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<', . . .. . Temporomandibular Joint Dysfurtction · '' ·':" " arid Myofascial Pain Dysfunction Syndromes: : ··· · Parameters, Etiology, and Treatment

( . . Robert A. Moss, James Garrett, and June F. Chiodo·

University of Georgia ·

Temporomandibular joint (TMJ) dykfunction syndrome and myofascial pain dysfunction (MPD) syndrome have been primarily viewed as dental problems and have orily recently received close attention by psychologists. The literature reviewed here reveals that a substantial portion of the population is affected by thClle tflsordtrs. Nevertheless, a great deal of confusion exists in relation to their , , '··. etiology and treatment. This article represents an attempt to clarify the cUrrent· '''#'

understanding of these disorders. It begins with a discussion of the symptoms that constitute. each syndrome and the proposed physiological mechanisms al· sociated with each symptom. The etiological theories for each syndrome are ,,

. reviewed and critically evaluated, aDd treatments that,have been derived from . , . each theoretical model are discussed. Finally, methodological considerations in-.

volving classification, assessment, and treatment are presented, and future re-. se~rch needs are outlined.

Myofascial pain dysfunction (MPD) syn­dl'Ohltand temporomandibular joint (TMJ) dysfunction syndrome have become topics of increasing interest in the psychological field over the past two decades. This increas­ing interest may be attributable to the fact that these disorders affect a large portion of the population (Helkimo, 1976), and the etiologies of these disorders are not yet clearly defined (McNeil et al., 1980; Mikhail & Rosen, 1980).

The first comprehensive description of . symptoms involving the temporomandibular jOint was· :presented by an otolaryngologist named Costen in 1934. On the basis of a sample of 11 subjects, he identified a number of symptoms including impaired hearing, dizziness, tinnitus, headache, popping noises in the TMJ, stuffiness, earache, dryness of tbo mouth, and burning sensation of the tongue and throat. This constellation of symptoms became known as .. Costen's syn­drome." Over the years, various authors pro­posed additional symptoms associated with

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the syndrome; others proposed the exc:lusiolf of certain other symptoms originally de- . scribed by Costen (Rugh & Solberg, 1976). The term Costen's syndrome eventually· fell into disuse and was replaced by th~ term TMJ dysfunctidn syndrome.

In their review· of the TMJ dysfulletibtt literature, Rugh and Solberg ( 1976) found some consensus on three symptoms that con· stitute TMJ dysfunction syndrome: (a) pain · and tenderness of the muscles of masti­cation and the TMJ, (b) sounds during con­dylar movements (i.e., popping, clicking, or crepitus of the jaw), and (c) limitati6111·of mandibular movements. Currently, the di­agnosis of TMJ dysfunction may be made when one or more of these symptoms is pres• ent, but it cannot be made on condylar move­ment sounds alone (Laskin, 1980; Rugh cl Solberg, 1976). Other symptoms such u sublaxation/dislocation of the mandible; tin­nitus, and dizziness may also be priRnt (Greene, Lerman, Sutcher, & Laskin, 1969) but are not considered necessary for the di­agnosis of TMJ dysfunction syndrome; · ·

The term MPD syndrome was originally proposed to identify a subgroup of TMJ pa-: . ' ' tients whom Laskin (1969) thought repre-' sented the majority of patients teporting

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pain and dysfunction ~ttle~inastica:tory sys- ployed in a Swedish shipyard. These authors tern. The criteria for MPD included the com- reported that 79% of the subjects had some moo TMJ dysfunction symptoms with the TMJ-related muscular symptoms, and 30% exception that pain is unilateral. In addition, had two or more such symptoms. The most

· two other criteria should be met: (a) absence frequent symptom was clicking of the tern­of clinical or radiographic evidence of or- poromandibular joint, which was found in ganic changes in the TMJ and (b) lack of 65% of the subjects. tenderness in the TMJ when this area is pal- Following a review of the epidemiological pated in the external auditory meatus. studies of masticatory symptom dysfunction,

During the course of our review of the Helkimo {1976) concluded that no apparent literature, it became evident that a great deal sex differences occurred in the frequency of of confusion exists regarding the differential dysfunction in the general population. Only diagnosis ofTMJ dysfunction and MPD syn- one study (Solberg, Woo, and Houston, dromes. Specifically, the terms have been 1979) reported slightly higher levels of used synonymously by some authors, which symptoms in women. Helkimo also con­presents problems in cross-study compari- eluded that the symptoms of mandibular sons. lh addition, there is a paucity of re- dysfunction were found in all age groups, search on the validity of differentiating be- with a slightly greater frequency in older tween TMJ dysfunction syndrome and MPD individuals. syndrome patients in terms of etiology and Clinic populations show two interesting differential responsiveness to treatments. discrepancies from the epidemiological data. Moreover, the present classification system The first is a fairly consistent agreement on for both disorders requires the presence of a sex-distribution difference. A number of only one of the three basic symptoms com- studies have reported that the majority moo to both disorders. As a result, hetero- ( 65%-80%) of the clinical patients are fe­geneous populations could have the same male (Campbell, 1958; Carraro, Caffesse, diagnosis (Greene et al., 1969 ), or, if the & Albano, 1969; Franks, 1965b; Gelb, Cald­additional criteria for MPD syndrome have erone, Gross, & Kantor, 1967; Schwartz been ignored, homogeneous populations could & Cobin, 1959; Thompson, 1959; Weinberg have different diagnoses. Therefore, any con- & Lager, 1980). Second, there appears to elusions drawn on the basis of prior research be fairly consistent age distribution, with the must be regarded cautiously. Although we 20-40-year-old group predominating (Car­acknowledge the problems concerning the raro et al., 1969; Franks, 1965b; Schwartz differential diagnoses of TMJ dysfunction & Cobin, 1959; Weinberg & Lager, 1980). and MPD syndromes, we report studies ac- The reasons for these discrepancies are un­cording to the diagnoses given by the original clear and require further systematic inves-authors. tigation.

