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REVIEW

Myofascial trigger points and sensitization: an updated painmodel for tension-type headache

C Fernndez-de-las-Peas1,2, ML Cuadrado2,3, L Arendt-Nielsen4, DG Simons5 & JA Pareja2,31Department of Physical Therapy, Occupational Therapy, Physical Medicine and Rehabilitation and 2Aesthesiology Laboratory, Universidad

Rey Juan Carlos, 3Departments of Neurology, Fundacin Hospital Alcorcn and Universidad Rey Juan Carlos, Alcorcn, Madrid, Spain,4Centre for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Aalborg University, Aalborg, Denmark and5Rehabilitation Medicine at Emory University, Atlanta, GA, USA

Fernndez-de-las-Peas C, Cuadrado ML, Arendt-Nielsen L, Simons DG &Pareja JA. Myofascial trigger points and sensitization: an updated pain model fortension-type headache. Cephalalgia 2007; 27:383393. London. ISSN 0333-1024

Present pain models for tension-type headache suggest that nociceptive inputs

from peripheral tender muscles can lead to central sensitization and chronictension-type headache (CTTH) conditions. Such models support that possibleperipheral mechanisms leading to pericranial tenderness include activation orsensitization of nociceptive nerve endings by liberation of chemical mediators(bradikinin, serotonin, substance P). However, a study has found that non-specific tender points in CTTH subjects were not responsible for liberation ofalgogenic substances in the periphery. Assuming that liberation of algogenicsubstances is important, the question arising is: if tender muscle points are notthe primary sites of on-going neurogenic inflammation, which structure can beresponsible for liberation of chemical mediators in the periphery? A recent studyhas found higher levels of algogenic substances, and lower pH levels, in activemyofascial trigger point (TrPs) compared with control tender points. Clinicalstudies have demonstrated that referred pain elicited by head and neck muscles

contribute to head pain patterns in CTTH. Based on available data, an updatedpain model for CTTH is proposed in which headache can at least partly beexplained by referred pain from TrPs in the posterior cervical, head and shouldermuscles. In this updated pain model, TrPs would be the primary hyperalgesiczones responsible for the development of central sensitization in CTTH. Algo-genic substances, central sensitization, myofascial trigger points, peripheral nociception,tension-type headache

Csar Fernndez de las Peas, Facultad de Ciencias de la Salud, Universidad ReyJuan Carlos, Avenida de Atenas s/n, 28922 Alcorcn, Madrid, Spain. Tel. +34 91488 8884, fax +34 9 1488 8957, e-mail [email protected], [email protected]

Introduction

Headache is one of the most common problemsseen in medical practice. Among the many types ofheadache disorders, tension-type headache (TTH) isone of the most prevalent in adults. Population-based studies suggest 1-year prevalence rates of38.3% for episodic TTH and 2.2% for chronic TTH

(1). In addition, the prevalence of TTH hasincreased in recent years (2).

Despite some advances, the pathogenesis of TTHis not clearly understood. It has been demonstratedthat the most prominent clinical finding in bothadults and children suffering from TTH is anincreased tenderness to palpation of pericranialtissues (37). The increased tenderness seems to be

doi:10.1111/j.1468-2982.2007.01295.x

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uniformly increased throughout the pericranialregion and both the muscles and tendon insertionshave been found to be excessively tender (6, 7). Inaddition, it has also been reported that pressurepain threshold (PPT) levels are lower in patientswith chronic tension-type headache (CTTH) com-pared with control healthy subjects (810).

