscles
Quadratus Plantae
• Functie
Schok absorptie en balans tijdens
wandelen
Zorgt voor stabiliteit tijdens afzet
Quadratus plantae, helpt dig long met flexie
van distale phalanx
Interossei
Lumbricales; flexie prox. phalanx
Lumbricales geeft stabiliteit als de tenen
buigen bij lopen in zacht zand
Spieren fungeren als een geheel
Adductor hallucis flexor
hallucis brevis
Deep intrinsic footmuscles
Quadratus Plantae
houden T.P’s
Interossei
– Verminderde mobiliteit
van gewrichten
– In zacht zand lopen
– Trauma
– Incorrect schoeisel
Adductor hallucis flexor
hallucis brevis
TP deactivatie is belangrijk bij
onder andere
Thoracic outlet
Carpal tunnel
Ischias
Post operatief
Na immobilisatie
Laterale knie pijn
Whiplash
Hoofdpijn
TMJ
Tennis elleboog
Achillespees
ontsteking
Een alternatieve manier om iets veilig van de grond te
pakken als soleus T.P’s de gangbare manier niet
toestaan
TP deactivatie in relatie tot
ademhaling
Spieren die overbelasten bij incorrecte
ademhaling
• Pectoralis minor
• Scalenis
• Pectoralis major
• Serratus posterior
superior
• Trapezius
• Iliocostalis thoracis
Incorrect ademen doet alle TP de-activatie teniet.
Ademen moet gecorrigeerd worden voor permanent
resultaat!!
Anamnese en onderzoek
Thoracic outlet syndrome
Pijn in de bil
Tennis elleboog
Voor deze drie klachten, beantwoord de
volgende vragen
– Welke spieren zou jij onderzoeken voor TPs en
waarom?
– Welke andere behandelings technieken zou je
combineren met de TP behandeling?
The Journal of Manual & Manipulative Therariy
a peer-reviewed journal
Volume 14 Number 4
2006
Special Topic Issue: Myofascial Trigger Points
GUEST EDITORIAL
Neuromusculoskeletal Medicine-Dawning of A New Day
David G. Simons
MANUAL THERAPY AWARDS
199
202
ARTICLES
Myofascial Trigger Points: An Evidence-Informed Review
Jan Dommerholt, Carel Bron, Jo Franssen
In this hand out pages
203
73-92
Contributions of Myofascial Trigger Points to Chronic Tension Type Headache
Cesar Fernandez-de-las-Penas, Lars Arendt-Nielsen, David G. Simons
222
Myofascial Trigger Points: Translating Molecular Theory into Manual Therapy
John M. McPartland, David G. Simons
232
ONLINE-ONLY ARTICLES www.jmmtonline.com
Trigger Point Dry Needling
Jan Dommerholt, Orlando Mayoral del Moral, Christian Grobli
E70
Physical Therapy Diagnosis and Management of a Patient with
Chronic Daily Headache: A Case Report
Tamer S. Issa, Peter A. Huijbregts
E88
Myofascial Trigger Points and Myofascial Pain Syndrome: A Critical Review
of Recent Literature (With an Introduction by the Editor-in-Chief)
David G. Simons, Jan Dommerholt
ABSTRACTS: AAOMPT Conference, 2006 (Addendum)
BOOK, CD, AND TAPE REVIEWS
THESIS REVIEWS
MANUAL THERAPY ANNOUNCEMENTS
INFORMATION FOR AUTHORS
AUTHOR INDEX
SUBJECT INDEX
E124
240
241
245
248
249
250
251
Copyright: All papers published in this journal remain the property of The Journal of Manual & Manipulative Therapy and should
not be reproduced without the permission of the Editor.
Contact us via E-mail: jmmt@telus.net
Myofascial Trigger Points: An Evidence-Informed Review
Jan Dommerholt, PT, MPS, FAAPM
Caret Bron, PT
Jo Franssen, PT
Abstract: This article provides a best evidence-informed review of the current
scientific understanding of myofascial trigger points with regard to their etiology,
pathophysiology, and clinical implications. Evidence-informed manual therapy
integrates the best available scientific evidence with individual clinicians' judgments, expertise, and clinical decision-making. After a brief historical review,
the clinical aspects of myofascial trigger points, the interrater reliability for
identifying myofascial trigger points, and several characteristic features are discussed, including the taut band, local twitch response, and referred pain patterns. The etiology of myofascial trigger points is discussed with a detailed and
comprehensive review of the most common mechanisms, including low-level muscle contractions, uneven intramuscular pressure distribution, direct trauma, unaccustomed eccentric contractions, eccentric contractions in unconditioned muscle,
and maximal or sub-maximal concentric contractions. Many current scientific
studies are included and provide support for considering myofascial trigger
points in the clinical decision-making process. The article concludes with a summary of frequently encountered precipitating and perpetuating mechanical, nutritional, metabolic, and psychological factors relevant for physical therapy practice.
Current scientific evidence strongly supports that awareness and working knowledge of muscle dysfunction and in particular myofascial trigger points should be incorporated into manual physical therapy practice consistent with the guidelines for
clinical practice developed by the International Federation of Orthopaedic Manipulative Therapists. While there are still many unanswered questions in explaining
the etiology of myofascial trigger points, this article provides manual therapists
with an up-to-date evidence-informed review of the current scientific knowledge.
Key Words: Myofascial Pain Syndrome, Trigger Points, Myofascial, Etiology,
Pathophysiology
During the past few decades, myofascial trigger points
(MTrPs) and myofascial pain syndrome (MPS) have
received much attention in the scientific and clinical
literature. Researchers worldwide are investigating
various aspects of MTrPs, including their specific etiol
ogy, pathophysiology, histology, referred pain patterns,
and clinical applications. Guidelines developed by the
International Federation of Orthopaedic Manipulative
Addressallcorrespondenceand requestfor reprintsto;
JanDommerholt
BethesdaPhysiocare,Inc.
7830OldGeorgetownRoad,SuiteC15Bethesda, MD 208142440
dommerholt@bethesdaphysiocare,com
Therapists (IFOMT) confirm the importance of
muscle dysfunction for orthopedic manual therapy
clinical practice. The IFOMT has defined orthopedic manual therapy as "a specialized area of
physiotherapy/physical therapy for the management of neuromusculoskeletal conditions, based
on clinical reasoning, using highly specific treatment approaches -including manual techniques
and therapeutic exercises." The educational standards of IFOMT require that skills will be demonstrated in-among others-"analysis and specific
tests for functional status of the muscular system," "a high level of skill in other manual and
physical therapy techniques required to mobilize the articular, muscular or neural systems,"
and "knowledge of various manipulative therapy
approaches as practiced within physical therapy,
medicine, osteopathy and chiropractic".
However, articles about muscle dysfunction in the
manual therapy literature are sparse and they generally
focus on muscle injury and muscle repair mechanisms 2 or
on muscle recruitment 3 . Until very recently, the current
scientific knowledge4_7and clinical implications of MTrPs
.
were rarely included It appears that orthopedic manual
therapists have not paid much attention to the pathophysiology and clinical manifestations of MTrPs. Manual
therapy educational programs in the US seem to reflect
this orientation and tend to place a strong emphasis on
joint dysfunction, mobilizations, and manipulations with
only about 10%-15% of classroom education devoted to
muscle pain and muscle dysfunction.
This review of the MTrP literature is based on
current best scientific evidence. The field of manual
therapy has joined other medical disciplines by embracing evidence-based medicine, which proposes that the
results of scientific research need to be integrated into
clinical practice 8 . Evidence-based medicine has been
defined as "the conscientious, explicit, and judicious
use of current best evidence in making decisions about
the care of individual patients "9' 10 . Within the evidencebased medicine paradigm, evidence is not restricted to
randomized controlled trials, systematic reviews, and
meta-analyses, although this restricted view seems to be
prevalent in the medical and physical therapy literature.
Sackett et a1 9" 0 emphasized that external clinical evidence
can inform but not replace individual clinical expertise.
Clinical expertisee determines whether external clinical
evidence applies to an individual patient, and if so, how
it should be
integrated into clinical decision-making.
1
Pencheon ' shared this perspective and suggested that
high-quality healthcare is about combining "wisdom
produced by years of experience" with "evidence produced
by generalizable research" in "ways with which patients
are happy." He suggested shifting from evidence-based
to evidence-informed medicine, where clinical decisionmaking is informed by research evidence but not driven
by it and always includes knowledge from experience.
Evidence-informed manual therapy involves integrating the best available external scientific evidence with
i ndividual clinicians' judgments, expertise, and. clinical decision-making 12 . The purpose of this article is to
provide a best evidence-informed review of the current
scientific understanding of MTrPs, including the etiology,
pathophysiology, and clinical implications, against the
background of extensive clinical experience.
Brief Historical Review
While Dr. Janet Travell (1901-1997) is generally credited for bringing MTrPs to the attention of health care
providers, MTrPs have been described and rediscovered 13for4
several centuries by various clinicians and researchers "
As far back as the 16th century, de Baillou (1538-1616),
as cited by Ruhmann, described what is now known as
myofascial pain syndrome (MPS) 15 . MPS is defined as
204 I The
Journal of Manual & Manipulative Therapy, 2006
the "sensory, motor, and autonomic symptoms caused
by MTrPs" and has become a recognized medical diagnosis among pain specialists 16 " 7 In 1816, British physician Balfour, as cited by Stockman, described "nodular
tumors and thickenings which were painful to the touch,
18
and from which pains shot to neighboring parts" . In
1898, the German physician Strauss discussed "small,
tender and apple-sized nodules and painful; pencil-sized
to little-finger-sized palpable bands". The first trigger
point manual was published in 1931 in Germany nearly
2
a decade before Travell became interested in MTrPs o
While these early descriptions may appear a bit archaic
and unusual-for example, in clinical practice one does
not encounter "apple-sized nodules" -these and other
historic papers did illustrate the basic features of MTrPs
quite accurately 14 .
In the late 1930s, Travell, who at that time was a
cardiologist and medical researcher, became particularly
i nterested in muscle pain following the publication of
several articles on referred pain 21 . Kellgren's descriptions
of referred pain patterns of many muscles and spinal
ligaments
after injecting these tissues with hypertonic
22-25
saline
eventually moved Travell to shift her medical
career from cardiology to musculoskeletal pain. During
the 1940s, she published
several articles on injection
2628
. In 1952, she described the
techniques of MTrPs
myofascial genesis of pain with detailed referred pain
29
patterns for 32 muscles . Other clinicians also became
interested in MTrPs. European physicians Lief and Chaitow
developed a treatment method, which they referred to as
neuromuscular technique" 30 . German physician Gutstein
described the characteristics of MTrPs and effective manual
therapy treatments in several papers under
the names
313
of Gutstein, Gutstein-Good, and Good 4. In Australia,
Kelly produced a series of articles
about fibrositis, which
35-3s
paralleled Travel's writings
39
In the US, chiropractors Nimmo and Vannerson
described muscular "noxious generative points," which
were thought to produce nerve impulses and eventually
result in "vasoconstriction, ischaemia, hypoxia, pain, and
cellular degeneration." Later in his career, Nimmo adopted
the term "trigger point" after having been introduced
to Travell's writings. Nimmo maintained that hypertonic
muscles are always painful to pressure, a statement that
later became known as "Nimmo's law." Like Travell,
Nimmo described distinctive referred pain patterns and
recommended releasing these dysfunctional points by
applying the proper degree of manual pressure. Nimmo's
receptor-tonus control method" continues to be popular
among chiropractic physicians39,4o According to a 1993
report by the National Board of Chiropractic Economics,
over 40% of chiropractors in the US frequently apply
Nimmo's techniques41 . Two spin-offs of Nimmo's work
are St. John Neuromuscular Therapy (NMT) method and
NMT American version, which have become particularly
popular among massage therapists30
In 1966, Travel! founded the North American Academy of
Manipulative Medicine, together with Dr. John Mennell, who also
published several articles about MTrPs4 ,43. Throughout her
career Travel! promoted integrating myofascial treatments
with articular treatments16. One of her earlier papers
described a technique for reduc-ing sacroiliac displacement44.
However, Travel!, as cited by Paris45, maintained the opinion
that manipulations were the exclusive domain of physicians
and she re-jected membership in the North American Academy
of Manipulative Medicine by physical therapists.
In the early 1960s, Dr. David Simons was introduced to
Travel! and her work, which became the start of a fruitful
collaboration eventually resulting in several pub-lications,
including the Trigger Point Manuals, consist-ing of a 1983 first
volume (upper half of the body) and
a 1992 second volume (lower half of the body)46,47 The
first volume has since been revised and updated and a second
edition was released in 199916. The Trigger Point Manuals are
the most comprehensive review of nearly 150 muscle referredpain patterns based on Trave!!'s clinical observations, and
they include an extensive review of the scientific basis of
MTrPs. Both volumes have been translated into several
foreign languages, including Russian, German, French,
Italian, Japanese, and Spanish. Several other clinicians
worldwide have also published their own trigger point
manuals4 -54.
Z
observed significant lowering of the pain threshold over
active MTrPs when measured by electrical stimulation, not
only in the muscular tissue but also in the overlying
cutaneous and subcutaneous tissues. In contrast, with latent
MTrPs, the sensory changes did not involve the cutaneous and
subcutaneous tissues57-59. Autonomic aspects of MTrPs may
include, among others, vasoconstriction,
vasodilatation, lacrimation, and piloerection16,60-63
A detailed clinical history, examination of movement
patterns, and consideration of muscle referred-pain pat-terns
assist clinicians in determining which muscles may harbor
clinically relevant MTrPs64. Muscle pain is perceived as aching
and poorly localized. There are no laboratory or imaging tests
available that can confirm the presence of MTrPs. Myofascial
trigger points are identi-fied through either a flat palpation
technique (Figure 1) in which a clinician applies finger or
thumb pressure to muscle against underlying bone tissue, or a
pincer palpation technique (Figure 2) in which a particular
muscle is palpated between the clinician's fingers.
g
Clinical Aspects of
Myofascial Trigger Points
An MTrP is described as "a hyperirritable spot in skeletal
muscle that is associated with a hypersensitive palpable nodule
in a taut band"16. Myofascial trigger points are classified into
active and latent trigger points16. An active MTrP is a
symptom-producing MTrP and can trigger local or referred pain
or other paraesthesiae. A latent MTrP does not trigger pain
without being stimulated. Myofascial trigger points are the
hallmark characteris-tics of MPS and feature motor, sensory,
and autonomic components. Motor aspects of active and latent
MTrPs may include disturbed motor function, muscle weakness as a result of motor inhibition, muscle stiffness, and
restricted range of motion55,56 Sensory aspects may include
local tenderness, referral of pain to a distant site, and
peripheral and central sensitization. Peripheral sensitization
can be described as a reduction in threshold and an increase in
responsiveness of the peripheral ends of nociceptors, while
central sensitization is an increase in the excitability of
neurons within the central nervous system. Signs of peripheral
and central sensitization are allodynia (pain due to a stimulus
that does not normally provoke pain) and hyperalgesia (an
increased response to a stimulus that is normally painful).
Both active and latent MTrPs are painful on compression.
Vecchiet et al57-59 described specific sensory changes over
MTrPs. They
Fig. l: Flat palpation
Fig. 2: Pincer palpation
Myofascial Trigger Points: An Evidence-Informed Review / 205
By definition, MTrPs are located within a taut band of
contractured muscle fibers (Figure 3), and palpating for
MTrPs starts with identifying this taut band by palpating
perpendicular to the fiber direction. Once the taut band is
located, the clinician moves along the taut band to
Fig. 3: Palpation of a trigger point within a taut band
(reproduced with permission from Weisskircher H-W. Head Pains
Due to Myofascial Trigger Points. CD-ROM, www. triggerpoint.com, 1997)
find a discrete area of intense pain and hardness.
Two studies have reported good overall interrater
reliability for identifying taut bands, MTrPs, referred pain, and
local twitch responses65 66 The minimum criteria that must be
satisfied in order to distinguish an MTrP from any other
tender area in muscle are a taut band and a tender point in
that taut band65. Although Janda maintained that systematic
palpation can differentiate between myofascial taut bands and
general muscle spasms, electromyography is the gold standard to
differentiate taut bands from contracted muscle fibers67,68.
Spasms can be defined as electromyographic (EMG) activity as
the result of increased neuromuscular tone of the entire
muscle, and they are the result of nerve-initiated
contractions. A taut band is an endogenous localized
contracture within the muscle without activation of the
motor endplate69. From a physiological perspective, the term
"contracture" is more appropriate then "contraction" when
describing chronic involuntary shortening of a muscle
without EMG activity. In clinical practice, surface EMG is used
in the diagnosis and management of MTrPs in addition
to manual examinations67,7o,71. Diagnostically, surface
EMG can assist in assessing muscle behavior during rest and
during functional tasks. Clinicians use the MTrP referred
pain patterns in determining which muscles to examine
with surface EMG. Muscles that harbor MTrPs responsible
for the patient's pain complaint are examined first. EMG
assessments guide the clinician with postural training,
ergonomic interventions, and muscle awareness training67.
The patient's recognition of the elicited pain further
guides the clinician. The presence of a so-called local twitch
response (LTR), referred pain, or reproduction of the
person's symptomatic pain increases the certainty and
specificity of the diagnosis of MPS. Local twitch responses are
spinal reflexes that appear to be unique to MTrPs. They are
characterized by a sudden contrac-tion of muscle fibers within
a taut band, when the taut band is strummed manually or
needled. The sudden contractions can be observed visually,
can be recorded electromyographically, or can be visualized
with diag-nostic ultrasound 72. When an MTrP is needled with
a monopolar teflon-coated EMG needle, LTRs appear as highamplitude poly-phasic EMG discharges73-7s.
In clinical practice, there is no benefit in using needle
EMG or sonography, and its utility is limited to research
studies. For example, Audette et a179 established that in 61.5%
of active MTrPs in the trapezius and levator scapulae muscles,
dry needling an active MTrP elicited an LTR in the same
muscle on the opposite side of the body. Needling of latent
MTrPs resulted in unilateral LTRs only. In this study, LTRs
were used to research the nature of active versus latent MTrPs.
Studies have shown that clinical outcomes are significantly
improved when LTRs are elicited in the treatment of patients
with
dry needling or injection therapy74'80'81 The taut band,
MTrP, and LTR (Figure 4) are objective criteria, identified
solely by palpation, that do not require a verbal response
from the patient82.
Active MTrPs refer pain usually to a distant site. The
referred pain patterns (Figure 5) are not necessarily
>
206 / The Journal of Manual & Manipulative Therapy, 2006
Fig. 4: Local twitch response in a rabbit trigger spot. Local
twitch responses are elicited only when the needle is placed
accurately within the trigger spot. Moving as little as 0.5 cm
away from the trigger spot virtually eliminates the local
twitch response (reproduced with permission from Hong C-Z,
Torigoe Y. Electrophysiological characteristics of localized twitch
responses in responsive taut bands of rabbit skeletal muscle. J
Musculoskeletal Pain 1994;2:17-43)
Fig. 5. MTrP referred pain patterns (reproduced with per-mission
from MEDICLIP, Manual Medicine 1 & 2, Version 1. Da,1997,
Williams & Wilkins)
restricted to single segmental pathways or to periph-eral
nerve distributions. Although typical referred pain patterns
have been established, there is considerable
variation between patients16,4s
Usually, the pain in reference zones is described as "deep
tissue pain" of a dull and aching nature. Occasion-ally, patients
may report burning or tingling sensations, especially in
superficial muscles such as the platysma muscle83 ,84. By
mechanically stimulating active MTrPs, patients may report
the reproduction of their pain, either immediately or after a
10-15 second delay. Normally, skeletal muscle nociceptors
require high intensities of stimulation and they do not respond
to moderate local pressure, contractions, or muscle stretches".
However, MTrPs cause persistent noxious stimulation, which
results in increasing the number and size of the receptive fields
to which a single dorsal horn nociceptive neuron responds,
and the experience of spontaneous and referred pain86.
Several recent studies have determined previously unrecorded referred pain patterns of different muscles and
MTrPs87-90. Referred pain is not specific to MPS but it is relatively
easy to elicit over MTrPs". Normal muscle tissue and other body
tissues, including the skin, zygapophyseal joints, or internal
organs, may also refer pain to distant regions with
mechanical pressure, making referred pain elicited by
stimulation of a tender location a nonspecific
finding84"2-95 Gibson et a196found that referred pain is actually easier to elicit in tendon-bone junctions and tendon than
in the muscle belly. However, after exposing the muscle to
eccentric exercise, significantly higher referred pain frequency
and enlarged pain areas were found at the muscle belly and the
tendon-bone junction sites following injection with hypotonic
saline. The authors suggested that central sensitization may
explain the referred pain
frequency and enlarged pain areas97.
While a survey of members of the American Pain Society
showed general agreement that MTrPs and MPS exist as
distinct clinical entities, MPS continues to be one of the
most commonly missed diagnoses 17"8. In a recent study of
110 adults with low back pain, myofascial pain was the most
common finding affecting 95.5% of patients, even though
myofascial pain was poorly defined as muscle pain in the
paraspinal muscles, piriformis, or tensor fasciae latae99. A
study of adults with frequent mi-graine headaches diagnosed
according to the International Headache Society criteria showed
that 94% of the patients reported migrainous pain with
manual stimulation of cervical and temporal MTrPs, compared
with only 29% of controls' °°"°1 In 30% of the migraine group,
palpation of MTrPs elicited a "full-blown migraine attack that
required abortive treatment." The researchers found a
positive relationship between the number of MTrPs and the
fre-quency of migraine attacks and duration of the illness100
Several studies have confirmed that MTrPs are common not
only in persons attending pain management clinics but also in
those seeking help through internal medicine and dentistryl°21°7 In fact, MTrPs have been identified with nearly every
musculoskeletal pain problem, includ-ing radiculopathies104,
joint dysfunction108, disk pathol-ogy109, tendonitis110,
craniomandibular dysfunction"-113,
migraines' 00"4, tension-type headaches7,87, carpal tunnel
syndrome115, computer-related disorders116, whiplash-associated disorders'°"7, spinal dysfunction118, and pelvic pain
and other urologic syndromes" 122. Myofascial trigger points are
associated with many other pain syndromes123, including, for
example, post-herpetic neuralgia124"25, complex regional pain
syndrome126"27, nocturnal cramps128, phantom pain129"3°, and
other relatively uncommon diagnoses such as Barre-Lieou
syndrome131 and neurogenic pruritus132. A recent study
suggested that there might be a relationship between MTrPs in
the upper trapezius muscle and cervical spine dysfunction at the
C3 and C4 vertebrae, although a cause-and-effect relationship
was not established in this correlational study133. Another
study described that persons with mechanical neck pain had
significantly more clinically relevant MTrPs in the upper
trapezius, sternocleidomastoid, levator scapulae, and
suboccipital muscles as compared to healthy controls5.
Etiology of MTrPs
Several possible mechanisms can lead to the development of MTrPs, including low-level muscle contrac-tions,
uneven intramuscular pressure distribution, direct trauma,
unaccustomed eccentric contractions, eccentric contractions
in unconditioned muscle, and maximal or submaximal
concentric contractions.
Low-level muscle contractions
Of particular interest in the etiology of MTrPs are lowlevel muscle exertions and the so-called Cinderella
Myofascial Trigger Points: An Evidence-Informed Review 1207
Hypothesis developed by Hagg in 1988134. The Cinderella
Hypothesis postulates that occupational myalgia is caused by
selective overloading of the earliest recruited and last derecruited motor units according to the ordered
recruitment principle or Henneman's "size principle"134,135
Smaller motor units are recruited before and de-recruited after
larger ones; as a result, the smaller type 1 fibers are
continuously activated during prolonged motor tasks135.
According to the Cinderella Hypothesis, muscular force
generated at sub-maximal levels during sustained muscle
contractions engages only a fraction of the motor units
available without the normally occurring substitution of
motor units during higher force contractions, which in turn
can result in metabolically overloaded motor units, prone to
loss of cellular Cat-homeostasis, subsequent activation of
autogenic destructive processes, and muscle
pain136"37 The other pillar of the Cinderella Hypothesis is
the finding of an excess of ragged red fibers in myalgic
patients136. Indeed, several researchers have demonstrated the
presence of ragged red fibers and moth-eaten fibers in
subjects with myalgia, which are indications of struc-tural
damage to the cell membrane and mitochondria and a change
in the distribution of mitochondria or the
sarcotubular system respectivelyl3s-142
There is growing evidence that low-level static muscle
contractions or exertions can result in degeneration of
muscle fibers143 Gissell144"45 has shown that low-level
exertions can result in an increase of Cat-release in skeletal
muscle cells, muscle membrane damage due to leakage of the
intracellular enzyme lactate dehydrogenase, structural damage,
energy depletion, and myalgia. Low-level muscle stimulation
can also lead to the release of
interleukin 6 (IL-6) and other cytokines146"47
Several studies have confirmed the Cinderella Hypothesis and support the idea that in low-level static
exertions, muscle fiber recruitment patterns tend to be
stereotypical with continuous activation of smaller
type 1 fibers during prolonged motor tasksl 4s-152. As
Hagg indicated, the continuous activity and metabolic
overload of certain motor units does not occur in all
subjects 136. The Cinderella Hypothesis was recently
applied to the development of MTrPs116. In a well-de-signed
study, Treasters et a1116 established that sustained low-level
muscle contractions during continuous typing for as little as
30 minutes commonly resulted in the formation of MTrPs.
They suggested that MTrPs might provide a useful
explanation for muscle pain and injury that can occur from
low-level static exertions116. Myo-fascial trigger points are
common in office workers, musicians, dentists, and other
occupational groups exposed to low-level muscle
exertions153. Chen et a1154 also suggested that low-level
muscle exertions can lead to sensitization and development
of MTrPs. Forty piano students showed significantly reduced
pressure thresholds over latent MTrPs after only 20 minutes
of continuous piano playing154.
208 I The Journal of Manual & Manipulative Therapy, 2006
Intramuscular pressure distribution
Otten155 has suggested that circulatory disturbances
secondary to increased intramuscular pressure may also lead
to the development of myalgia. Based on mathemati-cal
modeling applied to a frog gastrocnemius muscle, Otten
confirmed that during static low-level muscle contractions,
capillary pressures increase dramatically especially near the
muscle insertions (Figure 6). In other words, during lowlevel exertions, the intramuscular
Fig. 6: Intramuscular pressure distribution in the gastroc-nemius
muscle of the toad (reproduced with p e r m i s s i o n from E.
Otten, 2006)
pressure near the muscle insertions might increase
rapidly, leading to excessive capillary pressure, decreased
circulation, and localized hypoxia and ischaemia155. With
higher level contractions in between 10% and 20% of
maximum voluntary effort, the intramuscular pressure
increases also in the muscle belly156"57. According to Otten,
the increased pressure gradients during low-level exertions
may contribute to the development of pain at the
musculotendinous junctions and eventually to the formation
of MTrPs (personal communication, 2005).
In 1999, Simons introduced the concept of "attach ment
trigger points" to explain pain at the musculoten-dinous
junctions in persons with MTrPs, based on the assumption that
taut bands would generate sufficient sustained force to
induce localized enthesopathies16"5s More recently, Simons
concluded that there is no con-vincing evidence that the
tension generated in shortened sarcomeres in a muscle belly
would indeed be able to generate passive or resting force
throughout an entire taut band resulting in enthesopathies,
even though
there may be certain muscles or conditions where this could
occur (personal communication, 2005). To the contrary, force
generated by individual motor units is always transmitted
laterally to the muscle's connective tissue matrix, involving at
least two protein complexes containing vinculin and dystrophin,
respectively159. There is also considerable evidence that the
assumption that muscle fibers pass from tendon to tendon is
without basisl6o Trotterl6o has demonstrated that skeletal
muscle is comprised of in-series fibers. In other words, there is
evidence that a single muscle fiber does not run from tendon to
tendon. The majority of fibers are in series with inactive
fibers, which makes it even more unlikely that the whole
muscle length-tension properties would be dictated by the
shortest contractured fibers in the muscle161
In addition, it is important to consider the mechanical and
functional differences between fast and slow motor units162"63
Slow motor units are always stiffer than fast units, although
fast units can produce more force. If there were any
transmission of force along the muscle fiber, as Simons initially
suggested, fast fibers would be better suited to accomplish this.
Yet, fast motor units have larger series of elastic elements,
which would absorb most of the force displacement164"65 Fast
fibers show a progressive decrease in cross-sectional area and
end in a point within the muscle fascicle, making force
transmission even more unlikely163. Fast fibers rely on
transmitting a substantial proportion of their force to the
endomysium, transverse cytoskeleton, and adja-cent muscle
fibers162"63 In summary, the development of so-called
"attachment trigger points" as a result of increased tension
by contractured sarcomeres in MTrPs is not clear and
more research is needed to explain the clinical observation that
MTrPs appear to be linked to pain at the musculotendinous
junction. The increased tension in the muscle belly is likely to
dissipate across brief sections of the taut band on both sides of the
MTrP and laterally through the transverse cytoskeleton166-168.
Instead, Otten's model of increased intramuscular pressure the
muscle insertions provides an alternative model for the
clinically observed pain near the musculotendinous junction
and osseous insertions in persons with MTrPs, even though
the model does not explain why taut bands
are commonly present155.
Direct trauma
There is general agreement that acute muscle over-load
can activate MTrPs, although systematic studies are lacking169.
For example, people involved in whiplash injuries commonly
experience prolonged muscle pain
and dysfunction17o -173. In a retrospective review, Schul-ler et
a1174 found that 80% of 1096 subjects involved in
low-velocity collisions demonstrated evidence of muscle pain
with myogeloses among the most common find-
ings. Although Schuller et a1174 did not define these
myogeloses, Simons has suggested that a myogeloses
describes the same clinical entity as an MTrPl75. Baker117
reported that the splenius capitis, semispinalis capitis, and
sternocleidomastoid muscles developed symptomatic MTrPs in
77%, 62%, and 52% of 52 whiplash patients, respectively. In a
retrospective review of 54 consecutive chronic whiplash
patients, Gerwin and Dommerholt176 reported that clinically
relevant MTrPs were found in every patient, with the
trapezius muscle involved most often. Following treatment
emphasizing the inactivation of MTrPs and restoration of
normal muscle length, ap-proximately 80% of patients
experienced little or no pain, even though the average time
following the initiating injury was 2.5 years at the beginning
of the treatment regimen. All patients had been seen
previously by other physicians and physical therapists who
apparently had not considered MTrPs in their thought
process and
clinical management176. Fernandez-de-las-Penas et a1177"7'
confirmed that inactivation of MTrPs should be included in the
management of persons suffering from whiplashassociated disorders. In their research-based treatment
protocol, the combination of cervical and thoracic spine
manipulations with MTrP treatments proved superior to more
conventional physical therapy consisting of massage,
ultrasound, home exercises; and low-energy high-frequency
pulsed electromagnetic therapy177.
Direct trauma may create a vicious cycle of events wherein
damage to the sarcoplasmic reticulum or the muscle cell
membrane may lead to an increase of the calcium
concentration, a subsequent activation of actin and myosin, a
relative shortage of adenosine triphosphate (ATP), and an
impaired calcium pump, which in turn will increase the
intracellular calcium concentration even more, completing the
cycle. The calcium pump is responsible for returning
intracellular Cat+ to the sar-coplasmic reticulum against a
concentration gradient, which requires a functional energy
supply. Simons and Travell179 considered this sequence in the
development of the so-called "energy crisis hypothesis"
introduced in 1981. Sensory and motor system dysfunction have
been shown to develop rapidly after injury and actually may
persist in those who develop chronic muscle pain and in
individuals who have recovered or continue to have persistent
mild symptoms172" ° S co tt e t a !" de -termined that
individuals with chronic whiplash pain develop more
widespread hypersensitivity to mechanical pressure and
thermal stimuli than those with chronic idiopathic neck pain.
