Local myalgia
Myofascial pain with referral
Arthralgia
Headache attributed to TMD (DC/TMD)
Headache attributed to TMD (ICHD – 3)
Description
Pain of muscle origin as described for myalgia with localization of pain only at the site of palpation when using the myofascial examination or protocol
Pain of muscle origin as described for myalgia with referral of pain beyond the boundary of the muscle being palpated when using the myofascial examination protocol. Spreading pain may also be present
Pain of joint origin that is affected by jaw movement, function, or parafunction, and replication of this pain occurs with provocation testing of the TMJ
Headache in the temple area secondary to pain-related TMD (see Note) that is affected by jaw movement, function, or parafunction, and replication of this headache occurs with provocation testing of the masticatory system
Headache caused by a disorder involving structures in the temporomandibular region
History
Positive for both of the following:
1. Pain in the jaw, temple, in the ear, or in front of ear
2. Pain modified with jaw movement, function, or parafunction
Positive for both of the following:
1. Pain in the jaw, temple, in the ear, or in front of ear
2. Pain modified with jaw movement, function, or parafunction
Positive for both of the following:
1. Pain in the jaw, temple, in the ear, or in front of ear
2. Pain modified with jaw movement, function, or parafunction
Positive for both of the following:
1. Headache of any type in the temple
2. Headache modified with jaw movement, function, or parafunction
A. Any headache fulfilling criterion C
B. Clinical and/or imaging evidence of a pathological process affecting the temporomandibular joint (TMJ), muscles of mastication, and/or or associated structures
C. Evidence of causation demonstrated by at least two of the following:
1. Headache has developed in temporal relation to the onset of the temporomandibular disorder
2. Either or both of the following:
(a) Headache has significantly worsened in parallel with progression of the temporomandibular disorder
(b) Headache has significantly improved or resolved in parallel with improvement in or resolution of the temporomandibular disorder
3. The headache is produced or exacerbated by active jaw movements, passive movements through the range of motion of the jaw, and/or provocative manoeuvres 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 temporomandibular disorder
Exam
Positive for all of the following:
1. Confirmation of pain location(s) in the temporalis or masseter muscle(s)
2. Report of familiar pain with palpation of the temporalisor masseter muscle(s)
3. Report of pain localized to the site of palpation
Positive for all of the following:
1. Confirmation of pain location(s) in the temporalis or masseter muscle(s)
2. Report of familiar pain with palpation of the temporalisor masseter muscle(s)
3. Report of pain at a site beyond the boundary of the muscle being palpated
Positive for both of the following:
1. Confirmation of pain location in the area of TMJ(s)
2. Report of familiar pain in the TMJ with at least one of the following provocation tests:
(a) Palpation of the lateral pole or around the lateral pole
Positive for both of the following:
1. Confirmation of headache location in the area of the temporalis muscle(s)
2. Report of familiar headache in the temple area with at least one of the following provocation test:
(a) Palpation of the temproalis muscle(s)
Not available
(b) Maximum unassisted or assisted opening, right or left lateral, or protrusive movement(s)
(b) Maximum unassisted or assisted opening, right or left lateral, or protrusive movement(s)
Comments
The pain is not better accounted for by another pain diagnosis. Other masticatory muscles may be examined as dictated by clinical circumstances, but the sensitivity and specificity for this diagnosis based on these findings have not been established
The pain is not better accounted for by another pain diagnosis. Other masticatory muscles may be examined as dictated by clinical circumstances, but the sensitivity and specificity for this diagnosis based on these findings have not been established
The pain is not better accounted for by another pain diagnosis
The headache is not better accounted for by another headache diagnosis
Not better accounted for by another ICHD-3 diagnosis
From a purely anatomical perspective, all types of painful TMDs are obviously “headaches” as the jaw and orofacial region are part of the head. Therefore, merely based on this fact, it is perhaps unsurprising that painful TMDs and headaches frequently overlap. However, a more careful examination of the specific criteria for painful TMDs per the DC/TMD reveals that these diagnoses are only justified if patients outline their pain in specific parts of the jaws/temple and if this can be verified by the examiner based on further questions to the patients. Moreover, the pain complaints need to be reproduced by either jaw movements or standardized palpation of the jaw muscles or TMJs, i.e. emphasis is devoted to the clinical feature of “familiar pain”. In contrast to the DC/TMD specifications, no particular emphasis is given to pain distribution in TTH except that it is usually bilateral, affects the temple and that the quality may be “pressing”. TTH is mainly subdivided according to the temporal characteristics into infrequent episodic, frequent episodic and chronic types. Furthermore, there are subsets of TTH which are associated with pericranial tenderness. In the DC/TMD, specific recommendations for clinical palpation of muscles with 1 kg and the TMJ with 0.5 kg are provided, whereas the ICHD criteria give no two such specifications, and the evoked response includes “tenderness” and not only “pain”. Such differences in criteria may indeed be important when the overlap between conditions is examined.
