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CRANIO®The Journal of Craniomandibular & Sleep Practice

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Graded exposure and orthopedic manual physicaltherapy for kinesiophobia and function in chronictemporomandibular dysfunction: A case report

Leanna Blanchard , Steven Goostree & Alison Duncombe

To cite this article: Leanna Blanchard , Steven Goostree & Alison Duncombe (2020): Gradedexposure and orthopedic manual physical therapy for kinesiophobia and function in chronictemporomandibular dysfunction: A case report, CRANIO®, DOI: 10.1080/08869634.2020.1779483

To link to this article: https://doi.org/10.1080/08869634.2020.1779483

Published online: 18 Jun 2020.

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CASE REPORT & LITERATURE REVIEW

Graded exposure and orthopedic manual physical therapy for kinesiophobia and function in chronic temporomandibular dysfunction: A case reportLeanna Blanchard PT, DPT, CLT, OCS, FAAOMPT a, Steven Goostree PT, DPT, Cert.MDT, OCS, FAAOMPTb, and Alison Duncombe PT, DPT, OCS, FAAOMPTa

aDepartment of Rehabilitation Services, University of Illinois Hospital and Health Sciences System, Chicago, IL, USA; bLuna Physical Therapy, Chicago, IL, USA

ABSTRACTBackground: This case report describes the successful use of multi-modal physical therapy (PT), including orthopedic manual physical therapy (OMPT) and graded exposure, in a patient with chronic temporomandibular dysfunction (TMD).Clinical Presentation: A 41-yr old female presented with a five-year history of bilateral chronic myofascial TMD and comorbid neck/right arm pain. The patient was treated for 12 weeks with a focus on OMPT and graded exposure. The patient demonstrated clinically significant improve-ments on the Tampa Scale of Kinesiophobia-TMD, maximal mouth opening, Global Rating of Change, and Jaw Functional Limitation Scale.Clinical Relevance: Mechanisms underlying chronic TMD are complex. Current evidence supports PT management of physical impairments; however, neglecting central drivers or psychosocial factors may result in suboptimal outcomes. Physical therapists are able to address both peripheral and central mechanisms of pain, and future research should examine the utilization of multi-modal PT to improve kinesiophobia and function in patients with chronic TMD.

KEYWORDS Temporomandibular joint dysfunction; physical therapy; manual therapy; chronic pain; central sensitization

Introduction

Temporomandibular joint dysfunction (TMD) is the second-most common musculoskeletal complaint after chronic low back pain [1], with prevalence estimates of 30–44% [2,3] and peak incidences at 20–40 years of age [4]. TMD contributes significantly to health-care expendi-tures and financial burden. A study by White et al. [5] found mean health-care costs over 6 years for TMD patients to be 15,996.26 USD versus 10,173.90 USD in the comparison group, indicating a 1.6x difference in costs. The overall expenditure for TMD in the United States is 4 USD billion [1]. Females are more likely than males to experience TMD, with ratios of 1.5:1, which increases to 8:1 in individuals seeking treatment for TMD [6]. Patients with TMD present with more social disturbance, decreased satisfaction with life, and decreased quality of life [7–9]. In a study by Boggero et al. [7], patients with masticatory myofascial pain, local myalgia, centrally mediated myalgia, disc displacement, capsulitis/synovitis, and continuous neuropathic pain were found to have differences in reported life satisfaction, with significantly lower

satisfaction reported in patients with centrally mediated myalgia. Higher affective distress, but not pain unpleasant-ness, was associated with poor life satisfaction. Patients with TMD and associated migraine have demonstrated increased disability days, pain intensity, and disability scores compared to patients with TMD or migraine alone [8]. Patients with myofascial TMD have higher incidences of self-reported migraine and chronic fatigue syndrome, as compared to their non-myofascial TMD counterparts [10]. A systematic review by Dahlström and Carlsson [9] of 12 studies examining oral health-related quality of life (OHRQoL) in patients with TMD found that the most common negatively impacted areas included psychological discomfort and disability, and subjective reports showed a greater association with decreased OHRQoL than clinical findings. Other studies have described associations between TMD and depression, stress, kinesiophobia, and anxiety [11–14]. Lastly, a study by Mingarelli et al. [15] found that alexithymia was correlated to pain severity in patients with TMD, which was related to social difficulties, such as interference in daily activities, difficulty in

CONTACT Leanna Blanchard BlanchardDPT@gmail.com Department of Rehabilitation Services, University of Illinois Hospital and Health Sciences System, Chicago, IL 60612, USACLT - Certified Lymphedema Therapist Cert.MDT - Credentialed in Mechanical Diagnosis and Therapy OCS - Board-Certified Clinical Specialist in Orthopaedic Physical Therapy FAAOMPT - Fellow of the American Academy of Orthopaedic Manual Physical Therapists

CRANIO®: THE JOURNAL OF CRANIOMANDIBULAR & SLEEP PRACTICE https://doi.org/10.1080/08869634.2020.1779483

© 2020 Taylor & Francis Group, LLC

employment, and difficulty in communication (speaking, laughing, kissing).

