7 Otolaryngologic Aspects of Orofacial Pain

Table 7-8 Diagnostic criteria for vestibular migraine Diagnostic criteria Notes A. At least five episodes fulfilling criteria C and D B. A current or past history of Code also for the underlying migraine diagnosis. 1.1 Migraine without aura or 1.2 Migraine with aura C. Vestibular symptoms of Vestibular symptoms, as defined by the Bárány Society’s Classification of moderate or severe intensity, Vestibular Symptoms and qualifying for a diagnosis of A1.6.5 Vestibular lasting between 5 minutes migraine, include: and 72 hours a. Spontaneous vertigo: i. Internal vertigo (a false sensation of self motion) ii. External vertigo (a false sensation that the visual surround is spinning or flowing) b. Positional vertigo, occurring after a change of head position c. Visually induced vertigo, triggered by a complex or large moving visual stimulus d. Head motion–induced vertigo, occurring during head motion e. Head motion–induced dizziness with nausea (dizziness is characterized by a sensation of disturbed spatial orientation; other forms of dizziness are currently not included in the classification of vestibular migraine) Vestibular symptoms are rated moderate when they interfere with but do not prevent daily activities and severe when daily activities cannot be continued. Duration of episodes is highly variable. About 30% of patients have episodes lasting minutes, 30% have attacks for hours, and another 30% have attacks over several days. The remaining 10% have attacks lasting seconds only, which tend to occur repeatedly during head motion, visual stimulation, or after changes of head position. In these patients, episode duration is defined as the total period during which short attacks recur. At the other end of the spectrum, there are patients who may take 4 weeks to recover fully from an episode. However, the core episode rarely exceeds 72 hours. D. At least 50% of episodes One symptom is sufficient during a single episode. Different symptoms may are associated with at least occur during different episodes. Associated symptoms may occur before, one of the following three during or after the vestibular symptoms. migrainous features: Phonophobia is defined as sound-induced discomfort. It is a transient and 1. Headache with at least bilateral phenomenon that must be differentiated from recruitment, which is two of the following four often unilateral and persistent. Recruitment leads to an enhanced perception characteristics: and often distortion of loud sounds in an ear with decreased hearing. a. Unilateral location b. Pulsating quality Visual auras are characterized by bright scaintillating lights or zigzag lines, c. Moderate or severe often with a scotoma that interferes with reading. Visual auras typically expand intensity over 5–20 minutes and last for less than 60 minutes. They are often, but not d. Aggravation by routine always restricted to one hemifield. Other types of migraine aura, for example physical activity somatosensory or dysphasic aura, are not included as diagnostic criteria 2. Photophobia and because their phenomenology is less specific and most patients also have phonophobia visual auras. 3. Visual aura E. Not better accounted for by History and physical examinations do not suggest another vestibular disorder another ICHD-3 diagnosis or such a disorder has been considered but ruled out by appropriate or by another vestibular investigations or such a disorder is present as a comorbid or independent disorder condition, but episodes can be clearly differentiated. Migraine attacks may be induced by vestibular stimulation. Therefore, the differential diagnosis should include other vestibular disorders complicated by superimposed migraine attacks.

190 Vestibular Syndromes Related to Orofacial Pain or Structures tion, and susceptibility to motion sickness may jects, indicating that those with migraine have a be associated with vestibular migraine. Howev- lowered threshold for crosstalk between these er, they also occur with various other vestibular neighboring brainstem structures.95 disorders, so they are not included as diagnos- Migraine is more common in patients with tic criteria. Ménière’s disease than in healthy control sub- The prevalence of vestibular migraine is vari- jects. Many patients with features of both able and probably underdiagnosed, as shown Ménière’s disease and vestibular migraine have by a study from a dizziness clinic in Switzer- been reported. In fact, migraine and Ménière’s land, where vestibular migraine accounted for disease can be inherited as a symptom clus- 20.2% of the diagnoses in young patients but ter. Fluctuating hearing loss, tinnitus, and au- was suspected by the referring physicians in ral pressure may occur in vestibular migraine, only 1.8%.92 In a community-based sample but hearing loss does not progress to profound of middle-aged women in Taiwan, vestibular levels. Similarly, migraine headaches, photo- migraine was identified in 5%, and in 30% of phobia, and even migraine auras are common all women with migraine.93 Vestibular migraine during attacks of Ménière’s disease. The patho- has a female preponderance, and the reported physiologic relationship between vestibular female-to-male ratio is between 1.5 and 5 to 1.88 migraine and Ménière’s disease remains uncer- Familial occurrence is not uncommon, probably tain. In the first year after onset of symptoms, based on an autosomal-dominant pattern of in- differentiation between them may be challeng- heritance with decreased penetrance in men.94 ing, as Ménière’s disease can be monosymp- In most patients, migraine begins earlier in life tomatic with only vestibular symptoms in the than vestibular migraine. Not infrequently, mi- early stages of the disease. When the criteria for graine headaches are replaced by vertigo at- Ménière’s disease are met, particularly hearing tacks in women around menopause. loss as documented by audiometry, Ménière’s Patients with vestibular migraine typically disease should be diagnosed, even when mi- report spontaneous or positional vertigo. Some graine symptoms occur during the vestibular experience a sequence of spontaneous vertigo attacks. Only patients who have two different transforming into positional vertigo after several types of attacks, one fulfilling the criteria for ves- hours or days. This positional vertigo is distinct tibular migraine and the other for Ménière’s dis- from benign paroxysmal positional vertigo with ease, should be diagnosed with both disorders. regard to duration of individual attacks (often The therapeutic recommendations for ves- as long as the head position is maintained in tibular migraine are currently based on the treat- vestibular migraine versus seconds only in be- ment guidelines for migraine (see chapter 10). nign paroxysmal positional vertigo), duration of Zolmitriptan is recommended for acute vestibu- symptomatic episodes (minutes to days in ves- lar migraine.96 Non-pharmaceutical approaches tibular migraine versus weeks in benign parox- in the treatment of vestibular migraine should ysmal positional vertigo), and nystagmus find- not be neglected and may be even more effec- ings. Vertigo can precede headache, as would tive than drugs in individual patients. A thorough be typical for an aura; may begin with headache; explanation of the migraine origin of the attacks or may appear late in the headache phase. can relieve unnecessary fears. Avoidance of Auditory symptoms, including hearing loss, identified triggers, regular sleep, regular meals, tinnitus, and aural pressure have been reported and exercise have a firm place in migraine pro- in up to 38% patients with vestibular migraine.88 phylaxis. Selected patients, particularly those Genetic and neural mechanisms have been with persistent symptoms between attacks, described for vestibular migraine. The only hy- may profit from vestibular rehabilitation.97 pothesis that is actually based on a human ex- perimental model of vestibular migraine relates to the known reciprocal connections between Mastication-induced vertigo the trigeminal and vestibular nuclei. Trigeminal activation by painful electrical stimulation of the and nystagmus forehead produced spontaneous nystagmus in Various maneuvers may trigger vertigo and nys- patients with migraine but not in control sub- tagmus according to the pathology involved.

191 7 Otolaryngologic Aspects of Orofacial Pain

Although reciprocal connections exist between 5. Harvey H. Diagnosing referred otalgia: The ten Ts. the trigeminal and vestibular systems, induc- Cranio 1992;10:333–334. 6. Yanagisawa K, Kveton JF. Referred otalgia. Am J tion of dizziness or oscillopsia by mastication Otolaryngol 1992;13:323–327. has been reported only as a mechanical or vas- 7. Kim DS, Cheang P, Dover S, Drake-Lee AB. Dental cular steal phenomenon.98–100 otalgia. J Laryngol Otol 2007;121:1129–1134. Mastication-induced vertigo and nystagmus 8. Wazen JJ. Referred otalgia. Otolaryngol Clin N Am are rare phenomena. Park et al101 determined in- 1989;22:1205–1215. 9. Jaber JJ, Leonetti JP, Lawrason AE, Feustel PJ. Cer- duction or modulation of nystagmus in two index vical spine causes for referred Otaligia. Otolaryngol patients with mastication-induced vertigo, 12 Head Neck Surg 2008;138:479–85. healthy control subjects, and 52 additional pa- 10. Nestor JJ, Ngo LK. Incidence of facial pain caused tients with peripheral or central vestibulopathy by lung cancer. Otolaryngol Head Neck Surg 1994;111(1):155-156. during their acute or compensated phase. Both 11. Morgan NJ, Skipper JJ, Allen GM. Referred otalgia: index patients developed mastication-induced An old lesson. Br J Oral Maxillofac Surg 1995;33:332– vertigo after near-complete resolution of the 333. spontaneous vertigo from presumed acute 12. Mulwafu W, Fagan J, Lentin R. Suprahyoid approach unilateral peripheral vestibulopathy. The nys- to base-of-tongue squamus cell carcinoma. S Afr J Surg 2006;44:120–124. tagmus and vertigo gradually built up during 13. Amundson LH. Disorders of the external ear. Prim mastication and dissipated slowly after cessa- Care 1990;17:213–231. tion of mastication. Mastication did not induce 14. Gergely P Jr, Poór G. Relapsing polychondritis. Best nystagmus in healthy control subjects. Howev- Pract Res Clin Rheumatol 2004;18:723–738. 15. Puéchal X, Terrier B, Mouthon L, Costedoat-Chalumeau er, mastication-induced nystagmus appeared N, Guillevin L, Le Jeunne C. Relapsing polychondritis. in five (24%) of the 21 patients without sponta- Joint Bone Spine 2014;81:118–124. neous nystagmus who had a previous history of 16. Staats BA, Utz JP, Michet CJ Jr. Relapsing polychon- a vestibular syndrome, and mastication either dritis. Semin Respir Crit Care Med 2002;23:145–154. increased (21/31, 68%) or decreased (7/31, 17. Michet CJ Jr, McKenna CH, Luthra HS, O’Fallon WM. Relapsing polychondritis. Survival and predictive 23%) the spontaneous nystagmus in almost role of early disease manifestations. Ann Intern Med all the patients (28/31, 90%) with spontaneous 1986;104:74–78. nystagmus. They concluded that mastication 18. Sander R. Otitis externa: A practical guide to treatment may induce significant vertigo and nystagmus and prevention. Am Fam Physician 2001;63:927– 36;941–942. in patients with a prior history of acute vestib- 19. Hirsch BE. Infection of the external ear. Am J Otolar- ulopathy. The induction or modulation of nys- yngol 1992;13:145–155. tagmus by mastication in both peripheral and 20. Handzel O, Halperin D. Necrotizing (malignant) exter- central vestibulopathies supports trigeminal nal otitis. Am Fam Physician 2003;68:309–312. modulation of the vestibular system in humans. 21. Kim YH, Chang MY, Jung HH, et al. Prognosis of Ramsay Hunt syndrome presenting as cranial poly- The gradual buildup and dissipation suggest a neuropathy. Laryngoscope 2010;120:2270–2276. role of the velocity storage mechanism in the 22. Shim HJ, Jung H, Park DC, Lee JH, Yeo SG. Ramsay generation of mastication-induced vertigo and Hunt syndrome with multicranial nerve involvement. nystagmus. Acta Otolaryngol 2011;131:210–215. 23. Ko JY, Sheen TS, Hsu MM. Herpes zoster oticus treated with acyclovir and prednisolone: Clinical man- ifestations and analysis of prognostic factors. Clin References Otolaryngol Allied Sci 2000;25:139–142. 24. Goldani LZ, da Silva LF, Dora JM. Ramsay Hunt syn- 1. Israel HA, Davila LJ. The essential role of the oto- drome in patients infected with human immunodefi- laryngologist in the diagnosis and management of ciency virus. Clin Exp Dermatol 2009;34:e552–e554. temporomandibular joint and chronic oral, head, 25. Kinishi M, Amatsu M, Mohri M, Saito M, Hasegawa and facial pain disorders. Otolaryngol Clin North Am T, Hasegawa S. Acyclovir improves recovery rate of 2014;47:301–331. facial nerve palsy in Ramsay Hunt syndrome. Auris 2. Murtagh J. The painful ear. Aust Fam Physician Nasus Larynx 2001;28:223–226. 1991;20:1779–1783. 26. Morrow MJ. Bell’s palsy and herpes zoster oticus. 3. Conover K. Earache. Emerg Med Clin North Am Curr Treat Options Neurol 2000;2:407–416. 2013;31:413–442. 27. de Ru JA, van Benthem PP. Combination therapy is 4. Headache Classification Committee of the Interna- preferable for patients with Ramsay Hunt syndrome. tional Headache Society. The International Classifi- Otol Neurotol 2011;32:852–855. cation of Headache Disorders, 3rd edition (beta ver- 28. Harmes KM, Blackwood RA, Burrows HL, Cooke JM, sion). Cephalalgia 2013;33:629–808. Harrison RV, Passamani PP. Otitis media: Diagnosis and treatment. Am Fam Physician 2013;88:435–440.

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194 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia 8 Peter Svensson, DDS, PhD, Dr Odont Yair Sharav, DMD, MS Rafael Benoliel, BDS

This chapter focuses on pain felt primarily in the regional muscles. The most common types in our experience are myofascial pain (MFP) and tension-type headaches (TTHs), which may have a very similar clinical phenotype. Indeed, it is feasible that these conditions may share a common underly- ing pathophysiology, possibly faulty pain modulation, with varying clinical expressions. In this con- text, the relationships between MFP, TTH, and fi bromyalgia are examined. The common features of chronic daily headaches (CDHs) are reviewed, expanding on chronic TTH and new daily persistent headache in its differential diagnosis. Other types of CDHs such as chronic migraine (see chapter 10); chronic trigeminal autonomic cephalalgias, including hemicrania continua (see chapter 11); and medication-overuse headache (see chapter 14) are covered in designated chapters. MFP is one of the entities found within a diagnostic umbrella termed temporomandibular disorders (TMDs), a clas- sifi cation that includes ailments of the temporomandibular joints (TMJs) and masticatory muscles1,2 (TMJ disorders are reviewed in chapter 9). In its most recent classifi cation, the International Headache Society (IHS) has signifi cantly changed the approach to TMDs as a possible cause of head or facial pain.3 Disorders of the TMJ and masticatory muscle are now included as possible causes of secondary headache, and refer- ence is made to the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) (Table 8-1). Nevertheless, for TMDs the IHS classifi cation is limiting, and orofacial pain specialists have tended to use the DC/TMD based on the original Research Diagnostic Criteria for Temporomandibular Dis- orders (RDC/TMD)1,2,4 (Table 8-2). In the current classifi cation, muscle pain is subdivided into three categories based on the degree of referred pain: (1) myalgia, when pain is only elicited locally; (2) MFP, when there is pain referral within the boundaries of the muscle examined; and (3) MFP with referral, when pain referral is to a distant site beyond the muscle boundaries. The original RDC/TMD system has been extensively tested and translated into various languages so that it has wide uni- versal acceptance. In addition to the physical diagnosis (Axis I), the RDC/TMD system is unique be- cause it also assesses psychologic, behavioral, and psychosocial factors (Axis II). Axis II parameters

195 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

Table 8-1 Diagnostic criteria for headache attributed to TMDs* Diagnostic criteria Notes A. Any headache fulfilling criterion C B. Clinical and/or imaging evidence of a pathologic process Clinicians should use the DC/TMD. Most affecting the TMJ, muscles of mastication, and/or prominent in the preauricular areas of the face, associated structures masseter muscles, and/or temporal regions. Some overlap exists between headache C. Evidence of causation demonstrated by at least two of attributed to a TMD as a result of muscular the following: tension and TTH. When the diagnosis of a TMD 1. Headache has developed in temporal relation to the is uncertain, the headache should be coded onset of the TMD as TTH, presumably with pericranial muscle 2. Either or both of the following: tenderness. a. Headache has significantly worsened in parallel with progression of the TMD b. Headache has significantly improved or resolved in parallel with improvement in or resolution of the TMD 3. The headache is produced or exacerbated by active jaw movements, passive movements through the range of motion of the jaw, and/or provocative maneuvers applied to temporomandibular structures such as pressure on the TMJ and surrounding muscles of mastication 4. Headache, when unilateral, is ipsilateral to the side of the TMD D. Not better accounted for by another International Classification of Headache Disorders, third edition diagnosis *Reproduced with permission from the International Headache Society.

are further discussed later in this chapter and in chapter 4. The Axis II questionnaires used Clinical Approach in the DC/TMD have clinically relevant and ac- ceptable psychometric properties for reliability, A thorough pain histo ry must be recorded, in- validity, and utility as instruments for identify- cluding specific questions on masticatory dys- ing patients with TMDs who have high levels of function. Pain location should be augmented distress, pain, and disability that can interfere by drawings that outline the extent and referral with treatment response and course of Axis I pattern of pain (Case 8-1; Fig 8-1). The referral disorders.5 Research on TMDs should therefore patterns are also subject to particular investi- use the DC/TMD criteria, although for routine gations during a clinical examination using the situations clinicians can use the screening ver- DC/TMD system. sion of the DC/TMD. A routine head and neck examination must TMDs are among the most common orofacial be performed, including cranial nerve assess- pain conditions in the general population. TTH ment. Specifically, the interincisal mouth open- is the most common primary headache,6 and re- ing should be recorded in millimeters and any ferral of pain to the orofacial region is suspected deviation or accompanying pain adequately de- in some cases. General dentists and orofacial scribed. The DC/TMD system offers operational- pain specialists are therefore regularly required ized guidelines for the specific examination pro- to diagnose and manage these patients. cedures for the jaw muscles, TMJs, and opening

196 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Clinical Approach

Table 8-2 DC/TMD diagnostic criteria for myalgia* Axis I : • Minimum of 2 lb (range 2 to 3 lb) for masseter and temporalis sites Methodology • Pressure is held for 2 seconds for myalgia and 5 seconds for myofascial pain • Pain on palpation in one or more of the following sites, at least one of which is ipsilater- al to the pain complaint (right/left muscles count for separate sites): ººRight/left temporalis anterior ººRight/left temporalis middle ººRight/left temporalis posterior ººRight/left masseter origin ººRight/left masseter body ººRight/left masseter insertion History 1. Pain in the jaw, temple, in front of the ear, or in the ear AND 2. Pain modified with jaw movement, function, or parafunction Examination 1. Confirmation of pain location(s) in the temporalis or masseter muscle AND 2. Report of familiar pain in the temporalis or masseter muscle with at least one of the following provocation tests: a. Palpation of the temporalis or masseter muscle OR b. Maximum unassisted or assisted opening Sub­class­ifications 1. Local myalgia AND: (additional 3. Pain with muscle palpation with pain localized to the immediate site of the examination criteria to palpating finger(s) the aforementioned 2. Myofascial pain AND: for specific diagnosis) 3. Pain with muscle palpation with spreading of the pain beyond the location of the palpating finger(s) but within the boundary of the muscle 3. Myofascial pain with referral AND: 3. Pain with muscle palpation beyond the boundary of the muscle Axis II: • Pain intensity and pain-related disability Psychosocial ººGraded chronic pain scale comorbidity ººJaw disability checklist • Depression and somatization ººSymptom Checklist for Depression and Somatization (SCL-90) *Adapted from Schiffman et al.2

patterns.7 In all patients seeking musculoskeletal close conformity with accepted classification cri- treatment, it is imperative to carefully palpate the teria and thorough self-calibration are essential.8 regional muscles (masticatory/pericranial, cervi- Examiner calibration rather than professional ex- cal) and TMJs to locate painful areas or trigger perience seems to be the most important factor points. Muscle trigger points refer pain and are for reliable measurement of TMD symptoms.9 distinct from muscle tenderness, which reflects The DC/TMD system suggests that pressure ap- a generalized sensitivity over the affected mus- plication be standardized to 1 kg at the masse- cle. The patient’s reaction and assessment of re- ter and temporalis muscles and to 0.5 kg and 1 sultant pain or tenderness should be recorded, kg at the TMJ.7 Other intraoral or extraoral sites and it may be important to distinguish between should be approached with 0.5 kg of pressure. pain and tenderness on palpation. Particularly in Practicing pressure application on weight scales MFP, the examination is crucial in diagnosis; it using the fingers or thumbs is advisable, but re- is therefore essential to develop a reliable tech- cent research has clearly shown a huge variabil- nique whereby even and consistent pressure is ity of manually applied forces, which can almost applied across all patients.7 Clinical signs are dif- be eliminated using simple palpometer devic- ficult to measure with consistency, and interrater es.10 For neck and shoulder muscles, a some- reliability is not good for some signs of MFP, so what higher force should be applied, aiming at a

