Cognitive-Behavioral Treatment for Depression: Relapse Prevention

Transcription

1 Journal of Consulting and Clinical Psychology, Vol., No., -8 Copyright by the Americ; i Psychological Association, Inc X/8/S.00 Cognitive-Behavioral Treatment for Depression: Relapse Prevention Eric Tomas Gortner and Jackie K. Gollan University of Washington Neil S. Jacobson University of Washington Keith S. Dobson University of Calgary This study presents -year follow-up data of a comparison between complete cognitive-behavioral therapy for depression (CT) and its major components: behavioral activation and behavioral activation with automatic thought modification. Data are reported on participants who were randomly assigned to of these treatments for up to 0 sessions with experienced cognitivebehavioral therapists. Long-term effects of the therapy were evaluated through relapse rates, number of asymptomatic or minimally symptomatic weeks, and survival times at -, -, -, and -month follow-ups. CT was no more effective than its components in preventing relapse. Both clinical and theoretical implications of these findings are discussed. To investigate the theory of change as formulated by Beck and colleagues in the cognitive theory of depression (Beck, Rush, Shaw, & Emery, ), we conducted a component analysis of cognitive-behavioral treatment (CT) for depression. CT is based on a theory of change that posits cognitive structures as the active ingredient. However, the techniques used to alter cognitive structures are many, and alternative interpretations for the efficacy of CT abound. We were primarily interested in two alternative hypotheses: (a) the activation hypothesis, which was tested by treating depressives with that component of CT that focuses exclusively on behavioral activation (BA), and (b) the coping skills hypothesis, which was tested by treating other depressives with a component of CT that added to BA an attempt to modify automatic dysfunctional thinking (AT). The rationale for choosing these particular component treatments is described elsewhere (Jacobson et al. ). The overall aim of the component analysis was to assess the short- and long-term outcomes of these three specific forms of treatment (Jacobson et al., ). We randomly assigned depressed outpatients to one of the three treatments: (a) BA, (b) AT, or (c) a treatment that allowed the full range of CT interventions, including the modification of depressive cognitive structures. Because Beck and colleagues () hypothesized that change in CT is uniquely connected to explicitly cognitive interventions, one would expect that the full CT treatment would significantly outperform the other two conditions: BA and AT. Eric Tomas Gortner, Jackie K. Gollan, and Neil S. Jacobson, Department of Psychology, University of Washington; Keith S. Dobson, Department of Psychology, University of Calgary, Calgary, Alberta, Canada. This article was part of Eric Tomas Conner's doctoral dissertation under the supervision of Neil S. Jacobson. Preparation of this article was supported by National Institute of Mental Health Grants R0 MH0-0 and K0 MH We gratefully acknowledge the contributions of Michael E. Addis, Kelly Koerner, Stacey E. Prince, and Paula A. Truax to this project. Correspondence concerning this article should be addressed to Neil S. Jacobson, Department of Psychology, University of Washington, NE th Street, Suite, Seattle, Washington 8-. Further, the AT condition, with a partial cognitive package, should perform better than the BA condition, which offered no direct cognitive interventions. In contrast to predictions following Beck et al.'s () cognitive theory, we found nonsignificant differences in outcome between the three treatments. Participants exposed to the complete CT treatment did not fare better than those with the partial package of cognitive interventions (AT) and those with no cognitive interventions (BA). At least with regard to the immediate outcome, BA performed remarkably well in comparison to CT. These results are inconsistent with the cognitive theory of change (Beck) but serve as a discovery that could lead to a more parsimonious treatment for depression (see Jacobson et al., ). However, it is possible that CT, when presented in isolation, prevents relapse to a greater degree than either of the component treatments. Indeed, the cognitive theory of depression suggests that the modification of dysfunctional schema should pay its greatest dividends in relapse prevention. It may not be surprising that differences did not emerge during acute treatment, because the primary purpose of CT is to produce fundamental changes in the way depressives view themselves, their world, and their future. Perhaps such schematic changes would only reveal themselves in studies that monitor participants for a significant period of time after treatment termination. Similar studies, reviewed by Hollon, Shelton, and Loosen (), suggest that CT may have a superior relapse prevention effect relative to pharmacotherapy that has been discontinued. Therefore, acute treatment findings may not provide the strongest test of Beck's theory. The primary purpose of the present study was to examine the relapse prevention potential of the three treatments (BA, AT, and CT) first reported by Jacobson et al. (). Comparisons were made of those who responded favorably during the acute treatment phase as well as those who did not at -, -, -, and -month follow-up evaluations. We examined the proportion of participants in each treatment condition who reported at least one relapse by the time each follow-up evaluation was conducted, the number of weeks that participants in each treatment