Comorbid conditions within TMD are common, with 53% of patients reporting comorbid migraines/headaches and 54% of patients reporting comorbid neck pain [16]. Patients who have sustained whiplash-type injuries have also been found to have an increased incidence of TMD compared to patients with chronic orofacial pain but no history of whiplash injury [17,18]. Patients with TMD often present with malocclusion, although the relationship between malocclusion and TMD-related pain has not been proven [19–22]. These patients may report a variety of symptoms, such as headache, clicking/popping, grinding, pain and/or fatigue with chewing, speaking, and yawning, and parafunctional habits such as bruxism, gum-chewing, fingernail chewing, or resting with the jaw in the hands [17,23–26]. Objective examination of these patients may reveal limited maximal mouth opening, clicking on open-ing and/or closing, hypomobility of accessory motions of the temporomandibular joint (TMJ) and cervical spine, decreased cervical range of motion, and trigger points/ tenderness in masticatory and cervical musculature [24,26,27]. Objectively, patients with TMD may also have reduced local and widespread pressure pain thresholds (PPT), heat pain sensitivity, temporal summation, and impaired conditioned pain modulation [26,28–35]. Risk factors for the development of TMD include parafunc-tional activities, such as daytime clenching and grinding, female gender [36], increased number of comorbidities, such as irritable bowel syndrome, migraine, chronic fatigue syndrome, interstitial cystitis, and restless leg syndrome [37], whiplash injury [18], bruxism [19,38], prior craniofa-cial trauma, history of orthodontic or oral surgery proce-dures [39], and history of craniofacial malignancy with or without radiation therapy [40].

There are a variety of proposed classification systems for orofacial pain and TMD [41]. Patients with TMD can be generally classified into three groups: masticatory muscle disorders, disc displacements, or joint dysfunction, although more detailed subgroupings exist within these classifications [24]. More specifically, patients with TMD can also be classified according to the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) under Axis I for Physical diagnosis, and Axis II for Psychosocial diag-nosis [42]. Axis I diagnoses include “arthralgia, myalgia, local myalgia, myofascial pain, myofascial pain with refer-ral, four disc displacement disorders, degenerative joint disease, subluxation, and headache attributed to TMD” [42]. Axis II includes assessment of chronic pain, general health, functional limitation, and anxiety to determine distress and pain disability [24,42]. A full description of each of the classifications is beyond the scope of this report. Readers are encouraged to review both the Harrison et al.

[24] and Schiffmann et al. [42] papers for further under-standing of TMD classification.

Studies have reported the use of physical therapy inter-ventions, such as therapeutic exercise, manual therapy, dry needling, and education in patients with TMD [17,43–64]. However, there is still a paucity of high- quality evidence to describe the efficacy and outcomes of physical therapy management of patients with chronic TMD and other regional symptoms, particularly as it relates to kinesiophobia, fear, and anxiety. Additionally, few studies explicitly report full resolution of TMD symp-toms, indicating that further innovation is needed in the care of these patients. The purpose of this case report was to describe the successful use of multi-modal physical therapy management, including orthopedic manual phy-sical therapy (OMPT), graded exposure, exercise, and education in a patient with chronic TMD, with emphasis on the outcomes of kinesiophobia and function.

Clinical case

Case description/methods

A 41-yr old female presented to physical therapy (PT) with a five-year history of bilateral TMD. She also reported a history of intermittent ear fullness as well as neck/right arm pain that was aggravated by a motor vehicle collision 2 years prior to the evaluation Figure 1. The patient stated that she had been undergoing constant splinting therapy for approximately 4 years, during which the TMD symp-toms worsened. She also reported the presence of dental prosthetics to approximate the posterior aspect of her bite. She had sought a second opinion regarding dental manage-ment approximately 1 year prior, and was instructed to discontinue splinting. The patient noted subjective improvement in ear fullness and TMJ clicking since dis-continuing the splints; however, she still experienced pain and fatigue in the bilateral TMJs and right neck/arm. She also reported paresthesia in the right arm, as well as fear of functional use of the jaw, including eating hard or crunchy foods. Regarding the 24-hr pattern, she woke with jaw soreness in the morning, and jaw, neck, and arm symptoms would worsen with functional use throughout the day. She reported that she would frequently avoid eating for an extended period of time, due to either fear of eating or being occupied by household and childcare responsibilities. She noted that, eventually, she would binge-eat any food available, regardless of the effect it might have on her symptoms. Aggravating factors included eating chewy, hard, or crunchy foods, speaking for prolonged periods, lifting, driving, sleeping, and performing household chores. Alleviating factors were use of a cold pack on the jaw, moving or shaking the right arm, cervical stretching, and

2 L. BLANCHARD ET AL.

use of non-steroidal anti-inflammatory drugs (NSAIDs). Pain at rest was rated as 0/10 on the Numeric Pain Rating Scale (NPRS), and at worst, up to an 8/10 in all painful areas. The patient’s primary goal was to be able to eat normal foods. She was not presently employed but was caring for her 11- and 15-yr-old daughters and assisting her husband in the administrative aspects of his contracting/ carpentry business. Depression screening was performed using the Patient Health Questionnaire-2 (PHQ-2). The PHQ-2 has a maximum score of 6 points, with higher scores indicating more severe/frequent symptoms [65]. Kroenke et al. [65] reported a cutoff of ≥3 points as the best compromise between sensitivity and specificity to screen for depressive disorders but noted that, as the pre-valence of depression varies depending on geographic loca-tion, numbers may differ. The patient responded “Yes – Several days” to both questions, which equates to a score of 2. Per Kroenke et al. [65], a score of 2 holds a positive predictive value of 21.1% for major depressive disorder and 48.3% for any depressive disorder, indicating that the patient could be at risk for depressive disorders.