197 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

CASE Masticatory myofascial pain in a 27-year-old woman. 8-1 Present complaint: Pain on the right side of the face, particularly around the angle of the man- dible and the preauricular region (Fig 8-1a). The pain is constant, and recently the pain severity became worse, graded around 6 on a 10-cm visual analog scale (VAS). Pain severity fl uctuates throughout the days and is worse in the afternoon or after chewing or yawning. Other than mild neck discomfort, the patient reports no generalized symptoms. The patient has no record of absenteeism from work and reports that she sleeps well. Pain has occasionally referred to the teeth, but her dentist has not detected pathology. Descriptors for pain quality are pressure, dull, and annoying. History of present complaint: Present for the past 4 months but before that has occurred and remitted for some months. Physical examination: Extraoral examination revealed regional muscle tenderness (Fig 8-1b) bilaterally but more pronounced in the ipsilateral masseter and temporalis muscles. Interincisal mouth opening was 34 mm and accompanied by pain. Examiner-assisted opening was 39 mm with severe pain. No TMJ sounds were detected, and the joints were not tender. Cranial nerve examination was normal. Intraoral examination and full-mouth radiographs revealed no dental problems. Relevant medical history: The patient was diagnosed with hypothyroidism 4 years ago and has been taking 100 μg of thyroxine daily. Diagnosis: Masticatory muscle myofascial pain. Diagnostic and treatment considerations: Conservative treatment options were discussed with the patient, and therapy was initiated with analgesics (ibuprofen 400 mg three times daily for 10 days) and physiotherapy for the jaw and neck muscles (see text). The patient was also referred to her family physician to check on her thyroid status. Over the next 6 weeks, the patient report- ed no signifi cant improvement and began to complain of disturbed sleep and increased neck discomfort (Fig 8-1c). Thyroid hormone and thyroid-stimulating hormone levels were normal. Amitriptyline (10 mg at bedtime) was therefore initiated, together with continuing physiotherapy. Based on response and side effects, the dose was increased to 20 mg at bedtime, and over a period of 15 weeks the pain severity decreased to a mean VAS score of 1. The patient reported increasingly longer periods during the day when she was pain free. On examination, the masti- catory muscles were not signifi cantly tender, and unassisted, pain-free mouth opening was 41 mm. The patient was then lost to follow-up for about 12 weeks and subsequently returned and requested that the amitriptyline be withdrawn. She also commented that pain was aggravated during intensive work at her desk. The amitriptyline was withdrawn, and the patient was instruct- ed to continue physiotherapy and obtain advice regarding ergonomics in her immediate work en- vironment. Over the next 4 or 5 weeks, the patient reported no signifi cant pain and was released.

pressure of about 4 kg.11 The authors’ approach as refl ected in the different subgroups of MFP in is to begin by applying pressure on unaffected the new DC/TMD (see Table 8-2). Most masti- regions (eg, forehead, shoulder) so the patient catory muscles are examined extraorally, except becomes familiar with the technique. Patient re- for the lateral pterygoid, which is approached sponse can be recorded for each muscle or joint from the maxillary retromolar region. However, and graded on a scale from 0 to 3, where 0 is palpation of the lateral pterygoid is notoriously no pain, 1 is mild, 2 is moderate, and 3 is severe associated with false-positive responses (eg, pain.12 Pain ratings may then be summated to pain due to stimulation of the oral mucosa) and give a total pain score.11,13 Patients with MFP or has low inter- and intraexaminer reliability. The fi bromyalgia consistently display more pain and temporalis muscle has an insertion to the coro- have more involved muscles than control sub- noid process, and the tendon may be palpated jects, but the fi ndings for TTH are inconsistent intraorally. Patients should be questioned about and vary among patients. Radiation of pain or re- other body pains and these areas examined if ferral to particular sites is not a constant feature, need be.

198 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Clinical Approach

3

1 1 1 3

1 2

Fig 8-1a Pain location for the patient Fig 8-1b Muscle pain in the same patient. Tenderness is described in Case 8-1. graded from 1 to 3 (mild to severe). The ipsilateral masseter and temporal muscles were the most tender (scored 3). The contralateral masseter muscle was also mildly tender. Addi- tionally, the suboccipital and sternocleidomastoid muscles were mild to moderately tender bilaterally.

Physiotherapy analgesics

7 Amitriptyline 10 mg/d 6 Amitriptyline 5 20 mg/d 4 Amitriptyline stopped 3

Mean weekly VAS 2 1 0 0 5 10 15 20 33 38 43 Time (weeks)

Fig 8-1c The pain diary of the patient in Case 8-1.

In the general population, clicking or pop- joint sounds are often transduced to the op- ping jaw joints are very common and may posite side, so careful examination is required. occur during opening and/or closing; often, Lateral and protrusive movements of the jaw this is an isolated symptom that requires no should be examined and irregularities or con- treatment. The interincisal opening at each comitant pain recorded. Joint pain should also click and associated deviation in the mouth be examined and recorded under ipsilateral opening should be recorded. At times, joint and contralateral loading (biting a bite stick). sounds may be pathognomonic of underlying Guidelines, manuals, and clinical examination disease; for example, crepitation (a sound or forms for a systematic and standardized ex- feeling like sand or walking on snow) com- amination may be downloaded from the In- monly occurs in degenerative joint disease. ternational RDC-TMD Consortium (www.rdc- Because the mandible connects the TMJs, tmdinternational.org).

199 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

Intraoral examination should rule out dental representative. The case could be made that pathology as the source of pain or referred pain instead of performing univariate analyses and to the musculoskeletal structures. Furthermore, looking for specific and dominant risk factors, the occlusion/articulation should be checked a more fruitful approach would be to recog- for gross problems and/or recent changes that nize the complex interactions among multiple may have been associated with or caused by factors and adopt a multivariate analytic ap- a TMD. The dentition and periodontal tissues proach. Ascertaining the parameters the study should be assessed for possible pathology. assessed is important, that is, patient report or physical findings of signs and symptoms by ex- amination. The examination usually uncovers more physical findings than the patient is aware Temporomandibular of.14 The physical assessment of patients in Disorders TMD studies requires standardization of meth- ods, reliability data, and interrater calibration. Study design and reliability The double-blind placebo controlled trial is the gold standard for therapeutic interventions but Depending on the specific subdiagnosis, the may be problematic in some physical therapy cardinal features of TMDs include muscle modalities. Comparative studies of different in- and/or joint pain, joint sounds, and mastica- terventions are needed to identify the more effi- tory dysfunction. Many studies have therefore cacious treatments. Evidence-based therapies focused on the prevalence of TMD signs and in TMDs are rare, and expert opinion or person- symptoms without knowing their clinical signif- al preference often replaces a sound scientific icance. Moreover, because studies address a approach. Although clinical experience and in- number of symptoms, conclusions about the dividual judgment are important in the assess- behavior of any one sign or symptom should be ment and treatment of patients, incorporating arrived at with care. Other studies have report- evidence-based principles is essential. ed on samples of patients seeking treatment or on convenience samples that are misrepre- sentative of the population, that is, they have Epidemiology selection bias. A major historical problem has TMDs are recognized as the most common been the use of diverse inclusion and exclusion chronic orofacial pain condition, and only minor criteria by different groups. This is reflected in differences are found among racial groups.15,16 the diverse terminology used in the literature: As previously mentioned, TMDs refer to a group mandibular dysfunction, craniomandibular dis- of pain conditions and dysfunctions, and not orders, myofascial pain dysfunction syndrome, all epidemiologic studies have used the same etc. These terms have been substituted with classification or differentiated between muscle TMD throughout this chapter (see Peck et al1 and joint disorders. Indeed, inclusion criteria and Schiffman et al7). The universal use of ac- used in studies before modern classifications cepted research criteria will no doubt increase grouped a number of disorders into one enti- practitioners’ understanding of the processes ty. This raises questions about the current va- and epidemiology involved in TMDs and our lidity of much of the epidemiologic research diagnostic skills. The use of the term TMD is performed before criteria and diagnoses were widespread; however, research on epidemiolo- standardized. gy, treatment response, natural history, and ge- netic factors must clearly differentiate among the diagnostic subgroups. Signs and symptoms versus When examining the literature, it is important treatment need to assess the study design, statistical power, Studies reveal that 6% to 93% of the general and presence of confounding variables. For ex- population have or report signs and symptoms ample, studies of pain and bruxism often ignore of TMDs. Study results show great disparity, confounding parameters, such as stress and however, and prevalences of common signs, anxiety, and therefore the results may be mis- such as clicking joints, range from 6% to 48%,

200 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Temporomandibular Disorders

which suggests that the methodology and defi- some extent genetic risk factors.16,25,26 Taking nitions account for the observed variability. findings from the Orofacial Pain: Prospective Moreover, data are lacking on the signif- Evaluation and Risk Assessment (OPPERA) icance of these highly prevalent signs and study into account, it seems inappropriate to symptoms. Thus, practitioners cannot reliably consider TMD solely as a localized orofacial predict which signs and symptoms will deterio- pain condition.16,25,26 rate and therefore justify early treatment. Clini- cal judgment alone is relied on to decide which signs and symptoms will be treated, but clinical Age distribution of TMDs judgment varies, and in the absence of clear cri- Signs and symptoms of TMDs have been found teria, this alone should not be relied on. Based in all age groups, peaking in 20- to 40-year- on available data, clear indications for treat- olds. Signs of TMDs have been described in ment are pain and/or significant dysfunction. children and adolescents but are usually mild.27 The data should therefore reflect the se- In a group of adolescents, treatment need was vere cases (pain and/or dysfunction) that assessed at 7%.28 TMDs may also occur in need treatment. For example, although signs edentulous patients.29 Accumulated evidence or symptoms of dysfunction are extremely suggests that symptoms in the elderly may be common, only 3% to 11% of patients are as- lower than in the general population, but some sessed as needing treatment.17 TMD-related studies show a slight elevation in the preva- facial pain has been found to occur in 4% to lence of some signs in this age group, includ- 12% of the population,18,19 and severe symp- ing asymptomatic joint sounds (eg, crepitation) toms are reported by 10% of subjects. These and limited mouth opening.30 In a longitudinal figures are compatible with the data on the study of elderly patients, signs and symptoms percentage of people who seek treatment of TMDs tended to decrease over the follow-up (1.4% to 7%).20 In a large population, mastica- period.31 These data suggest that TMDs are not tory muscle and TMJ tenderness were found progressive and most symptoms resolve with in 15% and 5% of patients, respectively,21 but increasing age. were self-reported only by about 4% and 6% to 8% of patients, respectively, which suggests that muscular tenderness is less bothersome Sex to patients or that examination techniques TMD signs and symptoms have a female pre- are resulting in overdiagnosis.22,23 Longitudi- ponderance, especially those of muscular or- nal studies suggest that symptoms of TMDs igin.17 Most studies also report that the vast fluctuate considerably, particularly in patients majority of patients (up to 80%) who seek with MFP, and progression to severe pain and treatment are girls or women.32,33 Back pain, dysfunction of the masticatory system is rare.17 headache, and TMD-related pain were found MFP has been clearly shown to be a chron- to increase significantly with increasing puber- ic or fluctuating pain condition; over 5 years, tal development in girls.34 Additionally, women 31% of patients suffered continuous MFP, with TMDs generally have more severe physi- 36% experienced recurrent pain, and 33% cal and psychologic symptoms than do men.35 remitted.24 Clinical experience confirms that TMD pain and related symptoms appear to im- there is extreme symptom fluctuation, and new prove over the course of pregnancy and are not symptoms appear as often as old ones disap- paralleled by improvements in psychologic dis- pear. Significant predictors of persistence were tress.36 This is most likely associated with the high baseline pain frequency, painful palpation dramatic hormonal changes during pregnancy. sites, and other body sites with pain.24 First, Indeed, TMD pain in women is highest at times onset of any painful TMD has recently been re- of lowest estrogen and may also be related to ported to be about 4% per annum and is influ- periods of rapid estrogen change.37 A recent enced by multiple factors, such as sociodemo- study identified only a slightly greater incidence graphic characteristics, health status, clinical of first onset of any painful TMDs for women.16 orofacial factors, psychologic functioning, pain Sex-related effects are examined further in the sensitivity, cardiac autonomic features, and to section on TMD pathophysiology.

201 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

Personal and societal impact of TMDs patient; Table 8-2 lists clinical criteria for di- agnosis. No classification system is perfect, Although progression to severe TMD-related however, and clinical diagnosis needs to rely pain and dysfunction is rare, the personal and on more than just a list of criteria. For example, societal impact of TMDs is significant. Patients most clinicians would be comfortable with di- with TMDs request sick leave significantly agnosing a patient with MFP in the presence of more often, visit a physician more frequently, chronic orofacial pain and dysfunction and only and use more physical therapy services than two painful muscle sites, whereas the original control subjects. Disabling TMDs cause an RDC/TMD criteria required three or more pain- estimated 18 lost workdays annually for ev- ful muscle sites. This criterion has been revised ery 100 working adults in the United States.38 in the new DC/TMD,7 demonstrating the need During the early 1990s, it was calculated that for critical reflections and continuous adjust- approximately 3.6 million acrylic splints were ment of all classification systems guided by constructed yearly in the United States to treat high-quality clinical research. TMDs and bruxism, accounting for an annual expenditure of US $990 million (not adjusted for inflation), or about 3% of the total US den- Location and quality tal health care expenditure.39 Subjects with By definition, MFP is characterized by re- TMDs use significantly more health care ser- gional, and often unilateral, pain; however, it vices than control subjects—about 50% more is important to check for more systemic pain in mean costs for drug utilization, outpatient complaints. Patients typically localize the pain visits, and specialist services.33 Most of the to areas around the ear, the angle/body of the increased costs were accounted for by about mandible, and the temporal region (Fig 8-2). 10% of those with TMDs, probably the most Referral patterns include intraoral, auricu- severely affected.33 lotemporal, supraorbital, and maxillary areas depending on the muscles involved and the intensity of the pain, and perhaps reflecting in- Myofascial Pain dividual propensity for pain spread and refer- ral.11,40–42 Intraoral referral of pain is well docu- mented and may be the prime complaint from Clinical features the patient.11 At times the pain refers diffusely The masticatory muscles involved in jaw clo- throughout one side of the face, compounding sure include the masseter, temporalis, and diagnosis.11,40 Although MFP is typically a unilat- medial pterygoids. The lateral pterygoids are eral pain condition, it may also occur bilaterally, involved in opening, in laterotrusive and pro- particularly when associated with generalized trusive movements, and, to some extent, in disorders such as fibromyalgia and trauma.11,43 articular disc/condylar stabilization, whereas Pain quality is dull, heavy, tender, or aching and the digastric muscles assist in mouth opening. rarely throbbing.44 Emotive descriptors, such as Other pericranial and cervical muscles are con- “tiring” and “troublesome” are often reported comitantly involved or provide support and sta- by patients with MFP.44 Pain severity may fluc- bility during mastication, speech, and swallow- tuate during the day but is usually about 3 to 5 ing. MFP is characterized primarily by pain and on a 10-cm visual analog scale (VAS); however, tenderness from the jaw-closing muscles. The it varies considerably across patients.44,45 Some specialized function of the masticatory mus- patients may report more severe pain (VAS 7), cles, the presence of bilateral joints with oc- but this is rare.11 More severe pain in patients cluding teeth, and their important roles in chew- with MFP is associated with increased reports ing produce specific clinical features, such as of pain-related awakenings.46 significant masticatory dysfunction. In addition, the intimate anatomical relationships produce Temporal pattern complex and overlapping referral patterns. At present, the diagnosis of MFP is based Some patients experience the most intense pain on the history and clinical examination of the in the morning (21%) or late afternoon (79%),

202 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Myofascial Pain

TTH MFP

Fig 8-2 Typical pain location in TTH and MFP.

though others have no fixed pattern; fortunate- in the new DC/TMD system, one of the criteria ly, the pain rarely wakes the patient.45 Pain-free for MFP is that pain is changed (not necessarily days may be reported, and on a painful day increased) during jaw function. Further studies average pain duration ranges from 5.5 to 18 are needed to determine the clinical signifi- hours.11,45 Typically and per definition, MFP is cance of this apparent dilemma in the clinical characterized by chronicity with reported onset examination. being months to several years previously.24,44 The temporal pain pattern varies considerably among patients but should be carefully explored during Associated signs the pain history. Pain occurring on most days of In addition to pain, there may be deviation of the the month is typical of patients with MFP.11 mandible on opening, fullness of the ear, dizzi- ness, and soreness of the neck. Dizziness has been associated with pain in the sternocleido- Triggers mastoid muscle and ear stuffiness with spasm Pain may be aggravated during jaw function, of the medial pterygoid. Some patients may with transient spikes of pain occurring sponta- report tinnitus that is correlated with a number neously; indeed, pain on function may be the of tender muscles.47,48 Tinnitus often improves patient’s primary complaint. Nevertheless, a with treatment, together with other TMD signs subset of patients may also experience relief of and symptoms. Interestingly, tinnitus is also as- pain during function such as mastication, sug- sociated with depression levels, thus indicating gesting different phenotypes of MFP. Note that complex and multifactorial relationships.49

203 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

Physical findings of chronic musculoskeletal conditions such as fibromyalgia, myofascial pain, and probably Examination usually reveals limited mouth MFP.56 Patients will often have extratrigemi- opening (< 40 mm, interincisal)11 with a soft- nal pain and tenderness, and the presence of end feel. The presence of limited mouth open- widespread body tenderness is associated ing in a patient with MFP may also indicate TMJ with more severe TMDs and increased somatic pathology that may be clinically difficult to di- symptoms.57,58 agnose.50 Pain to palpation is usually present in ipsilateral masticatory muscles and is a dis- tinguishing feature of MFP. The masseter is the Differential diagnosis muscle most commonly involved (> 60%), and MFP needs to be differentiated from other con- the medial pterygoid and temporalis muscles ditions that may affect the masticatory muscles. are painful in about 40% to 50% of patients, Inflammation of a muscle and myositis second- often unilaterally.11 The sternocleidomastoid, ary to infection or trauma are commonly seen trapezius, and suboccipital muscles are usually in dental practice. Myositis is usually associat- painful in a small number of patients, very often ed with a pertinent history or significant clinical bilaterally.11 findings, such as muscle or regional swelling, Typically, there are localized tender sites and redness, and dental or periodontal infection. trigger points in muscle, tendon, or fascia.42,51 The affected muscles are tender, located in the A so-called hypersensitive bundle or nodule vicinity of the inflammation, and accompanied of muscle fiber of harder-than-normal consis- by limitation of mouth opening. Myositis may tency is the physical finding most often asso- precede or be associated with a painful con- ciated with a trigger point. Trigger points are traction or myospasm in the regional muscles traditionally described to be associated with a that is of acute onset. Treatment of these in- twitch response when stimulated. Additionally, volves the effective eradication of the initiating trigger point palpation may provoke a charac- cause and analgesics in accordance with pain teristic pattern of regional referred pain and/ intensity (see chapters 6 and 16). Active phys- or autonomic symptoms. The importance of iotherapy helps restore normal mouth opening. trigger points remains controversial, and an al- Local muscle pain may occur 24 to 48 hours ternative interpretation is that they may simply after acute overuse of the masticatory muscles; be epiphenomena of deep tissue pain. Areas this delayed-onset muscle soreness is simi- of referred pain may include perioral and intra- lar to that observed in patients with TMDs or oral (teeth) structures and may depend on the in other body muscles after exercise.59 Treat- muscles involved and the intensity of pain.52,53 ment should be tailored to reported symptom- Referral to the teeth may be prominent and atology and usually includes analgesics and may often cause misdiagnosis as dental pa- physiotherapy. thology. Referral of pain from trigger points in Pain referral to intraoral structures has of- the deep part of the masseter muscle includes ten caused serious misdiagnosis and unwar- the TMJ and ear, which causes possible mis- ranted dental treatment, but this can be easily diagnosis with intra-articular or ear disorders avoided by careful clinical and radiographic (see chapters 7 and 9). Trigger points may be examination. The differentiation from painful active (ie, induce clinical symptoms) or latent, TMJ disorders may also be complex because in which case they only induce pain on stimu- of the overlapping symptomatology; regional lation. Some researchers suggest that muscle pain, pain-referral patterns, and pain evoked overload may activate latent trigger points.54,55 by mandibular movement are common to both In the authors’ experience, tender or painful MFP and TMJ disorders (see chapter 9). Careful points are far more common in patients with clinical assessment and follow-up are essential. MFP than are trigger points; the DC/TMD cri- Clinicians must be alert to the possible contri- teria relate to this by including the diagnosis of bution of systemic comorbidities. Hypothyroid- myofascial pain with referrals. Indeed, as dis- ism, statin use, connective tissue disease, and cussed later, the presence or absence of trig- AIDS may cause a diffuse myalgia and there- ger points seems unnecessary in the diagnosis fore require investigation in relevant situations.

