Myofascial pain syndromes in the maxillofacial area: a ... Myofascial pain syndromes (MPS) are a...

YIJOM-1399; No of Pages 10

Invited Review PaperFacial Pain

Int. J. Oral Maxillofac. Surg. 2008; xxx: xxx–xxxdoi:10.1016/j.ijom.2008.04.023, available online at http://www.sciencedirect.com

Myofascial pain syndromes inthe maxillofacial area: acommon but underdiagnosedcause of head and neck painLeonidasManolopoulos, Petros V. Vlastarakos, LucasGeorgiou, IoannisGiotakis,AnthonyLoizos, Thomas P. Nikolopoulos: Myofascial pain syndromes in themaxillofacial area: a common but underdiagnosed cause of head and neck pain. Int. J.Oral Maxillofac. Surg. 2008; xxx: xxx–xxx. # 2008 International Association of Oraland Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Abstract. Myofascial pain syndromes (MPS) are a large group of muscular disorders,characterized by the presence of hypersensitive spots called trigger points (TP). Themaxillofacial region is a high-frequency area for developing TPs. The aim of thispaper was to review and summarize the most important methods of management. Aliterature review was carried out from Medline and database sources. A range ofstudy types were selected for analysis. TP formation and activity result in areverberating circuit of sustained neural activity. Central mechanisms, primarilyassociated with psychosocial factors, lead to chronicity. Other synergistic factorsare metabolic disorders, nutritional imbalances and regional anatomic disorders. Adetailed history and physical examination are important for proper diagnosis. Theaim of MPS management is pain relief and restoration of full muscle function.Treatment may require enhancing central inhibition, using pharmacological and/orbehavioural techniques, and reducing peripheral inputs, using physical therapy.There are various effective methods of inactivation of TPs. Recognition andreduction of synergistic factors may be important. MPS have a very high prevalencein the general population, despite low awareness among physicians, affectingpatients’ quality of life. There is a need for interdisciplinary teams of healthprofessionals to achieve proper diagnosis, management and sustainable outcomes.

Please cite this article in press as: Manolopoulos L., et al., Myofascial pain syndromes

underdiagnosed cause of head and neck pain, Int J Oral Maxillofac Surg (2008), doi:10.1

0901-5027/000001+010 $30.00/0 # 2008 International Association of Oral and Maxillofacial Surgeo

Leonidas Manolopoulos1,Petros V. Vlastarakos1,Lucas Georgiou2, IoannisGiotakis1, Anthony Loizos2,Thomas P. Nikolopoulos1

1ENT Department, Hippokrateion GeneralHospital of Athens, Athens, Greece; 2PainClinic, Hippokrateion General Hospital ofAthens, Athens, Greece

Keywords: myofascial syndromes; head andneck pain; muscular disorders; trigger points;maxillofacial; treatment.

Accepted for publication 29 April 2008

Head and neck pain may be associated withinflammation, neoplasm, certain types ofarteritis, ophthalmic diseases, orthopedicproblems, neurological or psychiatric con-ditions, and other disorders. Differentialdiagnosis can be very difficult, and patients

may be left under long-term pain-relieftreatment without proper diagnosis.

Myofascial pain syndromes (MPS)form a large group of muscular disordersthat are not well known by clinical practi-tioners and are usually underestimated or

misdiagnosed, leaving a significant num-ber of patients without proper treatment.The aim of the present study was to reviewthe existing literature on MPS and sum-marize their most important features andmethods of management.

in the maxillofacial area: a common but

016/j.ijom.2008.04.023

ns. Published by Elsevier Ltd. All rights reserved.

http://dx.doi.org/10.1016/j.ijom.2008.04.023


2 Manolopoulos et al.


Materials and methods

An extensive search of the literature wasperformed in Medline and other availabledatabase sources, using the keywords‘‘myofascial’’, ‘‘pain syndromes’’,‘‘maxillofacial’’, ‘‘trigger points’’, ‘‘tautbands’’ ‘‘motor end-plates’’, ‘‘nocicep-tors’’ and ‘‘treatment’’. Information fromelectronic links and five related books wasincluded in the analysis of data.

Results

Twenty-four randomized controlled trials,eight controlled clinical trials, 19 clinicaltrials, 11 laboratory studies, three retro-spective studies, 31 reviews and four casereports met the defined criteria and wereincluded in the study selection.

