Differential diagnosis and management of masticatory myogenous pain and dysfunction
16.1 Understanding Muscle Pain Classification and Causation
The first section of this chapter deals with the differential diagnostic process and the criteria for the various painful masticatory myogenous pain (MMP) subgroups that patients present with. The current system for classifying myogenous disorders is an anatomically based system; therefore, the differential diagnosis process is relatively easy since it mostly involves careful palpation of the muscles and joint tissues (Table 16.1). However, above and beyond the clinical examination, an expert clinician must also strive to determine the etiology and pathophysiologic changes that occur with the various types of muscle pain. This determination is based on a thorough history and an in-depth understanding of the muscle pain research. Unfortunately, no valid additional diagnostic testing methods (radiographic, serologic, or electromyographic [EMG]) are available that will help to further classify subgroups of myogenous pain. In Section 16.2, we focus on treatment which is largely a self-directed treatment physical medicine and behavioral intervention approach that the patient needs to perform daily. We also review the current medications that have been used for myogenous pain disorders.
|Focal myalgia due to direct trauma||
|Primary myalgia due to stress and/or parafunction||
|Secondary myalgia due to active local pathology or recent medications||
|Widespread chronic muscle pain and fibromyalgia||
16.1.A Diagnosis with Muscle Palpation
Logically, the first component of the differential diagnostic process is to conduct a thorough review of the patient’s history, looking for the most likely etiology or etiologies that might be causing or maintaining the pain. The second component, which is covered in this section, is to fully verify and document the anatomic extent and character of the myogenous pain using palpation. The third or last component is to decide, based on the examination and history gathered, which pathophysiologic changes would best explain the patient’s current muscle pain disorder. How to gather a medical history and various etiologies and pathophysiologic processes associated with them are discussed in the following subsections.
How Do You Palpate the Craniomandibular Muscles?
There are several articles that review how to properly conduct a muscle and trigger point palpation examination.1 Unfortunately the literature suggests that reproducibility of this examination between examiners is low.2–4 In spite of this limitation muscle palpation is the accepted clinical examination when diagnosing a myogenous disorder. The palpation pressure used in the masticatory system varies (in the range 1–2 kg) but is generally lower than is used when palpating large leg, arm, shoulder, or neck muscles, where 4 kg of pressure is commonly recommended.5 This palpation is done with the index finger being moved over the muscle of concern when in the relaxed state. The pressure used should be steady firm pressure (2 kg of pressure) applied for at least 1–2 seconds. While doing this palpation, ask the patient to rate the tenderness (if any) that is produced with this pressure, using 0 for none, 1 for mild, 2 for moderate, and 3 for severe tenderness. The level of tenderness at each muscle site should be recorded. When you palpate the muscle you must not only check for tenderness but also examine the muscle to see if it has a taut band (they always run parallel to the direction of the muscle fibers). Once you find the band, make sure you examine it for a trigger point and determine if this point produces referred pain to a nearby site. To do this examination it is presumed the examiner knows the landmarks needed to identify the underlying muscle. The common sites of palpation for the jaw closers are are the superficial and deep masseter muscles and the anterior, middle, and posterior temporalis muscles. The cervical muscles that should be palpated are the sternocleidomastoid muscle and the upper and oblique portion of the trapizius muscle (just under the occiput and at the top of the shoulder). Note that the medial pterygoid can be best palpated at the angle of the mandible just inside the inferior edge of the mandible, but the lateral pterygoid cannot effectively be palpated.
Confirming that the patient’s primary pain complaint can be reproduced by palpation of the muscle(s) is essential to the diagnosis of myogenous pain. However, getting a patient to report that your palpation pressure replicates their primary pain complaint is not proof that another source for the pain is not present. In fact, the opposite is true: if you cannot replicate the pain complaint by palpation, you have a high chance some othere pain-inducing disease process is present and unaccounted for.
