UC Berkeley

Objective

The goal of the current study was to examine mechanisms of change in prolonged exposure (PE) therapy for posttraumatic stress disorder (PTSD). Emotional processing theory of PTSD proposes that disconfirmation of erroneous cognitions associated with PTSD is a central mechanism in PTSD symptom reduction; but to date, the causal relationship between change in pathological cognitions and change in PTSD severity has not been established.

Method

Female sexual or nonsexual assault survivors (N = 64) with a primary diagnosis of PTSD received 10 weekly sessions of PE. Self-reported PTSD symptoms, depression symptoms, and PTSD-related cognitions were assessed at pretreatment, each of the 10 PE treatment sessions, and posttreatment.

Results

Lagged mixed-effect regression models indicated that session-to-session reductions in PTSD-related cognitions drove successive reductions in PTSD symptoms. By contrast, the reverse effect of PTSD symptom change on change in cognitions was smaller and did not reach statistical significance. Similarly, reductions in PTSD-related cognitions drove successive reductions in depression symptoms, whereas the reverse effect of depression symptoms on subsequent cognition change was smaller and not significant. Notably, the relationships between changes in cognitions and PTSD symptoms were stronger than the relationships between changes in cognitions and depression symptoms.

Conclusions

To our knowledge, this is the 1st study to establish change in PTSD-related cognitions as a central mechanism of PE treatment. These findings are consistent with emotional processing theory and have important clinical implications for the effective implementation of PE.