Tem p o ro m a n d i b u l a r D i s o rd e r s and Headaches Steven B. Graff-Radford,
DDS
a,b
, Jennifer P. Bassiur,
DDS
c,
*
KEYWORDS Temporomandibular disorder Migraine Tension-type headache Bruxism KEY POINTS Temporomandibular disorders (TMDs) and headache are common and may be reported as single or separate entities. There is no single cause for TMDs. Patients with asymptomatic clicking, often do not require treatment. Therapy is indicated if pain, significant limitation in mandibular range of motion, or both are present. The pain associated with TMD is frequently of muscular origin. Imaging alone should not dictate treatment. The symptoms of TMD are often self-limiting.
INTRODUCTION
Temporomandibular disorders (TMDs) are a major cause of nondental pain in the orofacial region, and may cause headache.1 The International Classification of Headache Disorders, 3rd edition (ICHD-3) recognizes headache attributed to TMDs2 but, because headache and TMD are prevalent, have multifactorial origins, and have similar or overlapping symptoms, diagnosis is often confused. It is often difficult to differentiate these disorders when they coexist.3 Overlap may also result from shared environmental and genetic factors involving abnormal pain processing and trigeminal sensitization. The trigeminal nerve is the final conduit of face, neck, and head pain,4 which may be generated by musculoskeletal, vascular, or neural structures. Once pain is established, referral anywhere in the trigeminal and cervical complex can occur through central sensitization. Management of TMD may reduce nociception, ameliorate sensitization, and reduce primary headache. However, this does not mean there
a
The Pain Center, 444 South San Vicente #1101, Los Angeles, CA 90048, USA; b Section of Oral Medicine and Orofacial Pain, UCLA School of Dentistry, 10833 Leconte Avenue, Los Angeles, CA 90024, USA; c Columbia University College of Dental Medicine, Division of Oral & Maxillofacial Surgery, 630 West 168th Street, Vanderbilt Building, 7th Floor, New York, NY 10032, USA * Corresponding author. Columbia University College of Dental Medicine, Division of Oral & Maxillofacial Surgery, 630 West 168th Street, Vanderbilt Building, 7th Floor, New York, NY 10032. E-mail address: [email protected]
Neurol Clin 32 (2014) 525–537 http://dx.doi.org/10.1016/j.ncl.2013.11.009 neurologic.theclinics.com 0733-8619/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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is a direct cause-and-effect relationship between TMD and primary headache; they can coexist and relate to each other through common neural circuits. Understanding the relationship between TMD and primary headache, as well as headache secondary to TMD, is important. Management is best achieved by addressing each individually and realizing that one can perpetuate the other. TEMPOROMANDIBULAR DISORDERS
TMDs include musculoskeletal and neuromuscular conditions that involve the temporomandibular joints (TMJs), the masticatory muscles, and all associated tissues.5 Common painful TMDs are generated from myogenous and/or arthrogenous components. A painful TMD may occur in 10% of the population and other signs and symptoms of TMD (eg, clicking, limited range of motion, pain on function) have been reported in 46.1% of the United States population.6,7 Studies of nonpatient populations have found that up to 75% of people studied have at least one sign of joint dysfunction and nearly one-third of the population has at least one TMD symptom.8 These data may be affected by differences in diagnostic criteria and data collection methods in the cross-sectional epidemiologic studies on the prevalence of TMDs. In 1992, the Research Criteria for TMD (RDC/TMD) introduced the use of standardized diagnostic criteria to improve consistency among studies. The RDC/TMD has provided researchers with a standardized process for examining, diagnosing, and classifying patients with TMD for the most common TMD subtypes.9 A systematic review including only those studies using RDC/TMD reported prevalences up to 12.9% for masticatory muscle pain, 15.8% for disc derangements, and 8.9% for inflammatory-degenerative or painful TMJ disorders.10 Less than 7% of individuals with TMDs need therapeutic intervention,11 and an even smaller percentage complain of headache. Headache and TMD are common and may therefore be reported as a single or as separate entities. The TMJ, masticatory muscles, and associated orofacial structures may act as triggering or perpetuating factors for primary headache. A primary headache disorder may similarly trigger or perpetuate pain in the masticatory muscles or TMJ. Ciancaglini and Radaelli3 reported that headache occurs significantly more frequently in patients with TMD