Biobehavioral Pain Management in TMD
Condition: Temporomandibular Joint Disorder
MeSH terms: Joint Diseases; Temporomandibular Joint Disorders; Temporomandibular Joint Dysfunction Syndrome
Study type: Interventional

Summary: 
      TMD is a poorly understood chronic pain disorder that affects up to 15% of the adult
      population, notably impacting women, is linked to greater healthcare utilization, and
      associated with multiple pain-related co-morbidities. Pain-related catastrophizing (CAT) and
      sleep continuity disturbance (SCD) are well established modifiable risk factors for TMD and
      other idiopathic pain conditions. Neither the causal status nor the neurobiological
      mechanisms by which these factors exert their effects on clinical pain have been established.
      We propose that CAT and SCD influence clinical pain through shared alterations in pain
      modulation and key neurobiological pathways, including amplified inflammatory activity,
      autonomic activity, and adrenocortical functioning. Beyond these shared mechanisms, however,
      we propose to determine whether pre-sleep CAT increases cortical arousal during sleep. The
      cognitive dimensions of pre-sleep arousal, particularly rumination and negative sleep-related
      thoughts, are central to the phenomenology of insomnia. Extending this notion, we propose
      that CAT in those experiencing ongoing clinical pain fosters sleep disturbance owing to
      increased pre- and peri-sleep cognitive arousal. Moreover, we propose that pre-sleep CAT is
      related to subtle variations in objective indices of fragmented sleep (e.g., cortical
      arousal). We will examine key hypotheses derived from this framework using a brief,
      prospective randomized experiment, which will permit careful analysis of the temporal
      patterning of how changes in either CAT or SCD influence each other and contribute to
      alterations in pain modulatory systems, key nociceptive mechanisms, and clinical pain.

      Women experiencing at least moderate chronic TMD pain (N=225) who demonstrate at least mild
      trait catastrophizing and meet at least subclinical insomnia criteria (SCD) will be randomly
      assigned to: 1) cognitive therapy for catastrophizing (CT-CAT); 2) behavior therapy for sleep
      disturbance (BT-SCD); or 3) TMD education (Control). Assessments of clinical pain, sleep
      disturbance, catastrophizing, pain sensitivity and modulatory systems, and indices of
      inflammatory activity, adrenocortical function and autonomic balance will be completed at
      baseline, 4 weeks (mid-manipulation) and 8 weeks (post-manipulation). Clinical pain, sleep,
      catastrophizing and covariates will additionally be measured at 16 weeks (follow-up).
    

Detailed description: 
      Temporomandibular Joint Disorder (TMJD) is a poorly understood chronic pain disorder
      characterized by pain and dysfunction in the jaw joint and the muscles that control jaw
      movement. TMJD affects up to 15% of the adult population, differentially impacts women, is
      linked to greater healthcare utilization, and is associated with multiple pain-related
      co-morbidities. Pain-related catastrophizing (i.e., the tendency to exaggerate the threat
      value of pain and negatively evaluate one's ability to deal with pain; CAT) and sleep
      continuity disturbance (i.e., disturbance in the speed with which sleep is initiated and the
      degree to which it is consolidated; SCD) are two well established modifiable risk factors for
      TMJD and other idiopathic pain conditions. SCD is defined in this protocol as at least
      moderate trouble initiating or maintaining sleep, which significantly impacts daytime
      function. SCD is common in chronic pain, including TJMD, and poor sleep predicts both the
      development and exacerbation of pain. CAT, a negative cognitive-emotional predilection and
      response to pain, prospectively predicts the onset and exacerbation of pain, as well as
      numerous pain-related outcomes. Surprisingly, neither the causal status nor the
      neurobiological mechanisms by which these factors exert their effects on clinical pain have
      been established. Preliminary data from our group and others suggest that CAT and SCD are
      independently associated with alterations in laboratory indices of pain modulation,
      exaggerated pain-evoked pro-inflammatory cytokine responses and amplified clinical pain.