2 8 GORTNER, GOLLAN, DOBSON, AND JACOBSON condition remained free of depression over the -year period, and the relative effectiveness of each treatment, taking into account both acute and long-term treatment response. A secondary purpose of this study was to examine the longterm outcomes of CT on an absolute basis. Surprisingly, few well-designed investigations go back as far as years posttreatment for their research (Blackburn, Eunson, & Bishop, ; Evans et al., ; Gallagher-Thompson, Hanley-Peterson, & Thompson, 0). The studies that have conducted long-term follow-ups are difficult to interpret because of their small sample sizes and high attrition rates (see Hollon et al., ). Furthermore, there is wide divergence in the relapse rates reported, ranging from 0% (Evans et al., ) to % (Gallagher- Thompson et al., 0). There is similar divergence in reported relapse rates in those studies that examined - or -month follow-ups (Elkin et al., ; Kovacs, Rush, Beck, & Hollon, ; Simons, Murphy, Levine, & Wetzel, ; Thase et al., ) with a range from 0% (Simons et al., ) to % (Kovacs et al., ) at the -year follow-up. Given the divergence about the long-term outcomes of CT, we sought to revisit this issue in the present study. Sample Method Details about participant selection, exclusion criteria, treatment assignment, therapy conditions, interrater reliabilities, and assessment of outcome during the acute treatment phase have been described elsewhere (see Jacobson et al., ) and are only summarized here. One hundred fifty-one participants were entered into the study according to the following criteria: major depression according to the Diagnostic and Statistical Manual of Mental Disorders (third edition, revised [DSM-III-R]; American Psychiatric Association, ), a score of 0 or higher on the Beck Depression Inventory (BDI; Beck et al., 8), and a score of or higher on the -item Hamilton Rating Scale for Depression (HRSD; Hamilton, T). DSM-III-R diagnoses were made using the Structured Clinical Interview for the DSM-III-R (Spitzer, Williams, & Gibbons, ). Once the individual qualified for the study, they were matched on a number of variables and then randomly assigned to one of three treatment conditions: BA, AT, or CT. Participants met for up to 0 sessions over a -week period with one of four experienced therapists who were trained to provide treatment in all three conditions. Treatments All three treatments are based on the techniques and descriptions in the Beck et al. () CT manual and are described in our previous report (Jacobson et al., ). The BA treatment focused primarily on identifying specific life problems and prescribing a set of semi structured activities that helped participants make contact with natural reinforcers in the environment. Therapists encouraged participants to monitor daily activities, assess their pleasure and mastery in activities, discuss problematic life situations, and make contact with potential reinforcers. The AT condition began with BA and moved into the identification and modification of dysfunctional thinking. Participants focused on identifying and modifying negative patterns of thinking in specific situations that were related to depressive actions. Some techniques included recording dysfunctional thinking, examining the validity and basis of each thought, empirically testing beliefs, and practicing more functional responses to them. The CT treatment included BA and dysfunctional thought modification, but also incorporated the identification and structural modification of generalized core beliefs that were presumed to be the major causes of dysfunctional thinking and depressive reactions. Outcome Measures To assess the longitudinal course of psychiatric disorders and depression severity, all participants were evaluated after treatment and at -, -, -, and -month follow-up sessions using the Longitudinal Interval Follow-Up Evaluation (LIFE-II; Keller et al., ). The LIFE-II is a semistructured interview specifically designed to assess DSM-III-R psychopathology over the previous months. We used the LIFE s psychiatric status ratings to measure weekly changes in the participant's reports of depressive symptoms, which helped us to measure the degree of recovery from previous or new episodes, the occurrence and degree of relapse, and severity of past and current depressive symptoms. Participants were also given the -item HRSD (Hamilton, ) at each follow-up evaluation, administered by a clinical ^valuator (Whisman et al., ). This is a widely used interviewer-based measure of depression severity. As a second self-report measure of depression severity, the BDI (Beck et al., ) was administered at each follow-up evaluation, This is another widely used measure of depression severity that correlates highly with the HRSD. Data Analysis We conducted most of our follow-up analyses on only recovered