J. Behav. Ther. & Exp. Psychiat.

45 (2014) 319e329

Contents lists available at ScienceDirect

Journal of Behavior Therapy and

Experimental Psychiatry
journal homepage: www.elsevier.com/locate/jbtep

Schema therapy for patients with chronic depression: A single case

series study
Ioannis A. Malogiannis a, b, *, Arnoud Arntz c, Areti Spyropoulou a, Eirini Tsartsara a, b,
Aikaterini Aggeli b, Spyridoula Karveli b, Miranda Vlavianou b, Artemios Pehlivanidis a,
George N. Papadimitriou a, Iannis Zervas a, b
a
1st Department of Psychiatry, Eginition Hospital, Athens Medical School, Athens, Greece
b
Greek Society of Schema Therapy, 10555 Athens, Greece
c
Maastricht University, The Netherlands

a r t i c l e i n f o a b s t r a c t

Article history: Background and objectives: This study tested the effectiveness of schema therapy (ST) for patients with
Received 26 November 2013 chronic depression.
Received in revised form Methods: Twelve patients with a diagnosis of chronic depression participated. The treatment protocol
6 February 2014
consisted of 60 sessions, with the rst 55 sessions offered weekly and the last ve sessions on a biweekly
Accepted 9 February 2014
Available online 24 February 2014
basis. A single case series AeBeC design, with 6 months follow-up was used. Baseline (A) was a wait
period of 8 weeks. Baseline was followed by introduction to ST and bonding to therapist (phase B) with
individually tailored length of 12e16 sessions, after which further ST was provided (phase C) up to 60
Keywords:
Chronic depression
sessions (included the sessions given as introduction). Patients were assessed with Hamilton Rating Scale
Schema therapy for Depression three times during baseline, at the end of phase B, then every 12 weeks until the end of
CBT treatment and at 6 months follow-up. Secondary outcome measures were the Hamilton Rating Scale for
Single case series Anxiety and the Young Schema Questionnaire.
Early maladaptive schemas Results: At the end of treatment 7 patients (approximately 60%) remitted or satisfactorily responded. The
mean HRSD dropped from 21.07 during baseline to 9.40 at post-treatment and 10.75 at follow-up. The
effects were large and the gains of treatment were maintained at 6-month follow-up. Only one patient
dropped out for reasons not related to treatment.
Limitations: The lack of control group, the small sample and the lack of a multiple baseline case series.
Conclusions: This preliminary study supports the use of ST as an effective treatment for chronic
depression.
2014 Elsevier Ltd. All rights reserved.

1. Introduction health care utilization, hospitalization and economic costs (Berndt

Approximately 20% of all depressed individuals develop a chronic
course (Arnow & Constantino, 2003; Gilmer et al., 2005). This im-
plies that 2.5e6% of the adult population in the community suffers
from chronic depression (Kessler et al., 2005, 1994). Chronic
depression is associated with increased functional impairment
(Klein, Schwartz, Rose, & Leader, 2000; Klein, Shankman, & Rose,
2006; Wells, Burnam, Rogers, Hays, & Camp, 1992), higher levels of
* Corresponding author. Greek Society of Schema Therapy, 10555 Athens, Greece.
Tel.: 30 6945898082.
E-mail address: imalog@hol.gr (I.A. Malogiannis).
et al., 2000; Gilmer et al., 2005; Howland, 1993; Klein et al., 2000;
Smit et al., 2006) compared with non-chronic forms of depression.
Four types of chronic depression are usually distinguished in the
literature: 1) dysthymic disorder, 2) chronic major depressive dis-
order (MDD), 3) double depression (MDD superimposed on a
dysthymic disorder) and 4) recurrent major depressive disorder
with incomplete remission between the episodes (Torpey & Klein,
2008). There are consistent ndings supporting the idea that the
various manifestations of chronic depression do not represent
distinct disorders (Cuijpers et al., 2010; Klein, Shankman,
Lewinsohn, Rohde, & Seeley, 2004; Klein et al., 2006; McCullough
et al., 2003, 2000). The DSM-5 (American Psychiatric Association,
2013) diagnosis of persistent depressive disorder (dysthymia)

