Sudden Gains in Cognitive Therapy of Depression and Depression Relapse/Recurrence

Journal of Consulting and Clinical Psychology Copyright 2007 by the American Psychological Association 2007, Vol. 75, No. 3, 404 408 0022-006X/07/$12.00 DOI: 10.1037/0022-006X.75.3.404 Sudden Gains in Cognitive Therapy of Depression and Depression Relapse/Recurrence Tony Z. Tang Northwestern University Steven D. Hollon Vanderbilt University Robert J. DeRubeis University of Pennsylvania Jay Amsterdam University of Pennsylvania Richard Shelton Vanderbilt University Cognitive therapy (CT) may have significant advantages over antidepressants in preventing depression relapses. Many CT patients experience sudden gains: large symptom improvement in 1 between-session interval. Past studies have associated CT sudden gains with in-session cognitive changes but not with life events. This study examined sudden gains and depression relapse/recurrence among 60 CT clinical-trial patients. Survival analyses showed that only one third of sudden-gain-responders relapsed in 2 years, and they had 74% lower relapse risks than did non-sudden-gain-responders. Among patients with sustained responses, 73% experienced sudden gains. The authors also replicated J. R. Vittengl, L. A. Clark, and R. B. Jarrett s (2005) finding that sudden gains identified with their unique criteria did not predict relapse. The current authors findings suggest that CT sudden gains are not measurement artifacts, and that sudden gains and their causes and consequences might be important in preventing relapses. Keywords: depression, sudden gain, cognitive therapy, depression relapse, relapse prevention Antidepressant medication (ADM) is the most popular treatment for depression. However, the majority of ADM responders relapse within 1 year if withdrawn from medication (Hollon et al., 2005). Treatment guidelines recommend that ADM responders remain on medication long after acute treatment (American Psychiatric Association, 2000). Studies have suggested that cognitive therapy (CT) of depression might have a significant advantage over medication in preventing relapses or recurrences (Hollon et al., 2005). Such advantages might be crucial to the future of psychotherapy: Psychotherapy for depression is usually more expensive than medication during acute treatment, but the cost of long-term medication continuation might eventually make CT more cost effective. The mechanism of CT s preventative benefit is not yet well understood, and it might become a focus of future research. A course of CT comprises 16 20 sessions, but about 40% of CT patients have more than half of their total symptom improvement Tony Z. Tang, Department of Psychology, Northwestern University; Robert J. DeRubeis, Department of Psychology, University of Pennsylvania; Steven D. Hollon, Department of Psychology, Vanderbilt University; Jay Amsterdam, Department of Psychiatry, University of Pennsylvania; Richard Shelton, Department of Psychiatry, Vanderbilt University. The dataset of this study came from a clinical trial supported by National Institute of Mental Health Grants MH50129(R10), MH55875(R10), and MH01697(K02). GlaxoSmithKline provided medications and placebos for the trial. Correspondence concerning this article should be addressed to Tony Z. Tang, Department of Psychology, Northwestern University, 2029 Sheridan Road, Evanston, IL 60208. E-mail: ttang@northwestern.edu concentrated in one between-session interval (Hardy et al., 2005; Tang & DeRubeis, 1999; Tang, DeRubeis, Beberman, & Pham, 2005). These large symptom improvements in one betweensession interval have been named sudden gains, and a set of quantitative criteria has been designed to identify them (Tang & DeRubeis, 1999; Tang et al., 2005). These sudden gains tend to average about 10 13 points on the Beck Depression Inventory (BDI; Beck, Steer, & Garbin, 1988), and their occurrence has predicted better end-of-treatment outcomes (Hardy et al., 2005; Tang & DeRubeis, 1999; Tang et al., 2005). Most CT sudden gains appear unrelated to positive life events (Hardy et al., 2005); instead, they seem to be associated with the correction of patients negative beliefs in the therapy session immediately preceding the sudden gain (Tang & DeRubeis, 1999; Tang et al., 2005). Intuition might suggest that such sudden gains should be unstable and that CT responders who experienced sudden gains during treatment (sudden-gain-responders) should relapse more frequently than should other responders. However, Tang and DeRubeis (1999) found that sudden-gain-responders were significantly less depressed than were other responders at 6 and 18 months (but not 12 months) after treatment. This suggests that CT sudden gains might be associated with the preventative benefits of CT. This finding also has important implications for CT suddengains mechanisms. Some sudden gains could be merely measurement artifacts. For example, if the real BDI score of a patient declined 2 BDI points per session, its time course would be 30, 28, 26, 24, 22, and so on, and there would be no sudden gain. However, if a measurement error of 3 points occurred at Session 404