participants who completed at least of the 0 therapy sessions offered {"completed ) and had complete follow-up data. We had remarkably low attrition rates during both acute treatment and follow-up: % of participants who entered the study went on to complete at least sessions or more. We were able to obtain complete follow-up data across years for 0% to % of treatment respondcrs (attrition rate varies depending on recovery criterion). The rates of attrition during acute treatment and follow-up were comparable in the three conditions. We used three different criteria to determine whether participants had recovered after treatment: (a) BDI scores of less than after treatment and minimal or no depressive symptoms on the LIFE-II instrument after treatment (i.e., ratings of or on the LIFE-n for the previous weeks directly preceeding posttreatment evaluation); (b) HRSD scores of less than 8 and minimal or no depressive symptoms on LIFE-II at posttreatment evaluation; (c) a minimum of 8 consecutive weeks after the end of treatment with minimal or no depressive symptoms on the LIFE-II instrument. These three criteria, although arbitrary, were recommended by Frank et a]. () to standardize measurement of recovery in depression research. The inclusion of outcome results based on these three different criteria allows us to better compare our results with previous studies that used similar criteria. Relapse was defined as a period consisting of at least consecutive weeks during which the recovered participant subsequently met DSM- IH-R criteria for depression (psychiatric status ratings of or on the LIFE-II instrument). We also considered a return to treatment for depression as a relapse, whether or not the participant reported the return of depressive symptoms on the LIFE-II. Total number of "well weeks" was defined as the number of weeks during follow-up that recovered participants had no or only minimal symptoms of depression (psychiat- This definition has been slightly altered from our previous report (Jacobson et al., ) to match exactly the recovery definition used in the National Institute of Mental Health (NIMH) Collaborative Depression Study (Shea et al., ). Whereas our earlier definition allowed recovery to occur before treatment termination, this definition, as in the Treatment of Depression Collaborative Research Program, makes recovery contingent on maintaining treatment gains for 8 consecutive weeks after treatment termination.

3 RELAPSE PREVENTION ric status ratings of or on the LIFE-II instrument). We also used our primary measures of depressive symptoms (BDI and HRSD) to assess severity of depression at the time of follow-up for all participants in the sample. Although the assessment of depressive symptoms at follow-up does not tell us much about how participants were doing in between the follow-up assessments, it does allow us to retain all participants in the sample for follow-up analyses, thus preserving randomization. By comparing participants at posttreatment with those at the various follow-up points, we were able to provide a parametric assessment of change in depressive severity during the follow-up period. More important, by comparing participants at pretreatment and at the follow-up points, we were able to determine the "ultimate" impact of therapy, because such comparisons take into account both acute and long-term treatment response. We examined long-term outcomes for responders in three ways. First, we used contingency table analyses to compare relapse rates for treatments at each follow-up time period. Second, analyses of variance were used to compare treatments in the cumulative number of well weeks at each follow-up period. Third, survival analyses were used to compare relapse rates among the treatments. We used the Kaplan-Meier product limit to generate survival curves for each treatment. These survival analyses allow us not only to consider differential relapse rates in each condition but also to take into account the amount of time that participants remained well before relapse. We also conducted a series of parametric analyses that retained all participants in the sample throughout the follow-up period whether or not they responded positively during the acute treatment phase. Using both the BDI and the HRSD as outcome measures, analysis of covariance (ANCOVAs) were conducted with the follow-up scores as criterion for depressive severity and posttest scores as covariates. This provided a comparative analysis of depression severity after treatment completion, controlling for posttreatment levels of depression. In addition, we conducted ANCOVAs with pretreatment scores used as covariates to determine the ultimate impact of therapy at each of our follow-up assessments. Table Recovery Rates for Each of the Three Criteria by Treatment Conditions After Treatment Recovered (BDI < )' Recovered Not recovered Recovered (HRSD < 8)" Recovered Not recovered Recovered (LIFE-II) C Recovered Not recovered Note. Recovered (BDI < ) included those participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who had scores of less than on the BDI after treatment termination. Recovered (HRSD < 8) included those participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who also had scores of less than 8 on the HRSD. Recovered (LIFE-II) included those participants who were either symptom-free or minimally symptomatic for at least 8 consecutive weeks on the LIFE-II interview. BA = behavioral activation; AT = automatic thoughts; CT = cognitive-behavioral therapy; BDI = Beck Depression Inventory; HRSD = Hamilton Rating Scale for Depression; LIFE-II = Longitudinal Interval Follow-Up Evaluation II. 