symptoms (27.4% vs 15.2%). Individuals with myogenous TMDs are more likely than those with arthrogenous TMDs to have headache, and the prevalence of TMD in patients with migraine and tension-type headache is higher than in a nonheadache population.12 According to Glaros and colleagues,13 individuals with chronic headache were more likely than nonheadache controls to meet criteria for an RDC/TMD diagnosis of myofascial pain. The potential for headache secondary to TMDs is recognized in the ICHD-3 with diagnostic criteria for 11.7 Headache attributed to temporomandibular disorder (TMD) (Box 1). Jaw movement or pressure applied to the TMJ or surrounding musculature frequently exacerbates the secondary headache. The described pain typically manifests ipsilaterally when the TMJ is the pain generator, but may be bilateral with muscular involvement.2 Peripheral and central mechanisms are likely involved in myogenous TMDs.14 Painful TMDs may increase central sensitization, inducing, exacerbating, or contributing to the chronification of headache. Regardless of whether or not evidence of causation can be shown, ignoring TMDs as peripheral triggers of headache often results in a poor clinical outcome. CAUSES OF TMD
There are many factors associated with TMDs but no universal cause has been identified. There is no single cause for all TMDs. Inflammation of the TMJs’ synovial lining or capsule may account for joint pain, and may be associated with an incoordination of
Temporomandibular Disorders and Headaches
Box 1 ICHD-3 (beta) criteria for headache attributed to TMD (11.7) Description: Headache caused by a disorder involving structures in the temporomandibular region Diagnostic criteria: A. Any headache fulfilling criterion C B. Clinical and/or imaging evidence of a pathologic process affecting the TMJ, muscles of mastication, and/or associated structures C. Evidence of causation shown by at least 2 of the following: 1. Headache has developed in temporal relation to the onset of the TMD 2. Either or both of the following: 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 ICHD-3 diagnosis From the Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalgia 2013;33(9):629–808; with permission.
the disc-condyle complex. Bone degeneration or disc displacement may occur, resulting in the incoordination during movement. Predisposing, initiating, or perpetuating factors for TMD may include parafunctional behaviors (clenching, bruxism) causing microtraumas, direct or indirect trauma, changes in occlusion, and systemic, genetic, and psychosocial factors. Although parafunctional habits have been implicated in TMD, their relationships with headache remain unknown. Of all the parafunctional activities of the stomatognathic system, bruxism is regularly, if incorrectly, assumed to be the most damaging and a major risk factor for TMDs.15 Bruxism involves diurnal or nocturnal parafunctional activity, including clenching, bracing, gnashing, and grinding of the teeth. It is common, occurring in 5% to 8% of the population, and independent of frequency in 31% of the population.16–20 The reported prevalence data are variable, subject to identification (sleep or awake bruxism or both). Sleep bruxism (SB) is an oromandibular sleeprelated movement disorder of repetitive gnashing of the teeth that is usually nocturnal, occurs during sleep, and is associated with arousals.18,19,21 SB is affected by smoking, the use of drugs such as antidepressants, caffeine, alcohol,16,22 type A personality and/or anxiety, as well as sleep-related breathing disorders.22 Up to 65% of patients with SB report frequent headache.23,24 A systematic literature review from 1998 to 2008 by Mandfredini and Lobbezoo15 supported an association between selfreport/questionnaire-diagnosed bruxism and TMD symptoms. In most of the selfreport studies reviewed, the association was with myofascial pain or symptoms of muscle disorders. The investigators also described a positive association between
527
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myofascial pain and clinically diagnosed bruxism, With the caution that the bruxism diagnosis was pain dependent,15 but only some bruxers have facial pain. Neither tooth wear nor polysomnogram-confirmed bruxism was predictably associated with TMD.15 In the absence of control for other causes, tooth wear cannot reliably predict bruxism.20 Evidence of SB on polysomnographic or electomyographic recordings may not represent activity that fluctuates over time. Experimental, sustained clenching can cause muscle pain, but it is usually short-lived.15 Clenching that is not experimentally induced has not been shown to cause muscle pain. Fernandes and colleagues25 found a significant increase in the risk for chronic migraine, episodic