It has been postulated that increased pericranialtenderness and decreased PPT levels in CTTHsubjects may be due to an increased sensitivity(hyperexcitability) in the central nervous systemor in the periphery. However, the demonstrationof a relation between pericranial tenderness andcentral sensitization does not reveal the causeeffect relationship between these factors. Bendtsenet al. (11) established a pain model in which themain problem in CTTH is the sensitization ofcentral pathways due to prolonged nociceptiveinputs, possibly provoked by the liberation of

algogenic substances at the periphery, from peri-cranial myofascial tender tissues. The presence ofprolonged peripheral inputs can be a mechanismof major importance for the conversion of episodicinto chronic TTH (11). The proposed modelexplains the sensitization at the level of the spinaldorsal horn/trigeminal nucleus, the slightlyincreased supraspinal hypersensitivity, the slightlyincreased muscle activity, the increased musclehardness, the chronic pain and the absence ofobjective signs of peripheral pathology in patientswith CTTH with increased pericranial tenderness.

However, the model does not account for themechanisms that initiate the central sensitization,i.e. the structures responsible for the nociceptiveinput from the periphery (11).

The aims of the present paper were: (i) to reviewthe fundamental neurophysiology of central sensi-tization in CTTH; and (ii) to update the pain modelfor CTTH based on recent histochemical andclinical studies on referred muscle pain in TTHpatients.

Central sensitization in CTTH

Sensitization of peripheral muscle nociceptors byliberation of algogenic substances

Spinal dorsal horn neurons that receive inputsfrom myofascial tissues can be classified as high-threshold mechano-sensitive (HTM) neurons, whichrequire noxious intensities of stimulation for acti-vation, or as low-threshold mechano-sensitive(LTM) neurons, which are activated by innocuous

stimuli (12). It has been demonstrated that HTMdorsal horn neurons have a positively acceleratingstimulusresponse function, whereas LTM neuronshave a linear stimulusresponse function (13). Thisfinding suggests that the linear stimulusresponsefunction in human muscles may be caused by activ-ity in LTM afferents, although at first this seemsunlikely. Furthermore, several studies have demon-strated that prolonged noxious input from theperiphery is capable of sensitizing spinal dorsalhorn neurons, showing that LTM afferents canmediate pain (12, 1416).

It is known that chemical mediators may sen-sitize the nociceptive nerve endings. Particularlyeffective stimulants for skeletal muscle nociceptorsare endogenous substances such as bradykinin orserotonin (12). Several studies have found thatsensitization of nociceptive nerve endings isgreater with the combination of both substances

rather than with each substance alone (17, 18).Therefore, muscle pain is produced mainly bynoxious stimuli that lead to increased synthesisand release of endogenous algogenic substancessuch as serotonin, bradykinin, histamine or pros-taglandins. Such stimuli may cause the antidromicrelease of neuropeptides from the nerve endingsof C fibres which contain neuropeptides such ascalcitonin gene-related peptide, substance P orneurokinin A (19, 20). The liberation of algogenicsubstances would lower tissue pH and then acti-vate the arachidonic acid cascade that produces a

number of unsaturated lipid products. Sensitiza-tion of nociceptors would cause spontaneous neu-ronal discharge, a lowered threshold to stimulithat normally provoke pain and an increasedfiring to stimuli that are not ordinarily perceivedas painful. Previous studies have confirmed thepresence of sensitization of peripheral musclenociceptors in both chronic (11) and episodic TTH(21, 22). Finally, other inflammatory chemicalsbelieved to be involved include bradykinin fromplasma, serotonin (5HT) from platelets andglutamate, which are known to affect the mem-branes of polymodal nociceptors to produce sen-

sitization (23).In addition, activation of silent peripheral noci-

ceptors might result in a qualitatively changedstimulusresponse function, explaining the abnor-mal stimulusresponse function seen in patientswith chronic myofascial pain (24). Further, it hasbeen recently found that the displacement of thestimulusresponse function is closely associatedwith frequency of headache in CTTH sufferers(25).

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Sensitization of second-order neurons inthe dorsal horn and in the trigeminalnucleus caudalis

Central sensitization can be generated by prolongednociceptive inputs from the periphery (26). Thismechanism is particularly important in patientswith chronic myofascial pain, since inputs frommuscle nociceptors are more effective in inducingprolonged changes in the behaviour of dorsal hornneurons than inputs from cutaneous nocicep-tors (27).