Discussion

MPS are characterized by the presence ofhypersensitive spots called trigger points(TPs). Such a syndrome is a regional dis-order concerning the muscle, its fascia orboth, and is accompanied by pain in anaffected area and/or a zone of reference,autonomous phenomena and malfunctionof the affected muscle30,95. The presenceof MPS in the maxillofacial area mainlyconcerns the masseter, temporalis, lateraland medial pterygoid muscles.

A TP elicits pain after palpation and/orcauses pain radiation towards a zone ofreference, and a local twitch response2. Itcan be active or latent. Active TPs causespecific pain during muscle movement,impeding full extension of the muscleand decreasing the range of motion. Theyalso display pain during relaxation, result-ing in continuous pain in the zone ofreference which can be accompanied byautonomous phenomena. The final out-come may be muscle degeneration. LatentTPs are pressure sensitive and becomepainful only during palpation. They canbe a predisposing factor for muscular mal-function. This state of latency can remainfor years, resulting in acute painful boutswhen activation occurs.

Pain in the reference zone originatesfrom a TP and is perceived in a distantlocation. It can be accompanied by regio-nal vasoconstriction, perspiration, sialor-rhea and pilomotor phenomena. Thecharacteristics of MPS may long outlastthe initiating events, setting up a self-induced pain cycle that is perpetuatedthrough continuing muscle tension andpain-reinforcing behavior, improper treat-ment and failure to reduce other synergis-tic factors.

Please cite this article in press as: Manolop

underdiagnosed cause of head and neck pai

Bibliographic references to MPS havemade since the 16th century under variousterms, such as muscular rheumatism,myalgic nodules, myalgia, myositis andfibrosis. MPS seem to be very common inthe USA25, as approximately 15% of thegeneral population are estimated to havemyofascial pain98, and 21%–93% of peo-ple with localized pain may have MPS25.The prevalence has been seriously under-estimated in current clinical practice, as aconsiderable number of physicians maynot even know of the existence of MPS.

Although the presence of MPS is inde-pendent of age, the prevailing opinion isthat the risk of developing active TPs isconcomitant with age with a peak between40 and 50 years, and there is a higherincidence among women. In older people,when activity is diminished, latent TPsappear prevalent. Nearly every Americancitizen develops a TP at some point in hislife, and 25%–54% of people withoutsymptoms have latent TPs. The maxillo-facial region is considered a high-fre-quency area for developing active TPs,along with the neck area, shoulders, gluteiand spinal muscles. A lower incidence isobserved in the upper trapezius, scalene,sternocleidomastoid, levator of scapulaand illiocostal muscle of the loins.

Women face almost three times the riskof developing chronic masticatory myo-fascial pain than men97. Research onfemale twins has supported the importanceof environmental influence, as no differ-ence in frequency of symptoms related tomyofascial pain dysfunction syndromeswas found between monozygous (identi-cal) and dizygous (non-identical) femaletwins43.

MPS are without doubt among the mostcommon painful syndromes. When theybecome chronic, they are one of the pri-mary causes of functional disability, leaveof absence and compensation claims in thelabor force.

Biopsies have shown that TPs are dis-crete spots, ranging from 2 to 5 mm indiameter, found within hard palpablebands of skeletal muscle and the fascialstructure of tendons and ligaments30.Within each TP there is a hyperirritablespot, the ‘taut band’, which is composed ofhyper-contracted extrafusal musclefibres98. As well as the distinction betweenactive and latent TPs, the terms satelliteand secondary are used to describe TPswithin the pain reference zone of anotherTP and those developed in either syner-gists or antagonists of the primarilyaffected muscle, respectively.

The structural changes that occur in aTP are visible only using electron micro-

oulos L., et al., Myofascial pain syndromes

n, Int J Oral Maxillofac Surg (2008), doi:10.1

scopy. Biopsies of patients with palpableand very painful TPs showed both musclefibre changes, in the form of local muscledystrophy and complete disruption ofcross striation, and alterations in the inter-stitial spaces, such as increases in mastcells, lymphocytes and leucocytes, withconnective tissue proliferation66. A ‘moth-eaten’ appearance of type I and type IIfibres was discovered in a later studyconducted by YUNUS et al.106. Ultra-micro-scopic findings in 12 patients demon-strated significant changes, such asmyofibrillar lysis with deposition of gly-cogen and abnormal mitochondria as wellas subsarcolemmal accumulation of gly-cogen and mitochondria, and in 11 of thempapillary projections of the sarcolemmalmembrane. More recently, biopsies ofmyofascial tissue in the vicinity of TPshave revealed ‘contraction knots’,described as large, rounded, darkly stain-ing muscle fibres, and a statistically sig-nificant increase in the average diameterof muscle fibres65. In another study, biop-sies demonstrated segmental shortening ofgroups of sarcomeres in individual musclefibres, and possibly waves of contractedsarcomeres to account for palpable tautbands86. Other morphological disordersinclude formation of hyaline bodies inmuscle fibres and deposition of non-spe-cific inflammatory factors.