The International Association for the Study of Pain Subcommittee on Taxonomy has classified myofascial pain as pain in any muscle with trigger points that are very painful to compression during palpation and causes referred pain.6 Essentially the term “myofascial pain” is used only when specific criteria are satisfied. These criteria are both subjective (history based) and objective (examination based). The three subjective criteria that patients should endorse include (1) spontaneous dull aching pain and localized tenderness in the involved muscle(s), (2) stiffness in the involved body area, and (3) easily induced fatigueability with sustained function. The four objective criteria are (1) a hyperirritable spot within a palpably taut band of skeletal muscle or muscle fascia, (2) upon sustained compression of this hyperirritable spot, the patient reports new or increased dull aching pain in a nearby site, (3) decreased range of unassisted movement of the involved body area, and (4) weakness without atrophy and no neurological deficit explaining this weakness. Many have included the presence of referred autonomic phenomena upon compression of the hyperirritable spot and/or a twitch response to snapping palpation of the taut bands as additional diagnostic criteria.7–11 However, inclusion of the last criterion is not endorsed by all since it is not a reliably present physical finding.12 The interesting aspect of this study was that taut muscle bands and muscle twitches were common and noted equally in all three diagnostic groups (fibromyalgia, regional myofascial pain, and healthy control subjects). This finding suggests that the clinical examination-based criteria for myofascial pain are not reliable and myofascial pain patients are best identified using a combination of historical and clinical criteria. This research report suggests that additional work is needed to establish a reliable set of diagnostic criteria for this disorder.
The American College of Rheumatology (ACR) has set forth criteria for the diagnosis of fibromyalgia.13 These criteria include specific (1) duration, (2) location, and (3) examination findings that must be satisfied. The duration criterion specifies that a history of widespread pain has to be present for at least 3 months. For pain to be considered widespread, it must involve (a) both sides of the body and (b) be located above and below the waist. Moreover, the location criteria state that the pain must involve multiple areas of the axial skeleton, including the cervical spine, anterior chest, and thoracic spine or lower back regions. If the patient has low back pain, this will satisfy the criterion for below-the-waist pain. Finally, the examination-findings criteria specify that a “painful” response must be elicited in 11 of 18 tender-point sites on digital palpation. The ACR criteria specify the exact location of these tender-point sites; they also specify that a manual finger palpation force of approximately 4 kg is to be used during the examination and that the allowable responses to palpation are no pain, tender, and painful.
Why Are the Same Muscles Always Tender?
Nontraumatic primary myogenous pain occurs in roughly the same anatomic locations from patient to patient in the masticatory and craniocervical systems. It was recently described that the slow time to peak motor units, which are presumably the slow twitch type 1 fibers, are clearly more sensitive to ischemia than the “fast” time to peak group.14 That would explain why postural muscles, which have a much higher proportion of slow twitch (type 1 fibers), are much more likely to exhibit diminished perfusion and show ischemic injury sites.15–17 Studies have shown that pH values of 6 or lower can be reached during ischemia and sustained contractions or exhaustive exercise.18,19
16.1.B Subtypes of Myogenous Pain
Myalgia (of all types) requires the following additional criteria to be satisfied: (1) the patient has an awareness of pain in the muscle on function; (2) this pain must be replicated by palpation. Based simply on its extent, the myogenous masticatory pain (MMP) can be divided into several subcategories. There are those patients with (1) focal masticatory myalgia, those with (2) regional craniocervical and masticatory myalgia (involving several muscles of the jaw and neck on the same side), and (3) those with a widespread chronic musculoskeletal pain that also involves the masticatory system. This anatomically based categorization system is inadequate, however, and a more logical system would be to have additional categories based on a combination of anatomic features and etiology: (1) myalgia due to direct muscle injury; (2) secondary local and regional myalgia; (3) primary local and regional myalgia; (4) myofascial pain; and (5) widespread chronic muscle pain and fibromyalgia.
Myalgia Due to Direct Muscle Injury
Local myalgia can develop as a result of muscle damage resulting in histologically evident changes within the muscle called myositis.20,21 Such injuries are not common in the masticatory system, but when they do occur they are quite dramatic. Patients typically report strong focal pain and severely limited opening due to secondary trismus.22
Secondary Local and Regional Myalgia
Sometimes local and even regional myalgia and trismus will develop in response to a local painful pathologic process such as an acute arthritis affecting the temporomandibular joint (TMJ). In local pathology cases the muscle pain develops unilaterally (on the side of the pathology, assuming it is one-sided). The pain in the muscle tissue is secondary, probably due to local hypoxia from the trismus reaction in these muscles. Also, a secondary myalgia can develop as a direct result of certain medications that activate the extrapyramidal system, such as psychological stimulants and certain types of antidepressants (e.g., serotonin selective reuptake inhibitors [SSRIs]).
