jurnal psikologi klinis

Sudden Gains in the Treatment of Generalized
Anxiety Disorder
m
Julie Present, Paul Crits-Christoph, Mary Beth Connolly
Gibbons, Bridget Hearon, Sarah Ring-Kurtz, and Matthew
Worley
University of Pennsylvania
m
Robert Gallop
West Chester University
The objective of this study was to investigate the prevalence and
timing of sudden gains over the course of brief, psychodynamically
oriented treatment for generalized anxiety disorder (GAD). Data were
used from two studies of brief (i.e., 16-session) supportive-expressive
psychotherapy for GAD. Anxiety symptoms were measured at every
weekly treatment session. Sudden gains in anxiety symptoms were
defined to parallel previous research on sudden gains in major
depressive disorder (MDD). Overall, sudden gains were found for 11
of 68 participants (16.2%), with 4 (36.4%) of these patients
experiencing reversals of these gains and losing over 50% of the
sudden gain during subsequent treatment sessions. Applying a
baseline severity cutoff and a duration criteria similar to those used
in previous studies of sudden gains resulted in 10 of 29 (34.5%)
patients showing sudden gains. Of these sudden gainers, 4 (40.0%)
experienced a reversal and 7 (70%) experienced an upwards spike in
symptoms during their psychotherapy course. When defined in a
parallel fashion, rates of sudden gains in GAD are similar to those
found in MDD, although anxiety symptoms are highly variable. & 2007
Wiley Periodicals, Inc. J Clin Psychol 64: 119–126, 2008.
Keywords: generalized anxiety disorder; sudden gains; brief psychotherapy;
psychodynamic treatment; symptom variability
The phenomenon of sudden gains—a dramatic improvement from one treatment
session to the next—has recently been explored in several studies examining patients
The preparation of this article was funded in part by National Institute of Mental Health Grant R21-
MH56018.
Correspondence concerning this article should be addressed to: Paul Crits-Christoph, Room 650, 3535
Market St., Philadelphia, PA 19104; e-mail: crits@mail.med.upenn.edu
JOURNAL OF CLINICAL PSYCHOLOGY, Vol. 64(1), 119--126 (2008) & 2007 Wiley Periodicals, Inc.
Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/jclp.20435
with major depressive disorder (MDD). Sudden gains have been found to be
common in both cognitive-behavioral (CBT; 39% of patients) and supportiveexpressive
(SE; 43% of patients) treatments for depression (Tang & DeRubeis, 1999;
Tang, Luborsky, & Andrusyna, 2002). In the study of CBT, sudden gainers had
significantly better outcomes at posttreatment than did nonsudden gainers, and the
sudden gainer’s improvements persisted 6 and 18 months after treatment (Tang &
DeRubeis, 1999). Similar results were found in the study of SE therapy, where
sudden gainers displayed significantly better outcomes at the end of treatment and a
better recovery rate (Tang et al., 2002); however, compared to Tang and DeRubeis’
(1999) CBT sudden gainers, the SE sudden gainers showed higher rates of reversal of
the sudden gain and less stable and less robust long-term gains.
The findings for manual-based CBT of depression have been replicated several times
in both clinical trial (Tang, DeRubeis, Beberman, & Pham, 2005; Tang, DeRubeis,
Hollon, Amsterdam, & Shelton, 2007; Vittengl, Clark, & Jarrett, 2005) and practice
settings (Hardy et al., 2005). Stiles et al. (2003) discovered that sudden gains occur for
diverse non-manual-based therapy delivered in routine clinic settings, but at a lower
prevalence and with higher rates of reversal. Still, the outcomes of sudden gainers were
significantly better than those of nonsudden gainers. Sudden gains also have been
observed for CBT treatment of social anxiety disorder (Hofman et al., 2006).
The phenomenon of sudden gains is potentially important from both a research
and a clinical perspective. To make progress in understanding the mechanism of how
psychotherapy works, Tang and DeRubeis (1999) argued that it is useful to first
understand the nature of the pattern of change over time. For example, researchers
who examine psychotherapy process in relation to outcome typically utilize change
from baseline to treatment termination as their outcome. But if the change process
primarily involves critical events in key sessions inducing sudden gains, it would be
more fruitful to study process predictors of these immediate sudden gains rather than
distal outcomes. In fact, Tang et al. (2005) found that clinically meaningful cognitive
changes in sessions precede a sudden gain, although others have not found cognitive
changes to precede sudden gains (Kelly, Roberts, & Ciesla, 2005). If research
establishes the importance of sudden gains and their causes as part of the overall
change process, clinicians can use sudden gains as markers of change, as well as
develop and implement interventions that might facilitate sudden gains.