Incidence Rate

Though· the exact nature of MPD and TMJ dysfunction syndromes is poorly de­fined, a number of studies have evaluated the existence of specific symptoms in various populations. Thiel ( 1970) examined 500 oral surgery patients and found that 52% pro­duced TMJ sounds, and 5% complained of facial pain. In a group of 269 young dental nurses Posselt ( 1971 ) found that 41% exhib­ited TMJ sounds, and 6% reported facial pain. Using a larger subject sample, Hansson and Nilner (1975) examined 1,069 persons ranging in age from 20 to 65 who were em-

Symptom Mechanisms

Pain

The most common complaint in clinical patients is pain (Greene et al., 1969 ). Clin­ical descriptions of the reported pain vary considerably. The pain is most often reported to be unilateral (Christensen, 1981 ), al­though bilateral pain is common (Weinberg, 1980a; Weinberg & Lager, 1980). The qual­ity of pain is usually a dull ache, although it can become sharp and acute (Meklas, 1971; Weinberg, 1980a). Further, the locations of the pain may range from the back of the head and neck to the temporal

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TMJ /MPD SYNDROMES 333

area to the angle of the jaw, with the most frequently cited location being the area in front of the ear (Bell, 1969; Laskin, 1969; Perry, 1957; Weinberg & Lager, 1980). Fi­nally, variations in the pain patterns over time may differ. Some authors (e.g., Laskin, 1969; Toller, 1976) suggest that for most patients pain is most intense in the morning; others (e.g., Perry, 1957) report that pain is minimal in the morning and progresses and intensifies in the course of the day.

The first theory addressing the physiolog­ical basis fot facial pain was proposed by Costen (1934). He hypothesized that facial, muscle, and joint pain resulted from pressure applied by the TMJ on articulotemporal and chorda tympani nerves. These pressures were considered to occur because defects in the dental occlusion permitted the mandible to overclose. In a review questioning Costctn's hypotheses, Zimmerman ( 1951) reported that it was anatomically improbable for the chorda tympani to be affected; moreover, even if affected, this nerve failed to contain fibers that could produce the described pains. Zimmerman suggested that the sensory end­ings of the articulotemporal nerve located in the posterior portion of the capsular lig­ament could produce pain owing to posterior condylar displacement. Sieber (1955), how­ever, maintained that direct condylar pres­sure on the articulotemporal nerve was un­likely. He proposed that the pain results from pressure applied to the sensitive soft tissue posterior to the condyle. More re­cently, Weinberg (l979a) suggested that su­perior condylar displacement can cause pain as a result of compression of nerve fibers located in the periphery of the articular disc. In relation to anterior condylar displace­ment, Ram fjord and Ash ( 1966) reported that pain can be caused by pressure applied to the articular disc if it is caught between the condyle and articular eminence. Finally, Weinberg (1979b) suggested that inflam­mation of the capsular ligament may be an additional source of pain.

The hypothesis that spasm in the muscles of mastication is responsible for the pain was originally proposed by Schwartz ( 1955, 1956, 1958) and continues to be advocated by many investigators (e.g., Chaco, 1973; Grif­fin & Munro, 1971 ). The masticatory mus-

cles implicat~ include the masseter, tem­poral, medial pterygoid, and lateral ptery­goid. Others that may be associated with the syndromes include the sternocleidomastoid and trapezius muscles (Sharav, Tzurkert, & Refaeli, 1978). Travell (1960) reported that the involvement of each of these muscles is capable of directly or indirectly (i.e., re­ferred pain) producing the pain associatCld with these symptoms. The lateral pterygoid is the muscle most frequently found to be tender and painful (Franks, 1965b; Sharav et al., 1978). Furthermore, Sharav et al. (1978) presented some data suggesting that dizziness may be related to problems of the sternocleidomastoid.

Yemm (1976) criticized the muscle spasm hypothesis, as he observed no difference· in right and left masseter electromyographic (EMG) levels during experimental stress tasks, even when one of the muscles was painful and tender. He contended that only a portion of the muscle may be damaged and that this region may not be aligned with muscle fibers. As a result, tenderness might be expected to be distributed along the whole length of fibers. Although Yemm's propo­sition is interesting and other authors (A wad, 197 3; Rais, 1961) have suggested the exis­tence of microtraumatic lesions within the muscles, tendons, and joints, no objective evidence has been produced to support this hypothesis. Furthermore, Yemm's failure to find elevated masseter EMG levels may have been because masticatory muscles other than the masseter could have been the source of spasm and pain.

Another hypothesis of the pain mecha­nism is based on the TMJ analogue study by Christensen ( 1971 ). Christensen observed an increase in fluid pressure following 30 minutes of unilateral grinding by non-TMJ f MPD subjects and suggested that edema fol­lowing sustained muscle contraction may be the cause of pain (Christensen, 1975). Yemm (1976) stated that edema arises from in­creased capillary permeability and is a con­sequence of inflammation. In an investiga­tion of an inflammatory state in TMJ dys­function syndrome patients, Betry and Yemm (1971, 1974) measured infrared emission and found that the skin overlying the tender region of the masseter muscle was

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334 R. MOSS, J. GARRETT, AND J. CHIODO

hotter than that of the corresponding area on the opposite side. They interpreted this as an indication of locally raised blood flow· due to inflammation. These differences be­tween clinically normal and abnormal sides tended to diminish during treatment and were reported to have disappeared shortly after the symptoms cleared.