Primary Local and Regional Myalgia
When a direct muscle injury explaining the muscle pain cannot be found and the patient does not have another adjacent pathology in the area that would cause secondary muscle guarding effects (e.g., arthritis of the TMJ or internal derangement of the TMJ), then one of the criteria for a primary myalgia is satisfied. Pain in these cases is most likely related to stress and parafunction inducing a localized hypoxia, but eventually sensitization of muscle nociceptors will result. Using the term “myalgia” means that taut bands and active trigger points are not identified in the muscle.
If palpation reveals taut bands, trigger points within the taut band, and referred pain sensations upon sustained compression of the trigger point, then the term “myofascial pain” should be used instead of “myalgia.” Several authors have offered explanations for the referred-pain phenomena.23–27 However the more interesting question is, “What are trigger points and how do they develop?” Needle-EMG-based studies have reported that a sustained spontaneous EMG activity can be found within 1–2 mm of hyperirritable or “trigger” points in a muscle but not from control nonpainful sites or from the surface above the muscle.28 That this activity is influenced (increased) by the sympathetic nervous system was recently demonstrated by using a Valsalva maneuver to induce a transient sympathetic activation. This research suggests that that sympathetic neural outflow increases painful-area motor nerve activity and this may be contributing to a focal contraction (palpable taut band) at the painful trigger point site.
Widespread Chronic Muscle Pain and Fibromyalgia
For widespread chronic musculoskeletal pain, if the appropriate criteria are satisfied, then the term “fibromyalgia” is used.29 A small percentage of the population develops widespread chronic musculoskeletal pain. Based on epidemiologic studies, syndromes of diffuse musculoskeletal pain are reported to occur in 4–13% of the general population.30–32 Fibromyalgia (FM) is a specific disorder with published diagnostic criteria and it is less common, with a prevalence of 2% in the community. Widespread diffuse musculoskeletal pain syndromes, in particular FM, often occur in concert with several additional diseases, most notably chronic fatigue syndrome, irritable bowel syndrome, temporomandibular disorders, and headaches. In general, fibromyalgia is treated using multimodal approaches that simultaneously target the biological, psychological, and environmental–social factors that maintain the pain. With regard to the underlying differences between focal–regional myalgia and myofascial pain versus fibromyalgia, there is substantial evidence that fibromyalgia sufferers have central neuronal changes in their pain system. For example, fibromyalgia patients show clear-cut altered sensory processing versus normal subjects. Normals show an increase in their pain threshold with repeated skin stimulation, but this does not occur in fibromyalgia, which suggests a reduced descending inhibitory pain suppression system. Moreover, functional CNS changes can be demonstrated in fibromyalgia by several different imaging techniques. For example, one study reported that fibromyalgia patients have a decreased thalamic and caudate blood flow compared with healthy controls on single-photon-emission computed tomography (SPECT) imaging.33
16.1.C Etiologic Agents Underlying Myogenous Pain
Of course, the anatomically based classification of masticatory muscle pain described previously does not account for the etiology, so this must be appended, if known, to the diagnostic subgroup. An example of this type of classification would be “local masticatory myalgia secondary to temporomandibular joint osteoarthritis.” The most common etiologies for myogenous pain are (1) direct muscle trauma, (2) adverse effects from medications, (3) secondary pathology-induced trismus, (4) parafunctions (both waking and sleeping), and (5) stress-induced hypoperfusion. In addition, while they are not etiologies per se, it is necessary to determine to what extent any secondary neurogenic effects have occurred: (6) peripheral muscle motor nerve and nociceptor sensitization and (7) central pain pathway sensitization. These etiologies and neurogenic adverse effects are discussed in the following subsections.