http://dx.doi.org/10.1016/j.jbtep.2014.02.003
0005-7916/ 2014 Elsevier Ltd. All rights reserved.
320 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329
includes both the DSM-IV diagnostic categories of chronic major
depression and dysthymia.
It is suggested that the determinants of chronic depression do
not necessarily differ qualitatively, but only quantitatively from
those of acute depression, with involvement of increased levels of
these determinants in chronic forms (Riso, Miyatake, & Thase,
2002). Among the several possible determinants of chronic
depression that have been investigated so far, the strongest support
has been found for the role of developmental antecedents and early
adversity (Bifulco, Brown, Lillie, & Jarvis, 1997; Brown, Craig, &
Harris, 2008; Brown, Craig, Harris, Handley, & Harvey, 2007;
Brown, Harris, Hepworth, & Robinson, 1994; Brown & Moran,
1994; Klein et al., 2009; Lizardi et al., 1995; Riso et al., 2002).
Family problems, anxious personality in childhood and low self-
esteem and mastery in early adulthood have been associated
with chronicity (Angst, Gamma, Rossler, Ajdacic, & Klein, 2011). A
recent meta-analysis reported that childhood maltreatment is
associated with elevated risk of developing chronic depression and
lack of response during treatment (Nanni, Uher, & Danese, 2012).
Several studies have emphasized the close relationship between
chronic depression and Axis II personality disorders (Garyfallos
et al., 1999; Klein et al., 1995; Maddux et al., 2009; Pepper et al.,
1995; Riso et al., 1996, 2002). Among dysthymic patients the rates
of personality disorders tend to be high, up to 65% (Klein et al.,
1995; Riso et al., 2002). Cluster C personality traits in patients
with chronic depression predict poor outcome in a naturalistic
study at 5 (Hayden & Klein, 2001) and 10-year follow-up (Klein,
Shankman, & Rose, 2008).
According to the cognitive theory of depression negative core
beliefs or cognitive schemas represent key vulnerability factors to
depression (Beck, 1976; Beck, Rush, Shaw, & Emery, 1979). Young,
inuenced by cognitive and attachment theory, elaborated the
schema concept (Young, 1994; Young, Klosko, & Weishaar, 2003)
and proposed that Early Maladaptive Schemas (EMS) are broad,
pervasive, trait-like, cognitive and emotional self-defeating pat-
terns, regarding oneself and ones personal relationships (Young
et al., 2003). EMS are hypothesized to develop as a result of toxic
childhood experiences and unmet core emotional needs, and to
underlie the development of psychopathology and chronic psy-
chological disorders (Young et al., 2003). To date 18 EMS have been
identied and grouped in ve domains: disconnection and rejec-
tion; impaired autonomy and performance; other directedness;
over-vigilance and inhibition; and impaired limits (Young et al.,
2003). EMS remain stable over time (Renner et al., 2013; Wang,
Halvorsen, Eisemann, & Waterloo, 2010) and relate to depressive
symptoms in depressed patients (Halvorsen et al., 2009; Hawke,
Provencher, & Arntz, 2011; Petrocelli, Glaser, Calhoun, &
Campbell, 2001). EMS of the domains impaired autonomy & per-
formance and disconnection & rejection relate to depressive
symptoms severity (Renner, Lobbestael, Peeters, Arntz, & Huibers,
2012), and EMS of the domains impaired autonomy & perfor-
mance and over-vigilance & inhibition distinguish patients with
chronic depression from patients with non-chronic major depres-
sive disorder (Riso et al., 2003). The emotional deprivation schema
mediates the relation between physical abuse and anhedonic
depressive symptoms whereas social isolation and self-sacrice
schemas mediate the relation between emotional maltreatment
and anhedonic depressive symptoms (Lumley & Harkness, 2000).
In conclusion, the evidence so far suggests that EMSs play a role in
chronic depression.
A schema model for chronic depression has been described
proposing the interplay between distal factors (early adversity,
personality pathology), which are mediated by proximal factors
(EMS) triggered by life events (loss, failure) and maintained by
avoidant coping strategies (Renner, Arntz, Leeuw, & Huibers, 2013).
Pharmacological (Kocsis, 2003; Kocsis et al., 2009) and psy-
chotherapeutic (Keller et al., 2000; Markowitz, 1994) interventions
have been developed for the treatment of chronic depression.
Cognitive Behavior Analysis System of Psychotherapy (CBASP)
(McCullough, 2000) is a model incorporating cognitive behavioral
and interpersonal techniques, which was developed for the treat-
ment of chronically depressed patients. Studies have supported its
effectiveness (Keller et al., 2000; Schatzberg et al., 2005) suggesting
equivalence to pharmacotherapy (Keller et al., 2000; Kocsis, 2009)
and superiority to pharmacotherapy for chronically depressed pa-
tients with a history of childhood trauma (Klein et al., 2009;
Nemeroff et al., 2003). Although the initial effects of the imple-
mentation of CBASP were good, when it comes to long-term effects,
CBASP does not seem to do better than continued antidepressant
medication (Gelenberg et al., 2003; Kocsis et al., 2009; Renner,
Arntz et al., 2013).
A meta-analysis examining the effects of psychotherapy on
chronic depression reported that the length of the studied psy-
chotherapies may not be sufcient to treat dysthymia (Imel,
Malterer, McKay, & Wampold, 2008). Indeed, the efcacy of psy-
chotherapeutic interventions increases with the number of sessions
(Cuijpers et al., 2010). Klein et al. (2008) suggests that chronically
depressed patients with comorbid personality disorders may
require a modied and more intensive course of treatment.
The above-mentioned literature suggests the crucial causal role
of early adversity, EMS and comorbid personality disorders in the
development of chronic depression. Moreover the effectiveness of
the existed treatment interventions remains limited. A qualitatively
different psychotherapeutic intervention lengthier and more
intensive, which focuses on underlying psychological factors like
childhood adversity and schemas might lead to improvement of
treatment of chronic depression.
Schema therapy (ST) has been developed as the clinical impli-
cation of Young (1994) schema theory. It is an integrative therapy,
which combines elements of cognitive behavior therapy, attach-
