Biobehavioral Pain Management in TMD (TMD)
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).
|Temporomandibular Joint Disorder||Behavioral: Cognitive Therapy for Catastrophizing Behavioral: Behavioral Therapy for Sleep Continuity Disturbance|
|Study Design:||Allocation: Randomized
Intervention Model: Single Group Assignment
Masking: Single Blind (Outcomes Assessor)
Primary Purpose: Treatment
|Official Title:||Biobehavioral Pain Management in TMD|
- To investigate a proposed causal chain for TMJD pain based on changes in pain modulation, inflammatory profile and clinical pain. [ Time Frame: Pain modulation and Inflammatory profile: Visit 6-8; Clinical Pain: Visit 8 to 3 month follow up ]
Two interventions that experimentally manipulate TMJD pain risk factors (behavioral therapy focusing on sleep continuity disturbance [BT-SCD] and cognitive therapy focusing on pain-related catastrophizing [CT-CAT]) will be compared with a control (education about TMJD and its treatments), to assess changes in and temporal relationships of pain modulation, pain-evoked inflammatory activity and clinical pain.
PAIN MODULATION: Mid change (Visit 6 to Visit 8) in temporal summation and Conditioned Pain Modulation (CPM) INFLAMMATORY PROFILE: Mid change (Visit 6 to Visit 8) in plasma levels of Interleukin-6(IL-6) in blood samples obtained before, during and after Quantitative Sensory Testing (QST) CLINICAL PAIN: Late change (Visit 8 to 3 month follow-up) in the Brief Pain Inventory (BPI) rating of pain severity
- Impact of pre-sleep cognitive arousal on autonomic and cortical arousal during sleep [ Time Frame: at end of 5 year long study ]We propose that pre-sleep cognitive arousal disrupts sleep in TMJD due to its association with cortical and autonomic arousal. Dr. Smith previously showed that pre-sleep cognitive arousal was more closely associated with sleep disturbance than somatic arousal. He further found that pain-related pre-sleep thoughts predicted subsequent self-reported nocturnal awakenings, after controlling for depression and pain severity. Chronic insomnia (with or without pain) is associated with elevations in cortical arousal during sleep. However, increased alpha activity during sleep is not specific to chronic pain and can be observed in depressed patients and some asymptomatic controls. We believe the lack of specificity of these physiologic markers is in part attributable to ignoring pre-sleep cognitive arousal. In our study, we will examine treatment related changes in pre-sleep cognitive arousal and determine whether these changes map onto cortical and autonomic arousal during sleep.
- Determine if manipulation of TMJD pain risk factors (SCD and CAT) reduces autonomic/cortical arousal. [ Time Frame: at Visit 8 per participant (day 63 +/- 1 week) ]
We hypothesize that any reduction in sleep disturbance associated with CT-CAT will be mediated by reductions in pre-sleep (CAT) cognitive arousal.Our proposal to examine indices of cortical and autonomic arousal provides a robust test of whether BT-SCD changes cortical and autonomic arousal in TMJD and directly associates these changes with changes in pre-sleep arousal.
AUTONOMIC AROUSAL: Heart Rate Variability (HRV): Low Frequency/High Frequency (LF/HF) ratio CORTICAL AROUSAL: Quantitative Electroencephalography (QEEG)-derived relative alpha and beta power during Non-Rapid Eye Movement (NREM) sleep
- Determine if BT-SCD and CT-CAT treatments alter clinical pain and inflammatory activity relative to control. [ Time Frame: at Visit 6 (Day 35 +/- 2 weeks) to Visit 8 (Day 63 +/- 2 weeks) per participant ]To determine whether the two interventions that experimentally manipulate pain risk factors (BT-SCD and CT-CAT) alter temporal relationships between secondary measures of pain-evoked inflammatory activity and clinical pain relative to the control. INFLAMMATORY PROFILE: Mid change (Visit 6 to Visit 8) in plasma levels of IL-10 and IL-1ra in blood samples obtained before, during and after QST
|Study Start Date:||April 2013|
|Estimated Study Completion Date:||July 2017|
|Estimated Primary Completion Date:||December 2016 (Final data collection date for primary outcome measure)|
Active Comparator: Cognitive Therapy
Cognitive Therapy for Catastrophizing
Behavioral: Cognitive Therapy for Catastrophizing
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.
Active Comparator: Behavioral Therapy
Behavioral Therapy for Sleep Continuity Disturbance
Behavioral: Behavioral Therapy for Sleep Continuity Disturbance
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.
No Intervention: TMJD Education
6-sessions of TMJD disease education/support control
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01794624
|Contact: Mary Reddingemail@example.com|
|Contact: Lauren Swedbergfirstname.lastname@example.org|
|United States, Maryland|
|University of Maryland Dental School: Brotman Facial Pain Clinic||Recruiting|
|Baltimore, Maryland, United States, 21201|
|Contact: Sharon Gordon 410-706-1656 SGordon@umaryland.du|
|Contact: Katie Bisordi 410-706-6345 Katharine.Bisordi@som.umaryland.edu|
|Sub-Investigator: Sharon Gordon|
|Johns Hopkins Bayview Meidical Center: Behavioral Medicine Research Laboratory||Recruiting|
|Baltimore, Maryland, United States, 21224|
|Contact: Mary Redding 410-550-8099 email@example.com|
|Contact: Michelle Polley 410-550-9057 firstname.lastname@example.org|
|Principal Investigator: Jennifer A Haythornthwaite|
|Principal Investigator: Michael T Smith|
|Principal Investigator:||Jennifer A Haythornthwaite||Johns Hopkins University|
|Principal Investigator:||Michael T Smith||Johns Hopkins University|
|Principal Investigator:||Sharon A Gordon||University of Maryland, School of Dentistry|