The present study examined the relationship between posttraumatic and depressive symptoms during prolonged exposure therapy for PTSD among youth. Consistent with previous studies (e.g., Gilboa-Schechtman et al., 2010
), PE significantly reduced both posttraumatic and depressive symptoms (Paths A and C in ). Moreover, we found support for the reciprocal influence model (model C). However, changes in posttraumatic symptoms accounted for 64.1% of the changes in depressive symptoms, whereas changes in depressive symptoms accounted for only 11.0% of the changes in posttraumatic symptoms. Our findings indicate that reciprocal relations exist between posttraumatic and depressive symptoms during treatment, but changes in posttraumatic symptoms lead to changes in depressive symptoms to a greater extent than vice versa.
According to the tripartite model (Clark & Watson, 1991
), anxiety and depression share a higher-order factor of negative affect. Although it is possible that trauma-focused treatment would target shared posttraumatic and depressive factors leading to reciprocal, simultaneous reductions, our findings suggest that such treatment primarily affects posttraumatic symptoms, which in turn lead to reductions in depressive symptoms. This has important implications for treatments of PTSD, and indicates that treatments do not need to target shared posttraumatic and depressive factors in order to reduce depressive symptoms.
The helplessness/hopelessness theory (Alloy, Kelly, Mineka, & Clements, 1990
) may account for the effect of posttraumatic symptoms on subsequent depressive symptoms during treatment. This theory posits that feelings of helplessness are primarily related to anxiety, whereas feelings of hopelessness are primarily related to depression. According to this theory, experiencing helplessness repeatedly or for long periods of time, can lead to hopelessness (Alloy et al., 1990
). Thus, as individuals begin to better cope with their symptoms during treatment, their helplessness is reduced, which results in subsequent reductions in hopelessness. Alternatively, the anhedonia model of depression (Loas, 1996
) may also account for the findings of the present study. It is possible that diminishing anxiety and avoidance levels during treatment, may lead to the increased experience of pleasurable life events, thus reducing anhedonia and subsequent depression (Loas, 1996
Our findings are congruent with those of Moscovitch et al. (2005)
, who found that social anxiety reduction leads to depression reduction to a greater extent than vice versa during treatment for social anxiety disorder. However, it remains unclear if the relationship found in the present study holds in other treatments. For example, since cognitive biases play an important role in both PTSD and depression, treatments that are more cognitively-focused and less exposure-based than PE may lead to a more reciprocal relationship between posttraumatic and depressive symptoms. Future studies may examine the relationship between posttraumatic and depressive symptoms in various treatments for PTSD in order to elucidate whether different treatments for PTSD work through similar mechanisms. In addition, future studies may also examine the relationship between anxiety and depressive symptoms in individuals with primary depression. Examining such a group of patients can indicate whether the relationship found in the present study is a result of primary PTSD or whether it represents a general anxiety-depression relationship during treatment.
In closing, we would like to note several limitations of the present study. First, we did not include a control condition and therefore cannot assess whether our findings are specific to processes that occur during PE or capture more naturalistic processes underlying changes in PTSD and depression. Second, the present study focused solely on the interplay between posttraumatic and depressive symptoms and did not assess mechanisms that could account for the findings. Future studies may investigate mechanisms by which posttraumatic symptoms can affect depressive symptoms (e.g., cognitions, hopelessness, anhedonia, positive and negative affect, physiological arousal) in order increase our understanding of the pathways connecting posttraumatic symptoms and depressive symptoms.
Despite these limitations, the present study represents the first multilevel mediational study of the longitudinal relationship between posttraumatic and depressive symptoms, during the treatment of PTSD. Our findings extend previous research on treatment for PTSD, by indicating that PE affects depressive symptoms primarily through its effect on posttraumatic symptoms.