The existing literature has primarily focused on sudden gains in the treatment of
MDD, with only one study examining sudden gains in the treatment of anxiety
disorders (Hofmann et al., 2006). Limited research has focused on sudden gains
occurring across modalities of psychotherapy treatment; with the exception of Tang
et al. (2002), most studies have focused only on sudden gains in CBT.
The purpose of the present study was to investigate sudden gains among patients
with generalized anxiety disorder (GAD) who were receiving brief SE psychodynamic
therapy. The first goal was to document the prevalence of sudden gains among
these patients. The second goal was to examine when the sudden gains occurred in
treatment. The last goal was to evaluate treatment outcomes, comparing patients
with and without sudden gains.
Methods
The data analyzed in the present study were obtained from two previous studies
involving patients enrolled in psychodynamic-interpersonal therapy for GAD. The
first study involved 46 patients who received brief (i.e., 16 once-per-week sessions
120 Journal of Clinical Psychology, January 2008
Journal of Clinical Psychology DOI 10.1002/jclp
followed by 3 once-per-month booster sessions) SE therapy for GAD. The second
study involved 22 patients with a principal diagnosis of GAD according to the
Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition
(DSM-IV; American Psychiatric Association, 1994) who were treated with SE
therapy for 16 once-per-week sessions. Using data from these studies, a combined
database consisting of 68 patients (33 men, 35 women) treated with SE therapy was
created for the current analyses examining sudden gains. The majority of the sample
was Caucasian (87%); more than half were married (59%) and employed (60%).
Comorbidity was common in these patients; 35% (i.e., 24 of 68) had comorbid
MDD. Further details of the combined study sample are described in Crits-
Christoph, Connolly Gibbons, Narducci, Schamberger, and Gallop (2005).
Criteria for selecting participants were similar across both studies. Patients had to
have a principal diagnosis of GAD [according to the Diagnostic and Statistical
Manual of Mental Disorders, Third Edition-Revised (DSM-III-R; American Psychiatric
Association, 1987) for the first study and DSM-IV for the second] and be
between 18 and 65 years of age. Patients had to be available for the 16 weeks of study
treatment, they had to provide written informed consent and understand the nature
of the study, and if they were on medication for more than 3 months they had to
agree not to increase the dosage for the rest of the study.
Patients were excluded from both studies if they had begun a psychotropic
medication within the last 3 months or if they displayed any acute, unstable, and
Axis III medical disorder that might interfere with either study safety or analysis of
study results. They also were excluded if they had any current report of bipolar
disorder, schizophrenic disorders, or Cluster ‘‘A’’ Axis II personality disorders (i.e.,
schizoid, schizotypal, or paranoid), or any current or past report of seizure disorder
(other than febrile seizure as an infant). In addition, patients who in the past 12
months met criteria for alcohol or substance dependence or abuse, obsessive
compulsive disorder, eating disorder, or borderline personality disorder were
excluded and referred elsewhere.
A detailed account of the SE treatment approach as applied to GAD is explained
elsewhere (Crits-Christoph et al., 1997; Crits-Christoph et al., 1998). The treatment
was based upon the general SE treatment manual of Luborsky (1984), supplemented
with a more specific SE for GAD guide (Crits-Christoph, Crits-Christoph, Wolf-
Palacio, Fichter, & Rudick, 1995). SE treatment for GAD aims to understand the
anxiety symptoms of a patient in the context of interpersonal conflicts formulated by
the therapist using the core conflictual relationship theme method.
A detailed description of selection, training, certification, and competence
evaluation of therapists from the first study can be found elsewhere (Crits-
Christoph, Connolly, Azarian, Crits-Christoph, & Shappell, 1996). Therapists for
the second study had 2 years of training in SE therapy with GAD patients. Therapist
training included instructional presentation of the treatment manual, training cases,
and training discussions. During their training cases, the therapists were rated by
their supervisor on an adherence/competence scale and judged to be adequately
implementing SE therapy.
Axis I and II diagnostic assessments were obtained using trained interviewers who
administered the Structured Clinical Interview for the DSM-III-R or DSM-IV
(SCID) and SCID II (First, Spitzer, Gibbon, & Williams, 1994, 1997; Spitzer,
Williams, Gibbon, & First, 1990a, b).
Treatment outcomes were assessed using the Hamilton Anxiety Rating Scale
(HAM-A; Hamilton, 1959), administered at intake and posttreatment, and the Beck
Sudden Gains in GAD 121
Journal of Clinical Psychology DOI 10.1002/jclp
Anxiety Inventory (BAI; Beck, Epstein, Brown, & Steer, 1988), administered at every
treatment session as well as at intake (i.e., baseline) and termination (i.e., 16 weeks).