The patient’s resting blood pressure was 110/ 60 mmHg, and heart rate was 69 bpm. Red flag screening questions for cord compression, cancer, and cauda equina were negative.

Consent to publication was obtained from the patient.

Initial examination

The initial examination took place during the first visit, with further assessments completed at the subsequent two visits during the following week.

Posture screen/general observation

The patient demonstrated a normal body habitus and pleasant demeanor. Sitting posture demonstrated for-ward head positioning, rounded/protracted shoulders, increased upper thoracic kyphosis, and decreased lum-bar lordosis. She was in no apparent distress.

Neurologic screening and cranial nerve exam

Neurologic screening was unremarkable. Sensation test-ing of dermatomes and peripheral nerves of bilateral upper extremities revealed no deficits. Upper extremity myotomes were grossly intact and equal bilaterally. Biceps, brachioradialis, and triceps reflexes were +2 bilaterally. Babinski, Hoffman, and Inverted Supinator reflex testing were negative, and only one beat of ankle clonus was noted on the left. Assessment of cranial nerves I–XII was unremarkable.

Vertebrobasilar insufficiency screening

While seated, the patient was assessed at end range left and right cervical rotation. The patient denied nystagmus, dys-arthria, diplopia, or other visual changes, although she did report dizziness that resolved upon return to neutral.

Movement screens

Cervical active range of motion and overpressure was performed in all cardinal planes and was not provocative of the patient’s TMJ or neck/arm pain. Upper cervical extension provoked familiar neck pain, and combined lower cervical extension with right rotation and side bend-ing reproduced familiar ear fullness and right arm pain (Table 1).

Passive joint accessory mobility assessment

The patient demonstrated hypomobility with inferior and anterior/inferior glides of the left TMJ. Hyoid mobility was normal. The patient also demonstrated hypomobility throughout the cervical spine during central posterior- anterior (CPA) and left and right unilateral posterior- anterior (UPA) assessment. CPA and UPA glides/mobili-zations are manual therapy assessment techniques utilized throughout the spinal column over the spinous process (CPA) and facet joints (UPA) to assess segmental joint mobility and pain provocation both centrally and unilat-erally. This allows for more specific information regarding the movement and sensitivity of the facet joints in the area of assessment. These techniques have been described in detail by Geoffrey Maitland in many books and papers, and readers are encouraged to review any texts by Maitland if wanting more information on this technique. If hypomo-bility or pain is identified, these techniques are also often used as manual therapy interventions. Hypomobility was

Table 1. Cervical assessment.Cervical – active with overpressure Range Pain response

Flexion Within Normal Limits (WNL)

x

Extension WNL xLateral Flexion Left WNL xLateral Flexion Right WNL xRotation Left WNL xRotation Right WNL xUpper Cervical Extension WNL Familiar neck

painUpper Cervical Extension with

rotation/lateral flexionWNL x

Upper Cervical Flexion WNL xLower Cervical Extension WNL xLower Cervical Extension Quadrant

RightWNL Ear fullness and

neck painLower Cervical Extension Quadrant

LeftWNL x

CRANIO®: THE JOURNAL OF CRANIOMANDIBULAR & SLEEP PRACTICE 3

most evident in the upper cervical spine (C1–3), and pro-vocation of familiar arm pain was noted with right UPA at C5. Tenderness was reported throughout the cervical spine. There was no reproduction of jaw or facial pain with cervical CPA or UPA assessment, although the patient did report some posterior ear pain with upper cervical UPA assessment and familiar dizziness with UPA assess-ment at C1.

Temporomandibular motion assessment

Actively, the patient was able to achieve 30 mm of maximal mouth opening with difficulty and reports of fatigue (Table 2). Mean maximal mouth opening in adult populations has been reported at 44.3 ± 6.7 mm [66], and the minimum detectable difference has been reported as 9 mm [67]. There was an observable “S” curve upon opening. Lateral deviation to each side was approximately one-fourth of the opening range of motion, which is generally considered to be within normal limits. The patient achieved an edge-to- edge bite with protrusion but was extremely apprehensive and refused to attempt further protrusion, due to self- reported fear “of the jaw going out.”

Palpation

There was no audible or palpable click with mouth opening or closing; however, the patient reported tenderness over bilateral (left greater than right) TMJs, bilateral suboccipital muscles, bilateral masseter, and bilateral lateral pterygoid, which reproduced familiar jaw pain on the left. Temporalis and digastric were nontender bilaterally.

Special tests

Cervical flexion rotation test was within normal limits for mobility bilaterally and without pain provocation. In supine, the patient’s cervical spine is passively brought into maximal flexion and then rotated left and right while this position is maintained. Flexing the cervical spine aims to reduce lower cervical spine contribution and better assess the rotational mobility of C1-C2. Upper limb neural provocation testing with median, ulnar, and radial nerve biases reproduced the patient’s usual arm pain. These tests are also performed in supine,

with the clinician passively moving the patient’s extre-mity into specific positions of increased excursion for each nerve. The clinician assesses side-to-side differ-ences in motion or provocation of familiar symptoms.