No conclusions have been reached about the physiological mechanisms . responsible for pain in MPD and TMJ dysfunction syn­dromes. Each mechanism proposed must be viewed cautiously because it is improbable that one explanation can accommodate the wide range of reported differences in the location, quality, and temporal variations of the pain. Furthermore, complete under-· standing of an individual's perception of pain probably cannot be achieved within a strictly physiological framework. Other factors such as anxiety, attention, suggestion, and 'prior learning history appear to be related to pain perception (Christensen, 1980; Melzak, 1974; Sternbach, 1968) and thus warrant atten­tion.

Sounds During Condylar Movements

Another commonly observed symptom is sounds during condylar movements (Greene et al., 1969 ). The sounds occur in the TMJ and are diagnosed by listening with a stetho­scope while the patient opens and closes his or her mouth. The noises have been de­scribed as clicking, popping, and crepitus (Weinberg, 1980a).

Vamvas (1977) reported that clicking of the TMJ is the result of the condylar head colliding with the edge of the articular disc at the beginning or end of mandibular open­ing and closing. In normal opening, the con­dylar head always holds a constant relation to the central part of the disc such that the disc moves forward with the condylar head during the opening of the qtouth. Toller ( 1976) suggested that a frictional impedi­ment may occur between the condyle and the meniscus during early rotational move­ments, giving rise to hesitations in the move­ment of the articular disc in the joint as a whole. Therefore,

the initial opening movement of the jaw would be ac­companied by a small forward slide in the upper joint

cavity while the meniscus remains stuck to the c:otldyle. On further opening in the jaw the friction between the condyle and disc would suddenly be overcome, and rather strangely this would necessitate the disc slipping back suddenly in relation to the condyle. (p. 74)

The clicking noise would be the result of this process.

Weinberg (1980a) considers clicking that immediately follows opening and closure of the teeth to be the result of posterior dis­placement of the condyle on the affected side. He also considers the mechanism of the popping sound to be the same as that de­scribed by Toller (1976) and Vamvas (1977) in their discussion of clicking (i.e., slipping of the articular disc). Weinberg questions whether the change in the motion of the disc is caused by weakening of the attachment of the disc to the lateral and medial surfaces of the condyle and/or by uncoordinated function of the superior and inferior heads of the lateral pterygoid muscle. He reports that, anatomically, popping is associated with hypermobility of the condyle anteriorly. Finally, he reports that a crepitus sound is associated with perforations in the disc. There is some evidence that crepitus sounds are frequently associated with degenerative joint disease (Clark & Solberg, 1977; Mof­fett, Johnson, McCabe, & Askew, 1964). Weinberg further reports, on the basis of TMJ radiographs, that crepitus is frequently . associated with reduced joint spaces.

In conclusion, the direct causes of the changes in the disc and its motion have not been conclusively demonstrated (Toller, 1976; Weinberg, 1980a). There is also dis­agreement on the sounds (i.e., clicking vs. popping) associated with posterior and an­terior displacement of the condyle. This distinction is important because Wein­berg ( 1980b) suggested differential occlusal treatment for posterior and anterior dis­placement.

Limitations of Mandibular Movements

The symptom of limited mandibular movements can be classified into two cate­gories: restricted mouth opening (trismus) and deviations during mandibular move­ments. Toller (1976) suggested that trismus may be closely related to the mechanisms

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involving TMJ noises. He contends that tris­mus may result from a failure of a full for­ward sliding of the articular disc in the upper joint compartment. Thus, restricted mandib­ular movement results from the failure of the disc to slide fully down and over the em­inence articularus. Toller described this lim­ited opening as a "sort of undischarged click" that frequently occurs at the stage in mouth opening at which the click is normally observed.

Farrar ( 1978) contends that locking of the jaw results from the disc's being dislocated anteriorly. Bell (1969) suggested several ad­ditional causes of trismus other than jam­ming of the articular disc, including (a) shortened elevator muscles due to spasm, inflammation, and contracture; (b) ankylosis due to "fibrous adhesions or calcifications that join the articular surfaces; and (c) capsular ligament restriction due to inflammation or capsular fibrosis. In support of muscular in­volvement Sharav et al. (1978) found a di­rect relation between trismus and muscle pain, particularly pain associated with the medial pterygoid muscle. Thus, several dif­ferentmechanisms are implicated in trismus. Deviations during mandibular movements are not as frequently discussed in the liter­ature, although there appears to be some consensus that muscle spasms are probably responsible for this symptom (Bell, 1969; Day, 1977).

Given the variety of mechanisms proposed to account for each symptom, it is easy to understand the confusion over whether the TMJ or the masticatory muscles may be the originating factor in the facial pain dys­function syndromes. On the basis of the hy­pothetical causes of each symptom, several distinct etiological theories have been pro­posed to account for the constellation of symptoms observed in these syndromes. These theories can be divided into two groups: (a) theories advocating the TMJ as the originating factor and (b) theories re­garding muscular hyperactivity as the pri­mary causal factor.

Etiological Theories

Many authors (e.g., Laskin, 1969; Wein­berg, 1979a) suggest that TMJ dysfunction

syndrome is, by definition, associated with pathology of the TMJ. In like manner, MPD syndrome is concerned with abnormally in­creased and sustained muscle activity as the primary cause. Despite the problems asso­ciated with classifying these syndromes, we treat them from a theoretical standpoint as distinct and separate syndromes.

TMJ Dysfunction

A number of disorders unrelated to the TMJ result in pain that may resemble TMJ dysfunction syndrome. These disorders in­clude trigeminal neuralgia, cervico-occipital neuralgia, glossopharyngeal neuralgia, neo­plasm, vascular disorders (i.e., migraine, temporal arteritis), certain ear infections, diseases of the salivary glands, and sinusitis. A discussion of the differential diagnosis of these disorders has been presented elsewhere (Christensen, 1981; Rowe, 1977; Weinberg, 1979a).