SPECIAL SECTION: SUDDEN GAINS 405 2 and an error of 3 points occurred at Session 3, the reported time course would be 30, 31, 23, 24, 22, and so on. (Throughout the article, bold font is used to highlight the two sessions between which gains occurred.) The patient would then appear to have a sudden gain between Sessions 2 and 3. If most CT sudden gains were due to such measurement errors, then sudden-gainresponders would just be non-sudden-gain-responders in disguise, and they would probably have identical long-term outcomes. If their long-term outcomes do differ substantially, it would argue strongly against this measurement artifacts interpretation. However, the Tang and DeRubeis (1999) finding was preliminary and inconclusive. At 12 months after treatment, sudden gains did not predict significant differences in BDI scores and relapse rates. 1 Moreover, depression severity assessed at 6-month intervals misses relapse episodes between assessments, and it does not account for whether the patients dropped out or reentered treatments. The current state-of-the-art methodology calls for (a) using a structured interview procedure such as the Longitudinal Interval Follow-Up Evaluation II (LIFE-II; Keller et al., 1987) to track all depression episodes, reentry into treatments, and dropouts throughout the follow-up period and (b) using survival analyses to account for how long each patient survived before relapse and to adjust for attrition and reentry into treatment without documented relapses (Cox & Oakes, 1984). Vittengl, Clark, and Jarrett (2005) reported that the 2-year raw relapse/recurrence rates did not differ significantly between CT sudden-gain-responders (38%) and non-sudden-gain-responders (41%). They used direct comparisons of raw relapse rates instead of survival analysis. Also, their sudden-gain criteria differed from the original criteria in Tang and DeRubeis (1999) in two important ways. First, instead of session-by-session BDI scores, they used BDI scores of every other session for the first 16 sessions. (They assessed BDI weekly. The first 16 sessions were scheduled twice per week, and the last 4 sessions were scheduled once per week.) Whereas the original sudden-gains criteria required improvement in one between-session interval to meet the criteria, Vittengl et al. (2005) only required improvement accumulated over two intervals to meet the criteria before Session 16. This enables modest gains to pass the criteria. Vittengl et al. noted that two prior sudden-gains studies also used weekly data, but these studies had only one therapy session per week and were consistent with Tang and DeRubeis (1999) in using session-by-session data (Gaynor et al., 2003; Tang, Luborsky, & Andrusyna, 2002). Second, Vittengl et al. (2005) analyzed sudden gains only when 3 BDI data points existed before and after the gain, and none of the 6 points was missing. Other studies required only two BDI scores before and after the symptom change (Gaynor et al., 2003; Hardy et al., 2005; Tang & DeRubeis, 1999, p. 895). As a result, Vittengl et al. excluded all gains before Week 3 (Sessions 5 and 6). This is important because half of CT sudden gains tend to occur by Session 5 (Hardy et al., 2005; Tang & DeRubeis, 1999). This study reexamined sudden gains and long-term outcomes in 60 CT patients from a recent CT clinical trial (DeRubeis et al., 2005). Following Tang and DeRubeis (1999), we used the original sudden-gain criteria. Unlike Tang and DeRubeis, we directly assessed relapse/recurrence rates, attrition, and treatment reentry using LIFE-II (Keller et al., 1987) and analyzed the relationship between sudden gains and relapse/recurrence with survival analyses. To examine its impact, we also re-ran our analyses using the sudden-gain criteria of Vittengl et al. (2005). Participants and Treatment Method Patient characteristics, treatment, and outcomes have been detailed elsewhere (DeRubeis et al., 2005). All patients provided written informed consent prior to participating in the research protocol, which was approved by institutional review boards. Patients were moderately-to-severely depressed adult outpatients who scored 20 on the 17-item modified HRSD (Williams, 1988) at both screening and intake visits. 2 The trial randomized 60 of these 240 patients to receive CT and the rest to receive either ADM or inert placebo. CT was conducted, following Beck, Rush, Shaw, and Emery (1979), by six therapists with 5 21 years of experience. Both CT and ADM outperformed placebo, and both achieved response rates of 58%. Nine CT patients dropped out during acute treatment, and unless otherwise specified, analyses were based on the all-assigned sample with last observation carried forward. Responders at end of treatment (Week 16) were patients who had (a) 16-week HRSD 12 and either 14-week HRSD 14 or 10-week and 12-week HRSD 12 or (b) 12-, 14-, and 18-week HRSD 12. 