migraine, and episodic tension-type headache when SB was associated with TMD; however, SB alone did not increase the risk for headache. Although a causal relationship is not evident, SB is associated with TMDs and headache and may exacerbate TMD and/ or headache symptoms. Sensory innervation of the TMJ is mediated through the mandibular division of the trigeminal nerve. The TMJ capsule, posterior attachment, and discal ligaments are sensitive to pain. The articular disc, vital to maintaining condylar stability during mandibular movement, is not sensitive to pain because it is devoid of direct innervation or vascularization. The richly vascularized and innervated posterior attachment is often implicated in joint pain. Trauma to the TMJ may result in capsulitis. This acute inflammatory process tends to resolve quickly and without complication. By comparison, painful derangements of the TMJ are more likely to be associated with chronic joint disorders. The cause may be multifactorial or unclear, but often involves articular disc displacement. The TMJ is formed by the articular surfaces of the temporal bone and the mandibular condyle, bilaterally. Each TMJ is separated into an upper and lower compartment by a fibrocartilaginous disc. The TMJ is subject to the pathologic disorders that affect other synovial joints, but it is unique in several anatomic features. The TMJs move as a functional unit and, unlike most synovial joints, are lined by fibrocartilage, which is more resistant to degenerative change and has a greater capacity for repair than hyaline cartilage. The ability of the TMJ to adapt to various biomechanical stresses is well documented.26 Failure of this adaptive capacity mechanism may lead to tissue destruction and disc displacement and may be affected by age, stress, sex, systemic illness, or previous trauma. Incoordination of the disc-condyle relationship is a major component of TMDs. Articular disc displacement is the most common temporomandibular arthropathy and is characterized by an abnormal relationship or misalignment of the articular disc relative to the condyle.26 This condition, often referred to as an internal derangement, interferes with smooth movement of the TMJ, resulting in joint noises, brief sticking or catching, or locking. Disc displacements can be divided into disc displacement with reduction and disc displacement without reduction (Boxes 2 and 3).11 In disc displacement with reduction, the disc reduces, or is recaptured, on opening of the mouth. The disc reduction is accompanied by a sound that is often described as clicking or popping. With mandibular closure, a second sound called a reciprocal click or closing click may be audible as the disc moves off the condyle just before the teeth come together. Clicking sounds are not necessarily a sign of degeneration or an indication for treatment. Moderate to severe derangements have been observed on imaging in greater than one-third of an asymptomatic population,27 and as many as 25% of clicking joints show normal or slightly displaced discs.28 Irrespective of whether it is acute or chronic, disc displacement is not necessarily painful. Patients with pain-free clicking often do not require treatment. Therapy is indicated if pain, significant limitation in mandibular range of motion, or both are present.
Temporomandibular Disorders and Headaches
Box 2 Diagnostic criteria for disc displacement with reduction All of the following must be present: Reproducible joint noise that usually occurs at variable positions during opening and closing mandibular movements. Soft tissue imaging reveals displaced disc that improves its position during mandibular opening, and hard tissue imaging shows the absence of extensive degenerative bone changes (although the diagnosis of disc displacement can only be confirmed with soft tissue imaging, the temperate nature of the disorder does not warrant routine soft tissue imaging). Any of the following may accompany the preceding items: Pain, when present, is precipitated by joint movement Deviation during opening movement coincides with a click No restriction in mandibular movement Episodic and momentary catching during opening (
DDS
a,b
, Jennifer P. Bassiur,
DDS
c,
*
KEYWORDS Temporomandibular disorder Migraine Tension-type headache Bruxism KEY POINTS Temporomandibular disorders (TMDs) and headache are common and may be reported as single or separate entities. There is no single cause for TMDs. Patients with asymptomatic clicking, often do not require treatment. Therapy is indicated if pain, significant limitation in mandibular range of motion, or both are present. The pain associated with TMD is frequently of muscular origin. Imaging alone should not dictate treatment. The symptoms of TMD are often self-limiting.