Disorders of the TMJ include osteoar­throsis, rheumatoid arthritis, and condylar displacement (Carlsson, 1980; Weinberg, 1979a ). Osteoarthrosis has been defined as "a primarily non-inflammatory disease char­acterized by both deterioration and abrasion of the articular soft tissue surface and by simultaneous remodeling processes in the underlying bone" (Carlsson, 1980, p. 658 ). The disease usually affects the· center of the joint(s) and emanates peripherally. In TMJ problems, osteoarthrosis is most often uni­lateral. Crepitus sounds usually occur early in the course of the disease, and the diagnosis is made on the basis of radiography (Wein­berg, 1979a). Carlsson ( 1980) reported that the prevalence of osteoarthrosis in all joints increases with age, although the epidemiol­ogy of the disease in the TMJ is not known. Schwartz and Cobin (1959) studied 491 TMJ patients and noted that arthritis and neurologic conditions were present in only 8%. In patients seeking treatment for TMJ dysfunction, Kopp and Rockier ( 1978) found radiographic signs of osteoarthrosis in 20% of those examined. In relation to these stud­ies, Carlsson ( 1980) believes that there may have been many more cases of undiagnosed incipient osteoarthrosis because the disease had not progressed to the point allowing a

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diagnosis to be made radiographically. Al­though there appears to be strong support for the presence of osteoarthrosis in a large portion of TMJ dysfunction patients, a com­parable percentage of symptom-free patients (i.e., no TMJ dysfunction symptoms) also show radiographic evidence of osteoarthrosis in the TMJ (Ericson & Lundberg, 1968).

Another proposed cause of TMJ problems is rheumatoid arthritis. Rheumatoid arthri­tis involves the conversion of synovial cells to panus cells that secrete an enzyme that erodes the articular surface (Weinberg, 1979a). This process is associated with acute inflammation of the marrow spaces. In con­trast to osteoarthrosis, the pathological pro­cess erodes from the periphery toward the center and is usually bilateral. Other joints of the body are usually affected first (Wein­berg, 1979a); only rarely is the TMJ the first site to be affected (Carlsson, 1980). Diag~ nosis of rheumatoid arthritis is often difficult because erosive changes are usually not vis­ible radiographically during the first year of the disease (Carlsson, 1980 ).

The final theoretical cause of the symp­toms associated with TMJ dysfunction is condylar displacement in the glenoid fossa. Displacement may result from trauma, mal­occlusion, or certain oral habits such as bruxism. Trauma producing condylar dis­placement may result from direct blows to the mandible, iatrogenic effects associated with surgical and dental procedures in and around the mouth, and whiplash (Vamvas, 1977). Vamvas (1977} reported that the in­jury may be transitory or long-term joint symptoms may develop should permanent damage to the meniscus occur.

Malocclusion bas been one of the most frequently cited causes of both condylar dis­placement and masticatory muscle disor­ders. The relation between malocclusion and muscle disorders is discussed in the following section. In relation to TMJ problems, it has been proposed that malocclusion of the teeth results in mandibular displacement, usually in the posterior direction, and can cause compression of sensitive soft tissue. Contin­ued compression of this tissue could result in pain· as well as impairment of the blood supply to joint structures. This compression, therefore, could lead to degenerative changes

(Laskin, 1969). Support for the proposal that condylar displacements occur as a func­tion of malocclusion is drawn from two areas: (a) the finding that many TMJ dysfunction patients have malocclusion .(Ramfjord, 1961; Krogh~Poulsen & Olsson, 1968) and (b) the finding that alteration of occlusion is followed by clinical improve­ment in a high percentage of patients (Kopp, 1979; Perry, 1957).

Several criticisms of the malocclusion the­ory have been made. For instance, evidence about the relation between malocclusion, side of tooth loss, and the laterality of joint disturbance is contradictory (Franks, 1967; Thomson, 1971; Toller, 1976). Malocclusion has been suggested as a factor that may lead to destructive oral habits, such as bruxism, that may be related to TMJ dysfunction (Beyron, 1969; Graber, 1969; Meklas, 1971; Ramfjord, 1961), but this proposition has been criticized on the ground that not all bruxists have malocclusion and not all in­dividuals with malocclusion are bruxists (Glaros & Rao, 1977; Schultz, 1968; Thompson, Geiger, Wasserman, & Turgeon, 1972). Finally, the studies of altered occlu­sion in the treatment of TMJ dysfunction syndrome have largely been uncontrolled, as will be detailed later.

Despite the tenuous support for malocclu­sion as a causal factor in condylar displace­ment, Weinberg (l979c) maintains that the conflicting nature of prior research may be due to the lack of an operational definition of malocclusion. He argues that the criteria for malocclusion have never been satisfac­torily determined. Thus, Weinberg suggests that future studies provide an operational definition of malocclusion that includes ra­diographic evaluation of each condyle.

The final proposed cause of condylar dis­placement is destructive oral habits includ­ing nocturnal and diurnal bruxism; lip and lateral tongue biting; chewing on pens, pen· cils, or pipe; cupping the chin in the hand or resting the head with the hand on the side of the face; and playing musical instruments (e.g., violin, clarinet, trumpet) that require certain mouth and chin positions (Day, 1977). Of these, only nocturnal bruxism has received any degree of empirical support as being related to TMJ dysfunction syndrome.

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Toller (1976) estimated that approximately 40% of TMJ dysfunction patients exhibited nocturnal bruxism. oit the basis of dental examinations and self-report, Lupton (1966) reported that 77% of the TMJ patients were bruxists. In a better controlled study, Tren­outh ( 1979) compared three groups of sub­jects: A TMJ /bruxism group of 9 patients, a TMJ fnonbruxism group of 6 patients, and a non-TMJ /non bruxism group of l 0 student volunteers. Bruxism was diagnosed on the basis of tooth wear (Franks, l965b ). Brux­ism was operationally defined as the fre­quency and duration of tooth contact as measured by two stainless steel bands that were placed on opposing incisor teeth. The results indicated that the TMJ /bruxism group had significantly more frequent tooth contact than did the non-TMJfnonbruxism group.