204 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Myofascial Pain

Fig 8-3 Metastatic lesion to the left condyle mimicking a temporomandibular dis- order. The condylar anatomy is distorted, and a pathologic fracture is present. The patient had a previous adenocarcinoma of the breast.

The occurrence of regional primary or met- ters attempt to accurately assess pressure pain astatic tumors may induce TMD-like symptom- thresholds but are affected by rate of applica- atology and should be excluded. Although rel- tion, sex, and site.62 Neurophysiologic methods atively rare, reports in the literature continue to and quantitative sensory testing offer excellent suggest that such misdiagnosis is possible.60,61 tools in assessing trigeminal somatosensory Warning signs include pain of sudden onset or function and the contribution of the central ner- acute worsening of existing pain; focal neuro- vous system in orofacial pain conditions, which logic findings, such as disturbances in somato- makes them useful for research64 (see chap- sensory function; a lack of response to therapy; ter 3). Quantitative sensory testing techniques and atypical distribution or characteristics of measure pain and sensory thresholds to elec- the pain. Particularly, patients with a history of trical, mechanical, and thermal stimuli and are previous malignancy are at risk and should be able to distinguish TMJ from MFP cases, but referred for relevant imaging studies (Fig 8-3). they are time-consuming.65 Furthermore, movement disorders such as oro- A relatively understudied yet clinically useful facial dyskinesia and oromandibular dystonia and well-known technique is the use of differ- may sometimes be associated with muscle pain ential analgesic blocks and provocation tests.66 symptoms (see Peck et al1). Finally, fibromyal- Application of local anesthetics may help to gia (discussed later in this chapter) and wide- determine the peripheral nociceptive source, spread pain, whiplash-associated disorders, but sensitivity, specificity, and predictive values and headaches attributed to TMDs should be remain to be established. considered in the differential diagnosis. Treatment Additional diagnostic tools Treatment of TMDs with a variety of conser- The doubtful role of muscle hyperactivity in vative methods consistently results in high the pathophysiology of MFP, as discussed lat- (75% to 90%) success rates.32,67–70 In general, er, suggests that the use of electromyography treatment is aimed at palliation and is based (EMG) measurements is not useful in patient di- on clinical diagnosis; because the etiology is agnosis and management.62 Moreover, surface unclear, no treatment is curative. An interest- EMG recordings are often contaminated by the ing approach is to identify individual factors muscles of facial expression. Trigeminal reflex in specific patients and attempt to recognize recordings are valuable tools for assessing their roles as possible predisposing, initiating, neurologic disorders or pain mechanisms but and perpetuating factors. Individual factors hold little potential to be easily implemented in may serve any or all of these roles in different routine clinical examination.63 Pressure algome- patients.

205 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

Table 8-3 Treatment aims in masticatory myofascial pain Aims Examples of available therapies Reduce pain Simple analgesics, tricyclic antidepressants, rest Restore function and range of motion Physiotherapy, reduced pain Decrease aggravating or contributing Identify specific variables acting in the individual patient and attempt factors to eradicate; these may include emotional and physical variables Increase bite comfort Occlusal appliances (eg, guards) Increase muscle strength Physiotherapy, restored function Reduce physiologic distress Empathy, information; referral for counseling, cognitive-behavioral therapy when needed Prevent drug abuse Careful monitoring of drug use, efficient and prophylactic pain therapy Restore social functioning Cooperation with family physician, family members; referral for social and emotional help/counseling

Extensive research in the field of TMD ther- summarized in Table 8-3. The assessment of apy shows that there are no compelling data treatment outcomes should be based on accu- to support any intervention as being capable rate assessment of pain intensity and frequen- of disease eradication or modification. More- cy (see chapter 3) and the evaluation of chang- over, conservative therapies are consistently es in psychosocial comorbidity (see chapter 4). successful and are in no way inferior to more The Initiative on Methods, Measurement, and invasive or irreversible procedures, such as Pain Assessment in Clinical Trials (IMMPACT) surgery, occlusal adjustment, or prosthetic suggests that the following domains need to rehabilitation.32 The data support a conserva- be considered in the comprehensive analyses tive approach to the management of TMDs.71 of treatment outcomes: pain intensity, physical This is reinforced by findings that the natural functioning, emotional functioning, and partici- history of MFP includes an extensive number pant’s rating of overall improvement.74 of patients that will substantially fluctuate or remit over time and rarely progress to severe pain.17,24 A patient’s beliefs, medical status, Chronicity in myofascial pain type of employment, and personal preference The transition from acute to chronic MFP is may often dictate the treatment plan; the pa- dictated partly by response to initial treatment tient should therefore be actively involved in the and is therefore discussed in this section. High decision-making process. characteristic pain intensity, high disability Therapy for MFP falls into four main cate- score, higher scores of emotional distress, and gories—physical, pharmacologic, psychologic, being female with myofascial pain (versus TMJ or trigger point injection—and is often multi- disorders) are the most significant predictors of disciplinary.72,73 Treatment of MFP often com- chronicity. Patients developing chronicity differ bines conservative interventions, and different significantly in numerous biopsychosocial vari- centers have variable protocols depending on ables (eg, they suffer from more current anxiety patients’ signs, symptoms, and personal pref- disorders, mood disorders, and somatization erences. Treatment duration is usually 4 to 6 disorders). Patients with TMDs who did not re- months but in selected cases may be longer. spond to treatment were found to suffer from Most patients with MFP seek treatment to al- significantly higher rates of fatigue and sleep leviate pain; thus, significant reduction or eradi- disturbances.75 Researchers have suggested cation of pain must be one of the primary aims. that the development of chronicity involves However, treatment aims in MFP patients are neuroplastic changes in the medullary dorsal usually more complex and ambitious; these are horn, including functional and morphologic

206 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Myofascial Pain

changes. At the same time, endogenous fac- beneficial effects of physiotherapy are closely tors, such as descending inhibition, are work- linked to the more cognitive-behavioral aspects ing to attenuate these changes and may vary (eg, education and self-awareness) of a man- in effect between patients. These findings are agement program. consistent with the theory that prolonged and Muscle tenderness and pain may also be intense nociceptive input is one of the initiating treated with vapocoolant sprays and concom- factors for chronicity with decreased biopsy- itant stretching, known as spray and stretch.55 chosocial abilities, sex-related variables in pain This usually induces immediate relief and is of- modulation, and generalized symptomatology ten used as a diagnostic test, although sensi- possibly acting as perpetuating factors. Recent tivity, specificity, and predictive values have not research also emphasizes the contribution of been established (see Table 8-1). Other com- genetic factors and multisystem dysregulation monly used techniques, such as ultrasound for persistent pain conditions, including MFP.76 and thermal packs, have not been rigorously assessed. However, because these are con- servative approaches, individual patients who Physical and combined modalities benefit from their use should be encouraged to Most pain physicians with experience in the continue. Some evidence supports the use of field of MFP will attest to the success of con- low-level laser therapy in patients with TMDs, servative physical therapy, including muscle particularly MFP.79 When combined with an ex- exercise, thermal packs, and oral splints. How- ercise program, laser therapy significantly im- ever, few, if any, of these therapies have been proved symptoms more than exercise alone.80 unequivocally proven in controlled trials. Often, However, there was no advantage in adding reassurance and education of the patient, com- laser therapy when pain intensity was specif- bined with simple muscle exercises for masti- ically analyzed.80 Other systematic reviews do catory and neck muscles, will result in pain al- not offer much support in terms of clinical ef- leviation and restored mandibular function.67,69 ficacy oflow-level laser therapy,71,81 and it may Chewing exercises may be beneficial for some not be appropriate to include this in the first line patients with MFP, but there may be increased of treatment options. pain after vigorous exercise.77 Based on accept- A physical self-regulation program consist- ed principles,55 the authors have the patient per- ing of training in breathing, postural relaxation, form simple, active stretch exercises: two min- and proprioceptive re-education has been imal mouth openings followed by a gentle and shown to be superior to conservative therapy slow maximal opening (stretch) without causing (flat-plane intraoral appliance and self-care in- extreme pain. The patient may use wooden or structions) at a 6-month follow-up.82 In a fur- plastic tongue spatulas as a dynamic record ther study, conservative treatment by special- of maximal opening. These exercises are per- ists was compared with a structured self-care formed three or more times every 1 or 2 hours. program in patients with TMDs and minimal Patients with suboccipital and cervical muscle levels of psychosocial dysfunction.68 The spe- tenderness or chronic pain will benefit from the cialist treatments included splints, physiother- addition of active neck exercises. Rotation of apy, analgesics, muscle relaxants, and patient the head and ear-to-shoulder movements with education (diet and parafunctional habits). No mild stretching to each side (three times each) limitations were imposed on the combinations are similarly prescribed every 1 or 2 hours. Un- of treatments or the number of visits. The self- der normal conditions, patients will rotate the care program incorporated cognitive-behavioral head by about 70 degrees, whereas ear-to- therapy and self-care techniques, such as re- shoulder movements are inherently more limited laxation. One year later, both groups showed (40 degrees). Although clinical experience with improvement in all clinical and self-report cat- physiotherapy and exercises is usually good, a egories measured.68 However, the patients in recent study challenged this notion by showing the self-care program showed significantly no significant differences in outcome between decreased TMD pain, decreased pain-related a group receiving physiotherapy and a control interference in activity, and a reduced number group only receiving education.78 Perhaps the of painful masticatory muscles; they also re-

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quired fewer visits. These studies indicate the of repositioning the mandible in a new maxillo- importance of education and self-care in the mandibular relationship (repositioning splints). management of TMDs, and these strategies are Soft appliances are probably as efficacious as supported by systematic reviews.71 hard splints in the management of MFP but are difficult to adjust and repair.90 Reposition- ing appliances have been used extensively to Occlusal adjustments and the treat internal derangements of the TMJ and aim management of TMDs to recapture the disc (see chapter 9). Although There is no doubt that occlusion is of para- these appliances may successfully capture mount importance in restorative and prosthetic discs in internal derangement and provide re- dentistry (ie, oral rehabilitation). The question duction in the short term, they fail to do so at remains as to the relationship between TMDs all for internal derangement without reduction and occlusion/malocclusion. The historical im- or osteoarthritis.91 Moreover, long-term stabili- portance of occlusion in the etiology of TMDs, ty of successful treatment is usually not good, although largely unproven, led to the extensive and clicks or abnormal disc positions tend to use of occlusal adjustment. Occlusal adjust- recur.92,93 Recent studies show that reposition- ment may induce pain relief in some cases, but ing appliances have no significant benefit over the irreversible nature of this procedure is prob- stabilization appliances in the treatment of TMJ lematic. To date, opinions diverge concerning sounds.94 In addition, repositioning splints may occlusal and skeletal factors in TMDs. A large induce irreversible occlusal changes and are number of general and specialist dentists still therefore not recommended. When managing view occlusal factors as important in the patho- conditions like TMDs, it should be emphasized physiology and management of TMDs, and that the number needed to harm (NNH; that many continue to equilibrate the occlusion is, the number of patients to be treated before as therapy for TMDs. Based on published re- one patient will experience an unwanted or search, comprehensive reviews, and clinical side effect due to the treatment) value should experience, irreversible occlusal adjustment be extremely high. In the management of TMJ or rehabilitation for the treatment of TMDs is disorders, splints are sometimes constructed contraindicated.83–85 Patients with prosthodon- to reduce TMJ loading by providing occlusal tic needs will benefit from sound prosthodontic contacts in the posterior region only.95 This is rehabilitation, but that should not be confused further discussed in chapter 9. with the treatment of TMDs. Flat occlusal splints (relaxation or stabilizing The sum results of the studies supporting splints) are in widespread use and provide even adjustment are equivocal. Factors not consid- occlusal contacts; these may be constructed ered in these studies are the irreversible nature for the maxilla or the mandible. Stabilization of occlusal adjustments and that these ad- splints are effective in managing TMJ arthral- justments are not stable over time and tend to gia96 (see chapter 9). No difference in effect is partially recur.86 Moreover, occlusal adjustment apparent between flat splints and splints de- shows no advantage over any other conserva- signed to provide canine guidance on lateral tive and reversible therapy.71 Occlusion plays a excursions of the mandible.97 The authors are minor role, if any, in the etiology and therefore in reluctant to use partial-coverage splints be- the treatment of TMDs, including MFP.87,88 cause of the inherent potential to cause per- manent occlusal changes and the lack of ev- idence for any advantage over flat splints.98,99 Occlusal splints To avoid occlusal changes, all patients with Occlusal splints may be soft or hard and may any appliance must be instructed not to wear be fabricated with full or partial tooth cover- it all the time. Additionally, appliances must be age. A recent example of a new type of partial- regularly checked and repaired if need be. In coverage bite plate is the nociceptive trigeminal some cases, the splint has fractured in the area inhibition tension suppression system, which of the most-distal molars (the thinnest part) and has been advocated for the treatment of head- has allowed the selective overeruption of these ache.89 Some splints are designed with the aim teeth, therefore causing an anterior open bite.

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Meta-analyses consistently demonstrate act through nonspecific mechanisms prob- benefit for oral splints in TMDs in general.71,83,100 ably involving placebo and anticipation and The most recent meta-analytic review con- possibly involving some behavior-modifying cluded that “stabilization splint therapy may properties. be beneficial for reducing pain severity at rest and on palpation and depression when com- pared to no treatment.”101 Several studies have Pharmacologic investigated the efficacy of occlusal applianc- Simple analgesics. NSAIDs are used exten- es in the treatment of MFP.70,102,103 Most have sively in the management of pain and disability found improvement in the active and place- associated with musculoskeletal pain. Although bo arms (nonoccluding splints) of the trial but the antiplatelet and gastrointestinal safety pro- only marginal superiority of the active splint.90 file of selective cyclooxygenase-2 inhibitors is Similar effects of nonoccluding splints on TMJ superior, they still have potentially serious side pain and clicking have been observed.97 The effects on the renal and cardiovascular system presence of widespread pain reduces the ef- (see chapter 15). For the treatment of TMDs, cal- fectiveness of oral splints and suggests that culations of NNTs for drugs versus placebo re- they should only be prescribed for patients with veal encouraging figures of 2.7 to 3.5.100 Based regional myofascial facial pain.104 The number on current evidence, ibuprofen (400 mg three needed to treat (NNT) for occlusal appliances in times daily) or naproxen (250 mg twice daily) is the treatment of TMDs has been calculated.100 efficacious (see chapter 15). Simple analgesics The NNT calculates the number of patients that or combination analgesics (eg, codeine and ac- need to be treated to obtain one patient with etaminophen) may also provide good analgesia 50% or greater reduction of the worst pain. For and may be safer than NSAIDs. In patients with oral splints, an NNT of 6 was obtained for TMJ myofascial pain, ibuprofen combined with diaz- pain and 4.3 for MFP. The relatively good suc- epam is superior to ibuprofen. The use of ben- cess rate and generally conservative nature of zodiazepines as analgesics is of questionable splints accounts for their extensive use. Howev- value, however, and antidepressants, muscle er, splints entail substantial costs to manufac- relaxants, and anticonvulsant drugs are more ture and maintain. A recent study suggests that efficacious. splint therapy, whether high-cost laboratory- processed splints or chairside thermoplastic Antidepressants, benzodiazepines, mus- splints, offer no significant advantage over con- cle relaxants, and antiepileptic drugs. servative self-care strategies,105 including jaw Ami­triptyline at low doses (10 to 30 mg/day) relaxation, reduction of parafunction, thermal is superior to placebo109 and has been consis- packs, physiotherapy, stress reduction, and tently reported as beneficial for patients with the use of nonsteroidal anti-inflammatory drugs craniofacial myofascial pain, including predom- (NSAIDs).105 inantly muscular TMDs,110 and posttraumatic The exact mode of action of splints is un- myofascial pain.111 The use of clonazepam, a proven. Splints may reduce sleep bruxism, long-acting benzodiazepine with anticonvul- but both control and placebo splints induce sant properties, has been beneficial,112 but the similar reductions in muscle activity.106 In fact, muscle relaxant cyclobenzaprine has proven these effects appear to be temporary because superior to clonazepam in another study on muscle activity reaches baseline levels af- pain upon awakening.113 More recently, gab- ter about 6 weeks according to another con- apentin, an antiepileptic drug, has been test- trolled trial.107 After prolonged wear of splints, ed for the treatment of MFP in a randomized bruxing movements tend to recur in spite of double-blind study.114 Gabapentin was found to the fact that symptoms such as pain remain be clinically and statistically superior to place- improved.108 The aforementioned data and the bo in reducing reported pain, masticatory mus- lack of evidence for the role of muscle hyper- cle hyperalgesia, and the impact of MFP on dai- activity in TMDs confirm that reducing bruxism ly functioning. Reduction in muscle tenderness is not the mode of action of splints in the relief was observed after 8 weeks, but the effects on of TMDs. Currently, splints are considered to pain appeared only after 12 weeks of therapy at

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a mean dose of about 3,400 mg gabapentin per pain and to diminish distress and suffering (see day.114 The NNT was calculated at 3.4 for gab- chapter 4). Whether implemented separately or apentin in the treatment of MFP. Involvement of in combination with other pain treatments, CBT the sympathetic nervous system is suspected produced significantly decreased pain, emo- in MFP, similar to that observed in fibromyal- tional distress, and disability and is of proven gia (discussed in later sections). Recent find- efficacy in patients with TMD.120 Biofeedback is ings of genetically based abnormalities in the one such technique that aims to teach patients catecholamine pathophysiology of MFP115 the- to control behavior that is possibly part of the oretically support the treatment of MFP with pain etiology121 (see chapter 4). The lack of evi- adrenergic blockers; in fact, preliminary evi- dence for muscle hyperactivity in the etiology of dence from a randomized clinical trial suggests MFP raises questions about the validity of this that propranolol can decrease pain scores in method. Indeed, some studies have shown that patients with painful TMDs, depending on the headache improves whether patients increase catechol-O-methyltransferase (COMT) haplo- or decrease muscle activity.122 Biofeedback, type.116 More quality drug trials in craniofacial, however, is efficacious in regulating muscle ten- myofascial, and arthralgic pain and in patients sion in patients with TMDs and produces good with MFP are needed, and treatment remains long-term results,123 and the limited data avail- somewhat empiric. able support the efficacy of EMG biofeedback treatments for TMDs.71,121 This may be particu- larly useful for TMJ disorders associated with Biobehavioral therapy overloading (see chapter 9). Combining biofeed- Pain is a subjective experience with important back with CBT techniques significantly improves affective, cognitive, behavioral, and sensory treatment outcomes versus CBT alone.124,125 components (see chapter 4). Like other longer- lasting pain conditions, MFP is a complex enti- ty associated with changes in mood, behavior, Trigger point injections and needling and attitudes to life, in addition to drug abuse Clinical experience suggests that injections of and secondary psychologic gains. Therefore, local anesthetics into trigger points induce pain outcomes such as restoration of functional ac- relief that may be prolonged beyond the effect tivity, eradication of drug abuse and dependen- of the anesthetic agent.55 Few controlled stud- cy, and rehabilitation of residual emotional dis- ies have systematically tested this intervention tress need to be addressed. Careful review of for MFP, but the technique for the head and such parameters as lost work days, sleep dis- neck muscles is simple. The presumed trigger turbance, and general functioning provide valu- point is located and immobilized followed by able insight as to the emotional well-being of injection using a standard dental syringe and patients in accordance with IMMPACT propos- a 27-gauge needle, though other body areas als.117 Patients reporting a high degree of dis- may require thicker needles (Fig 8-4). Introduc- ability, psychologic distress, and drug or alcohol ing the needle into the trigger point may induce abuse may suffer from underlying psychosocial sharp pain, muscle twitching, or an unpleasant distress. Sleep disturbances are often part of sensation. Before injection, the overlying skin emotional disorders and are intimately related should be cleansed with an approved antisep- to a number of chronic pain conditions.118 Al- tic. Some suggest that the needle be inserted though experienced clinicians may obtain much 1 to 2 cm away from the trigger point and then information from an interview, it is generally advanced at an acute angle of 30 degrees to accepted that this is insufficient for a reliable the skin into the trigger point proper. Once an psychosocial assessment. The assessment of initial injection is performed (about 0.2 mL), the psychologic distress in patients with MFP may needle may be withdrawn to the level of the be performed with the DC/TMD questionnaire subcutaneous tissue, then redirected superi- or with established alternatives.7,117,119 orly, inferiorly, laterally, and medially, repeating Cognitive-behavioral therapy (CBT) is an op- the needling and injection process in each di- tion that aims to alter negative overt behavior, rection. All injections should be preceded by thoughts, or feelings in patients with chronic aspiration to ensure that the needle is not in