3 During the first year of the follow-up, CT responders were allowed, at most, three booster sessions scheduled at least 1 month apart. Relapse/recurrence criteria were met if a responder (a) scored 14 on HRSD for 2 consecutive weeks or (b) met the diagnostic criteria for major depressive disorder for 2 consecutive weeks. The relapse rate of CT responders was comparable to that of ADM responders who stayed on treatment dosage medication and significantly lower than that of ADM responders whose medication was gradually withdrawn after treatment (Hollon et al., 2005). Sudden-Gain Criteria The original sudden-gain criteria are based on BDI scores, measured immediately before every session, targeting symptom severity since the last visit (Tang & DeRubeis, 1999). Sudden gains should be (a) large in absolute magnitude, (b) large relative to pregain BDI severity, and (c) large relative to symptom fluctuation before and after the gain. These considerations were implemented in three criteria. A sudden gain occurred between Session n and Session n 1 if (a) the gain was 7 BDI points (absolute 1 Tang and DeRubeis could not report on whether CT sudden gains predicted relapse/recurrence rates at 6 and 18 months after treatment because they did not have access to relapse rates at these time points. 2 Their age ranged from 18 to 70 years, 33% were married or cohabitating, 82% were employed, 59% were women, 82% were Caucasian, 72% had Axis I comorbidity, and 48% had Axis II comorbidity. 3 This responder definition of DeRubeis et al. (2005) allows a patient to be classified as a responder even if he or she has a transient surge of symptom severity at Week 14 or Week 16. It differs from that in Vittengl et al. (2005), which requires termination HRSD 9. Switching to the Vittengl et al. responder definition does not change any of our conclusions.

406 TANG, DERUBEIS, HOLLON, AMSTERDAM, AND SHELTON magnitude), (b) the gain represented at least 25% of the pregain session s BDI score (relative magnitude), and (c) the difference between the mean BDI score of the three sessions before the gain (n 2, n 1, and n) and the three sessions after the gain (n 1, n 2, and n 3) was at least 2.78 times greater than the pooled standard deviations of these sessions BDI scores (relative to symptom fluctuation). When applied to Session 2, Session n 2 was not used, as there is no Session 0; for the third-to-last session, Session n 3 was not used. Thus, only changes following the first session and the second-to-last session were excluded. 4 A full course of CT usually produces about 12 15 points of improvements in mean BDI scores, and 7 points is about half of that. The standard deviation of BDI scores in clinically depressed samples is also about 7. Thus, the first criterion sets a high bar to select only unusually large improvements in one between-session interval. The second criterion addresses the concern that more severely depressed patients tend to have more volatile BDI scores. 5 The third criterion uses the pooled standard deviation of the three sessions before and after the gain to measure symptom fluctuation around the gain. It aims to select only gains that dwarf such fluctuations. For example, the third criterion would reject BDI time courses such as 30, 20, 30, 20, 30, 20, and so on or 30, 31, 30, 20, 31, 30, and so on. These gains are probably more likely to be mood fluctuations or random measurement errors. The 2.78 cutoff in the third criterion was retained to maintain compatibility with the original criteria of Tang and DeRubeis (1999), when this criterion was presented as a t-score calculation. Similar to those of Tang and DeRubeis (1999), our results are not sensitive to small variations in the cutoff values of these three criteria. Mishandling missing data can create false sudden gains. For example, if the actual BDI data time course is 30, 30, 30, (25), 20, 20, 20, and so on, and the score of Session 4 is missing (indicated here by parentheses), then some statistical software would delete the missing session and treat the time course as 30, 30, 30, 20, 20, 20. This creates a false sudden gain. Similar to using bisession BDI scores, this allows two consecutive moderate improvements to pass as a sudden gain. Only.8% of all data points are missing in this dataset, but because each patient has 10 20 BDI data points, this mistake can potentially affect more than 10% of the patients. We did not analyze the between-session changes before or after missing data, as we could not determine their sizes. However, we tolerated missing data when estimating symptom fluctuation in the third criterion. For instance, in time course 30, 30, 30, 20, 20, (missing), 20, we would analyze the gain from Sessions 3 to 4, using Session 7, instead of Session 6, in calculating the third criterion. Sudden-Gain Criteria in Vittengl et al. (2005) We attempted to replicate Vittengl et al. s (2005) analyses by following their sudden-gain criteria, which differed from the original criteria in two important ways. First, instead of session-bysession BDI scores, they used bisession BDI scores for the first 16 sessions. This change allowed modest symptom improvements to pass the first criterion (7 BDI points), if they occurred consecutively. For example, a