Myofascial trigger points are a likely source of ongoing
peripheral nociceptive input, and they contribute to both
peripheral and central sensitization, which may explain the
observation
of
widespread
allodynia
and
hypersensitivity60"2"3. In addi-tion to being caused by whiplash
injury, acute muscle overload can occur with direct impact,
lifting injuries, sports performance, etc."2
Eccentric and (sub)maximal concentric contractions
Many patients report the onset of pain and activation of
MTrPs following either acute, repetitive, or chronic
183
184
suggested that likely
mechanisms relevant for the development of MTrPs included
either unaccustomed eccentric exercise, ec-centric exercise
in unconditioned muscle, or maximal or sub-maximal
concentric exercise. A brief review of pertinent aspects of
exercise follows, preceding linking this body of research to
current MTrP research.
Eccentric exercise is associated with myalgia, muscle
weakness, and destruction of muscle fibers, partially because
eccentric contractions cause an irregular and
uneven lengthening of muscle fibers185-187. Muscle soreness and pain occur because of local ultra-structural damage,
the release of sensitizing algogenic substances, and the
subsequent onset of peripheral and central
sensitization85"88-19o Muscle damage occurs at the cytoskeletal level and frequently involves disorganization of the
A-band, streaming of the Z-band, and disruption of
cytoskeletal proteins, such as titin, nebulin, and desmin,
even after very short bouts of eccentric exercise 186"89-194
Loss of desmin can occur within 5 minutes of eccentric
loading, even in muscles that routinely contract eccen-trically
during functional activities, but does not occur after
isometric or concentric contractions193"95 Lieber and
Friden193 suggested that the rapid loss of desmin might
indicate a type of enzymatic hydrolysis or protein
phosphorylation as a likely mechanism.
One of the consequences of muscle damage is muscle
weakness196-198. Furthermore, concentric and eccentric
contractions are linked to contraction-induced capil-lary
constrictions, impaired blood flow, hypoperfusion, ischaemia,
and hypoxia, which in turn contribute to the development
of more muscle damage, a local acidic milieu, and an
excessive release of protons (H+), potassium (K+), calcitoningene-related-peptide (CGRP), bradykinin (BK), and substance
P (SP), and sensitization of muscle nociceptors184"88. There
are striking similarities with the chemical environment of
active MTrPs established with microdialysis, suggesting an
overlap between the research on eccentric exercise and MTrP
research184"99 However, at this time, it is premature to
conclude that there is solid evidence that eccentric and submaximal concentric exercise are absolute precursors to the
de-velopment of MTrPs. In support of this hypothesized
causal relation, Itoh et al200 demonstrated in a recent study
that eccentric exercise can lead to the formation of taut and
tender ropy bands in exercised muscle, and they hypothesized
that eccentric exercise may indeed be a useful model for the
development of MTrPs.
Eccentric and concentric exercise and MTrPs have been
associated with localized hypoxia, which appears to be one of
the most important precursors for the development of
MTrPs201. As mentioned, hypoxia leads to the release of
multiple algogenic substances. In this
m u s c l e o ve r l o a d
. Ge r w i n e t a 1
context, recent research by Shah et a1199 at the LAS N tional
Institutes of Health is particularly relevant. Shah et al
analyzed the chemical milieu of latent and active l 1TrPs and
normal muscles. They found significantly in-creased
concentrations of BK, CGRP, SP, tumor necrosis factor-a
(TNF-a),
interleukin-lei
(IL-lei),
serotonin,
and
norepinephrine in the immediate milieu of active MTrPs
only199. These substances are well-known stimulants for
various muscle nociceptors and bind to specific receptor
molecules of the nerve endings, including the so-called
purinergic and vanilloid receptors85,202
Muscle nociceptors are dynamic structures whose
receptors can change depending on the local tissue
environment. When a muscle is damaged, it releases ATP,
which stimulates purinergic receptors, which are sensitive to
ATP, adenosine diphosphate, and adenosine. They bind ATP,
stimulate muscle nociceptors, and cause pain. Vanilloid
receptors are sensitive to heat and respond to an increase in H+concentration, which is especially relevant under conditions
with a lowered pH, such as ischaemia, inflammation, or
prolonged and exhaustive muscle contractions85. Shah et a1199
determined that the pH at active MTrP sites is significantly
lower than at latent MTrP sites. A lowered pH can initiate and
main-tain muscle pain and mechanical hyperalgesia through
activation of acid-sensing ion channels203'204 Neuroplastic
changes in the central nervous system facilitate me-chanical
hyperalgesia even after the nociceptive input
has been terminated (central sensitization) 203,204Any
noxious stimulus sufficient to cause nociceptor activa-tion
causes bursts of SP and CGRP to be released into the muscle,
which have a significant effect on the local biochemical
milieu and microcirculation by stimulating "feed-forward"
neurogenic inflammation. Neurogenic inflammation can
be described as a continuous cycle of increasing
production of inflammatory mediators and neuropeptides and
an increasing barrage of nociceptive input into wide
dynamic-range neurons in the spinal
cord dorsal horn184
The Integrated Trigger Point Hypothesis
The integrated trigger point hypothesis (Figure 7) has
evolved since its first introduction as the "energy crisis
hypothesis" in 1981. It is based on a combination of
electrodiagnostic and histopathological evidence179"83
Already in 1957, Weeks and Trave11205 had published a
report that outlined a characteristic electrical activ-ity of an
MTrR It was not until 1993 that Hubbard et al206
confirmed that this EMG discharge consists of lowamplitude discharges in the order of 10-50 pV and intermittent
high-amplitude discharges (up to 500 PV) in painful MTrPs.
Initially, the electrical activity was termed "spontaneous
electrical activity" (SEA) and thought to be related to
dysfunctional muscle spindles206 Best available evidence now
suggests that the SEA is in fact endplate noise (EPN), which is
found much more
Fig. 7: The integrated trigger point hypothesis.
Ach- acetylcholine; AchE- acetylcholinesterase; A c h R acetylcholine receptor
commonly in the endplate zone near MTrPs than in an
endplate zone outside MTrPs2°7-209. The electrical discharges
occur with frequencies that are 10-1,000 times that of normal
endplate potentials, and they have been found in
humans, rabbits, and recently even in horses209,21o The
discharges are most likely the result of an abnormally
excessive release of acetylcholine (ACh) and indicative of
dysfunctional motor endplates, contrary to the com-monly
accepted notion among electromyographers that endplate
noise arises from normal motor endplates183 The effectiveness
of botulinum toxin in the treatment of MTrPs provides indirect
evidence of the presence of excessive ACh211. Botulinum toxin
(BoTox) is a neurotoxin that blocks the release of ACh from
presynaptic choliner-gic nerve endings. A recent study in
mice demonstrated that the administration of botulinum
toxin resulted in a complete functional repair of dysfunctional
endplates212. There is some early evidence that muscle
stretching and hypertonicity may also enhance the excessive
release of ACh213,214 Tension on the integrins in the
presynaptic membrane at the motor nerve terminal is
hypothesized to mechanically trigger an ACh release that does
not
require Ca2+ 213-215. Integrins are receptor proteins in the
cell membrane involved in attaching individual cells to the
extracellular matrix.
Excessive ACh affects voltage-gated sodium chan-nels of
the sarcoplasmic reticulum and increases the intracellular
calcium levels, which triggers sustained muscle contractures.
It is conceivable that in MTrPs, myosin filaments literally get
stuck in the Z-band of the sarcomere. During sarcomere
contractions, titin filaments are folded into a gel-like
structure at the Z-band. In MTrPs, the gel-like titin may prevent
the myosin filaments from detaching. The myosin filaments
may actually damage the regular motor assembly and prevent
the sarcomere from restoring its resting length216. Muscle
contractures are also maintained because of the relative
shortage of ATP in an MTrP, as ATP is required to break the
cross-bridges between actin and myosin filaments. The
question remains whether sustained contractures require an
increase of oxygen availability.
At the same time, the shortened sarcomeres compro-mise
the local circulation causing ischaemia. Studies of oxygen
saturation levels have demonstrated severe hypoxia in MTrPs201.
Hypoxia leads to the release of sensitizing substances and
activates muscle nociceptors as reviewed above. The
combined decreased energy supply and pos-sible
increased metabolic demand would also explain the common
finding of abnormal mitochondria in the nerve terminal and
the previously mentioned ragged red fibers. In mice, the onset
of hypoxia led to an immediate increased ACh release at the
motor endplate217.
The combined high-intensity mechanical and chemi-cal
stimuli may cause activation and sensitization of the
peripheral nerve endings and autonomic nerves, activate
second order neurons including so-called "sleep-ing" receptors,
cause central sensitization, and lead to the formation of new
receptive fields, referred pain, a long-lasting increase in the
excitability of nociceptors, and a more generalized
hyperalgesia beyond the initial nociceptive area. An expansion
of a receptive field means that a dorsal horn neuron receives
information from areas it has not received information
from previously218. Sensitization of peripheral nerve endings
can also cause pain through SP activating the neurokin-1
receptors and glutamate activating N-methyl-D-aspartate
recep-tors, which opens post-synaptic channels through which
Ca2+ ions can enter the dorsal horn and activate many enzymes
involved in the sensitization85.
Several histological studies offer further support for the
integrated trigger point hypothesis. In 1976, Simons and
Stolov published the first biopsy study of MTrPs in a canine
muscle and reported multiple contraction knots in various
individual muscle fibers (Figure 8)219. The knots featured a
combination of severely shortened sarcomeres in the
center and lengthened sarcomeres outside the immediate
MTrP region219.
Reitinger et a1220 reported pathologic alterations of the
mitochondria as well as increased width of A-bands
and decreased width of I-bands in muscle sarcomeres of
MTrPs in the gluteus medius muscle. Windisch et al221
determined similar alterations in a post-mortem histo-logical
study of MTrPs completed within 24 hours of time of death.
Mense et a1222 studied the effects of electrically induced muscle
contractions and a cholinesterase blocker on muscles with
experimentally induced contraction knots and found evidence of
localized contractions, torn fibers, and longitudinal stripes.
Pongratz and Spath223, 224 dem-onstrated evidence of a
contraction disk in a region of an MTrP using light microscopy.
New MTrP histopathological studies are currently being
conducted at the Friedrich
Fig. 8: Longitudinal section of a contraction knot in a canine gracilis
muscle (reproduced with permission from: Simons DG, Travell JG,
Simons LS. Travell and Simons'Mryofascial Pain and Dysfunction:
The Trigger Point Manual. Vol. 1. 2nd ed. Baltimore, MD:
Williams & Wilkins,1999)
Baur Institute in Munich, Germany. Gariphianova 225
described pathological changes with biopsy studies of MTrPs,
including a decrease in quantity of mitochondria, possibly
indicating metabolic distress. Several older histological
studies are often quoted, but it is not clear to what extent
those findings are specific for MTrPs. In 1951, Glogowsky and
Wallraff226 reported damaged fibril structures. Fassbender227
observed degenerative changes of the I-bands, in addition to
capillary damage, a focal accumulation of glycogen, and a
disintegration of the myofibrillar network.
There is growing evidence for the integrated trigger point
hypothesis with regard to the motor and sensory aspects of
MTrPs, but many questions remain about the autonomic
aspects. Several studies have shown that MTrPs are
influenced by the autonomic nervous system. Exposing
subjects with active MTrPs in the upper trapezius muscles
to stressful tasks consistently increased the electrical activity
in MTrPs in the upper trapezius muscle but not in control
points in the same muscle, while autogenic relaxation was
able to reverse
the effects228-231. The administration of the sympathetic
blocking agent phentolamine significantly reduced the
electrical activity of an MTrP228,232,233. The interactions
between the autonomic nervous system and MTrPs need
further investigation. Hubbard 228 maintained that the
autonomic features of MTrPs are evidence that MTrPs may be
dysfunctional muscle spindles. Gerwin et a1184 have suggested
that the presence of alpha and beta adrenergic receptors at
the endplate provide a possible mechanism for autonomic
interaction. In a rodent, stimulation of the alpha and beta
adrenergic receptors stimulated the release of ACh in the
phrenic nerve 234. In a recent study, Ge et al61 provided for
the first time experimental evidence of sympathetic facilitation
of me-
chanical sensitization of ! TrPs. which they attributed to a
change in the local chemical milieu at the MTrPs due to
increased vasoconstriction, an increased sympathetic release
of noradrenaline, or an increased sensitivity to noradrenaline.
Another intriguing possibility is that the cytokine
interleukin-8 (IL-8) found in the immediate milieu of active
MTrPs may contribute to the autonomic features of MTrP.
IL-8 can induce mechanical hyper-no-ciception, which is
inhibited by beta adrenergic receptor antagonists 235. Shah et
al found significantly increased levels of IL-8 in the
immediate milieu of active MTrPs (Shah, 2006, personal
communication).
The findings of Shah et a1199 mark a major milestone in
the understanding and acceptance of MTrPs and support parts of
the integrated trigger point hypothesis 183. The possible
consequences of several of the chemicals present in the
immediate milieu of active MTrPs have been explored by
Gerwin et a1184. As stated, Shah et al found significantly
increased concentrations of H+, BK, CGRP, SP, TNF-a, IL13, serotonin, and norepinephrine in active MTrPs only. There
are many interactions between these chemicals that all can
contribute to the persistent nature of MTrPs through various
vicious feedback cycles236. For example, BK is known to
activate and sensitize muscle nociceptors, which leads to
inflammatory hyperalgesia, an activation of high-threshold
nociceptors associated with C-fibers, and even an increased
production of BK itself. Furthermore, BK stimulates the
release of TNF-a, which activates the production of the
interleukins IL-13, IL-6, and IL-8. Especially IL-8 can cause
hyperalgesia that is independent from prostaglandin
mechanisms. Via a positive feedback loop, IL-13 can also
induce the
release of BK237. Release of BK, K+, H+, and cytokines
from injured muscle activates the muscle nociceptors,
thereby causing tenderness and pain184.
Calcitonin gene-related peptide can enhance the
release of ACh from the motor endplate and simultaneously decrease the effectiveness of acetylcholinesterase
(ACNE) in the synaptic cleft, which decreases the removal
ofACh238'239 Calcitonin gene-related peptide also upregulates the ACh-receptors (AChR) at the muscle and
thereby creates more docking stations for ACh. Miniature
endplate activity depends on the state of the AChR and on
the local concentration of ACh, which is the result of AChrelease, reuptake, and breakdown by ACNE. In summary,
increased concentrations of CGRP lead to a release of more
ACh, and increase the impact of ACh by reducing ACNE
effectiveness and increasing AChR efficiency. Miniature endplate
potential frequency is increased as a result of greater ACh
effect. The observed lowered pH has several implications as
well. Not only does a lower pH enhance the release of CGRP,
it also contributes to a further down-regulation of ACNE. The
multiple chemicals and lowered pH found in active MTrPs can
contribute to the chronic nature of MTrPs, enhance the
segmental spread of nociceptive input into the dorsal horn
of the
spinal cord, activate multiple receptive fields, and trigger
referred pain, allodynia, hypersensitivity, and peripheral and
central sensitization that are characteristic of active
myofascial MTrPs184. There is no other evidence-based
hypothesis that explains the phenomena of MTrPs in as much
detail and clarity as the expanded integrated trigger point
hypothesis (Figure 9).
Fig. 9: The expanded MTrP hypothesis (reproduced with
permission from: Gerwin RD, Dommerholt J, Shah J. An
expansion of Simons' integrated hypothesis of trigger point formation.
Curr Pain Headache Rep 2004;8:468-475). Ach- acet icholine;
AchE- acet icholinesterase; AchR-acet icholine receptor; ATPadenosine triphosphate; SP- substance P; CGRP- calcitonin
gene-related p e pti de ; MEPP- miniature endplate potential
Perpetuating Factors
There are several precipitating or perpetuating factors that
need to be identified and, if present, adequately managed to
successfully treat persons with chronic myalgia. Even
though several common perpetuating factors are more or
less outside the direct scope of manual physical therapy,
familiarity with these factors is critical especially
considering the development of increasingly autonomous
physical therapy practice. Simons, Travell, and Simons16
identified mechanical, nutritional, metabolic, and
psychological categories of perpetuating factors. Mechanical
factors are familiar to manual therapists and include the
commonly observed forward head posture, structural leg
length inequalities, scoliosis, pelvic torsion, joint
hypermobility, ergonomic
stressors, poor body mechanics, etc.16,102"16,240
In recent review articles, Gerwin241,242 provided a
comprehensive update with an emphasis on non-struc-tural
perpetuating factors. Management of these factors usually
requires an interdisciplinary approach, including
medical and psychological intervention64,82. Common
nutritional deficiencies or insufficiencies involve vitamin B1,
B6, B12, folic acid, vitamin C, vitamin D, iron, magnesium,
and zinc, among others. The term "insuf-ficiency" is used
to indicate levels in the lower range of normal, such as
those associated with biochemical or metabolic abnormalities
or with subtle clinical signs and symptoms. Nutritional or
metabolic insufficiencies are frequently overlooked and not
necessarily considered clinically relevant by physicians
unfamiliar with MTrPs and chronic pain conditions. Yet any
inadequacy that interferes with the energy supply of muscle is
likely to aggravate MTrPs242. The most common
deficiencies and insufficiencies will be reviewed briefly.
Vitamin B12 deficiencies are rather common and may
affect as many as 15%-20% of the elderly and approximately 16% of persons with chronic MTrPslo3,243
B12 deficiencies can result in cognitive dysfunction,
degeneration of the spinal cord, and peripheral neu-ropathy,
which is most likely linked to complaints of diffuse myalgia
seen in some patients. Serum levels of vitamin B12 as high as
350 pg/ml may be associated with a metabolic deficiency
manifested by elevated serum or urine methylmalonic
acid or homocysteine and may be clinically symptomatic244.
However, there are patients with normal levels of
methylmalonic acid and homocys-teine, who do present with
metabolic abnormalities of B12 function242. Folic acid is
closely linked to vitamin B12 and should be measured as well.
While folic acid is able to correct the pernicious anaemia
associated with vitamin B12 deficiency, it does not influence
the neuromuscular aspects.
Iron deficiency in muscle occurs when ferritin is
depleted. Ferritin represents the tissue-bound nones-sential
iron stores in muscle, liver, and bone marrow that supply the
essential iron for oxygen transport and iron-dependent
enzymes. Iron is critical for the genera-tion of energy through
the cytochrome oxidase enzyme system and a lack of iron may
be a factor in the develop-ment and maintenance of MTrPs242.
Interestingly, lowered levels of cytochrome oxidase are
common in patients with myalgia140. Serum levels of 15-20
ng/ml indicate a depletion of ferritin. Common symptoms are
chronic tiredness, coldness, extreme fatigue with exercise,
and muscle pain. Anaemia is common at levels of 10 ng/ml or
less. Although optimal levels of ferritin are unknown,
Gerwin242 suggested that levels below 50 ng/ml may be
clinically significant.
Close to 90% of patients with chronic musculoskeletal pain
may have vitamin D deficiency245. Vitamin D deficien-cies are
identified by measuring 25-OH vitamin D levels. Levels above
20 ng/ml are considered normal, but Gerwin242 suggested that
levels below 34 ng/ml may represent insuf-ficiencies.
Correction of insufficient levels of vitamin B12, vitamin D, and
iron levels may take many months, during which patients may
not see much improvement.
Even when active MTrPs have been identified in a
particular patient, clinicians must always consider that
MTrPs may be secondary to metabolic insufficiencies or other
medical diagnoses. It is questionable whether physical
therapy and-as an integral part of physical therapy
management-manual therapy intervention can be
successful when patients have nutritional or metabolic
insufficiencies or deficiencies. A close working relationship
with physicians familiar with this body of literature is
essential. Therapists should consider the possible
interactions between arthrogenic or neurogenic
dysfunction and MTrPs4'5"18'133'246'247
Clinically, physical therapists should address all
aspects of the dysfunction. There are many other conditions that feature muscle pain and MTrPs, including
hypothyroidism, systemic lupus erythematosis, Lyme
disease, babesiosis, ehrlichiosis, candida albicans infec-tions,
myoadenylate deaminase deficiency, hypoglycaemia, and
parasitic diseases such as fascioliasis, amoebiasis, and
giardia64'242 Therapists should be familiar with the
symptoms associated with these medical diagnoses64.
Psychological stress may activate MTrPs. Electromyographic activity in MTrPs has been shown to increase
dramatically in response to mental and emotional stress,
whereas adjacent non-trigger point muscle EMG activity
remained norma1229' 230 Relaxation techniques, such as
autogenic relaxation, can diminish the electrical activ-ity231.
In addition, many patients with persistent MTrPs are dealing
with depression, anxiety, anger, and feelings of
hopelessness248. Pain-related fear and avoidance can lead to
the development and maintenance of chronic pain249. Sleep
disturbance can also be a major factor in the perpetuation
of musculoskeletal pain and must be addressed. Sleep
problems may be related to pain, apnea, or to mood disorders
like depression or anxiety. Manage-ment can be both
pharmacologic and non-pharmacologic. Pharmacologic
treatment utilizes drugs that promote normal sleep
patterns and induce and maintain sleep through the night
without causing daytime sedation. Non-pharmacologic
treatment emphasizes sleep hygiene,
such as using the bed only for sleep and sex, and not for
reading, television viewing, and eating250. Therapists must be
sensitive to the impact of psychological and emotional
distress and refer patients to clinical social workers or
psychologists when appropriate.
The Role of Manual Therapy
Although the various management approaches are
beyond the scope of this article, manual therapy is one of
the basic treatment options and the role of orthope-dic
manual physical therapists cannot be overempha-sized 82'158
Myofascial trigger points are treated with manual
techniques, spray and stretch, dry needling, or injection
therapy. Dry needling is within the scope of physical therapy
practice in many countries including Canada, Spain, Ireland,
South Africa, Australia, the Netherlands, and. Switzerland.
In the United States, the physical therapy boards of eight
states have ruled that physical therapists can engage in
the practice of dry needling: New Hampshire, Maryland,
Virginia, South Carolina, Georgia, Kentucky, New Mexico, and
Colorado80. A promising new development used in the
diagnosis and treatment of MTrPs involves shockwave therapy,
but as of yet, there are no controlled studies
substantiating its use251'252
Summary
Although MTrPs are a common cause of pain and
dysfunction in persons with musculoskeletal injuries and
diagnoses, the importance of MTrPs is not obvious from
reviewing the orthopedic manual therapy litera-ture. Current
scientific evidence strongly supports that awareness and a
working knowledge of muscle dysfunc-tion; in particular,
MTrPs should be incorporated into manual physical
therapy practice consistent with the IFOMT guidelines for
clinical practice. While there are still many unanswered
questions with regard to explain-ing the etiology of MTrPs,
this article provides manual therapists with an up-to-date
evidence-informed review of the current scientific knowledge.
REFERENCES
1.
2.
IFOMT. Available at:http:lwww.ifomt.org/ifomt/about/standards.Accessed
November 15, 2006.
Huijbregts PA. Muscle injury, regeneration, and repair. JManual
Manipulative Ther 2001;9:9-16.
3. Urquhart DM, Hodges PW, Allen TJ, Story IH. Abdominal muscle recruitment
during a range of voluntary exercises. Man Ther 2005;10:144-153.
4. Fernandez-de-las-Penas C; Alonso-Blanco C, Alguacil-Diego IM,
Miangolarra-Page JC. Myofascial trigger points and postern-an-
terior joint hypomobility in the mid-cervical spine in subjects presenting with
mechanical neck pain: A pilot study. JManual Manipulative Ther
2006;14:88-94.
5. Fernandez-de-las-Penas C, Alonso-Blanco C, Miangolarra JC. Myofascial
trigger points in subjects presenting with mechanical neck pain: A blinded,
controlled study Man Ther (In press).
6. Lew PC, Lewis J, Story I. Inter-therapist reliability in locating latent
myofascial trigger points using palpation. Man Ther 1997;2:87-90.
7. Fernandez-de-las-Penas C, Alonso-Blanco C, Cuadrado ML, Pareja JA.
Myofascial trigger points in the suboccipital muscles in episodic
tension-type headache. Man Ther 2006;11:225-230.
8. Moore A, Petty N. Evidence-based practice: Getting a grip and finding a
balance. Man Ther 2001;6:195-196.
9. Sackett DL, Rosenberg WM. The need for evidence-based medi-cine. J R
Soc Med 1995;88:620-624.
10. Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS.
Evidence-based medicine: What it is and what it isn't. BMJ
1996;312:71-72.
11. Pencheon D. What's next for evidence-based medicine? EvidenceBased Healthcare Public Health 2005;9:319-321.
12. Cicerone KD. Evidence-based practice and the limits of rational
rehabilitation. Arch Phys Med Rehabil 2005;86:1073-1074.
13. Baldry PE. Acupuncture, Trigger Points and Musculoskeletal
Pain. Edinburgh, UK: Churchill Livingstone, 2005.
14. Simons DG. Muscle pain syndromes. Part 1. Am J Phys Med
1975;54:289-311.
15. Ruhmann W. The earliest book on rheumatism. BrJRheumatism
1940;11:140-162.
16. Simons DG, Travel! JG, Simons LS. Travell and Simons' Myo-fascial
Pain and Dysfunction: The Trigger Point Manual. Vol. 1. 2nd ed.
Baltimore, MD: Williams & Wilkins,1999.
17. Harden RN, Bruehl SP, Gass S, Niemiec C, Barbick B. Signs and symptoms
of the myofascial pain syndrome: A national survey of pain management
providers. Clin J Pain 2000;16:64-72.
18. Stockman R. The causes, pathology, and treatment of chronic
rheumatism. Edinburgh Med J 1904;15:107-116.
19. Strauss H. Uber die sogenannten, Rheumatische Muskelschwiele`
[German; With regard to the so-called myogelosis]. Klin Wo-chenschr
1898;35:89-91,121-123.
20. Lange M. Die Muskelharten (Myogelosen) [German; The Muscle
Hardenings (Myogelosen)]. Munich, Germany: J.F. Lehmann`s
Verlag,1931.
21. Travel! J. Office Hours: Day and Night. The Autobiography of
Janet Travel!, MD. New York, NY: World Publishing, 1968.
22. Kellgren JH. Deep pain sensibility. Lancet 1949;1:943-949.
23. Kellgren JH. Observations on referred pain arising from muscle.
Clin Sci 1938;3:175-190.
24. Kellgren JH. A preliminary account of referred pains arising
from muscle. British Med J 1938;1:325-327.
25. Simons DG. Cardiology and myofascial trigger points: Janet
G.
Travell's contribution. Tex Heart Inst J 2003;30(1):3-7.
26. Travel! J. Basis for the multiple uses of local block of somatic
trigger areas (procaine infiltration and ethyl chloride spray).
Miss Valley Med 1949;71:13-22.
27. Travel! J, Bobb AL. Mechanism of relief of pain in sprains by
local injection techniques. Fed Proc 1947;6:378.
28. Travel! JG, Rinzler S, Herman M. Pain and disability of the
shoulder and arm: Treatment by intramuscular infiltration with
procaine hydrochloride. J AMA 1942;120:417-422.
29. Travel! JG, Rinzler SH. The myofascial genesis of pain. Postgrad
M e d 1952;11:452-434.
30. Chaitow L, DeLany J. Neuromuscular techniques in orthopedics.
Techniques in Orthopedics 2003;18(1):74-86.
31. Good MG. Five hundred cases of myalgic in the British army.
Ann Rheum Dis 1942;3:118-138.
32. Good MG. The role of skeletal muscle in the pathogenesis of
diseases. Acta Medica Scand 1950;138:285-292.
33. Gutstein M. Common rheumatism and physiotherapy. BrJPhys
Med 1940;3:46-50.
34., Gutstein M. Diagnosis and treatment of muscular rheumatism. Br J
Phys Med 1938;1:302-321.
35. Kelly M. The nature of fibrositis. I. The myalgic lesion and its secondary
effects: A reflex theory. Ann Rheum Dis 1945;5:1-7.
36. Kelly M. The nature of fibrositis. II. A study of the causation of the
myalgic lesion (rheumatic, traumatic, infective). Ann Rheum Dis
1946;5:69-77.
37. Kelly M. The relief of facial pain by procaine (Novocaine) injec-tions. J
Am Geriatr Soc 1963;11:586-96.
38. Kelly M. The treatment of fibrositis and allied disorders by local
anesthesia. Med JAust 1941;1:294-298.
39. Schneider M, Cohen J, Laws S. The Collected Writings of Nimmo &
Vannerson: Pioneers of Chiropractic Trigger Point Therapy.
Pittsburgh, PA: Schneider, 2001.
40. Cohen JH, Gibbons RW. Raymond L. Nimmo and the evolution of
trigger point therapy, 1929-1986. JManipulative Physiol Ther
1998;21:167-172.
41. National Board of Chiropractic Examiners. Chiropractic Treat-ment
Procedures. Greeley, CO: NBCE,1993.
42. Mennell J. Spray-stretch for the relief of pain from muscle spasm and
myofascial trigger points. JAm PodiatryAssoc 1976;66:873-876.
43. Mennell J. Myofascial trigger points as a cause of headaches. J
Manipulative Physiol Ther,1989;12:308-313.
44. Travel! W, Travel! JG. Technic for reduction and ambulatory treatment
of sacroiliac displacement. Arch Phys Ther 1942;23:222-232.
45. Paris SV. In the best interests of the patient. Phys Ther
2006;86:1541-1553.
46. Travel! JG, Simons DG. Myofascial Pain and Dysfunction: The
TriggerPointManual. Vol. 2. Baltimore, MD: Williams & Wilkins, 1992.
47. Travel! JG, Simons DG. Myofascial Pain and Dysfunction: The
TriggerPointManual. Vol, l. Baltimore, MD: Williams & Wilkins, 1983.
48. Dejung B, Grobli C, Colla F, Weissmann R. Triggerpunkttherapie [German;
Trigger Point Therapy]. Bern, Switzerland: Hans Huber, 2003.
49. Ferguson LW, Gerwin R. Clinical Mastery in the Treatment of
Myofascial Pain. Philadelphia, PA: Lippincott Williams & Wilkins, 2005.
50. Kostopoulos D, Rizopoulos K. The Manual of Trigger Point and
Myofascial Therapy. Thorofare, NJ: Slack, 2001.
51. Prateepavanich P Myofascial Pain Syndrome:A Common Problem
in Clinical Practice. Bangkok, Thailand: Ammarind,1999.
52. Rachlin ES, Rachlin IS. Myofascial Pain and Fibromyalgia: Trigger
Point Management. St. Louis, MO: Mosby, 2002.
53. Cardinal S. Points Detente et Acupuncture: Approche Neurophysiologique [French; Trigger Points and Acupuncture: Neurophys iological Approach]. M ont real, Canada: Centre
Collegial de Developpement de Materiel Didactique, 2004.
54. Jonckheere PDM. Spieren en Dysfuncties, Trigger punten, Basisprincipes van de Myofasciale Therapie [Dutch; Muscles and
Dysfunctions, Basic Principles of Myofascial Therapy]. Brussels,
Belgium: Satas,1993.
55. Lucas KR, Polus BI, Rich PS. Latent myofascial trigger points: Their
effect on muscle activation and movement efficiency. J Bodywork
Mov Ther 2004;8:160-166.
56. Weissmann RD. Uberlegungen zur Biomechanik in der Myo-faszialen
Triggerpunkttherapie [German; Considerations with regard to the
biomechanics related to myofascial trigger point
Myofascial Trigger Points: An Evidence-Informed R e v i e w / 215
therapy]. Physiotherapie 2000;35(10):13-21.
