Muscle pain in the head: Overlap between temporomandibular disorders and tension-type headaches

Department of Clinical Oral Physiology, School of Dentistry, University of Aarhus, Denmark.
Current Opinion in Neurology (Impact Factor: 5.31). 07/2007; 20(3):320-5. DOI: 10.1097/WCO.0b013e328136c1f9
Source: PubMed


A variety of painful problems can affect the muscles in the head and face. Both temporomandibular disorders and tension-type headaches are believed to have a significant contribution from the skeletal muscles and have several clinical features in common. It still unclear, however, to what extent these two prevalent disorders are separate entities or have similar pathophysiological background.
There is now reasonably good evidence that myofascial temporomandibular disorder patients are more likely to have a tension-type headache problem and vice versa, but the overlap is not complete. Studies have documented similarities regarding sensitization of the nociceptive pathways, dysfunction of the endogenous pain modulatory systems as well as contributing genetic factors, but there are also a number of distinct differences between temporomandibular disorders and tension-type headaches that need to be considered.
Using the current classification systems, myofascial temporomandibular disorder pain and tension-type headache disorders do overlap and appear to share many of the same pathophysiological mechanisms, but it would be premature to consider them as identical entities since the importance of, for example, the affected muscles and associated function and genetic background needs to be established. Orofacial pain and headache specialists should collaborate to further develop diagnostic procedures and management strategies of temporomandibular disorders and tension-type headaches.

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    • "In either case, the pathophysiology and management are different [27] [28] [99]. Temporomandibular disorder (TMD) pain may also be connected to regional pain i.e. tension-type headache [113] [114] [133] [141] or cervical musculoskeletal pain [7]. In this review we focus on localised muscle pain. "
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    ABSTRACT: For the treatment of localised masticatory muscle pain, it is still unknown whether exercises have any efficacy. The understanding of these supposed biological effects is linked to the pathophysiological model of localised myofascial pain and dysfunction (MPD). (1) Motor activity: In MPD, the pain adaptation model implies that there is an agonist-antagonist co-activation. In healthy muscles, training exercises allow a tendency to a switch from agonist-antagonist co-activation towards reciprocal inhibition, either during isometric contractions or during isokinetic contractions. (2) Hemodynamics: In MPD, a hypoperfusion is supposed. In healthy muscle, training exercises enhance the functional hyperaemia. (3) Histology: (a) In females with localised trapezius myalgia, but not in males, there is a decrease in capillarisation. Exercises induce capillary angiogenesis in healthy muscles, and also in females with trapezius myalgia. (b) In myalgic females, but not in males, there is a tendency towards a higher proportion of type I fibres; exercises decrease the proportion of type I fibres, with a reciprocal increase of type IIA fibres (phenotypic conversion). (4) Biochemistry: There may be a cytochrome c oxidase (COX) deficiency that could explain the lower ATP concentrations in female patients. Exercises induce a decrease in the proportion of COX-negative fibres. Finally, a 10-week training program might have specific positive effects. Physiological mastication could be both a natural means of re-education and one of the goals of treatment. KeywordsLocalised muscle pain-Temporomandibular disorder-Exercise therapy-Efficacy-Motor activity-Mastication-Microcirculation-Hemodynamics-Capillary angiogenesis-Muscle fibres-Cytochrome C oxidase
    international journal of stomatology & occlusion medicine 12/2010; 3(3):150-158. DOI:10.1007/s12548-010-0064-2
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    • "Therefore, it is likely that increased P-p38 and P-ERK activity in neuronal and glial cells in the trigeminal ganglion may contribute to peripheral sensitization of primary sensory neurons. It is interesting to speculate that peripheral sensitization mediated by changes in trigeminal neurons and satellite glia may explain the higher incidence of comorbidity reported for individuals with TMJ disorders and other diseases that involve trigeminal nerve activation such as migraine and sinus pathologies (Cady et al., 2005, Graff-Radford, 2007, Svensson, 2007). "
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    ABSTRACT: Elevated nitric oxide (NO) and proton levels in synovial fluid are implicated in joint pathology. However, signaling pathways stimulated by these molecules that mediate inflammation and pain in the temporomandibular joint (TMJ) have not been investigated. The goal of this study was to determine the effect of NO-proton stimulation of rat trigeminal neurons on the in vivo expression of mitogen-activated protein kinases (MAPKs) and phosphatases (MKPs) in trigeminal ganglion neurons and satellite glial cells. Low levels of the active MAPKs extracellular signal-regulated kinase (ERK), Jun amino-terminal kinase (JNK), and p38 were localized in the cytosol of neurons and satellite glial cells in unstimulated animals. However, increased levels of active ERK and p38, but not JNK, were detected in the cytosol and nucleus of V3 neurons and satellite glial cells 15 min and 2 h following bilateral TMJ injections of an NO donor diluted in pH 5.5 medium. While ERK levels returned to near basal levels 24 h after stimulation, p38 levels remained significantly elevated. In contrast to MKP-2 and MKP-3 levels that were barely detectable in neurons or satellite glial cells, MKP-1 staining was readily observed in satellite glial cells in ganglia from unstimulated animals. However, neuronal and satellite glial cell staining for MKP-1, MKP-2, and MKP-3 was significantly increased in response to NO-protons. Increased active ERK and p38 levels as well as elevated MKP levels were also detected in neurons and satellite glial cells located in V2 and V1 regions of the ganglion. Our data provide evidence that NO-proton stimulation of V3 neurons results in temporal and spatial changes in expression of active ERK and p38 and MKPs in all regions of the ganglion. We propose that in trigeminal ganglia these cellular events, which are involved in peripheral sensitization as well as control of inflammatory and nociceptive responses, may play a role in TMJ pathology.
    Neuroscience 11/2008; 157(3):542-55. DOI:10.1016/j.neuroscience.2008.09.035 · 3.36 Impact Factor
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    ABSTRACT: Le concept d’algie orofaciale idiopathique (AOFI) regroupe plusieurs douleurs chroniques de l’extrémité céphalique qui sont souvent très invalidantes (algie faciale atypique, odontalgie atypique, stomatodynie, certaines douleurs musculosquelettiques). Ces pathologies localisées autour de la cavité buccale ne correspondent à aucune cause organique objectivable et pourraient être assimilées à des douleurs « fonctionnelles ». Elles pourraient constituer une seule et même entité physiopathologique affectant des tissus différents. Différents mécanismes physiopathologiques démontrés ou hypothétiques sont décrits. The concept of orofacial idiopathic pain groups together several chronic pain syndromes of the head, which are often very disabling (atypical facial pain, atypical odontalgia, stomatodynia, certain forms of musculoskeletal pain). These orofacial pathologies are not associated with somatic identifiable causes and could be considered as “functional” pain. Such entities might constitute a single pathophysiological entity affecting different tissues. Different pathophysiological mechanisms, already demonstrated or hypothetical, are presented.
    Douleur et Analgésie 06/2009; 22(2):89-95. DOI:10.1007/s11724-009-0130-y · 0.09 Impact Factor
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