ment theory, object relations theory and emotional-focused models
and was developed for the treatment of patients with chronic
emotional difculties (Young et al., 2003). ST is an effective treat-
ment for patients with borderline personality disorder (BPD)
(Farrell, Shaw, & Webber, 2009; Giesen-Bloo et al., 2006; Nadort
et al., 2009; Nordahl & Nysaeter, 2005) and for patients with cluster
C personality disorders, including comorbid depression (Bamelis,
Evers, Spinhoven, & Artntz, 2013). Recently a randomized clinical
trial compared ST and CBT for patients with a current major
depressive episode, in a protocol of weekly sessions for six months
and monthly sessions for another six months (Carter et al., 2013).
No difference was found between the two therapies. Brewin et al.
(2009) tested the use of imagery rescripting (a core technique of
ST) as a stand-alone treatment for chronically depressed patients
with intrusive memories and found large treatment effects, main-
tained at one-year follow-up. Renner, Arntz et al. (2013) currently
conduct a single case series study of ST for chronic depression
testing the model described above.
To the best of the authors knowledge so far no study has been
published on the application of schema therapy in chronic
depression. The aim of this study is to examine the effectiveness of
schema therapy in a sample of chronically depressed patients.
2. Methods
2.1. Participants
Inclusion criteria were a primary diagnosis of DSM-IV chronic
depression, age 18e65 years and a score of 15 or higher on
the 24-item Hamilton Rating Scale for Depression (HRSD24)
 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329
(Hamilton, 1967; Miller, Bishop, Norman, & Maddever, 1985) at two
baseline and the pre-treatment assessments.
Exclusion criteria were a secondary diagnosis of bipolar or
cyclothymic disorder, schizophrenia or other psychotic disorder,
borderline or antisocial PD, eating disorder, obsessive compulsive
disorder, psychiatric disorders secondary to medical conditions,
mental retardation, severe addiction needed detoxication and
presence of current suicidal ideation.
Patients could be on antidepressant medication, with the
treatment remaining stable, concerning dosage and medication, for
at least 1 month before the rst baseline assessment.
In case of severe suicidal ideation or medical conditions needing
hospitalization, the participant would be excluded from the trial
and appropriate treatment would be provided. This did not happen.
Patient ow is presented in Fig 1.
Twelve patients participated, all women, age 26e56 years old.
Table 1 presents their sociodemographic and clinical
characteristics.
2.2. Design
A single case series AeBeC design, with 6 months follow-up was
used. Baseline (A) was a wait period of 8 weeks during which the
Fig. 1. Consort ow chart of the participants.
321
primary outcome (HRSD) was taken three times every 4 weeks.
After baseline, an introduction to ST and bonding to therapist was
provided (phase B), with individually tailored length of 12 to
maximally 16 sessions, after which assessment was repeated and
ST was provided (phase C) up to 60 sessions (included the sessions
given as introduction). We assessed effects of phase B separately
like was done in Weertman and Arntz (2007) and Arntz, So, and
van Breukelen (2013).
All the participants were outpatients of the Womens Mental
Health Clinic of the 1st Department of Psychiatry, Eginition Hos-
pital, Athens Medical School. Therapists of the unit referred pa-
tients to the study, based on a clinical diagnosis of chronic
depression.
Patients were assessed using the Structured Clinical Interview
for DSM-IV Axis I (SCID-I, First, Spitzer, Gibbon, & Williams, 2002)
and Axis II (SCID-II, First, Gibbon, Spitzer, Williams, & Benjamin,
1997) Disorders. They were further screened using the HRSD; pa-
tients had to have a score of 15 or higher to be eligible for the study.
All the screening interviews were contacted by one experienced
psychiatrist.
After the screening the patients that were eligible for the study
entered phase A. An HRSD score of 15 or higher in the assessments
of phase A was mandatory for them to continue in phase B with the
initiation of the treatment (no participant was excluded for this
reason). Additionally the patients who received therapy were
assessed pre-treatment on the battery of the instruments of the
study. Assessment during treatment was conducted by the
administration of the HRSD and the other instruments used in the
study at 12the16th sessions, 24th session, 36 session, 48 session,
post-treatment (60th session) and follow-up (6 months after the
termination). The rst assessment during treatment was conducted
on session 12the16th to give therapists the exibility to complete
the rst stage of the treatment including assessment, education
and bonding with the patient.
The baseline, pre-, during, post-treatment and follow-up as-
sessments were conducted by an experienced psychiatrist (other
from the one conducted the screening interviews).
The study was approved by the Medical Ethics Committee. All
patients signed informed consent.
2.3. Outcome measures
The main outcome measure was the 24-item HRSD. Following
previous studies on chronic depression (Keller et al., 2000; Kocsis
et al., 2009) we dened remission as an HRSD score of no more
than 8 at post-treatment and follow-up assessments and satisfac-
tory response (but not remission) as a reduction of 50% in the HRSD
and a score of 15 or less, but of more than 8 at post-treatment and
follow-up assessments.
A second outcome measure was the Hamilton Rating Scale for
Anxiety. A score of 14 has been suggested as the threshold for
clinically signicant anxiety.
A third, treatment-specic measure, was the Young Schema
Questionnaire YSQ, Long form, 3rd version (YSQ-L3). The YSQ-L3 is
a 232-item self-report inventory that assesses the 18th schemas
proposed by Young (2003). We used the sum of the scores of the
schemas of each of the ve domains, dened as YSQ1e5
respectively.
2.4. Treatment protocol
The schema therapy treatment protocol consisted of 60 sessions
of 50 min duration each. The rst 55 sessions were offered weekly
and the last ve sessions on a biweekly basis. The whole treatment
was offered over a 20 months period.
322 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329