57. Vecchiet L, Giamberardino MA, De Bigontina P. Comparative sensory
evaluation of parietal tissues in painful and nonpainful areas in
fibromyalgia and myofascial pain syndrome. In: Gebhart GF, Hammond
DL, Jensen TS, eds. Proceedings of the 7th World Congress on Pain
(Progress in Pain Research and Management). Seattle, WA: IASP Press,
1994:177-185.
58. Vecchiet L, Giamberardino MA, Dragani L. Latent myofascial trigger
points: Changes in muscular and subcutaneous pain thresholds at
trigger point and target level. JManual Medicine 1990;5:151-154.
59. Vecchiet L, Pizzigallo E, Iezzi S, Affaitati G, Vecchiet J, Giamberardino MA. Differentiation of sensitivity in different tissues and
its clinical significance. J Musculoskeletal Pain 1998;6:33-45.
60. Dommerholt J. Persistent myalgia following whiplash. Curr Pain
Headache Rep 2005;9:326-330.
61. Ge HY, Fernandez-de-las-Penal C, Arendt-Nielsen L. Sympathetic
facilitation of hyperalgesia evoked from myofascial tender and trigger
points in patients with unilateral shoulder pain. Clin Neurophysiol
2006;117:1545-1550.
62. Lidbeck J. Central hyperexcitability in chronic musculoskeletal pain: A
conceptual breakthrough with multiple clinical implica-tions. Pain Res
Manag 2002;7(2):81-92.
63. Munglani R. Neurobiological mechanisms underlying chronic whiplash
associated pain: The peripheral maintenance of central sensitization. J
Musculoskeletal Pain 2000;8:169-178.
64. Dommerholt J, Issa T. Differential diagnosis: Myofascial pain. In: Chaitow
L, ed. Fibromyalgia Syndrome: A Practitioner's Guide to
Treatment. Edinburgh, UK: Churchill Livingstone,
2003:149-177.
65. Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz R. Inter-rater
reliability in myofascial trigger point examination. Pain 1997;69(12):65-73.
66. Sciotti VM, Mittak VL, DiMarco L, Ford LM, Plezbert J, Santipadri E,
Wigglesworth J, Ball K. Clinical precision of myofascial trigger point
location in the trapezius muscle. Pain 2001;93(3):259-266.
67. Franssen JLM. Handboek Oppervlakte Elektromyografie [Dutch; Manual
Surface Electromyography]. Utrecht, The Netherlands: De
Tijdstroom,1995.
68. Janda V. Muscle spasm: A proposed procedure for differential diagnosis.
JManual Med 1991;6:136-139.
69. Mense S. Pathophysiologic basis of muscle pain syndromes. In: Fischer
AA, ed. Myofascial Pain: Update in Diagnosis and Treat-ment.
Philadelphia, PA: W.B. Saunders Company, 1997:23-53.
70. Headly BJ. Evaluation and treatment of myofascial pain syndrome utilizing
biofeedback. In: Cram JR, ed. Clinical Electromyogra-phy for Surface
Recordings. Nevada City, NV: Clinical Resources, 1990:235-254.
71. Headly BJ. Chronic pain management. In: O'Sullivan SB, Schmitz IS, eds.
Physical Rehabilitation: Assessment and Treatment. Philadelphia,
PA: F.A. Davis Company, 1994:577-600.
72. Gerwin RD, Duranleau D. Ultrasound identification of the
myofascial trigger point. Muscle Nerve 1997;20:767-768.
73. Hong CZ. Persistence of local twitch response with loss of conduction to
and from the spinal cord. Arch Phys Med Rehabil 1994;75:12-16.
74. Hong C-Z, Torigoe Y. Electrophysiological characteristics of
localized twitch responses in responsive taut bands of rabbit
skeletal muscle. J Musculoskeletal Pain 1994;2:17-43.
75. Hong C-Z, Yu J. Spontaneous electrical activity of rabbit trig-
2 1 6 / T h e J o u r n a l o f M a n u a l & M a n i p u l a t i v e T h e r a p y, 2 0 0 6
gar spot after transaction of spinal cord and peripheral nerve. J
Musculoskeletal Pain 1998:6(4):45-58.
76. Fricton JR. Auvinen MD. Dvkstra D, Schiffman E. Myofascial pain
syndrome: Electrom yographic changes associated with local twitch
response. Arch Phys Med Rehabil 1985;66:314-317.
77. Simons DG, Dexter JR. Comparison of local twitch responses elicited by
palpation and needling of myofascial trigger points. J Musculoskeletal
Pain 1995:3:49-61.
78. Wang F, Audette J. Electrophysiological characteristics of the local twitch
response with active myofascial pain of neck compared with a control
group with latent trigger points. Am J Phys Med Rehabil 2000;79:203.
79. Audette JF, Wang F, Smith H. Bilateral activation of motor unit potentials
with unilateral needle stimulation of active myofascial trigger points. Am
J Phys Med Rehabil 2004;83:368-374, quiz 375-377,389.
80. Dommerholt J. Dry needling in orthopedic physical therapy practice.
Orthop Phys Ther Pract 2004;16(3):15-20.
81. Hong C-Z. Lidocaine injection versus dry needling to myofascial trigger
point: The importance of the local twitch response. Am J Phys Med
Rehabil 1994;73:256-263.
82. Gerwin RD, Dommerholt J. Treatment of myofascial pain syn-dromes. In:
Boswell MV, Cole BE, eds. Weiner's Pain Manage-ment: A Practical
Guide for Clinicians. Boca Raton, FL: CRC Press, 2006:477-492.
83. Vecchiet L, Dragani L, De Bigontina P, Obletter G, Giamberardino MA.
Experimental referred pain and hyperalgesia from muscles in humans.
In: Vecchiet L, et al, eds. New Trends in Referred Pain and
Hyperalgesia. Amsterdam, The Netherlands: Elsevier Science,
1993:239-249.
84. Vecchiet L, Giamberardino MA. Referred pain: Clinical significance,
pathophysiology and treatment. In: Fischer AA, ed. Myofascial Pain:
Update in Diagnosis and Treatment. Philadelphia, PA: W.B. Saunders
Company, 1997:119-136.
85. Mense S. The pathogenesis of muscle pain. Curr Pain Headache Rep
2003;7:419-425.
86. Mense S. Referral of muscle pain: New aspects. Amer Pain Soc J
1994;3:1-9.
87. Fernandez-de-las-Penal CF, Cuadrado ML, Gerwin RD, Pareja JA.
Referred pain from the trochlear region in tension-type headache: A
myofascial trigger point from the superior oblique muscle.
Headache 2005;45:731-737.
88. Fernandez-de-las-Penal C, Cuadrado ML, Gerwin RD, Pareja JA.
Myofascial disorders in the trochlear region in unilateral migraine:
A possible initiating or perpetuating factor. Clin J Pain 2006;22:548553.
89. Hwang M, Kang YK, Kim DH. Referred pain pattern of the pronator
quadrates muscle. Pain 2005;116:238-242.
90. Hwang M, Kang YK, Shin JY, Kim DH. Referred pain pattern of the
abductor pollicis longus muscle. Am J Phys Med Rehabil
2005;84:593-597.
91. Hong CZ, Kuan TS, Chen JT, Chen SM. Referred pain elicited by palpation
and by needling of myofascial trigger points: A comparison. Arch
Phys Med Rehabil 1997;78:957-960.
92. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns.
I: A study in normal volunteers. Spine 1990;15:453-457.
93. Giamberardino MA, Vecchiet L. Visceral pain, referred hyperal-gesia
and outcome: New concepts. Eur J Anaesthesiol (Suppl) 1995;10:61-66.
94. Scudds RA, Landry M, Birmingham T, Buchan J, Griffin K. The
frequency of referred signs from muscle pressure in normal healthy
subjects (abstract). JMusculoskeletalPain 1995;3 (Suppl. 1):99.
95. Torebjork HE, Ochoa JL, Schady W. Referred pain from intra-neural
stimulation of muscle fascicles in the median nerve. Pain
1984;18:145-156.
96. Gibson W, Arendt-Nielsen L, Graven-Nielsen T. Referred pain and
hyperalgesia in human tendon and muscle belly tissue. Pain
2006;120(1-2):113-123.
9 7 . Gibson W, Arendt-Nielsen L, Graven-Nielsen T. Delayed onset muscle
soreness at tendon-bone junction and muscle tissue is associated with
facilitated referred pain. Exp Brain Res 2006 (In press).
98. Hendler NH, Kozikowski JG. Overlooked physical diagnoses in chronic
pain patients involved in litigation. Psychosomatics 1993;34:494501.
99. Weiner DK, Sakamoto S, Perera S, Breuer P. Chronic low back pain in
older adults: Prevalence, reliability, and validity of physi-cal
examination findings. JAm Geriatr Soc 2006;54:11-20.
100. Calandre EP, Hidalgo J, Garcia-Leiva JM, Rico-Villademoros F
Trigger point evaluation in migraine patients: An indication of
peripheral sensitization linked to migraine predisposition? Ear J
Neurol 2006;13:244-249.
101. Headache Classification Subcommittee of the International
Headache Society: The international classification of headache
disorders. Cephalalgia 2004;24(Suppl l):9-160.
102. Fricton JR, Kroening R, Haley D, Siegert R. Myofascial pain syn-drome
of the head and neck: A review of clinical characteristics of 164
patients. Oral Surg Oral Med Oral Pathol 1985;60:615-623.
103. Gerwin R. A study of 96 subjects examined both for fibromy-algia and
myofascial pain (abstract). J Musculoskeletal Pain 1995;3(Suppl
1):121.
104. Rosomoff HL, Fishbain DA, Goldberg N, Rosomoff RS. Myofascial findings
with patients with chronic intractable benign pain of the back and neck.
Pain Management 1989;3:114-118.
105. Skootsky SA, Jaeger B, Oye RK. Prevalence of myofascial pain in
general internal medicine practice. WestfMed 1989;151:157-160.
106. Chaiamnuay P, Darmawan J, Muirden KD, Assawatanabodee P.
Epidemiology of rheumatic disease in rural Thailand: A WHO-ILAR
COPCORD study. Community Oriented Programme for the Control of
Rheumatic Disease. J Rheumatol 1998;25:1382-1387.
107. Graft-Radford B. Myofascial trigger points: Their importance and
diagnosis in the dental office. J Dent Assoc S Air 1984;39:249-253.
108. Bajaj P, Bajaj P, Graven-Nielsen T, Arendt-Nielsen L. Trigger points in
patients with lower limb osteoarthritis. J Musculosk-eletal Pain
2001;9(3):17-33.
109. Hsueh TC, Yu S, Kuan TS, Hong C-Z. Association of active myofascial
trigger points and cervical disc lesions. J Formosa Med Assoc
1998;97(3):174-80.
110. Wang C-F, Chen M, Lin M-T, Kuan T-S, Hong C-Z. Teres minor
tendinitis manifested with chronic myofascial pain syndrome in the
scapular muscles: A case report. J Musculoskeletal Pain
2006;14(1):39-43.
111. Fricton JR. Etiology and management of masticatory myofascial
pain. JMusculoskeletal Pain 1999;7(112):143-160.
112. Teachey WS. Otolaryngic myofascial pain syndromes. Curr Pain
Headache Rep 2004;8:457-462.
113. Dommerholt J. El syndrome de dolor miofascial en la region
craneomandibular. [Spanish; Myofascial pain syndrome in the
craniomandibular region]. In: Padros Serrat E, ed. Bases
diagnosticas, terapeuticas y posturales del functionalismo
craniofacial. Madrid, Spain: Ripano, 2006:564-581.
114. Hesse J, Mogelvang B, Simonsen H. Acupuncture versus
meto-prolol in migraine prophylaxis: A randomized trial of trigger
point inactivation. J Intern Med 1994;235:451-456.
115. Skubick DL, Clasby R, Donaldson CC, Marshall WM. Carpal tunnel
syndrome as an expression of muscular dysfunction in the neck. J
Occupational Rehab 1993;3:31-43.
116. Treaster D, Marras WS, Burr D, Sheedy JE, Hart D. Myofascial
trigger point development from visual and postural stressors during
computer work. J Electromyogr Kinesiol 2006;16:115-124.
117. Baker BA. The muscle trigger: Evidence of overload injury. J Neurol
Orthop Med Surg 1986;7:35-44.
118. Fruth SJ. Differential diagnosis and treatment in a patient with
posterior upper thoracic pain. Phys Ther 2006;86:254-268.
119. Doggweiler-Wiygul R. Urologic myofascial pain syndromes. Curr Pain
Headache Rep 2004;8:445-451.
120. Jarrell J. Myofascial dysfunction in the pelvis. Curr Pain
Head-ache Rep 2004;8:452-456.
121. Jarrell JF, Vilos GA, Allaire C, Burgess S, Fortin C, Gerwin R, Lapensee L, Lea
RH, Leyland NA, Martyn P, Shenassa H, Taenzer P, Abu-Rafea B.
Consensus guidelines for the management of chronic pelvic pain. J
Obstet Gynaecol Can 2005;27:869-887.
122. Weiss JM. Pelvic floor myofascial trigger points: Manual therapy for
interstitial cystitis and the urgency-frequency syndrome. J Urol
2001;166:2226-2231.
123. Dommerholt J. Muscle pain syndromes. In: Cantu RI, Grodin AJ, eds.
Myofascial Manipulation. Gaithersburg, MD: Aspen, 2001:93-140.
124. Weiner DK, Schmader KE. Postherpetic pain: More than sensory
neuralgia? Pain Med 2006;7:243-249; discussion 250.
125. Chen SM, Chen JT, Kuan TS, Hong C-Z. Myofascial trigger points in
intercostal muscles secondary to herpes zoster infection of the intercostal
nerve. Arch Phys Med Rehabil 1998;79:336-338.
126. Dommerholt J. Complex regional pain syndrome. Part 1: His-tory,
diagnostic criteria and etiology. J Bodywork Mov Ther 2004;8:167-177.
127. Rashiq S, Galer BS. Proximal myofascial dysfunction in complex
regional pain syndrome: A retrospective prevalence study.
Clin J Pain,1999;15:151-153.
128. Prateepavanich P, Kupniratsaikul VC. The relationship between
myofascial trigger points of gastrocnemius muscle and nocturnal calf
cramps. JMed Assoc Thailand 1999;82:451-459.
129. Kern KU, Martin C, Scheicher S, Muller H. Auslosung von Phan
tomschmerzen and -sensationen lurch Muskulare Stumpftriggerpunkte nach Beinamputationen [German; Referred pain from
amputation stump trigger points into the phantom limb]. Schmerz
2006;20:300-306.
130. Kern U, Martin C, Scheicher S, M ller H. Does botulinum toxin A
make prosthesis use easier for amputees? J Rehabil Med
2004;36:238-239.
131. Longbottom J. A case report of postulated "Barre Lieou syn-drome."
Acupunct Med 2005;23:34-38.
132. Stellon A. Neurogenic pruritus: An unrecognized problem? A
retrospective case series of treatment by acupuncture. Acupunct Med
2002;20:186-190.
133. Fernandez-de-las-Penas C, Fernandez-Carnero J, Miangolarra-
Page JC. Musculoskeletal disorders in mechanical neck pain:
Myofascial trigger points versus cervical joint dysfunction. J
Musculoskeletal Pain 2005;13(1):27-35.
134. Hagg GM. Ny forklaringsmodell for muskelskador vid statisk belastning
i skuldra och nacke [Swedish; New explanation for muscle damage
as a result of static loads in the neck and shoulder]. Arbete
Manniska Miljo 1988;4:260-262.
135. Henneman E, Somjen G, Carpenter DO. Excitability and inhibitability of motoneurons of different sizes. J Neurophysiol
1965;28:599-620.
136. Hagg GM. The Cinderella Hypothesis. In: Johansson H, et al, eds.
Chronic Work-Related Myalgia. Gavle, Sweden: Gavle University Press,
2003:127-132.
137. Armstrong RB. Initial events in exercise-induced muscular injury.
Med Sci Sports Exerc 1990;22:429-435.
138. Hagg GM. Human muscle fibre abnormalities related to occupational load. Ear J Appl Physiol 2000;83(2-3):159-165.
139. Kadi F, Hagg C, Hakansson R, Holmner S, Butler-Browne CS, Thornell
LE. Structural changes in male trapezius muscle with work-related
myalgia. Acta Neuropathol (Ben) 1998;95:352-360.
140. Kadi F, Waling K, Ahlgren C, Sundelin C, Holmner S, Butler-Browne CS,
Thornell LE. Pathological mechanisms implicated in localized female
trapezius myalgia. Pain 1998;78:191-196.
141. Larsson B, Bjork J, Kadi F, Lindman R, Gerdle B. Blood supply and
oxidative metabolism in muscle biopsies of female cleaners with and
without myalgia. Clin J Pain 2004;20:440-446.
142. Henriksson KG, Bengtsson A, Lindman R, Thornell LE. Morpho-logical
changes in muscle in fibromyalgia and chronic shoulder myalgia, In:
Vaeroy H, Merskey H, eds. Progress in Fibromyalgia and Myofascial
Pain. Amsterdam, The Netherlands: Elsevier, 1993:61-73.
143. Lexell J, Jarvis J, Downham D, Salmons S. Stimulation-induced damage
in rabbit fast-twitch skeletal muscles: A quantitative morphological
study of the influence of pattern and frequency. Cell Tissue Res
1993;273:357-362.
144. Gissel H. Cat+ accumulation and cell damage in skeletal muscle
during low frequency stimulation. EurfAppl Physiol 2000;83(23):175-180.
145. Gissel H, Clausen T. Excitation-induced Ca(2+) influx in rat soleus
and EDL muscle: Mechanisms and effects on cellular integrity. Am J
Physiol Regal Integr Comp Physiol 2000;279: R917-924.
146. Febbraio MA, Pedersen BK. Contraction-induced myokine
production and release: Is skeletal muscle an endocrine organ? Exerc
Sport Sci Rev 2005;33(3):114-119.
147. Pedersen BK, Febbraio M. Muscle-derived interleukin-6: A pos-sible
link between skeletal muscle, adipose tissue, liver, and brain. Brain
Behav Immun 2005;19:371-376.
148. Forsman M, Birch L, Zhang Q, Kadefors R. Motor unit recruit-ment in
the trapezius muscle with special reference to coarse arm movements.
JElectromyogr Kinesiol 2001;11:207-216.
149. Forsman M, Kadefors R, Zhang Q, Birch L, Palmerud G. Motor-unit
recruitment in the trapezius muscle during arm movements and in
VDU precision work. Int J Ind Ergon 1999;24:619-630.
150. Forsman M, Taoda K, Thorn S, Zhang Q. Motor-unit recruitment during
long-term isometric and wrist motion contractions: A study
concerning muscular pain development in computer operators. Int
11nd Ergon 2002;30:237-250.
151. Zennaro D, Laubli T, Krebs D, Klipstein A, Krueger H. Continu-ous,
intermitted and sporadic motor unit activity in the trape-
2 1 8 / Th e J o u r n a l of M a n u a l & M a n i p u l a t i v e T h e r a p y, 2 0 0 6
zius muscle
prolonged computer work. J Electromyogr
Kinesiol 2003:13:113-124.
152. Zennaro D, Laubli T. Krebs D. Krueger H, Klipstein A. Trapezius muscle
motor unit activity in symptomatic participants during finger
tapping using properly and improperly adjusted desks. Hum Factors
2004:46:252-66.
153. Andersen JH, Kaergaard A. Rasmussen K. Myofascial pain in different
occupational groups with monotonous repetitive work (abstract). J
Musculoskeletal Pain 1995;3(Suppl 1):57.
154. Chen S-M, Chen J-T, Kuan T-S, Hong J, Hong C-Z. Decrease in
pressure pain thresholds of latent myofascial trigger points in the
middle finger extensors immediately after continuous piano practice.
J Musculoskeletal Pain 2000;8(3):83-92.
155.Otten E. Concepts and models of functional architecture in skeletal
muscle. Exerc Sport Sci Rev 1988;16:89-137.
156. Sjogaard G, Lundberg U, Kadefors R. The role of muscle activity and
mental load in the development of pain and degenerative processes at
the muscle cell level during computer work. Ear J Appl Physiol
2000;83(2-3):99-105.
157. Sjogaard G, Sogaard K. Muscle injury in repetitive motion disorders.
Clin Orthop 1998;351:21-31.
158. Simons DG. Understanding effective treatments of myofascial trigger
points. J Bodywork Mov Ther 2002;6:81-88.
159. Proske U, Morgan DL. Stiffness of cat soleus muscle and tendon during
activation of part of muscle. JNeurophysiol 1984;52:459-468.
160. Trotter JA. Functional morphology of force transmission in skeletal
muscle: A brief review. Acta Anat (Basel) 1993;146(4):205-222.
161. Monti RJ, Roy RR, Hodgson JA, Edgerton VR. Transmission of forces
within mammalian skeletal muscles. J Biomech 1999;32:371-380.
162. Bodine SC, Roy RR, Eldred E, Edgerton VR. Maximal force as a
function of anatomical features of motor units in the cat tibialis
anterior. J Neurophysiol 1987;57:1730-1745.
163.Ounjian M, Roy RR, Eldred E, Garfinkel A, Payne JR, Armstrong A, Toga
AW, Edgerton VR. Physiological and developmental implications of
motor unit anatomy. J Neurobiol 1991;22:547-559.
164. Petit J, Filippi GM, Emonet-Denand F, Hunt CC, Laporte Y. Changes in
muscle stiffness produced by motor units of dif-ferent types in
peroneus longus muscle of cat. J N e u r o p h y s i o l 1990;63:190-197.
165. Petit J, Filippi GM, Gioux M, Hunt CC, Laporte Y. Effects of tetanic
contraction of motor units of similar type on the initial stiffness to
ramp stretch of the cat peroneus longus muscle. J N e u r o p hy s i o l
1990;64:1724-1732.
166. Altringham JD, Bottinelli R. The descending limb of the sarco-mere
length-force relation in single muscle fibres of the frog. J Muscle Res
Cell Motil 1985;6:585-600.
167. Street SF. Lateral transmission of tension in frog myofibers: A
myofibrillar network and transverse cytoskeletal connections are
possible transmitters. J Cell Physiol 1983;114:346-364.
168. Denoth J, Stussi E, Csucs C, Danuser C. Single muscle fiber
contraction is dictated by inter-sarcomere dynamics. J Theor Biol
2002;216(1):101-122.
169. Dommerholt J, Royson MW, Whyte-Ferguson L. Neck pain and
dysfunction following whiplash. In: Whyte-Ferguson L, Gerwin RD,
eds. Clinical Mastery of Myofascial Pain Syndrome. Balti-more, MD:
Lippincott, Williams & Wilkins, 2005:57-89.
170. Jull GA. Deep cervical flexor muscle dysfunction in whiplash. J
Musculoskeletal Pain 2000;8(112):143-154.
171. Kumar S, Narayan Y, Amell T. Analysis of low velocity frontal
impacts. Clin Biomech 2003;18:694-703.
172. Sterling M, Jull G, Vicenzino B, Kenardy J, Darnell R. Development of motor system dysfunction following whiplash injury.
Pain 2003;103(1-2):65-73.
173. Sterling M, Jull G, Vicenzino B, Kenardy J, Darnell R. Physical and
psychological factors predict outcome following whiplash injury. Pain
2005;114(1-2):141-148.
174. Schuller E, Eisenmenger W, Beier G. Whiplash injury in low speed car
accidents. JMusculoskeletal Pain 2000;8(112):55-67.
175. Simons DG. Triggerpunkte and Myogelose [German; Trigger points
and myogeloses]. Manuelle Medizin 1997;35:290-294.
176. Gerwin RD, Dommerholt J. Myofascial trigger points in chronic cervical
whiplash syndrome. JMusculoskeletal Pain 1998;6(Suppl. 2):28.
177. Fernandez-de-las-Penas C, Fernandez-Carnero J, Palomeque-del-Cerro
L, Miangolarra-Page JC. Manipulative treatment vs. conventional
physiotherapy treatment in whiplash injury: A randomized controlled
trial. J Whiplash Rel Disord 2004;3(2):73-90.
178. Fernandez-de-las-Penas C, Palomeque-del-Cerro L, Fernandez-Carnero
J. Manual treatment of post-whiplash injury. JBodywork Mov Ther
2005;9:109-119.
179. Simons DG, Travell J, Myofascial trigger points: A possible
explanation. Pain 1981;10:106-109.
180. Sterling M, Jull G, Vicenzino B, Kenardy J. Sensory hypersen-sitivity
occurs soon after whiplash injury and is associated with poor
recovery. Pain 2003;104:509-517.
181. Scott D, Jull G, Sterling M. Widespread sensory hypersensitiv-ity is a
feature of chronic whiplash-associated disorder but not chronic
idiopathic neck pain. Clin J Pain 2005;21:175-181.
182. Vecchiet L, Vecchiet J, Bellomo R, Giamberardino MA. Muscle pain from
physical exercise. J Musculoskeletal Pain 1999;7(112):43-53.
183. Simons DG. Review of enigmatic MTrPs as a common cause of
enigmatic musculoskeletal pain and dysfunction. JElectromyogr Kinesiol
2004;14:95-107.
184. Gerwin RD, Dommerholt J, Shah J. An expansion of Simons' integrated
hypothesis of trigger point formation. Curr Pain Headache Rep
2004;8:468-475.
185. Newham DJ, Jones DA, Clarkson PM. Repeated high-force ec-centric
exercise: Effects on muscle pain and damage. J Appl Physiol
1987;63:1381-1386.
186. Friden J, Lieber RL. Segmental muscle fiber lesions after repeti-tive
eccentric contractions. Cell Tissue Res 1998;293:165-171.
187. Stauber WT, Clarkson PM, Fritz VK, Evans WJ. Extracellular matrix
disruption and pain after eccentric muscle action. JAppl Physiol
1990;69:868-874.
188. Graven-Nielsen T, Arendt-Nielsen L. Induction and assessment of muscle
pain, referred pain, and muscular hyperalgesia. Curr Pain Headache Rep
2003;7:443-451.
189. Lieber RL, Shah S, Friden J. Cytoskeletal disruption after ec-centric
contraction-induced muscle injury. Clin Orthop 2002;403: 590-599.
190. Lieber RL, Thornell LE, Friden J. Muscle cytoskeletal disruption occurs
within the first 15 min of cyclic eccentric contraction. J Appl Physiol
1996;80:278-284.
191. Barash IA, Peters D, Friden J, Lutz GJ, Lieber RL. Desmin cytoskeletal
modifications after a bout of eccentric exercise in the rat. Am J Physiol
Regul Integr Comp Physiol 2002;283:
R958-R963.
192. Thompson JL, Balog EM, Fitts RH, Riley DA. Five myofibrillar
lesion types in eccentrically challenged, unloaded rat adductor longus
muscle: A test model. Anat Rec 1999;254:39-52.
193. Lieber RL, Friden J. Mechanisms of muscle injury gleaned from
animal models. Am JPhys MedRehabil 2002;81(11 Suppl):570-579.
194. Peters D, Barash IA, Burdi M, Yuan PS, Mathew L, Friden J, Lieber RL.
Asynchronous functional, cellular and transcriptional changes after a
bout of eccentric exercise in the rat. J Physiol 2003;553(Pt 3):947957.
195. Bowers EJ, Morgan DL, Proske U. Damage to the human quad-riceps
muscle from eccentric exercise and the training effect. J Sports Sci
2004;22(11-12):1005-1014.
196. Byrne C, Twist C, Eston R. Neuromuscular function after exercise-induced
muscle damage: Theoretical and applied implications. Sports Med
2004;34(1):49-69.
197. Hamlin MJ, Quigley BM. Quadriceps concentric and eccentric exercise.
2: Differences in muscle strength, fatigue and EMC activity in
eccentrically-exercised sore and non-sore muscles. J Sci Med Sport
2001;4(1):104-115.
198. Pearce AJ, Sacco P, Byrnes ML, Thickbroom GW, Mastaglia FL. The
effects of eccentric exercise on neuromuscular function of the biceps
brachii. J Sci Med Sport 1998;1(4):236-244.
199. Shah JP, Phillips TM, Danoff JV, Gerber LH. An in-vivo microanalytical technique for measuring the local biochemical milieu of
human skeletal muscle. J Appl Physiol 2005;99:1980-1987.
200. Itoh K, Okada K, Kawakita K. A proposed experimental model of myofascial
trigger points in human muscle after slow eccentric exercise. Acupunct
Med 2004;22(1):2-12; discussion 12-13.
201. Bruckle W, Suckfull M, Fleckenstein W, Weiss C, Muller W. Gewebep02-Messung in der verspannten Ruckenmuskulatur (m. erector
spinae) [German; Tissue p02 in hypertonic back muscles]. Z.
Rheumatol 1990;49:208-216.
202. McCleskey EW, Gold MS. Ion channels of nociception. Anna Rev Physiol
1999;61:835-856.
203. Sluka KA, KalraA, Moore SA. Unilateral intramuscular injections of
acidic saline produce a bilateral, long-lasting hyperalgesia. Muscle
Nerve 2001;24:37-46.
204. Sluka KA, Price MP, Breese NM, Stucky CL, Wemmie JA, Welsh MJ.
Chronic hyperalgesia induced by repeated acid injections in muscle is
abolished by the loss of ASIC3, but not ASIC1. Pain 2003;106:229-239.
205. Weeks VD. Travell J. How to give painless injections. In: AMA Scientific
Exhibits. New York, NY: Grune & Stratton, 1957:3 18-322
206. Hubbard DR, Berkoff GM. Myofascial trigger points show spontaneous needle EMG activity. Spine 1993;18:1803-1807.
207. Couppe C, Midttun A, Hilden J, Jorgensen U, Oxholm P, FuglsangFrederiksen A. Spontaneous needle electromyographic activity in
myofascial trigger points in the infraspinatus muscle: A blinded
assessment JMusculoskeletal Pain 2001;9(3):7-17.
208. Simons DG. Do endplate noise and spikes arise from normal motor
endplates? Am J Phys Med Rehabil 2001;80:134-140.
209. Simons DG, Hong C-Z, Simons LS. Endplate potentials are common
to midfiber myofascial trigger points. Am J Phys Med Rehabil
2002;81:212-222.
210. Macgregor J, Graf von Schweinitz D. Needle electromyographic
activity of myofascial trigger points and control sites in equine
cleidobrachialis muscle: An observational study. Acupunct Med
2006;24(2):61-70.
211. Mense S. Neurobiological basis for the use of botulinum toxin in pain
therapy. JNeurol 2004;251(Suppl.1):I1-7.
212. De Paiva A, Meunier FA, Molgo J, Aoki KR, Dolly JO. Functional repair of
motor endplates after botulinum neurotoxin type A poisoning: Biphasic
switch of synaptic activity between nerve sprouts and their parent
terminals. Proc Natl Acad Sci USA 1999;96:3200-3205.
213. Chen BM, Grinnell AD. Kinetics, Cat+ dependence, and biophysi-cal
properties of integrin-mediated mechanical modulation of transmitter
release from frog motor nerve terminals. JNeurosci 1997;17:904-916.
214. Grinnell AD, Chen BM, Kashani A, Lin J, Suzuki K, Kidokoro Y. The role of
integrins in the modulation of neurotransmitter release from motor nerve
terminals by stretch and hypertonicity. J Neurocytol 2003;32(5-8):489503.
215. Kashani AH, Chen BM, Grinnell AD. Hypertonic enhancement of
transmitter release from frog motor nerve terminals: Cat+ independence
and role of integrins. J Physiol 2001;530(Pt 2):243-252.
216. Wang K, Yu L. Emerging concepts of muscle contraction and clinical
implications for myofascial pain syndrome (abstract). In: Focus on Pain.
Mesa, AZ: Janet G. Travell, MD Seminar Series, 2000.