The BAI was used to define sudden gains in a manner parallel to previous
definitions of sudden gains using the Beck Depression Inventory (BDI; Beck, Ward,
Mendelson, Mock, & Erbaugh, 1961). The BAI was designed to be parallel
(i.e., same number of items; same rating scale) as the BDI, so a parallel definition
of sudden gains was feasible. Specifically, sudden gains were derived using
three criteria originally implemented by Tang and DeRubeis (1999). These criteria
mandated that the sudden gain be an improvement of 7 or more points on the BAI
from one session to the next and that the gain was at least 25% of the previous
session’s BAI score. In addition, the main difference between the BDI scores of the
three sessions before the gain and the three sessions after the gain had to be at least
2.78 times greater than the pooled standard deviations of these two groups’ BAI
scores (The use here of effect size rather than statistical significance was a further
modification by Tang et al., 2002.) To evaluate the stability and maintenance of these
gains, we examined reversals of sudden gains. In a parallel fashion to the criterion
used by Tang and DeRubeis, reversals were defined here as a loss of 50% or more of
the BAI sudden gain improvement over the course of the rest of treatment. A
‘‘spike’’ of anxiety symptoms was defined as an increase of 7 or more scale points on
the BAI from one session to the next at any point throughout the course of
treatment.
Tang and DeRubeis (1999) did not include sudden gains that occurred between
Sessions 1 and 2 because the first session in CBT is devoted primarily to history
taking and other practical matters pertaining to the overall treatment program. In
SE therapy, however, interventions (e.g., alliance building and initial interpretations)
can occur in the first session, and therefore the data were evaluated with and without
inclusion of sudden gains occurring immediately following the first session.
Moreover, Tang and DeRubeis excluded patients who attended less than eight
treatment sessions as well as patients who did not meet the 15 or greater severity
cutoff on the BDI at Session 1. Data were analyzed with and without this duration
and parallel severity criteria.
Results
The average number of treatment sessions attended (including booster sessions in the
first study) was 16.4 (SD53.8) for the 68 patients, with 84% completing treatment
(defined as 15 or more sessions). The outcomes of each of the two studies that were
pooled for the analyses reported here have been summarized previously (Crits-
Christoph et al., 1995; Crits-Christoph et al., 2005). For the combined sample
(N568), mean scores on the HAM-A decreased from 17.0 (SD55.9) at baseline to
9.5 (SD57.1) at 16 weeks. On the BAI, the mean at intake was 20.7 (SD59.9)
compared to 8.8 (SD59.9) at 16 weeks.
In the full sample, sudden gains were relatively uncommon. When sudden gains
were defined using all three criteria and excluding sudden gains occurring between
Sessions 1 and 2, a total of 11 of 68 (16.2%) participants displayed a sudden gain,
and 4 of these patients experienced reversals. The median session in which the
sudden gain occurred was Session 8. Including sudden gains occurring between
Sessions 1 and 2 resulted in two more sudden gains occurring within this same cohort
of 11 patients. Excluding the 24 patients who had comorbid MDD resulted in a
slightly lower rate (5 of 44; 11.4%) of sudden gains, but the rates of sudden gains
122 Journal of Clinical Psychology, January 2008
Journal of Clinical Psychology DOI 10.1002/jclp
among GAD patients without comorbid MDD were not significantly different than
the rates among GAD patients with comorbid MDD: w2(1)51.4, p5.23.
When severity and duration criteria were applied, sudden gains were more
frequent. Applying the 15 or over severity cutoff on the BAI at Session 1 excluded
patients who had already recovered quite significantly before starting therapy. This
changed the overall sample size from 68 to 31 patients (Unlike many studies of
MDD, these studies of GAD did not have a severity inclusion criteria.) Furthermore,
excluding 2 additional patients who received less than eight treatment sessions
reduced the sample to 29 patients. A total of 10 of these 29 patients (34.5%)
experienced a sudden gain throughout their treatment. Of these 10 patients, 4
(40.0%) experienced a reversal, losing over 50% of the sudden gain during
subsequent treatment sessions. Within this sample of 29 patients, the median session
in which a patient experienced the sudden gain was between Sessions 7 and 8.
Excluding patients with comorbid MDD from the sample of 29 meeting severity
and duration criteria resulted in a group of 16 GAD patients, of whom 4 showed
sudden gains (25.0%). For patients meeting duration and severity criteria, the rates
of sudden gains among GAD patients without comorbid MDD were not
significantly different than the rates among GAD patients with comorbid MDD:
w2(1)52.1, p5.14.
The average magnitude of the sudden gains was 11.5 BAI points for the 11 sudden
gainers in the full sample, and 11.9 BAI points for the 10 sudden gainers meeting
severity and duration criteria. For some patients, the sudden gain change was
actually larger than the change seen on the BAI from intake to termination
(reflecting the variability of anxiety scores over time). Setting a sudden gain change
that was larger than the pre–post change to 100%, the average percent of total
improvement accounted for by the sudden gain was 70% in the full sample and 75%
within the sample meeting severity and duration criteria.