INTRODUCTION
Temporomandibular disorders (TMDs) are a major cause of nondental pain in the orofacial region, and may cause headache.1 The International Classification of Headache Disorders, 3rd edition (ICHD-3) recognizes headache attributed to TMDs2 but, because headache and TMD are prevalent, have multifactorial origins, and have similar or overlapping symptoms, diagnosis is often confused. It is often difficult to differentiate these disorders when they coexist.3 Overlap may also result from shared environmental and genetic factors involving abnormal pain processing and trigeminal sensitization. The trigeminal nerve is the final conduit of face, neck, and head pain,4 which may be generated by musculoskeletal, vascular, or neural structures. Once pain is established, referral anywhere in the trigeminal and cervical complex can occur through central sensitization. Management of TMD may reduce nociception, ameliorate sensitization, and reduce primary headache. However, this does not mean there
a
The Pain Center, 444 South San Vicente #1101, Los Angeles, CA 90048, USA; b Section of Oral Medicine and Orofacial Pain, UCLA School of Dentistry, 10833 Leconte Avenue, Los Angeles, CA 90024, USA; c Columbia University College of Dental Medicine, Division of Oral & Maxillofacial Surgery, 630 West 168th Street, Vanderbilt Building, 7th Floor, New York, NY 10032, USA * Corresponding author. Columbia University College of Dental Medicine, Division of Oral & Maxillofacial Surgery, 630 West 168th Street, Vanderbilt Building, 7th Floor, New York, NY 10032. E-mail address: [email protected]
Neurol Clin 32 (2014) 525–537 http://dx.doi.org/10.1016/j.ncl.2013.11.009 neurologic.theclinics.com 0733-8619/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
526
Graff-Radford & Bassiur
is a direct cause-and-effect relationship between TMD and primary headache; they can coexist and relate to each other through common neural circuits. Understanding the relationship between TMD and primary headache, as well as headache secondary to TMD, is important. Management is best achieved by addressing each individually and realizing that one can perpetuate the other. TEMPOROMANDIBULAR DISORDERS
TMDs include musculoskeletal and neuromuscular conditions that involve the temporomandibular joints (TMJs), the masticatory muscles, and all associated tissues.5 Common painful TMDs are generated from myogenous and/or arthrogenous components. A painful TMD may occur in 10% of the population and other signs and symptoms of TMD (eg, clicking, limited range of motion, pain on function) have been reported in 46.1% of the United States population.6,7 Studies of nonpatient populations have found that up to 75% of people studied have at least one sign of joint dysfunction and nearly one-third of the population has at least one TMD symptom.8 These data may be affected by differences in diagnostic criteria and data collection methods in the cross-sectional epidemiologic studies on the prevalence of TMDs. In 1992, the Research Criteria for TMD (RDC/TMD) introduced the use of standardized diagnostic criteria to improve consistency among studies. The RDC/TMD has provided researchers with a standardized process for examining, diagnosing, and classifying patients with TMD for the most common TMD subtypes.9 A systematic review including only those studies using RDC/TMD reported prevalences up to 12.9% for masticatory muscle pain, 15.8% for disc derangements, and 8.9% for inflammatory-degenerative or painful TMJ disorders.10 Less than 7% of individuals with TMDs need therapeutic intervention,11 and an even smaller percentage complain of headache. Headache and TMD are common and may therefore be reported as a single or as separate entities. The TMJ, masticatory muscles, and associated orofacial structures may act as triggering or perpetuating factors for primary headache. A primary headache disorder may similarly trigger or perpetuate pain in the masticatory muscles or TMJ. Ciancaglini and Radaelli3 reported that headache occurs significantly more frequently in patients with TMD symptoms (27.4% vs 15.2%). Individuals with myogenous TMDs are more likely than those with arthrogenous TMDs to have headache, and the prevalence of TMD in patients with migraine and tension-type headache is higher than in a nonheadache population.12 According to