217. Bukharaeva EA, Salakhutdinov RI, Vyskocil F, Nikolsky EE. Spontaneous
quantal and non-quantal release of acetylcho-line at mouse endplate
during onset of hypoxia. Physiol Res 2005;54:251-255.
218. Hoheisel U, Mense S, Simons D, Yu X-M. Appearance of new receptive fields in
rat dorsal horn neurons following noxious stimulation of skeletal muscle:
A model for referral of muscle pain? Neurosci Lett 1993;153:9-12.
219. Simons DG, Stolov WC. Microscopic features and transient contraction
of palpable bands in canine muscle. Am JPhysMed 1976;55:65-88.
220. Reitinger A, Radner H, Tilscher H, Hanna M, Windisch A, Feigl W.
Morphologische
Untersuchung
an
Triggerpunkten
[German;
Morphological investigation of trigger points]. ManuelleMedizin
1996;34:256-262.
221. Windisch A, Reitinger A, Traxler H, Radner H, Neumayer C, Feigl W, Firbas
W. Morphology and histochemistry of myogelosis. Gun Anat 1999;12:266271.
222. Mense S, Simons DG, Hoheisel U, Quenzer B. Lesions of rat skeletal muscle
after local block of acetylcholinesterase and neu-romuscular stimulation.
J Appl Physiol 2003;94:2494-2501.
223. Pongratz D. Neuere Ergebnisse zur Pathogenese Myofaszi-aler
Schmerzsyndrom [German; New findings with regard to the etiology of
myofascial pain syndrome]. Nervenheilkunde 2002;21(1):35-37.
224. Pongratz DE, Spath M. Morphologic aspects of muscle pain syndromes.
In: Fischer AA, ed. Myofascial Pain: Update in Diagnosis and
Treatment. Philadelphia, PA: W.B. Saunders Company, 1997:55-68.
225. Gariphianova MB. The ultrastructure of myogenic trigger points in
patients with contracture of mimetic muscles (abstract). J Musculoskeletal
Pain 1995;3(Suppl 1):23.
226. Glogowsky C, Wallraff J. Emn Beitrag zur Klinik and Histologie der
Muskelharten (Myogelosen) [German; A contribution on clinical aspects and
histology of myogeloses]. Z Orthop 1951;80:237-268.
227. Fassbender HG. Morphologic and Pathogenese des Weichteilrheumatismus [German; Morphology and etiology of soft
220 / Th e J ou rn a l of M a n u a l & M a n i p u la t i ve Th era p y, 20 0 6
tissue rheurnati m]. Z eumaforsch 1973;32:355-374.
228. Hubbard DR. Chronic and recurrent muscle pain: Pathophysi-ology
and treatment. and review of pharmacologic studies. J
Musculoskeletal Pain 1' 6:4:123-143.
229. Lewis C, Gevirtz R, Hubbard D, Berkoff G. Needle trigger point and
surface frontal EMG measurements of psychophysiological responses
in tension-type headache patients. Biofeedback & Self Regulation
1994:3:274-275.
230. McNulty WH, Gevirtz RN. Hubbard DR, Berkoff GM. Needle
electromyographic evaluation of trigger point response to a
psychological stressor. Psychophysiology 1994;31:313-316.
231. Banks SL, Jacobs DW, Gevirtz R, Hubbard DR. Effects of auto-genic
relaxation training on electromyographic activity in active myofascial
trigger points. JMusculoskeletal Pain 1998;6(4):23-32
232. Chen JT, Chen SM, Kuan TS, Chung KC, Hong C-Z. Phentolamine effect on
the spontaneous electrical activity of active loci in a myofascial trigger
spot of rabbit skeletal muscle. Arch PhysMed Rehabil 1998;79:790794.
233. Chen SM, Chen JT, Kuan TS, Hong C-Z. Effect of neuromuscular blocking
agent on the spontaneous activity of active loci in a myofascial trigger
spot of rabbit skeletal muscle. JMusculosk-eletal Pain 1998;6(Suppl.
2):25.
234. Bowman WC, Marshall IG, Gibb AJ, Harborne AJ. Feedback control of
transmitter release at the neuromuscular junction. Trends Pharmacol
Sci 1988;9(1):16-20.
235. Cunha FQ, Lorenzetti BB, Poole S, Ferreira SH. Interleukin-8 as a
mediator of sympathetic pain. Br J Pharmacol 1991;104:765-767.
236. Verri WA, Jr., Cunha TM, Parada CA, Poole S, Cunha FQ, Fer-reira SH.
Hypernociceptive role of cytokines and chemokines: Targets for
analgesic drug development? Pharmacol Ther 2006 (In press).
237. Poole S, de Queiroz Cunha F, Ferreira SH. Hyperalgesia from
subcutaneous cytokines. In: Watkins LR, Maier SF, eds. Gytokines and
Pain. Basel, Switzerland: Birkhaueser,1999:59-87.
238. Fernandez HL, Hodges-Savola CA. Physiological regulation of G4 AChE
in fast-twitch muscle: Effects of exercise and CGRP. J Appl
Physiol 1996;80:357-362.
239. Hodges-Savola CA, Fernandez HL. A role for calcitonin gene-related
peptide in the regulation of rat skeletal muscle G4
acetylcholinesterase. Neurosci Lett 1995;190(2):117-20.
240. Fernandez-de-las-Penas C, Alonso-Blanco C, Cuadrado ML, Gerwin
RD, Pareja JA. Trigger points in the suboccipital muscles and forward
head posture in tension-type headache. Headache 2006;46:454-460.
241. Gerwin RD. Factores que promueven la persistencia de
mialgia en el syndrome de dolor miofascial y en la fibromyalgia
[Span-ish; Factors that promote the continued existence of myalgia in
myofascial pain syndrome and fibromyalgia]. Fisioterapia
2005;27(2):76-86.
242. Gerwin RD. A review of myofascial pain and fibromyalgia: Factors that
promote their persistence. Acupunct Med 2005;23(3):121-134.
243. Andres E, Loukili NH, Noel E, Kaltenbach G, Abdelgheni MB, Perrin
AE, Noblet-Dick M, Maloisel F, Schlienger JL, Blickle JF Vitamin B12
(cobalamin) deficiency in elderly patients. GMAJ 2004;171:251-259.
244. Pruthi RK, Tefferi A. Pernicious anemia revisited. MayoGumProc
1994;69:144-150.
245. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis
D in patients with persistent, nonspecific musculoskeletal pain.
Mayo Clin Proc 2003;78:1463-1470.
246. Bogduk N, Simons DG. Neck pain: Joint pain or trigger points. In: Vaeroy
H, Merskey H, eds. Progress in Fibromyalgia and Myofascial Pain.
Amsterdam, The Netherlands: Elsevier,1993:267- . 273.
247. Padamsee M, Mehta N, White GE. Trigger point injection: A neglected
modality in the treatment of TMJ dysfunction. JPedod 1987;12(1):72-92.
248. Linton SJ. A review of psychological risk factors in back and neck pain.
Spine 2000;25:1148-1156.
249. Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in
chronic musculoskeletal pain: A state of the art Pain 2000;85:317-332.
250. Menefee LA, Cohen MJ, Anderson WR, Doghramji K, Frank ED, Lee H.
Sleep disturbance and nonmalignant chronic pain: A comprehensive
review of the literature. Pain Med 2000;1:156-172.
251. Bauermeister W. Diagnose and Therapie des Myofaszialen
Triggerpunkt Syndroms lurch Lokalisierung and Stimulation
sensibilisierter Nozizeptoren mit fokussierten elektrohydraulische
Stosswellen (German; Diagnosis and therapy of myofascial trigger point
symptoms by localization and stimulation of sensitized nociceptors
with focused ultrasound shockwaves]. Medizinisch-Orthopadische
Technik 2005;5:65-74.
252. Muller-Ehrenberg H, Licht G. Diagnosis and therapy of myofascial pain
syndrome with focused shock waves (ESWT). MedizinischOrthopddische Technik 2005;5:1-6.
Myofascial Pain Syndrome
Trigger Points
David G. Simons
Jan Dommerholt
INTRODUCTION
This issue has what are, to our knowledge, a
number of noteworthy firsts. The Macgregor
and Graf von Schweinitz study of equine
myofascial trigger points [TrPs] not only introduces to the scientific literature the fact that
horses are quite prone to developing disabling
TrPs, but they also added substantiation to the
association of TrPs with endplate noise. Kao,
Hsieh, Kuo, and Hong did a well-controlled
study electromyographically establishing that a
pain acupuncture site was also always a TrP,
further strengthening the association of endplate
noise and TrPs. The fact that the reason ergonomics
is so critical for relieving musculoskeletal pain
in the workplace is because it addresses
perpetuating factors that aggravate the TrPs that
are causing the pain. Dainoff, Cohen, and Dainoff
reported the presence of TrPs and the tests that
detect restricted range of motion caused by them
in a remarkably thorough study of this all-toocommon pain problem with equally remarkable
results.
Five articles [with many more on the way]
from Spanish physical therapists are making it
unmistakably clear that for the first time, TrPs are
shown experimentally to be a major factor in
most headaches and from some previously
unidentified muscles. Several articles describ
ing the successful treatment of phantom and
stump pain with botulinum toxin injections in
TrPs by Kern and colleagues offer hope for
many patients with amputated limbs and persistent phantom pain. The systematic mapping of
TrPs responsible for phantom pain is another first!
The rate of progress [this is the result of
publications that have been newly identified in
only two months] in this field is most remarkable
[DGS and JD].
Each article review indicates whether it is
prepared by Simons [DGS] or Dommerholt
[JD].
RESEARCH STUDIES
Kao MJ, Hsieh YL, Kook FJ, Hong CZ:
Electrophysiological assessment of acupuncture points. Am J Phys Med Rehabil 85(5):
443-448, 2006.
Summary
Physiatrists in Taiwan examined by needle
electromyography [EMG] an acupuncture point and
a nearby non-acupuncture control site in a
randomly chosen tibialis anterior muscle for the
presence of endplate noise [EPN] characteristic
of myofascial trigger points [TrPs] in 10
David G. Simons, MD, Clinical Professor [voluntary], Department of Rehabilitation Medicine, Emory University,
Atlanta, GA.
Jan Dommerholt, PT, MPS, Bethesda PhysioCare, Bethesda, MD.
Address correspondence to: David G. Simons, MD, 3176 Monticello Street, Covington, GA 30014-3535 [E-mail:
loisanddavesimons @ earthlink. net] or Jan Dommerholt. PT, MPS. 7830 Old Georgetown Road, Suite C-15. Bethesda,
MD 20814 [E-mail: dommerholt@painpoints.com].
Journal of Musculoskeletal Pain, Vol. 15(1) 2007
Available online at http://jmp.haworthpress.com 2007 by
The Haworth Press, Inc. All rights reserved.
doi: 10. 1300/J094v 15n01 08
JOURNAL OF MUSCULOSKELETAL PAIN
male and 10 female normal volunteers. Each
site was explored for endplate noise by slowly
advancing the electromyographic needle as
previously described for TrPs. Following this, all
sites were examined for the following clinical
evidence of a TrP: the most tender spot in a
palpable taut band that referred pain to the ankle
and foot and responded to snapping palpation
with a local twitch. Endplate noise was found at
acupuncture sites in 25 percent of both male and
female subjects, and in non-acupuncture sites in six
percent of male and one percent of female subjects.
The difference between the two kinds of sites was
statistically significant [P < 0.001]. Every time
the needle approached one of the 127 acupuncture
sites and resulted in the appearance of EPN, the
subject reported pain, soreness, or an unpleasant
feeling. This experience is comparable to the
"Ah-Shi" [that's it] effect characteristic of
acupuncture sites and was reported in only seven
of the 826 times that the needle did not
encounter EPN. Subjects found the sensation
when a local twitch response was elicited by the
needling a TrP to be comparable to the "De-Qui"
effect of acupuncture.
Comments
The authors are to be highly congratulated for
this first controlled well-designed study
comparing acupuncture and TrP sites. This
study also, for the first time, provides an experimental answer to a tricky and controversial
question that the authors did not recognize.
They do point out how fatally and seriously
flawed previous studies have been that simply
review the literature and are based on false assumptions and they concluded that this study
demonstrates that the Stomach-36 acupuncture
sites [for treatment of pain] seem to be TrPs,
which supports the concept that some acupuncture
points are actually TrPs based primarily on the
strong, significant correlation between the
presence of EPN and the acupuncture points
compared to non-acupuncture points. This
conclusion is further supported by the correspondence of the Ah-Shi and De-Qui experiences
at both kinds of sites.
The authors also noted that this study
strongly supports the association of EPN with
TrPs, which is a basis for the integrated hypothesis
explanation of the cause of TrPs.
The fact that several non-acupuncture sites
showed EPN can be accounted for by another
interpretation. These sites may have been
subclinical TrPs that included a few muscle fibers
that had all of the dysfunctions of a TrP, but too
few of them were involved to be detected by
the limited sensitivity of the clinical examination
for TrPs. Not all TrP sites are also acupuncture
sites, but likely, most pain acupuncture sites are
also TrPs.
The data reported help to clarify another
controversial issue that was the used as the basis
for the rejection by one journal for the research
paper that established the close relationship
between EPN and TrPs. Is EPN only the result of
needle stimulation of a normal endplate, or does it
reveal an abnormality of endplate function that was
already present? It is not easy to design an
experiment to answer this question since the only
way you can detect the EPN is by placing the
needle close to the endplate and needle
pressure increases the amount of EPN.
The presence of EPN at acupuncture sites
demonstrated that they were in an endplate
zone, and the placement of the non-acupuncture
sites likely also placed them in the endplate zone.
Since exactly the same search procedure was
used at both kinds of sites, the needle should
have encountered a nearly equal numbers of
endplates. The fact that so few of the nonacupuncture [non-TrP] endplate encounters
responded to needle approach with EPN is strong
evidence that the presence of the needle alone was
usually inadequate mechanical stimulus to produce
EPN in most normal endplates. Therefore, the EPN
that was observed was usually preexisting and was
caused by the TrP abnormality, not just by the
presence of the needle. If this degree of mechanical
stimulation did happen occasionally, or the
needle encountered a particularly sensitive
endplate, it could account for the occasional
presence of EPN at non-acupuncture sites. [DGS]
Literature Reviews
Macgregor J, Graf von Schweinitz D: Needle
electromyographic activity of myofascial
trigger points and control sites in equine
cleidobrachialis muscle-an
observational
study. Acupunct Med 24(2): 61-70, 2006.
Summary
allow the activity to stabilize. The needles in the
control and TrP sites were connected to a twochannel EMG machine and recorded
simultaneously.
Three items were listed: the appearance of
continuous spontaneous electrical activity [EPN] of
at least 10 pV more than control baseline activity
[generally 20 pV greater], the appearance of
irregular spike activity [usually negative first and
biphasic] of at least 100 pV, and the occurrence of
local twitch responses. These three data were
combined for all four horses. Differences of P <
0.05 between TrP and control sites were considered
statistically significant.
Endplate noise sometimes reached 80 pV, and
endplate spikes, 1,000 pV. A typical recording is
included. All three phenomena observed were
significantly more common at the TrP sites than at
control sites. Although the authors used the
outmoded SEA [spontaneous electrical activity]
terminology instead of the more specific EPN
designation for the first item reported, they did
recognize from the literature that they were actually
dealing with EPN. They were not aware of the
more recent literature that has adopted the EPN
designation and the paper that justifies that
change (1,2). The presence at control sites of
EMG recordings typical of TrPs may have been
because the horse muscle is large enough that early
or small or deep TrPs may not be clinically
identifiable. The surprisingly high level [four
times what has usually been seen in human and
rabbit studies] of background noise at control sites
may have been because the horses were
standing, fully alert, on the legs being tested. The
EPN often disappeared if the needle was advanced
or withdrawn a few millimeters, consistent with
its endplate origin. Although there were only
four subjects, the results- were statistically
significant. The authors also noted that blinding of examiners would be desirable.
A veterinary physiotherapist and acupuncturist in the United Kingdom explored the
electromyographic [EMG] and other characteristics of myofascial trigger points [TrPs] in
equine muscle compared to normal muscle. They
examined the cleidobarachialis division of the
brachiocephalic muscle of four thoroughbred
horses that had been retired from active duty and
were being seen for treatment of chronic pain
signs and impaired performance. The muscle was
examined bilaterally at two acupuncture sites for
TrPs. The sites were approved, with the owners'
informed consent, for the administration of
acupuncture-like treatment with an EMG needle
exploring for endp late noise and local twitch
responses without equine sedation. Initially, a very
tender spot in a palpable taut band in the muscle
identified a TrP. Its precise location was found by
the very limited range along the taut band that responded with a maximum twitch response to
snapping palpation. Of course, the location of
induced pain and its familiarity could not be determined, but it is unlikely the horses would fake
the local sensitivity, the twitch response is objective
evidence, and the musculoskeletal functional
disability for which the horses were being seen for
treatment was very real to the owners. Needles
were inserted only at acupuncture sites that were
suitable for treatment, which were LI16 and LI17
using the transpositional acupoints system. L116
was chosen as the MTrP site in all four horses, and
for a clinically TrP-free EMG control site, L117
was chosen in three horses, and ST 10 was used in
one horse that had a TrP at L117.
A 50 mm long concentric Teflon coated dis- Comments
posable EMG needle was used to record EMG
activity at each test site. Each TrP region and each
This is, to my knowledge, the first research
acupuncture control site was explored for electrical paper ever published on the presence of TrPs in
activity by inserting the needle in five directions: horses and earns our hearty CONGRATUperpendicularly, and at 45 degrees in four
quadrants. Each needle insertion was tested for
EMG at five depths, roughly 1 cm
apart, and was advanced slowly with rotation to
minimize insertional activity and twitch responses [instead of endplate noise [EPN]. When
activity appeared the needle was left in situ to
LATIONS. Dr. Janet Travell often described her
treatment of TrPs in her beloved horses. This
paper takes a large second step of further EMG
substantiation of the strong association of
EPN with TrPs. This part of the paper reinforces
the basic concept of the integrated hypothesis,
which still needs much additional research to fully
complete the picture (1). The
descriptions and illustration of EPN and spikes are
fully consistent with the extensive experience of
Hong, Lois Statham Simons, and me, when we
were intensively studying TrPs in human and
rabbit subjects from 1993 through 1995 (3). We
hope the authors will continue this kind of
research and make the considerable additional
effort required to conduct a controlled blinded
study of the effectiveness of acupuncture
treatment of TrPs in their horse patients. It would
be another major contribution to the veterinary and
TrP literature. [DGS]
Fernandez de las Peiias C, Cuadrado ML,
Gerwin RD, Pareja JA. Myofascial disorders
in the trochlear region in unilateral migraine: a
possible initiating or perpetuating factor. Clin
J Pain 22(6): 548-553, 2006.
Summary
This physiotherapist from Spain and three
neurologists report an unprecedented exami nation
of the superior oblique muscle [SOM] of the eye
bilaterally for myofascial trigger points [TrPs] in
20 patients [seven men and 13 women] with
unilateral migraine attacks and in 20 age and
gender matched healthy control subjects. All
subjects were examined by a blinded
examiner and patients examined at least one
week following a migraine attack to avoid
migraine-related allodynia and in a headache-free
status. The trochlear region of the eyeball was
examined for trochlear region [SOM]
tenderness, referred pain evoked by digital
pressure maintained for 30 seconds, increased
referred pain in response to contraction of the
SOM [downward and medial gaze], and increased
referred pain due to stretching it [upward and lateral
gaze]. A definite TrP was identified if both
contraction and stretching of the SOM increased
pain. Response to only one maneuver identified a
probable TrP. Patient rec
ognition of evoked referred pain as familiar
during a migraine attack identified an active TrP,
otherwise it was considered latent. Four visual
analog scale estimates of pain level were made by
subjects on initial trochlear pressure, after 30
seconds of pressure, and in response to contracting
or stretching the SOM.
All migraine patients had local trochlear-region
tenderness, more on the symptomatic side [VAS
4.8] compared to the asymptomatic side [VAS
2.2] [P<0.001]. Sixteen patients [80 percent]
perceived referred pain when pressure was
maintained for 30 seconds [VAS 5.2], described as
a tightening sensation in the retro-orbital region
that sometimes extended to the supraorbital
region and even the homolateral forehead. This
pain was evoked only from an eye on one side
in all patients. Fifteen patients [75 percent] had
definite TrPs, 10 of these patients had active TrPs,
and five had latent TrPs. In all of these cases, the
TrPs were ipsilateral to the side of the headache.
The presence of TrPs was essentially the same in
patients with or without aura. The intensity of
local pain responses to testing in controls was
significantly lower than patient responses on the
symptomatic side [P < 0.001], but equal to those
on the asymptomatic side. Five control subjects
reported local pain on SOM examination that
rated them as probable TrPs that were all Latent.
Future studies are needed to clarify the cause/
effect relationship between the SOM TrPs and
headaches. These studies include treatment
effects.
Comments
This outstandingly well-designed, innovative
study is a sequel to a previous report of SOM
TrPs in patients with tension type headache, that
described similar pain patterns (4).1 often
wondered why the extraocular muscles didn't have
TrPs that caused referred pain. I just didn't look
hard enough. Devin Starlanyl told me how she
screens for TrPs in the other extraocular muscles
and occasionally finds them by having the
patient gaze in each of the four directions [up,
down, left, and right] sequentially for painfully
restricted range of motion. Apparently there are
very few headaches, including migraine, that do
not have a significant TrP component (5). Eighty
percent of the
patients with migraine had clinical evidence of TrPs research group, it appears that suboccipital
muscles play a role in the etiology of episodic
in the SOM. [DGS]
tension-type headaches. As these muscles are not
directly palpable, it is conceivable that other
Fernandez de las Penas C, Alonso Blanco C,
structures in the suboccipital region could also
Cuadrado ML, Pareja JA: Myofascial trigger
contribute to the perception of referred pain even
points in the suboccipital muscles in episodic
though the authors attempted to minimize its
tension-type headache. Man Ther 11: 225-230,
likelihood. Future studies should be
2006.
expanded and
include other posterior neck muscles, a larger
Summary
sample size, and other types of headaches. [JD]
In this study, ten subjects with episodic tensiontype headaches [ETTH] and ten healthy age- and
sex-matched controls were examined for the
presence of myofascial trigger points [TrPs] in
the rectus capitis posterior minor, rectus capitis
posterior major, and oblique capitis superior by
an examiner who was blinded to the subjects'
condition using modified criteria by Simons,
Travell, and Simons, and by Gerwin et al. (6,7).
Since these suboccipital muscles are not directly
palpable, subjects were asked to extend the neck
from a neutral spine position, once the examiner
had elicited referred pain by compression in the
area between the occiput and the posterior arch of
the atlas. The active cervical-occipital extension
allowed the examiner to palpate for active
contractions. The presence or absence of familiar
referred pain similar to pain during headache
attacks determined whether TrPs were classified
as active of latent respectively. On the day of the
examination, all ETTH subjects received a
headache diary to record the daily headache
intensity, duration, and the days with headache for
a period of four weeks.
All ETTH subjects had TrPs in the suboccipital muscles; six subjects [60 percent] had
active and four subjects [40 percent] had latent
TrPs. Two control subjects [20 percnet] had latent
TrPs. Differences between groups were
significant for the presence of active TrPs. The
headache intensity, frequency, and duration in the
ETTH group did not depend on whether TrPs
were active or latent.
Fernandez de las Penas C, Alonso Blanco C,
Alguacil Diego IM, Miangolarra Page JC:
Myofascial trigger points and postero-anterior
joint hypomobility in the mid-cervical spine in
subjects presenting with mechanical neck
pain; a pilot study. J Manual Manipulative
Ther 14(2): 88-94, 2006.
Summary
Thirty patients with mechanical neck pain
referred by their primary care physician were
included in this study. Mechanical neck pain was
defined as "generalized neck and/or shoulder pain
with mechanical characteristics including
symptoms provoked by maintained neck
postures, by neck movement, or by palpation of the
cervical muscles." One physical therapist
examined each subject for the presence of
myofascial trigger points [TrPs] in the upper
trapezius, sternocleidomastoid, and levator muscles
according to the criteria by Simons, Travell, and
Simons, and by Gerwin et al. (6,7). The researchers
used an algometer to reproduce familiar referred
pain. A second physical therapist, blinded to the
findings of the first therapist, examined the
cervical spine from C3 to C7 for the presence of
posterior-anterior hypomobility as described by
Maitland (8).
The mean number of TrPs was 3.4 [2.3 latent and
1.1 active] with most TrPs in the sternocleidomastoid muscle [left: 66.6 percent, right:
83.3 percent], followed by the trapezius
[left: 70.0 percent, right: 63.3 percent], and the
Comments
levator scapulae [left: 30.0 percent, right: 26.6
The authors recognized that the limited sample percent]. Sixteen subjects had right-sided joint
size designates this study basically as a pilot study hypomobility and 14 presented with left-sided
hypomobility with the C3 segment most comwith limited power. Combined with the
many other headache studies by this monly involved [80 percent] followed by C4
[20 percent]. The authors could not determine a
statistically significant relationship between the
number of TrPs in the examined muscles and the
presence of hypomobility at the C3 and C4
vertebrae.
In the discussion section the authors addressed several aspects of muscle and joi nt dysfunction in the cervical spine and reviewed in
detail the discrepancies between the current
study and a previous study from the same research group reporting a significant relationship
between the number of TrPs in the upper
trapezius muscle and C3 and C4 hypomobility (9).
In the previous study, they employed the lateral
gliding test and included 150 subjects versus 30
in the current study [9].
Comments
It is encouraging to see that one of the world's
leading manual therapy journals published this
excellent article on the relationship between TrPs
and cervical hypomobility. Even though this study
could not determine statistical significance, the
authors emphasized that the mere presence of
TrPs and joint dysfunction dictates that in clinical
practice both muscles and joints need to be
addressed. It is our impression that until recently,
the manual physical therapy community has not
focused on TrPs. The many clinically relevant
studies by this Spanish research group certainly will
facilitate a re-orientation that can only benefit our
patients. [JD]
without referred pain with snapping palpation. A
point in the right tibialis anterior muscle was used as
a control point. Subjects rated their resting pain on a
visual analog scale before any measurements were
taken. The researchers determined the pressure
pain threshold [PPT] for all three points using an
algometer during normal respiration and during
induced elevated intrathoracic pressure [EITP],
which is described as a maneuver that increases
the sympathetic outflow to the skeletal muscle
when holding one's breath with the glottis
closed. With this maneuver it is possible to
determine the effect of increased sympathetic
outflow on the mechanical sensitivity of TrPs.
In the second phase of the study, the PPT and the
pressure threshold for eliciting referred pain
[PTRP] were determined in eleven subjects.
Next the local pain and referred pain intensities
were measured at the TrP during normal
respiration and during EITP during application
of pressure equal to 1.5 X PTRP. After all
measures were completed, a local twitch
response was elicited in the active TrP using an
acupuncture needle.
The authors concluded that increasing sympathetic outflow to the muscle decreased PPT,
PTRP, and increased local and referred pain intensities at both TeP and TrP [P < 0.001 for all
four comparisons]. They offered several conceivable mechanisms for the observed sensitivity,
including a change in the local chemical milieu at
the TePs and TrPs due to increased
vasoconstriction, an increased sympathetic release
of noradrenaline, or an increased sensitivity to
noradrenaline.
Ge HY, Fernandez de las Peflas C, ArendtNielsen L: Sympathetic facilitation of hyperalgesia evoked from myofascial tender and Comments
trigger points in patients with unilateral
This is an important study that provides for the
shoulder pain. Clin Neurophysiol 117(7):
first time experimental evidence of sympathetic
1545-1550, 2006.
facilitation of mechanical sensitization of TrPs.
Previous studies demonstrated that exposing
Summary
subjects with active TrPs in the upper trapezius
Twenty-one female subjects with chronic muscles to stressful tasks consistently increased
unilateral shoulder pain were included in this the electrical activity in TrPs, while autogenic
study. To be included in the study, the subjects relaxation was able to reverse the effects (10-13).
needed to have an active myofascial trigger The authors offer several possible mechanisms
point [TrP] in one of the infraspinatus muscles that differ from previous suggestions that the
using the criteria of Simons, Travell, and autonomic contributions
Simons (7). A tender point [TeP] in the contra
lateral infraspinatus muscle was identified. A TeP
was defined as a point within a taut band but
Literature Reviews
may be due to muscle spindle activity or activity of
adrenoreceptors on the motor nerve terminal.
(11,14).
The authors' choice of characterizing a tender
point in a taut band as a "TeP" is rather confusing, as
these points seem to meet the criteria for latent
TrPs as defined by Simons, Travel], and Simons
(7). It gets even more confusing when the authors
seem to equate these TePs or latent TrPs with
fibromyalgia TePs in the discussion section of
this paper. While it is conceivable that some
fibromyalgia syndrome TePs may indeed be
TrPs, the mixed use of these terms only contributes
to confusion (15). Notwithstanding the confusing
terminology, this study does offer support for
autonomic influences on TrPs. [JD]
stump end. The TrPs that caused toe projections were usually more distal than those with
tibia] referred pain/sensation patterns. Thirty
percent of the TrPs were located in the dorsolateral aspect of the stump and 18 percent were in
the medio-ventral part, presumable because of
greater muscle mass, but conceivably because of
more dorsal nerve dis tributions in the leg. Ventral
TrP did cause dor
sal phantom pain in some instances. The authors
concluded that latent TrPs may contribute to
phantom pain and sensations and speculated
whether TrP pain and phantom pain may develop
from a shared etiology.
Comments
This and other articles from the same authors [also
reviewed in this column] are very encouraging and
should provide hope for thousands of patients
suffering from daily phantom pain. A survey of
American veterans revealed that 78 percent of
respondents experienced phantom pain (16). To
the best of our knowledge, this is the first study that
systematically examined the role of TrPs in
phantom pain phenomena. While the exact
Summary
mechanism of action may require further studies,
the results of this study justify examining and
Based on their experiences with the treatment of
treating patients with phantom pain with
phantom and stump pain using botulinum toxin
inactivation of TrPs. [JD]
injections into myofascial trigger points [TrPs],
the authors completed a systematic analysis of the
local and referred pain patterns of stump TrPs. Arokoski JP, Surakka J, Ojala T, Kolari P,
Thirty subjects with leg amputations [ 12 Jurvelin JS: Feasibility of the use of a novel soft
transfemoral, 18 transtibial] were examined for tissue stiffness meter. Physiol Meas 26(3):
TrPs. After determining the five most symptomatic 215-228,2005.
TrPs, the subjects were asked to localize areas of
stump pain, phantom pain, and sensations in the Summary
phantom limb.
This is a form of tissue compliance meter.
Interestingly, patients were not aware of the
Usually
these meters measure the force required
presence of the TrPs. Yet, pain sensations were
commonly seen in as many as 20 out of 30 pa- to push a plunger a measured distance into the
tients with 60 out of 150 TrPs producing tissue, which is a measure of tissue stiffness. The
phantom sensations and 17 causing phantom pain. plunger usually is advanced step-wise through a
Fourteen TrPs caused involuntary stump hole in a footplate, which provides a skin-surface
movements and 10 produced stump fasci- reference for measuring the force of indentation.
culations. Phantom phenomena were most This provides data for constructing an X-Y plot of
commonly seen in the toes [62.8 percent] and the indentation distance versus force required.
midfoot [ 17.9 percent] with the remainder more These authors devised a similar device that
proximal. Approximately 70 percent of the TrPs measure both the amount of force being applied to
the skin with the plunger and to a footplate to keep
were in an area 3 to 7 cm from the
that presKern K-U, Martin C, Scheicher S, and Muller H:
Auslosung von Phantomschmerzen undsensationen durch muskulare Stumpftriggerpunkte nach Beinamputationen [in German:
Referred pain from amputation stump trigger
points into the phantom limb]. Schmerz
20(4): 300-306, 2006.
sure applied to the skin constant and then extended the plunger a fixed [unstated] distance for
the one measurement and recorded the re
sultant plunger force produce by that much indentation of the tissues with a measured constant
footplate pressure. The only variable available
with this system was a change in tissue pressure
against the plunger due to a change [or lack of
change] in the nature of what was being
measured.