'X (, JV = ) = 0.. b x' (, N = ) =.0. C X (,N= ) =.. Recovery Rates Results A more comprehensive description of our entire sample and the response to acute treatment is available in Jacobson et al. (). Table shows recovery rates, according to each of our recovery criteria, for the three treatment conditions after the end of treatment. Depending on the recovery criterion used, approximately 0% to 0% of treatment completers recovered at the end of treatment. There were no significant differences in recovery rates between the three treatment conditions, regardless of how recovery was denned. Relapse Rates Table, Table, Table, and Table show the percentage of treatment responders who had relapsed by each follow-up time period for the three treatment conditions. We report relapse rates for those participants who met relapse criteria on the LIFE- II interview and for those participants who either met LTFE-I relapse criteria or returned to treatment for depression during the time period up to the particular follow-up. Across all followup time periods, there were no significant differences in relapse rates between conditions regardless of how recovery or relapse were defined. As Table shows, by the -year follow-up, roughly % of the BA participants suffered a depressive relapse compared with roughly % of the CT participants. Well Weeks Table shows the mean cumulative number of well weeks at each follow-up period for the three conditions. The maximum number of well weeks for each time period was, with a maximum number of weeks across all follow-ups. There were no significant differences in the mean number of well weeks between the three conditions regardless of how recovery was defined. On average, participants reported no or minimal depressive symptoms for more than % of the weeks during the -year follow-up period. Although we previously have reported the recovery rates for the recovered BDI < group (Jacobson et al., ), we did not report recovery rates for the two other definitions of recovery. The relapse rates in Table are different from those previously reported in Jacobson et al., () for several reasons; (a) We now have complete follow-up data and report on those participants with data at all time points; (b) our relapse numbers are based on treatment completers versus all participants; and (c) an extensive clinical edit of our LIFE-II data revealed several clinical and data entry inconsistencies (e.g., participants who suffered from brief uncomplicated bereavement reactions were erroneously coded as having met relapse criteria). Well weeks data are difficult to interpret because they are often confounded with return to treatment. However, in our sample, total number of well weeks did not correlate significantly with return to treatment (r = -.).

4 80 GORTNER, GOLLAN, DOBSON, AND JACOBSON Survival Time to First Relapse We conducted survival analyses to compare the mean survival time in weeks before relapse for each of the three treatment conditions. Figure shows the time to first relapse in each condition for those participants meeting LIFE-II recovery criterion. Log-rank tests comparing the survival times between conditions revealed no significant differences between the three treatments, X (, N = ) =.0. The mean survival times in weeks for the weeks of follow-up were 8. weeks for BA,. weeks for AT, and 8. weeks for CT. BD and HRSD Scores at Each Follow-Up Period Table illustrates the results of our parametric analyses on BDI and HRSD scores. We conducted two series of ANCOVAs for each follow-up period. Our first series of ANCOVAs controlled for posttest BDI (or HRSD) scores and represent comparisons of depression severity from posttest to follow-up evaluation. As Table shows, there were, on average, no changes in depression from posttest evaluation to any of the follow-up points in any treatment condition. Moreover, CT was no more effective at preventing changes in depression from posttest to follow-up evaluation than either AT or BA. Our second series of ANCO\As takes into account acute treatment response by Table Percentage of Participant!, Who Through -Month Follow-Up Recovered (BDI < )" Recovered (HRSD < 8)" Recovered (LIFE-II)" *, L Note. Recovered (BDI < ) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who had scores of less than on the BDI after treatment termination. Recovered (HRSD < 8) included those participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who also had scores of less than 8 on the HRSD. Recovered (LIFE-II) included those participants who were either symptom-free or minimally symptomatic for at least 8 consecutive weeks on the LTFE-II interview. = participants who either returned to treatment for depression or met LIFE- II relapse criteria during follow-up; BA = behavioral activation; AT = automatic thoughts; CT = cognitive-behavioral therapy; BDI = Beck Depression