Table 1
Sociodemographic and clinical characteristics of the participants.

Participant Age Marital status Education Chronic depression Years of onset Medication Personality disorder (PD)
(years) diagnosis (SCID-I) of depression diagnosis (SCID-II)

1 47 Married 12 Chronic MDD 2 SSRI e

2 26 Single 15 Double Depression 10 SSRI NaSSA Dependent and Avoidant PD
3 35 Single 15 Dysthymic Disorder 3 SNRI Histrionic and Narcissistic PD
4 49 Divorced 16 Dysthymic Disorder 4 SSRI e
2 children
5 47 Married 4 Chronic MDD 3.5 SSRI e
2 children
6 54 Married 18 Chronic MDD 2 SNRI Histrionic and Narcissistic PD
1 child
7 32 Single 15 Dysthymic Disorder 6 NDRI (Bupropion) PD Not Otherwise Specied
8 56 Divorced 12 Double Depression 10 SSRI NaSSA Obsessive Compulsive and
Narcissistic PD
9 45 Divorced 12 Chronic MDD 3 SSRI
2 children
10 32 Single 15 Double Depression 14 SNRI Histrionic and Narcissistic PD
11 38 Divorced 12 Dysthymic Disorder 6 SSRI Avoidant PD
2 children
12 50 Married 12 Chronic MDD 3 SSRI e
2 children