Although these results suggest a relatipn between· nocturnal bruxism and TMJ dys­function syndrome, the operational defini­tion of bruxism in this study is of question­able validity. Reding, Zepelin, Robinson, Smith, and Zimmerman ( 1968) suggested that rhythmical bursts of electromyographic (EMG) activity were highly correlated with nocturnal bruxism, but forcible tooth con­tacts were not. Furthermore, using an op­erational definition of bruxism consisting of rhythmical EMG activity, Moss et al. ( 1982) found that a conditioning procedure effec­tively reduced nocturnal bruxism. In con­trast, DeRisi ( 1970) failed to reduce brux­ism using a conditioning procedure when tooth contacts were used as the operational definition of bruxism. Therefore, in the ab­sence of any measure of rhythmical EMG activity as a definition of bruxism, studies supporting the relation between nocturnal bruxism and TMJ syndrome must be re­garded cautiously.

The association between diurnal bruxism and TMJ dysfunction syndrome has received some attention. Moss, Wedding, and Sand­ers (in press) found, on the basis of self-mon­itored teeth clenching, that only one of five chronic . TMJ patients exhibited diurnal bruxism. Solberg and Rugh (1972) reported that 15 facial pain patients who frequently exhibited diurnal bruxism were unaware of its occurrence. When wearing a portable

EMG feedback device, the patients reported clenching their teeth during stressful events. Unfortunately, no measures of the frequency and duration of diurnal bruxism were ob­tained. As with nocturnal bruxism in TMJ dysfunction, the relation between diurnal bruxism and TMJ problems is inconclusive.

Masticatory Muscle Hyperactivity

Theories related to muscular hyperactivity are, by definition, associated with MPD syn­drome. Support for muscular involvement in facial pain has been drawn from studies in three basic areas: (a) studies that have in­duced pain similar to that of MPD syndrome in non-MPD patients via sustained contrac­tion of the masseter (Christensen, 1975) and the lateral pterygoid muscles (Scott & Lun­deen, 1980 ); (b) EM G assessment studies, which have reported elevated EMG activity levels in the masticatory muscles of TMJ patients (Chaco, 1973; Jarabak, 1956; Kydd, 1959) and increased periods of no EMG ac­tivity (i.e., .. silent periods") in the masti­catory muscles following the .. jaw jerk re­flex" (Bessette, Bishop, & M obi, 1971 ; Bes­sette, Mohl, & DiCosimo, 1974; McCall, Gale, & Uthman, 1981; Skiba & Laskin, 1981); (c) studies that have used treatment (e.g., EMG biofeedback) specifically de­signed to reduce masticatory muscle activity.

The theoretical approaches in the expla­nation of masticatory muscle hyperactivity can be divided into two categories: those that suggest a local cause and those that suggest a centrally mediated cause.

Local causes. The local factors that have been identified as possible causes of mus­cular hyperactivity are' essentially identical to those associated with condylar displace­ment in TMJ dysfunction. These include trauma and malocclusion that result in brux­ism. Many of the same criticisms of these proposed causal factors of condylar displace­ment also apply to muscular hyperactivity. In addition, another body of evidence ad• dresses the question of whether malocclusion can produce a sensory input arising from the periodontal mechanoreceptors that can re­sult in a long period of hyperactivity of the jaw closing muscles. Yemm (1976) pre­sented an extensive review of the literature

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related to this question and concluded that the evidence supports an inhibition instead of excitation of jaw closing muscles resulting from stimulation of the periodontal mecha­noreceptors.

On the basis of the experimental evidence, local factors other than trauma appear un~ likely to be the cause of increased mastica­tory muscle hyperactivity. This has led to the suggestion that muscular hyperactivity may originate centrally in the nervous sys­tem (Berry, 1967; Copeland, 1954; Yemm, 1976).

Centrally mediated causes. The most frequently cited cause of central activation of masticatory muscle hyperactivity is psy­chological and/or physical stress (Berry, 1967; Copeland, 1954; Franks, 1965b; Yemm, 1976), Support for this hypothesis has been provided by (a) studies of stress in MPD populations and (b) studies that have attempted to induce stress experimentally and to measure the physiological reactions of MPD patients.

Two studies found a high incidence of psy­chophysiological disorders in MPD syn­drome patients. Berry ( 1969) noted an in­cidence rate of migraine headache and back­ache that was I 0 times higher than that reported in prior studies of normal popula­tions. Similarly, Gold, Lipton, Marbach, and Gurion (1975) found that compared with a group of non-MPD controls, MPD syndrome patients reported more frequent low back and neck pain, nervous stomach, asthma, and history of ulcers. In a study of biochem­ical indications of stress, Evaskus and Laskin (I 972) examined urinary concentrations of catecholamines and 17-hydroxy steroids in a group of MPD patients and non-MPD con­trols and found that the MPD patients had significantly higher concentrations of both substances than did the controls. Although these results suggest that a stress factor is associated with MPD syndrome, causal fac­tors cannot be ascertained from correlational studies. Some studies (Franks, 1965b; Moody, Calhoun, Okeson, & Kemper, 1981; Weinberg & Lager, 1980) have inconclu­sively related stress levels of MPD patients with symptom onset and maintenance. These studies have relied on retrospective self-re­port of patients, a method that is subject to

- a number of problems (e.g., omissions, con­fabulations).