Quantitative sensory testing

Pressure pain threshold (PPT) assessment was initiated at follow-up visit 9, with an average of two trials per-formed at each site. Assessment was performed at the bilateral masseter, as well as the medial joint line of the right knee. PPT assessment at a contralateral, distant, non-painful site can provide an objective sensory profile, indicating more clearly whether central sensitization and resultant widespread hyperalgesia are present. Rolke et al. [68] determined a normative PPT value at the masseter as 223 kPa (2.27 kg/cm2) in females over age 40, as well as a normative value over the foot as 535 kPa (5.46 kg/cm2). The intra-rater minimum detectable change (MDC) for the upper trapezius in patients with neck pain has been reported at 47.3 kPa (0.48 kg/cm2) [69]. Cunha et al. [29] reported a cut-off value of 1.36 kg/ cm2 to diagnose TMD and orofacial pain. The patient’s PPT values were below normal in the masseter and at the knee, indicating widespread hyperalgesia (Table 3).

Outcome measures

The patient completed the Jaw Functional Limitation Scale (JFLS). The JFLS is a 20-item self-report question-naire of orofacial function comprising three constructs (mastication, mobility, and emotional and verbal com-munication) [70]. The 20 items are rated on a 10-point scale, with endpoints of “no limitation” (0) and “extreme limitation” (10) and a maximum possible score of 200, indicating extreme limitation in all functional areas [70]. The patient’s initial JFLS score was a total of 76/200, with individual component scores of 24 on the Mastication Scale, 17 on the Mobility Scale, and 35 on

Table 2. Temporomandibular joint assessment.Temporomandibular joint active motion Range Pain response

Opening 30 mm Apprehension and fatigue of jawClosing/Clenching WNL ApprehensionLateral Deviation Right WNL (~¼ of opening range) xLateral Deviation Left WNL (~¼ of opening range) xProtrusion Occlusion Apprehension

Table 3. Quantitative sensory testing.Pressure Pain Thresholds (average of 2 trials)

Visit Right masseter Left masseter Right medial knee

Visit 9 1.36 kg/cm2 0.79 kg/cm2 3.06 kg/cm2

Visit 10 1.58 kg/cm2 1.77 kg/cm2 4.56 kg/cmVisit 11 1.66 kg/cm2 1.72 kg/cm2 3.54 kg/cm2

4 L. BLANCHARD ET AL.

the Communication Scale. Lower scores on the JFLS indicate better function. The JFLS has been found to be valid and reliable in patients with TMD, but no mini-mum clinically important difference (MCID) or MDC has been reported [70,71]. The patient also completed the Tampa Scale of Kinesiophobia for TMD (TSK- TMD). The TSK-TMD has been modified to a 12-item version, each item rated from 1 to 4 on a Likert Scale, where 1 = strongly disagree, and 4 = strongly agree [72]. The patient’s initial score on the 12-item version was 35 out of a total possible 48, where a lower total score indicates less fear of jaw movement. Aguiar et al. [73] reported an MDC for the Brazilian translation of the 12- item TSK-TMD as 4.3 points. The TSK-TMD has also been validated in a Chinese population, though without MCID or MDC reported [74]. Lastly, the patient was periodically given the Global Rating of Change Scale (GROC). The GROC was described by Jaeschke et al. [75] as a 15-point self-report scale, ranging from “a very great deal worse” (−7) through “a very great deal better” (+7), with a mid-point of “about the same” (0). The MCID was reported as ± 3 points [75].

Imaging

The patient brought in a report of her previous MRI of the cervical spine and TMJ. Cervical MRI revealed small left paramedian C3–4 disc extrusion without evidence of neural impingement, right-sided small disc/osteophyte complex at C5–6 causing moderate right foraminal ste-nosis, and small bilateral posterior-lateral endplate uncovertebral joint hypertrophy causing mild foraminal stenosis at C6–7. The TMJ MRI revealed no condylar osteochondrosis, no bony injury or joint effusion, bilat-eral disc degeneration, condyles in centric position in closed-mouth position but with limited translation in the open mouth position, slight medial subluxation of the left intra-articular disc, and slight lateral subluxation of the right intra-articular disc.

The patient later underwent a CT scan of bilateral TMJs, and the results were unremarkable.

Clinical impression

The initial working hypothesis was myofascial TMD in the context of cervical facet dysfunction complicated by possible whiplash-associated disorder. The primary con-tributing drivers were felt to be masticatory muscle ten-sion, left TMJ capsular hypomobility, and upper cervical facet hypomobility. This hypothesis was based on the patient’s significant history of dental work, limited and apprehensive opening, provocation of pain with muscle palpation, findings of familiar neck and arm pain with

cervical motion and accessory assessment, and history of motor vehicle collision that facilitated the progression of her pain and dysfunction.

Based on this clinical impression, initial expected interventions included soft tissue mobilization to masti-catory and cervical muscles, joint mobilization to both the TMJ and cervical segments, education, and exercise progression.