Glaros and colleagues,13 individuals with chronic headache were more likely than nonheadache controls to meet criteria for an RDC/TMD diagnosis of myofascial pain. The potential for headache secondary to TMDs is recognized in the ICHD-3 with diagnostic criteria for 11.7 Headache attributed to temporomandibular disorder (TMD) (Box 1). Jaw movement or pressure applied to the TMJ or surrounding musculature frequently exacerbates the secondary headache. The described pain typically manifests ipsilaterally when the TMJ is the pain generator, but may be bilateral with muscular involvement.2 Peripheral and central mechanisms are likely involved in myogenous TMDs.14 Painful TMDs may increase central sensitization, inducing, exacerbating, or contributing to the chronification of headache. Regardless of whether or not evidence of causation can be shown, ignoring TMDs as peripheral triggers of headache often results in a poor clinical outcome. CAUSES OF TMD
There are many factors associated with TMDs but no universal cause has been identified. There is no single cause for all TMDs. Inflammation of the TMJs’ synovial lining or capsule may account for joint pain, and may be associated with an incoordination of
Temporomandibular Disorders and Headaches
Box 1 ICHD-3 (beta) criteria for headache attributed to TMD (11.7) Description: Headache caused by a disorder involving structures in the temporomandibular region Diagnostic criteria: A. Any headache fulfilling criterion C B. Clinical and/or imaging evidence of a pathologic process affecting the TMJ, muscles of mastication, and/or associated structures C. Evidence of causation shown by at least 2 of the following: 1. Headache has developed in temporal relation to the onset of the TMD 2. Either or both of the following: 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 ICHD-3 diagnosis From the Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalgia 2013;33(9):629–808; with permission.
the disc-condyle complex. Bone degeneration or disc displacement may occur, resulting in the incoordination during movement. Predisposing, initiating, or perpetuating factors for TMD may include parafunctional behaviors (clenching, bruxism) causing microtraumas, direct or indirect trauma, changes in occlusion, and systemic, genetic, and psychosocial factors. Although parafunctional habits have been implicated in TMD, their relationships with headache remain unknown. Of all the parafunctional activities of the stomatognathic system, bruxism is regularly, if incorrectly, assumed to be the most damaging and a major risk factor for TMDs.15 Bruxism involves diurnal or nocturnal parafunctional activity, including clenching, bracing, gnashing, and grinding of the teeth. It is common, occurring in 5% to 8% of the population, and independent of frequency in 31% of the population.16–20 The reported prevalence data are variable, subject to identification (sleep or awake bruxism or both). Sleep bruxism (SB) is an oromandibular sleeprelated movement disorder of repetitive gnashing of the teeth that is usually nocturnal, occurs during sleep, and is associated with arousals.18,19,21 SB is affected by smoking, the use of drugs such as antidepressants, caffeine, alcohol,16,22 type A personality and/or anxiety, as well as sleep-related breathing disorders.22 Up to 65% of patients with SB report frequent headache.23,24 A systematic literature review from 1998 to 2008 by Mandfredini and Lobbezoo15 supported an association between selfreport/questionnaire-diagnosed bruxism and TMD symptoms. In most of the selfreport studies reviewed, the association was with myofascial pain or symptoms of muscle disorders. The investigators also described a positive association between
527
528
Graff-Radford & Bassiur