When patients with different clinical TMD and headache diagnoses are asked to draw their painful areas on figures of the head, a close inspection, in addition to a more quantitative analysis, indicates that the location/specific sites differ between, e.g. myalgic TMDs, TMJ arthralgias, chronic tension-type headaches (CTTH) and migraine patients (Fig. 9.1). The possibility of the frequently observed overlap and comorbidity between painful TMDs and headaches being due to pure chance should be considered, since both conditions are highly prevalent and manifest in the head. Most studies describing this overlap are, in fact, cross-sectional and based on slightly different criteria for TMD and headaches, and keeping in mind some of the potential weaknesses of the ICHD to pinpoint location and amount of pressure for palpation, this, in addition to lack of blinding of examiners, may perhaps explain part of this overlap. Studies with concise and operationalized criteria for both TMD and headache will be needed together with sufficient blinding of examiners for clinical diagnosis.
Fig. 9.1
Superimposition of individual patient-based drawings of perceived areas of pain. Temporomandibular joint (TMJ) arthralgia (n = 10), temporomandibular disorder (TMD) myalgia (n = 13), mixed TMJ arthralgia and TMD myalgia (n = 13), and patients with chronic tension-type headache (TTH) (n = 22). The three TMD drawings are from Svensson (unpublished); the TTH drawing is from Schmidt-Hansen et al. 2005
With these caveats in mind, more recent and longitudinal studies have looked into the comorbidity between painful TMDs and headaches. One study found that first-onset TMD pain (not subdivided into muscle or TMJ pain) was significantly associated with reports of headache and headache severity [102]. It should be noted that first-onset TMD pain was also associated with pain in one or more bodily sites. However, this could lead to the challenging suggestion that the TMDs were attributed to headache in contrast to the DC/TMD and ICHD diagnoses of HATMD. So could there be a bidirectional relationship between painful TMDs and headaches, perhaps related to more basic characteristics of the nociceptive system? In the following, an overview on basic pain mechanisms from musculoskeletal tissues is provided, and the implications for TMD and headache are discussed.
9.2 Basic Pain Mechanisms
Both peripheral and central sensitization processes have been implicated in the pathophysiology of painful TMDs [24, 25] and headaches [7, 13, 14, 17, 21, 60, 68]. It should be noted that there is currently no accurate electrophysiological or imaging test of either peripheral or central sensitization of the nociceptive pathways in the human trigeminal system but rather a number of clinical “proxies” of these mechanisms, such as quantitative sensory testing (standardized application of thermal, mechanical, chemical or electrical stimuli and recording of patient-based responses or evoked physiological measures).
9.2.1 Peripheral Sensitization
In TMD, peripheral sensitization can occur through either activation of muscle or joint nociceptors [23, 99]. Several substances have been shown to activate peripheral muscle nociceptors [73, 74]. It is thought that the two most important factors in causing muscle pain are the release of adenosine triphosphate (ATP) and protons (H+). These substances activate receptors on free nerve endings causing depolarization of the nociceptive neuron. This activation in turn causes the release of neuropeptides from the free nerve endings such as substance P (SP), bradykinin (BK), calcitonin gene-related peptide (CGRP), serotonin and prostaglandin E2 (PGE2), what is termed neurogenic inflammation [122]. There are also other substances, such as tumour necrosis factor alpha (TNF-α) and nerve growth factor (NGF), that are released and can further stimulate nociceptors [74]. Because of this cascade of events, the sensitivity of the muscle nociceptors is increased causing hyperalgesia, and they are more susceptible to stimuli such as normal jaw function. In the case of the TMJ, inflammation is probably the most common driver of pain. It is thought that inflammation caused by increased loading and remodelling results in the release of pro-inflammatory substances such as TNF-α and interleukins [3, 111]. The release of these substances will, as with muscle pain, cause the release of more inflammatory substances, such as SP, BK, PGE2 and CGRP. This neurogenic inflammation will result in the hallmarks of inflammation such as redness, oedema, increase in temperature and pain [112]. It has also been shown in experimental models of headache as well as myalgic and arthralgic TMD that there is an increase in peripheral glial cells [22, 69, 118, 127] that may contribute to the peripheral sensitization that may be seen in the different types of TMD and headaches.