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a blood vessel. After the injection, the muscle should be gently mobilized. Stretch exercises and analgesics are prescribed postoperatively to ensure that mouth opening and muscle func- tion remain improved. In patients with myo­ fascial pain, bupivacaine (0.5%) is equally ef- ficacious to botulinum toxin in the relief of pain and cost-effectiveness, which would suggest the former’s preferential use.126 Furthermore, botulinum toxin injections have not been found to be superior to placebo injections in patients with MFP.127,128 The authors suggest that, ini- tially, mepivacaine (3%) should be used to test Fig 8-4 Trigger point injection. Identifiable trigger points patient response. If the results are encouraging are immobilized between two fingers, and local an- esthetic solution is then injected. Injection should be and the patient needs further injections, bupiv- performed at a number of points around the trigger. The acaine (0.5%) may then be used, although there needle should be retracted (but not withdrawn from the are reports of bupivacaine-induced damage to skin) and reinserted at each injection point. This tech- nique combines the effects of local anesthetic with the muscle fibers. However, based on an extensive effects of needling. literature review, direct (or dry) needling of myo- fascial trigger points appears to be an effective treatment, most likely because of the needle or placebo rather than the injection of saline or ac- tive drug.129 Thus, whether these needling ther- Chronicity of MFP is manifest by the in- apies have efficacy beyond placebo is unclear. creased need for long-term treatment of these Dry needling of trigger points is very similar to patients.130 However, prognosis in most pa- some acupuncture techniques. tients with MFP is moderately good, and remis- sion of pain and dysfunction is readily achieved for long periods. Complementary and alternative therapy Patient interest and demand for complemen- Pathophysiology of MFP tary or alternative medicine (CAM) is increas- The etiologic theory of TMDs, including MFP, ing (see chapter 17). Approximately 20% of much of which is based on deep-rooted histor- patients with facial pain in a referral center ical concepts, is clouded by controversy and had previously seen a CAM specialist, and up lack of stringent classification schemes. Current to 36% of patients with TMDs reported treat- evidence supports the belief that the appear- ing their symptoms with CAM techniques (see ance of myofascial pain involves the interplay chapter 17). The existing evidence supports the among a peripheral nociceptive source in mus- value of acupuncture for the management of cle, a faulty component of the central nervous idiopathic headaches and has shown promise system (sensitization), and decreased coping in the management of TMDs71 (see chapter 17). ability.131 In patients with MFP specifically, it is However, well-planned studies are needed to widely accepted that a complex interaction of assess the clinical value and cost-effectiveness variable intrinsic and extrinsic factors induces of acupuncture and other CAM therapies for fa- craniofacial pain and dysfunction. The clinical cial pain. presentation and symptoms of MFP resemble that of muscular pain disorders elsewhere in the body. Similarly, it is thought that the patho- Treatment: Summary and prognosis physiology of MFP may share mechanisms A clinician may choose from a number of con- with such entities as regional myofascial pain, servative therapeutic options that depend on TTH, and fibromyalgia. Figure 8-6 pre­sents a the history, physical findings, and comorbid conceptual model for understanding the many signs in the individual patient (Fig 8-5). factors involved in MFP.

211 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia injection Identifi able Identifi Trigger point Trigger trigger points Local anesthetic Dry needling • • splint Stabilization Regional MFP Comorbid arthralgia Medications contraindicated Occlusal splint Occlusal • • • Physiotherapy Medications contraindicated Limitation of mouth opening • • Physical Laser therapy TENS Medications contraindicated Adjunct to physiotherapy • • • • MFP CBT Relaxation Hypnosis Psychiatric referral Medications contraindicated cant Signifi psychologic distress present Biobehavioral • • • • • • Muscle Muscle relaxants Presence of muscle spasm muscle Psychotropics TCAs BDZ Widespread pain of more Failure conservative therapies sleep Poor Comorbid depression Pharmacologic • • • • • • • Simple analgesics Initial control of pain Comorbid TMJ pain • •

Fig 8-5 Treatment of masticatory myofascial pain. A wide variety of conservative treatment options are available. Symptomatology, comorbid medical or psychologic problems, and physician or patient preference dictate choice. TCA, tricyclic antidepressants; BDZ, benzodiazepine; TENS, transcutaneous electrical nerve stimulation.

212 Myofascial Pain

Psychosocial

Environment, function, comorbidities, Sleep Gender Mood and and life style, and catastrophizing disruption drug abuse ethnicity

Increased Autonomic pain nervous sensitivity system Nervous system Disturbed pain modulation Peripheral Central Trauma sensitization sensitization

Genetics and epigenetics

Fig 8-6 Conceptual model of the pathophysiologic factors influencing the development of MFP, which is considered a complex disease and is assumed to share features of other persistent pain conditions. Pain occurs within a frame- work of nervous system changes initiated by external events and modified by various intrinsic factors (mood, cognitive set, neurodegeneration) on the basis of genetic factors (and epigenetic changes). In essence, this is a gene by pain modulatory circuits by environment interaction. Multiple genes, for example, COMT, or α-adrenoreceptor 2, glucocor- ticoid receptors, protein kinase, muscarinic receptors, transcription coregulators, and phosphorylators of G proteins have been identified that carry an increased risk for higher pain sensitivity. Environmental factors can increase the risk through psychosocial mechanisms, physical factors such as trauma, or epigenetic modifications. The exact pain phenotype is determined by the interplay of several brain factors, such as context, cognition, mood, learning, memory, sleep, and neurodegeneration, that affect inhibitory circuits.132,133 Biologic sex and ethnicity may influence the balance among factors.

Historical perspective on TMD concepts TTH, regional myofascial pain, or fibromyalgia. However, data expressing common ground be- The first description of a TMD-like entity em- tween TTH and MFP is available, which sug- phasized the etiologic importance of tooth gests that we need to reexamine the present loss. This established the concept that regional nosologic separation. musculoskeletal pain was invariably associat- Historically, the diagnosis of pain associated ed with dental occlusion and other anatomical with TMDs has been approached under more factors, such as skeletal relationships. The re- than a dozen names, including temporoman- sultant structural and mechanistic concepts of dibular joint dysfunction syndrome and myofas- TMD etiology remain unproven but widely pub- cial pain dysfunction syndrome, which reflects licized. In view of such concepts, dentists have the confusion surrounding its etiology and often treated TMDs while other medical specialties its therapy. Research in the late 1950s attempt- have cared for additional chronic musculoskel- ed to shift attention from the TMJ to the mus- etal craniofacial pain such as TTH. Unfortunate- cles of mastication. Early studies also empha- ly, this has resulted in a separation of MFP from sized the contribution of psychologic factors to other chronic regional pain conditions, such as TMDs, which produced the psychophysiologic

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theory. Psychologic components as contrib- In the following section, possible factors that uting factors in TMDs were demonstrated by may be active in the initiation and maintenance extensive work on large patient populations, of chronic muscle pain are reviewed. These fac- and it was hypothesized that parafunctional tors act with genetics, proinflammatory states, activities to relieve psychologic stress led to cardiovascular and neuroendocrine function, muscle fatigue, spasm, and pain (see chapter trauma, and the social and environmental 4). Recent research has shown that patients makeup and may serve to protect or increase a with MFP consistently suffer higher levels of person’s risk132 (see Fig 8-6). distress than patients with articular TMDs.134,135 However, some patients with TMDs suffer from complex psychosocial disorders, and the role Nervous system alterations and pain of such influences as initiating factors remains modulation unclear, particularly in TMJ-related TMDs.136 The sensation of muscle pain is usually the Early theories offered one-cause, one- result of activation of polymodal muscle noci- disease hypotheses (that is, they were overly ceptors, groups III and IV, which are function- simplistic and univariate models), but accu- ally and anatomically equivalent to Aδ and C mulating data indicating a more complex TMD fibers, respectively. These fibers have a high etiology disproved these. Subsequently, new stimulation threshold and, under normal con- theories proposed a combination of stress and ditions, are therefore not activated to physi- occlusal disharmonies, but the focus remained ologic movement or normal muscle stretch. on occlusal adjustment as the preferred therapy. However, muscle nociceptors may be sensi- The most popular current theories are the multi- tized by peripherally released neuropeptides factorial,137 biopsychosocial,138 and multisystem that increase their response to suprathreshold vulnerability and dysregulation76 theories. All of stimuli and may induce long-term changes in these propose a complex interaction among en- the central nervous system, such as central vironmental, emotional, behavioral, genetic, and sensitization.131 Damage to individual muscle physical factors in the etiology of TMDs, which cells releases sufficient intracellular adenosine strongly suggests the need for multivariate ap- triphosphate to activate purinergic receptors proaches to study and understand these disor- and induce pain. ders. However, specific risk factors may or may In subgroups of patients with muscle pain, not be active in any given patient and therefore however, such as in fibromyalgia, pain may not do not answer the question of why an individual be dependent on any peripheral input. Indeed, patient develops a TMD. Thus, although these as discussed later, pain can occur secondary concepts are helpful at a population or group to a dysfunctional descending antinociceptive level, they may be limited for individual patients. system, an overactive descending facilitatory Some etiologic factors have received wide system, or loss of central inhibitory neurons acceptance. A proportion of patients with acute (see also chapter 12). TMDs report a clear association with trauma. In Evidence suggests that multiple mecha- chronic cases, initiation of pain is often associ- nisms are involved at the level of the periph- ated with a history of trauma, but whether this eral nervous system and the central nervous is the etiology, a cofactor, or a trigger is unclear. system. The complex and heterogenous clin- However, the patient’s psychologic status and ical phenotype of muscle pain (TTH, myofas- psychosocial functioning have emerged as cen- cial pain, fibromyalgia) probably involves dif- tral in determining the establishment of chronic ferent combinations of peripheral and central muscular pain and its treatment response.139 In nervous system mechanisms at different and support, baseline and longitudinal data from the even changing levels of activity. For example, OPPERA case-control study identify complex fibromyalgia may be mainly an expression of multifactorial conditions.16,140 Unfortunately, the central nervous system dysfunction, whereas patients in the OPPERA study largely (85%) suf- myofascial pain may initially involve peripheral fered from both MFP and TMJ disorders,16,141,142 mechanisms that may over time trigger central which limits the conclusions that can be drawn nervous system changes. Evidence of central specifically about MFP pathophysiology. sensitization was shown to be present in pa-

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tients with MFP and those with mixed MFP and suggest an additional component of enhanced TMJ disorders.143 pain facilitation that contributes to the greater Numerous studies have documented neu- pain sensitivity observed in patients with TMDs. rophysiologic characteristics of patients with In support of this concept, patients with TMDs TMDs. Unfortunately, many of these did not have repeatedly been shown to be more pain differentiate between muscular- versus joint- sensitive and to have concomitantly reduced based etiologies, so their usefulness is extreme- pain inhibition; these findings are similar to ly limited. Moreover, most of these studies were what has been demonstrated in patients with inconclusive and have largely been replaced other types of chronic pain, such as those with by quantitative sensory testing and functional irritable bowel syndrome.154 studies of the somatosensory system. Lowered pressure-pain thresholds in deep Complex behavioral influences, such as anx- tissues have been consistently reported in iety, depression, belief states, and cognition, patients with MFP, which suggests a failure in can separately influence pain perception and modulation and peripheral sensitization of mus- the pain experience. A key system that is able cle nociceptors.150,157–159 Because pressure-pain to directly change pain intensity is the brain- thresholds are changed not only in the painful stem’s descending modulatory network with its region but also at other sites, these studies pro- and antinociceptive components.133 suggest that those patients have central sensi- Altered pain modulation is suggested by tization.42,159,160 Activators of peripheral muscle findings of significantly more prevalent gen- nociceptors may include peripheral chemical eralized body pain (eg, fibromyalgia and back or mechanical agents and trigger point activity pain) and headache in patients with TMDs,144,145 (discussed later), in addition to reactive or even whereby most patients suffering from painful primary central mechanisms that can lead to joint or muscle pain report pain outside the neurogenic inflammation.41 craniocervical region.146,147 Patients with MFP The largest effects on experimental pain mea- display augmented central nervous system sures shown in patients with TMDs have been processing of pain (central sensitization) and on the pressure-pain thresholds at multiple body a deficit in endogenous pain inhibition.148–150 sites and on the cutaneous mechanical pain However, in other experiments151 no general- threshold. These results largely confirm previ- ized hypersensitivity has been shown in pa- ous studies that found that patients with chronic tients with MFP. This suggests that there may TMDs are more sensitive to many experimental be two clinical and possibly therapeutic sub- noxious stimuli at extracranial body sites, and types of MFP: those patients with and those they also provide clinicians with the ability to without extracranial muscle involvement.58 directly compare the case-control effect sizes Alternatively, multisite hyperalgesia may be a of a wide range of pain sensitivity measures graded, time-dependent phenomenon41; and for the first time.161 These data indicate gener- indeed, experimental studies have shown that alized hyperexcitability of the central nervous somatosensory sensitivity develops gradual- system and generalized upregulation of noci- ly in the presence of experimental jaw mus- ceptive processing, and thus, they suggest that cle pain.152 Additionally, in patients with MFP, these may be pathophysiologic mechanisms.156 widespread pain and tenderness are associat- Moreover, the response of patients with MFP ed with long-standing MFP.153 to experimental ischemic pain also depends Quantitative sensory testing studies have on their depression and somatization scores.162 been applied to the study of TMDs and fre- This complex interaction among psychosocial quently reveal evidence for abnormal somato- and biologic variables in MFP patients may sensory processing in patients with MFP58,64,65 occur independently or may share a common (see also chapter 3). Patients with TMDs exhibit biologic basis (see the section on psychosocial lower pain thresholds, greater temporal sum- factors). In any event, this clearly indicates the mation of mechanically and thermally evoked need for a combined therapeutic approach and pain, stronger aftersensations, and multisite for multivariate research approaches. A recent hyperalgesia.149,150,154–156 These findings indi- study demonstrated the potential for a multivar- cate faulty nervous system inhibition but also iate approach by showing that modulation of

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emotions by negative- or positive-loaded pic- did not influence pain-pressure thresholds or tures were only able to increase and decrease, EMG activity in the masseter and trapezius respectively, the pain sensitivity in people with muscles.176 In light of the evidence on the con- high expression of the serotonin transporter nections among the beta-adrenergic system, protein (this is a demonstration of gene × emo- COMT, and MFP177,178 (see the section on ge- tions × pain interactions).163 netics), it is reasonable to assume that future Molecular imaging studies are providing research will establish the involvement of sym- highly novel information regarding faulty pain pathetic dysfunction in patients with MFP.179 processing in patients with chronic pain. Al- though the data are not conclusive regarding causality, they clearly show that in patients suf- Neuropeptides and MFP fering chronic pain, the brain is fundamentally Little is known about pain and inflammatory disturbed and demonstrates faults and degen- mediators or neuropeptides in muscle tissue.131 erative changes in areas involved in pain modu- Serotonin and prostaglandin E are involved in 2 lation.143 They also show differences among pa- the development of pain and hyperalgesia/allo- tients with various orofacial pain conditions164 dynia of the masseter muscle in patients with and volumetric changes in gray and white mat- fibromyalgia, whereas local myalgia (myofascial ter in patients with chronic painful TMDs.165,166 pain) seems to be modulated by other as yet unknown mediators.180 Injection of neuropep- tides into muscle and the resultant changes Autonomic nervous system and MFP have provided important insight into the cas- The role of the autonomic nervous system cade of events that lead to persistent muscle has been investigated in persistent muscle pain. Inclusion of male and female subjects pain, particularly fibromyalgia. Although the also allows the analysis of sex differences. exact pathophysiology of fibromyalgia is un- Injection of glutamate into muscle is pain- clear, there is evidence of dysautonomia with ful181–184 and, acting through N-methyl-d- increased neural sympathetic activation and aspartate (NMDA) receptors and glutamate re- lack of an adequate sympathetic response to ceptors (GluR1), it has been shown to be import- stressor or cardiovascular challenges167 (see ant in producing muscle pain.185,186 Protein kinase the section on fibromyalgia). C activation is also required for this effect in cra- Patients with fibromyalgia suffer dysfunction niofacial muscle tissue.186 Glutamate excites and of the hypothalamic-pituitary-adrenal axis, sim- sensitizes rat masseter muscle afferent fibers ilar to that found in MFP,168 and this is thought through similar activation of peripheral recep- to partly underlie sleep disorders, some pain tors. However, the resultant afferent fiber activity symptoms, and autonomic nervous system im- is greater in female than male rats,181 an effect balance.169–172 Another view is that fibromyalgia observed in human subjects as well.184,187 These may represent a neuroplastic idiopathic pain studies clearly demonstrate sex-related differ- condition with similar neurobiologic changes ences in glutamate-evoked jaw-muscle activity but not specifically caused by a distinct lesion that are dependent on female sex hormones. or disease of the somatosensory system. Some of the mechanisms of muscle sensitiv- In a similar fashion, these findings indicate ity to palpation (allodynia) have been elucidated statistically significant differences between pa- by extensive experiments by Svensson et al, tients with TMDs and control subjects across 188–192 particularly the powerful effects of nerve multiple autonomic constructs, particularly ele- growth factor on muscle sensitization and its vated heart rate, reduced heart rate variability, sex-selective effects (see below). These experi- and reduced baroreflex sensitivity at rest and ments indicate that human nerve growth factor– during physically and psychologically challeng- induced sensitization of masseter nociceptors ing conditions.173 Patients with MFP demon- results, in part, from the activation of tyrosine strate increased levels of catecholamines174 kinase receptors. In contrast to findings from and reduced COMT activity.175 In contrast, later previous experiments on pain, muscle sensitivi- experiments on patients with MFP found that ty does not appear to be mediated through en- beta-adrenergic sympathomimetic stimulation hanced peripheral NMDA receptor activity.193,194