The authors applied the device to a series of
elastamere samples of known elasticity, four
different neck and shoulder muscles bilaterally in
12 healthy subjects, and in 16 females with
chronic neck pain due to myofascial trigger
points [TrPs], during forearm voluntary muscle
contraction from rest to maximum effort, and
during different degrees of forearm venous
occlusion. Pressure pain thresholds and muscle
stiffness measures of the attachment TrP area of
the levator scapulae muscles were cornpared. A
linear relationship was found between indenter
force [muscle stiffness] and successive degrees
of voluntary muscle contraction [from 0 to
maximus] but a non-linear relationship with
different degrees of venous occlusion. The
indenter force recorded was different at different
muscle sites between about 5.5 [deltoid] to
about 7.5 [levator scapulae] Newtons. The
indenter force was 13.6 percent higher at the
levator scapulae sites that were on the side of the
smaller [more sensitive] pressure pain thresholds.
Assuming the text is correct and that the title of
Figure 2 is in error, the coefficients of variation
were nearly, or less than, 10 for inter- and intrarater stiffness readings on all muscles. The authors
concluded that this device is a simplified, reliable
way of taking tissue stiffness measurements.
Comments
This device is simpler but also provides a
more limited amount of information than previous
devices. The inter- and intra-reliability values
reported were good. Correlation coefficients
are simply the standard deviation corrected for
the average value and are most useful when you
are comparing sets of values for different
measurements that have different units. That
permitted comparison of reliability of pressure
pain thresholds with stiffness mea
sures. The fact that TrP sites in different muscles
have somewhat different stiffness values is no
surprise. The fact that the more tender TrPs exhibit
a greater stiffness is confirmation of the clinical
finding of a firmer palpable nodule in a more active
TrPs. The limited application of the device in this
study does not establish it as a reliable measure of
TrP activity because it did not test how well this
measure can distinguish the increased tension at
the TrP or of the taut band as compared to
surrounding tissue. It may or may not be as prone to
error as pain pressure threshold measurements
when the measurement i s not taken exactly the
point of maximum TrP tenderness, which would be
difficult to do. Properly administered, this factor
gives pain threshold measurements a high degree
of sensitivity to TrP activity. Being a different kind
of measure, this device may be useful in addition
to pain threshold measures for studying the
characteristics of taut bands throughout a
muscle. [DGS]
P. Dorsher: Trigger points and acupuncture
points: anatomic and clinical correlations.
Med Acupunct 17(3): 21-25, 2006.
Summary
This article compares the anatomical and
clinical relationships between myofascial trigger
points [TrP] described by Travell and Simons
and acupuncture points [AcP] described by the
Shanghai College of Traditional Medicine and
other acupuncture publications. An anatomical
correspondence was assumed when a TrP and
AcP were within a 2 cm radius of each other, and
the points entered the same muscle. A published
cross-sectional anatomic study of AcP was used
to determine whether AcPs were in the same
muscle as the corresponding TrPs. Differences in
depth were accepted. The author determined
whether AcPs with corresponding TrPs had
similar regional pain indications as the TrPs. In
addition, he determined whether there was any
overlap between the distributions of acupuncture
meridians and TrP referred pain patterns. The
degree of correspondences were graded on a
fivepoint scale ranging from excellent to none.
7
Literature Reviews
Of the 255 TrPs, only eight did not have an
anatomic correspondence with AcPs, and most of
these points were located in the medial
pterygoid, psoas, iliacus, subscapularis, and
obturator internus muscles, which the author
characterized as "not safely accessible by trigger
point injections." Fifteen percent of classical AcPs
with corresponding TrPs did not have similar
clinical pain indications. Referred pain patterns and
meridian distributions were nearly identical in 76
percent, partially identical in 14 percent, and had
no correspondence in 10 percent of comparable
points. After the author addressed possible
criticisms of this study, he concluded that "the
strong correspondence between trigger point
therapy and acupuncture should facilitate the
increased integration of acupuncture into
contemporary clinical pain management."
Comments
Dowsher has undertaken a very detailed and
consuming comparison between 255 TrPs and 386
AcPs. In addition to the current article, he
mentioned that he has prepared computer
graphic demonstrations of each of the 234 TrPAcP anatomic correspondences, and meridianreferred pain correlations. His findings are pretty
much in line with Melzack et al.'s conclusion
that there is a 71 percent overlap between TrPs and
AcPs (17). Dowsher dismissed Birch's arguments
that most AcPs are not used specifically for pain
indications (18).
Yet, it remains questionable whether it is
possible to assume distinct anatomical locations
of TrPs and use those in comparisons with other
points. In part the Trigger Point Manuals are to
blame for suggesting that TrPs have distinct
locations (7,19). Simons, Travell, and Simons
have described specific TrPs in numbered
sequences based on their "approximate order of
appearance," and may have contributed to the
widely accepted impression that indeed TrPs have
distinct anatomical locations (7). To this reviewer,
the detailed numbered descriptions of specific TrPs
in the Trigger Point Manuals are not consistent
with clinical practice. For example, Simons,
Travel], and Simons described seven TrPs in the
trapezius muscle. In clinical practice, one
frequently finds more TrPs in just the upper
part of the
muscle. The authors have used the terms "trigger
regions with distinctive pain patterns" and "TrPs"
somewhat interchangeable, which in fact may
add to the confusion.
The most striking aspect of this study are the
correspondences between known referred pain
patterns and described courses of meridians.
However, the same dilemma arises: Are referred pain patterns TrP-specific, or should they
be described for muscles in general or perhaps for
certain parts of muscles? Recent studies of
experimentally induced referred pain suggest
that individual referred pain patterns may be
characteristic of muscles rather than of TrPs
(20-23).
If one of the objectives of this paper is to increase the utilization of acupuncture into pain
management practice, it may be preferable to
conduct clinical outcome studies of the efficacy
of acupuncture in the treatment of persons with pain
conditions or investigate the nature of acupuncture
points as several researchers have attempted
(24-26). More research is needed to establish
whether TrPs can be categorized with distinctive
anatomical locations and whether referred pain
patterns are TrP-specific or muscle-specific,
before undertaking more such studies. As a side
note, all the muscles the author deemed not
safely accessible by TrP injections are
commonly needled in clinical practice. [JD]
TREATMENT STUDIES
Rodriguez Blanco CR, Hernandez J, Algaba C,
Fernandez M, de la Quintana M: Changes in
active mouth opening following a single
treatment of latent myofascial trigger points in
the masseter muscle involving post-isometric
relaxation
or
strain/counterstrain.
J
Bodywork Movement Ther 10(3): 197-205,
2006.
Summary
This study of 90 subjects [42 men, mean age 25
years] with a latent myofascial trigger point [TrP]
in the masseter muscle compared the immediate
effect on active mouth opening follow
ing a single treatment with either post-isomet-
ric relaxation or strain/counterstrain technique. The
subjects were healthy college students without
any restrictions in mouth opening. Trigger points
were identified using the Simons, Travell, and
Simons criteria (19). Subjects were excluded if
they had no TrP in the massetermuscle, a history
offibromyalgiasyndrome, whiplash, surgery in the
cranio-cervical region, or temporomandibular
disorders, or having undergone myofascial pain
therapy within the past month before the study.
Subjects were randomly assigned to one of
three groups. Groups one and two were treated
with post-isometric relaxation and strain/counterstrain, respectively, while the third group functioned as the control group that received no
treatment. Treatment by post-isometric relaxation
began with passive opening of the mouth to the
barrier, followed by a gentle isometric voluntary
contraction,
repeated
three
times.
Strain/counterstrain treatment began by the
therapist applying pressure to the masseter TrP by
pincer palpation until the subject felt pressure and
some pain. Then the subject was passively
positioned into a position of ease that reduced the
palpable tension and pain by around 75 percent,
which was usually ipsi-lateral side-flexion of
the cervical sine, and a slight mouth opening [5
to 8 mm]. Blinded evaluations of mouth opening
before treatment, and five minutes post-treatment
found an increase of 2.0 mm after postisometric
relaxation, 0.2 mm after strain/counterstrain, [P <
0.00 1], and 0.1 mm for the control group. Only
the group receiving post-isometric relaxation
showed a significant improvement in active mouth
opening.
Comments
Spain is becoming an important source of
high quality TrP research and this study follows the trend. To our knowledge, this is the
first blinded, randomized, controlled study
comparing the effectiveness of a manual treatment of TrPs that is comparable to strain/
counterstrain, and the results were more. dramatic than expected. The authors acknowledged that the results may not be typical of
symptomatic patient populations, as the subjects
were asymptomatic before the study. This
study had no assessment of follow-up results.
Yet, the study does demonstrate that latent TrPs may
be clinically relevant and can cause limitations in
range of motion consistent with Lucas et al.'s
findings (27). Several additional considerations
would have been of value in this study. Additional
measures of TrP tenderness [pressure pain
threshold] before and after treatment were lacking.
The authors did not include TrP examinations of
the temporalis and medial pterygoid muscles,
which share functions with the masseter. They
may have been more affected by the postisometric
relaxation
than
by
the
strain/counterstrain technique.
The question remains how actual patients
with limited mouth opening would respond to
either form of therapy, and we hope that this research team will consider this in future studies.
[DSG and JD]
Dainoff MJ, Cohen BGF, Dainoff MH: The
effect of an ergonomic intervention on
musculoskeletal, psychosocial, and visual
strain of VDT data entry work: the United
States part of the international study. Int J
Occup Saf Ergon 11(1): 49-63, 2005.
Summary
Twenty-six female employees of the Cincinnati Service Center of the United States Internal Revenue Service, who were entering data
from paper copy on old computer equipment that
required keyboard operation rather than mouse
operation, received extensive, intensive, and
relatively expensive ergonomic intervention and
training in three parts that also included
evaluation of multiple measures. Each subject
received optometrist-prescribed corrective lenses
whenever needed. Secondly, they were provided
a workstation ergonomically optimized with
fully adjustable ergonomic chairs, a push-button
motorized work surface height adjustment for
sitting or standing, a keyboards with three
interchangeable sections that could be lifted or
swiveled to fit the operators preferences, a
copyholder specially designed for this computer
application adjustable in viewing height and
angle; a custom-made monitor support, and an
adjustable footstool. Thirdly, training of subjects
in ergo-
nomic principles included classroom training.
initial on-site coaching, and subsequent followup coaching visits at workstations with receipt of a
periodic ergonomics newsletter. Measurements
were taken initially, one month after completion
of interventions, and six months after
completion of the study that included a final
interview.
Initial physical examinations were repeated by
blinded examiners at one month and one year
following all interventions. Examination for the
number of painful trigger points [TrPs] [no
additional details] reported 128, 34, and 17 on the
three successive examinations. Testing of
shoulder function endurance, palpation tenderness,
and mobility [no further details] for number of
positive responses, reported 13, 12, and 7 on
successive exams. Testing`the number of
participants who reported pain on passive
flexion, extension, side bending, or rotation of the
neck reported 19, 4, and I on successive exams.
Overall results for all three tests for all subjects
were statistically [P < 0.001] and clinically
significant. Pain scores [visual analog scale
0-100] were successively 36, 25, and 27 for pain
intensity, and 1.55, 0.97, and 0.92 for pain
frequency. Both measures showed statistically [P <
0.001] and clinically significant improvement
between initial values and at 30 days post
intervention, with no indication of return of pain
symptoms at one year. The estimated static load
obtained by observation of the subjects working
posture decreased significantly [P < 0.001] between
the first and second a d the improvement
maintained at the third evaluation. Head and
trunk postural angles showed similar improved
decreases, but should flexion increased, apparently
as an adaptation to the new keyboard. Frequency
of visual fatigue was reported as 11, 9 and 3;
burning/itching of eyes as 16, 5, 0; redness as 1 l,
3, 0; and hazy/double vision as 13, 7, 3. These are
statistically [P < 0.001 ] and clinically significant
improvements. Subject estimates of comfort resulting from ergonomic intervention improved
significantly [P < 0.001] between the first and
second examinations and maintained at the
third examination. Electromyographic evaluation
used a strange method of calculating muscle stress
from amplitude data that did not include power
spectrum analysis and got confusing results. At
the follow-up interview, all
2 3 available subjects were pleased with their
physical improvement and with this intervention:
several subjects experienced bolstered selfesteem because they had control of their work
environment.
The authors examined the economic value of this
intervention and discovered that the biggest gains
were in overhead costs such as training costs of
replacement employees, medical expenses, sick
leave, etc., items that are rarely included in
business organizational accounting systems and
are therefore unnoticed by management in this
context. The cost of this intervention was
estimated at $2,200 per employee, while the cost
of a single worker's compensation case could be as
high as $75,000. This does not include the value of
employee satisfaction and improvement in
lifestyle of employees who generalized the
ergonomic principles learned at work to their
home environment also.
Comments
This paper by members of the ergonomics
research center in Oxford Ohio is the most detailed, eloquent application of ergonomics I
have encountered. Most interestingly, a primary
set of results measures were examination for TrPs
per se, and two other musculoskeletal functional
measures that are widely recognized by clinicians
as being highly dependent on the activity level of
TrPs in the muscles being stretched.
Unfortunately the authors did not report the
criteria they used to identify an TrP. However,
this report is fully consistent with the experiences of
TrP-skilled clinicians working with this same type
of patient population. Since all of the ergonomic
interventions would also reduce TrP perpetuating
factors, although the authors did not point this out
in their paper and gave the subjects no specific
TrP therapy, the outstandingly good results
including marked reductions in the TrP counts and
the two associated physical examination
measures indicate that the muscle abuse imposed
by most current work station practices is a major
source of the musculoskeletal symptoms
responsible for the epidemic of workman's
compensation cases, lost work time, and workers'
musculoskeletal miseries. The results of this study
further indicate that effective resolution of this
problem
depends on ergonomic reform of much current
practice and most important that simply treating
the pain with analgesics or even inactivating just
the TrPs is not a long term solution unless the
perpetuating factors of work-station muscle
abuse are also eliminated. This study leaves
open the question of how much better the final
results would have been if the TrPs responsible for
the remaining musculoskeletal pain of these
subjects had also been inactivated by specific TrP
therapy. The remarkable and commonly
overlooked economic advantages to everyone
involved of investing in this level of ergonomic
practice were most impressive and need to
become a part of management thinking and
practice. Awareness of the role of TrPs in this
process helps everyone better understand the
basic nature of this common problem and the
appropriate solutions. [DGS]
Qerama E, Fuglsang-Frederiksen A, Kasch H,
Bach FW, Jensen TS: A double-blind,
controlled study of botulinum toxin A in
chronic myofascial pain. Neurology 67:
241-245,2006.
Summary
These neurologists and neurophysiologist from
Aarhus, Denmark have reported a randomized,
double-blind, controlled study by injecting either
botulinum toxin A [BTXA] or isotonic saline
solution into trigger points [TrPs] of the
infraspinatus muscle in 30 patients [18 female].
All patients had pain in shoulder referred to
the arm for at least six months with TrPs in the
ipsilateral infraspinatus muscle and a numerical
rating scale [NRS] of at least a 2 [0-10] level
pain. Exclusions included current alcohol or drug
abuse, participation in another research study,
reluctance to stop other therapies for project period,
and any TrPs in the ipsilateral trapezius,
supraspinatus, and teres muscles. A TrP was
identified by a painful spot in a palpable taut
band, recognition of current sensory complaints
with pressure applied to the tender spot, and if
referred pain was in the distribution expected
from a TrP in the infraspinatus muscle. The TrP
was considered stable if spontaneous pain scores
and range of motion improved by
less than 50 percent and pressure pain threshold and
tolerance increased less than 50 percent during
the one-week run-in period between the first and
second visit. At the second visit, each subject
received an injection at the TrP site, and fluid was
deposited in four sites in each of five directions.
Physical testing included limitation of the Mouth
Wrap-around Test and the Hand-to-shoulder
Blade Test. At the second visit, motor endplate
activity was recorded electromyographically in
10 of 13 patients and in 29 of 268 sites in the
BTXA group and a similar number in the
control group.
At the fourth [final] visit, there was a reduction
in the number of electromyographically active
[endplate noise] sites [P = 0.02] in the BTXA
group, but no change in the control group,
indicating that the BTXA had effectively
inactivated the motor endplates at that TrP.
There was no difference in the number of patients
in both groups who experienced at least 30
percent
pain
relief
following
treatment.
Examination of Figure E-F-1 available only at the
journal's website, showed that between the first
and fourth visits, spontaneous pain dropped in
median of NRS from 4.2 to 2.0 in BTXA subjects
and from 6 to 4 in control subjects [respectively
P < 0.05 and P < 0.01], which indicated a more
significant reduction of spontaneous pain reduction
in BTXA subjects. The NRS for evoked pain went
from 7.5 to 5.5 for BTXA subjects, and from 8 to
4.5 for control subjects. Both were statistically
significant [P < 0.01].
The following results were obtained by calculating the percentage change between the
measures at baseline and at the fourth visit from the
data listed in the tables available only from the
journal's website. The results are presented in
percent change between the baseline and fourth
visit results for each examination. Subject groups
are identified as BTXA subjects or control
subjects. Percent reduction in pain during the
Mouth Wrap-around Test 57/33, Hand to
Shoulder Blade Test [distance between hand spine
of scapula in mm] 22/10, pain during same test
67/30, increase in pressure pain detection
threshold [kPa] 8.7/20 and increase in pressure
tolerance threshold [kPa] 0.7/24 percent. The text
indicated that there was no significant difference in
these results except that the
BTXA group showed significant improvement in
range of motion during Hand to Shoulder Blade
testing [22/10 percent decrease]. The other test
commonly showed what was likely clinically
significant improvement with BTXAfree needling.
Comments
This flawed-design randomized, doubleblind,
controlled and poorly interpreted study is, to my
knowledge, the first explicitly TrP study to be
published in a mainstream neurology journal and
illuminates some important considerations in TrP
research. Since both test and control subjects
showed marked and comparable improvement, the
selection of that control methodology was
inappropriate, as the previous studies indicate
that it would be. The authors report that all 30 of
their chronic pain [longer than six months]
subjects had active TrPs in their infraspinatus
muscles on one side, but no TrPs in the upper
trapezius, supraspinatus, teres major, and teres
minor muscles. Clinicians familiar with patients
with myofascial pain of that muscle for that long
find it incredibly remarkable that the authors
could find so many subjects with no active TrPs
in any of those other muscles among only 57 candidates. This raises a question in their minds as to
the credibility of the examinations. The criteria for
identifying a TrP were appropriate and well
described, and explicitly identified active TrPs.
These authors made the common mistake that so
many authors make by not screened for all of the
TrPs that are contributing to the subjects' pain
complaint. This failure introduces potentially
critical uncontrolled variables. In that case, the
results of treatment of the TrPs in only one of the
muscles can be highly contaminated by pain from
remaining active TrPs. This study likely suffered
from this factor due to the limited identification of
other muscles which one would expect to harbor
TrPs in subjects with myofascial pain of this
degree of chronicity.
The authors report, not surprisingly, that injecting normal saline into the TrPs was nearly
equally as effective at reducing patient pain reports
as injecting BTXA. They noted in their
discussion that it is well established that the
needling procedure alone [dry needling, which is
also the nature of acupuncture] is as effective as
injecting any substance, including BTXA. If both
procedures were already fully effective, it is
questionable how valid the conclusions are that
are based on differences in the outcome. The
surprising thing was that the BTXA did provide
as much improvement as the saline. The one
item not reported that would have helped
greatly to evaluate the needle effect is how
frequently the needling in either group elicited
either a marked pain response and/or a local
twitch response. When this occurs the needling
is far more effective than when it does not occur. If
this was comparable in the two groups [and
based on the rigid protocol and total amount of
needling at each TrP site, it very likely was], one
would expect the needling to have been equally
and significantly effective in both groups.
The inclusion of the detection of endplate
noise as part of the protocol is to be highly complimented and assures us that the authors were
dealing with TrPs. Unfortunately, their reference
to the second edition of Volume I of the Trigger
PointManual had the right date, but the wrong first
author and an outmoded title. Two other papers
reviewed in this issue used that same measure.
The authors question the adequacy of the integrated hypothesis because they contend that if
the relief of pain was equally effective with or
without endplate noise, this indicates that pain
relief is not dependent on abnormal endplate
function. Although there was less difference
than the authors called to our attention or recognized,
we strongly agree that additional mechanisms very
likely contribute to the clinical phenomena
associated with TrPs. Pain is only one of them. It
appears that the serious motor dysfunctions [e.g.,
inhibition causing increased fatigability and
weakness_] that are common in latent TrPs do not
produce a clinical pain complaint. Why, at this
point, is anyone's guess. We only have a
hypothesis that serves as a starting point for the many
questions that need to be resolved before we have a
fully satisfactory understanding of TrPs and
heartily welcome any research that contributes
to that objective. [DGS]
Huuenin L, Brukner PD, McCroryg P,
Comments Smith P, Wajswelner H, Bennell K:
Effect of dry needling of gluteal muscles on
straight leg raise: a randomized, placebo
controlled, double blind trial. Br J Sports
Med 39(2): 84-90, 2005.
Summary
Fifty-nine athletes with hamstrings pain recruited
from Australian Rules football clubs,
advertisements, flyers, and private referral were
included in this study, which aimed to evaluate
the effects of therapeutic and placebo dry needling
on hip straight leg raising [SLR],
internal rotation [IR], muscle pain, and muscle
tightness. The symptoms had to be reproducible
with pressure over gluteal myofascial trigger points
[TrPs]. The SLR and IR were measured with
standardized methods validated for their reliability
before the start of the study. Pain and tightness
in the hamstrings and gluteals were assessed on
four unmarked 10 cm visual analog scales.
The dry needling procedures were performed
by the same researcher. The TrPs were identified
mostly in the upper outer buttock quadrant with
three to five TrPs per subject. Therapeutic
needling was performed with 0.30 tnm diameter
and 25 mm long acupuncture needles.
Reproduction of recognizable pain or visualization
of a local twitch response were used as indicators
of correct needle placement. The needle was
partially withdrawn and repeatedly advanced until
the pain resolved and no further twitches were
observed. Placebo needles were modified
acupuncture needles. The tip had been removed
and the needle was glued back into the shaft.
Placebo needling involved applying the tip of the
blunted needle to the skin over TrPs. The placebo
needling had been assessed for reliability in 10
volunteers and found to be reliable.
There were no significant changes in range of
motion in either group. The VAS scores did not
change significantly either for any of the resting
variables or for gluteal pain. Both groups did
have significant improvements in hamstrings
tightness, hamstrings pain, and gluteal tightness.
Measurements were taken before, immediately
after, and again after 24 and 72 hours.
This study is somewhat difficult to understand
and to evaluate. Both the therapeutic and placebo
group had similar outcomes. The authors raised the
possibility that limited range of motion may not
necessarily be associated with symptoms. But there
are other, more fundamental problems with this
study. Unfortunately, the authors did not indicate
which gluteal muscles were included in the
assessment or in the interventions. Which
particular gluteal TrP reproduced the hamstrings
pain? According to Travell and Simons, only TrPs
in the deeper portion of the gluteus mimimus refer
pain to the hamstring (19). Did the authors provoke
the familiar pain by applying pressure on a gluteus
minimus TrPs? If so, it would be impossible to
reach this TrP with a 25 mm long acupuncture
needle, especially in well-trained athletes with
presumably conditioned gluteal muscles.
There may have been other structures contributing to hamstrings pain, such as the sacrotuberous ligament, or sacroiliac joints, even
though the latter were excluded based on clinical
evidence. At the same time, there are many other
muscles that may need to be treated before
changes in range of motion would be measurable,
including the piriformis and other hip rotators, the
abductor magnus, and of course the hamstrings
themselves. Hamstrings pain is frequently due to
TrPs in the hamstrings or the adductor magnus, and
not from gluteal TrPs (28).
Another issue is whether the placebo needle
really provided a true placebo. The researchers did
stimulate the skin overlying TrPs, which may
implicate a-beta fibers, which in turn may have an
impact on the observed outcomes. Placebo needling
is inherently difficult to accomplish. The authors
suggested that the placebo stimulus may have
been equivalent to a needle penetration. [JD]
CASE STUDIES
Longbottom J: A case report of postulated
`Barre Lieou syndrome.' Acupunct Med
23(1): 34-38, 2005.
Summary
This United Kingdom physiotherapist describes a case diagnosed as Barre Lieou syn-
Literature Reviews
drome with severe occipital and temporal headaches
of 9-10 intensity on a verbal score of 0 to 10, visual
disturbances, and breathing difficulty after a fall on
her left outstretched arm two years ago. At the age of
10 she fell out of a tree, fractured her skull, and
remained unconscious for several weeks, but was
deemed to have fully recovered. Recent referrals to
the Chronic Pain Clinic, ear nose throat
specialists, and for chiropractic and osteopathic
treatments had been of no help. Lately she had
overwhelming physical inability to cope with
even minor chores and reported a feeling
helplessness and loss of control with impaired
memory. Her general practitioner gave her the
diagnoses of depression and anxiety, and she
reported panic attacks and a feeling of inability to
cope.
She had symptoms and findings consistent with
the diagnoses of Barre Lieou syndrome and of
complex regional pain syndrome of the left arm,
serious articular dysfunctions from T2 to T8, and
active myofascial trigger points [TrPs] in three
neck muscles, which on palpation, reproduced
labored breathing and swallowing difficulties with
increased occipital pain. Previous chiropractic
manipulations were of no help at best. Treatment
began with acupuncture treatments selected to relieve
her high level of anxiety and poor sleep, and it
specifically avoided spinal manipulation because
of the severely restricted range of motion imposed by
both joint and muscle involvements. By the third
treatment additional acupuncture sites were
included to reduce pain and normalize her breathing.
The patient had improved in these issues sufficiently
that during the 12th through 15th treatments the
therapist needled TrPs in the sternocleidomastoid,
scalene, trapezius, and levator scapulae muscles
bilaterally. The procedure elicited a jump reaction.
The patient required daily myofascial stretch and
exercise regimes in order to keep pain and anxiety at
reasonable levels. On reassessment at 18 weeks,
the patient was again working full time, sleeping,
and maintaining an improved lifestyle with control of
her pain without opioids. Although the TrPs were
not active, they were threateningly latent.
Comments
This is an outstanding example of effective
management of a very complex neuromusculoskeletal pain and dysfunction problem that
combined judicious selection of a combination of
acupuncture and TrP treatments with avoidance of
counterproductive spinal manipulation in this case.
No mention was made of investigation of
perpetuating factors of the remaining TrPs such as
foot dysfunctions, unequal leg or pelvic lengths,
vitamin inadequacies, anemia, or low thyroid
function that could very likely have needed
attention. Patients benefit greatly by close
cooperation between a competent physical
therapist like this and a patient-orientedphysician
sensitive to these systemic perpetuating factors.
[DSG]
Kern U, Martin C, Scheicher S, Muller H:
Langzeitbehandlung von Phantom- and
Stumphschmerzen mit Botulinumtoxin Typ A
uber 12 Monate. Eine erste klinische
Beobachtung [in German: Long-term treatment
of phantom- and stump pain with Botulinum
toxin type A over 12 months. A first clinical
observation]. Nervenarzt 75(4): .336-340, 2004.
Summary
A male patient with a right-sided abovethe-knee
amputation suffered from severe phantom and
stump pain over a period of more than five years. The
phantom pain started about six weeks after the
amputation and was described as "cutting like a
knife." He experienced eight attacks per day rated
at an intensity of 10 on a visual analog scale from
0-10 and lasting several hours. Stump pain was so
severe that the patient could not tolerate any touch.
The patient's quality of life was very poor, in spite
of taking high doses of gabapentin and intrathecally
administered morphine and clonidine.
Five years after the amputation, the patient was
treated with botulinum toxin [BTX] injections into
four very painful myofascial trigger points [TrPs] in
the stump musculature. The injections were
extremely painful. After two
days, the patient experienced a significant reduction in pain. The intensity of the phantom
pain was only 2/10 and pain attacks occurred
only once per day, lasting a few minutes. After
14 weeks, the severe pain returned within a
matter of days. The BTX injections were repeated, again with dramatic reductions in pain. The
pattern repeated itself several times and the injection
therapy was administered every I I to 14 weeks.
The patient discontinued the clonidine and
significantly reduced the morphine therapy. In
the discussion section, the authors discussed
several possible mechanisms of the dramatic
reduction in phantom and stump pain following
BTX injections into TrPs.
Comments
Already in 1980 did Sherman include the
treatment of TrPs in the treatment of patients
with phantom pain (29). The work by Kern and
colleagues follows in the footsteps of Janet
Travell, who already reported incorporating
TrPs in the treatment of persistent and severe
phantom and stump pain (7). In Volume 1, 2nd
edition of the Trigger Point Manual, Travell reported the successful treatment of a patient
with upper limb phantom pain by inactivating
scalene TrPs (7). In this study, the authors
elected to use BTX injections and were able to
give the patient significant relief and an unparalleled quality of life he had not experienced
since the amputation. It is conceivable that
phantom pain may be another manifestation of
TrP referred pain. The treatment with BTX
clearly gave the patient i n this case his life back. That
leaves the question whether TrP manual
treatments, dry needling, or injections with an
anesthetic would be effective in the treatment of
individuals with phantom and stump pain. [JD]
REVIEWS AND COMMENTS
Kern U, Martin C, Scheicher S, Muller H:
Does botulinum toxin A make prosthesis use
easier for amputees? J Rehabil Med 36(5):
238-239, 2004.
Kern and colleagues described four more
brief case reports of the successful treatment of
phantom and stump pain using botulinum toxin
injections into myofascial trigger points. Not only
were the patients able to tolerate wearing their
prostheses after the treatment, secondary
symptoms including hyperhidrosis also improved significantly. Further studies are needed
to determine the optimum dosage, number of
injections, and should include non-botulinum toxin
treatments. [JD]
Staud R: Are tender point injections beneficial:
the role of tonic nociception in fibromyalgia.
Curr Pharm Des 12(l):23-27,2006.
This fibromyalgia syndrome [FMS]-oriented
rheumatologist in Florida reviewed the nature of
FMS and myofascial pain. He clearly
distinguished tender points of fibromyalgia from
trigger points of myofascial pain and reviewed
the literature reporting injections in both
locations and concluded that the literature indicates
injections seem to reduce local FMS pain, but
need to focus less on tender points and more on
trigger points. We heartily agree. [DGS]
Fabiano JA, Fabiano AJ, Anders PL, Thines TJ:
Trigeminal neuralgia with intraoral trigger
points: report of two cases. Spec Care
Dentist 25(4): 206-213, 2005.
The authors' use of the term "trigger points" is
confusing here, because they were not referring to
myofascial or any other kind of trigger point, but
to a trigger area or region in the mouth that
contributed to attacks of trigeminal neuralgia.
[DGS]
REFERENCES
1. Simons DG: Review of enigmatic TrPs as a common
cause of enigmatic musculoskeletal pain and dys
function. J Electromyogr Kinesiol 14, 95-107, 2004.
2. Simons DG: Do endplate noise and spikes arise
from normal motor endplates? Am J Phys Med Rehabil
80: 134-140, 2001.
3. Simons DG, Hong C-Z, Simons LS: Endplate
potentials are common to midfiber myofasciai trigger
points. Am J Phys Med Rehabil 81(3): 212-222, 2002. 4.