patient whose BDI scores consistently declined 3 4 points per session in the first 10 sessions would not come close to meeting the original criteria. This patient would have been a prototypical non-sudden-gain-responder. However, this patient would likely meet the Vittengl et al. criteria, as many of the two-session intervals would show 7 8 points of improvement. Thus, sudden gains identified this way might no longer fit the definition of sudden and substantial symptom improvement in one between-session interval (Tang & DeRubeis, 1999, p. 894). Furthermore, switching to bisession scores affects the third criterion. It stretched the relevant time periods from three sessions before and after the gain to six sessions before and after the gain. This can increase the mean difference between the 3 BDI points before and after the gain, because BDI scores typically decline with more time in treatment. Second, Vittengl et al. (2005) analyzed sudden gains only when there were 3 BDI data points before and after the gain and none of the 6 points was missing. This excludes all gains before Week 3 (Sessions 5 and 6), as too few weekly BDI points exist before the gain. It also excluded all gains after the last three sessions, as too few BDI points exist after the gain. In datasets with many missing data, this change might have even greater impact. For instance, in time course 30, 30, 30, 20, 20, (missing), 20, Vittengl et al. would conclude that no sudden gain occurred at Session 3 because Session 6 is missing. Survival Analysis During the 24-Month Follow-Up Survival curves were estimated using the Cox proportional hazards model (Cox & Oakes, 1984). We censored 1 sudden-gainresponder and 1 non-sudden-gain-responder, who dropped out, and 1 sudden-gain-responder who reentered treatment without coming close to meeting relapse criteria before or after reentering treatment (Hollon et al., 2005). 6 Results According to the original sudden-gain criteria, 24 of the 60 CT patients (40%) experienced sudden gains during treatment, with 8 patients experiencing more than one sudden gain. The sudden gains averaged 11 BDI points in magnitude, and the median session for them to occur was Session 5. At intake, patients who later experienced sudden gains did not differ from the other patients on HRSD: 24 versus 23, t(58) 0.96, p.34. At termination, patients who experienced sudden gains had significantly lower HRSD scores than did the other patients: 7.8 versus 14, t(58) 3.2, p.002, Cohen s d 0.8. 7 Among the 24 patients who experienced sudden gains, 19 met responder criteria; among the 36 patients who did not experience sudden gains, only 16 met 4 Gains after the first session are excluded also because first sessions in CT clinical trials typically focused on practical matters such as scheduling (Hardy et al., 2005; Tang & DeRubeis, 1999). 5 The second criterion can be seen as inconsistent with the ordinal nature of the BDI scale. It also has little impact in selecting sudden gains and can be omitted (Tang et al., 2005). In this dataset, the second criterion changed the classification of 1 patient and made no difference to the results. We included the second criterion to be consistent with both Tang and DeRubeis (1999) and Vittengl et al. (2005). 6 Although some patients reenter treatments anticipating relapses, they could be mistaken in their judgment; patients do reenter treatments for other reasons. 7 BDI scores showed identical patterns.

SPECIAL SECTION: SUDDEN GAINS 407 responder criteria; the difference is statistically significant, 2 (1) 6.9, p.01, estimated effect size measure r.3. Nine sudden-gain patients experienced a reversal before the end of treatment, defined as an increase of BDI scores back to higher than the mean of the pregain- and postgain-session BDI scores (Tang & DeRubeis, 1999). Only 1 of these 9 patients became a nonresponder. Of the 35 CT responders, 19 (54%) experienced sudden gains. These findings generally resemble those of prior CT suddengains studies (Hardy et al., 2005; Tang & DeRubeis, 1999; Tang et al., 2005). Figure 1 shows the survival curves during the 24-month followup, and sudden-gain-responders were significantly less likely to experience relapse/recurrence than were the non-sudden-gainresponders, 2 (1) 5.0, p.02. This remained true after controlling for end-of-treatment HRSD, 2 (1) 6.3, p.01. The adjusted relapse/recurrence rate over 2 years was 34% for suddengain-responders, versus 73% for non-sudden-gain-responders. After controlling for end-of-treatment HRSD, the risk ratio of sudden gains was.26, corresponding to a 74% reduction in relapse/ recurrence risk. Among the 15 patients who showed sustained response (responders without relapse/recurrence; Hollon et al., 2005), 11 (73%) experienced sudden gains during treatment. The Vittengl et al. (2005) sudden-gain criteria identified 15 patients as having had sudden gains. Their criteria and the original criteria differed on 19 patients: 5 met only the Vittengl et al. criteria, and 14 met only the original criteria. Similar to Vittengl et al. (2005), Figure 2 shows that sudden