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In a study examining the levels of serotonin unclear.212 A neurobiologic basis is supported in masseter muscle in a heterogenous group of by prospective studies showing that about a fibromyalgia and MFP patients, it was found that third of patients develop TMJ arthralgia after serotonin is present in the human masseter mus- neck injury, despite not showing any structural cle in a steady state and that it is associated with damage to the TMJ.213 Patients with whiplash pain and allodynia. The origin of the serotonin demonstrate changes in thermal sensitivity in seems to be partly from the blood, but results facial regions, suggesting cervically driven neu- indicate that peripheral release also occurs.195 roplastic changes in the trigeminal system.214 Although most of these neuropeptide exper- An increased incidence of facial or jaw pain iments were performed with only one agent, the in patients after whiplash trauma has been in vivo milieu includes the interaction among a shown.213,215 MFP and neck pain are often co- number of neuropeptides and amines that may morbid,216 but they may also be confounders, act synergistically to increase sensitivity and because one of the features of MFP is neck pain in muscle.196 Indeed, combined admin- muscle pain. Moreover, patients with headache istration of bradykinin, serotonin, histamine, and facial pain frequently report concomitant

prostaglandin E2, and adenosine triphosphate cervical pain and vice versa, probably because in healthy subjects produces prolonged moder- of convergence of trigeminal and cervical affer- ate levels of pain and tenderness and has been ents on second-order neurons in the brainstem suggested as a useful model to mimic myofas- trigeminocervical complex.217 This bidirection- cial pain and TTHs.197,198 ality of pain referral has been experimentally demonstrated.218 Additionally, masseter pain can alter the strategy for jaw-neck motor con- Trauma trol, which further underlines the functional in- Researchers have increasingly recognized that tegration between the jaw and neck regions.219 trauma to the craniofacial region can lead to Functional findings in the masticatory ap- MFP.199 The exact mechanisms of how this re- paratus in patients after whiplash include de- sults in MFP are unclear but may include direct/ creased range of motion, disturbed coordina- invasive muscle damage, stretch injuries to tion, and impaired endurance.220–223 Although muscle, or long-term immobilization (eg, with functional impairment may be present in pa- fractured jaws). Indirect injury of brain tissue tients with a history of whiplash, long-term may also lead to persistent head and facial pain, follow-up of these patients does not indicate an although there is no correlation between the increased risk for persistent MFP.224–226 degree of injury and the incidence or severity of Many studies have assessed the presence the pain. Shear forces applied to the brain may of TMDs (both MFP and TMJ disorders)227 or result in severe damage. After even relatively have solely assessed the TMJ,213 making inter- minor head trauma, progressive and extensive pretation of the literature difficult. Moreover, it axonal injury can occur, which is commonly has been suggested that whiplash can lead to known as diffuse axonal injury.200,201 A history widespread body pain and that TMDs may be of trauma is present in significant numbers of just one expression rather than a specific out- patients with TMDs.199,202–205 Dental surgery has come of whiplash.228 Notwithstanding, recent also been found to increase the prevalence and systematic reviews conclude that whiplash symptomatology of TMDs.206,207 trauma is a clear comorbid condition in patients Whether patients with posttraumatic TMDs with TMDs but could also be an initiating and/ suffer more severe symptoms or are more re- or aggravating factor for TMDs.229,230 The exact sistant to treatment is unclear.208–210 Indications role of whiplash in TMD/MFP remains unclear.209 suggest that early intervention with a conser- vative approach (physical therapy, tricyclic an- tidepressants, NSAIDs) significantly improves Psychosocial factors the prognosis in cases of posttraumatic pain.111 Persistent pain, from whatever source, is asso- Whiplash, a hyperextension-flexion injury ciated with psychologic distress and psychoso- to the neck, has been implicated in the etiol- cial disturbances in many patients. These lev- ogy of TMDs,211 but how it can lead to MFP is els of distress may significantly affect patient

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compliance and treatment outcomes. Several ing factors.151,204,237,241 More recently, evidence methods have been designed to measure the suggests that global psychologic and somatic emotional results of stress or the intensity of symptoms emerge as one of the most robust environmental stress. These methods are used risk factors for incident TMD pain.242 Dysregu- as secondary end points in the assessment of lation in terms of enhanced negative feedback outcomes in the treatment of chronic pain. The suppression of the hypothalamic-pituitary- methodologies have recently been reviewed, adrenal axis exists in chronic myogenous fa- and the Depression Inventory and the Profile of cial pain. These results suggest a more central Mood States questionnaires are recommend- etiology, with dysregulation in the stress- and ed for the assessment of treatment outcomes pain-modulating systems.168 Indeed, patients and for research in chronic pain.117 For TMDs, with TMDs who have increased self-efficacy the RDC/TMD and DC/TMD Axis II criteria have measures suffered lower levels of pain, disabili- been extensively applied. ty, or psychologic distress and reported greater The level of psychologic and psychosocial use of an active, adaptive pain-coping strate- disturbance often predicts treatment demand gy.243 These findings form the justification and and outcome in patients with MFP139,231,232 (see basis for biobehavioral interventions. chapter 4). Patients with persistent pain who seek treatment usually have more severe pain and distress and a poorer prognosis. Cognitive Occlusion coping abilities in response to injury and pain The relationship between occlusion and MFP are also thought to be important. Recently, is based on the vicious cycle theory in which stress, negative affectivity, global psychoso- an occlusal interference is supposed to in- cial symptoms, and active and passive pain duce hyperactivity and spasm of the affect- coping have been significantly associated ed muscles, which in turn leads to ischemia with TMDs.233 Two aspects of coping emerge secondary to blood vessel compression. Ac- as therapeutically relevant in TMDs: control or cording to this rather old theory, the ischemic adjustment in response to pain and the recruit- contractions are painful and activate muscle ment of maladaptive coping strategies, such as nociceptors, thereby completing the vicious catastrophizing, in an attempt to control pain.139 cycle. Although the extent of the occlusal in- A positive response to TMD treatment has been terference may be minute, it supposedly upsets correlated with increased coping abilities.234 proprioceptive feedback and triggers bruxism Psychologic status and psychosocial func- and spasm of the masticatory muscles. These tioning of the patient have also been implicat- assumptions have been refuted by experiments ed in determining the establishment of MFP.139 demonstrating that artificial occlusal discrep- Patients with TMDs will manifest significant- ancies tend to reduce rather than enhance ly higher levels of psychosocial symptoms, bruxism244,245 and by the lack of correlation affective distress, somatic awareness, and between oral parafunction and pain intensity pain catastrophizing.233 Patients with MFP are in patients with TMDs.246,247 Clinically, no cor- frequently found to suffer from other stress- relation has been found between bruxism and related disorders, such as migraine headache, muscle tenderness.248 Interestingly, however, backache, nervous stomach, and gastrointes- the effect of occlusal interferences appears to tinal ulcers.235,236 Patients with MFP consistent- be dependent on the self-reported levels of oral ly suffer higher levels of distress than those parafunctions.244 with articular TMDs.134,135 Depression and lack Several long-term follow-up studies have of sleep have also been found to be signifi- also shown no consistent pattern between cantly increased in patients with TMDs.204,237–239 occlusal variables and TMDs,249,250 although Depression and chronic widespread pain are some show weak associations.251 In patients significant risk factors for the onset of MFP.240 awaiting full dentures, no statistically signifi- Earlier studies suggest that stress-related cant correlations were found between signs disorders may underlie or contribute to the de- and symptoms of TMDs and occlusal errors or velopment of TMD chronicity and may therefore freeway space.29 Malocclusion in adolescents be viewed as perpetuating rather than initiat- is not associated with TMDs.252 However, some

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rare malocclusions have been associated with Skeletal morphologic features and signs or symptoms of TMDs, including unilater- orthodontics al open bite, some crossbites, negative overjet, unilateral scissors bite in men, and edge-to- The association between certain skeletal mor- edge bite in women.253 Some of these maloc- phologic features and the prevalence of TMDs clusions are more significant in the presence of has been the focus of some controversy. Most bruxism.254 In several large population studies, research has focused on derangements and such malocclusions (and functional occlusion degenerative changes in the TMJ as they relate factors) accounted for only a small part of the to skeletal morphology, so few data are avail- differences between the control population and able on MFP.262 Nevertheless, data presented the study population with signs or symptoms in early reviews and in recent research indicate of TMDs.255,256 Patients with deep bite, in par- that the distribution of major skeletal/occlusal ticular those with retroclined maxillary incisors, categories in patients with TMDs does not differ frequently reported jaw stiffness and muscle significantly from the clinically normal popula- disorders, and this may represent a risk factor tion and that no single skeletal/occlusal prob- for TMDs.257 However, this is tempered by the lem can accurately predict the possibility of fact that somatization scores were significantly myogenous or arthrogenous TMD onset.263,264 higher in the deep bite group compared with The possibility that orthodontic treatment in the control group and that all patients were re- any of its many forms can lead to the initiation ferred for treatment.257 The data indicate that or deterioration of TMDs has been a topic of support for a causal relationship is weak. Only great concern within the orthodontic commu- bruxism, loss of posterior support, and unilater- nity.83 However, research consistently indicates al posterior crossbite show some consistency that orthodontic treatment does not entail an across studies, and these may be more import- increased risk for developing signs or symp- ant in TMJ disorders than in MFP.85 toms of a TMD.256,263–269 Therefore, the rela- Recent studies have reexamined the ef- tionship of TMDs to occlusion and orthodontic fects of acute artificial occlusal interferences treatment is minor. One review concluded that on such parameters as facial pain, chewing because signs and symptoms of TMDs occur ability, and jaw fatigue.258 Acute malocclusions in healthy people and increase with age, partic- usually cause variable amounts of discomfort ularly during adolescence, TMDs that originate in clinically normal subjects. However, this ex- during various types of dental treatment may perimental design does not parallel the clinical not be related to the treatment but may be a situation in patients with MFP, where purported naturally occurring phenomenon.270 Moreover, malocclusions occur slowly and are accompa- in two meta-analyses, no study was found in- nied by skeletal growth and adaptation. Other dicating that traditional orthodontic treatment experimental results seem to indicate that pa- increased the prevalence of TMDs.268,271 An in- tients with MFP have less adaptive capabilities teresting preliminary observation reported that to both active and control interventions, but subjects with a pain-sensitive variant of the they leave the precise relationship between COMT gene who underwent orthodontic treat- TMD pain and occlusion unanswered,258 and no ment were more likely to report subsequent studies have yet demonstrated a specific effect TMD pain,272 indicating a complex interaction of occlusal interferences rather than a more between genetics and environmental factors in generalized hypervigilance response. accordance with the conceptual model for MFP In conclusion, studies of this relationship (see Fig 8-6). have shown no functional occlusal factors to Orthodontic therapy aimed at improving or be consistently associated with TMD onset, resolving a symptomatic TMD condition also and no specific type of malocclusion has been has largely no supporting data266,269,273 apart found to be an accurate predictor of TMD inci- from correction of unilateral open bite, which dence.259–261 Taken together, these data indicate has a weak association with TMD improve- that occlusal factors seem to be of minor, if any, ment. However, this finding needs further importance in the etiology of TMDs.85 confirmation.88

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TMJ disorders Excessive bruxism with insufficient relax- ation, as in jaw clenching, is thought to lead to Theoretically, trauma or noxious stimulation muscle ischemia and pain. In this context, the of TMJ tissues can produce a sustained exci- most widespread belief is that repetitive tooth tation of the masticatory muscles, which may clenching, grinding, or abnormal posturing of serve to protect the masticatory system from the jaw induces MFP. However, these habits are potentially damaging stimuli and movements. extremely common and statistically have not This has been shown in animal models.274 Clini- been proven to induce MFP. cally, the frequent comorbidity of arthralgia and Exogenous models of muscle pain involve myalgia202 has led to hypotheses linking their the injection of algesic substances into mus- etiologies, but these have not been proven.275 cle. Endogenous models of experimental pain Such comorbidity may reflect sensitization have been studied extensively and involve the and referral patterns mediated by primary af- persistent contraction or exercise of the mas- ferents in the TMJ and muscles of mastication ticatory muscles.41,284–291 These experiments, co-synapsing on dorsal horn neurons (conver- although not identical to the chronic parafunc- gence).276,277 Moreover, experimental injection tional activities that occur in patients, have pro- of algesic chemicals into the rat TMJ resulted duced inconsistent, nonspecific, and inconclu- in a sustained reflex increase in EMG activity sive results, raising questions about the role of of the jaw-opening muscles. Excitatory effects muscle hyperactivity/overload in the etiology were also seen in the jaw-closing muscles, of MFP. A more clinically applicable situation but these were generally weaker.278 The weak is chronic low-level clenching, which does in- effects in jaw-closing muscles and the stron- duce muscle pain but, again, only in a subset ger effects in the antagonist muscles suggest of patients.292 Similarly, self-reported clenching associations more in keeping with protective, is more consistently associated with MFP than withdrawal-type reflexes, at least in animal grinding, although no cause-and-effect rela- models.274 Based on the present available data, tionship has been established.205 In this con- it seems that pain originating in the TMJ con- text, the Cinderella hypothesis, which provides tributes minimally to the development of MFP. a possible explanation for tissue damage after long-lasting and low-level muscle contrac- tions,293,294 may be relevant.295 This hypothesis Muscle hyperactivity, bruxism, postulates that some motor units containing and MFP type I fibers remain contracted throughout the A thorough understanding of bruxism is es- motor task and lead to localized overload, dam- sential to fully appreciate the implications of age, subsequent inflammation, and muscle no- the ongoing debate relating to its role in the ciceptor sensitization. These motor units have pathophysiology of MFP.279–283 The etiology of been demonstrated in the masseter muscle, sleep bruxism is probably related to arousal but so far no correlation has been found with responses and changes in the central/auto- postexperimental pain.295 Work is currently un- nomic nervous system that may be modulated derway to attempt to more closely reproduce by stress279 (see also chapter 5). The etiology naturally occurring long-lasting and low-level of awake bruxism is unclear and may involve masticatory muscle activity and relate this to stress in predisposed persons. the Cinderella hypothesis. Bruxism can cause muscle hypertrophy and Population studies suggest that self-reported severe damage to the dentition. The parafunc- tooth grinding (bruxism) may cause myal- tional forces applied during bruxism have also gia.204,296,297 Investigations based on self- been suggested as a cause of dental implant fail- reported bruxism generally show a positive as- ure, periodontal tissue damage, and tooth frac- sociation with TMD pain, but they are charac- ture. Hypothetically, the repetitive overloading terized by bias and confounders.298 For exam- of the TMJ and masticatory muscles by bruxing ple, the reliability of self-reported bruxing habits movements may cause tissue damage leading is problematic; 85% to 90% of the population to TMDs. Muscle overload may also initiate or report that at some time they have ground or reactivate trigger points in susceptible persons. clenched their teeth.282 Many patients who

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self-report tooth grinding admit that this was ise that pain acts as a homeostatic emotion first brought to their attention by their dentist. that requires a behavioral response. It involves Moreover, the reliability of clinician judgments an optimized recruitment of motor units, which of bruxism has been found to be extremely represents a person’s integrated response poor.299 Notwithstanding all of these limitations, to the sensory-discriminative, motivational- self-reported clenching and grinding have fre- affective, and cognitive-evaluative components quently been associated with MFP.202,300 In con- of the pain. This recruitment strategy aims to trast, and raising further questions about the minimize pain and maintain homeostasis and association between bruxism and MFP, studies puts more emphasis on how patients perceive based on more quantitative and specific meth- and cope with their muscle pain. ods to diagnose bruxism showed a much lower It is important to appreciate that rhythmic association with TMD symptoms.247 masticatory muscle activity (RMMA) produces In summary, available data do not support positive EMG findings that may occur with no the traditional concept of MFP being induced tooth grinding.283 RMMA is extremely common or maintained by muscle hyperactivity (ie, the and occurs in 60% of healthy control subjects vicious cycle theory).301 Little evidence is avail- and may easily be mistaken for tooth grind- able to support sleep bruxism in the etiology ing.305 Yet the number of RMMA episodes in of MFP, but the role of bruxing and clenching bruxers is three times higher than in control habits, particularly in the daytime, are as yet un- subjects and is associated with tooth grinding clear.205,292,295,296 Based on the data, the vicious in 33% of episodes.283 However, two recent cycle theory is untenable, and an alternative studies suggested an inverse relationship be- model—the pain adaptation model—has been tween sleep bruxism RMMA activity and mea- proposed to explain motor changes in patients sures of TMD pain and a positive relationship with muscle pain and disorders. between background non-RMMA activity and TMD pain.306,307 If muscle dysfunction is not the cause of Muscle hyperactivity and the pain pain, but rather part of the spectrum of a pain adaptation model adaptation response, then some parafunctions, The pain adaptation model is based on data including some bruxing habits, can no longer from persistent musculoskeletal pain condi- be considered primary etiologic mechanisms tions (including MFP), and it proposes that in MFP.301 However, the precise association the observed changes in motor function are between bruxism and MFP remains unclear at secondary to persistent pain and are mediat- this stage. Further refinement of how bruxism ed at the spinal or brainstem level.301 Changes is being assessed and quantified is obviously in masticatory muscle function secondary to needed. experimental muscle pain, as previously de- scribed, support this model and confirm the clinical complaints of dysfunction in patients Trigger points and the sympathetic with MFP.41 Injection of hypertonic saline into nervous system the jaw muscles induces pain with a significant Myofascial pain, whether in the facial area, reduction in jaw movements and in EMG activity head, or other body parts, is often characterized during the agonist phase; this is accompanied by the presence of painful trigger points.54,55 by a small increase in antagonist muscle activ- Pressure on a trigger point will activate intense ity.302,303 The pain adaptation model suggests pain and induce referral to characteristic sites. that pain will inhibit alpha motor neurons during The muscle around a trigger point is usually jaw closing and facilitate them during antago- hard and may be nodular or a taut band. Data nist (opening) activity.301 This model accurately suggest that trigger points are found in the area fits the currently available data. More recently, a of unchecked electrophysiologic activity at the broader model, termed the integrated pain ad- neuromuscular junction in the motor end plate. aptation model, has been suggested304 that in- This results in localized contraction, which, cludes the existing pain adaptation model as a together with the adjacent active motor end subset. This new model is based on the prem- plates, contributes to the formation of the taut

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band or nodule.54 Continued contraction in the of an organized nutritional schedule was found area of trigger points leads to localized hypoxia, significantly less frequently in patients with lowered pH, and the accumulation of proinflam- MFP.315 The potential future applications of es- matory mediators.55,308 Lowered pH increases tablished lifestyle risk factors in MFP are partic- the activity of the peripheral receptors, further ularly interesting as they may be relatively easy sensitizing the muscle nociceptors.131 Howev- avenues for initial and conservative treatment. er, the localized contraction in trigger points is not associated with generalized muscle hy- peractivity, so this phenomenon should not be Genetics confused with the muscle hyperactivity theory. No heritability has been found in humans for Furthermore, controlled studies have not been any TMD. In a study on monozygotic and di- able to identify more spontaneous EMG activity zygotic twins, no concordance in TMD signs in trigger points of patients with TTH compared and symptoms was found.316 A study on fe- with healthy control subjects.309 The appear- male patients with MFP and their first-degree ance of active trigger points is thought to be relatives also revealed no evidence of familial related to muscle trauma, particularly eccentric aggregation.317 However, genetic influences muscle lengthening during contraction.54 How- on TMD development have been found.115,318 A ever, experiments directed at inducing such significant association between polymorphisms damage have been largely inconclusive. in the serotonin transporter gene and TMD has Some researchers have suggested that mus- been shown in a Japanese population.318 A rela- cle hypoperfusion (diminished blood flow) may tionship between clinical phenotypes of TMDs be the primary factor in initiating muscle pain, (joint versus muscle) and COMT polymorphisms possibly because of changes in sympathetic has also been reported,319 but neither the clin- control.310 Moreover, the unchecked motor end ical criteria used nor the terminology (myofa- plates previously described develop sensitivity cial versus myofascial) are in line with current to sympathetic nervous system activity.54 Sim- thinking. Further work on COMT has identi- ilarly, sensitized nociceptors may be activated fied three genetic variants (haplotypes) of the by sympathetic activity. Thus, the sympathet- COMT-encoding gene, which were designated ic nervous system is capable of independently as low pain sensitivity, average pain sensitivi- initiating all the features of MFP.310,311 However, ty, and high pain sensitivity. These haplotypes there is still insufficient data at present to entire- encompass 96% of the human population, and ly endorse or refute this hypothesis. five combinations of these haplotypes were shown to be strongly associated with sensitivi- ty to experimental pain. The presence of even a Lifestyle single low pain sensitivity haplotype diminished Very little research has been performed on the the risk of developing MFP by as much as 2.3 relationship between various lifestyle habits, times. The low pain sensitivity haplotype pro- such as nutrition, exercise, and smoking, and duces much higher levels of COMT enzymatic the presence and treatment of MFP. In one pa- activity compared with the average pain sen- tient population study, current tobacco use was sitivity or high pain sensitivity haplotypes. In- associated with unfavorable demographic vari- hibition of COMT in rats results in a profound ables and more pain interference in subjects increase in pain sensitivity. Thus, COMT activ- with TMDs, but these effects were less pro- ity substantially influences pain sensitivity, and nounced in the case of myofascial pain.312 Cig- the three major haplotypes determine COMT arette smoking and its extent have been posi- activity in humans, which inversely correlates tively correlated with pain intensity in patients with pain sensitivity and the risk of develop- with TMDs, though there were no differences ing MFP.115 In a further study examining beta- between articular pain and MFP.141,313,314 In a adrenergic receptor haplotypes, positive or recent, population-based questionnaire study, negative imbalances in receptor function in- current tobacco use was significantly greater in creased the vulnerability to persistent pain patients with MFP relative to those with pain- conditions such as TMDs.320 The same group ful TMJs or to control subjects.315 Maintenance later showed the first direct evidence that low