The formation of TPs is believed tooccur as a consequence of biomechanicalfactors63 that act either acutely, followinga sudden muscle overload (acute trauma),or contribute to a more gradual develop-ment, following prolonged contractions orrepetitive activity (repetitive micro-trauma). TP development secondary torheumatoid arthritis, lupus erythematosus,scleroderma, nerve injuries36 and visceraldiseases has been observed. Regardless ofthe cause, these injuries are thought torelease cytokines, especially bradykinin,histamine, serotonin and prostaglandins,which stimulate nociceptors near the end-plate region. A great concentration ofsensitive loci can be found in this area45

which may contain one or more of thesensitized nociceptive nerve endings.

The correlation between motor end-plates and TPs was first elucidated byGUNN and MILBRANDT

41. The pathophysio-logical and biochemical mechanisms thatoccur in the dysfunctional end-plate areaare thought to include presynaptic disor-ders in the a-motor neurons leadingto excessive acetylcholine (ACh)release65,87, as well as synaptic andpost-synaptic dysfunction due to pro-longed ACh presence following acetyl-cholinesterase (AChE) deficiency and


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MPS and head and neck pain 3


nicotine ACh receptor (nAChR) hyperac-tivity or hypersusceptibility, respectively.These dysfunctions can be genetic oracquired56,58,72,76. Excessive ACh releasein the synaptic cleft following Ca++ chan-nel dysfunction, sarcoplasmic reticulumdestruction, prolonged ACh presencedue to AChE deficiency, or even constantor extremely sensitized activity of thenAChR post synaptically leads to a viciouscircle: excessive muscle contractioncompresses the local sensory nerves andreduces the axoplasmic transport of mole-cules that normally inhibit AChrelease34,44.

Compression of local blood vessels canalso occur when muscle contraction isprolonged, resulting in a reduction in thelocal supply of oxygen. The combinationof poor oxygen supply and increasedmetabolic demand results in the rapiddepletion of local ATP reserves, generat-ing an ATP energy crisis87. ATP shortageresults in decreased inhibition of AChrelease in the a-neuron and impairs thenormal function of the Ca++ pump in themuscle cell, decreasing the re-uptake ofCa++ and perpetuating the cycle. Thishypothetical model is supported by bio-chemical findings, such as decreasedlevels of ATP, ADP and phosphoryl crea-tine, and increased levels of AMP andcreatine in muscle biopsy samples6, alongwith evidence of abnormal tissue oxyge-nation59. Other biochemical findingsinclude localized increases of tissue water,chloride and acid mucopolysaccharides,decreased levels of serum lactic dehydro-genase fraction 1 (LDH1), and increasedlevels of LDH3, LDH4, LDH5 and musclealdolase47, indicative of inflammatorychanges similar to polymyositis duringTP development.

Focal demyelination of sensory nervesmay be a result of the local production ofsensitizing substances, creating abnormalimpulse-generating sites capable of gen-erating ectopic nociceptive impulses10.Dysregulation of the g-motoneuron circui-try, leading to muscle disinhibition, is alsoproposed as a mechanism for the devel-opment of TP activity. The outcome of thisdysregulation may be muscle hyperactiv-ity after contraction, excessive electricalactivity during movement, and/or inap-propriate co-activity with other musclesduring movement16.

TP formation and consequent activityresult in sensitization of the dorsal horns incertain spinal cord segments, and theestablishment of a reverberating circuitof sustained neural activity98. Sensitiza-tion of the central nervous system is accel-erated in the presence of abnormal



impulse-generating sites63, while the sen-sitized dorsal horns also receive nocicep-tive signals, concerning somatic orvisceral dysfunctions, which converge inthe same spinal cord segment63. Sensitiza-tion of second-order neurons in the brain-stem, due to the activation of N-methyl-D-aspartate receptors, may be involved.