      While the effects of CAT and SCD are independent of depression and psychological distress, no
      longitudinal or experimental studies have evaluated the potential interplay between CAT and
      SCD and how this interplay contributes to pain outcomes. There is a strong theoretical reason
      to hypothesize interplay between these seemingly disparate constructs among patients with
      chronic pain. We have developed a novel, integrated theoretical framework positing that CAT
      and SCD influence clinical pain through shared alterations in pain modulation and key
      neurobiological pathways, including amplified inflammatory activity, sympathetic activity,
      and adrenocortical functioning. Beyond these shared mechanisms, however, we propose to
      determine whether presleep CAT increases autonomic and cortical arousal during sleep measured
      by polysomnography (PSG)-derived indices of Heart Rate Variability (HRV) and average relative
      power in the alpha and beta bands on quantitative electroencephalography (QEEG). The
      cognitive dimensions of pre-sleep arousal, particularly rumination and negative sleep-related
      thoughts, are central to the phenomenology of insomnia. Extending this notion, we propose
      that CAT in those experiencing ongoing clinical pain fosters sleep disturbance owing to
      increased pre- and peri-sleep cognitive arousal. Moreover, we propose that pre-sleep CAT is
      related to subtle variations in objective indices of fragmented sleep (e.g., cortical
      arousal). We will examine key hypotheses derived from this framework using a brief,
      prospective randomized experiment, which will permit careful analysis of the temporal
      patterning of how changes in either CAT or SCD influence each other and contribute to
      alterations in pain modulatory systems, key nociceptive mechanisms, and clinical pain.

      In this 5 year study, 300 women with chronic TMJD and reporting at least mild trait
      catastrophizing and at least mild sleep continuity disturbance will complete a randomized,
      parallel group experiment comparing cognitive therapy for catastrophizing (CT-CAT) and
      behavior therapy for sleep disturbance (BT-SCD) to TMJD disease education (TMJD-ED). Subjects
      will be randomized in a ratio of 1:1:1 to one of the three interventions. Each subject will
      participate in the study for up to 30 weeks. The study includes three phases: 1) screening
      and baseline (up to 10 weeks), 2) intervention (approximately 7 weeks), and 3) follow-up
      (ends approximately 12 weeks after the final intervention visit). Assessments of outcome
      measures (inflammatory activity, pain modulation, clinical pain, pre-sleep cognitive arousal,
      cortical and autonomic arousal) will be made during the interventions and after completion of
      the interventions, and will be compared with baseline assessments. It is anticipated that
      enrollment will be completed over four years.
    

Intervention name(s): Cognitive Therapy for Catastrophizing; Behavioral Therapy for Sleep Continuity Disturbance
Intervention type(s): Behavioral; Behavioral
Intervention description(s): Cognitive Therapy for Catastrophizing will involve a standardized, 6-session cognitive intervention, focusing on cognitive restructuring techniques for managing pain and reducing catastrophic thinking and includes some general coping skills training. Cognitive restructuring includes identifying patterns of dysfunctional thinking which can give rise to emotional distress, physiological arousal, or maladaptive behaviors. Patients are taught to identify and replace distorted thinking with balanced, realistic thinking. Patients learn to identify these thoughts as they occur in daily life and challenge their own negative thoughts.; Behavioral Therapy for Sleep Continuity Disturbance (BT-SCD) will involve 6-sessions of standardized interventions on sleep restriction therapy (SRT), stimulus control therapy (SCT), and sleep hygiene education. Sleep Restriction curtails the amount of time in bed so that it matches the average baseline amount of total sleep time. Stimulus Control Therapy re-establishes the bed and bedroom as cues for sleep by insuring the patient does not spend significant time in bed awake and/or engaging in sleep-incompatible behaviors. Sleep Hygiene Education uses motivational interviewing to teach subjects about environmental and behavioral factors which may influence sleep. SRT and SCT alone or combined have demonstrated overwhelming efficacy and effectiveness.
Other intervention name(s): CT-CAT; CT; CAT; BT-SCD; SCD; BT
Allocation: Randomized
Intervention model: Single Group Assignment
Masking: Single (Outcomes Assessor)
Primary purpose: Treatment
Keywords: TMD; TMJD; Temporomandibular Joint Disorders; Sleep Continuity Disturbance; Pain Catastrophizing; Cognitive Therapy; Behavioral Therapy