Taken into account recent developments in ST for PD that focus
more on schema modes than schemas (Arntz, 2012) and the close
relation between chronic depression and PDs we followed a mode
approach of ST similar to that described by Arntz (2012) for appli-
cation of ST in patients with cluster C PDs. Whereas schemas are
trait-like constructs, schema modes are state-like, and denote the
current affective-cognitive behavioral state of the person. Schema
modes can be understood as the combination of an activated
schema and specic coping (Lobbestael, Arntz, & Sieswerda, 2005;
Lobbestael, Van Vreeswijk, & Arntz, 2008). ST based on a mode
model has specic techniques for each mode (Young et al., 2003;
Arntz & Jacob, 2012). Change in ST is achieved through a range of
emotional-focused, cognitive and behavioral techniques focus on
(1) therapeutic relationship, (2) past (traumatic) experiences, (3)
daily life outside therapy (Nadort et al., 2009). Central to the ther-
apeutic relationship is limited reparenting, a therapeutic stance
characterized by warmth, nurturance and providing patients,
within the limited professional boundaries, corrective emotional
experiences that meet partially the unmet core emotional needs
that led to the development of the EMS (Young et al. 2003).
The protocol consisted of three phases: a rst, from the beginning
up to the 12the16th session, during which the schema case
conceptualization and patients education was completed. This was
the stage where the bond between therapist and patient was
created. The second phase, up to the 40th session, focused on
childhood memories and the change of schemas and modes through
experiential work and limited reparenting. The last phase focused on
behavioral change in the everyday life of the patient. The only dif-
ference between our protocol and the one described by Renner,
Arntz et al. (2013) was the use of limited reparenting even from
the rst sessions of the study with the therapist being extremely
empathic and nurturing in an attempt to bond to the patient. This
phase followed the protocol described by Young et al. (2003) for ST in
BPD, mainly promoting the formation of a secure attachment to
support the remaining treatment and to prevent dropout.
2.5. Therapists and treatment integrity
Four therapists participated in the trial. All were psychologists
with MSc degrees, one had also a PhD degree. All therapists were
trained in the training program of the Greek Society of Schema
Therapy and were certied on advanced level by the International
Society of Schema Therapy (2013) (www.isst-online.com).
Treatment integrity was monitored by means of supervision.
Therapists were provided with 3 h group supervision weekly dur-
ing the rst 12 months of the treatment and biweekly during the
last eight months of the treatment. The supervisor was an experi-
enced psychiatrist and schema therapist, accredited by the ISST.
All sessions were audiotaped. One audiotape between sessions 16
and 50, from each of the 12 patients, was randomly selected and rated
by the supervisor, using the Schema Therapist Rating Scale (Young,
2005). An adequate level of competency was dened as a mean
score of 4 or 4.5 for standard or advanced level certied therapists
respectively (Nadort, Genderen, & Behary, 2012). A cut off score of 4.5
was chosen, as therapists were all certied in advanced level.
Adherence to ST for methods and techniques used was excellent
(mean 5.12; SD 0.15) and no non-ST techniques were observed.
2.6. Statistical analysis
SPSS version 21 mixed regression was used to analyze the HRSD
results, using all available data. For the separate analysis of the
three HRSD baseline assessments an unstructured covariance
structure for the repeated part was used. For the other analyses,
involving more repeated assessments, the optimal covariance
structure for the repeated part was determined comparing
ARMA11, AR1, and AR1 heterogeneous structures. The last one was
found to be optimal and was used in these analyses. The analytic
strategy for analyzing treatment effects was similar to those
described in (Arntz et al., 2013). First the main effect of time was
tested (i.e., the linear time effect), by entering assessments (starting
with zero) as covariate. In the second step, condition and time-
within-treatment (centered) were added. Condition had three
levels: baseline (reference), introduction (the assessment imme-
diately after the introduction phase), and treatment (the four as-
sessments after 24, 36, 48 and 60 sessions). If the general linear
time effect was non-signicant, it was deleted as predictor. Addi-
tion of random intercepts and slopes was tried but estimations
failed to converge. The 6 months follow-up was separately tested
against baseline, also by means of mixed regression, with an un-
structured covariance structure for the repeated part, and time
within baseline (centered) as covariate.
For the HRSA, only one baseline assessment was available, just
before introduction to treatment. Therefore no change during
baseline could be assessed, but the other analyses were similar as
with the HRSD.
 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329 323

For the YSQ, only assessment just before introduction to treat-
ment, after 24 sessions, and post-treatment were available. Because
of the skewed distributions, changes were tested with mixed
gamma regression with a log-link, using an unstructured repeated
part. Assessment was entered as factor, with the baseline-24 ses-
sions and the baseline-post-treatment assessment contrasts.
Three versions of Cohens d as effect size for the nal change as
result of treatment were calculated based on the mean change in
estimated means from the mixed regression analysis from the
(average) baseline assessment(s) to the 60 months assessment,
respectively the half year follow-up, and three SD estimates: (1) the
baseline SD; (2) the pooled standard deviation of the assessments
involved in the pertinent change; the SD of the change score. All
necessary statistics were derived from the mixed regression results.
3. Results
heterogeneous variances). However, after adding condition and
time-within-treatment as predictors, overall time became non-
signicant, B 0.50, se 0.63; t (23.64) 0.81, p 0.43 (based
on rst order autoregressive covariance structure with heteroge-
neous variances). After deleting the overall time effect, the condi-
tion effect was signicant, F (2, 21.14) 22.29, p < 0.001. The
assessment after the introduction phase showed signicantly lower
HRSD scores than during baseline (m 20.87 vs. m 10.87, t
(8.92) 4.78, p 0.001). The mean HRSD score during treatment
(m 12.29) also differed signicantly from baseline, t
(24.32) 5.83, p < 0.001. During treatment there was a signicant
linear decrease in HRSD scores, B 1.94, se 0.854, t
(23.25) 2.28, P 0.032. At post-test the estimated HRSD mean
was 9.40 (SD 7.17), signicantly lower than during baseline
(m 20.87, SD 3.61). Effect size estimates (Cohens d) were 2.01
(pooled SD); 2.84 (baseline SD); and 2.02 (SD of change score).