Direct Muscular Trauma
The most common traumatic cause of myositis in the jaw system is an inadvertent intramuscular injection of local anesthetic during dental treatment. In these cases, the nature of the injury is influenced by the amount of injected material, the type of anesthetic used, and more important, whether a vasoconstrictor such as epinephrine was included in the anesthetic solution. Several authors have described and documented the effect of an inadvertent anesthetic injection into muscle tissue.34–37 Other forms of local muscle injury can occur (e.g., neck musculature can be injured during a low-velocity rear-end collision) that produces a regional cervical muscle strain and secondary cervical and masticatory myalgia. Current data suggests that the jaw closing and opening muscles themselves are not stretched or torn during a low-velocity rear-end motor vehicle collision, but they may become involved as a secondary phenomenon after the craniocervical muscles are injured. It has been claimed that actual muscle tearing type damage and tissue inflammation can occur as a result of high levels of sustained clenching and eccentric bruxism-like contraction in some patients, but the evidence does not support this claim. Several researchers have tried to induce this type of muscle pain in volunteers who performed prolonged sustained centric and eccentric exercises of the jaw.38–41 The data from these experiments do show that some acute pain is inducible during and shortly after the exercise task, and some mild increased tenderness can be demonstrated, but overall the masticatory motor system is actually quite resistant to this form of muscle injury. If a direct muscle trauma is suspected as the etiology, then the traumatic event is usually easily identified in the patient’s history. The standard treatment for traumatic focal or regional myalgia is rest, ice, NSAIDs, and then frequent daily active mobilization of the jaw and neck muscles until normality of range movement is maintained.42 The latter is important because traumatic myositis frequently induces a substantial trismus of the jaw in an attempt to prevent movement. This trimus is a logical and appropriate acute injury response but, if prolonged, it can lead to chronic loss of jaw motion due to contracture development.43 Most healthy patients manage to overcome these injuries and achieve normal function with the minimal amount of disruption, but poorly treated patients often end up with significant long-term limitations of jaw opening.
Trismus-Induced Secondary Myogenous Pain
That the nociceptors inside a joint and even a tooth can induce a secondary motor reaction in the anatomically adjacent muscles has been clearly demonstrated in the literature.44–46 When a patient presents with one-sided muscle pain in the absence of trauma or a strong stress or parafunction history, the clinician would be wise to carefully examine the TMJ, oral mucosal tissues, and teeth for local disease or dysfunction. In these cases it is logical and appropriate to manage or minimize the local pathology first and then re-examine the myogenous pain for resolution or persistence. As with injection-induced trismus, in some cases, acute secondary trismus can convert to chronic contracture of the involved muscle.47
First, if a patient is using psychological stimulant medication or is using an SSRI, then a medication-induced myalgia would be suspected. The various medications that can induce muscle pain are reviewed in Chapter 19 and are not discussed here.
Although most oral parafunctions do not induce myalgia, if the behavior is prolonged, occasionally they can. Parafunction-induced myalgia should be suspected when a patient admits to, or if the clinician observes, repetitive oral habits. Oral parafunctions may be present both during waking and sleeping hours and during specific activities such as chronic gum chewing.48 Several studies have reported that there is a moderately strong positive association between self-reported clenching and chronic masticatory myofascial pain (MMP).49–51 Unfortunately, these studies do not specify whether the clenching is occurring during waking or sleeping periods because to do so accurately would require an actual recording of the jaw motor behaviors in question over moderately long periods of time (minimum, 2 weeks). A 2003 study examined various potential contributing factors such as clenching, grinding, head–neck trauma, psychological factors using the Symptom Check List 90 Revised Questionnaire (SCL-90R), and various sociodemographic characteristics for their effect on chronic masticatory myofascial pain.52 They used a case–control designed study with 83 patients with MMP, selected from the dental clinics of the Jewish General and Montreal General Hospitals, Montreal, Canada, and 100 concurrent controls. Using unconditional logistic regression analysis they found that self-reported clenching or grinding either in association with an elevated anxiety score (OR = 8.48) or an elevated depression score (OR = 8.13) was statistically associated with chronic MMP. They concluded that tooth clenching, trauma, and female gender strongly contribute to the presence of chronic MMP even when other psychological symptoms are similar between subjects. Interestingly, grinding-only behavior, age, household income, and education were not related with chronic MMP. This report of no association between tooth grinding and chronic muscle pain is in conflict with other studies. For example, one study performed a questionnaire-based epidemiologic cross-sectional study and another used a clinical-based case–control design.53,54 These two studies found a positive relationship between self-reported nocturnal tooth grinding and self-reported jaw pain. This conflict will require additional data to resolve.