Inventory; HRSD = Hamilton Rating Scale for Depression; LIFE-IT = Longitudinal Interval Follow-Up Evaluation II. X b (. N = 8) =.8. x (, JV = ) = 0.. ' x~' (, N = ) =.. Table Percentage of Participants Who Through -Month Follow-Up Recovered (BDI < )' Recovered (HRSD < 8) b Recovered (LIFE-II) Note. Recovered (BDI < ) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who had scores of less than on the BDI after treatment termination. Recovered (HRSD < 8) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who also had scores of less than 8 on the HRSD. Recovered (LIFE-II) included participants who were either symptom-free or minimally symptomatic for at least 8 consecutive weeks on the LIFE-II interview. = participants who either returned to treatment for depression or met LIFE-II relapse criteria during follow-up (or previous follow-up evaluations); BA = behavioral activation: AT = automatic thoughts; CT = cognitive-behavioral therapy; BDI = Beck Depression Inventory; HRSD = Hamilton Rating Scale for Depression; LIFE-II = Longitudinal Interval Follow-Up Evaluation II. "X (, /V = 8) = 0.. b r (, N = ) = 0., m. "X (, N = ) =.. controlling for pretest BDI (or HRSD) scores and, therefore, shows the ultimate impact of therapy. As Table indicates, CT was no more effective than either treatment component over the course of the follow-up period than either AT or BA regardless of the follow-up point examined. In short, parametric analyses revealed that all of the treatments led, on average, to lasting change, but CT was no more effective at bringing about such change than either BA or CT. Discussion This article extends the scope of our findings from acute treatment response to longer term outcomes, including up to years posttreatment. Our results regarding the relative effectiveness of different components of cognitive therapy for depression indicate that there were nonsignificant differences in long-term outcomes between the BA. AT, and CT conditions regardless of the recovery definition used or how relapse was operationalized. The three treatment conditions were virtually identical on every criterion measure, including recovery and relapse rates, number The survival analysis results were virtually identical across all three recovery criteria.

5 RELAPSE PREVENTION 8 Table Percentage of Participants Who Through -Month Follow-Up Recovered (BDI < )' Recovered (HRSD < 8)* Recovered (LIFE-II)' Note. Recovered (BDI < ) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who had scores of less than on the BDI after treatment termination. Recovered (HRSD < 8) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who also had scores of less than 8 on the HRSD. Recovered (LIFE-I) included participants who were either symptom-free or minimally symptomatic for at least 8 consecutive weeks on the LIFE-n interview. participants who either returned to treatment for depression or met LIFE-TI relapse criteria during follow-up (or previous follow-up evaluations); BA = behavioral activation; AT automatic thoughts; CT = cognitive-behavioral therapy; BDI - Beck Depression Inventory; HRSD = Hamilton Rating Scale for Depression; LIFE-TI = Longitudinal Interval Follow-Up Evaluation II. 'X (, N = 8) = 0.. " r (, N = ) = 0.. " x (, N = ) = 0.0. of well weeks, and survival time to relapse. In other words, the full CT package was no more effective at preventing depressive relapse or recurrence than either of its component parts. These results necessarily raise important questions about the theory of change offered by Beck and his associates (). They attributed the active ingredients of CT to the cognitive interventions allowed only in one of these conditions. These interventions are viewed as necessary in permanently altering depressogenic schema. Schematic change in cognitive structures is seen as necessary to preventing relapse. However, the present findings do not support this theory of change; the inclusion of cognitive interventions did not have any additive positive effect in either acute treatment response or relapse prevention. Also, as reported by Jacobson et al. (), changes in cognitive mechanisms were not related to treatment improvements in the CT condition. This finding has implications for the way that cognitive therapy is practiced. If the BA treatment is as effective as the AT and CT treatments, then there is no added reason to engage in cognitive strategies when treating depression; strictly activation strategies may be sufficient. Because BA involves fewer intervention options than CT and is a relatively uncomplicated treatment, it may be particularly well suited for paraprofessional or self-administered implementations, making BA uniquely cost effective (cf. Christensen & Jacobson, ). However, despite the apparent equivalence of BA to CT, our study does not explain the basis for this equivalence. Several interpretations are possible, and exploring them all is beyond the scope of this article. For example, certain types of depressives are less likely to benefit from BA than others (Addis & Jacobson, ), and there may be a number of other client variables that have the potential to predict differential treatment response. Future research should explore such possibilities. Moreover, by definition, participants in the BA condition