In the context of headaches and TMDs, it is significant that these changes in the normal conduction of somatosensory information from the joint and muscle structures may contribute to a spread and referral of pain that could be perceived as a “headache” by the patients due to the close anatomical relationship between the TMJs, masticatory muscles and the usual sites where headaches are felt such as the temple, frontal and occipital areas.
Despite this, clinically, the concentrations of ATP, PGE2, glutamate and other inflammatory mediators have not been shown to differ in tender points of patients with CTTH when compared to healthy controls [5]. The authors concluded that tender points are not sites of ongoing inflammation. On the other hand, Shah et al. found that there was inflammation in active trigger points (TrPs) in the trapezius of neck pain subjects as well as a remote site and that these were substantially different from controls [100]. However, such studies need to be replicated in larger sample sizes and with blinded observers.
In patients with myalgic TMD and in experimental models of myalgia, lower mechanical and thermal thresholds have been shown in the painful area when compared to controls [49, 70, 89, 103, 107–109, 116]. In patients with TTH, such signs or “proxies” of peripheral sensitization have also been demonstrated. Studies assessing pressure pain threshold (PPT) in patients with TTH have found, with some exceptions, that PPTs in the cranial region are lower in patients with episodic TTH (ETTH) when compared to controls, and these same thresholds are more robustly decreased in patients with CTTH [2, 6, 42, 98]. Furthermore, it is clinically evident that TTH consists of various subgroups where muscle triggers such as TrPs may play a role. No studies have so far addressed the question of how TrPs may help stratifying different populations, but a number of papers have shown an association between the number of trigger points and the severity of TTH attacks [38–40, 43]. Interventional studies (needling, toxins, local analgesics) targeting the TrPs have resulted in very different outcomes, and many of these studies lack controls and proper patient profiling.
Regarding arthralgic TMD, it is thought that the process of peripheral sensitization can occur much in the same way as with myalgic TMD. Despite this, arthralgic TMD appears to have low prevalence among headache sufferers [48, 51]. Gonçalves et al. reported that a muscular component seems to be needed to cause mixed TMD or myalgic TMD and that both of these were more associated with chronic daily headache and migraine than with ETTH [51]. This could be due to the fact that most of the time if arthralgic TMD is severe enough, it may cause a protective reflex of the jaw muscles (e.g. a splinting effect) and could eventually lead to myalgic TMD as well [119]. More research will be needed to demonstrate the importance of such possible reflex mechanisms in TMD pain and HATMD.
In summary, peripheral sensitization is believed to be an important mechanism in both TMDs and headaches. In general it is shown that peripheral sensitization may play a role in decreasing somatosensory thresholds (mechanical, thermal). The increased tenderness upon palpation of muscles for both TMD and headaches is thought to be due to sensitization of muscle nociceptors although more studies are needed.
9.2.2 Central Sensitization
Strong excitation of nociceptive-specific fibres such as C fibres, and in particular those from deep tissues such as muscles and joints, can in turn lead to prolonged excitability of neurons in central nociceptive pathways that is referred to as central sensitization, and this phenomenon may be responsible for allodynia [120]. If central sensitization is limited to the trigeminal second-order neurons, pain will be limited to the areas innervated by the trigeminal nerve [21]. On the other hand, if this sensitization advances to the third-order neurons in the thalamus, the phenomenon could be responsible for the widespread pain that is reported in some subgroups of painful TMDs and headaches [21, 62]. As a result of widespread hypersensitivity, there are many comorbidities among different pain syndromes with a high prevalence of, for example, TMD in fibromyalgia [63] and chronic low back pain [9] as well as TTH [29] and migraine [117]. The more widespread a musculoskeletal pain problem becomes, the more somatosensory signs of generalized hypersensitivity are found [26].
Clinically, this widespread hypersensitivity has been shown both through patient report of pain [115] and also through lowered pain thresholds both cranially and extracranially [20, 45, 70, 84, 116]. For example, patients with myalgic TMD pain have generally lower pain thresholds to mechanical stimuli applied to the painful area when compared to control subjects [70, 107, 110, 116]. However, it has also been shown that myalgic TMD patients have decreased pain thresholds outside the painful area and have a greater temporal summation (TS) of nociceptive cutaneous input [44, 70, 116]. These latter observations are difficult to explain with peripheral sensitization and clearly implicate the central nociceptive pathways. A generalized hyperexcitability of central nociceptive processing in TMD patients has been indicated by the finding of more pronounced TS of pain and greater after-sensations following repetitive painful mechanical stimulation of the fingers versus control subjects [94], and similarly widespread mechanical pain hypersensitivity has been reported in both myalgic TMD [44] and TMJ arthralgia patients [8]. It has also been shown that specific subgroups of TMD patients with widespread tender points present with lowered pressure and thermal pain thresholds both in trigeminal and extra-trigeminal areas when compared to TMD patients with less widespread tender points [84].