Stress-Related Muscle Hypoperfusion
Stress-associated myalgia should be suspected if a patient reports a prolonged increase in their environmental (job or personal) stress levels. With regard to stress, psychological factors have been associated with chronic facial and jaw pain.55 Unfortunately we cannot be sure if the chronic pain is influencing the psychologic factors or visa versa. Chronic muscle pain is known to be highly prevalent and induces daily-life disability in humans.56,57 Although significant effort has been devoted to determining its pathophysiology, the exact mechanisms have not been firmly established. In recent years, localized intramuscular hemodynamic disturbance has been recognized as one of the possible mechanisms that cause or sustain this pain condition.58 Several studies evaluated intramuscular hemodynamics using near infrared (NIR) spectroscopy to understand muscle pain mechanisms and discovered some interesting findings. For example, dynamic muscle blood flow in fibromyalgia has been studied by numerous researchers using different methods to monitor blood flow.59–61 These studies have found there is a significantly reduced intramuscular perfusion in the focal myalgia subjects. These differences in vasodilative response in focal myalgia cases might be related to desensitization of beta-adrenergic receptors, which occurs with long-term exposure to the stress-associated neurotransmitter epinephrine. Overall, these studies suggest there are demonstrable changes in intramuscular perfusion of chronic regional myalgia involving the masseter and trapezius muscles. This hypoperfusion occurs in these subjects both during and after muscle activity. One study reported that intramuscular blood flow increases provoked by cold pressor stimulation, which increases systemic sympathetic nervous activity and produces a vasodilation reaction, was significantly diminished in painful muscles compared with healthy individuals.62 This hemodynamic response to cold pressor stimulation in chronic localized muscle pain is very similar to the hemodynamic response observed in normal subjects who are intravenously administrated a nonselective beta-adrenergic antagonist.63 In all subtypes of beta-adrenergic receptor (βAR), the beta-2-adrenergic receptor (β2AR) is known to be abundantly localized on smooth muscle cells in skeletal muscles.64 This receptor induces vasodilation when the sympathetic system is activated, and the preceding findings support the notion that β2AR activity is diminished in chronic muscle pain patients. Additionally, research has provided the evidence that β2AR is easily desensitized or downregulated by chronic βAR agonist exposure.65,66 For these reasons, we have speculated that β2AR abnormality is associated with chronic muscle pain pathophysiology. In a prior study on β2AR function on mononuclear cells it was demonstrated in fibromyalgia patients that a β2AR abnormality is associated with the chronic fibromyalgia state. However, it is still unknown whether this association is also present in the localized myalgia state.
Peripheral Muscle Nociceptor Sensitization
Considering what is now known about muscle pain mechanisms, specifically about jaw muscle activity, intramuscular blood flow, and the effect of prolonged stress on masticatory muscle blood flow, the following hypothesis has been put forth: (1) prolonged stress causes local intramuscular hypoperfusion, which seems to selectively target muscles with higher proportions of type 1 (slow twitch) fibers that are involved in postural maintenance; (2) this focal hypoperfusion induces a local partial ischemic condition and endogenous chemicals accumulate in the muscle, causing local muscle pain; (3) once the pain develops to a sufficient level in the muscle, this causes reactive neurogenic changes; (4) the neurogenic changes include focal hyperactivity of motor nerves, and sensitization of muscle nociceptors adjacent to the motor end plates. These neurogenic changes induce taut bands and painful foci in the muscle, called trigger points. If multiple areas of the muscle are affected, then whole muscle splinting or trismus can result. The central neurogenic effects of this process are described in the next subsection; there is some evidence to suggest that some patients may have a genetic susceptibility to this central sensitization process. Evidence for this theory comes from several sources. First, one study concluded that the electrical activity characteristics of trigger points are similar to those described from needle EMG recording in and around motor end plates.67 The authors speculated that the spontaneous activity recorded from a trigger point is probably related to excessive release of acetylcholine (ACh) at the end plate, suggesting a hyperactive motor nerve. They also speculated that these end plates were the source of trigger-point pain because the sensory nerve fibers that surrounded these end plates were sensitized and were spontaneously active or active during stressful periods of the day and in turn caused local pain and more focal motor nerve activity in the end plate. Focal hypoxia is the most likely mechanism that causes pain and muscle nociceptor sensitization. The basis of this focal hypoxia is that the release of acetylcholine produces a muscle contraction, which among other things causes a compression of