Other theories explaining the persis-tence of pain in MPS include spinalreflexes that alter the biochemical envir-onment of the nociceptors in the skeletalmuscles64 and differences in muscle phy-siology71. A neural basis involving centralpain, and/or peripheral hyperalgesia, hasbeen considered75. Muscle dysfunction inMPS may be regarded as myospasticactivity52 and MPS may represent focaldystonia80. The fact that disturbance innon-rapid eye movement sleep has beenrelated to a temporary appearance of mus-culoskeletal symptoms suggests that myo-fascial pain may be a non-restorative sleepsyndrome68. MPS can be perpetuated byprotective splinting of the affected muscleand by avoiding painful stretching. If nor-mal muscle length is not restored and thepainful process continues, the muscleband initially responds with hypertrophy,which later evolves to dystrophic changesand localized fibrosis.

Certain aspects of the above theories onthe pathology of MPS have received criti-cism. Since the painful muscles in MPSare electrically silent, the suggestion ofmyofibrillar or myofascicular contractionis considered highly improbable18. Therecovery from muscle injuries in normalsubjects is complete, unless muscle tearsor deep haematomas exist67. This debateand related research continue.

Biomechanical strain seems to be impli-cated in the onset of MPS, but centralmechanisms primarily associated withpsychosocial factors lead to the chronicityof the syndromes29. A large survey inIsrael demonstrated that 1 in 6 patientswith chronic widespread pain were foundto have a mental disorder9, and anotherstudy has suggested that MPS patientshave a remarkable hypochondriac ten-dency and irrational way of thinking53.Evidence from electromyogram (EMG)responses indicates that patients withMPS display a stereotypic response tostress via increased activity in the facialmuscles51. Although it is difficult to estab-lish solid evidence of a direct relationshipbetween stress and MPS, higher than nor-mal levels of urine catecholamines and 17-hydroxycorticosteroids, which are usuallyindicative of stressful situations, werefound in a group of patients withMPS21. Stress-related muscle habits, such



as bruxism, result in myofascial pain35

through augmented contraction of themasticatory muscles, and abnormal swal-low patterns may predispose to the devel-opment of MPS due to hyperactivity of thedigastric muscles38. Anxiety and depres-sion have also been associated with mas-ticatory myofascial pain97.

The presence of metabolic disorders,such as McArdle’s disease94, may facil-itate the development of MPS, while otherdisturbances such as hypothyroidism,hyperuricaemia, increased creatine levels,oestrogen deficiency, mild iron deficiency,anaemia, and low potassium and calciumreserves seem to be involved to someextent95. Nutritional disorders, such aslow levels of C, E and B complex vitaminsin the blood along with decreased plasmafolic acid (common in chronic alcohol-ism), are also considered to be synergisticfactors for the development of TPs95.Temporomandibular joint disorders(TMD), internal derangements, cervicalosteoarthritis and disc disease can contri-bute to the development of TPs, mainly asa result of reflex muscle splinting to pro-tect the joint from aggravating move-ment95.

Some of these factors may be a resultand not the cause, and the old ‘chicken–egg’ question is valid in many cases ofMPS. For example, is stress a contributingfactor to these syndromes, or are thesesyndromes causing stress to the patients?

At present, there is no reliable, objectivetest to confirm the presence of myofascialTPs57 and therefore no gold-standard diag-nostic criterion exists84. The diagnosis ofMPS in the maxillofacial area is basedupon the history and physical examinationof the patient, which can be furtherassisted by laboratory findings indicativeof predisposing or synergistic factors, suchas hypothyroidism, vitamin deficiencies,hyperuricaemia, McArdle’s disease, etc.

Imaging methods include ultrasonogra-phy, which has shown significant differ-ences in the thickness at rest, and theincrease ratio by contraction, betweenpatients and control groups, possiblyrelated to muscle oedema3. Temperaturemeasurements of the skin overlying theupper trapezius muscle, using liquid crys-tal thermography, in patients with TMDhave showed increased temperature on thesymptomatic side78. The diagnostic valueof this method has not been well docu-mented92.

Although routine EMG studies havefailed to show significant abnormalitiesassociated with TPs18, such as evidenceof denervation or focal muscle spasm,some specialized EMG studies have


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Fig. 1. Physical examination.

revealed certain differences. End-platenoise is significantly more prevalent inmyofascial TPs than at other sites withinthe end-plate zone, suggesting that it maybe a characteristic of the TP region but notrestricted to it85. An interesting EMGdifference appears between active andlatent TPs during TP needling. The formershow bilateral or mirror-image EMGactivity associated with unilateral needlestimulation4.