Interventions

At the evaluation, the patient was given education on self-soft tissue mobilization to the masseter, both exter-nally and intraorally, as well as education on seated cervical retraction to address postural impairments. She was then seen 1 to 2 times per week for the next 8 weeks. Table 4 specifically outlines the progression of manual therapy, exercise, and education.

Treatment during the first 2 weeks initially focused on addressing the mobility deficits in the upper cervical spine, which progressively alleviated her neck pain and reduced the discomfort with maximal mouth opening and jaw closing. The patient was further instructed on self-management strategies at these visits, including thoracic extension self-mobilization over a foam roll for posture, self-suboccipital mobilization using tennis balls, and education regarding fear reduction with eat-ing, as well as pacing eating throughout the day to avoid periods of binging.

During the third week, intraoral TMJ mobilization was initiated, which led to pain-free maximal mouth opening, as well as increases in the range of maximal opening. A graded eating program was also initiated. The patient in this case reported fear of eating hard and crunchy foods, due to the pain that was provoked. The patient self-selected walnuts to begin the graded eating program and was educated to progress by one walnut per day, as tolerated.

The patient returned during week 4, having self- progressed to eating almonds, stating that walnuts had become too easy for her. She had noted pain with eating three almonds and was subsequently educated to decrease to two almonds for several days before re-attempting three. A systematic review by Macedo et al. [76] described the differences between graded activity and graded exposure.

Graded exposure was initially described in reference to low back pain [77,78]. The intervention is designed to expose patients to specific situations of which they are fearful, encouraging a confrontation response [77,78]. Patients learn that feared activities will not harm them or cause tissue damage, and they develop an under-standing of the negative effects of avoidance behavior. Graded exposure is performed as a hierarchy, in which

CRANIO®: THE JOURNAL OF CRANIOMANDIBULAR & SLEEP PRACTICE 5

the first step is for the patient to identify feared activities. The program then progresses from least to most feared activities. The progression for this patient included com-ponents of both graded exposure and graded activity, in that feared foods/activities were identified, a hierarchy was created, and irrational beliefs were consistently addressed (graded exposure); healthy behaviors were reinforced, and goals were based upon function (graded activity) [76]. Manual therapy was again performed to address mobility deficits in the left TMJ and the cervical spine, and centralization of arm symptoms occurred with right unilateral PAs at C7-T1. Graded exposure continued, and she was able to eat a quarter cup of salad, progressing as previously instructed.

During week 5, she reported a flare-up in jaw pain after eating at a friend’s house, and therefore, had not progressed the eating program. TMJ mobility deficits were addressed via joint and soft tissue mobilization, and functional maximal mouth opening was now con-sistently in the range of 40 mm. At this time, a specific weekly schedule of home exercises was developed to give more structure and guidance on self-management.

During weeks 6 and 7, manual therapy to the TMJ was performed; however, the emphasis shifted toward upper quarter exercises and jaw motor control exercises to facilitate the appropriate use of the new range of mouth opening. The patient reported being able to eat

romaine lettuce and chips and stated she no longer felt she had to overthink what she was eating. Education related to continued stress management, activity pacing, and graded exposure was provided.

During week 8, the patient was able to focus primarily on exercise and education interventions and, as she was doing well, the patient and therapist agreed to have her return in 4 weeks for reassessment.

At that time (week 12) the patient stated that she had experienced a few flare-ups and noted that these flare-ups mostly occurred when she had not been consistent with her home exercises. She had not had to regress her eating program and had not experi-enced any headache or dizziness. Opening range of motion had been maintained, and there was no pro-vocation of neck or arm symptoms during reassess-ment. The patient and therapist again agreed to trial another 4 weeks of independence, with the under-standing that improved consistency of home exercises was needed to assist in preventing flare-ups and facil-itate self-progression.

Outcomes/results

The patient was first formally reassessed at visit 7 (Tables 5 and 6). At this time, she was able to eat a quarter cup of lettuce and six walnuts without

Table 4. Interventions.Manual therapy Therapeutic exercise and home exercise program (HEP)

Evaluation (Week 1)

-Education on self-soft tissue mobilization to masseter

-Seated cervical retraction/chin tuck

Visit 1 (Week 2) -Upper cervical joint mobilization -Reviewed chin tucks, added submaximal biting to HEP -Education on decreasing fear with eating

Visit 2 (Week 2) -Upper cervical mobilization -Soft tissue mobilization of suboccipitals -Self-assisted opening mobilization

-Thoracic extension over foam roller, self-suboccipital soft tissue/AP with tennis balls

Visit 3 (Week 3) -Upper cervical mobilization - L TMJ mobilization -Self L TMJ glides

-Graded exposure to eating -Education on decreasing fear with eating

Visit 4 (Week 4) -Upper and lower cervical joint mobilization -L TMJ mobilization

-Continue with graded exposure to eating -Education on decreasing fear with eating

Visit 5 (Week 4) -Upper and lower cervical mobilization -L TMJ mobilization -Self-masseter and lateral pterygoid massage

-Isometric lateral deviation -Progression of graded exposure – ¼ cup of salad

Visit 6 (Week 5) -Soft tissue mobilization to L lateral pterygoid -Upper cervical joint mobilization

-Review of HEP, continue with graded eating exposure -Education on decreasing fear with eating

Visit 7 (Week 5) -L TMJ mobilization -Review chin tucks -Development of HEP weekly schedule -Continue graded exposure -Education on decreasing fear with eating