local vasculature in the area and produces reduction in the local supply of oxygen. This impaired circulation, combined with the increased metabolic demands generated by contracted muscles, results in a rapid depletion of local adenosine triphosphate (ATP). One study showed that ATP directly inhibits ACh release, so depletion of ATP increases ACh release.68 In the muscle cell, ATP powers the calcium pump, which returns calcium to the sarcoplasmic reticulum. Hence, loss of ATP also impairs the reuptake of calcium, which increases contractile activity.69 Finally, the ATP energy crisis causes a local release of a variety of chemicals, peptides, and cytokines (i.e., bradykinins, cytokines, serotonin, histamine, potassium, prostaglandins, leukotrienes, somatostatin, and substance P) that have the potential to activate and sensitize nociceptive nerves in the region and more centrally.70
When a patient exhibits widespread chronic myalgia and or fibromyalgia, the patient’s pain is usually so long-standing by the time fibromyalgia has developed that the original etiology that triggered the cascade of events leading to this disorder is not discoverable. The one scientific fact that everyone agrees upon is that central sensitization and aberrant central nervous system processing of pain is the predominant issue and a major perpetuating factor in fibromyalgia.71–73 This means that patients have developed an increased response to painful stimuli (hyperalgesia) and experience pain from normally non-noxious stimuli (allodynia). Both hyperalgesia and allodynia reflect an enhanced CNS processing of painful stimuli that is characteristic of central sensitization.74 In fact, fibromyalgia patients show substantially elevated levels of substance P in their cerebral spinal fluid, which would enhance the likelihood of sensitization of second-order spinal neurons.75,76 Muscle nociceptor sensitization in fibromyalgia77,78 is known to be an important contributor to pain pathogenesis.79 How nociceptors become altered or “sensitized” has been presented in several recent reviews.80–82 One theory suggests that dysfunction in serotonin and norepinephrine in these pain-inhibitory pathways may contribute to the central sensitization and hyperexcitability of the spinal and supraspinal pain transmitting pathways and is manifest as persistent pain associated with fibromyalgia and some other chronic pain conditions.83–88 Another theory suggests that chronic muscle pain patients have an associated abnormal sympathetic system function.89,90
How Do You Determine Etiology?
Etiologies often prove far more difficult to discover than “where the pain is located and what physical characteristics are revealed by palpation.” To a large degree the information gathered during the medical interview is the process by which an etiologic discovery is made. Of course, establishing the chief complaint is the starting point and, after identifying this, the history of the present illness must be established. These details include (1) location, (2) severity (use a 0–10 score here), (3) duration, and most important (4) causation (if known). Under duration, make sure you include the course of the symptom(s) over a 24-hour period and the course since the symptoms first developed. Under causation (whether or not an exact cause is known), it is important to detail any event or situation which now precipitates or aggravates the symptoms. Also include all alleviating factors. If trauma is a cause, establish the details of the injury or iatrogenic trauma. Next the patient’s past medical history must be reviewed (current diagnosed diseases; general health; last physical examination; the exact types and daily dosage of any medications; all prior, recent, or ongoing treatments being rendered, including success, failure, compliance, and adverse reactions of these prior treatments; and all recent surgical interventions and hospitalizations). Added to this information, a thorough review-of-systems (ROS) questionnaire that includes at least nine systems should be filled out by the patient and reviewed during the interview. Next, probe for any family history of similar problems in the patient’s sibling(s) or parents, and ask about any ongoing serious medical problems in the family. At the end of the medical questions, ask several questions about the patient’s current job and home responsibilities, how many sick days, if any, are directly related to his or her problem, and how it interferes with desired social activities. Ask about recent change in stress, anxiety, or depression levels in the patient’s life and about the presence of a counselor, therapist, or confidant, if any. Be sure to ask about the patient’s awareness of any waking or sleeping clenching, night grinding (bruxism), facial tension, gum chewing, or abnormal jaw–tongue–face muscle posture habit. Observation of the patient for repetitive orofacial habits during the interview is an important feature of this aspect of the social history. Finally, as a part of the social history, ask about any disability claims that are pending or planned and establish if any litigation related to the patient’s complaints is pending or planned. There is no guarantee that the information gathered during a medical interview will pinpoint probable etiologies, but it is certain that a poor or incomplete history will not help.