Since laboratory testing and imagingtechniques cannot reliably diagnoseMPS, a detailed history and physicalexamination are essential. The latterrequires specific skills, such as innatepalpation ability, authoritative trainingand extensive clinical experience86. Pro-blems of reliability concerning findings oftaut bands, muscle twitch and active TPs



Fig. 2. Physical examination for TPs in the ma

occur, even among experts104. Pain onpalpation of a TP can be prompt or delayedfor a few seconds. Usually this pain is deepand blunt, causing muscular dysfunctionand reducing the range of muscle move-ment, but its intensity depends on theirritability of the TP rather than the sizeof the affected muscle. The pattern of painreferral is both reproducible in the samepatient and consistent between patients,enabling the clinician to use the zone ofreference to pinpoint the TP in question.The patient’s behavioural reaction to firmpalpation of a TP is characterized as apositive ‘jump sign’ and is a distinguish-ing feature of MPS. Attention should bepaid during physical examination toabnormalities, such as malocclusion andprotective or restricted movements, duringjaw opening. Taut bands can be felt either



sseter muscle.

by exerting pressure with the fingertipsalong the muscle (Fig. 1A, left hand) orby ‘cupping’ the muscle venter betweenthumb and index finger and rolling for-wards and backwards (Fig. 1B and C).

TPs in the superficial layers of themasseter muscle cause referral pain inthe mandible, molars and related gingivae,whereas the pain from deep-layer TPsreflects at the temporomandibular joint(TMJ) and into the ear. Inspection of themasseter muscle is performed with anopen mouth in order not to cause painas a result of muscle tension. Palpationwith regard to the superficial layers isperformed either by pressing the muscleagainst the mandible (for anterior TPs,Fig. 2A), or by ‘cupping’ the musclebetween thumb and index finger(Fig. 2B). Deeper TPs may be found along


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Fig. 3. Physical examination for TPs in thetemporalis muscle.

the ramus of the mandible or the floor ofthe maxillary sinus.

TPs in the temporalis cause pain in thesupraorbital area and incisors of the max-illa (anterior section), premolar area (mid-dle section) or upper molars and occipitalarea (posterior section). Inspection of thetemporalis muscle is facilitated when thejaws are wide open so that the muscle isslightly tensed. The anterior and middlesection can be checked on the upper limitof the zygomatic arch, and the posteriorsection over the ear (Fig. 3). The inspec-tion is completed from inside the mouth,with palpation of the temporalis insertionon the coronoid process.

TPs of the medial pterygoid musclecause pain in the tongue, hard palate,TMJ and cervical muscles, swallowingdifficulties and decreased jaw opening,



Fig. 4. Physical examination for TPs in the pte

whereas TPs of the lateral pterygoid causedeep pain in the TMJ and maxilla andmastication disorders. The former can bepalpated either outside (Fig. 4A) orthrough the open mouth (Fig. 4B). Thelatter require a jaw opening of 5–8 mmwith the muscle palpated between the cystof Stafne and the zygomatic process(Fig. 4C and D).

The differential diagnosis of MPS in themaxillofacial area includes TMD, arthri-tis, fibromyalgia, temporal arteritis, fibro-sitis and polymyositis.

MPS may settle without medical inter-vention within 5–10 days, but if theybecome chronic can be quite disabling.Early diagnosis and targeted treatmentmay prevent chronicity occurring27. Theaim of MPS management is pain relief andrestoration of full-muscle function, whichis associated with complete muscle length,posture and full joint range of motion, toavoid chronic complications such as mus-cular dystrophy and permanent disability.Treatment may require enhancing centralinhibition, with the use of pharmacologi-cal and/or behavioural techniques, andreducing peripheral inputs, using physicaltherapy (exercises and TP-specific treat-ment)40. Recognition and reduction ofother synergistic factors33 or correctionof possibly unconscious postural habits19

may be important.Methods of inactivation of TPs include

non-invasive mechanical disruption(using massage, acupressure or ultra-sound), skin and muscle temperaturechanges (using vapour coolants, moist



rygoid muscles.

heat application, magnetic stimulation,electrical stimulation or laser therapy),and direct mechanical or chemical treat-ment (TP injections, acupuncture oranaesthetic patches).