Two studies have attempted to induce stress directly in experimental situations while monitoring the physiological changes in facial pain populations. Yemm (1969) reported that normal subjects exhibit a ten­dency to reduce EMG activity across ~xper­imental trials, whereas no such reduction was observed with TMJ patients. Mercuri, Olson, and Laskin (1979) compared the physiological effects of laboratory stress in 20 MPD patients and 20 non-MPD controls and found that the MPD patients had sig­nificantly higher masseter and frontalis EMG activity. The authors concluded that the re• suits supported the existence of a response­specific reaction to stress in MPD patients. Unfortunately, these studies suffered frotn a number of methodological flaws: the ab­sence of adaptation periods for physiological stabilization, the use of motor tasks that re­quired head and/or eye movement, a lack of controls for EMG movement artifacts, and the use of questionable statistical pro­cedures (e.g., multiple t tests).

Centrally mediated causes of masticatory pain and dysfunction other than those re­lated to stress have been suggested. One group of studies is based on classical psy­choanalytic theory about facial pain. Dun­bar ( 1935 ), Engel ( 1951 ), Lefer ( 1966), and Moulton (1955) contend that TMJ dysfunc­tion is best explained as an hysterical con­version reaction resulting from an individ­ual's unconscious emotional conflicts. But because classical psychoanalytic theory has yielded neither experimentally verifiable ex­planations nor replicable treatment meth­odologies (Rugh & Solberg, 1976), any ap­plication to TMJ /MPD patients must be considered tenuous.

A number of studies have attempted to determine personality correlates for facial pain patients. Such studies have described patients as anxious (Kydd, 1959; Schwartz, 1974; Shipman, 1973), perfectionistic(Lesse, 1956), domineering (Greider, 1973; Lupton, 1969 ), narcissistic, responsible; autocratic, overgenerous (Lupton, 1966), emotional, neurotic (Gross & Vacchino, 1973), as well as insecure, hostile, aggressive (Molin, Ed­man, & Schalling, 1973). As Rugh and Sol-

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·berg (1976) emphasized, these studies are correlational in nature and thus exclude causal influences. ~n addition, many of the dependent measures that are used show low levels of diagnostic reliability and validity.

·Finally, there is disagreement regarding specific personality characteristics related to TMJ fMPD patients. Other studies (Schwartz, Greene, & Laskin, 1979; Sol­berg, Flint, & Brantner, 1972) have reported that the MMPI profiles of facial pain pa­tients as a group are within normal limits.

A final area of study related to centrally mediated causes of MPD syndrome is the evaluation of threshold/tolerance levels of experimentally induced pain. Out of three studies of pain tolerance (Lupton & John­son, 1973; Mercuri et al., 1979; Molin et al., 1973), only Molin et al. (1973) reported quantitative scores of comparisons between MPD patients and non-MPD controls. Using noxious electrical stimulation that was ·in­creased in discrete steps, Molin et al. found that MPD patients demonstrated signifi­cantly lower pain thresholds than did the controls. There was no significant difference between groups in pain tolerance. Although this area of investigation is potentially valu­able, no conclusions can be drawn regarding the differences in pain perception in MPD patients on the basis of these limited data.

Conclusions on Etiological Theories

There is a paucity of methodologically sound studies of all the etiological theories. Thus, as each theory lacks strong empirical support, advocacy of any one theory is pre­mature. Quite possibly, several of the theo­ries may be correct for certain portions of this patient population. The current classi­fication system (i.e., TMJ dysfunction vs. MPD), however, may result in heteroge­neous populations with the same diagnosis, which would necessarily complicate the identification of specific etiologies. In addi­tion, the intimate relation between the mas­ticatory muscles and the temporomandibu­lar joint as a functional unit presents further complications because dysfunction of the TMJ can reportedly occur secondarily to masticatory muscle hyperactivity and vice versa (Weinberg, 1979c). These problems

have led to the position of several authors (Rugh & Solberg, 1976) that TMJ dys­function and MPD syndromes are best viewed as the result of a number of inter­locking factors of occlusal, neurophysiolog­ical, and psychological origin. Within the current classification system, a multifacto­rial view of etiology seems to be the most · useful and reasonable approach. Neverthe­less, through 'the application of a more em­pirical classification scheme, distinct etiolo­gies might become apparent. This issue is addressed more fully following a review of the treatment studies.

Treatment

A number of· treatments have been ad· vocated for TMJ /MPD patients. Each treat­ment is rooted in at least one of the previ­ously described etiological theories. For the sake of parsimony, these treatments are di­vided into dental and psychological ap­proaches.

Dental Approaches

A widely recommended treatment in­volves the use of occlusal appliances (Beard & Clayton, 1980; Carraro & Caffesse, 1978; Greene & Laskin, 1972). Courant (1967) advocated the use of occlusal splints, or bite · guards, in the treatment of TMJ dysfunction syndrome because the coverage of occlusal surfaces by the splint distributes the forces of nonfunctional movements (e.g., bruxism) to a maximum area of tooth support. Theo­retically, this procedure prevents excessive movement by individual teeth and helps oc­clusal trauma. Some support has been fur­nished to show that occlusal splints reduce masticatory muscle activity. Kawazoe, Ko­tani, Hamada, and Yamada (1980) reported that masseter muscle activity was signifi­cantly reduced during maximal clenching in MPD patients wearing a biteplate. In a study of nocturnal muscle activity, Fuchs (197 S) reported significantly greater levels of mas­seter EMG activity in TMJ patients than in non-TMJ controls; this difference became nonsignificant when the TMJ patients wore occlusal splints during the night.

Another dental procedure used in the .. ..,.