16.2 Treatment of Masticatory Myogenous Pain
This section of the chapter covers self-applied treatment, office-based treatment, pharmacologic treatment, and behavioral treatment. Because it is a relatively new therapy, we report on botulinum toxin injections for myofascial pain. Finally, where no substantive scientific evidence is available, current best clinical practice as understood by the author is described and identified clearly as clinical opinion. The most respected form of scientific evidence available for assessing a specific treatment effect is a randomized, blinded clinical trial (RBCT). Even better is when there are several RBCTs assessing the same method; the conclusions that can be drawn across several RBCT studies are usually described in a systematic review of the literature. Typically the reviews considered most valuable are those which qualify for inclusion in the Cochrane Library database, an international collaboration that promotes evidence-based reviews of the literature (www.cochrane.org). Where they were available we report on Cochrane review results. Here we have endeavored to find those review articles that specifically deal with local or regional myogenous pain in the craniocervical or temporomandibular region. However, if such information was not available, we looked at low back pain treatment outcome reviews hoping to generalize the data on this regional musculoskeletal disorder to masticatory myogenous pain. Finally, we examined systematic reviews on the treatment of fibromyalgia or, in some cases, chronic pain disorders if no systematic myogenous pain review was available. The hope is that, although such collecting together of disparate information has its disadvantages, the advantages and overall conclusions will outweigh the limitations of the data.
16.2.A Self-Directed Treatment
Whether the masticatory musculoskeletal pain is localized, regional, or generalized, the first line of treatment is almost always self-treatment; this includes education about the specific masticatory muscle disorder the patient is experiencing and an individualized self-treatment program. This self-treatment program generally includes four elements: (1) identify and avoid activities that are potentially harmful to the jaw system; (2) increase local blood flow in the muscles which are painful; (3) stretch stiff and painful muscles to try to decrease postural tone in the sore muscle; and (4) when the patient is able, encourage the patient to start a daily nonimpact exercise program.91 Each of these four elements will be discussed in this section. With regard to education about the disease process of chronic musculoskeletal pain, there are severeal patient-driven self-help groups which host helpful websites and meetings. For example, the National Fibromyalgia Association (NFA) is a patient-run nonprofit group and it recommends strongly that fibromyalgia sufferers make many lifestyle accommodations to manage their pain. The NFA endorses vitamin supplements, relaxation–meditation techniques (e.g., yoga, relaxation exercises, breathing techniques, aromatherapy), daily exercise (e.g., gentle aerobic exercise and stretching), avoidance of stimulants (caffeine, sugar, and alcohol), participation in a local fibromyalgia support group, and thermal therapy for pain relief. Of course, the extent to which a patient incorporates these self-directed treatments into daily life will largely depend on the training received and the severity of the problem. Fortunately, patients with focal and even regional myalgia or myofascial pain will have far less disability and life interference.92
This treatment approach also has four elements; it is one of the treatment methods that has little or no hard scientific evidence and is largely based on common sense. For musculoskeletal pain, common sense dictates that, if it hurts, avoid the behavior that causes the pain. In the case of jaw pain, the four elements of avoidance behaviors are as follows:
- Clenching avoidance Clenching avoidance is best done by instructing the patient to hourly find a relaxed position of the jaw, tongue, and lips. The most commonly used instructions to achieve this position are to say the letter N and then hold this position for as long as possible. Additionally patients are told that they should bring their teeth together only when swallowing, eating, or talking and they should practice recognizing when they are clenching their teeth and be more vigilant during these times (such as when they are undergoing emotional stress). Patients are also known to clench when concentrating on a specific task such as driving, watching television, working on the computer, or exercising.