Fernandez de las Peflas CF, Cuadrado ML, Ger
win RD, Pareja JA: Referred pain from the trochlear
Literature Reviews
region in tension-type headache: a myofascial trigger point from
the superior oblique muscle. Headache 45(6): 73 1737,
2005.
5. Calandre EP, Hidalgo J, Garcia-Leiva JM. RicoVillademoros F: Trigger point evaluation in migraine
patients: an indication of peripheral sensitization linked to
migraine predisposition? Eur J Neurol 13(3): 244249,2006.
6. Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz
R: Interrater reliability in myofascial trigger point
examination. Pain 69(1-2): 65-73, 1997.
7. Simons DG, Travel] JG, Simons LS: Travell and Simons'
Myofascial Pain and Dysfunction: The Trigger Point
Manual, 2 ed, Vol. 1. Williams & Wilkins. Baltimore,
1999.
8. Maitland G, Hengeveld E, Banks K, English K:
Maitland's Vertebral Manipulation, 6 ed. Butterworth
Heineman, London. 2000.
9. Fernandez de las Penas C, Fernandez Carnero J,
Miangolarra-Page JC: Musculoskeletal disorders in mechanical neck pain: myofascial trigger points versus
cervical joint dysfunction. J Museuloskele- Pain 13(1):
2
7-35,2005.
10. Banks SL, Jacobs DW, Gevirtz R, Hubbard DR: Effects
of autogenic relaxation training on electromyographic
activity in active myofascial trigger points. J
Musculoskele Pain 6(4): 23-32, 1998.
11. Hubbard DR, Berkoff GM: Myofascial trigger points
show spontaneous needle EMG activity. Spine 18:
1803-1807, 1993.
12. Lewis C, Gevirtz R, Hubbard D, Berkoff G: Needle trigger
point and surface frontal EMG measurements of
psychophysiological responses in tension-type headache
patients. Biofeedback & Self-Regulation 3: 274275, 1994.
13. McNulty WH, Gevirtz RN, Hubbard DR, Berkoff GM:
Needle electromyographic evaluation of trigger point
response to a psychological stressor. Psychophysiology
31(3): 313-316, 1994.
14. Gerwin RD: A review of myofascial pain and
fibromyalgia-factors that promote their persistence. Acu
punct Med 23(3): 121-134, 2005.
15. Dommnerholt J, Issa T: Differential diagnosis: myofascial
pain. Fibromyalgia Syndrome: A Practitioner's Guide to
Treatment. Edited by L Chaitow. Churchill Livingstone,
Edinburgh, 2003, pp. 149-177.
16. Sherman RA, Sherman CJ, Parker L: Chronic phantom
and stump pain among American veterans: results of a
survey. Pain 18(1): 83-95, 1984.
17. Melzack R, Stillwell DM, Fox EJ: Trigger points and
acupuncture points for pain: Correlations and implications.
Pain 3(1): 3-23, 1977.
18. Birch S: Trigger point-acupuncture point correlations
revisited. J Altern Complement Med 9(1): 91103,2003.
19. Travell JG, Simons DG: Myofascial Pain and
Dysfunction: The Trigger Point Manual, Vol. 2. Baltimore: Williams & Wilkins, 1992.
20. Cornwall J. Harris AJ, Mercer SR: The lumbar multifidus
muscle and patterns of pain. Man Ther 11(1): 40-45, 2006.
21. Ge HY, Madeleine P, Wang K, Arendt-Nielsen L:
Hypoalgesia to pressure pain in referred pain areas
triggered by spatial summation of experimental muscle
pain from unilateral or bilateral trapezius muscles. Eur J
Pain 7(6): 531-537, 2003.
22. Hwang M, Kang YK, Kim DH: Referred pain pattern
of the pronator quadratus muscle. Pain 116(3): 238-242,
2005.
23. Hwang M, Kang YK, Shin JY, Kim DH: Referred
pain pattern of the abductor pollicis longus muscle. Am J
Phys Med Rehabil 84(8): 593-597, 2005.
24. Kao MJ, Hsieh YL, Kuo FJ, Hong CZ: Electrophysiological assessment of acupuncture points. Am J
Phys Med Rehabil 85(5): 443-448.2006.
25. Langevin HM, Bouffard NA, Badger GJ. Churchill DL,
Howe AK: Subcutaneous tissue fbroblast cytoskeletal
remodeling induced by acupuncture: evidence for a
mechanotransduction-based mechanism. J Cell Physiol
207(3): 767-774, 2006.
26. Macgregor J, Graf von Schweinitz D: Needle
electromyographic activity of myofascial trigger points
and control sites in equine cleidobrachialis muscle-an
observational study. Acupunct Med 24(2): 61-70, 2006.
27. Lucas KR, Polus BI, Rich PS: Latent myofascial trigger
points: their effect on muscle activation and movement
efficiency. J Bodywork Movement Ther 8: 160-166,
2004.
28. Gerwin RD: A standing complaint: inability to sit; an
unusual presentation of medial hamstring myofascial pain
syndrome. J Musculoske Pain 9(4): 81-93, 2001.
29. Sherman RA: Published treatments of phantom limb
pain. Am J Phys Med Rehabil 59: 232-244, 1980.
doi:10.1300/J094v 15 n01 08
LITERATURE REVIEW
Myofascial Pain Syndrome-Trigger Points
Jan Dommerholt, PT, MPS
David G. Simons, MD
INTRODUCTION
This issue has a double first.
Two
rheumatologists
have
published informative papers in
prestigious rheumatology journals
on the subject of myofascial trigger
points [TrPs], a subject that has
been commonly neglected by that
specialty. A paper by a third
rheumatologist stands in stark
contrast to the papers by the other
two. The review starts off with a
new TrP reliabil ity study from the
Netherlands, which confirms that
trained examiners can reliably
palpate TrPs. The importance of
TrPs in migraine, abdominal and
pelvic pain, shoulder pain, and
tinnitus was examined in several
papers. Unfortunately, TrPs were
sometimes poorly defined without
clear definitions and criteria.
Several studies explored injection
and dry needling of TrPs.
Research
papers
from
11
different countries are included
in this review [Table 1). As usual,
each article review indicates
whether Dommerholt [JD] or
Simons [DGS] prepared it
RESEARCH STUDIES
Bron, C, Franssen, J,
Wensing, M, Oostendorp,
Rab: Interrater Reliability
Of Palpation Of Myofascial
Trigger Points I n Three
Shoulder Muscles. J Manual
Manipulative Ther 15(4):
203-215, 2007
Summary
Thirty-two
patients
with
unilateral or bilateral shoulder
pain and eight asymptomatic
subjects were included in this
study of the interraterreliability
of palpating myofascial trigger
points [TrPs]. Patients had been
diagnosed
with
subacromial
impingement, rotator cuff disease,
tendonitis, tendinopathy,
and
chronic
subdeltoidsubacromial
bursitis. To be considered for the
study, subjects were between 18
and 75 years of age with an
ability to read and understand the
Dutch
language.
Exclusion
criteria
included
serious
rheumatologic,
neurological,
orthopedic, or internal diseases.
Jan Dommerholt. PT, MPS, Bethesda Physiocare, Bethesda, MD.
David G. Simons, MD, MS, DSc (Hon x 2), Clinical Professor (voluntary), Department of
Rehabilitation Medicine, Emory University, Atlanta, GA; and Adjunct Professor, Department of Physical
Therapy, Georgia State University, Atlanta GA [E-mail: loisanddavesimonsCearthlink.netj.
Address correspondence to: Jan Dommerholt, PT, MPS. Bethesda Physiocare, 7830 Old
Georgetown Road, Suite C-15, Bethesda, MD 20814-2440 [E-nail:
dommerholt@bethesdaphysiocare.coml.
Journal of Musculoskeletal Pain, Vol. 16(3), 2008
Available online at http://jnip.haworthpress.com
C 2008 by Informa Healthcare USA. Inc. All rights reserved.
doi: 10.1080/ 10582450802162059
J O U R N A L O F M U S C U L O S K E L E TA L P A IN '
TABLE 1- Country of Origin of Reviewed
Papers
Country of Origin
Number of Papers
Brazil
1
Canada
1
Greece
1
Italy
1
Japan
1
Korea
1
The Netherlands
1
Spain
2
Taiwan
1
United Kingdom
1
United States
5
Three physical therapists with experience in the
identification and management of TrPs examined the
subjects for the presence of TrPs in the
infraspinatus, anterior deltoid, and biceps brachii
muscles for a total of 12 TrPs. The muscles were
examined for the presence of a taut band with a
nodule, a painful sensation during compression of the
palpable nodule in comparison to established
referred pain patterns, the presence of a visible
or palpable local twitch response during snapping
palpation, and the presence of a general pain
response during palpation. referred to as a jump sign.
The therapists were blinded to the status of the
patients and did not know whether they were
symptomatic. As a result of the study design, the
examiners did not distinguish between active and
latent TrPs, and the subjects were not allowed to report whether they recognized the elicited pain. An
observer was present during all examination to verify
correct implementation of the testing procedures, but
the observers did not interfere with the examination.
Both the examiners and observers participated in a
total of eight hours of training and reached consensus
about all aspects of the examination.
The researchers determined both the percent
ages of agreement [PA] and the pair-wise Cohen
Kappa values [yi]. The PA value for identifying
a palpable nodule in a taut band ranged from 45
percent in the medial head of the biceps to 90
percent in the infraspinatus muscle. The fi varied
from O.I l to 0.75. PA scores for eliciting referred
pain were over 70 for most muscle locations with
-values ranging from --0.13 to 0.64. The presence of
a jump sign varied between muscles.
The raters reached a PA of 93 percent for the
infraspinatus muscle and 6 3 percent for another part
of the infraspiniatus and biceps brachii muscles. Thenvalues ranged from 0.07 to 01.68. The overall
agreement on TrP presence or absence was
acceptable for the infraspinatus muscle with PA
values exceeding, 70 percent. In the anterior deltoid
and biceps brachii muscles the PA value was below
70 percent.
In the discussion section of the paper. the authors concluded that referred pain and a jump sign
were the most reliable indicators of the presence of a
TrP. There were clear differences in between various
muscles and even in between different locations in
the same muscle, especially for the nodule in the
taut band, the local twitch response, and the jump
sign. Compared with other commonly used
examination tests, including muscle strength or the
assessment of intervertebral motion, the interrater
reliability was found to be acceptable. They noted that
in clinical practice, the degree of agreement may increase as patients would be able to identify the
clinical significance of the elicited pain.
Comments
This study from the Netherlands performed by a
group of physical therapists is a welcome addition to
the TrP literature and confirms the conclusions from
o t h e r reliability studies that TrPs can be reliably
palpated by trained and experienced examiners (1-3).
The authors decided to blind the examiners to
whether patients had active or latent TrPs and
correctly concluded that in clinical settings, trained
clinicians most likely would h a v e reached higher
degrees of agreement based on patients' feedback. In
the era of evidence-based medicine, this study contributes to the body of literature firmly establishing
TrPs as reliable clinical entities. The authors are
congratulated on the publication of this well executed
study [JD].
Cannon DE, Dillingham TR, Miao H, Andary MT,
Pezzin LE: Musculoskeletal Disorders in Referrals
for Suspected Cervical Radiculopathy. Arch Phys
Med Rehabil 88: 1256-1259,2007
Summary
A total of 191 subjects with suspected cervical
radiculopathy were included in this study.
The researchers determined the prevalence of
several other musculoskeletal disorders, including
myofascial pain, shoulder impingement syndrome,
de Quervain's tenosynovitis, and lateral
epicondytis. Dependent on which muscles and
myofascial trigger points [TrPs] are involved,
myofascial pain can mimic cervical radiculopathy at
several levels. A shoulder impingement may
resemble a C5 radiculopathy. De Quervain's
tenosynovitis and lateral epicondylitis may be
confused for a C6 radiculopathy. In addition to
determining the prevalence of these disorders, the
authors were also interested in examining the
influence of these disorders on electrodiagnostic
study outcome prediction. Four US medical centers
participated in the study.
All subjects completed a questionnaire and were
examined using a standardized protocol. Myofascial
pain was diagnosed if palpation of the neck or
shoulder region produced symptoms. Shoulder
impingement was diagnosed if crossed adduction,
flexion, or abduction with internal rotation caused
symptoms. Lateral epicondylitis was diagnosed if
palpation of the wrist extensor muscles reproduced
pain, and a positive Finkelstein test was determined
to be indicative of de Quervain's tenosynovitis. A
standard electrodiagnostic study was completed and
included at least an upper limb motor nerve
conduction study, one upper limb sensory nerve
conduction study, and needle electromyography with
either monopolar or concentric needles of 10
predetermined muscles. Additional tests were completed at the discretion of the electrodiagnostician.
The study outcome was considered either normal,
indicative of cervical radiculopathy, or indicative of
another
diagnosis.
Irrespective
of
the
electrodiagnostic outcome, all subjects were
examined for the other musculoskeletal disorders.
Fifty-two percent of subjects included in the study
had confirmed cervical radiculopathy, 24 percent
had a normal study, and 25 percent had another
diagnosis identified through electrodiagnosis, such
as plexopathy; median, ulnar, or radial neuropathy;
or polyneuropathy. The total prevalence of the
other musculoskeletal disorders was 42 percent.
The prevalence of subjects with a normal study was
69 percent, and 29 percent in subjects with cervical
radiculopathy [P 0.001], and 45 percent in subjects
with another diagnosis [P = 0.02]. Myofascial pain
was very
common among subjects with a normal electrodiagnostic study [53 percent] but also significantly more common in subjects with cervical
radiculopathy [17 percent, P < 0.001] and in
subjects with other diagnoses [19 percent, P <
0.001], suggesting that many subjects with myofascial pain may be referred for electrodiagnostic
studies. Shoulder impingement was also common in
normals [31 percent] and in subjects with another
diagnosis [30 percent] but not as common with
cervical radiculopathy [nine percent, p < 0.001 ].
The diagnoses of lateral epicondylitis and de
Quervain's was similar across the three groups
and more common than in the general population.
The presence of myofascial pain indicated
approximately one fourth the likelihood of having
cervical radiculopathy [P = .0021 and one third the
likelihood of having another diagnosis [P =
0.017] compared with a normal study. The
presence of shoulder impingement indicated one fifth
the likelihood of having cervical radiculopathy
compared with a normal study [P = 0.007]. It
remains difficult to predict the outcome of
electrodiagnostic studies based on the presence of
musculoskeletal
disorders.
The
authors
acknowledged potential limitations of the study.
Comments
Though the authors concluded that myofascial
pain was very common among all three groups,
the criteria used to diagnose myofascial pain were
poorly defined. Presumably they attempted to
palpate active TrPs to reproduce patients'
symptoms, but there was no mentioning of
palpating for taut bands or any indication of the
level of experience of the examiners in
identifying TrPs. The authors suggested that there
may have been different levels of expertise and that
more specific diagnostic criteria would have made
the diagnosis more objective. The diagnosis of
lateral epicondylitis was based on palpation of the
wrist extensor muscles. Epicondylalgia may be due
to TrPs, but again, the authors did not specify how
the palpation was performed ...(4). Even the
diagnosis of de Quervain's syndrome based on a
positive Finkelstein test may not always be accurate.
In the reviewer's clinical practice, a patient with pain
in the first dorsal compartment had a positive
Finkelstein test when the test was performed with
the elbow extended. However. when the
Finkelstein test
JOURNAL OF MUSCULOSKELETALL PAIN
was performed with the elbow flexed, the test was
negative. The patient was later diagnosed with an
entrapment syndrome of the posterior interosseus
nerve.
In summary, the results of this study would have
been much more reliable if the diagnostic criteria were
better defined and if the various examiners would have
standardized
their
examinations
techniques.
Nevertheless, myofascial pain is a common
differential diagnosis for cervical radiculopathy [JD].
patients reported no pain or pain much alleviated.
Visual analog scores reduced from 7.6 pre treatment
to 1.8 one week later [P < 0.001 ]. At three-month
follow up, 86.5 percent of patients had complete or
nearly complete relief with an average visual analog
scale score of 2.1, that is P < 0.001 compared to
pretreatment. These are also clinically very
significant and long-lasting improvements.
The authors emphasized that all physicians
examining patients with lower abdominal pain
complaints for abdominal wall should look for TrPs
and make sure they are effectively treated.
TREATMENT STUDIES
Comments
Kuan LC, Li YT, Chen FM, Tseng CJ, Wu SF,
Duo TC: Efficacy of Treating Abdominal Wall
Pain By Local Injection. Taiwanese J Obstet
Gynecol45(3): 239-243, 2006
Summary
This study by authors from the departments of
obstetrics, gynecology, and nursing in Taiwan
presented what is essentially a multiple case report of
140 patients with lower abdominal pain complaints.
The patients 1139 women and one man] showed
evidence of myofascial trigger points [TrPs] that
patients were able to identify rather accurately as the
abdominal location of their pain. These patients had
often received previous abdominal surgery and
erroneous diagnoses of abdominal adhesions,
pelvic inflammatory disease. and three nerve
entrapments. On examination, they exhibited
exquisite point tenderness at the designated location,
particularly when tested for a positive Carnett's sign.
In that case, lifting the feet and head off the table
intensifies the sensitivity to local pressure and identifies abdominal wall tenderness as compared with
visceral tenderness. The diagnosis of TrPs was
then confirmed without mentioning how.
Patients received a fan-shaped injection of a
mixture of 2 ml 0.5 percent bupivicaine, 3 ml 2
percent lidocaine, and 4 mg of betamethasone in the
TrP using a 23-gauge needle. At the follow-up exam
in seven days, a second injection was given if the first
did not provide relief, with one or more subsequent
weekly injections in some cases. Eventually 133
patients [95 percent] experienced no pain or mild pain
following this treatment. Follow-up exams were
done after three months. After one week, 68 percent
of
This is a clinically useful and informative multiple
case report on lower abdominal pain and its
management even though it rates poorly as scientific
research of TrPs. I fully agree with the authors'
conclusions.
It is unfortunate that the authors failed to identify
what diagnostic criteria they used to confirm the
presence of TrPs and that they had such a poor
understanding of TrPs. The latter is no surprise
considering that their references did not include one
publication on the subject of TrPs, although that
was the subject of the paper even if the title did
not say so. Which abdominal wall muscles were
being treated was not indicated. It is very doubtful if
there was any advantage to injecting three
medications, especially a corticosteroid that is
contraindicated, when dry needling is known to be
equally effective. The discussion of the nature of TrPs
left much to be desired. There was no mention of
eliciting a local twitch response when the needle
encountered a TrP. However, one must be careful
not to throw the baby out with the bath water [DGS].
Garcia-Leiva, JM, Hidalgo J,
R ico- Villademoros F, Moreno V, Calandre
EP: Effectiveness of Ropivacaine Trigger
Points Inactivation in The Prophylactic
Management of Patients With Severe Migraine.
Pain Med 8(l): 65-70, 2007
Summary
A PhD and four MDs from Granada, Spain.
reported injecting myofascial trigger points
215
[TrPs] weekly in 52 patients who suffered migraine
headaches with 10 mg of ropivacaine. In every
patient, TrPs were identified by manual palpation of
the scalp and neck by a trained expert in this field
during a headache-free period with a finger
pressure of not more than 4 kg. They reported
examining the supraciliary arch, medial and anterior
fibers of the temporal is muscle, parietal muscle, both
the occipital and suboccipital areas, and the upper
trapezius muscle. Every patient had TrPs with at
least one TrP in the temporalis muscle. Eighty
percent of the patients had at least one TrP in the
suboccipital region, Forty-two percent of the patients
had four TrPs, and one had as many as 13, In addition
to TrPs, 9 patients had fibromyalgia syndrome
[FMS], 10 had temporomandibular dysfunction, and
one had mixed anxiety and depression syndrome.
Two patients with chronic migraine, multiple
tender points, and generalized allodynia [probably
FMS] withdrew because of unbearable pain with
injections and no improvement. Sixty per cent of patients
were much or very much improved based on
Clinical Global Impression [GGI] scares. Twentyseven percent of the 30 patients with chronic migraine
advanced to only episodic migraine. The patients
with severe migraine improved from an average
visual analog scale [VAS] reading of 7 to 4 [P =
0.0013], moderately severe migraine improved
slightly from 6.5 to only 6 VAS, and those with
mild migraine got more severe attacks and increased
VAS readings from 5 to 5.5. Thirty-two percent of
patients reported pain during ropivacaine injections.
Patients with generalized allodynia did poorly. Only
one of these patients reached 50 percent reduction in
attack frequency, none reported improvement in
GGI scores, and only two reduced rescue
medication. Thirty-two percent of patients found the
ropivacaine injections painful and 42 percent
complained of post injection soreness.
The CGI scores indicated much more improvement
than reduction in frequency of attacks. Migraine
attacks were better tolerated after treatment, and the
patients welcomed the reduced need for rescue
medication and shorter attacks. The authors thought
that the degree of central sensitization contributed to
the severity of symptoms and that TrP injections are
a valuable therapeutic tool in prophylaxis of
migraine: however, they did not recommend it
as first-line
treatment because of the demands injection
treatment made on the patient. They recommended
drug therapy instead, unless drugs were ineffective.
Comments
This good-sized study of a clinical condition for
which there are only a few other published peer
reviewed articles is an important pioneering
publication in this field (5-7). The finding that the
more severe the migraine symptoms the more
effective inactivation of TrPs was is a very important
additional clinical guide. The authors applied only
one injection procedure for this study, but in
clinical practice, numerous other TrP treatments
may be less demanding of patients' tolerance.
They concluded the inactivation of TrPs is a
valuable procedure for prophylaxis of migraine
and then contradicted themselves by saying drugs
are a preferable way to go. Drugs have
undesirable side effects, and there were no
adverse reactions to the injections and less
likelihood from manual therapy treatments. The
basis for this conclusion is not clear, especially
because other studies recommended in activation
of TrPs without reservations for these patients.
The lack of a control group in this study is
largely covered by the fact that some patients
greatly improved and others got worse, which
eliminates placebo reactions as the cause for
improvement. This is actually more valuable to
clinic practice than a control group, but was
serendipitous good luck in this case.
As a research study of TrPs, this paper leaves
much to be desired. There is no complete description of the specific diagnostic criteria employed
to confirm the identification of TrPs, but the paper as
a whole confirms that for the most part that is what
they were treating. The understanding of TrPs was
hazy, which is not surprising because the only TrP
references cited were clinical treatment studies and
none dealt with the nature of TrPs, such as the
1999 edition of The Trigger Point Manual (8). The
authors wisely emphasized the important role of
central sensitization with a chronic pain input like
this [DGS]
Giainberardino IJ A, Tafuri E', Savini A,
Fabrizio A, Affaitati G, Lerza R, Di lanni L ,
Lapenna D, ,Vea etti A: Contribution of
_11yofascial Trigger Points to Migraine
Symptoms. J Pain 8(11): 869-878,2007
Summuarv
group 1, pain threshold measurements to electrical
stimulation in skin, subcutis, and muscle in the TrPs
and referred pain area were determined before the
initial TrP infiltration with 0.5 mL of
bupivacaine [5 mg/mL] and before each subsequent
infiltration on the 3rd, 10th. 30th, and 60th day after
the initial treatment. Only one TrP was injected in
each subject following a standardized methodology.
Patients were not told that the treatment could reduce
their migraine pain. Subjects in group 2 did not
receive any treatment. The researchers determined
the number and maximal intensity of migraine attacks during a two-month period prior to the interventions and the number of times they had
to take "rescue medication" consisting of 1000 mg
paracetemol during the study. Normal subjects were
evaluated in the same intervals as the subjects. Other
potential complicating factors, such as the phase of
the menstrual cycle in fertile women or possible
cutaneous allodynia following a migraine episode,
were considered in the study design. The researchers
also included a second phase to control for a
possible placebo effect. Twelve subjects, meeting
the inclusion criteria for group 2, received injections
outside TrP areas during a 30-day period with followup interventions scheduled at the 3rd, 10th, and 30th
day after the initial injection.
As previously established in research by the main
author and the late Dr. Vecchiet, the subjects in both
groups presented with skin, subcutis, and muscle
hyperalgesia at the beginning of this study (9,10).
Only subjects in group 1, who were treated with TrP
injections, showed a progressive reduction of tissue
hyperalgesia, especially at the skin and subcutis
level. At the same time, migraine symptoms
decreased only in group 1. Subjects in the
"placebo-control" group who received injections
outside TrP areas did not show any significant
improvements. The authors concluded that TrPs are
strong sources or peripheral nociceptive input and
cervical TrPs may contribute to migraine symptoms.
Treatment of TrPs lowers the peripheral input from
TrPs.
Seventy-eight migraine patients with myofascial
trigger points [TrPs] in the cervical muscles and
referred pain consistent with frontal and temporal
migraine sites were included in this study from Italy.
The objective of the study was to compare the
efficacy of TrP treatment with local anesthetic vs. no
treatment in patients as compared with sensory
assessment in normal subjects. The subjects were
divided into two groups. Inclusion criteria for
group 1 [N = 54] were an age range of 18 to 50
years, either sex, a history of migraine at least a year
before the examination and diagnosed by a specialist
using the 2004 criteria of the International Headache
Society, a number of migraine attacks equal to or
greater than six per month in the preceding two
months, a negative history for any condition known
to affect general pain sensitivity, the presence of
active TrPs in the cervical region with referred pain
into typical migraine pain areas, poor responsiveness
to classic migraine treatments, and written consent.
The subjects in this ,group had unilateral frontal or
temporal migraine with TrPs in the stem
ocleidomastoid [N = 19], semispinalis cervicis [N=
23], or splenius cervicis [N = 12] muscles with
referred pain patterns consistent with the migraine
pain locations.
Subjects assigned to group 2 [N = 24] had the
same inclusion criteria as well as an intolerance or
allergy to local anesthetics. They also presented with
TrPs in the stemocleidomastoid [N = 10].
semispinalis cervicis [N = 8], or splenius cervicis
[N = 6] muscles. Normal subjects [N = 20] had to
have an age range of 18 to 50 years and either sex,
a negative history for migraine and am
cenicocranial pain, a negative history for any
condition known to affect general pain sensitivity. a
negative clinical examination for the presence of
TrPs in the cervicocranial region and written Comments
informed consent to participate in the study.
This is a very well-designed study that offers
Trigger points were identified using standardized
criteria consistent with guidelines by Simons. Travell, strong support that TrPs can contribute to symptoms
associated with migraine. Even though
and Simons (8). For subjects in
Dornmerholt and Simons
only one TrP was treated, tissue hyperalgesia,
migraine symptoms, and use of rescue medication
was significantly. We welcome such excellent TrP
research by Giamberardino and her colleagues.
There should be no doubt anymore that TrPs are
essential in the treatment of patients with
migraines. This study joins a growing number of
other studies confirming the role of TrPs in migraine
headaches and the effectiveness of TrP therapy
(5,6,11,12). As a side note, Travell discussed the
relationship between TrPs and headaches already in
1967 (13)! In clinical practice, multiple TrPs in
various muscles are treated along with other
therapeutic measures, such as posture corrections,
restoration of joint mobility and proprioception, and
psychological management for depression, stress.
anger, and anxiety. Dr. Giamberardino and
colleagues are congratulated on designing and
publishing one of the best studies to date on the
subject of TrPs and migraine. Hopefully Dr.
Giamberardino will consider extending the current
research study to other pain syndromes, as we fully
anticipate that similar correlations exist between TrPs
and other pain syndromes, including low back and
pelvic floor pain, shoulder and arm pain, among
others [JD].
Ga H, Koh H-J, Choi J-H, Kim CH:
Intramuscular and Nerve Root Stimulation vs
Lidocaine Injection of Trigger Points in Myofascial
Pain Syndrome. J Rehabil Med 39:374378,2007
Summary
Forty-three subjects with myofascial trigger points
[.TrPs] in the upper trapezius muscle were included
in this study from Korea. The subjects were
randomly assigned to one of two groups: an
intramuscular stimulation [IMS] group and a TrP
injection [TPI] group. The subjects and the
examiner were blinded to the group assignment.
Exclusion criteria included previous treatment with
either modality in the past six months; a history of
neck or shoulder surgery within one year
preceding the study: opioid medicine intake within
one month prior to the study; a diagnosis of
fibromyalgia, cervical radicalopathy, or myelopathy;
severe cardiovascular or respiratory disease;
allergies for drugs or injections:
cognitive deficits or communication problems,
among others. Subjects in the TPI group were
treated with 0.5 percent lidocaine injections using
0.2 ml per TrP into a taut band in the upper
trapezius muscle "until all the TrPs were
inactivated." A 25-gauge, 38-mm long needle was
used. Subjects in the IMS group also were treated
in a similar fashion using a 60-mm long
acupuncture needle with a 0.30-mm diameter. In
addition, subjects in the IMS group were nee-died
at the C3-5 level as described by Gunn ...(14).
The authors referred to the paraspinal needling as
"nerve
root
stimulation."
Following
the
intervention, all subjects were instructed to perform
self-stretching exercises for the upper trapezius
muscle three times per day until the next treatment.
Follow-up treatments were scheduled one and two
weeks later, although the authors also mentioned
that outcome measures were determined on "days 0,
7, 14, and 28 just before treatment," leaving it unclear
whether subjects were treated three or four times.
The results section suggests that all subjects were
treated four times. Outcome measures included the
visual analog scale [VAS], the Wong-Baker FACES
pain scale, range of motion, pain pressure threshold
using digital palpation, depression, postneedling
soreness, hemorrhage, and dizziness.
Both groups showed significant improvements
in the VAS and Wong-Baker Faces scales, although
there were differences. For example, the TPI group
did not show any improvement on the VAS between
days 14 and 28 or on the Wong-Baker FACES
between days 0-7 and 1428 compared with the IMS
group that showed improvements on all follow-up
visits, except on the pressure threshold measures
between days 0 and 7. The authors argued that the
IMS group had better pain relief, based on reported
inconsistencies in the VAS for pain scales and a preference for the FACES Pain scales. Depression
scores improved only in the IMS group, which the
authors hypothesized could be related to the greater
time requirement to administer the IMS technique
when compared with TrP injections. Local twitch
responses were elicited in 81.4 percent of all
treatment during the first treatments. Fourty-two out
of the 43 subjects [97.7 percent] had at least one local
twitch response during the course of treatment. Both
the IRIS and TRI group improved in passive range of
JOURNAL OF MUSCULOSKETETAL PAIN
motion. The IMS group achieved greater improvement the American Academy of Family Physicians
in extension. There were no differences in advocated that the TrP injection codes can be used
even when performing dry needling (http://
posttreatment soreness between the two groups.
www.aafp.org/fpm/20041000/coding.html): "the
intent . . . is to identify the procedure of performing
Comments
the trigger point injection, regardless of whether an
To the best of this reviewer's knowledge, this is injectable is supplied." Insurance companies have not
the first study that compares TrP injections with dry uniformly followed the same guidelines [JD].
needling using acupuncture needles. Previous studies.
which were referenced properly by the authors,
compared TrP injections with dry needling using Ga H, Choi J-H, Park C-H, Yoon H-I': Dry
syringes, and it should come as no surprise that dry Needling Q f Trigger Points With and Without
needling using a syringe caused more postneedling Paraspinal Needling in Myofascial Pain
soreness than injections with lidocaine (15,16). This Syndromes in Elderly Patients. J Alters Compl
study confirms our clinical impression that dry Med 13(6): 617-623,2007,
needling does not cause more postneedlin g soreness
when compared with injection therapy. It is not clear Summary
from the study whether the authors attempted to
This study is a variation of the previously repurposefully elicit local twitch responses when they
inactivated TrPs. It appears that LTRs were a viewed paper that compared trigger point [TrP]
coincidental finding and not the focus of the needling injection therapy with combined peripheral TrP and
paraspinal dry needling. The exclusion criteria,
procedures.