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340 R. MOSS, J. GARRETT, AND J. CHIODO

treatment of TMJ /MPD problems is equil­ibration (Franks, 1965a; Kopp, 1979; Perry, 1957). Equilibration procedures involve the selective grinding and restoration of teeth as an attempt to restore optimal occlusion (Beyron, 1969). The final procedure involves the use of various medications ,(e.g., diaze­pam, meprobamate, amitriptyline) to reduce .anxiety andfor muscle tension (Cohen, 1978; Gessel, 197 5; Greene & Laskin, 1971).

On the basis of the treatment studies, the dental procedures appear to be effective in reducing or eliminating facial pain and man­dibular dysfunction in the majority of TMJ f MPD patients. On closer inspection, how­ever, this body of research is rather poorly controlled. The influence of placebo effects for each of the treatments has been dem­onstrated (Goodman, Greene, & Laskin, 1976; Greene & Laskin, 1972; Laskin & Greene, 1972 ), but the majority of studies have failed to include controls fqr placebo effects. Furthermore, the uncertain course of symptoms and the lack of adequate fol­low-up are major issues that have not been addressed in many of these studies. There­fore, any definitive statements of the differ­ential effectiveness of these treatments is im­possible at the present time.

Psychological Approaches

Because TMJ dysfunction syndrome has been interpreted as a conversion reaction, psychoanalysis has been recommended to identify the underlying emotional conflicts. Several descriptive studies have been re­ported (Engel, 1951; Lefer, 1966; Moulton, 1966), but controlled outcome studies are unavailable.

Another psychological approach has been use of EMG biofeedback and progressive muscular relaxation training, the assump­tion being that muscle hyperactivity is the cause of pain and dysfunction. Three studies have used progressive relaxation training either alone (Gessel & Alderman, 1971) or in combination with other treatments (Moss et al., in press; Stenn, Mothersill, & Brooke, 1979). Each has provided limited support for this procedure. A number of studies have used EMG feedback either to reduce mas­seter, temporal, and frontalis EMG levels

1

(Carlsson & Gale, 1976, 1977; Carlsson,· Gale, & Ohman, 1975; Gessel, 1975; Moss et al., in press; Olson, 1977; Peck & Kraft, 1977; Stenn et al., 1979) or at night to re­duce bruxism (Clarke & Kardachi, 1977). Of these, only two (Moss et al., in press; Peck & Kraft, 1977) failed to support the use of EMG feedback. What is important, however, is that the study by Moss et al. (in press) was one of the few to u·se exper­imental controls.

Several methodological criticisms of these studies have been offered by Scott and Gregg ( 1980): (a) There is little evidence to suggest that reduced pain ratings of patients were accompanied by lower EMG levels; (b) de­pendent measures have been restricted to self-reported changes in pain and have ex­cluded other symptoms (i.e., joint sounds and trismus); and (c) few studies have used placebo control groups. In addition, there has been a lack of follow-up data allowing for further analysis of treatment effective­ness. As with the dental treatments, no firm conclusions can be drawn regarding relax­ation training and EMG feedback except that these procedures appear to be effective with some TMJ /MPD patients.

Methodological Considerations

Classification Issues

A number of the confusing aspects of ' MPD and TMJ dysfunction syndromes may well be the result of the classification scheme used to define them. The scheme is disjune .. tive and requires only one or more of the three basic symptoms to be presertt for the diagnosis of each syndrome. Pain is consid­ered one category, although the descriptions of quality, location, temporal patterns, and chronicity vary widely between patients with the same diagnosis. Although different mechanisms may be associated with the tem­poromandibular joint sounds or popping, clicking, and crepitus, all of these symptoms are similarly classified within the TMJ dys­function or MPD syndrome diagnosis. Therefore, it is obvious that a number of patients can have one or more similarly clas­sified symptoms that possibly represent dif­ferent causal mechanisms. Finally, other symptoms (e.g., dizziness, tinnitus) may be

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TMJ/MPD SYNDROMES 341

present, although they have no particular influence on differential diagnosis or impli­cations for alternative or supplemental forms of treatment.

There is clearly a need for a more useful and reliable classification scheme for dys­function and pain associated with the mas­ticatory system. One approach is to classify operationally defined symptoms into con­junctive categories (cf., Adams, Doster, & Calhoun, 1977). Thus, separate symptoms would constitute mutually exclusive and

. jointly exhaustive categories. Combinations of symptoms could be evaluated in a similar fashion by requiring that each symptom be present before a specific diagnosis can be made. Within such a system, care should be taken to ensure the reliability of the opera­tional definition of each symptom. This would permit clear comparisons to be made between studies. Such a classification system would allow for the identification of homo­geneous populations. Once accurately iden­tified, investigation of these homogeneous populations may reveal the existence of sep­arate etiologies and differential responsive­ness to various treatments. Results could be better evaluated to determine the utility for each of the separate diagnostic categories. Eventually, it might become possible to com­bine the diagnostic categories on an empir­ical basis and, thereby, to yield a few specific categories that differ qualitatively.

Assessment Issues

The assessments for each symptom cate­gory are of extreme importance for two rea­sons. First, they permit a clear definition of a symptom; second, they allow evaluation of various treatments. Each symptom reported by TMJ /MPD patients should be thor­oughly assessed at both a subjective and an objective level. Subjective assessment tech­niques rely on retrospective and self-moni­tored reports. Objective techniques include dental examination for occlusion, muscle tenderness, and mouth-opening distance; ra­diographic tests; EMG assessments of most or all of the masticatory muscles; and reports from significant others (e.g., spouse).

The variables of interest when assessing pain include intensity, temporal patterns,

recurrence, and qualitative characteristics (e.g., dull, throbbing). In addition, objective pain behavior can be assessed and include somatic interventions (e.g., medication in­take), impaired functioning, and both verbal and nonverbal pain behavior (Frederikson, Lynd, & Ross, 1978 ). The variables of in­terest in relation to joint sounds include qualitative descriptions, frequency, temporal patterns, and the point at which these symp­toms occur in relation to mouth opening and closing. All other symptoms (e.g., dizziness) should be assessed in similar fashion .