Increased excitability of the dorsal horn neuronswould alter pain perception significantly. In thissensitized state, previously ineffective low-threshold Abfibre inputs to nociceptive dorsal hornneurons may become effective (28. 29). In such away, pain could be generated by low-threshold Abfibres, which clinically will manifest as allodynia.

It has been suggested that the major cause ofincreased pain sensitivity in chronic pain is anabnormal response to inputs from low-threshold Abfibres (30). In addition, the response to activation ofhigh-threshold afferents would be exaggerated,which clinically will manifest itself as hyperalgesia.Decreased PPT levels, i.e. local hyperalgesia, hasbeen found in both cephalic (9, 10) and extracepha-lic (8, 31) sites in CTTH, and other chronic muscu-loskeletal conditions such as whiplash (32).

Further, in the sensitized state, the afferent Abfibres, which normally inhibit Ad and C fibres by

presynaptic mechanisms in the dorsal horn, will, onthe contrary, stimulate the nociceptive second-orderneurons. Therefore, the effect of Ad and C fibrestimulation of the nociceptive dorsal horn neuronswill be promoted and the receptive fields of thedorsal horn neurons will be expanded (33). Thenociceptive input to supraspinal structures willbe considerably increased and, if more spatialinput exists, may result in increased excitability ofsupraspinal neurons (34) and decreased inhibitionor increased facilitation of nociceptive transmissionin the spinal dorsal horn (35), which will manifestclinically as generalized pain hypersensitivity. Gen-

eralized hyperalgesia has been recently demon-strated in CTTH patients (36), and other chronicmusculoskeletal conditions, i.e. osteoarthritis (37)and fibromyalgia (38).

Which peripheral structure is responsible for theliberation of algogenic substances?

Actual pain models for TTH establish that pro-longed nociceptive inputs from myofascial tender

tissues, i.e. peripheral sensitization of musclenociceptors provoked by the liberation of algogenicsubstances, could lead to central sensitization inCTTH (11). The question arising is: which structuresand mechanisms are responsible for initiating theliberation of algogenic substances in the periphery?

Bendtsen et al. have suggested that pericranialtender points could lead to central sensitizationin CTTH (11). However, Ashina et al. found nodifference in change in interstitial concentration ofadenosine 5-triphospate (ATP), glutamate, bradiki-nin, prostaglandin E2, glucose, pyruvate and ureafrom baseline to exercise and post-exercise periodsbetween non-specific tender points of CTTH sub-jects and controls (39). Authors of that study con-cluded that tender points in CTTH subjects are notresponsible for liberation of algogenic substances inthe periphery (39). On the other hand, significantlyhigher levels of algogenic substances, i.e. bradyki-

nin, calcitonin gene-related peptide, substance P,tumour necrosis factor-a, interleukin-1b, serotoninand norepinephrine, and lower pH levels, havebeen found in active but not in latent myofascialtrigger points (TrPs) (40). Since tender points(increased tenderness, local but not referred pain)and myofascial TrPs (hypersensitive spot, taut bandin a skeletal muscle, both local and referred painpattern) are different disorders, we can update thepain model for TTH based on peripheral sensitiza-tion of muscle nociceptors provoked by myofascialTrPs.

In conclusion, intense afferent nociceptive inputfrom peripheral muscle sensitization may alter thedorsal horn circuitry by unmasking, or activating,previously ineffective synapses to form novel syn-aptic contacts between low-threshold afferentsand high-threshold mechanosensitive dorsal hornneurons (41). Therefore, in these patients the pro-longed nociceptive input from muscle TrPs maylead to sensitization of nociceptive second-orderneurons at the level of the spinal dorsal/trigeminalnucleus.