myofascial pain and clinically diagnosed bruxism, With the caution that the bruxism diagnosis was pain dependent,15 but only some bruxers have facial pain. Neither tooth wear nor polysomnogram-confirmed bruxism was predictably associated with TMD.15 In the absence of control for other causes, tooth wear cannot reliably predict bruxism.20 Evidence of SB on polysomnographic or electomyographic recordings may not represent activity that fluctuates over time. Experimental, sustained clenching can cause muscle pain, but it is usually short-lived.15 Clenching that is not experimentally induced has not been shown to cause muscle pain. Fernandes and colleagues25 found a significant increase in the risk for chronic migraine, episodic migraine, and episodic tension-type headache when SB was associated with TMD; however, SB alone did not increase the risk for headache. Although a causal relationship is not evident, SB is associated with TMDs and headache and may exacerbate TMD and/ or headache symptoms. Sensory innervation of the TMJ is mediated through the mandibular division of the trigeminal nerve. The TMJ capsule, posterior attachment, and discal ligaments are sensitive to pain. The articular disc, vital to maintaining condylar stability during mandibular movement, is not sensitive to pain because it is devoid of direct innervation or vascularization. The richly vascularized and innervated posterior attachment is often implicated in joint pain. Trauma to the TMJ may result in capsulitis. This acute inflammatory process tends to resolve quickly and without complication. By comparison, painful derangements of the TMJ are more likely to be associated with chronic joint disorders. The cause may be multifactorial or unclear, but often involves articular disc displacement. The TMJ is formed by the articular surfaces of the temporal bone and the mandibular condyle, bilaterally. Each TMJ is separated into an upper and lower compartment by a fibrocartilaginous disc. The TMJ is subject to the pathologic disorders that affect other synovial joints, but it is unique in several anatomic features. The TMJs move as a functional unit and, unlike most synovial joints, are lined by fibrocartilage, which is more resistant to degenerative change and has a greater capacity for repair than hyaline cartilage. The ability of the TMJ to adapt to various biomechanical stresses is well documented.26 Failure of this adaptive capacity mechanism may lead to tissue destruction and disc displacement and may be affected by age, stress, sex, systemic illness, or previous trauma. Incoordination of the disc-condyle relationship is a major component of TMDs. Articular disc displacement is the most common temporomandibular arthropathy and is characterized by an abnormal relationship or misalignment of the articular disc relative to the condyle.26 This condition, often referred to as an internal derangement, interferes with smooth movement of the TMJ, resulting in joint noises, brief sticking or catching, or locking. Disc displacements can be divided into disc displacement with reduction and disc displacement without reduction (Boxes 2 and 3).11 In disc displacement with reduction, the disc reduces, or is recaptured, on opening of the mouth. The disc reduction is accompanied by a sound that is often described as clicking or popping. With mandibular closure, a second sound called a reciprocal click or closing click may be audible as the disc moves off the condyle just before the teeth come together. Clicking sounds are not necessarily a sign of degeneration or an indication for treatment. Moderate to severe derangements have been observed on imaging in greater than one-third of an asymptomatic population,27 and as many as 25% of clicking joints show normal or slightly displaced discs.28 Irrespective of whether it is acute or chronic, disc displacement is not necessarily painful. Patients with pain-free clicking often do not require treatment. Therapy is indicated if pain, significant limitation in mandibular range of motion, or both are present.
Temporomandibular Disorders and Headaches
Box 2 Diagnostic criteria for disc displacement with reduction All of the following must be present: Reproducible joint noise that usually occurs at variable positions during opening and closing mandibular movements. Soft tissue imaging reveals displaced disc that improves its position during mandibular opening, and hard tissue imaging shows the absence of extensive degenerative bone changes (although the diagnosis of disc displacement can only be confirmed with soft tissue imaging, the temperate nature of the disorder does not warrant routine soft tissue imaging). Any of the following may accompany the preceding items: Pain, when present, is precipitated by joint movement Deviation during opening movement coincides with a click No restriction in mandibular movement Episodic and momentary catching during opening (