received more BA than did those in the other treatment conditions. Although one might be tempted to infer from this study that cognitive interventions are nonessential, our study does not directly address the validity of such an interpretation. All we can conclude is that adding cognitive interventions to BA is no more effective than using that time to add more BA. This study also provides information about the absolute longterm effectiveness of cognitive therapy. Almost half of those who recovered by the end of treatment had suffered a relapse by the -month follow-up. Are these relapse rates artificially inflated? Was the CT administered in this study inferior to that administered in other trials? We tried to provide an optimal test of CT. First, adherence ratings demonstrated that therapists did practice CT but only in the CT condition; cognitive interventions Table Percentage of Participants Who Through -Month Follow-Up Recovered (BDI < )" Recovered (HRSD < 8)" Recovered (LIFE-TI) C Note. Recovered (BDI < ) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who had scores of less than on the BDI after treatment termination. Recovered (HRSD < 8) included participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who also had scores of less than 8 on the HRSD. Recovered (LIFE-II) included participants who were either symptom-free or minimally symptomatic for at least 8 consecutive weeks on the LIFE-II interview. = participants who either returned to treatment for depression or met LIFE-II relapse criteria during follow-up (or previous follow-up evaluations); BA = behavioral activation; AT = automatic thoughts; CT = cognitive-behavioral therapy; BDI = Beck Depression Inventory; HRSD = Hamilton Rating Scale for Depression; LIFE-II = Longitudinal Interval Follow-Up Evaluation II. X (, N = 8) = 0.. b * (. N = ) = 0.. "X (, N = ) -..

6 8 GORTNER, GOLLAN, DOBSON, AND JACOBSON Table Mean Number of Well Weeks During All Follow-Up Periods by Condition Well week M SD M SD M SD Recovered (BDI < ) months months months months Recovered (HRSD < 8) months months months months Recovered (LIFE-II) months months months months F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < F(, ) < Note. Recovered (BDI < ) included those participants who were either symptom free or minimally symptomatic for at least weeks immediately before posttest and who had scores of less than on the BDI at posttest. Recovered (HRSD < 8) included those participants who were either symptom-free or minimally symptomatic for at least weeks immediately before posttest and who also had scores of less than 8 on the HRSD. Recovered (LIFE-II) included those participants who were either symptom-free or minimally symptomatic for at least 8 consecutive weeks on the LIFE-II interview directly before posttest. Well weeks are defined as weeks in which the psychiatric status rating was coded (no depressive symptoms) or (minimally symptomatic) on the LIFE-II interview. BA = behavioral activation; AT = automatic thoughts; CT = cognitive-behavioral therapy; BDI = Beck Depression Inventory; HRSD = Hamilton Rating Scale for Depression; LIFE-II = Longitudinal Interval Follow-Up Evaluation II. did not "slip" into the BA condition. We also had a recognized expert in cognitive therapy (Keith S. Dobson) supervise CT therapists and determine that they performed competent cognitive therapy. Perhaps the best testament to the quality of our cognitive therapy is the CT recovery rates at posttreatment; our 0% recovery rates are entirely consistent with previous studies conducted by recognized cognitive therapy experts (cf. Hollon et al., ; Simons et al., ). If our cognitive therapy was inferior in any way, the effects were certainly not evident at posttreatment. A close examination of our relapse rates at each time period shows that the results are consistent with other findings on longterm outcomes for CT. For instance, at the -year follow-up, we found that roughly 0% of the recovered participants in our CT condition had experienced a relapse. This 0% figure is equal to or better than that of other CT studies that monitored participants up to year (Kovacs et al., ; Shea et al., ; Simons et al., ; Thase et al., ). Only two other studies reported a -month follow-up (Blackburn et al., ; Evans et al., ). However, one of them (Blackburn et al., ) U 0 ' No. of well weeks before first relapse Figure. Survival curves for time to first relapse by condition. CT = cognitive-behavioral therapy; AT = automatic thoughts; BA = behavioral activation. We subsequently had two outside experts in cognitive therapy independently rate of our CT sessions to see whether their ratings agreed with Keith S. Dobson's ratings. The results were contradictory and point to the problems with operationalizing and measuring the construct of competence. Even though the two outside experts rated identical tapes, their competence ratings were not significantly correlated with each other (r =.0). One expert rated our therapists as being as highly competent as rated by Dobson, whereas the other expert rated our therapists as being significantly less competent than did Dobson. However, only Dobson's competence ratings correlated significantly with outcome, as measured by posttest BDI scores (r = -.).