Muscle referred pain and myofascialtrigger points

Convergence of nociceptive inputs on thetrigeminal nucleus caudalis explaining musclereferred pain to the head

Small diameter group III and IV fibres from neckand shoulder muscles terminate mainly on neuronslocated in the superficial and intermediate dorsalhorn (laminae I and V) of the spinal cord (42, 43).

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Myofascial afferents from several different areasconverge onto the same second-order nociceptiverelay neurons in the spinal cord and the trigeminalnucleus caudalis. Animal (44) and human (45, 46)studies have clearly shown the convergence of cer-vical and trigeminal afferents in the trigeminalnerve nucleus caudalis, constituting the anatomicalbasis for the referred head pain from neck andshoulder muscles. Since nociceptive somaticafferents from muscles of the upper cervical roots,particularly C1 to C3, and the trigeminal nerve,particularly V1 (oftalmic) and V3 (mandible)nerves, converge on the same relay neurons, it isassumed that the message to supraspinal structurescan be misinterpreted and localized as pain in otherstructures distant from the site of painful stimulus(muscle referred pain).

In addition, dorsal horn neurons that receiveafferents from muscles frequently receive input

from other structures (47, 48). This extensive con-vergent input to dorsal horn neurons may accountfor the often diffuse and poorly localized natureof deep pain sensation in humans, particularlywhen pain is intense. In addition, animal studieshave demonstrated spinal level spread of the painmessage from one dorsal horn cell to another that isinitiated by strong input from muscle nociceptors(29, 49) and can be interpreted as a likely contrib-uting cause of muscle referred pain (50).

Different experimental pain models have beenproposed in order to elicit referred pain from peri-

cranial muscles. Hypertonic saline injections inducefiring in a large proportion of Ad and C fibres andcause deep, aching, referred pain in humans, simi-larly to clinical muscle pain (51). Schmidt-Hansenet al. have recently demonstrated that referred painelicited by the infusion of hypertonic saline into theanterior or posterior temporalis muscles is per-ceived as head pain (trigeminal or cervical der-matomes) in healthy subjects (52). Further, Ge et al.have demonstrated that injection of hypertonicsaline into the upper trapezius muscle elicited areferred pain to the neck and to the head in asymp-tomatic subjects (53, 54).

Clinical and physiological presentation ofmyofascial trigger points

Simons et al. define a TrP as a hyperirritable spotassociated within a taut band of a skeletal musclethat is painful on compression, and usually res-ponds with a referred pain pattern distant from thespot (a TrP) (55). From a clinical viewpoint, activeTrPs cause pain symptoms, and their local and

referred pain is responsible for patients complaints.In patients, the referred pain elicited by active TrPreproduces at least part of their clinical painpattern. Latent TrPs also evoke referred pain withmechanical stimulation or muscle contraction, butthis pain is not a usual or familiar pain for thepatient. Both active and latent TrPs can provokemotor dysfunctions, e.g. muscle weakness orimbalance, altered motor recruitment (56), in eitherthe affected muscle or in functionally relatedmuscles (55).

The formation of TrPs may result from a varietyof factors (e.g. muscle overuse, mechanical overloador psychological stress). Under normal conditions,pain from TrPs is mediated by thin myelinated (Ad)fibres and unmyelinated (C) fibres (57). Variousnoxious and innocuous events, such as mechanicalstimuli or chemical mediators, may excite and sen-sitize Adfibres and C fibres and thereby play a role

in the development of TrPs (58). Recent studieshave hypothesized that the pathogenesis of TrPscould result from injured or overloaded musclefibres (59). This could lead to endogenous (invol-untary) shortening, loss of oxygen supply, loss ofnutrient supply and increased metabolic demandon local tissues (60). However, these events havenot been completely proven and more research isneeded.