Massage therapy is considered moreeffective than ultrasound application inreducing the number and intensity ofTPs31, but when combined with neck-stretching techniques ultrasound treatmenthas been found to be as effective as TPinjection20. When a high level of coopera-tion between the patient and therapist wasestablished, a high-power, pain-threshold,static ultrasound technique, before stretch-ing the muscle, was found to be moreeffective than conventional ultrasound inacute MPS60.

With the stretch-and-spray technique, amild application of vapour coolant spray isfollowed by passive stretching, providingimmediate reduction in pain (Fig. 5). TPinactivation may be more attributable tothe muscle stretching than freezing. Thistechnique can be applied in cases of multi-ple TPs where injection may be difficult toperform. Moist heat application afterstretching may further aid muscle relaxa-tion. Passive stretching of the masticatorymuscles can be accomplished by placing atrimmed and sterile cork between the inci-sors. During active stretching, rapid move-ments of the muscles should be avoided inorder to reduce risk of injury.

Transcutaneous electrical nerve stimu-lation is one of the most frequentlyemployed treatments in MPS, resultingin significant improvement in TP charac-


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Fig. 5. Stretch-and-spray technique.

teristics and range of motion of theaffected muscles. Modified therapeuticregimens, such as frequency-modulatedneural stimulation, seem more effectivewith regard to medium-term outcomesor algometry measurements23. Peripheralrepetitive magnetic stimulation was alsofound to be more effective in terms ofalgometry measurements and medium-to-long-term outcomes88.

Low-level laser therapy could be effec-tive in pain relief and improvement ofmuscle function and quality of life inpatients with MPS42. The decrease in painat rest and during activity has been eithertemporary48 or not statistically significantcompared to placebo1,17, but no double-blind randomized studies have to dateincluded the maxillofacial area.



Fig. 6. Injection of local anaesthetic.

TP injections have been found to reducepain and increase both range of motionand exercise tolerance. When a TP isneedled, a sudden contraction of the mus-cle called ‘local twitch response’ isobserved, as well as a temporary intensi-fication of pain over the muscle or in thezone of reference. Relief of pain shouldoccur within a few minutes, after whichfull-range manual stretching of the musclecan be attempted. The presence of persis-tent pain, 2–8 h after needling, is frequentand attributed to microscopic haemor-rhage which may occur during penetra-tion. This phenomenon can be avoidedusing a local anaesthetic such as procaine0.5% or lidocaine 0.5% or 1% (Fig. 6).Although local anaesthetics should inducea nerve conduction block that facilitates



muscular activity, in one study they werenot found to be superior to normal sal-ine96. More recently, lidocaine 0.5% injec-tion has been considered as the treatmentof choice in MPS50. Some clinicians sug-gest adding corticosteroids to the localanaesthetic to increase effectiveness overinflamed fascial structures, such as jointsand ligaments.

Chemical treatment of a TP includesbotulinum toxin (BTX) and topisetroninjection. BTXs have clinical applicationwhen sustained focal muscle relaxation isrequired, and can be advised for pain reliefin cases of predominant dystonia and spas-ticity5. In principle, their action inhibitsmuscle contraction by blocking the releaseof ACh from peripheral nerves. There is apossibility that BTXs block g-motor end-


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Fig. 7. A flow chart for MPS management.

ings in addition to a-motor endings. Thismay reduce spindle inflow to a-motoneur-ons resulting in a decrease of the reflexmuscular tone24,81,101. The non-toxic com-ponents of the BTX complex may haveunrecognised clinical significance in termsof retarding tissue diffusion or impartingstability to the complex8.

Serotype A (BTX-A), which produces adose-dependent relaxation28, is the onlyBTX currently used for TP injections55.BTX-A injections can significantlyreduce spasticity- and dystonia-relatedlocal pain49,103 or focal muscular pain,and in many cases the benefit outlaststhe expected action of the toxin99. Resultsfrom a double-blind, placebo-controlledstudy showed at least a 30% reduction inpain in four out of six patients withchronic MPS following injection withBTX-A but not normal saline, as esti-mated by visual analog scales, verbaldescriptors for pain intensity and unplea-santness, palpable muscle firmness, andpressure pain thresholds11.

