Symposia
Trauma and Stressor Related Disorders and Disasters
Philip Held, Ph.D.
Assistant Professor
Rush
Chicago, Illinois
Dale Smith, PhD
Statistician
Rush University Medical Center
Chicago, Illinois
Debra Kaysen, ABPP, Ph.D.
Professor
Stanford University
Palo Alto, California
Although evidence-based PTSD treatments, such as Cognitive Processing Therapy (CPT), have been demonstrated to be effective and produce large symptom reductions, not everyone responds favorably. To date, there is little clinical research to help identify optimal subsequent courses of treatment for initial non-responders. Examining the engagement of previously identified treatment mechanisms, such as changes in negative posttraumatic cognitions, among non-responders could provide important information to guide future treatment selections.
To determine trauma cognition change trajectories among non-responders, we utilized a sample of 502 veterans who completed a 3-week CPT-based intensive PTSD treatment program and completed repeated measures. We previously identified four different PTSD symptom trajectories. For this study, we selected 244 veterans who did not experience a meaningful PTSD symptom reduction (hereafter referred to as “non-responders”). The subsample of these non-responders did not differ from the overall sample based on demographic characteristics (ps >.05). We then used group-base trajectory modeling to examine trauma cognition change trajectories based on the Posttrauma Cognitions Inventory (PTCI).
A two-trajectory group solution fit the data well based on Nagin’s guidelines (e.g., odds of correct classification >5). Approximately 35.80% (n=87) of the non-responders exhibited slow trauma cognition change whereas 64.20% (n=156) exhibited no trauma cognition change over the course of treatment. Trauma cognition change did not exactly match PTSD severity change, suggesting that they are distinct constructs.
The presentation will conclude with a discussion about ways in which trauma cognition change patterns may be used to identify the optimal subsequent course of treatment for initial non-responders. For example, individuals whose trauma cognitions do not change during the initial course treatment may indicate that individuals could benefit from a subsequent treatment which engages the identified mechanism differently. On the other hand, individuals who exhibit slow trauma cognition change during the course of treatment may benefit from additional time in the same treatment as the purported mechanism appears to be engaged, albeit slowly.