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.
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).