gains identified with their criteria did not predict relapse/recurrence. The adjusted relapse rates were 57% for sudden-gain-responders, versus 48% for nonsudden-gain-responders, 2 (1).52, p.5, risk ratio 1.4. To further explore this issue, we divided responders into four subgroups with both the original sudden-gain criteria and the Vittengl et al. criteria. The two subgroups that met the original sudden-gain criteria both had low relapse rates of 34%, regardless of whether they met the Vittengl et al. criteria (n 9) or whether they did not (n 10). The two subgroups that did not meet the original criteria had high relapse rates, regardless of whether they met the Vittengl Figure 1. The CT responders who experienced sudden gains during treatment were much less likely to have depression relapse/recurrence than were the CT responders who did not experience sudden gains. Figure 2. Sudden gains identified by the sudden gain criteria in Vittengl et al. (2005) did not predict relapse/recurrence rates. et al. criteria (100%, n 4), or whether they did not (63%, n 12). Discussion In our dataset, CT sudden gains identified by the original sudden-gain criteria were associated with substantial reduction in relapse/recurrence risks. These results are broadly consistent with the long-term outcome results from Hardy et al. (2005) and the 6- and 18-month results from Tang and DeRubeis (1999), although their 12-month results did not show any significant difference in relapse. Similar to the 6- and 18-month results of Tang and DeRubeis (1999), our results also show that sudden-gain-responders and non-sudden-gain-responders are very different. These findings contradict the hypothesis that most CT sudden gains are just measurement artifacts, because such a hypothesis would predict identical long-term outcomes for sudden-gain-responders and nonsudden-gain-responders. We replicated the Vittengl et al. (2005) finding that sudden gains identified by their criteria did not predict relapse/recurrence. Thus, the Vittengl et al. criteria and the original criteria lead to divergent findings in our dataset. It remains unclear what the results of Vittengl et al. (2005) would have been had they used the original criteria. The two studies differed in main analyses and in patient samples. In addition, some responders in Vittengl et al. received 8 months of continuation CT during follow-up, but responders in the present study received only three booster sessions. The best sudden-gain criteria probably differ for different purposes. For the purposes of predicting long-term outcomes and identifying pregain sessions where therapeutic breakthroughs occurred, the accumulated evidence seems encouraging for the original criteria (Andrusyna, Luborsky, Pham, & Tang, 2006; Tang & DeRubeis, 1999; Tang et al., 2005). Sudden gains have been discovered in other psychotherapies and routine clinical practices (Gaynor et al., 2003; Hardy et al., 2005; Stiles et al., 2003; Tang et al., 2002). Some of these sudden gains appear unrelated to cognitive changes, and they did not predict BDI scores 6 months after treatment (Andrusyna et al.,

408 TANG, DERUBEIS, HOLLON, AMSTERDAM, AND SHELTON 2006; Tang et al., 2002). Vittengl et al. (2005) studied sudden gains in ADM and placebo with their criteria, but their conclusions might not generalize to sudden gains identified with the original criteria. Such analyses are impossible in our dataset: As in most drug trials, our ADM and pill-placebo patients were not assessed frequently enough for sudden-gain analyses. In ADM, pill-placebo, or wait-list samples, there might be many sudden gains. Pill-placebo is powerful in relieving depression, as it typically matches 70 80% of the efficacy of ADM (Kirsch, Moore, Scoboria, & Nicholls, 2002). Spontaneous recovery and other nontreatment factors in wait lists can probably generate some sudden gains as well. Receiving medication, placebo, or promises of free future treatments can also drastically change beliefs and expectations. For example, a patient might have believed that his depression would never get better. During the trial, he might become convinced that he is getting the active medication, which would restore his brain chemistry imbalance and heal him. If such changes occur suddenly, like belief changes in CT pregain sessions, their impact might manifest as sudden gains. Our sample size is modest, and replication in other datasets would be informative. Our main findings are correlational predictions, and they are open to two classes of interpretations. First, both sudden gains and low relapse/recurrence risks might be caused by other variables such as therapy process variables, patient characteristics, and therapist characteristics. Second, CT sudden gains might have initiated a causal process that directly reduced relapse risks. Preliminary findings suggested that CT sudden gains trigger an upward spiral, with more cognitive changes, better therapeutic alliance, and sustained symptom relief mutually reinforcing each other (Tang & DeRubeis, 1999). 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