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COMT activity leads to increased pain sensi- pain perception. Moreover, it was recently tivity via a beta-adrenergic mechanism.178 This suggested that poor sleep may interfere with study was a major breakthrough, but it must endogenous pain modulation.325,326 Some pain be stressed that the genetic variation in COMT conditions, such as cluster headache and fibro- seems to be specific not to MFP but rather to myalgia, present with disturbed sleep as an ex- pain sensitivity and the development of per- pression of a common pathophysiology. sistent pain in general,321 and it acts via the opi- In general, pain severity seems to be a ma- oid system.322 Several new genetic risk factors jor parameter in the occurrence of disturbed for TMDs, including glucocorticoid receptors sleep.327 Indeed, pain disturbances and pain- (NR3C1), protein kinase (CAMK4), muscarinic related awakenings are common in persistent receptors (CHRM2), transcription coregulators orofacial pain and are related to pain intensi- (IFRD1), and phosphorylators of G proteins ty.328–330 Patients with MFP often report poor (GRK5) have been recently identified.323 More- sleep and have been objectively shown to have over, the OPPERA study demonstrated that poorer sleep quality than patients with painful nonspecific orofacial symptoms, but not TMD TMJs or CDH.145,151,239,331,332 These data suggest pain itself, were associated with voltage-gated that in some patients with MFP, sleep disrup- sodium channel, type I, alpha subunit, and an- tion may not just be a result of the pain but, as giotensin I-converting enzyme 2 and that global in fibromyalgia, may form part of the disease psychologic symptoms, stress, and negative process itself. Pain-related awakenings occur affectivity were associated with prostaglandin- in about a quarter of patients with MFP and are endoperoxide synthase 1 (PTGS1) and related to pain intensity and the degree of mus- amyloid-β (A4) precursor protein (APP), indicat- cle pain.328 Primary insomnia has been associ- ing new genetic pathways influencing the risk ated with reduced mechanical and thermal pain of TMDs.25 thresholds in the orofacial muscles even after Although these findings need to be replicat- controlling for multiple potential confound- ed in independent cohorts, the genes potential- ers.333 Chapter 5 specifically deals with the rela- ly represent important markers of risk for TMDs, tionship between sleep and facial pain. and they identify potential targets for therapeu- tic intervention. For example, pain conditions resulting from low COMT activity and/or ele- Comorbidities vated catecholamine levels can be treated with MFP has been significantly associated with a pharmacologic agents that block both beta number of comorbidities, such as irritable bowel (2)- and beta (3)-adrenergic receptors. Adren- syndrome,334 fibromyalgia,335,336 migraine,337–339 ergic dysregulation has been seen in patients vulvodynia,145 and TTH.340,341 Some patients with TMDs or fibromyalgia,177 and acute treat- with MFP present with widespread pain and ment with low-dose propranolol has led to some do not, and they seem to respond to short-term improvement. However, the clinical therapy differently.104 Some indications suggest effectiveness of propranolol is dependent on that these comorbidities and MFP share a basic the COMT haplotype.116 These studies lead the disorder in pain modulation and psychosocial way in establishing pharmacogenomics in the factors. The study of these associations will no management of MFP. doubt shed new light on the pathophysiology of MFP. MFP is possibly a graded phenomenon from regional to widespread with other comor- Sleep disturbance bidities; or alternatively there may be two sub- Associations between pain and sleep distur- sets of MFP—people with and people without bance have been documented in several sam- widespread pain and comorbidity. ples of patients with persistent pain, usually in association with depression.324 Recent research suggests bidirectional interactions between the Pathophysiology: Summary experience of pain and the process of sleep. Clearly, many factors may be active in the eti- Pain interferes with the ability to obtain sleep, ology of TMDs in general and MFP in particular and disrupted sleep contributes to enhanced (see Fig 8-6). Host susceptibility plays a role

223 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

in MFP at a number of levels. Some patients tries.342 In Europe, TTH has a 1-year prevalence may be more prone than others to develop trig- in adults of more than 80%, an incidence that is ger points secondary to muscle injury; that is, higher than migraine, and a lifetime prevalence they may have a genetically influenced injury of more than 80%.6 In North America, the prev- response. Other genetically influenced physi- alence is around 38%; taking world statistics cal traits, such as pain modulation and phar- together, the global prevalence of TTH is much macogenomics, may then interact with psy- lower at around 30%.342 chologic traits to determine disease onset and European population studies indicate that progression and indeed whether pain develops. infrequent episodic TTH that occurs on aver- Additionally, environmental parameters such as age once per month is most common (48% ethnicity, culture, and stress are essential vari- to 59%) but does not usually require medical ables in the patient’s coping abilities and de- attention.343,344 One-year prevalence of frequent mand for treatment. The effects of sex are par- episodic TTH is 18% to 43%, and 10% to 25% amount and may be expressed via interactions report weekly headaches.344,345 between hormones and nociceptive pathways The frequency and severity of TTH attacks as well as environmental and cultural issues. are fundamental in estimating socioeconomic Any of the etiologic agents discussed may and personal impact. By definition, patients contribute to MFP in one patient but not in an- with frequent episodic TTH suffer more than other; some require a single etiologic factor and one attack monthly but less than a headache some a combination of etiologic factors to de- every other day, which can have a significant velop MFP in accordance with the suggestion effect on quality of life. Indeed, patients with of heterogenous multisystem dysregulations in frequent episodic TTH report missing, on aver- TMD pain.76 Clinicians, however, are still unable age, 3 days of work per month.346 In one study, to accurately identify these factors in individual 12% of patients with TTH reported absence patients so as to tailor a focused, mechanism- from work during the previous year because based treatment plan. of headache.347 Considering the high prev- alence of TTH, this is a significant problem. TTH, in particular chronic TTH, is thought to Tension-Type Headaches account for more than 10% of disease-related absenteeism in Denmark.348 Chronic TTH has TTHs are extremely common, and most people a profound negative effect on the well-being will experience at least one in their lifetime. The of patients and significantly reduces quality of IHS subclassifies TTH into episodic (infrequent life.349 and frequent), chronic, and probable TTH (see The average onset age of TTH is 20 to 30 Tables 8-4 and 8-5). The individual attacks in years, and peak prevalence is in the 30s to these subentities have similar clinical features 50s.343 However, up to 25% of schoolchildren with some subtle differences; severity and the report having TTH,347 and in the older popu- occurrence of mild nausea tend to increase lation (> 60 years), the prevalence is 20% to with frequency. Pericranial muscle tenderness 30%. Postadolescent women are only slightly is an extremely common feature in patients more affected than men (ratio of 5:4).343,345 with TTH, but because some patients do not Genetic studies reveal that first-degree rela- demonstrate this feature, the IHS subclassifies tives of sufferers of chronic TTH are three times TTH as with or without pericranial tenderness. as likely to also suffer headaches relative to the Note that there is a perhaps somewhat overlap- population.350 This suggests that chronic TTH ping diagnosis of headache attributed to TMD has important genetic factors. Frequent epi- in accordance with the DC/TMD criteria7 and sodic TTH is significantly affected by environ- the IHS criteria. mental factors, and there is evidence for only a minor genetic contribution.351 For example, it has been shown that variants of the COMT Epidemiology and genetics of TTH gene (see previous sections) do not contribute Evidence indicates that TTH varies across con- specifically to the predisposition to suffer from tinents and is most common in European coun- chronic TTH in children.

224 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Tension-Type Headaches

Episodic tension-type headache TTH or chronic TTH experienced remission over a follow-up period of 12 years, which suggests Clinical features that some patients with TTH have a good long- term prognosis.359 Negative prognostic factors Location. Episodic TTH is almost exclusively for TTH included not being married, no physi- bilateral (> 90%) and is usually described as cal activity, and poor sleep.359 Episodic TTH is bandlike or caplike. It affects, in order of fre- a chronic condition with an average duration quency, the occipital, parietal, temporal, and before treatment of 9 to 12 years.354,359 frontal areas (see Fig 8-2). Pain site may vary with intensity and among patients.352 Precipitating or aggravating factors. Epi- sodic TTH is commonly precipitated by a num- Quality and severity. The vast majority of pa- ber of factors; stress, fatigue, disturbed meals, tients describe the quality of pain as pressure- menstruation, alcohol, and lack of sleep.360,361 like, dull, or a sensation of tightness. A throb- These are similar to those reported by mi- bing character is rare in TTH, but it has been graineurs (see chapter 10). reported in 14% to 20% of patients, particularly TTH is usually not aggravated by physical during more severe attacks.353 activity.352 This has been considered a major Pain of TTH is considered milder than mi- differentiating factor from migraine, with more graine pain, but the differences may not always than 95% of migraineurs reporting aggravation be as striking as expected. Usually TTH is mild by exercise.362 However, there are reports that to moderate in intensity and graded at around exercise may aggravate pain in 16% to 28% of 5 to 7 on a VAS,354,355 but it may become mod- patients with TTH.363,364 erate to severe with an increase in headache frequency. This is in contrast to the pattern Associated signs. A proportion of sufferers observed in migraine, an all or none phenom- from episodic TTH experience significant dis- ena where pain severity is largely unaffected ability related to pain severity, frequency, and by headache frequency (see chapter 10). Many accompanying features, such as poor sleep.365 patients with TTH suffer from pain in the neck Sleep disturbances are common in persons and shoulder muscles, and this increases in with TTH,366 and fatigue is reported very often. chronic TTH.356 Lack of sleep is a common precipitant of TTH. Accompanying symptoms are rare in the Temporal pattern. The temporal features of less frequent forms of TTH, but mild to moder- individual episodic TTHs are extremely vari- ate anorexia is reported by 18% of patients.367 able both within and among patients. TTH du- Occasional and mild photophobia (10%) or ration may range from 30 minutes to 7 days, phonophobia (7%) has been observed.352,367 and the reported median duration ranges from Many patients will suffer from both migraines 4 to 13 hours.346,357 The median frequency in and TTHs that may further affect quality of life. the population ranges from one headache ev- Interestingly, episodic TTH in migraine sufferers ery 2 months to two headache days per month, responds to sumatriptan, a migraine-specific whereas in a clinic population it is expectedly drug, whereas in nonmigraine patients it does higher at 6 days per month.346,354 The IHS classi- not.368 This may suggest that mild migraines fication lists five diagnostic criteria for episodic may be phenotypically very similar to episodic TTH (listed A through E), with the first criterion TTH (see chapter 10). (A) distinguishing, by temporal features, be- tween infrequent and frequent episodic TTH (Table 8-4). Chronic tension-type headache Long-term follow-up indicates that most Chronic TTH is one of the subtypes of a more patients (75%) with episodic TTH continue to recent diagnostic family simply termed chron- suffer episodic attacks, but 25% report evolv- ic daily headaches. The umbrella diagnosis of ing into chronic TTH.345,358 However, in another CDH is based on the daily or near-daily occur- study, 45% of patients with frequent episodic rence of headaches.

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Table 8-4 Diagnostic criteria for episodic TTH* Infrequent episodic TTH Notes A. At least 10 episodes of headache occurring on Patients with TTH often present with clinical pericranial < 1 day per month on average (< 12 days per muscle tenderness. However, some patients do not, year) and fulfilling criteria B through D and the role of muscle tenderness and hyperactivity is unclear. Infrequent episodic TTH and frequent episodic Frequent episodic TTH TTH have therefore been subclassified as with or without A. At least 10 episodes occurring 1 to 14 days per pericranial tenderness. month on average for > 3 months (≥ 12 and < 180 days per year) and fulfilling criteria B through D Both infrequent and frequent episodic TTH B. Headache lasting from 30 minutes to 7 days C. At least two of the following four characteristics: Accumulating evidence suggests that some TTHs may 1. Bilateral location be aggravated by exercise (see text). The diagnostic 2. Pressing or tightening (nonpulsating) quality difficulty most often encountered is to discriminate 3. Mild or moderate intensity episodic TTH from mild migraine without aura. This is 4. Not aggravated by routine physical activity, such especially so because patients with frequent headaches as walking or climbing stairs often suffer from both disorders. Criteria D are very common in migraines. D. Both of the following: 1. No nausea or vomiting 2. No more than one of photophobia or phonophobia E. Not better accounted for by another International Secondary headache has been excluded by history, Classification of Headache Disorders, third examination, and imaging if appropriate. edition diagnosis *Reproduced with permission from the International Headache Society.

Chronic daily headache tially induce headache, the primary CDH must occur without drug abuse. The concept of CDH The diagnosis of CDH is based on specific is clinically and epidemiologically useful, but criteria that have been shown to accurately because it represents a family of entities with classify most cases.369 Most importantly, CDH different therapeutic responses, a specific diag- is defined as headaches occurring on at least nosis is essential for successful management. 15 days per month and may be subdivided The prevalence of CDH in the population, into two forms: primary or secondary (attribut- from children to the elderly, is about 2.5% to able to specific pathology). The most common 5% and remains consistent across global stud- secondary type of CDH is medication-overuse ies.347,371,372 Chronic TTH has a global preva- headache (see chapter 14). Primary CDH may lence of 2% to 3%,344,345 and chronic migraine be short or long lasting (> 4 hours per attack) has been estimated to occur in 1.3% to 2.5% of and include chronic migraine (see chapter 10); the population (see chapter 10). Therefore, the chronic trigeminal autonomic cephalalgias, in- vast majority of CDH patients in the population cluding hemicrania continua (see chapter 11); suffer from chronic TTH or chronic migraine. chronic TTH; and new daily persistent headache CDH is very common in headache clinics. In (NDPH). The latter two entities are phenotypi- one study, 45% of 171 patients with a primary cally similar and are described in this section. complaint of headache were diagnosed as suf- The diagnosis of NDPH is reserved for patients fering from CDH; 62% of them had chronic mi- with daily headache and strictly no history of graine, 34% had chronic TTH, 2.6% had NDPH, episodic migraine or episodic TTH. As most and 1.3% were diagnosed with hemicrania con- patients with daily headache have a tendency tinua.373 In pediatric headache clinics, CDH may to abuse analgesics370 that themselves poten- be rare and account for about 5% of primary

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Table 8-5 Diagnostic criteria for chronic TTH* Diagnostic criteria Notes

A. Headache occurring on ≥ 15 days per month on average Chronic TTH evolves from episodic TTH. Chronic for > 3 months (≥ 180 days per year), fulfilling criteria B headache starting de novo should be classified as through D NDPH (see Table 8-7). B. Headache lasting hours to days or unremitting C. At least two of the following four characteristics: Chronic TTH is subdivided into with or without 1. Bilateral location pericranial tenderness. 2. Pressing/tightening (nonpulsating) quality 3. Mild or moderate intensity 4. Not aggravated by routine physical activity such as walking or climbing stairs D. Both of the following: These criteria may complicate differentiation with 1. No more than one of photophobia or phonophobia or chronic migraine (see chapter 10), and patients mild nausea may need careful follow-up (pain diaries) to 2. Neither moderate/severe nausea nor vomiting accurately diagnose their headaches. Chronic TTH is bilateral. E. Not better accounted for by another International Secondary headaches have been ruled out. Classification of Headache Disorders, third edition Medication overuse is common in chronic diagnosis headache and may lead to medication-overuse headache (see text and chapter 14). *Reproduced with permission from the International Headache Society.

headaches.374 Most studies demonstrate that cated in the frontal, temporal, or frontotemporal 25% to 38% of patients with CDH are abusing regions.367,379,380 Headaches limited to the oc- analgesics.375–377 This would require persistence cipital region have also been reported.381 of symptoms after cessation of drug abuse and Pain quality is similar to that reported in epi- before final diagnosis. Treatment of CDH de- sodic TTH and is mostly pressure-like and bilat- pends on the specific diagnosis and is based eral.367 Severity of chronic TTH in population and on prophylactic regimens involving many class- clinic studies reveal that most patients (78%) es of drugs (see chapters 10, 11, and 14 on the suffer moderate pain, some (14.8% to 16%) relevant disorders and chapters 16 and 17 on mild, and very few (4% to 7.4%) severe.367,382 the drugs commonly used). Temporal pattern. Chronic TTH is character- ized by a continuous or daily headache. Mean Clinical features of chronic TTH frequency obtained from patient diaries is 23 to Classically, the typical patient with chronic TTH 30 headache days per month.380,383 is a middle-aged woman with a long headache history who originally had episodic headaches Associated signs. Many patients with chron- 10 to 20 years previously that slowly increased ic TTH demonstrate increased pericranial in frequency.370,378,379 The clinical features of tenderness in regional muscles. This is more chronic TTH are largely similar to those in fre- severe in trapezius, neck, and sternocleido- quent episodic TTH, but there are differences mastoid muscles but is also detectable in in accompanying features, treatment response, masseter and temporalis muscles.384 Extra- and impact on quality of life (Table 8-5). cranial tenderness may also be present.385 Headaches are often accompanied (32% of Location and quality. In 80% to 98% of pa- patients) by photophobia or phonophobia.381 tients, chronic TTH is bilateral and usually lo- As reported for episodic TTH, physical activ-

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ity may worsen pain in a subgroup of patients etaminophen and aspirin and provides better with chronic TTH.367,382 and faster pain relief.390 Low-dose diclofenac Persons who suffer from TTH report a lack is comparable with 400 mg of ibuprofen.391 The of sufficient and restorative sleep, but this is a more rapidly absorbed naproxen formulation, common finding in patients with chronic pain naproxen sodium (375 to 550 mg), is effective and may also be related to depression.386 In- in TTH, and the higher dose was superior to deed, as observed in other chronic pain con- 1 g of acetaminophen.392 Overall, however, on- ditions, depression and anxiety are common in set of pain relief is delayed in most of these patients with chronic TTH.387 drugs.393 Based on efficacy and safety profiles, Photophobia or phonophobia was reported expert recommendations suggest ibuprofen by 17% of a population and 32% of subjects or naproxen sodium as drugs of choice393,394 in a clinic-based study on patients with chron- (see Table 8-6). The exact dosages should ic TTH.367,381 Nausea was reported by 25% of be titrated individually according to response patients with chronic TTH in the population. and adverse effects. Combination analgesics Chronic TTH may be diagnosed in patients with are often used but may offer small advantage only one of the conditions of photophobia, pho- over single drugs and may increase the risk of nophobia, or mild nausea (see Table 8-5).388 medication-overuse headache. However, caf- feine at doses up to 200 mg has been proven to increase the efficacy of ibuprofen and other Treatment of TTH mild analgesics in the treatment of TTH, but Patient education is essential, and there are caffeine carries a high addiction profile and websites that explain headaches and their should be carefully monitored.395 In patients treatment (eg, www.achenet.org/). The dangers with chronic TTH, or coexisting migraine and of analgesic drug abuse must be made clear episodic TTH, triptans have induced significant to the patient and every effort made to control pain relief.396,397 it. Many patients with frequent episodic TTH or Tricyclic antidepressants have been ex- chronic TTH suffer from impaired function and tensively studied as prophylactic agents and quality of life, often accompanied by emotional are superior to serotonin-selective agents in distress and drug abuse that needs careful and TTH.398 Amitriptyline is consistently efficacious professional attention. in prophylactically reducing frequency, dura- tion, and severity of chronic TTH.399 Interpreting these results and applying them to clinical prac- Pharmacologic tice and patient expectations require extreme The pharmacologic management of TTH may care; often, statistically significant reductions be subdivided into abortive (individually treat in headache duration (eg, from 11 to 8 hours) the acute attack) or prophylactic approaches; may be of doubtful value to the patient.12 Nev- the choice depends on headache frequency, ertheless, amitriptyline and other tricyclic anti- patient preference, and other factors. Abortive depressants are widely used for chronic TTH. approaches are largely pharmacologic, whereas Indeed, amitriptyline is effective in chronic TTH psychologic, physiotherapeutic, and TMD-aimed but not in episodic TTH, which suggests dif- treatments have all been used in the prophylactic ferent pathophysiologic mechanisms. Amitrip- treatment of TTH with varying degrees of suc- tyline should be initiated at 10 mg daily taken cess. Abortive pharmacotherapy should not be just before bedtime (see chapter 17) and then used in chronic TTH because the high headache titrated according to response and side effects. frequency may lead to analgesic abuse and Studies on patients with chronic TTH show that medication-overuse headache (see chapter 14). a higher dose is often needed (75 mg).12 Ven- As abortive therapy, mild analgesics or lafaxine (150 mg/day), a serotonin noradrena- NSAIDs have been consistently proven effi- line reuptake inhibitor, may be a good second cacious and are considered the first choice choice.394 Based on the high frequency of peri­ (Table 8-6). Mild headaches may respond fa- cranial muscle tenderness in TTH, investigators vorably to 1 g of acetaminophen or aspirin.389 have tried muscle relaxants such as tizanidine Ibuprofen (200 to 400 mg) is superior to ac- with mixed results.400

228 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Tension-Type Headaches

Table 8-6 Evidence-based recommendations for the abortive therapy of TTH* Drug Dose (mg) Notes Ibuprofen 200–800 Gastrointestinal irritation, bleeding risk Aspirin 500–1,000 Gastrointestinal irritation, bleeding risk Naproxen 275–825 Gastrointestinal irritation, bleeding risk Acetaminophen 1,000 Hepatic considerations Caffeine in analgesic 65–200 Increased efficacy of ibuprofen and acetaminophen but combinations addictive and increases risk of medication-overuse headache *Reproduced with permission from the International Headache Society.