Visit 8 (Week 6) -L TMJ mobilization -Self TMJ anterior internal glide (HEP)

-Seated latissimus pull downs, seated rows -Education on stress management

Visit 9 (Week 7) -Soft tissue mobilization to B masseter at end of session

-Neuromuscular Re-education: controlled opening and biting -Education on progressing eating exposure -Education on decreasing fear with eating, stress management

Visit 10 (Week 8) -None -Upper quarter exercise and stretching -Education on frequency of HEP, progressing food, stress management

Visit 11 (Week 12) -Upper cervical joint mobilization -Reviewed chin tucks at patient request -Encouragement to maintain consistency with HEP

6 L. BLANCHARD ET AL.

provocation of symptoms and had achieved 40 mm of mouth opening with 2/10 pain on the NPRS, exceeding the MDC of 9 mm [67]. The TSK-TMD 12-item score had improved to 29 points, exceeding the MDC of 4.3 points [73]. The JFLS total score had improved from 76 to 41, a 46% improvement (see Table 6 for the break-down of component scores). She subjectively rated her-self as 50% improved overall and reported a score of +4 on the GROC, exceeding the MDIC of ± 3 [75].

She was again reassessed at visit 10. She was now able to eat romaine lettuce, a small amount of almonds and chips without complaints, and had achieved pain-free maximal mouth opening of 42 mm. The TSK-TMD 12- item score had further improved from 29 to 25 points, again nearly matching the MDC of 4.3 [73]. The JFLS total score had improved to 23 points, a 43% improve-ment since the last assessment, and a 70% improvement since the initial evaluation. She subjectively rated herself as 80% improved overall. She reported very occasional arm pain, almost no headaches, and no dizziness in the previous week. Pressure pain thresholds had improved, particularly in the left TMJ and right medial knee joint line, both exceeding the MDC of 0.48 kg/cm2 reported by Walton [69].

After a four-week break from therapy, she was again reassessed at visit 11. There were no changes in food intake; however, maximal mouth opening was 45 mm and pain-free. The TSK-TMD 12-item score had improved to 23 points. JFLS total score had improved to 18 points, a 22% improvement since the previous assessment and a 76% overall improvement since the initial evaluation. She again subjectively rated herself as 80% improved overall and reported a GROC score of +7, meeting the MDIC of ± 3 [75]. She reported no

headaches, dizziness, or arm pain over the previous 4 weeks, and only intermittent flare-ups of neck and jaw pain. No significant changes in pressure pain threshold were seen from visit 10 to visit 11. The most notable change over the course of 11 visits was the improvement of the patient’s TSK-TMD score from 35 (at initial evaluation) to 23 points (at visit 11 reassessments), far exceeding the MDC of 4.3 points as reported by Aguiar [73], and indicating significantly reduced kinesiophobia.

Discussion

Evidence for splinting vs physical therapy management of TMD

The patient in this case report was initially managed with splinting therapy for 4 years without improvement in symptoms. The patient stated that the goal of splint-ing was to improve occlusion and reposition the mand-ible anteriorly, and that she had used both types of splints. Specifically, occlusal splinting is thought to alter afferent activity from intraoral tissues, alter TMJ position by increasing the vertical dimension, and alter motor control via changes in activity patterns of cranio-facial muscles during closing or clenching activities [79]. However, occlusal splint therapy is typically not specific, and therefore, mechanisms of efficacy are largely unknown [79]. While splinting therapy is a common first-line management strategy of TMD, there is a growing body of evidence to suggest that providers reconsider this treatment option in patients with myo-genic/myofascial TMD [50,79–84].

In a systematic review with meta-analysis, splinting was not shown to have significant effects on quality of life or depression [80]. Randomized controlled trials comparing various types of splinting therapy to physical therapy management generally find slightly superior short- and long-term outcomes with physical therapy, or at the very least, no significant benefit with the addi-tion of splinting to physical therapy or education [50,79,81–84]. Specifically, van Grootel et al. [79] com-pared physical therapy to occlusal splinting in patients with myogenous TMD and found similar short- and long-term success rates. Physical therapy was successful after a shorter duration than splinting (average of 10.4 weeks less); whereas, splinting was successful in

Table 5. Outcomes.

VisitMouth

opening

Tampa Scale of

Kinesiophobia (TSK-TMD)

total

Global rating

of change Food intake

Evaluation 30 mm 35 – Soft foods and smoothies only

Visit 7 40 mm 29 +4 ¼ cup soft lettuce, walnuts

Visit 10 42 mm 25 – Chips, almonds, romaineVisit 11 45 mm 23 +7 No further progression

Table 6. Jaw Functional Limitation Scale.Visit Total Mastication Mobility Communication

Evaluation 76 24 17 35Visit 7 41 (46% improvement from evaluation) 16 12 13Visit 10 23 (70% improvement from evaluation) 7 6 10Visit 11 18 (76% improvement from evaluation) 18 0 0

CRANIO®: THE JOURNAL OF CRANIOMANDIBULAR & SLEEP PRACTICE 7

fewer visits than physical therapy (average of 7.1 fewer visits) [79]. The authors concluded that, as the shorter duration of physical therapy achieved success, it may be more beneficial for patients with myogenous TMD to initiate treatment with physical therapy and have the option to initiate splinting later if therapy is unsuccessful [79]. Given that this patient reported 80% improvement after 10 visits of therapy over 8 weeks, and at visit 11 reported +7 (a very great deal better) on the Global Rating of Change Scale, the patient may have benefited from physical therapy treatment earlier on and may have been able to avoid years of progressive pain and dysfunction.