The same evidence of central sensitization has been found in patients with TTH even though, similarly to TMD, specific subgroups of patients present with different findings. These studies have found, with some exceptions, that PPT are lower in patients with ETTH when compared to controls [2], and these same thresholds are more robustly decreased in patients with CTTH, both in cephalic and extra-cephalic regions [2, 98]. Regarding TS studies, the results are fickle as they either show a small increase in TS of CTTH patients or no difference between these and controls [7, 95]. Taken together, these findings suggest that central sensitization may play a role in patients with CTTH but not to the same extent in ETTH [12]. Furthermore, evidence of central sensitization has also been found in migraine [19, 67] and cluster headache [45] both in cephalic and extra-cephalic regions.
These findings of central sensitization have been confirmed in both human and animal experimental studies. Activation of subnucleus caudalis neurons has been found in experimental animal models of both myalgic and joint TMD [28, 61, 90] as well as headache [16, 20]. In human experimental models, intramuscular injection of hypertonic saline into the masseter muscles causes localized pain around the injection site as well as spread and referral of pain to the temple, teeth and ear both in patients with myalgic TMD pain and healthy controls. Moreover, patients with myalgic TMD reported a larger pain area and more pain intensity than controls [110]. A similar study was done in frequent ETTH and CTTH patients. Both groups showed increased pain levels and larger pain areas when compared to healthy controls. Furthermore, and differently from the TMD study, increased sensitization of extra-trigeminal sites was also found [98]. This is in line with another recent study on CTTH patients showing a generalized hyperalgesia to single and repetitive electrical stimuli [7]. An important finding is that since the distinction between infrequent episodic (IETTH) and frequent episodic (FETTH) TTH, it has been reported that pain thresholds in FETTH are lowered when compared to the IETTH but do not differ from CTTH [98]. These findings imply that FETTH and CTTH are part of a continuum and not separate entities and that central sensitization is perhaps necessary for chronification [17, 18].
In summary, both myalgic TMD and headache patients have several clinical features which are compatible with both peripheral and central sensitization of the nociceptive pathways. This increased sensitivity is reflected into different pain conditions such as fibromyalgia, TMD and headache, and thus it is important for the clinician to be aware of this overlap between conditions [126].
9.3 Endogenous Pain Modulatory Systems
There is increasing evidence that the balance between the descending pain inhibition and facilitation may be disturbed in some chronic pain conditions and that this phenomenon has a role in maintaining central sensitization and spontaneous pain [86, 106, 125]. It has been observed for some time now that wide dynamic range neurons (convergent neurons) are inhibited by nociceptive stimuli applied to a segment remote from the excitatory receptive fields [59]. This phenomenon of diffuse noxious inhibitory control-like effects can also be triggered in humans and is termed conditioned pain modulation (CPM) [124]. CPM can be assessed as the analgesic effect to a given painful test stimulus when applied together with a tonic painful stimulus (the conditioning stimulus). CPM is assumed to be the net sum of the descending pain inhibition and pain facilitation, and this net sum is shown to result in reduced pain inhibition in many chronic pain conditions [105, 123].
Regarding patients with painful TMD, the results have been equivocal as some studies have shown that the endogenous pain modulatory system (EPMS) is not compromised [47, 59]. The results may however depend on the technique used to assess CPM as other studies with different types of conditioning stimuli have shown impaired CPM in painful TMD [56, 81] as well as the heterogeneity of the TMD group that can include patients with arthralgia, myalgia or with both. Other findings indicate that CPM could be impaired in TMD pain patients especially at sites with chronic pain but not at pain-free sites and that the clinical pain characteristics do not influence CPM [59]. Similar deficiencies in CPM have been shown in patients with TTH and migraine [27, 35, 85, 93]. Again this may have implications for the overlap between painful TMDs and headache as impaired endogenous control systems may contribute to the spreading and referral of pain. Another consideration is whether the pain condition occurs due to a deficient EPMS or if the pain condition causes the deficiency in the EPMS. It has been shown that CPM can change over time and that these changes may be related to the absence or presence of pain as well as sleep disturbances [53, 58, 64]. With this in mind, the interaction between painful TMD and headaches becomes even more complex as it could be argued that a deficient EPMS could facilitate both conditions but also that the presence of one or the other could weaken the EPMS and thus contribute to the presence of the other. Clearly there is a need for developing more sophisticated CPM techniques to better understand the potential contribution of EPMS in painful TMDs and headaches.