Of 16 patients referred for the study, 4 (25%) were not eligible for
participation: 1 did not meet inclusion criteria (had no chronic
depression), 3 met exclusion criteria (1 bipolar disorder, 1 psychotic
disorder, 1 BPD). 12 patients (75%) were included in the study. Of
the 12 patients who began treatment one participant (8.33%)
dropped out at session 50 due to business reasons (had to move to
another city). No participant was excluded during treatment due to
need of hospitalization or suicidal ideation.
At post-treatment assessment ve out of the twelve patients
(41.6%) fully remitted (participants 2, 4, 5, 6, 8) and another two
patients (16.6%) responded satisfactory (participants 9, 11). Of the
fully remitted patients, at the follow-up assessment one relapsed
(participant 6) and the others maintained the result while in the
same period of the 6-month follow-up, one patient (7) who had not
responded by the end of the treatment, exceeded satisfactory
response and also one patient (9) who had responded satisfactory
by the end of the treatment, exceeded remission, leading to ve
remitters and an additional three responders at follow-up.
Table 2 presents the estimated means from mixed regression
analysis for HRSD and HRSA.
3.1.3. Six months follow-up vs. baseline
The six months follow-up (estimated mean 10.75) differed
signicantly from baseline, t (10.62) 4.57, p 0.001. Effect size
estimates (Cohens d) were 2.24 (pooled SD); 2.60 (baseline SD);
and 1.40 (SD of change score).
3.2. Anxiety symptoms: HRSA
3.2.1. Change in anxiety during treatment
The linear time effect was signicant, B 1.49, se 0.478, t
(27.90) 3.12, p .004. However, after entering condition, the
time effect became non-signicant, B 1.00, se 0.83, t
(23.83) 1.20, p 0.24. After deleting the general time effect,
condition was signicant, F (2, 19.90) 5.67, p 0.011. Introduction
differed signicantly from baseline, t (18.14) 2.37, p 0.029, as
was the average during treatment, t (20.53) 3.26, p 0.004. The
change during treatment failed to reach signicance, p 0.24. The
estimated post-treatment mean was 9.56, compared with the
baseline mean 17.29. Effect size estimates (Cohens d) were 1.22
(pooled SD); 1.35 (baseline SD); and 1.04 (SD of change score).

3.2.2. Six months follow-up vs. baseline

3.1. Depressive symptoms: HRSD
The six months follow-up (estimated mean 9.63) differed
signicantly from baseline, t(11.05) 2.84, p 0.016. Effect size
3.1.1. Change in depression during baseline
estimates (Cohens d) were 1.33 (pooled SD); 1.36 (baseline SD);
Using an unstructured covariance structure for analyzing the
and 0.83 (SD of change score).
three baseline assessments, it was found that there was a signi-
Table 3 presents the estimated means from mixed regression
cant linear increase in HRSD scores during baseline, B 0.52,
analysis for HRSD and HRSA.
se 0.186, t (11) 2.81, P 0.017. Thus, during wait, depression
symptoms increased.
3.3. Maladaptive schemas: YSQ domain scores

3.1.2. Treatment effects on depression 3.3.1. Change in domain scores during treatment
The model with time as single predictor revealed a signicant Table 3 gives an overview of the results of the mixed gamma
effect of time, B 1.50, se 0.271, t(27.40) 5.53, p < 0.001 regression for the ve YSQ domain scores and the total YSQ sum. As
(based on rst order autoregressive covariance structure with can be seen, the change from baseline to 24 sessions was modest
Table 2
and NS in the majority of the contrasts, whereas the change from
Estimated means from mixed regression analysis for HRSD and HRSA. baseline to post-treatment was large and highly signicant.
The scores on the standardized measures at baseline, Pre-
Assessment HRSD HRSA
treatment, 12the16th session, 24th session, 36th session, 46th
m SD m SD session, Post-treatment and 6-month follow-up are presented in
Baseline 1 20.57 3.19 NA NA Fig. 2 (YSQ scales were divided by 10 for better presentation).
Baseline 2 21.07 3.22 NA NA
Baseline 3 21.58 4.30 17.29 5.71
4. Discussion
ST introduction 10.89 8.64 12.32 6.35
ST session 24 15.23 6.49 12.56 5.29
ST session 36 13.28 8.60 11.56 7.39 This study found that sixty sessions of ST produced statisti-
ST session 48 11.34 5.37 10.56 4.58 cally and clinically signicant improvements in the symptom-
ST session 60 9.40 7.17 9.56 6.94 atology of chronically depressed female outpatients. This
6 Months follow-up 10.75 5.50 9.63 5.92
improvement concerns depression and anxiety as measured by
324 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329

Table 3
Results of mixed gamma regression analyses of YSQ domain and total score.