- Poor head and neck posture avoidance The common sense rationale underlying this treatment is that reducing the abnormal strain that bad head and neck posture has on muscles and joints of the spine will reduce upper cervical muscle pain and possibly even jaw muscle pain. The best approach to avoiding bad posture is to teach the patient what is a good posture. This is done by showing the the patient how to keep their head up, with their ears aligned with their shoulders and also to keep their shoulders back so that the head is centered, upright, and relaxed. One commonly used self-treatment exercise to try to achieve good head and neck posture is to ask the patient to sit in a chair and pull their shoulders back at the same time as turning their hands outward. Both the “N”-position exercise and the head-and-neck postural position exercises are performed for a count of 10 (or four slow breaths) and then repeated 5–6 times every 2 hours or at least 6 times a day.
- Jaw joint clicking avoidance Once a temporomandibular disk is out of place it cannot be put back; avoidance of any motion or food that induces clicking is presumed to reduce wear and tear on the disk. Fortunately, the jaw joint can hinge open two fingers’ width (25 mm) without sliding forward, so teaching a patient how to open without clicking is not that hard. First you instruct the patient to put their hands over their jaw joints to feel whether the joint is sliding forward or rotating. Next you insist that the patient only take small food bites and eat only soft foods. For those who have a one-sided click it is also often possible to eat even medium- hard food in one area of the mouth (often on the same side as the click) without inducing a jaw click. To monitor how successful these steps are, the patient should keep track of how many times a day the joint clicks.
- Other habit avoidance This involves having the patient consciously identify and avoid any repetitive habits that might strain or load the jaw muscles and joints, such as wide-open yawning, nail biting, cheek or lip chewing, pen or pencil chewing, gum chewing. ice cube chewing, or even repeatedly snapping the neck vertebrae or opening the mouth to “equalize middle ear pressure.”
Increased Intramuscular Blood Flow Therapy
With regard to self-applied methods of stimulating blood flow in the jaw system, most patients report benefit from either heat or ice packs applied to the painful site. In addition, they will often say they feel better after a hot bath or shower. Many find that a hot bath or shower can be more effective than an analgesic medication for headache, body pain, and stiffness. The local application of heat or ice will both increase circulation and relax muscles in the region. Cold applications rather than heat are preferred by some patients. Although not specific to the masticatory system, a review of the scientific literature on thermal therapy for chronic rheumatic diseases involved 15 published papers which tested thermal and spa therapy on a mixed group of rheumatic diseases.93 The results of this review suggested that this form of treatment produces a consistent positive result. Of course caution must be exercised in those patients who are hypotensive and heat intolerant. The following are specific methods useful to increase blood flow in a patient with jaw and neck muscle pain:
- Thermal (hot bath or shower) therapy Hot bath or shower therapy is a practical and inexpensive treatment method that increases intramuscular blood flow, reduces muscle tension, and generally relieves muscle pain for a period of time. Like avoidance therapy, no study has systematically examined the long-term benefits of 3 weeks of daily 20-minute hot bath soaking for masticatory muscle pain, but this treatment recommendation makes sense. Common sense dictates that bath therapy is a better vasodilator induction method than showers, but for obese patients or patients on hypertension medication, a hot bath increases the risk of causing a lowered blood pressure and precipitating syncope. This therapy should not be initiated in the hypotensive, syncope-prone patient. In general, the hot bath water should be warm enough that the patient does not feel substantial burning when first getting in. This would be about 90°F, depending on the patient’s preference. After entering the tub, add more warm water and let the temperature rise until it is between 103 and 104°F. Duration of the soak, once it reaches temperature, should be 15–20 minutes. Repeat this three times per week for 3 weeks, while conducting the stretching and strict avoidance therapy components of the self-treatment protocol. Alcohol consumption and any opioid medications or any drug that alters blood pressure substantially taken before or during hot bath use should be totally avoided. Individuals suffering cardiac medical conditions such as heart disease, blood pressure and circulatory system problems, or diabetes should check with a physician before using the hot bath; pregnant women can use the hot bath at temperatures below 100°F. In addition to syncope, hyperthermia (heat stroke) is a dangerous condition brought about by excessive heat. It especially affects the very young, the elderly, individuals under the influence of alcohol or drugs, and those who are on certain medications. The symptoms of hyperthermia are sweating, dizziness, nausea, faintness, convulsions, increased pulse rate, and shallow breathing—and, in the extreme, unconsciousness.
- Local hot pack therapy This involves applying a hot pack to the painful />