7 RELAPSE PREVENTION 8 Table Mean BD and HRSD Scores at Each Follow-Up Follow-up period (months) BA Condition AT CT Controlling for pretest F Controlling for posttest F BDI HRSD F(, ) < F(, ) < F(, ) < F(, 8) < f(, ) < F(, ) < F(, ) < F(, 8) < F(, ) < F(, ) < F(, ) < F(, 8) < F(, ) < F(, ) < F(, ) < F(, ) < Note. BA = behavioral activation; AT = automatic thoughts; CT = cognitive-behavioral therapy; BDI = Beck Depression Inventory; HRSD Hamilton Rating Scale for Depression. relied on subjective, retrospective chart reviews for the last months of follow-up. Moreover, bolh studies had very small sample sizes (see Hollon et al., ). Finally the Evans et al. () study had high attrition rates, especially during acute treatment. This is important because it is reasonable to assume that dropouts are at higher risk for relapse than completers. Because we were so successful at retaining participants, we may have included those at high risk for relapse who were not part of the follow-up pool in Evans et al. (). In short, our results compare favorably with others at the - and -month follow-up evaluations, and our survival curves for CT through months map onto those from the NIMH Collaborative Depression Study, which is the only other CT study to use the LIFE-II interview as its primary measure of relapse. With our low rate of attrition, our relatively large sample size, and our long-term follow-up, we may have produced the closest approximation to date of the true long-term outcomes of CT. The findings themselves suggest three things. First, it may take participants longer to relapse after CT than after discontinued pharmacotherapy, but in the end the probabilities of ultimate relapse are quite similar. Second, unlike the previous research findings showing that depressives are at highest risk for relapse during the first months after acute treatment, our survival curves indicate a rather constant probability of relapse as time goes on, at least for outpatients. Third, as Shea et al. () noted, given the growing body of evidence that major depression is a chronic condition in which one can expect recurrence, it may be incorrect to assume that any short-term treatment will be effective over the long term after one administration. Nevertheless, there is enough suggestive evidence that CT prevents recurrence to explore further the potential of psychosocial treatments to be prophylactic, and BA deserves more exploration, as does CT. However, our results do raise important questions about the long-term gains from what is considered a valuable psychosocial treatment for depression. If only % of clients entering cognitive therapy recover by the end of treatment and continue to maintain treatment gains for years thereafter, as found here, one can question CT's reputed prophylactic effects. However, the reality is that there is wide variability in relapse figures across studies; therefore, the long-term effectiveness of CT remains an open question. Because we had no control group, we are not sure whether our findings indicate equal efficacy or equal inefficacy. Moreover, we cannot claim that BA works as well as CT simply because we failed to reject the null hypotheses. However, we can rule out several alternative interpretations, lending credence to the possibility that BA is equivalent to CT in efficacy. We know that the lack of significant differences was not due to an allegiance effect or to unwanted overlap between treatment. As stated earlier, the BA treatment is relatively simple to administer; compared with CT, its intervention options are fewer, and therapists can be trained to competence quickly. Because of this, BA is potentially amenable to inexpensive service delivery formats. Therefore, if these findings can be replicated with adequate statistical power and proper pharmacotherapy comparison groups, we may find that BA, not CT, is the psychosocial treatment that offers the cost-effective, prophylactic potential that discontinued pharmacotherapy clearly lacks. We do not include Gallagher-Thompson et al.'s (0) study in this discussion because it involved a geriatric population, which may have different relapse profiles from our sample. References Addis, M. E., & Jacobson, N. S. (). Reasons for depression and the process and outcome of cognitive-behavioral psychotherapies. Journal of Consulting and Clinical Psychology,, -. American Psychiatric Association (). 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