The authors maintained that they compared overall study design, and outcome measures were
intramuscular stimulation described by Gunn identical in both studies. In this study, the authors
with TrP injections described by Simons. As a compared TrP dry needling without paraspinal
certified PMTS practitioner, this reviewer does not needling to TrP dry needling with paraspinal
agree that the needling procedure used in this needling. Forty subjects, ranging in age between 63
study represents Gunn's approach. Although the and 90 years, with TrPs in the upper trapezius
authors describe Gunn's ideas accurately, according muscles, were randomly assigned to either a dry
to the quoted reference and this reviewer's needling group [N = 18] or to a dry needling
education in the Gunn Approach to Chronic Pain. group with additional paraspinal needling, which the
Gunn's IMS approach does not include inactivating authors referred to as the intramuscular stimulation
peripheral TrPs (14). Therefore, it would have been [IMS] group [N = 22]. The authors equated TrP dry
more accurate if the authors had acknowledged that needling with paraspinal dry needling to Gunn's IMS
they compared TrP injections with peripheral TrP dry techniques.
needling combined with paraspinal dry needling
Peripheral TrPs were treated in the same fashion in
It is noteworthy that in spite of some differences. both groups. Subjects were positioned in the prone
both injection therapy and dry needling were position. The taut band was held in between the thumb
effective for several of the outcome measures, and index finger and was needled using a 0.30
which brings up the question why injection therapy diameter, 60-mm length acupuncture needle fixed by
continues to be the leading choice of many physicians a plunger-type needle holder. The needling continued
when treating patients with TrPs. Could it be that the until there were no further local twitch responses
existence of insurance codes for TrP injections, at [LTR]. The IMS group was also needled in the
least in the United States, would persuade multifidi muscles at the C3-5 levels, using what
physicians to use injections rather than dry Gunn has described as the "grasping and winding
needling, for which there are no specific codes? up" method. which involves turning the needle after
There is controversy whether TrP injection codes can a `grasping" of the needle was perceived. The
he used when dry needling procedures are LTRs were observed in 80 percent of all subjects
performed. In 2004.
during the first treatments, with 97.5 percent of
subjects demonstrating
Donnnierholr and Sirnons
at least one LTR during the entire course of
treatment.
After one month, subjects in both groups showed
significant improvements in the scores on the visual
analog scale for pain, the WongBaker FACES pain
scale, and pain pressure thresholds using digital
palpation. The IMS group improved more
continuously throughout the month. There was a
borderline significant interaction between time and
type of treatment in the FACES scores. The authors
speculated that perhaps with a greater number of
subjects, the differences would be greater.
Depression scores improved only in the IMS
group. All passive range of motion scores improved
except cervical extension in the dry needling group.
There were no differences in postneedling soreness.
The authors concluded that dry needling of TrPs
with paraspinal needling is a better method than
dry needling of TrPs only.
219
paraspinal needling." Nevertheless, after reviewing
the data, it was noted that the changes were very
small, although statistically significant. That greater
numbers of subjects would confirm the current
findings is not at all clear. The authors stated that
"further studies with more subjects are needed for
verification." Until such studies have been completed,
it suffices to conclude that both peripheral TrP
needling and "dry needling of TrPs with paraspinal
needling" are effective treatment modalities in the
treatment of individuals with pain and dysfunction
associated with TrPs. The authors are commended
for starting this line of inquiry. There are not many
papers in support of TrP dry needling and good
research is very much needed. Both papers by Ga et
al. demonstrate that dry needling is a valid
modality for the treatment of TrPs [JD].
Itoh K, Katsumi Y, Hirota S, and Kitakoji H:
Randomised trial of trigger point acupuncture
compared with other acupuncture for treatment of
Compared to with TrP injection paper reviewed chronic neck pain. Complement Ther Med
above, the authors used both the term IMS or 15(3):172-179,2007
intramuscular stimulation and the descriptive "dry
needling of TrPs with paraspinal needling" Summary
interchangeably. Throughout the paper, they
Forty patients [29 women, 11 men; age range: 47
referred to the "dry needling of TrPs with
paraspinal needling" as the IMS group. As to 80 years] with nonradiating neck pain for more
summarized in the comment section of the preceding than six months and a normal neurological
review, the term IMS is strongly associated with the examination were included in this study from Japan
work of Chan Gunn, as the authors mentioned comparing standard acupuncture, trigger point [TrP]
several times. However, the IMS approach as Gunn acupuncture, non-TrP needling, and sham
described does not include the systematic acupuncture. The subjects were randomly assigned
inactivation of peripheral TrPs. In Gunn's to a group. All subjects received two phases of
hypothesis, TrPs are always the result of neuropathic treatment of three weeks each, for a total of six 30changes consistent with Cannon and Rosenblueth's minute treatments, once per week. Outcome
Law of Denervation, which maintains that the measures included pain intensity measured with a
function and integrity of innervated structures visual analog scale [VAS] and pain disability
depends upon the free flow of nerve impulses. Gunn measured with the Neck Disability Index [NDI]. An
speculated that needling the multifidi would facilitate independent and blinded examiner performed the
the resolution of any myofascial dysfunction. Gunn outcome measures.
Subjects assigned to the standard acupuncture
does not promote needling peripheral TrPs and
therefore, this study does not really compare IMS group were treated at acupuncture points GB 20
with peripheral needling. The descriptive "dry and 21, BL 10 and 11, S12 and 13, TE 5. LI 4
needling of TrPs with paraspinal needling" is the and SI 3. The needle was inserted and moved
back and forth until the subjects felt dull pain or
more appropriate term to use in this paper.
Regarding the outcomes, the authors found the acupuncture sensation referred to as "de qi," at
statistically significant changes in favor to the group which point the needle was left in place for 10
more minutes. Subjects in the trigger
that received "dry needling of TrPs with
Comments
point acupuncture group were examined for TrPs in
the splenius capitis, trapezius, sternocleidomastoid.
scalenes, levator scapulae, paraspinal, and
suboccipital muscles. An acupuncture needle was
inserted into the skin overlying a TrP and advanced to
20 mm into the muscle. A local twitch response was
elicited and the needle was left in place for 10
additional minutes. Subjects in the TrP group received
a mean of 2.3 insertions. Subjects in the non trigger
point group were treated at non tender points 50 mm
away from TrPs for a mean of 2.4 needle insertions.
Subjects in the sham acupuncture group were treated
over TrPs using the same criteria as in the TrP group.
The tips of the acupuncture needles used in the sham
group were cut off and smoothed to prevent
penetration of the skin. After 10 minutes, a
simulation of needle extraction was performed. All
subjects were asked to describe the needle insertion to
determine the efficacy of the blinding technique used
in this study.
The results were overwhelmingly positive for the
TrP group after three weeks and nine weeks both for
the pain intensity and pain disability. The VAS
scores reduced from 67 to 11 for the TrP group but
did not change significantly for the other groups [P <
0.01 ]. Pain disability scores on the NDI reduced from
13 to 3.1 for the TrP group and again did not change
significantly for the other groups IP < 0.01 ]. The
blinding technique was found to be reliable. The
authors concluded that treatment of TrPs has a better
analgesic effect than treatment of non-TrPs or
acupuncture points, presumably because of
polymodal-type nociceptor activation.
Comments
This paper from Japan is the second study by this
research group comparing various needling
approaches (17). The authors express a good understanding of TrPs and the requirements for effective dry needling techniques. Direct treatment of
TrPs was far superior to treatment of acupuncture
points or non-TrPs even though only one local twitch
response was elicited per TrP. This study supports the
use of TrP dry needling in the treatment of chronic
neck pain. The authors used the term TrP acupuncture,
which may be an appropriate term for acupuncture
practitioners treating TrPs. When nonacupuncture
practitioners, such as physical therapists. treat TrPs
with acupuncture needles, this reviewer prefers the
term dry needling [JD].
Srbely JZ, Dickey JP: Randomized Controlled
Study of The Antinociceptive Effect of Ultrasound
on Trigger Point Sensitivitti~: Novel Applications in
Myofascial Therapy? Clin Rehabil 21: 411-417,
2007
Summary
After a brief introduction discussing the
prevalence of musculoskeletal pain and the nature of
myofascial trigger points [TrPs], the authors reviewed
the few papers that have been published about the
effects of ultrasound on TrPs. The objective of this
study from Canada was to determine whether
ultrasound can modulate the sensitivity of TrPs.
Forty-four subjects [22 males and 22 females.
mean age 48 years, age range of 28 to 65 years] with
an active TrP in the right trapezius muscle were
selected from a rehabilitation clinic. The criteria used
to identify a TrP included a well-defined, palpable
tender nodule within a taut band with deep, achy, diffuse, and poorly localized discomfort radiating into
the lateral aspect of the ipsilateral arm after 10 to 20
seconds of prolonged pressure. Subjects with a
history of recent trauma to the neck or shoulder,
any form of medication, or subjects with a
preexisting neuromuscular condition were excluded
from the study. The primary outcome measure
was the pain pressure threshold measured by
applying direct pressure over a TrP using a
dynamometer. Subjects in the experimental group
received a 5-minute ultrasound treatment over the
trapezius TrP with a 1 W/cm', 1 MHz continuous
wave form. compared with a 5-minute 0.1 W/cm',
1 MHz continuous wave form for the control
group. The same person who administered the
treatment measured pain pressure thresholds
immediately following the intervention.
Subjects in the experimental group demonstrated a
significant 44.1 percent increase in their pain pressure
thresholds compared with 1.4 percent of the control
group [P < 0.05]. No differences were observed
between male and female subjects. In the discussion
section, the authors emphasize that in the clinical
setting ultrasound ma\ offer an alternative or
complement to
Dommerholt and Simons
other treatments, due to its ability to reduce TrP
sensitivity.
Comments
The authors acknowledged that the lack of a
blinded observer is a major limitation of this study.
Yet, the short term decrease in sensitivity may be
useful in preparing patients for other, potentially more
painful therapies, such as manual TrP release or
even TrP dry needling. The authors devoted a few
paragraphs on the possible mechanisms of ultrasound
analgesia, quoting a recent paper by Hsieh, who
established that ultrasound may modify the number
of neuronal nitric oxide synthase-like neurons in the
dorsal horn in rodents, thereby reducing pain via direct modulation of central pain pathways. There is
no evidence that ultrasound applied to TrPs would
have any long-term effect, a topic which the authors
aim to address in future studies [JD].
Zaralidou AT, Amaniti EN, Maidatsi PG,
Gorgias NK, Vasilakos DF: Comparison
Between Newer Local Anesthetics For
Myofascial Pain Syndrome Management.
Methods Find Exp Clin Pharmacol 29(5):
353-357,2007
day by a research fellow not otherwise involved in
the study and were asked to rate their pain. The
period of time until the pain returned to the preinjection value was used as an outcome measure. The
researchers did not find any statistically significant
differences in between the two
groups.
Levobupivacaine had slightly lower pain ratings than
ropivacaine. The authors concluded that both
anesthetics are equally effective, but because of its
lower pain rating, levobupivacaine might be
preferable.
Comments
This comparison study of the effects of trigger
point injections with 0.25 percent levobupivacaine
and 0.25 percent ropivacaine did not find any
significant differences between the two substances
for pain during injection, efficacy of the treatment,
and duration of pain relief. The substances were
equally effective. The diagnostic criteria for the
identification of TrP used in this paper are poorly
defined. The authors use the terms tender point
and TrP but make no mention of palpating for taut
bands. It is not clear whether they made a
distinction between active and latent TrPs [JD].
REVIEWS & C OM MEN T S
Summary
Bennett R: Myofascial Pain Syndromes and Their
Evaluation. Best Pract Res Clin Rheumatol 21(3):
In this study from Greece, 68 patients with 427-445, 2007
myofascial pain were randomly assigned to one of
two groups. Subjects received three to five trigger
point [TrP] injections with either 0.25 percent
levobupivacaine or with 0.25 percent ropivacaine.
Myofascial pain was defined as the presence of
musculoskeletal pain, localized tender points.
referred pain without symptoms of fatigue.
paresthesias, sensation of swelling with and without
the coexistence of headaches, poor sleep. or irritable
bowel syndrome. Patients did not have any analgesic
medication during the course of the study. The
clinician administering the injections and the patients
were blinded to the type of local anesthetic. Outcome
measures included a numerical rating scale for pain.
Measurements were obtained prior to any injection.
during. immediately after, and 15 minutes after each
TrP injection by an independent and blinded
investigator. Following the intervention, subjects v,
ere contacted by telephone every other
Summary
Throughout this paper, Bennett repeatedly focused
on the huge discrepancy between the high prevalence
and importance of myofascial trigger points [TrPs]
compared with the lack of attention many physicians
pay to them. He begins with definitions and follows
with a list of eight common musculoskeletal
complaints that are usually assigned other diagnoses
but are largely caused by TrPs. The list includes
tension headaches, low back pain, neck pain,
temporomandibular pain, forearm and hand pain,
postural pain, and pelviclurogenital pain problems.
Summarizing the history and physical examination,
he emphasized the important clinical difference
between active and latent TrPs,and the critical
importance of adequate training and experience
needed to
JOURNAL OF MUSKULOSKELETALPAIN
confidently delineate TrPs. He attributed the
common finding of muscle weakness associated v ith
TrPs to disuse or pain inhibition. While emphasizing
pain aspects of the examination. he noted the
importance of finding a tender spot in a palpable taut
band when it is within reach. Discussing reliability of
the diagnosis, he identified the studies that established
the importance of training and practice and the dire
need for a set of validated diagnostic criteria.
Muscle pain experiments have demonstrated the
importance of central sensitization to the pain of TrPs.
The current understanding of the histopathology of
TrPs was well summarized. The scope of
neurophysiology was well covered but was weak in
the
understanding
and
interpretation
of
electrodiagnostic studies. The section on the
biochemical milieu included a full description of the
2005 study by Shah et al. with illustrations (18).
The section on common clinical syndromes of
myofascial pain included common diagnoses that in
fact are due largely to TrPs for head and jaw pain
with pain illustrations, neck and shoulder pain,
low back pain with illustrations, hip pain, pelvic pain,
upper limb pain, lower limb pain, and chest and
abdominal pain. The section on treatment included
postural and ergonomic perpetuating factors,
stretching, strengthening of weakness due to pain
inhibition. Consideration of TrP injections noted the
value of dry needling and medications based on the
author's clinical experience. He wisely emphasized
the fact that anxiety and depression need to be treated
as a result of persistent pain and are usually not the
cause of it.
Comments
Robert Bennett, MD is a rheumatoloaist in
Portland. Oregon who, to our knowledge, has been
for many years one of the first rheumatologists to
fully appreciate the importance of TrPs for the
fibromyalgia syndrome. He is recognized among
rheumatologists as a leading research investigator of
fibromyalgia. This paper is one of the best up-to-date
reviews, summaries, and literature citations of
TrPs that has been published lately-. It is a
noteworthy milestone of progress toward mainstream
medical recognition of TrPs that such a solid member
of the rheumatology profession should author this
outstanding paper on TrPs.
Recently, a series of papers have greatly enhanced
our understanding of the relationship between
headaches and TrPs. Dr. Ferndindezdc-las-Petzas of
Spain and colleagues have published controlled
studies of prevalence of active or latent TrPs that
are strongly associated with restricted mouth
opening (19), tensiontype headache [TTH] from the
superior oblique extraocular muscle (20),
mechanical neck pain (21.22), TTH from
suboccipital muscles (23). and TTH from the
upper trapezius (24). In addition. Giamberardino
et al. of Italy did a controlled study of results of
treatment of migraine headaches that indicate TrPs
commonly act as triggers of symptoms (7).
The serious lack of validated diagnostic criteria is
currently under research investigation by a Spanish
physical therapist. The common finding of muscle
weakness associated with TrPs is likely more
frequently caused by inhibition from latent TrPs in
the same or neighboring muscles than to disuse or
pain inhibition. This is based on extensive surface
electromyographic studies by a competent physical
therapist but has been published only in book chapters
and not in peerreviewed literature (25,26). Another
motor disturbance from latent TrPs, loss of
coordination, has been published as a reviewed
article (27).
With regard to pathology, a new look at past biopsy
findings suggests that TrPs are essentially a myopathy.
Bennett's review emphasizes the importance of
studies to explore genetic factors. The findings and
results of electrodiagnostic examination of TrPs are
well described with an understanding of the integrated
hypothesis and shows why the spontaneous electrical
activity and endplate potentials are abnormal (28).
The Trigger Point Manual (8) fully explains why
muscle spindles cannot be the source of these
potentials. It is hard to see how TrPs could be
considered a focal dystonia. A dystonia produces
repetitive involuntary twisting movements. A focal
dystonia describes "a variety of musculoskeletal
problems that are particularly applied to the fine
muscle problems encountered by professional
musicians" (29,30). This condition lacks the spot
tenderness in a palpable taut band that is
characteristic of TrPs.
The section on Common Clinical Syndromes
leaves no doubt that TrPs are a pervasive and
widespread source of musculoskeletal pain. The fact
that the usual treatment for muscle weakness focuses
only on strengthening makes the fact
that the weakness is usually caused by inhibition
from a latent TrP an important issue. Starting with
inactivation of the latent TrP cause of the weakness
avoids the usual mistake of starting strength training
first, thus resulting in teaching the patient to use
substitute muscles instead of the inhibited muscle,
which unfortunately makes muscle function more
abnormal [DGS].
Staud R: Future perspectives: Pathogenesis of
Chronic Muscle Pain. Best Pract Res Clin
Rheumatol21(3): 581-596,2007.
Summary
This scholarly review by a rheumatologist in
Gainesville, Florida, describes in detail his understanding of myofascial trigger points [TrPs] and
fibromyalgia syndrome [FMS]. It emphasizes what
we don't know as much as we think we know. The
author begins by wondering if abnormal input from
deep nociceptors is essential for the development
and maintenance of FMS symptoms.
His review of TrPs summarized clinical characteristics, but defined active TrPs as responding to
needle insertion with a local twitch response, and
latent TrPs as not associated with either
spontaneous or referred pain. Under pathogenesis,
the author summarized and effectively integrated
throughout this paper the seminal paper of Shah et al_
(18). Staud was unsure of the etiology of TrPs but
presented the essentials of the integrated hypothesis,
quoting a number of studies that reinforce that
hypothesis.
The review of FMS started with the 1990
American College of Rheumatology diagnostic
criteria. With clear insight, Staud characterized it as
a syndrome with no single specific feature that
represents a symptom complex of self-reported or
elicited findings that appear to depend on
nociceptive input from deep tissues, particularly
muscle. The author specifically lists and discusses
in detail the response to stress events that alter
neuroendocrine and autonomic nervous systems'
functions. hyporeaction of the hypothalamicpituitary-adrenal axis to stress. and the direct
effects of the stress.
The source of the tenderness of tender points
appears to be enigmatic to this author. However. he
never mentions TrPs as a factor from this FNIS point of
view in spite of the fact that most tender
points are in muscles at locations that are common
TrP sites-facts that are well documented in both
sets of literature (31). One would expect at least
latent TrPs to frequently be present at those sites.
Interestingly, the author notes that patients
characteristically do not complain of total body pain,
but of specific regional pains like neck,
temporomandibular, and back pain, and of headache.
Each of these pain areas has its characteristic TrP
cause. Stand notes the progression of persistence of
these regional pains, especially whiplash injury, to
FNIS.
The author's review of the pathology of FMS is
confusing because he often overlooks the fact that
FMS research literature is highly contaminated by
lack of appreciation of TrPs and by terminological
confusion. It is important to remember that the
most common site of TrPs is the upper trapezius
muscle, the muscle that is usually biopsied for FMS
studies. Similarly, it can be misleading to assume
that microcirculation studies on the trapezius muscle
in subjects with the diagnosis of myalgia is caused by
FMS rather than TrPs. Staud presented a knowledgeable review of the mechanisms of hyperalgesia in
FMS.
Comments
By presenting so much interest and understanding of TrPs coming from a rheumatologist not
well known in the field of myofascial pain in a
prestigious rheumatology journal, this paper is a
breath of fresh air. The author is heartily congratulated. He is a true scholar and presented an upto-date summary of current knowledge and
understanding. This is illustrated in his review of the
mechanisms of hyperalgesia in FMS. Also, he
characterized FMS as a symptom complex with no
specific diagnostic feature that stems from
dysfunctions of multiple organ systems and appears
to depend on nociceptive input from deep tissues.
This looks to me like a harbinger of the growing
understanding of FMS.
The problems 1 encountered in this paper are
endemic among most rheumatologists and also many
others, but nevertheless are worthy of note. We avoid
using the term myofascial pain syndrome because
there is accumulating evidence that it a disease not a
syndrome and simply identify it as myofascial pain, or
more specifically TrPs (30).
Active TrPs are generally recognized as causing a
clinical pain complaint that is reproduced by digital
pressure on the TrP Latent TrPs do not cause a clinical
pain complaint but on examination can produce all the
pain symptoms characteristic of active TrPs. This
distinction is clinically very important. and we need to
reach agreement regarding these two definitions. The
definitions the author uses differ substantially from
the usage of Shah et al. and our publications (8.18).
The lack of consideration of TrPs in FMS
research has resulted in a whole body of literature
highly contaminated by unrecognized TrP effects that
renders it not only incomplete but also sometimes
seriously misleading. This stems from the early
erroneous report, by a rheumatologist unskilled at
finding TrPs, that TrPs are rarely found in patients
with FMS, which has become gospel truth to many
rheumatologists. Unfortunately. to date, there has
been no competent study published to correct this
misinformation.
The other serious source of confusion is the
multiplicity of names that have been used to de-
scribe patients with symptoms caused by TrPs going
back to muscular rheumatism, myogelosis. and
fibrositis thatt metamorphosed to FMS (32). Stand
quoted two papers as sources of biopsy
information on FMS, one of which attributed latent
TrP pathology to FMS. and he attributed the findings
in myogelosis to FMS. but the clinical symptoms of
myogelosis are much more specific to TrPs than
FMS (33,34).
Readers interested in this review of TrPs by a
rheumatologist will not want to miss the paper by
Robert Bennett reviewed above in this column I DGS].
syndrome. This justifies considering this group of
diagnoses as a syndrome that serves as an
umbrella syndrome. He lists 13 diagnoses that fit
under this umbrella and includes myofascial pain
syndrome as one of them.
He very seriously questions and unequivocally
rejects the validity of the current construct of what he
calls myofascial pain syndrome and uses the term
regional sofa-tissue pain syndrome as an equivalent.
The author's terminology identifies this disease as a
regional pain condition with tender points in the
absence of structural pathology, This issue is
considered under the comments following this
summary.
The erudite summary of the current understanding
of central sensitization with as many as 237 literature
references proceeds to a detailed analysis of how it
applies to FMS, chronic fatigue syndrome, irritable
bowel syndrome, tension type headache, migraine,
temporomandibular disorders, myofascial pain
syndrome, restless legs syndrome, multiple channel
sensitivity, primary dysmenorrhea, interstitial
cystitis, and traumatic stress disorder. Because it
is solidly established that any sustained pain input
produces central sensitization, the only specific
feature common to this listing of diagnoses is lack of
pathology that satisfies the author. We differ with the
author's opinion on four of the items, which will he
covered in the Comments section. The author
proceeds to list factors that may trigger or contribute
to central sensitization, a list that contains no
surprises, but reviews thoroughly the wellestablished literature.
Comments
Yunus MB: Fibromyalgia and Overlapping
Disorders: The Unifying Concept of Central
Sensitivity Syndromes. Semin Arthritis Rheum
36(6): 339-356, 2007.
Summarv
This rheumatologist author from Peoria, Illinois,
has been a leader in the field of fibromyalgia
syndrome [FMS] for many years, His thesis is that
lack of a demonstrated characteristic pathology and
presence of central sensitization is common to the
symptoms of FMS, irritable bowel syndrome.
headaches. and chronic fatigue
I fully agree with the author that the time has
come to find a new definition and understanding of
FMS. His suggestion is headed in the same direction
as the one Staud proposed that is also reviewed in
this column. The search for the cause of FMS has
been futile. Both authors agree that FMS also has
critically important neuroendocrine aberrations,
which is the issue that Staud emphasized. The
concept that FMS is a syndrome caused by many
interacting organ dysfunctions is the approach that
looks most promising to many clinicians familiar
with FMS. The importance of central sensitization to
the three conditions that Yunus addresses is
indisputable and is also a critically component of
chronic trigger points [TrPs].
The position that myofascial pain syndrome has
no pathological basis is untenable if one looks at
three reports of muscle biopsies done on patients with
myogelosis (33,35,36). Myogelosis has the same
essential diagnostic criteria as TrPs (37.38). These
papers demonstrate that TrPs have muscle pathology
fully consistent with, and explanatory of, the clinical
picture of TrPs. We prefer the term myofascial
trigger points [TrPs] instead of myofascial pain syndrome because the diagnosis of TrPs fully qualifies
for the dictionary definition of a disease rather than a
syndrome (30). When one recognizes this fact, then
conditions in which the pain component is largely
associated or caused by TrPs no longer fit under
the author's umbrella syndrome because they do
now have an identifiable pathological foundation. In
addition to TrPs, this consideration includes his
listings of tension type headache, migraine, temporomandibular dysfunction, and interstitial cystitis.
A recent series of well-designed papers established TrPs as a major factor in tension type
headache (20,23.24.39). Several of them emphasize
the important role of central sensitization that
enhances the basic TrP problem. Two similar papers
established the close association of migraine with
TrPs (5,6) and another identified the TrPs as a
significant trigger mechanism by effective treatment
of them (7).
One extensive paper by a dentist identified how
frequently which TrPs reproduced the pain pattern
of the temporomandibular-dysfunction patients for
all of the masticatory muscles including some neck
muscles (40). Members of the avant-garde Tuffs
Orofacial Pain Society at Tufts University in Boston,
Massachusetts, are among the increasing number of
dentists tuned in to TrPs and they told me [while I
was there on 8 September 2007 to receive an award
for my pioneering in the field of TrPs] that well over
half of the many temporomandibular dysfunction
patients that they see are there because of their
TrPs.
Interstitial cystitis is one of a number of enigmatic
pelvic pain complaints for which there are now
credible clinical research papers that identify TrPs as
the chief culprit (41). Other previously enigmatic
pelvic pain conditions include female pelvic pains
and nonbacterial prostatitis (42-44).
In addition. poor muscle coordination was
clearly demonstrated in a well-controlled study
to be due to TrPs. a conclusion further substantiated in a PhD thesis on the subject (27). Epicondylitis [tennis elbow] has now been well reported
as closely associated with TrPs (4). It is only a
matter of time until TrPs will also be identified
as the culprit source of common enigmatic
musculoskeletal complaints such as low back pain
and frozen shoulder by research investigators as
well as clinicians. Trigger points are being accepted
by mainstream medicine in many other countries.
The Trigger Point Manual has now been translated
into eleven (11) foreign languages including
German, Spanish, French, Italian, Russian,
Japanese, Chinese, and Korean.
In summary, it is not clear to this reviewer
whether the author's proposed syndrome serves any
useful purpose and whether his refusal to recognize
TrPs for what they are is at all helpful to the medical
community and to their patients [DGS].
Chaitow L: Chronic Pelvic Pain: Pelvic Floor
Problems, Sacro-iliac Dysfunction and The
Trigger Point Connection. J Bodywork
Movement Ther ll: 327-339, 2007
Summary
After presenting pertinent epidemiological data
and definitions, illustrating how common various
pelvic floor dysfunctions are, Chaitow provides a
succinct review of several pelvic dysfunction studies
where myofascial trigger points [TrPs] played a
significant role in the etiology or maintenance
of the problem. He discusses several
controversies in the literature, such as whether the
muscle tone of dysfunctional pelvic floor muscles
is increased or decreased. Citing recent research,
Chaitow reviews established connections between
breathing dysfunction, pelvic floor dysfunction, and
sacroiliac stability. The role of TrPs is
emphasized especially in cases where muscle tone is
inadequate to provide functional support for urethral
and sacroiliac stability. Chaitow suggests that the
development of TrPs may be a physiological
response to restore muscle tone in damaged,
dysfunctional, or denervated tissues. He concludes
that there is much evidence of intricate links
between pelvic floor muscle dysfunction and lumbopelvic or sacroiliac dysfunction without necessarily
knowing the etiological
JOURNAL OFMUSCULOSKELETAL PAIN'
relationships, He recommends including manual
treatment methods, including Thiele massage,
TrP inactivation, dry needling, biofeedback, and
relaxation or toning of the pelvic floor muscles.
Manual treatments need to be combined with
correcting postural and breathing pattern disorders and
normalising joint and soft tissue imbalances
Comments
Too often, clinicians and researchers focus on one
particular aspect of musculoskeletal pain and
dysfunction, including pelvic floor dysfunction. For
some, the main focus may be TrPs, while for
others sacroiliac dysfunction or motor planning may
get the overriding emphasis. Chaitow has synthesized
many current insights into pelvic floor dysfunction
into one of the most comprehensive reviews on the
topic. The paper illustrates nicely that any one
approach is always limited and that patients need to
be approached from a broad clinical perspective.
During the recent 6th World Congress on Low
Back and Pelvic Pain in November 2007 in
Barcelona, Spain. Chaitow moderated a panel of
myofascial experts. and the TrP concepts were
introduced to an audience that previously has been
more concerned about sacroiliac dysfunction. The
article is well referenced and offers plenty
opportunity to study the topic of pelvic floor
dysfunction in more detail [JD]
Ferruindez-de-las-Penas C , Simons DG, Cuadrado
ML, Pareja JA: The role of myofascial trigger
points in in usculoskeletal pain syndromes of the
head and neck. Current Headache Pain Reports
11: 365-372, 2007
Anyone interested in getting a quick and comprehensive review of the TrP literature relevant for
head and neck pain should consider reading this
paper. It is an excellent summary not only of the
authors' extensive contributions to the literature but
also of many other relevant studies. papers, case
reports, and chapters. The primary author is a PhDlevel Spanish physical therapist. The other three
coauthors are physicians from Spain and the United
States [JD].
Rocha CAAB, Sanchez TG: Myofascial Trigger
Points: Another Way of Modulating Tinnitus.
Progress Brain Res 166(18): 209-214,2007
Summary
In this paper from Brazil, the authors established a
strong correlation between tinnitus and myofascial
trigger points [TrPs] particularly in the masseter,
splenius capitits, sternocleidomastoid, and temporalis
muscles. The authors used the criteria for TrPs
Simons. Travel], and Simons suggested (8). More
than 72 percent of 94 patients with tinnitus had
relevant TrPs compared with 36 percent in a control
group of individuals without tinnitus. Compression of
the TrP modulated the symptoms of tinnitus in 55.9
percent of subjects. In more than 65 percent of
these subjects, the tinnitus was aggravated by stimulation of TrPs, while in others stimulation of the
involved TrP completed resolved the symptoms. Of
particular interest is the observation that compression
of both active and latent TrPs modulated tinnitus. The
paper includes a brief discussion about the
similarities between tinnitus and pain.
Comments
Summon'
This review article discusses the scientific evidence
that myofascial trigger points ITRPs] play a role in
common disorders of the head and neck, including
migraine and tension-type headaches, whiplashassociated disorders, and mechanical neck pain.
After a brief introduction with definitions of TrPs and
their clinical presentation: the paper reviews the
literature and summarizes the possible mechanisms
underlying the correlations between TrPs and pain
in the head and neck region.
This review paper, which was published as a
chapter in the periodical Progress in Brain Research,
is an important summary of the research of the
primary author who previously established that
individuals with tinnitus are more likely to complain
of chronic pain in the head, neck, and shoulder
girdle. The observation that tinnitus can be directly
linked to TrPs has many implications for the clinical
practice of primary
care physicians, internists, dentists. and earnose-andthroat physicians. Unfortunately, few physicians in
these disciplines have been trained to recognize the
signs of TrPs and to examine patients for the presence
of relevant TrPs. This study confirms other studies on
the subject of tinnitus and TrPs (45). The authors
misquoted the Simons, Travell, and Simons
reference [JD].