As previously stated, the mechanisms underlying the use and efficacy of occlusal splinting have not been well studied or understood. However, a study by Nitecka- Buchta et al. [85] examined plasma levels of calcitonin gene-related peptide (CGRP) after a month of splinting therapy in patients with myofascial TMD. The authors found significantly increased levels of plasma CGRP post-splinting therapy but no significant changes in the control group [85]. CGRP is known to play a role in the expression of brain-derived neurotrophic factor (BDNF), particularly from trigeminal nociceptors, which are likely involved in patients with TMD and other craniofacial pain syndromes [86]. Binding of BDNF facilitates C-fiber activity via n-methyl- D-aspartate (NMDA) receptors, leading to further acti-vation of spinal cord pathways and facilitating central sensitization [86]. The patient in this case report under-went splinting therapy for a significant period of time, which raises the question of whether these inflammatory markers were potentially elevated and may have con-tributed to persistent pain and dysfunction.

Evidence for central mechanisms, central sensitization, and impact of psychosocial factors

Per Courtney et al. [87], central sensitization is defined as “the increased response of nociceptive neurons in the central nervous system to noxious stimuli, mediated by amplification of signaling to the central nervous system, potentially at both spinal and supraspinal levels.” Central sensitization generally occurs by two known mechanisms: excitation of the central nervous system due to ongoing barrage of peripheral nociceptive input, as well as impaired descending pain modulation/inhibi-tion [88]. This barrage of nociceptive input by primary afferent neurons is known as peripheral sensitization, “a reduction in threshold and amplification in the respon-siveness of nociceptors that occurs when the peripheral terminals of these high-threshold sensory neurons are exposed to inflammatory mediators and damaged

tissue” [86]. According to Woolf [88], TMD has been associated with generalized pain sensitivity, indicative of central sensitization mechanisms. In theory, patients with TMD may experience this nociceptive barrage via persistent splinting or malocclusion, leading to abnor-mal bite force, or possibly a single particularly noxious stimulus during dental procedures [17]. Key players in the pathophysiology of central sensitization include the aforementioned NMDA receptors and CGRP, as well as glutamate, substance P, 5-HT, tumor necrosis factors (TNF-α), and interleukins (IL-1β), among many others [86]. The increased presence of these inflammatory fac-tors is typically referred to as neurogenic inflammation and can occur both at the joint and muscle [89]. With continued neurogenic inflammation, sensitization of nociceptors and wide dynamic range neurons in the spinal cord can occur, resulting in central sensitization [89]. Various studies have attempted to clarify the con-tribution of central mechanisms in patients with TMD, examining the presence or absence of these inflamma-tory mediators, and facilitation or inhibition of central pathways [6,33,35,85,90–95].

Chen et al. [90] induced TMJ inflammation and demonstrated the upregulation of transient receptor potential cation channel 4 (TRPV4) receptors, further correlating this with attenuation of bite force in mice. Not only were TMJ innervating trigeminal ganglion neurons upregulating TRPV4, but all trigeminal gang-lion neurons demonstrated upregulation, providing a possible mechanism for secondary or widespread hyperalgesia in TMD [90]. Another study demonstrated excitatory changes in bilateral masseter muscles and spinal cord dorsal horn neurons after inducing inflam-mation unilaterally, suggesting that contralateral hyper-algesia is mediated via spinal cord connections [92]. Studies have found increased plasma inflammatory mar-kers present in patients with TMD, including dopamine, glutamate, and pro-inflammatory cytokines (IL-1β and IL-6, TNF-α, C-reactive protein), as well as increased interstitial 5-HT and glutamate in the masseter [91,93,96,97]. These studies found that these markers correlated to lower pressure pain thresholds, higher perceived mental stress, increased muscle pain, allody-nia, impaired stretch reflexes, daytime sleepiness, and poor sleep quality [91,93,94]. Additionally, Castrillon et al. [96] noted that the increase in glutamate can facilitate NMDA receptor expression and contribute to changes in sensitization and pain perception. The impaired stretch reflexes demonstrated by Wang et al. [94] were present in the jaw and the neck, regardless of whether glutamate-induced inflammation was provoked in the masseter or splenius muscle, indicating likely convergence of craniofacial and cervical inputs and

8 L. BLANCHARD ET AL.

another possible mechanism for spinal cord-mediated pain. Wiesinger et al. [95] sought to further elucidate the relationship between pain and jaw/neck motor strategy and found that induction of masseter pain led to increased contribution of neck movement during jaw opening/closing tasks with no change in jaw amplitude, indicating a change in movement strategy.

