This study has a single overall aim: to identify patient predictive markers that determine who benefits most from two CIH treatments (hypnotic cognitive therapy \[HYP-CT\] and Mindfulness-Based Cognitive Therapy \[MBCT\]) and the current gold standard non-pharmacological treatment (CBT) vs. usual care (UC). This aim will be addressed in the context of a clinical trial in which participants with chronic pain will be randomized to one of the three active chronic pain treatments or UC. Based on findings from prior research, the investigators hypothesize that five primary predictive markers assessed at pre-treatment (alpha power, beta power, hypnotizability, nonreactivity \[a mindfulness domain\], and catastrophizing) will modify subsequent treatment-related changes in pain intensity following MBCT, HYP-CT, and CBT, relative to usual care.
The primary clinical endpoint is reduction (change) in average pain intensity from pre- to post-treatment; the post-treatment assessment point is the primary endpoint. Average pain intensity will be measured using a composite of up to 4 separate pain ratings assessed within a 1-week period at each study assessment window. Although there are up to four ratings, each from a different day in a 7-day window, that are used to compute post-treatment average pain severity score, these variables will be used to compute a single score representing average pain during the post-treatment period; therefore, there is only a single primary post-treatment end point.
The primary predictive markers are EEG-assessed alpha and beta power, researcher-measured hypnotizability, and self-reported-pain catastrophizing and non-reactivity mindfulness, all of which will be assessed at pre-treatment.
The five primary study hypotheses are as follows:
Hypotheses 1a, 1b, and 1c: Baseline alpha power will predict pre- to post-treatment change in pain intensity, such that, relative to UC, more alpha power predicts greater change (reduction) in pain intensity in response to HYP-CT (1a), and lower levels of alpha power predict greater pain intensity change (reduction) in response to both CBT (1b) and MBCT (1c).
Hypothesis 2: Baseline beta power will predict pre- to post-treatment change in pain intensity, such that, relative to UC, more beta power predicts greater change (reduction) in pain intensity in response to CBT.
Hypotheses 3a and 3b: Baseline hypnotizability will predict pre- to post-treatment change in pain intensity, such that, relative to UC, more hypnotizability predicts greater change (reduction) in pain intensity in response to HYP-CT (3a), and predicts less change (reduction) in pain intensity in response to CBT (3b), relative to UC.
Hypothesis 4a and 4b: Baseline catastrophizing and the nonreactivity domain of mindfulness will predict pre- to post-treatment change in pain intensity, such that lower levels of baseline catastrophizing (4a) and greater levels of nonreactivity (4b) will predict greater pain intensity change (reduction) in response to MBCT, relative to UC.
Hypothesis 5: Baseline mindfulness will predict pre- to post-treatment change in pain intensity, such that higher levels of baseline mindfulness will predict greater pain reduction in response to MBCT.
Secondary study objectives include:
* Understand the zero order associations between predictive markers and pre- to post-treatment pain reductions for participants in each treatment condition separately.
* Understand the predictive role of the primary predictive markers on longer-term outcomes (i.e., 3 and 6-months post-treatment follow-ups) for the four treatment conditions.
* Understand any differences in clinical outcomes between the three active treatments, relative to usual care.
* Determine if there are any effects of "dose" of treatment on clinical outcomes.
Tertiary/exploratory study objectives include:
* Identify additional potential predictive markers of treatment-related improvements in pain.
* Identify potential predictive markers of treatment effects on secondary outcomes.
* Develop initial treatment matching algorithm.