BTX-A injection can be considered aneffective treatment for patients withMPS14 and may be selectively used inpatients resistant to conventional methodsof treatment50, but the cost effectivenessshould be further assessed. Two rando-mised trials showed BTX-A injections tobe as efficient as topical anaesthetics(bupivacaine 0.5%, lidocaine 0.5%) interms of duration or magnitude of painrelief, function and quality of life, but less



cost effective39,50. Other randomized trialsdo not support a specific antinociceptiveand analgesic effect of BTX-A comparedto placebo (normal saline)79, although thisdiscrepancy may be partially attributableto adverse events that occur in the treat-ment group due to the nature of the toxin(i.e. weakness)100. Efforts to reduce theprevalence of such events by the employ-ment of low-dose protocols were notfound to be successful in terms of treat-ment efficiency73. Dose-ranging studies todetermine the optimal treatment as well aspotential immunoresistance from repeatedinjections, and the value of EMG guidanceregarding the outcome of treatment,remain important clinical issues to beaddressed93. The prevalence of end-platenoise in the myofascial TP region maywork as an objective indicator of the ther-apeutic effectiveness of BTX-A injec-tion54.

Local injections of topisetron, a 5-hydroxytryptamine3 receptor antagonist,may contribute to rapid and prolongedrelief, with an analgesic effect far superiorto the action of local anaesthetics70. Theefficacy of this drug has also been attrib-uted to its antiphlogistic effect, which maybe related to the inhibited release of sub-stance P and other neuropeptides fromnociceptors, and the blocked release ofphlogistic substances from macrophages,monocytes, etc22,69,70,91.

Chemical TP blockage with topicallidocaine 5% patches was also found to



be effective in reducing average painintensity and improving quality of life(P < 0.05), and can be used in the man-agement of myofascial pain12,13.

Acupuncture exerts a positive influenceon the signs and symptoms of MPS90, andprovides statistically significant short-term pain reduction in chronic orofacialpain (P < 0.0001)37. During rehabilita-tion, an appropriate exercise regimeshould also be followed to restore flex-ibility and balance to the muscles, in orderto avoid high recurrence rates105.

A variety of factors (social, psycholo-gical, economic, regarding substanceabuse, etc.) may influence the treatmentoutcome of TPs, confirming the multidi-mensional aspect of MPS46. Multidimen-sional rehabilitation programs that includecognitive behaviour therapy show a sta-tistically significant decrease in painintensity, duration and frequency com-pared to baseline measurements in patientswith MPS7, and a significant increase inquality of life over time102.

Physical manoeuvres may also be aneffective therapy82. Due to the difficultyin isolating a sole aetiologic factor forMPS, their employment seems quite rea-sonable, especially at the beginning oftreatment74. Exercise protocols for themasticatory muscles show a statisticallysignificant reduction in pain compared tocontrols (P = 0.019), and produce objec-tive physiologic results on EMG duringmaximal voluntary clench (P = 0.007)32.


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When physical therapy is combined withcounselling it may result in a significantimprovement in pain and jaw function15,as chronic pain is often a product of bothphysical and psychosocial factors thatcomplicate convalescence98.

Pharmacologic treatment of MPS mayinvolve alpha-2 agonists that have myor-elaxant properties, such as tizanidinehydrochloride89. A significant decreasein pain intensity and disability comparedto baseline measurements (P < 0.001) andan improvement in pressure thresholdsand sleep during treatment (P < 0.001)were reported in a clinical trial thatassessed the efficacy of tizanidine. Thisdrug has been rated as good to excellent inrelieving pain by 89% of patients and 79%of their doctors61. In another study, 54% ofMPS patients treated with tizanidineshowed absence of clinical symptomsand 23% showed improvement62. Otherdrugs that have antinociceptive effects inMPS-associated pain and may be used inchronic refractory situations include clo-nazepam26 and tricyclic antidepressants77.Interventions concerning dietary trypto-phan uptake have also been attempted83.

In conclusion, MPS have a high preva-lence in the general population despite thelow level of awareness among doctors,and affect patients’ quality of life. Themanagement of MPS is a long-term pro-cess that requires close cooperationbetween patients and physicians (Fig. 7).Difficulties in diagnosis and managementthat may influence long-term results lienot only in treating TPs but in changingfactors related to the patient’s attitudes,way of living, and social and physicalenvironment. There is a great need forinterdisciplinary teams of various healthprofessionals in order to achieve properdiagnosis, management and sustainableoutcomes.

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