Patients who present with central sensitization typi-cally demonstrate exaggerated temporal summation, indi-cating central facilitation at the dorsal horn, and impaired conditioned pain modulation, indicating decreased ability to inhibit painful stimuli [87]. In a literature review by Sarlani and Greenspan [6], it was stated that patients with TMD often do not present with peripheral tissue damage or abnormalities, supporting the likely contribution of a central mechanism in the persistence of pain and dys-function. Studies have shown increased temporal summa-tion in patients with TMD, indicating hyperexcitability of central pathways [33,35]. Maixner et al. [33] found lower pressure pain thresholds, increased perceived magnitude of heat stimuli, and increased temporal summation to heat stimuli in patients with TMD compared to controls. The results demonstrate support for the role of central mechanisms over, or in addition to, peripheral mechan-isms: 1) the thermal detection thresholds were not differ-ent between TMD patients and controls, indicating that the thermal nociceptors themselves were not sensitized; and 2) patients with TMD gave higher magnitude esti-mates of the heat stimulus, indicating impaired central pain inhibition [33]. Sarlani et al. [35] performed a similar study looking at temporal summation to mechanical sti-muli on the finger in patients with TMD compared to controls and again found increased temporal summation in the experimental group, as well as greater trends toward depression and anxiety.

Psychosocial factors are well associated with chronic pain conditions and central sensitization, including anxi-ety, depression, hypervigilance, catastrophizing, and poor emotional functioning [17,87,89,98]. There is consider-able evidence to suggest that psychological factors play a role in TMD, particularly in chronic presentations [89]. Given the observed relationships between dopamine levels and stress [91,93] and inflammatory cytokines and sleep dysfunction [93], it is clear that psychosocial factors and central sensitization are inherently linked. A meta- analytic review by Burke et al. [99] found that patients with chronic pain syndromes reported significantly more issues with depression, anxiety, anger, somatization, self- efficacy, self-esteem, and general emotional functioning. Burke et al. [98] also described the mechanisms of central nervous system inflammatory dysregulation that link depression and chronic pain states, noting that depression and chronic pain co-occur in up to 80% of patients. The

patient in this case report presented with kinesiophobia and anxiety relating to normal, functional use of the jaw. The presence of top-down sensitizers likely contributed to the facilitation of central pathway excitation and impaired descending inhibition/modulation of pain. Addressing this fear was an important component of successful man-agement and, in this case, was accomplished via education and graded exposure to eating. The inclusion of graded exposure programs may help impact pathways mediated by the amygdala, a region responsible for fearful mem-ories [89]. The patient also presented with decreased pressure pain thresholds, further providing evidence that central mechanisms were at least partly responsible for the persistent pain. It is possible that the persistent stimu-lation via prolonged splinting led to peripheral sensitiza-tion of the masticatory muscles, which may have provided the barrage of nociceptive input to the dorsal horn neu-rons necessary to facilitate central sensitization. This pro-cess was potentially further amplified by the motor vehicle collision she experienced, resulting in further sensitiza-tion of not just the TMJ region, but also the cervical spine, and contributing to trigeminocervical convergence. In this case, had the patient only been managed by addres-sing the peripheral components of her presentation, she likely would not have achieved successful outcomes. Addressing the psychosocial aspects of patients present-ing with persistent TMJ pain and dysfunction is a key component of successful physical therapy management.

Limitations

There are limitations within this case report. First, a definitive cause and effect relationship cannot be deter-mined from a single case report. Second, quantitative sensory testing was not initiated until visit 9; therefore, the authors cannot say whether these deficits were pre-sent earlier on. Earlier assessment of these central mechanisms would have provided further support for comprehensive management and evidence of change or dysfunction in central pain processing. It may also have been beneficial to perform pressure pain threshold mea-surements at the hand to assess regional hyperalgesia.

Conclusion

This case report aimed to describe the successful manage-ment of a patient with chronic TMD using multi-modal physical therapy, including graded exposure, and to describe the possible peripheral and central mechanisms that contribute to this presentation and impact patient management. The mechanisms by which TMD occurs and persists are complex and still emerging in the litera-ture. While the current evidence suggests that pain and

CRANIO®: THE JOURNAL OF CRANIOMANDIBULAR & SLEEP PRACTICE 9

function have successfully been impacted by manual ther-apy, exercise interventions, and education on activity modification, addressing psychosocial contributing fac-tors and providing patients with clear and direct guidance on graded exposure to feared activities or foods may be necessary to impact anxiety and kinesiophobia. Treating only the perceived peripheral drivers of a patient’s pain and dysfunction may cause neglect of possible central mechanisms and may result in suboptimal patient out-comes. Clinicians should view these patients within a multivariate model to ensure consideration of the full picture of the patient and prevent neglect of psychosocial drivers and other external factors [89]. These patients may be subjected to a variety of management strategies, including dental and physical therapy interventions, and should be closely monitored throughout for signs and symptoms of developing central sensitization or lack of improvement, indicating that referral to another health- care provider or change in treatment strategy may be necessary. Physical therapists are uniquely equipped to manage these patients, and future research should attempt to better elucidate outcomes with multi-modal physical therapy management in patients with all classifi-cations of TMD, as well as better understand the need to specifically address top-down sensitizers/psychosocial factors in acute and chronic presentations.

Disclosure of interest

The authors report no conflicts of interest.

ORCID

Leanna Blanchard PT, DPT, CLT, OCS, FAAOMPT http:// orcid.org/0000-0001-9972-6319

Sources of support

No funding was received for this report.

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