YSQ Estimated means (95% CI) Time effect t Baseline-24 sessions t Baseline-post-treatment

Domain Baseline 24 sessions 60 sessions F d.f. p d.f. p d(1) d(2) d(3) d.f. p d(1) d(2) d(3)

1 206 (163; 260) 197 (154; 252) 155 (130; 185) 5.53 2, 29 0.009 1.08 29 0.29 0.16 0.13 0.19 3.18 29 0.004 1.00 0.83 0.95
2 119 (91; 156) 111 (85; 146) 80 (65; 98) 8.86 2, 29 0.001 1.62 29 0.12 0.21 0.18 0.21 4.09 29 <0.001 1.22 1.00 1.24
3 143 (117; 175) 136 (108; 170) 101 (81; 126) 9.79 2, 29 0.001 1.58 29 0.13 0.15 0.15 0.24 3.96 29 <0.001 0.98 1.00 1.20
4 177 (147; 213) 166 (138; 199) 116 (98; 138) 11.67 2, 29 <0.001 1.67 29 0.11 0.24 0.23 0.56 4.61 29 <0.001 1.53 1.43 1.42
5 81 (66; 99) 74 (62; 89) 53 (43; 65) 11.89 2, 29 <0.001 2.52 29 0.018 0.24 0.26 0.35 4.86 29 <0.001 1.24 1.24 1.50

Total 726 (595; 887) 686 (557; 845) 502 (422; 599) 10.40 2, 29 <0.001 2.23 29 0.034 0.17 0.17 0.68 4.55 29 <0.001 1.09 1.18 1.38

Note. d(1) Cohens d based on baseline SD; d(2) Cohens d based on pooled SDs of the involved assessments; d(3) Cohens d based on SD of the change score. Cohens
d calculated from mixed gamma regression parameters in the transformed scale.

