Mediation of Changes in Panic Symptom Severity over Time
Our multimediator model is displayed in . This model examines the three potential mediators of changes in PDSS simultaneously, thus calculating the effects of each while controlling for the effects of the other mediators. Below, we present the results for each mediator in turn, discussing its significance as a mediator and its specificity to treatment condition.
Examining the results for each mediator, we found that PCO2
was a moderated mediator of PDSS. The a
path (from Time to PCO2
) was moderated by treatment condition, bdiff
= –.16, t
(36) = –2.15, p
< .05. The a
path was significant for those in CART, b
= .23, t
(36) = 6.47, p
< .01, but not for those in CT, b
= .08, t
(36) = 1.25, p
= .21. The b
path (from PCO2
to PDSS) was not moderated by treatment condition (p
= .57) and was significant, b
= –.24, t
(57) = –2.39, p
< .05. Following Tein, Sandler, MacKinnon, and Wolchik (2004)
, we calculated the magnitude and significance of the mediated pathway from time to PDSS through PCO2
separately for each treatment condition. As expected, PCO2
was a significant mediator of changes in PDSS over time for patients in the CART condition, a
= –.070, 95% CI [–.139, –.009], PM
= .27, but not for those in the CT condition, a
= –.016, 95% CI [–.054, .008], PM
= .06. Reverse mediation analysis (employing PDSS as the mediator and PCO2
as the outcome) was not significant, suggesting that the mediation was unidirectional.
Symptom appraisal was also a moderated mediator of PDSS, because the path from ASI/BSQ to PDSS was moderated by treatment condition, bdiff = .40, t(57) = 2.55, p = .01. This path was significant for those in CT, b = .39, t(57) = 3.10, p < .005, but not for those in CART, b = –.01, t(57) = –.08, p = .93. The path from Time to ASI/BSQ was not moderated by treatment (p = 1.00) and was significant, b = –.16, t(38) = –4.19, p < .01. Calculating the significance of the mediated pathway (from Time to PDSS through ASI/BSQ) for each treatment condition, we found it to be significant for patients in the CT condition, a*b = –.059, 95% CI [–.118, –.014], PM = .23, but not for those in the CART condition, a*b = .002, 95% CI [–.037, .041], PM = –.01. Reverse mediation analysis indicated the PDSS was a moderated mediator of symptom appraisal, such that PDSS mediated changes in symptom appraisal in CT (p < .05) but not in CART (p = .65). Thus, the effect of symptom appraisal on PDSS appears to be specific to CT and bidirectional.
Neither segment of the mediated pathway involving perceived control (ACQ) was moderated by treatment (p = .92 for path a; p = .77 for path b). Therefore ACQ was not a moderated mediator of PDSS. However, both segments of the mediated pathway linking Time and PDSS through ACQ were significant: path a, b = .12, t(38) = 3.07, p < .01; path b, b = –.34, t(57) = –4.17, p < .001. The mediated pathway was significant across treatment conditions, a*b = –.039, 95% CI [–.077, –.011], PM = .15 for CART; a*b = –.045, 95% CI [–.093, –.010], PM = .17 for CT. Reverse mediation analyses indicated that PDSS also mediated changes in ACQ (regardless of condition, ps < .05), indicating that the relation between ACQ and PDSS was bidirectional.
Because a previous study indicated that RR was not related to symptom appraisal in CART (Meuret et al., 2009
), we sought to replicate these findings by adding RR to our mediation model for PDSS. Results confirmed that RR did not mediate changes in PDSS over time, a
= –.006, 95% CI [–.049, .034], PM
= .02 for CART; a
= .003, 95% CI [–.018, .027], PM
= –.01 for CT.
Finally, individual mediator analyses were conducted to examine whether each of these mediators by themselves, without controlling for the other mediators, would mediate changes in PDSS. These results replicated those from the multimediator analysis, except that ASI/BSQ was found to be a significant mediator of PDSS in CART as well as in CT in the single mediator analysis (p
To further explore this result, we performed two double mediator analyses, including ASI/BSQ in each and adding either PCO2
or ACQ as the second mediator. Results indicated that ASI/BSQ remained a significant mediator of PDSS in CART when combined with PCO2
< .05) but not when combined with ACQ. These findings suggest that the relation between ASI/BSQ and PDSS in CART is due to the relation between ASI/BSQ and ACQ.
Relations among the mediators
While the mediation model for PDSS establishes the direct relations between each mediator and PDSS, each mediator may also affect PDSS indirectly through its effect on the other mediators. The mediation model above did not explore the relations among the mediators. Thus, we examined the relations among the three mediators to determine if there was evidence for indirect effects of the mediators on panic symptom severity.
PCO2 and symptom appraisal
It was hypothesized that PCO2 would mediate changes in symptom appraisal in the CART condition. Mediation analyses indicated that PCO2 was a significant mediator of changes in symptom appraisal in CART, a*b = –.018, 95% CI [–.032, –.005], PM = .11, but not in CT, a*b = –.006, 95% CI [–.018, .003], PM = .04. Within-subject, cross-lag panel analyses supported this finding: Prior levels of PCO2 led to later levels of ASI/BSQ for CART but not for CT (see ). There was no evidence that symptom appraisal mediated changes in PCO2 (reverse mediation), a*b = .004, 95% CI [–.009, .018], PM = .02 for CART; a*b = .004, 95% CI [–.009, .018], PM = .05 for CT, and cross-lag analyses showed that earlier symptom appraisal was not a significant predictor of later PCO2 for either condition (see ).
PCO2 and perceived control
As hypothesized, PCO2 mediated changes in ACQ in the CART condition, a*b = .043, 95% CI [.014, .077], PM = .36, but not in the CT condition, a*b = –.001, 95% CI [–.011, .008], PM = –.01. Cross-lag panel analysis supported these findings: Earlier levels of PCO2 were related to later levels of ACQ in the CART condition but not in the CT condition (see ). ACQ did not mediate changes in PCO2, a*b = .008, 95% CI [–.011, .031], PM = .04 for CART; a*b = –.006, 95% CI [–.025, .011], PM = –.07, for CT, nor did the cross lags indicate that earlier ACQ led to later PCO2 for either condition (see ). Thus, the mediation and reverse mediation analyses, as well as the cross-lag analyses, support PCO2 as a unidirectional mediator of changes in perceived control.
Symptom appraisal and perceived control
Mediation analyses showed that ASI/BSQ mediated changes in ACQ regardless of condition, a*b = .075, 95% CI [.036, .123], PM = .62 for CART; a*b = .036, 95% CI [.016, .062], PM = .30 for CT, and that ACQ mediated changes in ASI/BSQ, a*b = –.049, 95% CI [–.088, –.017], PM = .31 for both conditions. However, cross-lag panel analyses showed only that earlier levels of ASI/BSQ were related to later levels of ACQ, but only in CART, and that earlier levels of ACQ were not related to later levels of ASI/BSQ in either condition (see ). These findings suggest that symptom appraisal is generally bidirectionally related to perceived control; however, the lack of consistent cross-lag relations between the two suggests that they do not “cause” each other but are related in some other way (e.g., due to a mutual relation to a third variable or to construct overlap). The exception may be for CART, in which symptom appraisal preceded and affected perceived control. Although symptom appraisal and perceived control may have some construct overlap, the fact that ASI/BSQ mediated PDSS in CT when controlling for perceived control suggests that they also have some separate underlying components that differentially impact PDSS.