The most credible aetiological suggestion of TrPsis the integrated hypothesis, which hypothesizesthat abnormal depolarization of motor endplates

and sustained muscular contraction give rise to alocalized ATP energy crisis associated with sen-sory and autonomic reflex arcs that are sustained bycentral sensitization (61). A recent study foundhigher levels of pain when a noxious stimulus wasapplied to the motor endplate region comparedwith silent muscle sites (62). In addition, painevoked from motor endplate regions was describedas throbbing, sharp or aching; similar descriptionsto TrP referred pain sensations (55). It has beensuggested that a higher density of muscle nocicep-tors in the vicinity of the motor endplate regionmay account for the observed differences in pain

(62), but this has not been confirmed in otherstudies. Furthermore, endplate noise and endplatespikes [electromyographic (EMG) signal from dys-functional motor endplate regions] has been iden-tified and significantly associated with TrPs (63, 64).Findings from these studies support the theory thatTrPs could be dysfunctional motor endplates (65);however, further studies are required.

Further, it has been previously assumed that con-traction of head, neck or shoulder muscles could




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play a relevant role in the development of TTH.However, numerous surface EMG studies havereported normal or, more often, only slightlyincreased muscle activity in TTH (6672). A pioneerstudy analysing EMG activity with needle elec-trodes found an increased EMG activity in TrPscompared with an adjacent non-tender point (73).Furthermore, spontaneous EMG activity (endplatenoise) in the TrPs was significantly higher inpatients with CTTH than in healthy controls (73).Since the endplate region of a muscle fibre is only0.1 mm at the most in diameter, the increased EMGactivity (motor endplate noise and spikes) could bedetected only with needle electrodes preciselyplaced within the TrP. A histopathological cause oftaut bands in human trPs has not been convincinglydemonstrated. Many findings confirm the presenceof excessive muscle-fibre tension, but fail to identifyadequately what causes the tension. Also, there is

scientific evidence showing that increased auto-nomic activity increases endplate noise and clinicalsymptoms caused by TrPs, but the specific mediatorof this link is conjectural; norepinephrin is a likelycandidate. Finally, although there is evidence tosupport the integrated hypothesis of an aetiologicalorigin of TrPs, the above-mentioned studies haveseveral shortcomings which should be addressed infuture studies in order to confirm definitively thisetiological hypothesis as the genesis of TrPs.

Finally, it has been recently demonstrated thatactive TrPs may cause peripheral sensitization of

muscle nociceptors, since higher levels of algogenicsubstances and lower pH levels have been found inactive TrPs compared with both latent TrP andtender points (40).

Myofascial trigger points referred painin TTH

In their comprehensive text, Simons et al. havedescribed the referred pain patterns from differentTrPs in several head and neck muscles which havethe potential to refer pain to the head: upper tra-pezius, temporalis, sternocleidomastoid, spleniis

capitis, suboccipital muscles, etc. (Fig. 1) (55). SinceTTH is characterized by bilateral, pressing or tight-ening pain; pressure or band-like tightness; and/or increased tenderness on palpation of neck andshoulder muscles (74), these pain features resemblethe descriptions of referred pain originating in TrPs(55).

Recent studies have demonstrated clinical evi-dence of the presence of TrPs in certain neck andshoulder muscles in CTTH. Marcus et al. found, in

a non-blinded study, that TTH subjects had agreater number of either active or latent TrPs thanhealthy subjects (75). However, these authors didnot specify in which muscles TrPs were observedmore frequently. Similar findings have been re-ported for osteoarthritis patients (37). We recentlydemonstrated, in blinded controlled studies, thatCTTH is associated with active TrPs in the suboc-cipital muscles (76), and in the upper trapezius,sternocleidomastoid and temporalis muscles (77).All CTTH patients had active TrPs which, whenpressed, elicited referred pain that reproduced thesame head pain as during their headache attacks(Fig. 2). We also found that those CTTH patientswith active TrPs had greater headache intensity andfrequency than those with latent TrPs, which can beconsidered as temporal integration of the nocicep-tive barrage from TrPs (76, 77). In addition, inanother study we also found that patients with