Nonpharmacologic interventions al muscles are reasonably effective in frequent episodic TTH and may be an alternative or ad- Commonly used behavioral interventions for junctive treatment.355 Additionally, acupuncture TTH include relaxation training, biofeedback has emerged as a valuable nonpharmacologic training, and cognitive-behavioral (stress- tool in patients with frequent episodic TTH or management) therapy.394,401 These treatments chronic TTH.406 attempt to influence the frequency and sever- ity of headaches and emphasize the prevention Temporomandibular disorder therapies of headache episodes. Relaxation and EMG in the treatment of TTH. Interpretation of biofeedback therapies are effective mainly in the relevant literature is hampered by the over- episodic TTH and provide on average a 50% whelming majority of studies (> 95%) that are reduction in headache activity.402 However, in not randomized, controlled, or blinded. Uncon- patients with chronic TTH, the combination of trolled studies show a reduction in severity and stress management with a tricyclic antidepres- frequency of headaches after use of occlusal sant (amitriptyline ≤ 100 mg/day or nortriptyline splints, occlusal adjustments, or physiothera- ≤ 75 mg/day) was more likely to produce clin- py.407 With no placebo control and poor defi- ically significant reductions in headache index nition of headache types, these studies are of scores than each therapy alone or placebo.403 limited applicability. The newest version of the Physical or manual therapies are often inte- IHS and DC/TMD should help clinicians and re- grated into the treatment plan of those suffering searchers to better characterize and phenotype from TTH. Physiotherapy is more effective than their patients with overlapping signs and symp- massage therapy or acupuncture for the treat- toms of headache and TMDs. The use of stabi- ment of TTH and appears to be most beneficial lization splints in headache patients with con- for patients with a high frequency of headache current TMDs resulted in a significant reduction episodes. Chiropractic manipulation may be in headache frequency and analgesic use beneficial for TTH, but the evidence is weak. relative to a group treated by a neurologist.408 Data are lacking regarding the efficacy of these This would seem to make sense in that com- treatments in reducing headache frequency, prehensive treatment planning to include all intensity, duration, and disability in many com- pain-related problems is more likely to produce monly encountered clinical situations. Many of beneficial results. Moreover, the splint group the published case series and controlled stud- was examined more often by the treating physi- ies are of low quality, and there is very little rig- cian, which may have subconscious beneficial orous evidence clearly supporting the use of effects on treatment outcome. No significant these modalities.404 effect of occlusal adjustment was observed on Botulinum toxin injection has not been of headache frequency.409 The use of a new type any significant benefit to those suffering from of bite plate, the nociceptive trigeminal inhibi- TTH.405 Repeated local lidocaine injections tion tension suppression system, for the treat- into the trigger points located in the pericrani- ment of migraines and TTH has recently been

229 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

proposed.89 The original studies were all open peripheral afferents onto second-order neurons and have not been duplicated. Moreover, the in the subnucleus caudalis, central sensitization nociceptive trigeminal inhibition tension sup- with expansion of receptive fields,414 and acti- pression system provides occlusal contacts in vation of convergent thalamic neurons.415 the anterior region only and may, with overuse, cause permanent occlusal changes. Muscle hyperactivity. Excessive contraction In summary, standard TMD therapies may of pericranial muscles has been thought to play help some patients with TTH, particularly those a major role in the pathophysiology of many with concomitant MFP. However, as previously myofascial disorders, including TTH. Pericrani- stated, irreversible destruction of tooth struc- al muscle activity in patients with TTH has been ture, as in occlusal adjustment, does not have shown to be variably normal or increased. Later enough evidence in the authors’ view. In select- studies have similarly been inconclusive, but in ed cases, a trial with a flat occlusal splint may summary, there is no substantial evidence to be justified. support a causal relationship between pericra- A later section has a brief discussion of nial muscle hyperactivity and TTH. Some pa- NDPH as it represents a differential diagnosis tients with TTH do have increased muscle ac- to CDH and chronic TTH. tivity, but this may be in line with the protective mechanisms proposed by the pain adaptation Pathophysiology of TTH. Interrelationships model.301 Moreover, contamination of EMG re- among peripheral and central mechanisms cordings by the muscles of facial expression is probably underlie the initiation of TTH, but an important confounding variable. the exact etiology is uncertain. Note that the Experimental chewing (concentric exercises) same etiologic factors are considered in TTH with or without temporal artery ischemia induc- and in MFP, which further suggests a common es a bilateral dull head pain.416 TTH was induced pathophysiology. by prolonged tooth clenching with muscle ten- derness that preceded the onset of headache Pericranial muscles as a source of pain. by several hours.417 Prolonged experimental Whether the presence of pericranial muscle frontalis muscle contraction, however, failed to tenderness is the cause or the result of the produce headaches in a group with relatively headache is unclear. Moreover, many patients frequent TTHs.418 Moreover, a further study on with TTH present without pericranial myofascial patients with TTH showed no significant differ- tenderness. Notwithstanding, many patients ences in the induction of headache between with TTH display increased myofascial sensi- active clenching and holding a toothpick be- tivity, and this is considered important in the tween their lips as a control procedure.419 Both pathophysiology of this group of patients.3,410 groups, however, developed more headaches Human experiments with intramuscular in- than did patients without TTH under the same jection of algesic substances (usually hyperton- experimental conditions. This would suggest ic saline) induce pain and referral patterns char- that abnormalities in central pain transmission acteristic of craniofacial myofascial conditions. or modulation alter the susceptibility of patients Injections into the sternocleidomastoid and to develop headache and are more important trapezius muscles produce localized pain with than muscle strain induced, for example, by jaw referral to regions associated with TTH loca- clenching. Similar conclusions may be derived tion.53,411–413 In contrast, injection into the mas- from an experiment testing headache onset af- seter, medial, or lateral pterygoids refers pain ter static contraction of the trapezius muscle; al- to the teeth, angle of the mandible, and TMJ though more patients with TTH developed head- and resembles the pain pattern observed in ache than did control subjects, there was no MFP.53,412 Quality and intensity of resultant pain significant difference in headache development do not differ significantly among injection sites. between the active and the placebo procedure This would suggest a prominent role for muscle (tibial muscle contraction) in patients or control nociceptors in the location and referral patterns subjects.420 Eccentric exercises are proposed of reported pain in TTH and MFP. Pain-referral to induce ultrastructural muscle damage and patterns also involve central convergence of thus lead to inflammatory pain. This has been

230 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Tension-Type Headaches

postulated to involve abnormalities in muscle there is a high proportion of patients with ten- blood flow, but experiments show this is nor- derness of the myofascial tissues (including mal in patients with chronic TTH.421 During static tendons) that is present during and between contraction, diminished flow was noted but was attacks, which suggests peripheral sensiti- unassociated with ischemia or inflammation.421 zation.419,427 Interestingly, muscle tenderness Headache has been produced after various ex- correlates with frequency and intensity of TTH, perimental muscle exercises but is usually short and often the relief of TTH is accompanied by lasting, even after prolonged exercises.422 Thus, reduced muscle tenderness.428 Once again, the the role of pericranial muscle tenderness in TTH peripheral mechanism associated with these remains unclear; in patients with TTH and mus- findings remains unclear. cle tenderness, it has been suggested that the However, it has been suggested that sensi- mechanisms involve persistent nociceptive in- tivity in the pericranial muscles may be second- put leading to central sensitization that is neg- ary to changes in the central nervous system. In atively affected by faulty central modulation. a trial on the initiation of TTH by tooth clenching, This hypothesis is very similar to that proposed it was found that patients with frequent episodic for MFP but leaves the origin of the peripheral TTH who did not develop headache developed nociceptive activity unanswered. Most likely, a increased pressure-pain thresholds, which combination of and interaction among several suggests that clenching activated their antino- factors will be needed in accordance with the ciceptive system.417 Interestingly, the patients conceptual model presented in Fig 8-6. who did develop headache had no change in pressure-pain thresholds, which suggests that Biopsychosocial parameters. The complex patients unable to recruit endogenous antino- relationships between chronic pain and psy- ciceptive pathways are more likely to develop chosocial pathology have been increasingly headache.417 This lends support to the hypoth- investigated, including in the field of headache. esis that muscle tenderness may be secondary Significant psychopathology is observed in a to central sensitization and/or faulty supraspi- minority of headache patients in the popula- nal inhibitory or facilitatory mechanisms.429 The tion, although those with significant problems presence of central sensitization in chronic TTH are more likely to seek treatment for their head- is supported by findings of increased sensitivity aches.423 For example, patients with recurrent to pressure, electrical stimuli, and thermal stim- headaches (eg, TTH or migraines) exhibit sig- uli at craniofacial and general body sites.384,430 nificantly more psychiatric comorbidity.424 Sig- In most studies, pain detection and tolerance nificant psychopathology complicates head- thresholds are also reduced in patients with ache management and is associated with a chronic TTH.384,430 In contrast, patients with reduced prognosis. People with recurrent TTH episodic TTH, other than those with frequent report more stressful events and judge them to episodic TTH, demonstrate normal pain- have more impact on their lives.425 Those suffer- detection thresholds.357,431 In chronic TTH, there ing from TTH also seem to use different coping is a significant correlation between generalized strategies for stress and pain.425 However, there sensitivity and pericranial tenderness.384,432 Be- is little evidence of differences in physiologic re- cause chronic TTH is most often a progression sponses to stressful events.425 Recent findings from frequent episodic TTH, it is likely that cen- suggest that stress contributes to headache, in tral sensitization in patients with chronic TTH is part, by aggravating existing hyperalgesia.426 induced by prolonged nociceptive inputs from Coping abilities have not been extensively myofascial tissues.433 Increased pain sensitivi- studied in TTH, but catastrophizing may be ty seems to accompany the transformation of more common in persons suffering from TTH. episodic TTH to chronic TTH, but it is most like- In summary, the cause-and-effect relationship ly a result rather than the cause of increased between TTH and psychosocial problems is un- headaches.434,435 Impairment of endogenous clear but may affect treatment outcome. supraspinal pain-modulation systems after experimental pain has been shown in patients Peripheral and central neural mecha- with chronic TTH,436,437 and there is significant nisms. In both episodic TTH and chronic TTH, gray-matter decrease in regions known to be

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Table 8-7 Diagnostic criteria for NDPH* Diagnostic criteria Notes A. Persistent headache fulfilling Headache is daily from onset and very soon unremitting. Prior headache criteria B and C is not contraindicated, but onset of NDPH is not preceded by increasing frequency of migraine or TTH. B. Distinct and clearly remembered Essential for accurate diagnosis. If headache evolves from TTH, the onset, with pain becoming diagnosis should be chronic TTH. continuous and unremitting within 24 hours

C. Headache present for > 3 months There are two subforms: a self-limiting subform that typically resolves within several months without therapy, and a refractory form that is resistant to aggressive treatment regimens. D. Not better accounted for by Secondary headaches have been ruled out. Medication overuse is another International Classification common in chronic headache and may lead to medication-overuse of Headache Disorders, third headache (see text). edition diagnosis *Reproduced with permission from the International Headache Society.

involved in pain processing.438 The evidence reported by 40% of patients.441 Occipital areas thus suggests that peripheral mechanisms play are involved in 40% to 60% of cases, and a mi- a major role in episodic TTH, whereas central nority will describe pain throughout the head.441 mechanisms such as faulty inhibitory mecha- nisms and central sensitization are prominent in chronic TTH. Quality and severity Pressure (54%) and throbbing (10% to 55%) New daily persistent headache. The NDPH qualities are the individual descriptors most type of chronic headache was previously termed commonly reported.441,442 Pain quality is var- chronic headache with acute onset. Presentation ied, and many patients describe their pain with may be heterogenous, as exemplified by case combinations of descriptors such as pressure studies.439 The headache, as defined by the IHS, and tightening (73%).442 Stabbing (45%), aching must become chronic within 3 days of onset (Ta- (43%), dull (37%), and tightness (36%) are also ble 8-7), and this is the major differentiating fea- frequently used. More rarely, burning (23%) or ture in relation to chronic TTH388 (compare with searing (4%) pain is reported. Tables 8-4 and 8-5). In the current definition, Most patients (66%) report headache se- patients with a history of migraine or TTH are verity as usually moderate (4 to 6 on a 10-cm not excluded from the diagnosis of NDPH, but VAS); some (21%), however, report persistently the NDPH headache should take on a sudden severe pain (> 6 VAS).441 In a series of 30 Jap- daily frequency without any gradual increase in anese patients with NDPH, all reported severe frequency of the underlying headache.3,440 unbearable pain.442 These cases excluded post-viral cases (discussed later), so the differ- ences in pain severity may reflect a diagnostic Clinical features subgroup or cultural differences.442 Location Pain is bilateral in most patients.441–443 Location Temporal features involves the temporal region alone (20% of pa- Many patients can accurately recall the exact tients) or in combination with other sites (46% date of headache onset with a subsequently of patients). In one series, retro-orbital pain was rapid progression to chronic pain (< 3 days).441

232 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Tension-Type Headaches

The vast majority will report headache that is As discussed previously, CDH has a prevalence present continuously, but about one-fifth suf- of about 2.5% to 5% in the general population. fer from a daily headache lasting a number of In a Spanish population, NDPH was found in hours.441,442 More recent characterization of 0.1% of patients and formed only 2% to 6.7% these patients suggests they may be subdivid- of all the cases of CDH identified.375,449 In spe- ed based on temporal pattern and prognosis: cialist clinics, the proportion of CDH cases diag- (1) persistent type with a continuous headache nosed as NDPH increases to 11% to 14%.370,450 from onset, (2) remitting type with complete resolution of headaches that occur fewer than 5 days per month for 3 months, and (3) relapsing- Treatment remitting type with pain-free breaks between NDPH seems to have two subgroups: those bouts of continuous headache.444 refractory to treatment442 and those who have a benign progression and will improve, with or without therapy, within a few months.3,440 Com- Headache onset plete resolution was reported in 86% of male A recent infection or flulike illness is reported in patients and 73% of female patients over a pe- 30% of patients.441 Extracranial surgery (12%) riod of 2 years. or a stressful life event (12% to 20%) are also Specifically for patients with post-viral common precipitators, but 46% to 80% of NDPH, early treatment with methylprednisone patients had no identifiable precipitating fac- may be effective.451 Based on case reports, tors.441,442 One series excluded patients with botulinum toxin may provide relief for some post-viral NDPH, so the contribution of viral patients.440,452 infections to NDPH onset and phenotype re- Elevated levels of tumor necrosis factor al- mains unclear.442 pha in the cerebrospinal fluid (CSF) of patients with NDPH led to a successful trial of doxycy- cline and subsequently nimodipine (anti–tumor Accompanying signs/symptoms necrosis factor alpha properties).440,453 Associated migrainous symptoms may be pres- Anecdotal evidence suggests that the nov- ent in more than 50% of patients.445,446 These el antiepileptic drugs, such as gabapentin and include nausea or vomiting, phonophobia, and topiramate, may be useful in the prophylactic photophobia.441,442,447 Other more general symp- treatment of NDPH.440 Using a stepped ap- toms include lightheadedness, stiff neck, blurred proach that began with muscle relaxants and vision, and vertigo. Aura-type symptoms have progressed through tricyclic antidepressants, been observed in a small fraction of patients.441 selective serotonin reuptake inhibitors, and Patients with NDPH commonly report a history of antiepileptic drugs, it was found that 30% of anxiety/panic disorder and/or depression.444,448 patients graded the result as moderate or very improved, but only two patients were cured.442 The drugs that were moderately to very suc- Aggravating/relieving factors cessful were tricyclic antidepressants in 33% Stress, physical exertion, and bright light were of patients and antiepileptic drugs or muscle reported as aggravating factors in a third to 40% relaxants in 22% of patients each.442 However, of patients.441 Headache relief was obtained by gabapentin and topiramate were not tested. lying down in two-thirds of patients or by be- Positive findings for the use of naratriptan for ing in a dark room by almost half of patients.441 the treatment of CDH, including some patients Massage relieved pain in about a quarter and that may have had NDPH, suggest its utility in sleep only in a minority of patients (9%).441 the treatment of NDPH.454–456 Naratriptan was used for 3 months to 1 year in these patients. Epidemiology Based on available studies, a female preponder- Differential diagnosis ance is apparent.441,442 Age of onset in women NDPH is phenotypically similar to chronic TTH, (20s to 30s) occurs earlier than in men (50s).441 but onset of NDPH is independent of episod-

233 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

ic TTH or migraine that increases in frequen- herpes simplex virus infection and cytomeg- cy, and NDPH may be very refractory to treat- alovirus, have also been identified in patients ment.457 Both NDPH and hemicrania continua with NDPH.461 Moreover, bacterial agents have are continuous from onset. Hemicrania conti- been associated with NDPH, but the highly nua is usually accompanied by ipsilateral au- frequent reports of fever (34.2%) and painful tonomic signs and responds to treatment with cervical lymphadenopathy (56.5%) reported in indomethacin. other studies suggests that this may be a dis- A number of disorders may also give rise tinct subgroup.462 In a pediatric population with to NDPH-like headaches.458,459 Low CSF- NDPH, 43% reported onset of their symptoms volume headache is commonly encountered during an infection, and positive Epstein-Barr after lumbar puncture and is characteristically virus serology was detected in half of these. relieved by bed rest. Patients with chronic CSF However, how a viral infection leads to NDPH leaks may report a history of lumbar puncture is unclear. Some suggest that subclinical men- or epidural injection or vigorous exercises that ingitis may be involved,458 and in support, involve strong Valsalva maneuvers (eg, lifting new onset headache after meningitis is quite heavy objects). Headache is absent on waking common.463 and worsens during the day; lying down rapid- Minor head injuries (23%) and surgery were ly improves pain. Magnetic resonance imaging also common precipitators of headaches, which with gadolinium enhancement will usually iden- suggests that posttraumatic mechanisms may tify the leak. Raised CSF pressure may occur also be involved (see chapter 12). Stressful life secondary to tumors and induce headache. events are also frequently reported in patients Subarachnoid hemorrhage may be present with with NDPH, but it is unclear how these cause a normal or near normal neurologic examination onset of headache. and cause headache of moderate to severe in- In view of the heterogenous presentation of tensity. Onset of subarachnoid hemorrhage NDPH, the unreliable response to treatment, headache may be instantaneous in about half and the relationship between onset and a vari- of patients or develop over about 5 minutes.458 able list of triggers, it has been suggested that Benign thunderclap headache is also of sud- NDPH be viewed as a syndrome rather than a den onset, reaching maximum intensity within discrete disorder.464 30 seconds. The headache may last several hours, but a less severe headache may persist for weeks. Some consider benign thunderclap headache to be symptomatic of subarachnoid Headache, Myofascial hemorrhage, cervical artery dissection (see Pains, and Fibromyalgia chapter 14), or cerebral venous thrombosis.388 These entities should therefore be excluded in Masticatory muscle pain has been suggest- patients suspected of secondary NDPH. ed to be a localized expression of a spectrum of myofascial disorders with many similarities among MFP, TTH, and fibromyalgia; it is not un- Pathophysiology usual that these entities coexist in patients.465 Because about one-third of patients describe a Indeed, the segregation of MFP from other my- viral illness before headache onset, it has been ofascial pain disorders of a more generalized hypothesized that NDPH has an infectious eti- type, such as fibromyalgia, has been ques- ology. In support, more than 80% of patients tioned.466 The new DC/TMD7 has suggested with NDPH had evidence of active Epstein-Barr a distinction among local myalgia, myofascial virus infection, a percentage significantly high- pain, and myofascial pain with referral based er than in control subjects.460 More than 60% on the response to standardized palpation of of patients with NDPH were actively excret- the masseter and temporalis muscle: In local ing Epstein-Barr virus in the oropharynx. Past myalgia there is only pain specifically locat- but not active Epstein-Barr virus infection was ed to the site of palpation, in myofascial pain found in five of seven patients tested in a later there is a spread of pain on palpation but within study.441 Other viral infections, such as recent the boundaries of the muscle being palpated,