The assessment of stress in. TMJ /MPD patients has been addressed by Haber, Moss, Kuczmierczyk, and Garrett (in press). These authors suggest that both the antecedents and consequences of pain be monitored in an attempt to elucidate precipitating and maintaining factors for changes in reported pain levels. This necessitates a careful as­sessment of positive and negative reinforce­ment of the pain behavior. Such assessment as well as a history of similar pain problems (i.e., modeling) in significant others would be important in ascertaining the possibility of a conversion disorder in some patients.

In conclusion, future studies need to at­tend to each symptom and its associated characteristics so that more complete infor­mation can be obtained.

Treatment Issues

Each form of treatment for TMJ /MPD problems is supported to a degree, although the majority of these studies have been un­controlled. The fact that many patients re­spond to placebo treatments makes it diffi­cult to evaluate the efficacy of any form of treatment at the present time. Clearly, treat­ment research needs to control for placebo effects. The frequent finding that in the ab­sence of treatment many patients report symptom-free periods emphasizes the need for no-treatment control procedures and ex­tended follow-up for from· 6 months to 1 year.

Studies that use EMG biofeedback pro­cedures need to assess and report EMG lev­els carefully from each of the masticatory muscles. Only the medial and lateral pter­ygoids cannot be recorded by surface elec-

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342 R. MOSS, J. GARRETI, AND J. CHIODO

trodes; recordings from these muscles re­quire intrusive procedures, necessitating the assistance of medical staff. The rationale for multiple recording sites is that one or more of the masticatory muscles may show ele­vated levels of EMG activity while others reflect normal EMG levels. The ineffective­ness of masseter EM G feedback with certain patients may be accounted for if muscles other than the masseter are associated with the symptoms. Research investigating the generalizability of relaxation from a treated muscle group to untreated muscle groups has not been favorable (Surwit & Keefe, 1978).

Most treatment interventions with TMJ I MPD patients have been directed toward the physiological component (i.e., muscle hy­peractivity, occlusion). If, however, a thor­ough assessment reveals situational variables that precipitate and maintain masticatory pain or dysfunction, then it would seem rea­sonable to assess and modify each of these variables. This approach has been more fully addressed elsewhere (Haber et al., in press).

Recommendations for Future Research

A ·number of areas require extensive .in­vestigation if the present confusion about TMJ' dysfunction and MPD syndromes is to be alleviated.

1. Possible physiological (e.g., EMG lev­els, radiography of the TMJ) differences within and between groups of subjects who report the same symptom(s) need to be de­termined. In addition, psychometric exami­nations, detailed histories, and reactions dur­ing laboratory tests (e.g., pain threshold/ tolerance) may provide valuable information regarding quantitative and qualitative dif­ferences in these subjects.

2. No suitable explanations of the sex and age pr~ominance factors found with TMJ / MPD patients have been provided. Other variables that may be associated with these syndromes also require investigation. One possible v.ariable would be a history of sim­ilar problems among patients' family mem­bers or significant others. Another that has received little attention is racial variations ,in incidence rate.

3. Longitudinal studies of selected groups of subjects, particularly children and ado-

lescents, may be useful· in determining the actual incidence rate of TMJ /MPD symp­tomatology. In addition, this information may identify "at risk" populations.

4. Normative data on EMG levels of the muscles implicated in the dysfunction syn­dromes are needed to provide an empirical basis for determining abnormally high EMG levels. Such information would prove useful in both assessment- and treatment-oriented research.

5. Assessment of the relation between TMJ /MPD symptoms and certain oral hab­its, particularly bruxism, is needed. Noctur­nal bruxism studies should use an opera­tional definition consisting of thytlnnical · bursts of EMG activity, and the use of ex­perimental groups simila·r to Trenouth's ( 1979) is recommended. The assessment of diurnal bruxism and TMJ /MPD problems is more difficult owing to the possible reac­tivity associated with any assessment tech­nique. Present techniques include self-mon­itoring and the use of portable EMG devices. More innovative and less reactive recording procedures are needed.

6. The involvement of stress needs to be evaluated further. More carefully controlled research in both laboratory and natural en­vironment is required. Possible avenues of research include additional correlational studies of biochemical indicants of stress, self-monitoring of stressors and the presence or absence of masticatory pain and dysfunc­tion, and the effects of laboratory-induced stress on physiological recordings during pain and nonpain states.

7. Well-controlled treatment outcome studies are needed to evaluate the efficacy of each treatment for specific symptoms. In addition, psychological approaches directed toward teaching more effective coping skills (e.g., assertion training, problem solving) and cognitive pain control techniques (e.g., imagery training, cognitive restructuring) merit evaluation.

We hope that this review will provide a basis for better understanding TMJ dys­function and MPD syndromes. There is clearly a need for more systematic research of these disorders at all levels: classification, assessment, etiology, and treatment. Psy­chologists possess the necessary research

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TMJ/MPD SYNDROMES 3.43

skills needed to provide more definitive an­swers at each level. The statement made by Glaros and Rao ( 1977) in relation to psy­chology's involvement with bruxism applies equally well to TMJ dysfunction and MPD syndromes: "Psychologists' involvement in research on these 'dental' problems could well prove fruitful and could also widen the scope of psychology's influence on other dis­ciplines" (p. 778). Given that a great deal of confusion in this area is rooted in ques­tionable classification systems and inade­quate research methodology, psychology's impact can be dramatic and is limited only by psychologists' interest in, and motivation to deal with, what have been thought of as traditional dental problems.

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TMJ/MPD SYNDROMES 345

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Received August 6, 1981 •

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