BRIEF REPORTS
Botwin IMP, Patel BC: Electrontygraphically
Guided Trigger Point Injections in The
Cervicothoracic Musculature of Obese Patients:
A New and Unreported Technique. Pain
Physician 10: 753-756, 2007.
This report from two physiatrists from Florida
describes a previously unreported technique of
trigger point [TrP] injections in obese patients.
After a brief description of myofascial pain and
TrPs, the authors described an electromyographyguided injection technique, which assures the
clinician that the needle tip is placed in muscle
tissue and not in adipose tissue or in lung tissue.
The authors mentioned that electromyographyguided botulinum toxin injections have been
described previously. Palpation of TrPs can be
difficult in obese patients. The described
technique offers no assurance, however, that the
needle is placed directly in the TrP [JD].
REFERENCES
1. Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz R:
Interrater reliability in myofascial trigger
point examination. Pain 69(1-2): 65-73, 1997.
2. Hsieh CY, Hong CZ, Adams AH, Platt KJ, Daniel
son CD, Hoehler FK, Tobis JS: Interexaminer reliability of the
palpation of trigger points in the trunk and lower
limb muscles. Arch Phys Med Rehabil 81(3): 258-264, 2000.
3. Sciotti VM, Mittak VL, DiMarco L, Ford LM, Plezbert J,
Santipadri E,et al.: Clinical precision of my
ofascial trigger point location in the trapezius muscle. Pain
93(3): 259-266, 2001.
4. Femandez-Camero J, Femandez-de-las-Penas C. de la
Llave-Rincon Al, Ge HY, Arendt-Nielsen L: Preva
lence of and referred pain from myofascial trigger points in the
forearm muscles in patients with lateral
epicondylalgia. Clin J Pain 23(4): 353-360, 2007.
5. Femandez-de-las-Pefias C, Cuadrado NIL,
Gerwin RD. Pareja JA: Myofascial disorders in the
trochlear region in unilateral migraine: a possible
initiating or perpetuating factor. Clin J Pain 22(6): 548553.2006.
6. Femandez-de-Las-Penas C, Cuadrado ML, Pareja JA:
Myofascial trigger points, neck mobility and forward head
posture in unilateral migraine. Cephalalgia 26(9): 1061-1070,
2006.
7 . Giamberardino MA, Tafuri E, Savini A. Fabrizio A,
Affaitati G, Lerza R,et al.: Contribution of Myofascial Trigger
Points to Migraine Symptoms. J Pain 8(11): 869-878.2007.
8. Simons DG, Travel] JG. Simons LS: Travell and
Simons' Myofascial Pain and Dysfunction: The Trigger Point
Manual. 2 ed. Vol. 1. Williams & Wilkins, Baltimore, 1999.
9. Vecchiet 1. ., Giamberardino MA, Dragani L: Latent
myofascial trigger points: Changes in muscular and
subcutaneous pain thresholds at trigger point and target level,
J Manual Medicine 5: 151-154, 1990.
10. Vecchiet L, Giamberardino MA, Saggini R:
Myofascial pain syndromes: Clinical and pathophysiological
aspects. Clin J Pain 7(Suppl 1): 516-22, 1991.
11. Calandre EP, Hidalgo J, Garcia-Leiva JM, and RicoVillademoros F: Trigger point evaluation in migraine
patients: an indication of peripheral sensitization linked
to migraine predisposition? Eur J Neurol 13(3): 244249,2006.
12. Garcia-Leiva JM, Hidalgo J. Rico-Villademoros F,
Moreno V. Caiandre EP: Effectiveness of ropivacaine trigger
points inactivation in the prophylactic management of patients
with severe migraine. Pain Mcd 8(1): 65-70,200T
13. Travell J: Mechanical headache. Headache 7: 2329.1967.
14. Gunn CC: The Gunn Approach to the Treatment of
Chronic Pain. 2rsd ed. Churchill Livingstone, New York, 1997.
15. Hong CZ: Lidocaine injection versus dry needling to
myofascial trigger point. The importance of the local twitch
response. Am J Phys Med Rehabil 73(4): 256-263, 1994.
16. Karnanli A, Kaya A, Ardicoglu 0, Ozgocmen S, Zengin
FO. Bayik Y: Comparison of lidocaine injection, botulinum
toxin injection, and dry needling to trigger points in
myofascial pain syndrome. Rheumatol Int 25(8): 604611, 2005.
17. Itch K, Katsumi Y, Kitakoji H: Trigger point acupuncture
treatment of chronic low back pain in elderly patients-a
blinded RCT. Acupunct Med 22(4): 170-177, 2004.
18. Shah JP, Phillips TM, Danoff J V. Gerber LH: An invivo microanalytical technique for measuring the tocal
biochemical milieu of human skeletal muscle. J AppI Physiol
99: 1980-1987, 2005.
19. Blanco CR. Fernandez-de-las Penas C, Xumet JEH,
Algeba CP, Rabada MF, Lillo de la Quintana MC:
Changes in active mouth opening following a single treatment
of latent myofascial trigger points in the masseter muscle
involving post-isometric
.IOURNAL OF MUSCULOSKELETAL PAIN
relaxation or strain/counterstrain. J Bodywork Movement The
10: 19 7-205.2006.
20. Femandez-de-las-Penal CF, Cuadrado ML. Genvin RD.
Pareja JA: Referred pain from the trochlear region in tensiontype headache: A myofascial trigger point from the superior
oblique muscle. Headache 45(6): 7 31 - 7137,2005.
21. Femandez-de-Las-Penal C, Alonso-Blanco C.
NiiangolalTa JC: Myofascial trigger points in subjects
presenting with mechanical neck pain: A blinded, controlled
stud'. Man Ther, 12(1):23-33, 2007.
22. Femandez-de-las-Penas C. Femandez-Carnero J, and
Miangolarra-Page.IC:
Musculoskeletal
disorders
in
mechanical neck pain: Myofascial trigger points versus
cervical joint dysfunction. J Musculoske Pain 13) 1): 2735,200-9.
23. Fernandez-de-las-Pefas C, Alonso-Blanco C, Cuadrado
M1,Gerwin RD, Pareja JA: Trigger points in the suboccipital
muscles and forward head posture in tension-type headache.
Headache 46(3): 454-460, 2006.
24. Femandez-de-las-Pc6as C. Ge HY, .Arendt Nielsen
L. Cuadrado ML. Parcja JA: Referred pain from trapezius
muscle trigger points shares similar characteristics with
chronic tension type headache. Eur J Pain 1 1(4):475-182.
2007.
25. Headley BJ: Evaluation and treatment of myofascial
pain
syndrome
utilizing
biofeedback.
Clinical
Electromyography for Surface Recordings. Edited by JR
Cram Clinical Resources, Nevada City, 1990, pp. 235-254.
26. Headley BJ: The use of biofeedback in pain
management. Phys Ther Pract 2(2)-. 29-40, 1993.
27. Lucas KR, Polus BI, Rich PS: Latent myofascial trigger
points: Their effect on muscle activation and movement
efficiency. J Bodywork Movement Ther 8: 160V166. 2004.
28. Simons DC: Review of enigmatic MTrPs as a common
cause of enigmatic musculoskeietal pain and dysfunction. J
Electromyogr Kinesiol 14: 95-107, 2004.
29. Byl NN: What can we learn from animal models of focal
hand dystonia? Rev Neurol (Paris) 159(10 Pt l ) : 8 5 7 73,200I
30. Stedman's Medical Dictionary. Lippincott, Williams &
Wilkins, Baltimore, 2006.
31. DomrnerholtJ,Issa T:Differential diagnosis:Myofascial pain. Fibrornyalgia Syndrome: A Practitioner's
Guide to Treatment. Edited by L Chaitow. Churchill
Livingstone. Edinburgh. pp. 149-177. 2003.
32. Dornnterholt J: Fibromyalgia: Time to consider a new
taxonomy' J Musculoske Pain 8(4): 41-47. 2000.
33. Fassbender HG: Non articular rheumatism. Pathology of
Rheumatic Diseases. Springer, New York, pp. 303-314,
1975.
34. Yunus MB. Kalvan-Raman UP, Masi AT, Aldag JC:
Electron microscopic studies of muscle biopsy in primary
fibromyalgia syndrome: A controlled and blinded study. J
Rheurnatol 16(l): 97-101. 1989.
35. Reitinger A. Radner H, Tilschcr 1-1, Hanna M, Windisch
A, Feigl W: Morphologische Untersuchung an
Triggerpunkten. Manuclle Medizin. 34: 256-262. 1996.
36. Windisch A, Reitinger A, Traxler H, Radner H,
Neumayer C. Feigl W. Firbas W: Morphology and histochemistry of myogelosis. Clin Anat. 12(4): 266-271,
1999.
37. Lange M: Die Muskelhlirten (Myogelosen). Miinchen:
J.F. Lehmann's Verlag, 1931.
38. Simons DC: Triggerpunkte and Myogelose.
Manuelle Medizin 35: 290-294, 1997.
39. Femandez-de-las-Penas C. Cuadrado IMIL, ArendtNielsen L. Simons DG, Pareja )A: Myofascial trigger point,
and sensitization: An updated pain model for tension-type
headache. Cephalalgia 27(5): 383-393, 2007.
40. Wright EF: Referred craniofacial pain patterns in
patients with temporomandibular disorder. JADA 131: 13071315,2000.
41. Weiss JM: Pelvic floor myofascial trigger points:
Manual therapy for interstitial cystitis and the urgencyfrequency syndrome. J Urol 166(6): 2226-2231, 2001.
42. Anderson RU, Wise D, Sawyer T, Chan C: Integration of
myofascial trigger point release and paradoxical relaxation
training treatment of chronic pelvic pain in men. J Urol
174(l): 155-160, 2005.
43. Anderson RU. Wise D, Sawyer T. Chan CA: Sexual
dysfunction in men with chronic prostatitis/chronic pelvic
pain syndrome: Improvement after trigger point release and
paradoxical relaxation training. J Urol 176(4):15341538.2006.
44. Doggweiler-Wiygul R: Urologic rnyofascial pain
syndromes. Curr Pain Headache Rep 8(6): 445-451, 2004
45. Teachey WS: Otolarvngic myofascial pain syndromes.
Curr Pain Headache Rep 8(6):457-362, 2004
Myofascial Pain Syndrome-Trigger Points
Jan Dommerholt, PT, DPT, MPS
INTRODUCTION
Myofascial trigger points [TrPs] continue to attract
clinicians and researchers from around the world.
This review includes contributions from Brazil,
Canada, Denmark, Spain, Switzerland. Taiwan, and
the United States. A paper by Chang, Chen, and
Chang illuminates an important aspect of the
integrated TrP hypothesis and suggests that a
disintegration of spinal motor neurons may
contribute to the development of TrPs. Other papers
investigated TrPs and whiplash injury, urinary
incontinence, muscle cramps, shoulder pain, and
tinnitus. The research team of Fernandez-de-lasPenas explored preliminary clinical prediction rules
with trigger point therapy, which may assist in
determining which patients are most likely to benefit
from trigger point therapy.
RESEARCH STUDIES
Ettlin 1; Schuster C, Stoffel R, Briiderlin A ,
Kischka U: A distinct pattern of myofascinl
findings inpatients after whiplash injury. Arch
Phys Med Rehabil 89:1290-1293, 2008.
Summary
They were symptomatic for at least 6 months.
Exclusion criteria were age over 60 years, insufficient knowledge of German, and significant
internal or neurologic diseases.
A physical therapist specialized in the manual
diagnosis and treatment of TrPs performed all
examinations. The following muscles were included
in the examination: semispinalis capitis. trapezius
pars descendens, levator scapulae, scalenus medius,
sternocleidomastoid, and masseter. The therapist
was blinded to the diagnosis of the subjects.
Criteria for TrPs included a palpable hardening in
the muscle belly, pressure pain, referred pain with
manipulation of the hardening, and recognition of
the elicited pain. Three out of four criteria were
required to diagnose a TrP. In addition, all subjects
completed a visual analog scale for general pain level
and the German version of the Beck Depression
Index.
The results showed that the prevalence of TrPs in
the semispinalis capitis muscle was significantly
higher [85.1 percent] in the patients with whiplashassociated disorder then in any other group of
patients with 53.2 percent with bilateral TrPs. The
prevalence of TrPs in other muscles did not differ
from the patients with fibromyalgia syndrome [FMS]
or chronic cervical syndrome, but was significantly
higher compared to the patients with depression and
the healthy controls. Depression had no impact on
the outcome. Pain levels were higher for the patients
with whiplashassociated disorder and FMS
compared to the other groups.
This study from Switzerland compared the
prevalence and distribution of TrPs in the neck and
shoulder muscles of 47 patients with whiplashassociated disorder, 21 patients with fibromyalgia
syndrome [FMS], 17 with chronic cervical
syndrome, 1 with endogenous depression, and 24 Comments
control subjects [total number of patients = 100].
The researchers included one muscle each
Patients were recruited from three treatment centers
from
the upper cervical spine, lower cervical
in Switzerland and Germany.
Jan Dommerholt, PT, DPT, MPS, Bethesda Physiocare/Myopain Seminars, Bethesda, Maryland, USA Address
correspondence to: Dr. Jan Dommerholt, Bethesda Physiocare, 7830 Old Georgetown Road, Suite C-15, Bethesda, MD
20814-2440, USA. E-mail: dommerholt@bethesdaphysiocare.com
Journal of Musculoskeletal Pain, Vol. 17(1), 2009
Available online at http://jmp.haworthpress.com
C 2009 by Informa Healthcare USA, Inc. All rights reserved.
doi: 10.1080/10582450802675928
JOURNAL OF MUSCULOSKELET.AL PUY'
spine, neck, shoulder girdle, and face, and found a
distinct pattern of distribution of TrPs specifically
for whiplash injuries. They acknowledged that in
future studies other muscles should be examined as
well. Overall, this is an excellent study documenting
that TrPs are common after whiplash injury, and that
there may be distinct differences between groups of
patients. Patients with whiplash-associated disorder
should always be examined and treated for TrPs.
Ge H-Y, Fernande -de-las-Peiias C, Madeleine P,
Arendt-Nielsen L: Topographical mapping and
mechanical pain sensitivity of myofascial trigger
points in the infraspinatus muscle. Eur J Pain
12:859-865,2008.
Summary
This study from Denmark included nineteen
patients with unilateral shoulder pain. The researchers divided the area overlying the bilateral
infraspinatus muscles into 10 adjacent areas of 1 cm 2
and measured the pressure pain threshold in each
area. Next, an acupuncture needle was inserted into
each area five times in different directions to elicit
local twitch responses or referred pain.
The study revealed several interesting findings.
First, the pressure threshold was significantly lower
in the infraspinatus muscle on the painful side [p =
0.001]. Second, the pressure threshold was
significantly lower in the midfiber region of the
muscle compared to other parts [p < 0.05]. Third,
multiple TrPs were identified in the infraspinatus
muscle on the painful side. Fourth, multiple latent
TrPs were identified bilaterally. Fifth, the pressure
threshold of active TrPs was much lower than the
latent TrPs and again much lower than the nonTrPs.
The researchers concluded that bilateral mechanical hyperalgesia is common with unilateral
shoulder pain. It is likely that peripheral sensitization
plays a significant role in chronic myofascial pain.
Lastly, pressure pain threshold topographical
mapping and dry needling are sensitive techniques to
identify TrPs.
Comments
Part of the appeal of this study is its simplicity. The design of this study is not all that
sophisticated, yet, the results are dramatic and
they confirm the observations of clinicians. Trigger
points occur bilaterally in patients with unilateral
shoulder pain and are more prevalent in the midfiber
region of the muscle. The study also confirms that
TrP dry needling and pressure threshold
measurements can be used to identify trigger points.
Chang C-W, Chen Y-R, Chang K-F: Evidence of
neuroaxonal degeneration in myofascial pain
syndrome: A study of neuromuscular jitter by
axonal microstimulation. Eur J Pain 12:10261030, 2008.
Summary
Researchers from Taiwan used stimulated singlefiber electromyography [SFEMG] with 23 patients
with TrPs in the upper trapezius and levator
scapulae muscles and with 16 controls. The
SFEMG is a sensitive method to measure
neuromuscular jitter, assess the functional integrity
of peripheral nerves, and determine the stability of the
neuromuscular transmission function. The study
aimed
to
investigate
whether
neuroaxonal
degeneration and degeneration of motor neurons are
common in patients with myofascial pain.
Subjects had chronic myofascial pain with a
disease duration ranging from 6 months to 8
years [mean 2.6 years]. Subjects with a history of
diabetes, uremia, neck or shoulder trauma, cervical
radiculopathy,
neuritis,
myasthenia
gravis,
myasthenic syndrome, or muscular weakness related
to other neuromuscular diseases were excluded from
the study. Jitter or the mean consecutive difference
[MCD] was calculated as the mean of 30 consecutive
interpotential intervals between stimuli and singlefiber potentials.
Subjects with 1'rPs had significantly higher MCD
values than healthy controls with an abnormal
percentage of 74.3 and 70.7 for the trapezius and
levator scapulae muscles, respectively [p < 0.01],
which may indicate instability of the neuromuscular junction, post-synaptic damage, or
degeneration of motor neurons. The researchers
found a positive correlation between the jitter and the
duration of myofascial pain, which may support the
development of progressive neuronal degradation with
axonal neuropathy in more chronic cases. The authors
speculated that the noted degeneration of motor
neurons might
Dommerholt
trigger sensory nerve involvement and
hypersensitivity to pain.
Comments
Neuromuscular jitter is produced by fluctuations
in the time for endplate potentials at the
neuromuscular junction to reach the threshold for
action potentials. With a dysfunctional neuromuscular junction, muscle fibers of the same motor
unit may not always fire in the same sequence
causing jitter. This study confirmed that patients
with TrPs had a significantly increased MCD in the
trapezius and levator scapulae muscles compared to
controls. The integrated trigger point hypothesis is
based on dysfunction of the motor endplate and this
study suggests strongly that at least part of the
endplate dysfunction may be the result of
disintegration of spinal motor neurons. The
suggested link between motor and sensory neurons
is interesting and conceivable, but needs to be
supported with further research. The authors made a
very important contribution to the understanding of
the mechanisms underlying the development of
TrPs.
Ferndndez-de-las-Peiias C, Cleland JA, Cuadrado
ML, Pareja JA: Predictor variables for identifying
patients with chronic tension-type headache who
are likely to achieve short-term success with
muscle trigger point therapy. Cephalgia 28:264275, 2008.
Summary
Thirty-five subjects with chronic tension-type
headaches were included in this Spanish study, which
aimed to develop preliminary clinical prediction rules
with trigger point therapy. Clinical prediction rules
identify those patients at the time of the initial
evaluation who are most likely to benefit from a
particular intervention. In addition to evaluating range
of motion, head posture, pressure thresholds, and total
tenderness, all subjects were examined for active TrPs
in the upper trapezius, sternocleidomastoid, .
temporalis, and superior oblique muscles. The
therapy program consisted of a combination of
different trigger point techniques and a progressive
exercise program.
Outcome measures were determined as at least
a 50 percent reduction of at least one
headache parameter at I week and I month after
discharge from therapy. Twelve potential predictor
variables were entered into a logistic regression,
leaving four variables with the strongest predictive
value for short-term follow-up, including headache
duration [-<8.5 hr], headache frequency [<5.5
days/week], bodily pain [<47 on the medical
outcomes study 36-item short form (SF-36)], and
vitality [<47.5, on SF-36]. For long-term followup, two variables with the strongest predictive value
were determined, including headache frequency
[<5.5 days/week] and bodily pain [<47 on SF-36].
After 1 week, the chance of a successful outcome
was 80 percent with three of four variables present
and 87.4 percent if all the four variables were present.
After I month, if one of two variables was present, the
probability of success was 72 percent and if both
variables were present, it increased to 84 percent.
Comments
Being able to predict which patients are likely to
benefit from trigger point therapy following the
initial evaluation is a valuable and potentially costsaving utility. Clinical prediction rules have been
determined for other interventions for back and
neck pain. This study is a step in the right
direction, but is implicitly limited, because there are
no studies that have defined the effectiveness of the
therapy program used in this study. The authors
acknowledged this limitation and did not draw
definitive conclusions and labeled the outcome
correctly as "preliminary" prediction rules. It was
interesting to note that the number of active TrPs was
not identified as a strong predictor of successful
outcome.
Ge H-Y, Zhang Y, Boudreau S, Yue S-W,
Arendt-Nielsen L: Induction of muscle cramps
by nociceptive stimulation of latent myofascial
trigger points. Exp Brain Res 187(4): 623-629,
2008.
Summary
Fourteen healthy subjects received injections with
glutamate or isotonic saline in latent TrPs or non-TrP
muscle tissue of the gastrocnemius
JOURNAL OF MUSCULOSKEL ETAL PAIN
muscle in this Danish study on the association
between latent TrPs and muscle cramps. Latent
TrPs were identified manually and confirmed with
electromyography [EMG]. The presence of
spontaneous intramuscular electrical activity
registered with an EMG-guided injection needle and
the absence of surface EMG activity was interpreted
as a confirmation of a trigger point. Twenty minutes
later, a second injection was delivered in the noninjected site. Pain ratings were continuously recorded
on a visual analog scale. Muscle cramp was defined
as a significant increase in EMG activity as
measured by both the needle and surface EMG
electrodes.
The pain associated with glutamate injections was
rated as a 6.5 ~: 0.68 mm on a visual analog scale
compared to 1.8 ± 0.3 mm for the isotonic saline
injections. Following the injections, 92.86 percent of
subjects who were injected in latent TrPs
experienced muscle cramps compared to 0 percent
for non-TRP injections. None of the subjects
injected with isotonic saline experienced cramps
irrespective of the injection site. The researchers
concluded that noxious stimulation of latent TRPs
might result in muscle cramps.
Comments
Trigger points have associated with muscle
cramping in previous papers. The underlying
mechanisms of cramps are not well defined. This is
the first paper linking latent TrPs to the development
of muscle cramps. The authors suggested that
activation of nociceptive muscle afferents may
electrically induce muscle cramps by increasing the
response of group II spindle afferents and the afferent
input to motor neurons, realizing that this hypothesis
does not explain the induction of muscle cramps with
peripheral denervation. Another explanaton
suggests that noxious stimulation of latent TrPs
would decrease inhibitory input to motor neurons and
as a result induce muscle cramps. Therapeutically,
inactivating TrPs is one possible treatment of
muscle cramps.
TREATMENT STUDIES
Hains G, Hains F Descarreaux MMI, Bussiere A:
Urinary incontinence in women treated by
ischemic compression over the bladder area; a
pilot study. J Chiropractic Med 6:132-140,
2007.
Summary
From Canada comes this clinical study of the
effects of ischemic trigger point compression on
stress and mixed incontinence. Thirty-three women
with urinary incontinence were examined by a
chiropractor and randomly assigned to an
experimental group [N = 24] or a control group
[N = 9]. Subjects in the experimental group were
treated with ischemic compression therapy over TrPs
located on the bladder area, or as the authors
described, "deep behind the pubis." Subjects were
treated three times per week for a period of 5 weeks.
Trigger points were compressed starting with light
pressure with a gradual increase of pressure to
subjects' maximum pain tolerance levels for 15 s.
Subjects in the control group received ischemic
compression therapy over TrPs in the gluteus
maximus,
medius,
and
minimus
muscles.
Compression was maintained from 5 to 15 s per trigger
point. At the conclusion of the study, the subjects of
the control group were offered 15 more treatments
during which trigger pointTrP compression was
administered over the bladder area.
Outcome measures included modified versions of
the Urogenital Distress Inventory and the
Incontinence Impact Questionnaire, which were
administered after 15 treatments, 30 days after
treatments, 6 months later. Subjects in the
experimental group showed a significant decrease on
the scores for the questionnaires [from 23.3 to 10.2;
p < 0.001] compared to little change in the
control group [from 25.3 to 22.2]. After 30 days the
symptoms decreased further to a score of 6.9 and
increased to 11. 3 after 6 months. The crossover
group did not experience a significant improvement
in spite of receiving the same treatment as the
experimental group. All subjects were evaluated and
treated by the same chiropractic doctor.
Dommerholt
splenius
capitis,
stemocleidomastoid,
and
temporalis. All examinations were performed by the
This interesting study provides support for the same physical therapist who was not blinded. The
treatment of TrPs in females with urinary incon- authors concluded that both active and latent TrPs
tinence. The authors speculated that they were are associated with tinnitus.
treatise TrPs in the smooth musculature of the
bladder wall, a concept that has not received any
support in the literature. They did not mention Comments
whether they examined the patients for abdominal
Two of the authors have previously published
wall TrPs, including the pyramidalis muscle, which
some
of their findings (3), but this is their first solid
have been linked to pelvic floor disorders and
incontinence. The arguments in support of their study of the association between TrPs and tinnitus.
assumption are highly speculative. It is doubtful that A next logical study would be to examine the effect
the authors actually administered ischemic of different trigger point-treatment approaches on
compression. As TrPs are thought to be hypoxic, tinnitus, including manual TrP therapies, dry
needling, and injection techniques or stretching,
ischemic compression may not even be desirable.
muscle energy, and strain-counterstrain. This is a
very encouraging study from Brazil published in
Bezerra Rocha CAC, Ganz Sanchez T Tesseroli de an audiology and neurotology journal. Hopefully,
medical specialists involved in the diagnosis and
Siqueira JP Myofascial trigger point: A possible
treatment of tinnitus will take notice and incorporate
way of modulating tinnitus. Audiol Neurotol
TrPs in practices.
13:153--160, 2008.
Comments
Summary
Ninety-four patients with constant unilateral or
bilateral tinnitus during at least 3 months and an
equal number of controls were examined for the
presence of TrPs in the superficial masseter, splenius
capitis, sternocleidomastoid [sternal head], anterior
temporaiis, upper trapezius, posterior digastric,
scalenus
medius,
levator
scapulae,
and
infraspinatus muscles using the criteria suggested
by Simons, Travell, and Simons and by Gerwin et
al. (1, 2). The researchers examined whether
palpation of TrPs would alter the nature of tinnitus
in loudness or changes in the sound. The
evaluation of tinnitus loudness was assessed with a
visual analog scale. Palpation was performed once
with progressive and sustained deep single-finger
pressure up to 10 s.
Trigger points in at least one muscle were
much more common in the patient group [72.3
percent] then in the control group [36.2 percent: p
< 0001]. Laterality was observed in 56.5 percent
and modulation of tinnitus occurred in 55.9
percent of subjects in the experimental group.
Changes in tinnitus were mostly presented as
changes in loudness. Palpation of TrPs in all the
muscles included muscle-modulated tinnitus, but
much more pronounced in the masseter. followed
by the
REVIEWS & COMMENTS
Malanga G. Wolff E: Evidence-informed
management of chronic low back pain with
trigger point injections. Spine J 8(I): 2008.
Summary
This paper provides a comprehensive review of
the TrP literature with an emphasis on TrP injection
for the treatment of patients with chronic low back
pain. The authors included a brief historical section,
general descriptions of injection techniques, some
interpretations of insurance companies, and a
summary of possible mechanisms of action. To
support the use of UP injections for chronic low
back pain, the authors included the findings of
several Cochrane reviews.
Comments
It was encouraging that the North American
Spine Society sponsored a special issue of the
Spine Journal, which included this reasonably wellwritten article on TrPs as a nonsurgical approach
to chronic low back pain. Although the authors
advocated the use of TrP injections, they
excluded many recent studies, which substantiate
the trigger point concepts and the use of
injections. They mentioned that "a few states allows physical therapists to perform dry needling."
Dn needling is within the scope of physical therapy practice in 11 states in the United States,
and in many countries around the world, including Australia, Canada, Ireland, the Netherlands,
New Zealand, Norway, South Africa, Spain,
and the United Kingdom, among others.
The authors noted the limits some insurance
companies have imposed on the administration
of TrP injections, but they did not comment on
the significant discrepancies between arbitrary
insurance policies and clinical utility. One of the
insurance companies allows up to three injections per year, which for most patients with TrPs
and chronic pain conditions is very inadequate.
The authors suggested that trigger point injections should be considered when patients with
chronic low back pain have failed to respond
to medications or a course of active physical
therapy. This reviewer would argue that TrP injections or dry needling should be considered
early in the treatment of patients with chronic
low back pain and not just after other remedies
have failed.
Simons DG: New views of myofascial trigger points:
Etiology and diagnosis. Arch Phys Med Rehabil
89:157-159, 2008.
This article is a commentary on several studies
published in the Archives of Physical Medicine and
Rehabilitation. Dr. Simons emphasized the
importance of the recent studies by Shah et al. of
the chemical environment of active TrPs for the
integrated trigger point hypothesis (4, 5). The
finding
of
multiple
pro-inflammatory
inflammatory
cytokines,
serotonin,
and
bradykinin, among others, offers support for the
notion that noxious chemicals in the immediate
vicinity of motor endplates may indeed
stimulate nociceptors, contributing to pain from
TrPs. The other study by Chen et al. was
highlighted for its support of the presence of
taut bands using magnetic resonance elastography (6, 7). Although this technique does not
have direct clinical utilization, it is nevertheless
the first magnetic resonance elastography study
of trigger point phenomena. All papers already
have been reviewed in this column.
Clark GT.• Classification, causation and
treatment of masticatory myogenous pain and
dysfunction. Oral Maxillofacial Surg Clin N Am
20:145-157, 2008.
What a pleasant surprise to come across this
article published by an American dentist, who
actually mentioned TrPs in this overview article of masticatory muscle pain! As we have
commented many times earlier in this column
the dental literature frequently defines myofascial pain as "muscle pain with or without limited mouth opening" following the 1992 tempromandibular disorder criteria by Dworkin and
LeResche (8). Clark included basic information
about TrPs and briefly discussed the treatment
options for trigger points therapy. Hopefully, this
paper will contribute to expanding the TMD
criteria and include the current knowledge base
of TrPs.
REFERENCES
1. Gerwin RD, Shannon S, Hong CZ, Hubbard
D, Gevirtz R:lnterrater reliability in myofascial trigger
point examination. Pain 69(1-2): 65-73, 1997.
2. Simons DG, Travell JG, Simons LS: Travell and
Simons' Myofascial Pain and Dysfunction: The Trigger
Point Manual. 2 ed., Vol. 1. Williams & Wilkins,
Baltimore, 1999.
3. Rocha CA, Sanchez TG: Myofascial trigger
points: Another way of modulating tinnitus. Prog Brain
Res 166: 209-214, 2007.
4. Shah JP Danoff JV, Desai MJ, Parikh S,
Nakamura LY, Phillips TM, et al.: Biochemicals associated with pain and inflammation are elevated in sites
near to and remote from active myofascial trigger points.
Arch Phys Med Rehabil 89(1): 16-23, 2008.
5. Shah JP, Phillips TM, Danoff JV, Gerber LH: An
in-vivo microanalytical technique for measuring the local
biochemical milieu of human skeletal muscle. J Appl
Physiol 99: 1977-1984, 2005.
6. Chen QJ, Bas lord KN: An ability of magnetic resonance clastography to assess taut bands. Clin Biomech
23(5): 623-629, 2008.
7. Chen Q, Bensamoun S, Basford JR, Thompson
Jet, An KN: Identification and quantification of myofascial taut bands with magnetic resonance elastography.
Arch Phys bled Rehabil 88(12): 1658-1661, 2007.
8. Dworkin SF, LeResche L: Research diagnostic criteria for tcmporomandibular disorders: review,
criteria. examinations and specifications, critique. J
Craniomandib Disord Facial Oral Pain 6: 301-355, 1992.

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