234 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Headache, Myofascial Pains, and Fibromyalgia

and myofascial pain with referral is linked to a graine sufferers have been found to report sig- spread of pain outside the boundaries of the nificantly more clenching habits that may relate muscle during palpation. One simple view could to some forms of muscle pain.473 An associa- be that there is a progression from myalgia to tion between migraine and MFP is not clearly myofascial pain to myofascial pain with referral apparent; pathophysiology and clinical presen- and therefore that the suggested subdivision of tation are distinctly different. The role that neu- MFP may represent different stages and patho- rovascular mechanisms, such as neurogenic physiologic mechanisms, perhaps with clinical inflammation, play in MFP is not entirely clear. implications. However, another view is that pain Vascular headache is rapid eye movement spreading/referral could represent epiphenom- locked, and some data point to a rapid eye ena of deep nociceptive activity. Further stud- movement–locked destructive form of bruxism ies are needed to address these issues. that may link certain forms of muscle pain with TMDs, fibromyalgia, and some headaches vascular mechanisms.474,475 Moreover, recent are characterized by central sensitization associations between migraine and fibromyal- and have been termed central sensitivity syn- gia suggest that a relationship with MFP may dromes. These central sensitivity syndromes yet become apparent.476 also include irritable bowel syndrome, restless In spite of stated similarities, most patients legs syndrome, chronic fatigue syndrome, and with MFP have pain and muscle tenderness on other similar chronic painful conditions that are palpation unilaterally, whereas TTH and fibro- based on central sensitization.467 myalgia are predominantly bilateral pain con- ditions. Patients with TMDs report headaches significantly more frequently and of higher se- Headache and masticatory verity,468 and patients with MFP report a sig- nificantly higher incidence of TTH than control myofascial pain subjects.144 Limited evidence supports a find- Headache has been reported to be more com- ing of masticatory muscle tenderness (possibly mon in adult patients with TMDs than in those equivalent to MFP) in patients with TTH. How- without,235,468 but often these results are not ever, there is considerable overlap in the tender replicated in other studies or age groups.469 muscles needed for the diagnosis of MFP and Patients suffering from headache and those TTH, and this may suggest that MFP and TTH suffering from MFP show great similarities share pathophysiologic mechanisms and often and possible overlap. Age distribution, female coexist. Therefore, there is no convincing ev- preponderance, and contributing psychophys- idence for the role of TMDs in the initiation of iologic mechanisms are shared. Muscle ten- TTH. However, both the DC/TMD and IHS crite- derness is a frequent finding in patients with ria include a diagnostic subgroup termed head- migraine and TTH, the distribution of which ache attributed to TMD (see Table 8-1). may be distinctly similar to that in patients with MFP. Thus, two of the fundamental symptoms of MFP—daily occurrence of pain and tender- Fibromyalgia ness of muscles to palpation—fail to properly Diagnosis differentiate between patients with headache and those with MFP. Fibromyalgia is a common condition character- Migraineurs suffer no more TMDs than ized by widespread pain.477 In the past, diagno- control subjects, and this association does sis was made based on the physical finding of not change with increasing frequency of mi- at least 11 points of tenderness out of the 18 graine.470 The rate of migraine in patients with anatomical sites defined by the American Col- MFP does not differ from that in the general lege of Rheumatology.478 More recently, these population, so patients with MFP and those criteria have been revised, and the need for ten- with migraine seem to be separate groups.471 der points as a central element in diagnosis has Children with migraine and migraine-type head- been removed.479 Additionally, the new criteria aches were recently shown to have the highest introduce a quantitative measure of the num- incidence of more severe TMD signs.469,472 Mi- ber of sites with pain, termed the widespread

235 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

pain index (WPI), and a measure of the severity trigger points may be unnecessary.485 The oth- of symptoms associated with fibromyalgia, the er basic difference is the chronic, widespread, symptom severity scale (SSS). The WPI is the systemic character of fibromyalgia as opposed number of painful areas reported by the patient to the acute, localized nature of myofascial from a list of 19 sites, so the score may vary pains. However, fibromyalgia often begins as from 0 to 19. Notably, physical examination is a localized pain disorder and later becomes no longer required for diagnosis but is strongly widespread, whereas persistent myofascial recommended.480 The SSS is derived from the pains may involve multiple sites and cause sys- sum of a 0 to 3 scoring on the severity of as- temic symptoms.486 Many of the perpetuating sociated fatigue, waking unrefreshed, cognitive factors in myofascial pains are the modulating symptoms, and the overall extent of somatic factors of fibromyalgia: physical activity, cold, symptoms (scores thus range from 0 to 12). Im- stress, and weather changes. Indeed, it has portantly, these criteria recognize fibromyalgia been suggested that fibromyalgia and region- as a disease spectrum with altering and fluctu- al myofascial pains represent an overlapping ating symptoms.481 A diagnosis is justified when spectrum.465 the WPI ≥ 7 and the SSS ≥ 5, or the WPI = 2–3 and the SSS ≥ 9. In addition, symptoms have been present for 3 months or more and no bet- Clinical features ter diagnosis explains the patient’s symptoms. Fibromyalgia symptomatology is complex and These new criteria have not met with universal affects multiple modalities; widespread pain acceptance but have been widely applied.482 is universal, but other common complaints in- The Research Criteria, a self-report version of clude fatigue (75% to 90%), a feeling of swell- the 2010 criteria, was developed for research ing or paresthesia (50% each), vertigo (60%), purposes,483 and there is strong evidence that it nonrestorative sleep (70%), and psychologic accurately identifies fibromyalgia as diagnosed symptoms (60%). by clinicians. These criteria have comfortably Pain in fibromyalgia is usually located in the combined the WPI and the SSS into one scale, lower back, neck, shoulder, arms, hands, hips, the polysymptomatic distress scale (PSD). This thighs, knees, legs, and feet. Complaints of removes the need to calculate the ranges of the joint pains may accompany fibromyalgia and WPI and SSS; the case definition is then a PSD may be the prominent feature in some patients. score ≥ 12.483 In the vast majority (85%) of patients with fi- Without a clear diagnostic biomarker, fibro- bromyalgia, pain is accompanied by stiffness, myalgia remains controversial.56,484 Moreover, particularly in the morning. Both pain and stiff- the boundaries between fibromyalgia and re- ness are aggravated by cold or humid weath- gional myofascial pains, such as MFP, are at er, anxiety or stress, inactivity, and poor sleep. times poorly demarcated in spite of established Fatigue, usually expressed by patients as criteria. A major differentiating feature between feeling drained, is correlated to pain and poor fibromyalgia and regional myofascial pain is the sleep.487,488 presence of trigger points and a palpable band Paresthesias and swelling usually affect the of tight muscle in regional myofascial pain as extremities and need careful neurologic exam- opposed to multiple tender points in fibromy- ination. Vertigo or dizziness is considered to be algia. For MFP, trigger points are not an inte- central in origin and may be accompanied by gral part of the RDC/TMD or DC/TMD criteria. phonophobia or tinnitus. Sleep disturbances By definition, trigger points, on palpation, refer include difficulties in falling asleep (increased pain to a distant site, but this condition for trig- sleep latency), waking up during the night (de- ger points has been suggested as unnecessary, creased sleep efficiency), and feeling tired in and trigger points may be considered active the morning (nonrefreshing sleep). Poor sleep or latent, which further clouds the boundaries correlates with pain, psychologic distress, and between regional myofascial pain and fibro- fatigue.489,490 Anxiety, depression, and stress myalgia. Moreover, only regional pain and ten- are prevalent in patients with fibromyalgia, and derness have been validated in fibromyalgia psychologic distress correlates with disease and regional myofascial pain; the presence of severity.491 Rarer signs include Raynaud phe-

236 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia Headache, Myofascial Pains, and Fibromyalgia

nomenon, symptoms similar to those in Sjögren inhibition, all of which are characteristic of neu- syndrome, and cognitive dysfunction. In estab- ropathic pain.336,500 In support, imaging studies lished fibromyalgia cases, long-term follow-up suggest that there is less functional connectiv- shows that there is usually no further deteriora- ity in areas of the descending pain modulatory tion in symptomatology.492 system.501,502 Studies provide moderate evi- Studies indicate that the vast majority (84%) dence for increased activation of the pain ma- of patients with fibromyalgia suffer a significant trix and lowered pain thresholds.501 Specific de- medical comorbidity.493 Most commonly, they creases in gray matter volume with unchanged have other musculoskeletal conditions (67%), global gray matter are difficult to establish as psychologic disorders (35%), gastrointesti- a cause-and-effect relationship.501,502 However, nal disorders (27%), cardiovascular disorders clinical pain is correlated to the level of gray (23.5%), and endocrinologic disorders (19%). matter loss in the medial frontal gyrus.502 Oth- Patients with fibromyalgia are two to seven er consequences of these changes are unclear, times more likely to have one or more of the but patients with fibromyalgia experience more following comorbid conditions: depression, gray matter loss per year than control subjects anxiety, headache, irritable bowel syndrome, with possible deterioration in cognitive function chronic fatigue syndrome, systemic lupus ery- and pain processing.502 However, a peripheral thematosus, and rheumatoid arthritis.494 nociceptive input from sensitized nociceptors in deep tissues and muscle may produce all the observed central effects.503 In view of the evi- Epidemiology dence, a peripheral input in the pathophysiolo- The point prevalence of fibromyalgia is about gy of fibromyalgia cannot be ruled out. 2.7%; women (4.1%) are affected more than Patients with fibromyalgia have increased men (1.4%),487,495 and its prevalence increases neural sympathetic activation and lack an ade- with age.481,493 Most commonly, fibromyalgia quate sympathetic response to stressor or car- occurs in women aged 40 to 60 years.496 diovascular challenges.167,171 The data suggest that fibromyalgia may be a generalized form of sympathetically maintained neuropathic pain. Risk factors and pathophysiology As suggested, an alternative description for fi- The pathophysiology of fibromyalgia remains bromyalgia could be neuroplastic pain in order unclear.497 However, the risk of developing to differentiate it from the recently proposed symptoms is significantly affected by a number definition of neuropathic pain with emphasis on of factors, including physical trauma, sleep dis- a lesion or disease of the somatosensory sys- turbance, psychologic distress, socioeconom- tem and avoidance of the term dysfunction.504 ic status, lifestyle, genetics, and dysfunctional Dysfunction of the hypothalamic-pituitary- pain modulation.497 Fibromyalgia onset is often adrenal axis is thought to partly underlie sleep linked to a preceding viral infection or mental disorders, some pain symptoms, and autonom- stress.498 ic nervous system imbalance.171 Fibromyalgia may begin as a regional pain. In a prospective trial, back pain predicted fi- bromyalgia, whereas tender points and pain Management in the neck did not. Self-assessed depression, Many pharmacologic and nonpharmacologic long-lasting pain, and the presence of three or approaches have been used to treat fibromy- more associated symptoms were significant algia. Treatment aims at controlling pain and predictors for progression.499 associated signs and improving functional and Lack of consistent peripheral tissue abnor- psychologic disability. Nonpharmacologic man- malities has shifted the focus to the central agement involves the initiation of an aerobic nervous system as a source of pain and other exercise program, relaxation, CBT, and pacing features in fibromyalgia. Many patients display (matching activity to pain levels).505 Tricyclic or paresthesias, allodynia, augmented central other antidepressants and antiepileptic drugs nervous system processing of pain (central are probably the most effective pharmacolog- sensitization), and a deficit of endogenous pain ic agents.505–507 Combining these with aerobic

237 8 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia

exercise and CBT may increase efficacy.508 suggests that such local conditions of myofas- Acupuncture, hypnosis/guided imagery, and tai cial pain should be compiled to form one enti- chi may offer relief for some patients and are ty. Focusing on the one region in which pain is recommended modalities.509 Novel therapies greatest may account for a restricted diagno- that may find a place in the management of fi- sis, such as MFP, when in effect this disorder bromyalgia include cannabinoids and sodium can be a local symptom of a more generalized oxybate.510 condition. Findings of faulty pain processing in patients with MFP would seem to support this contention.148,150 However, not surprisingly, pa- Temporomandibular disorders tients with TMDs are distinguishable from pa- tients with fibromyalgia by a high prevalence of and fibromyalgia masticatory muscle tenderness and a reduced Early reports on MFP/fibromyalgia comorbid- prevalence of fatigue, muscle weakness, migra- ity suggested that a connection might exist tory arthralgias, and burning or shooting mus- between these entities. Fibromyalgia, by defi- cle pains.516 Patients with fibromyalgia may also nition, is characterized by widespread pain, demonstrate lower pain thresholds and lower so it is not surprising that many patients with tolerance levels to experimental facial pain than fibromyalgia have signs of MFP. Additionally, patients with TMDs, which suggests differential pain outside the craniofacial region is common processing of external stimuli.158 The vast ma- among patients with TMDs. Some patients with jority of patients with fibromyalgia (94%) report- MFP (18%) have signs suggestive of fibromy- ed local pain from the temporomandibular re- algia, and up to 75% of patients with fibromy- gion, most frequently the temple, the TMJ, and algia demonstrate comorbid MFP.43,335,467,511–513 the neck.518 About 50% of the patients com- Female patients with widespread pain are plained about difficulties in jaw movements, at significantly increased risk of developing and about three-quarters reported tiredness of TMDs, which suggests that TMDs may be re- the jaws. Generalized body pain had a signifi- lated, and in continuum, to generalized muscle cantly longer duration than the onset of TMD disorders.144,514 Indeed, patients with fibromyal- symptoms, suggesting that fibromyalgia starts gia, regional myofascial pain such as MFP, and in other parts of the body and later extends to chronic fatigue syndrome share many clinical the masticatory system. In a large study, jaw features, including myalgia, fatigue, and dis- pain was found in 35.4% of patients with fibro- turbed sleep, which suggests a common etiol- myalgia and in about 19% each of patients with ogy.515 Additionally, patients with fibromyalgia osteoarthritis and rheumatoid arthritis.519 Jaw and TMDs have significantly elevated preva- pain is associated with disease severity and lence rates of irritable bowel syndrome, sleep the presence of jaw pain in patients with fibro- disturbances, and concentration difficulties.516 myalgia, correlated with a significantly reduced Fatigued patients are four times more likely to quality of life relative to fibromyalgia without jaw suffer from TMDs than nonfatigued twin con- pain.519 trol subjects. Thus, fatigue and fatigue-related Female patients (n = 162) with a previous symptoms are common in TMDs but are also diagnosis of MFP were reexamined 7 years lat- frequently reported by all patients with chronic er to elicit a history of comorbid fibromyalgia.520 pain and are probably related to somatization Thirty-eight patients (23.5%) had a positive his- and depression.517 tory of fibromyalgia but showed no difference In many cases of MFP, muscle tenderness in presenting signs and symptoms relating to affects many sites in the head and neck, but MFP. However, patients with a positive histo- trigger points may be hard to find. These pa- ry of fibromyalgia reported more MFP symp- tients often have tender points and character- toms accompanied by more severe pain and istics associating them with fibromyalgia (eg, increased emotional distress. In conclusion, disturbed sleep, anxiety, and general fatigue). increased chronicity was observed for patients When the symptoms of patients with fibromy- with MFP and comorbid fibromyalgia, which algia are compared with those of patients with also seemed to be more resistant to occlusal MFP, no symptoms are specific to MFP, which splint treatment.104

238 Myalgia, Myofascial Pain, Tension-Type Headaches, and Fibromyalgia References

The data suggest similarities between MFP comorbidity was predicted by concomitant and generalized muscle disorders.76,145 Although depression and insomnia.526 A recent study on it is clear that in many cases MFP is a local pain 100 patients with fibromyalgia found that 76% condition with minimal complaints in other ar- had headaches, most of which began before eas of the body, many patients present with onset of fibromyalgia,476 and the most common complaints suggestive of a generalized wide- headache diagnosis was migraine alone or in spread disorder. Possibly, there are two distinct combination with TTH. Characteristics of fibro- MFP subgroups (with and without fibromyalgia/ myalgia patients with headache were not differ- widespread pain), or the MFP phenotype may ent from those without headache, so that they be part of a spectrum of a possible progression are not a distinct subgroup. The data suggest to fibromyalgia. However, which patients with that migraine may form part of the fibromyalgia MFP progress to fibromyalgia remains unclear. phenotype. Based on the data showing consid- erable overlap among migraine, MFP, fibromy- algia, and TTH, comorbidity in any given patient Headache and fibromyalgia is highly likely. The prevalence of fibromyalgia in patients at- tending a headache clinic with a diagnosis of pri- mary headache was between 6.9% and 59%.493 Future of MFP Data indicate that TTH is most commonly as- sociated with fibromyalgia.521 Similarities have In this chapter, the current knowledge of MFP been observed in the distribution of muscle pathophysiology and treatment implications tender points between patients with recurrent have been reviewed; however, it is evident that headache and those with fibromyalgia. A bidi- although the field has progressed substantial- rectional association between fibromyalgia and ly over the past decades, there are still signif- TTH is suggested by the finding that twins with icant gaps in the understanding of the neuro- chronic TTH have 6.6 times more fibromyalgia biologic mechanisms involved in the efficacy and patients with fibromyalgia have 5.0 times of treatment. The ultimate goal is to provide more chronic TTH.522 In patients with concom- mechanism-specific diagnosis of MFP and its itant CDH and fibromyalgia, there was signifi- overlapping phenotypic representations fol- cantly more insomnia and more incapacitating lowed by individualized management. A major headaches than in headache patients without fi- challenge is the integration of all the detailed bromyalgia.523 Within CDH, both migrainous and research-based information on the multiple nonmigrainous headaches have been similarly dimensions of pain into a sufficiently simple associated with generalized muscle pains.524 clinical context. A better understanding of the The most significant headache parameter asso- interactions and relative timing and significance ciated with muscle pain was headache frequen- of multiple risk factors is needed in order to cy and not headache diagnosis. These findings build treatment algorithms based on underlying may indicate that musculoskeletal pains and mechanisms. Important steps have been taken chronic headaches (irrespective of diagnosis) to allow this progression. First, the taxonomic may share central sensitization as a common classifications of TMDs and headaches have etiologic factor.521,524 In this and further studies, a improved, and second, longitudinal studies highly significant correlation was found between have been undertaken that may pave the road headaches and muscle pain in the upper body for further insights into MFP. area, which may suggest segmental effects. Data on central nervous system dysregula- tion and widespread allodynia in migraine (see References chapter 10) suggest that in some patients mi- graine may form part of more widespread pain 1. Peck CC, Goulet JP, Lobbezoo F, et al. Expanding disorders, such as fibromyalgia. Migraines oc- the taxonomy of the diagnostic criteria for temporo- cur frequently in patients with fibromyalgia.525 mandibular disorders. J Oral Rehabil 2014;41:2–23. 2. Schiffman EL, Velly AM, Look JO, et al. Effects of four Conversely, fibromyalgia was found in 36% of treatment strategies for temporomandibular joint closed patients with transformed migraine, and the lock. Int J Oral Maxillofac Surg 2014;43:217–226.

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