CTTH with bilateral TrPs in the upper trapeziusmuscle had greater headache pain, longer headacheduration and lowered pressure pain thresholdscompared with those with unilateral TrPs, whichcan be considered as spatial integration of nocice-ptive inputs from muscle TrPs (78). In these studiesactive TrPs, which referred a pain pattern thatreproduced the patients pain, were bilaterallylocated in CTTH (7578). In a recent study, wefound that patients with strictly unilateral migraineshowed a unilateral distribution of active TrPswhich were mostly located ipsilateral to migraine

headaches compared with the non-symptomaticside (79). These findings support that, in patientswith bilateral TTH, referred pain from active TrPscould be contributing to their headache perception,since TrPs were located on both sides in most ofthem (7578).

Although there is scientific evidence for a closerelationship between TrPs in certain head and neckmuscles and CTTH (7578), the type of researchdata reported to date does not establish a cause-and-effect relationship between TrPs and CTTH. Itis known that central sensitization may also beinvolved in the generation of muscle referred pain

from TrPs (80). Different studies have found that thearea of the referred pain correlated with the inten-sity of the muscle pain in patients with sensitizationof central pathways (81). It has been suggested thatreferred pain in deep somatic secondary hyperal-gesia areas resembles that found in secondary hype-ralgesic areas at the skin following, for example,capsaicin application (82). In that way, musclereferred pain may also correlate with the phenom-ena of secondary hyperalgesia and tenderness seen




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in CTTH patients (81). In addition, peripheral andcentral sensitization, and decreased descendinginhibition induced by long-term nociceptive stimulifrom TrPs, may also be involved in referred pain(83). Larger referred pain areas have been foundin chronic musculoskeletal conditions, e.g. fibro-myalgia (84), whiplash (85) and myofascial tem-poromadibular pain patients (86). These studieshave demonstrated that patients with central

sensitization showed larger referred pain areas inboth symptomatic areas and distant, not usuallysymptomatic areas (e.g. tibialis anterior muscle),which indicates that nociceptive inputs to thecentral nervous system may facilitate the referredpain mechanisms possibly resulting from centralsensitization (38). In addition, we have found largerreferred pain areas from upper trapezius muscleTrPs in CTTH patients compared with healthy

Upper trapezius Sternocleidomastoid

Semispinalis cervicis

Temporalis muscle

Splenius capitis muscle Splenius cervicis muscle

Suboccipital musclesClavicular divisionSternal division

Figure 1 Referred pain patterns from upper trapezius, sternocleidomastoid, suboccipital, splenius capitis, splenius cervicis,semispinalis capitis and temporalis muscle trigger points as described by Simons et al. Reprinted with permission fromSimons D, Travell J, Simons L. Travell & Simons myofascial pain and dysfunction: the trigger point manual, Vol. 1, 2ndedn. Baltimore: Williams & Wilkins, 1999.




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subjects (78). These studies support the hypothesisthat the area of muscle referred pain provoked byTrPs in neck and shoulder muscles could beenlarged in CTTH patients, contributing to sensiti-zation of central pathways.

Since active TrPs are related to several chronicconditions accounting for sensitization of centralpathways, the question arising should be: are activeTrPs the consequence of central sensitization? If thecentral sensitization were causing active TrPs, theywould not be expected in patients suffering from

episodic TTH (ETTH), in which central sensitizationhas not been demonstrated (11). Since there is alesser degree of central senzitisation in ETTH,because of the intermittent nature of the condition,one would expect fewer active and more latent TrPsin ETTH than in CTTH. We have demonstrated thatactive TrPs in the suboccipital, upper trapezius,sternocleidomastoid and temporalis muscles arealso present in ETTH (87, 88), to a similar degree asin CTTH (76, 77). However, active TrPs were notrelated to headache clinical parameters in ETTH,supporting the hypothesis that there was no tem-poral summation of peripheral nociceptive inputs

in patients with ETTH, due the intermittent natureof the condition. These findings indicate that activeTrPs are not the consequence of central sensitiza-tion, since they are also present in ETTH.