9.4 Genetics
Recently, it has been shown that different functional polymorphisms and haplotypes can cause differences in pain perception and sensitivity [34, 87]. The most promising avenue of research in the field of TMD is the variation in coding of the catechol O-methyltransferase (COMT). This enzyme metabolizes catecholamines such as epinephrine, norepinephrine and dopamine that play a critical role in pain perception, cognitive function and affective mood [34]. An association has been found between COMT haplotypes and sensitivity to experimental painful stimuli [33]; it has also been shown that carriers of the low pain sensitivity haplotype of the COMT gene have a 2.3 times lower risk of developing myalgic TMD when compared to individuals carrying the high pain sensitivity haplotype [34]. Furthermore, it has been shown that individuals carrying specific polymorphisms are also at a higher risk of developing TMD [75]. Finally, it has been demonstrated that the influence of COMT activity on pain sensitivity is, in part, mediated through adrenergic receptors beta 2 and 3 (ADRB2 and 3) [76] and that individuals who carry one haplotype coding for high and one coding for low ADRB expression display high positive psychological traits, have higher levels of resting arterial pressure and are about ten times less likely to develop TMD [32]. The activation of ADRB leads to the release of nitric oxide (NO) as well as several cytokines such as TNF-α, IL-1β and IL-6 [55], all of which have been implicated in painful TMD and TTH [4, 31, 57, 82, 101]. Moreover, selective treatment with an ADRB antagonist (propranolol) has been shown to decrease pain depending on the number of low pain sensitivity (LPS) alleles of the COMT gene [113]. However, numerous other genes coding for neurotransmitters and neuromodulators may obviously also have implications for pain sensitivity [113] and TMD [79, 104].
Regarding headaches, the genetic contribution to familial hemiplegic migraine (FHM) is well established [114], and some studies have shown a genetic contribution to regular migraine as well [37, 88]. Another recent study on twins concluded that genetic factors play a role in FETTH, while IETTH appears to be caused primarily by environmental factors [91]. Most studies regarding TTH have failed to show a relationship with specific genetic traits [41, 54], but most of these studies have not distinguished among the different types of TTH.
Furthermore, it has been shown that both dopamine receptor D3 (DRD3) and serotonin transporter gene polymorphisms can predict the efficacy of CPM [66, 87]. Considering that several studies have indicated that a less efficient CPM may be implicated in TMD [56, 81], migraine [77, 93], TTH [85, 93] and chronic post-traumatic headache [30], it would be important to consider that these genes may be indirectly involved in the development of TMD and headaches.
In summary, there is emerging evidence to support the notion of a genetic component involved in both myalgic TMD and TTH, and more studies may help to further identify vulnerable genes that interact with environmental factors, such as physical and emotional stress, to produce pain-prone phenotypes at risk for developing myalgic TMD pain and/or headache. These studies highlight the importance of individually tailored treatment plans for both TMD and headaches and further emphasize the idea that similar presenting conditions may have a different pathophysiology [11].
9.5 Clinical Evidence of Comorbidity Between TMD and Headaches
Several studies have looked at the association between TMD and headache with evidence of significant overlap between these conditions [51, 52, 65, 78]. A higher prevalence of TMD has been found in both episodic and chronic migraine patients when compared to controls [52]. Another study found that the presence of TMD increases the risk of chronic daily headache (CDH), migraine and ETTH. Furthermore, this increased risk was found for myalgic and mixed TMD but not for arthralgic TMD [51]. A study that investigated the frequency of TMD in 99 headache patients showed that the prevalence of TMD in the headache population is 56.1 % [10]. Moreover, the highest percentage of TMD was found in patients with a combination of migraine and TTH (75 %), followed by migraine alone (53.3 %) and TTH alone (45.4 %) [10]. Finally, several studies have shown that headaches are more severe and frequent as TMD pain increases [51] but also that TMDs are more severe in patients with headache [72]. Taken together these findings support our notion of a bidirectional relationship between painful TMDs and headache. At present, a temporal relationship between these two conditions cannot be inferred as most studies are cross-sectional. Despite this caveat one cross-sectional study showed that when asked through a questionnaire, adolescents reported that the onset of headache preceded the TMD pain [78]. On the other hand, a longitudinal study that followed the development of trigeminal and spinal pain for a period of 2 years showed that the baseline presence of spinal pain or TMD signs was more likely to cause headache occurrence than in subjects where these features were not present at baseline [71].
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