the Hamilton Rating Scales. Approximately 60% of the patients
remitted or satisfactorily responded in the ST treatment and the
Mean HRSD dropped from 21.07 during baseline to 9.40 at post-
treatment and 10.75 at follow-up. The effects were large and the
gains of treatment maintained in the 6-month follow-up
assessment. Only one patient relapsed while another two
exceeding response or remission, leading to a 67%
responders remitters rate at follow-up. Seven out of the 12
patients (58.33%) who participated had a diagnosis of at least one
PD (Table 1). Four of these patients (2, 7, 8, 11) fully remitted or
responded satisfactory. This nding is in accordance with the
effectiveness of ST for patients with PDs.
The design of this study includes a baseline wait period of 8
weeks. During this period no reduction in depression was observed.
Thus the sample seemed to be really chronically depressed, and this
suggests that changes during treatment can be attributed to ther-
apy. The introduction phase had a strong effect on HRSD and HRSA.
This deviates from ndings of others studies (Arntz et al., 2013;
Weertman & Arntz, 2007) where introduction had no therapeutic
effect. In these two studies, the introductory phase had a highly
explorative character. In our study a core element of the intro-
ductory phase was bonding, especially thru limited reparenting.
Along with the exploration of patients problems and construction
of the case conceptualization, therapists offered an extremely
nurturing environment, which may have relieved patients early in
therapy. Without further research it is unclear what lasting effects
this introductory phase would have, if provided as a stand-alone
treatment. ST argues that the rest of the treatment is needed to
bring about lasting change. This is indeed likely given the comor-
bidity with personality disorders and the need for lengthier treat-
ment protocols suggested for chronic depression (Cuijpers et al.,
2010; Klein et al., 2008; Imel et al,. 2008).
An interesting observation in this context is that most of the
patients who remitted or responded to treatment (participants 2,
4, 5, 6, 7, 9, 11) showed after this early improvement a trend to
deteriorate at the second (24th sessions) or later assessment.
This deterioration can perhaps be explained by the use of expe-
riential techniques for schema change, such as imagery and chair
work, which are crucial components of schema therapy in this
phase, and brings the patient in contact with the childhood early
adversity that underlies schema formation. This phase of ST
might be experienced initially as burdensome by patients and
may take time for clinical improvement to be translated into an
increase in quality of life (van Asselt et al., 2008). As therapy
progresses therapists help patients through experiential work
and reparenting to fulll the unmet core needs and change
schemas and modes resulting in more lasting change. This is
similar to descriptions of emotional processing in experiential
therapy [it gets worse before it gets better (Pascual-Leone,
2009) and the only way out is through (Hunt, 1998)]. Studies
examining the emotional process in the experiential therapy of
depression have found that high levels of emotional arousal in
mid-therapy are predictive of reduction in depressive symp-
tomatology and are related to positive outcome (Missirlian,
Toukmanian, Warwar, & Greenberg, 2005; Pos, Greenberg, &
Warwar, 2009). This emotional processing phase could explain
the nding of our study that all patients who exhibit remission or
satisfactory response showed this pattern of seeming deteriora-
tion at this phase of treatment.
Comparing the results of our study to those of CBASP studies,
Schema Therapy seems to be a promising new treatment. In the
study by Keller et al. (2000) the overall rates of response for the
intention-to-treat sample was 48% for CBASP group and 73% for
the combined-treatment group (nefazodone plus CBASP). Mean
HRSD scores dropped from 26.4 to 15.1 in the CBASP group and
from 27.4 to 9.7 in the combined treatment group (21.07e9.4 in
our study). A more recent study from the same group (Kocsis
et al., 2009) found that the addition of CBASP or Brief Support-
ive Psychotherapy (BSP) in chronically depressed patients
already treated with an algorithm of pharmacotherapy produced
an overall rate of response of 37.5% with the other 62.5%
remained depressed. Mean HRSD dropped from 19.5 to 11.2 in
the group received CBASP and from 19.4 to 12.8 in the group
received BSP. In difference with the CBASP studies, we provided a
much lengthier protocol of 60 sessions of psychotherapy. More-
over the control of the antidepressant medication was beyond
the scope of our study, but all of the participants were already on
antidepressant medication, which had to be stable at least three
months before the start of treatment and had not responded to it.
This concept is closer to the arms of the CBASP studies where
psychotherapy has been added (Kocsis et al., 2009) or provided in
combination with medication (Keller et al., 2000). Direct com-
parisons are needed to assess in what aspects the two ap-
proaches might yield different outcomes.
Our study along with the study by Carter et al. (2013) sup-
ports the suggestion of using ST for depressed patients. In the
study of Carter, the focus of interest was a current major
depressive episode, but 68% of the participants had also a diag-
nosis of chronic depression. The presence of chronic depression
did not impact the outcome of the study. These results could be
interpreted as an indication for the use of CBT for chronic
depression. On the other hand the study of Carter et al. lack of a
follow-up assessment and as mentioned in the introduction the
existing psychotherapeutic interventions suffer from low rates of
maintenance of their effects.
Regarding the EMS as measured with the YSQ inventory, in our
study, a statistically signicant reduction was observed in the
scores of the ve domains of the YSQ. Reduction of depression and
anxiety seems to precede reduction in the YSQ. This is similar with
the nding by Renner et al. (2013). An explanation for this could be
 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329 325

Fig. 2. Scores on standardized measures for HRSD, HRSA, YSQ1e5, for each participant (participants 1e12).
326 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329

Fig. 2. (continued).
 I.A. Malogiannis et al. / J. Behav. Ther. & Exp. Psychiat. 45 (2014) 319e329
Fig. 2. (continued).
that the YSQ, as a trait-instrument, might be not very suitable to
assess early changes in schemas. Alternatively, therapeutic changes
take rst place at emotional/symptom level, before they are shown
at schema level.
The reduction observed at the post-treatment assessment in
YSQ was especially manifest in the domains Impaired Autonomy
& Performance and Over-vigilance & Inhibition that characterize
chronically depressed patients (Riso et al. 2003) and the domain
of Disconnection & Rejection that is closely related to depressive
symptomatology (Renner et al. 2012). These changes at schema
level could explain the maintenance of the results in the 6-
month follow-up, but larger studies are needed to empirically
test this.
A number of factors limit the generalization of the results of
this study. One main limitation concerns the lack of control
group. A second one concerns the small number of the sample. A
third limitation is a weakness of the design, which does not
include a baseline phase of variable length, randomized over
participants (multiple baseline case series). With such a design,
especially when it is concurrent (participants start at the same
moment), better experimental control is achieved. On the other
hand the use of four therapists is strength of the study supporting
the feasibility of the treatment by different therapists. The con-
duction of the assessments by an independent rater, the super-
vision of therapists and the control for therapy adherence are
other strengths of this trial. The present study should be
considered as an indication and a preliminary test of the effec-
tiveness of ST for chronic depression. Future randomized
controlled studies should be conducted to conrm this effec-
tiveness of ST for chronic depression alone or in combination
with pharmacotherapy.
Declaration of interest
All the authors explicitly state that there is no interest to be
declared.
327
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