Upward spikes in anxiety were common. A total of 38 of the 68 patients (55.9%)
experienced a ‘‘spike’’ of 7 or more points between two sessions at some point during
the course of their treatment (And 76.3% of these 38 had a spike of 10 or more
points.) Of the 11 (of 68) patients who experienced a sudden gain, 7 (63.6%)
experienced a spike during treatment. Of the sample of 29 patients who met the
severity and treatment duration criteria, 7 of the 10 (70.0%) sudden gainers also had
an upward spike.
The 16-week outcomes for patients with and without sudden gains were compared
using analysis of covariance (ANCOVA). The HAM-A scores at termination served
as the dependent variable, and baseline HAM-A scores served as the covariate. For
the sudden gainers, with and without the addition of the severity and duration cutoff
criterion, no significant differences in outcome were apparent, F(1, 62)50.1, p5.82;
F(1, 27)50.01, p5.94, respectively.
Discussion
In this study of sudden gains among GAD patients receiving SE therapy, the
prevalence of sudden gains (34.5%) using all of the Tang and DeRubeis (1999)
criteria (including baseline severity and treatment duration criteria) yielded similar
results to those found in studies of MDD. Results from previous MDD studies have
produced rates of sudden gains from 39 to 43% (Hardy et al., 2005; Tang &
DeRubeis, 1999; Tang et al., 2005, 2007, 2002; Vittengl et al., 2005). The percent of
patients who experienced sudden gains, the median session of sudden gain
Sudden Gains in GAD 123
Journal of Clinical Psychology DOI 10.1002/jclp
occurrence, and the average magnitude of the sudden gain in BDI/BAI points were
similar across the studies.
Rates of reversals of sudden gains have varied across studies. Tang and DeRubeis
(1999) and Vittengl et al. (2005) reported low (17 and 19%, respectively) rates of
reversals. In contrast, Stiles et al. (2003) found 43% of sudden gains had reversals,
Hardy et al. (2005) found 30% had reversals, Tang et al. (2005) found 40% had
reversals, Tang et al. (2007) found 37.5% had reversals, Tang et al. (2002) found
46% of SE-treated MDD patients had reversals. Thus, the rate found in the current
study (i.e., 40%) is similar to that found in the majority of studies.
The most salient difference between our results and the results from all of the
aforementioned studies is that sudden gains did not predict a better end-of-treatment
outcome in our sample of GAD patients. The lack of better end-of-treatment
outcomes among GAD patients with sudden gains may be due to the highly variable
nature of anxiety symptoms. In fact, the phenomenon of large upward spikes
(occurring in 55.9% of the total population and 63.6% of the sudden gainers) and
high symptomatic changeability in anxiety, not reported in previous studies of
depression, illustrate how erratic anxiety symptoms can be. The definition of sudden
gains for GAD patients may need to be adjusted or redefined to account for the great
clinical variability of anxiety disorder symptoms. The ebb and flow in symptoms that
are common among those with GAD may be something quite different than the
sudden gains seen in the treatment of MDD. Research on the change process in
anxiety disorder may need to attend to a greater degree on the variability in anxiety
over time. Assumptions that change linearly over time, or that a single posttreatment
assessment can capture a patient’s typical level of symptoms, may be misguided.
Repeated assessments of outcome with alternative ways of integrating such
longitudinal data, such as examination of percent of relatively symptom-free weeks,
may be indicated for research on anxiety disorders.
The rates of sudden gains found here varied considerably depending on whether a
baseline severity cutoff was applied. When a cutoff was applied, rates of sudden
gains were similar to those found in studies of MDD that also applied severity
cutoffs. When a severity cutoff was not applied, rates of sudden gains were much
lower. Similarly, in a study of social anxiety disorder, Hofmann et al. (2006) found
that sudden gainers had higher baseline levels of social anxiety. Thus, to a certain
extent, the assessment of sudden gains is dependent on potential floor effects in
outcome measures. Future research on sudden gains clearly needs to attend to the
impact of baseline severity.
Limitations of this study include its exploratory nature and relatively small sample
size. The definition of sudden gains in treatment as defined by Tang and DeRubeis
(1999) may be less appropriate to the study of anxiety disorders, and GAD in
particular. Inclusion of a severity cutoff criterion at intake or at Session 1 may not
capture the ebb and flow of symptoms that are part of the course of GAD treatment.
Finally, the generalizability of the results to sudden gains experienced in treatments
for other Axis I disorders, and well as in other psychotherapeutic treatment
modalities for the treatment of GAD, is not known.
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