Based on available data, we can make twoassumptions: (i) myogenic referred pain elicited byactive TrPs in head, neck and shoulder musclescontribute to headache pain patterns in TTHpatients (7578, 87, 88); and (ii) persistent periph-eral sensitization provoked by algogenic substances

elicited by active TrPs (40), could lead to sensitiza-tion of nociceptive second-order neurons at thelevel of the spinal dorsal/trigeminal nucleus.

Updated pain model for TTH

Olesen (89) has suggested that perceived headacheintensity might be due to the sum of nociceptiveinputs from cranial and extracranial tissues con-verging on the neurons of the trigeminal nucleuscaudalis. Bendtsen (11) has suggested that the

barrage of peripheral nociceptive inputs is respon-sible for the development of central sensitization.Our updated model suggests that TrPs located inhead and neck muscles innervated by C1C3 (e.g.upper trapezius, sternocleidomastoid, suboccipitalmuscles) or by the trigeminal nerve (e.g. temporalis,masseter) are responsible for the peripheral nocice-ptive input and could produce a continuous affer-ent barrage into the trigeminal nerve nucleuscaudalis. Connections between afferents innervat-ing deep structures and second-order neuronscould be altered by these nociceptive afferent inputsfrom muscle TrPs. Convergent synaptic connections

on dorsal horn neurons, which are not usuallyfunctional, could be activated if intense nociceptiveinput reaches the dorsal horn. Changes in size andshape of peripheral receptive fields, and the forma-tion of new receptive fields, would occur if nocice-ptive barrage from muscle TrPs is maintainedduring time. This would result in temporal andspatial integration of neuron signals and might beone of the reasons for the central sensitization inCTTH.

Referred pain patterns from muscle TrPs TTH(a) (b)

Upper trapezius muscle

Sternocleidomastoid muscle

Suboccipital muscles

Head pain pattern inTTH

Figure 2 Similarities between the elicited referred pain from manual examination of upper trapezius, sternocleidomastoidand suboccipital muscle trigger point (TrP) in tension-type headache (TTH) patients (a) and the head pain patterndescribed by patients themselves (b).




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Based on new available data, an updated painmodel for TTH could be hypothesized as follows:TTH can at least partly be explained by referredpain from TrPs in the posterior cervical, head(including extraocular muscles) and shouldermuscles, mediated through the spinal cord and thebrainstem trigeminal nucleus caudalis, rather thanonly tenderness of the pericranial muscles them-

selves. In this updated pain model, we could con-sider TrPs as primary hyperalgesic zones in whichreferred pain areas to the head exhibit increasedtenderness and decreased pressure pain thresholds(secondary hyperalgesic zones). Figure 3 illustratesthe updated pain model for TTH.

Finally, a TrP role in headache does not negatethe importance of other physical (e.g. malalignmentof upper cervical vertebrae (90) or forward headposture (91)) or psychological (e.g. anxiety ordepression) factors in exacerbating and sustainingCTTH. It is of great clinical interest to note thatthese same factors are known to aggravate and

promote TrP activity. Many elements traditionallydeemed important in the genesis of CTTH mayresult from inadequate strategies devised to copewith TrP-induced head pain.

In conclusion, an updated pain model for CTTHhas been proposed in which headache can be atleast partly caused by referred pain from activeTrPs in the posterior cervical, head and shouldermuscles mediated through the spinal cord and thebrainstem trigeminal nucleus caudalis. In this

updated pain model, TrPs would be the primaryhyperalgesic zones responsible for the developmentof central sensitization in CTTH. If this model isvalid, every patient seen for TTH needs to beexamined for TrPs, which are often apparently con-tributing significantly to their symptoms.

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Peripheral sensitization

Sensitization of centralpathways

Myofascial TrPs (referred pain pattern)

Liberation of algogenicmediators

Updated pain model for TTH

Aand C fibres

Nociceptive barrage

Increased paintransmission

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