SCIENCE BRIEF
Treatment changes in the depressive
self-schema
Research examines effects of cognitive therapy and
medication on the structure of the self-schema.
The depressive self-schema
The depressive schema is a well-organized and interconnected negative
internal representation of self. Believed to develop through early life
experiences and to remain dormant until triggered by negative life events
(Beck, Rush, Shaw, & Emery, 1979), a depressive self-schema has long been identified
as a key factor associated with depression risk (see Beck & Dozois, 2011;
Dozois & Beck, 2008).
This deep level of cognition, once activated by negative life events (such
as loss, failure or rejection) purportedly impacts surface-level cognitions
(e.g., information processing, dysfunctional attitudes, automatic thoughts). As
such, the schema is considered a crucial variable in vulnerability models of
depression. The schema is believed to be characterized by both its content
(e.g., negative absolutist beliefs) and its structure or organization (Ingram,
Miranda, & Segal, 1998). Although many researchers have examined its
content, few studies have attempted to examine the structure of the
self-schema.
The Psychological Distance Scaling Task (PDST; Dozois & Dobson, 2001a,
2001b) was developed to measure the structure of the schema. Participants are
presented with a square grid divided into four quadrants on the computer
screen. The x-axis pertains to self-descriptiveness and is anchored with
"Very much like me" on the right and "Not at all like me"
on the left. The y-axis taps into the valence of the word and is anchored with
"Very positive" at the top and "Very negative" at the
bottom. Adjectives are displayed in the middle of the grid. Using the
computer mouse, participants consider both axes, and place each adjective on
the grid in terms of where it fits in psychological space for them. After
each response, a new grid and new adjective are displayed on the screen, until
all adjectives are presented. The computer records the X and Y
coordinate point for each adjective and calculates the interstimulus distance
among the positive schematic adjectives and among the negative schematic
adjectives. The computations used to derive self-relevant distances
entail dividing the sum of squared positive or negative self-relevant distances
by the total number of possible self-descriptive positive or negative distances
(see Seeds & Dozois, 2010). An assumption of this task is that less
distance among adjectives is indicative of greater interconnectedness or
consolidation of self-referent content, whereas greater distance among
adjectives is indicative of less interconnectedness or consolidation.
A number of studies have shown that a well-organized negative
representation of self (i.e., the organization of the self-schema) meets
sensitivity (Dozois & Dobson, 2001b, Lumley, Dozois, Hennig, & Marsh,
2012; Seeds & Dozois, 2010), specificity (Dozois & Dobson, 2001b,
Dozois & Frewen, 2006; Lumley et al., 2012) and stability (Dozois, 2007;
Dozois & Dobson, 2001a) criteria as a vulnerability factor for depression.
People with depression, for instance, show well-interconnected negative content
and loosely connected positive content. Studies using this method have also
been successful in differentiating the self-schema structures observed in
depression from those seen in anxiety (Dozois & Dobson, 2001b; Dozois &
Frewen, 2006). The interaction of cognitive organization and negative life
events also predicts depression prospectively (Seeds & Dozois, 2010).
The stability of negative cognitive organization has also been supported.
An early trial that examined this idea followed 45 depressed individuals over
a six month period. The hypothesis was that individuals who remitted from
depression would show a significant cognitive shift in information-processing
(e.g., deactivation of negative processing — for example, attention and
memory biases) but that temporal stability would be found on the PDST.
Individuals who improved from a depressive episode showed an increase in
positive processing and a decrease in negative processing over time. As
predicted, however, there was no significant change over time in negative
interpersonal structure (i.e., the
organization of negative adjective content; see Dozois & Dobson, 2001a).
This finding was replicated in an independent sample of 54 patients (Dozois,
2007). In this replication study, interpersonal content remained well-organized
even as patients moved from a depressed to a remitted state. Together, these
studies support one of the central tenets of Beck’s cognitive theory of
depression that negative self-schemas may be present but latent and that, once
activated they may proceed to impact various processing biases associated with
depressed mood (Beck et al., 1979; see Dozois & Beck, 2008).
Thus, cognitive structure or organization for interpersonal content appears
to be a stable vulnerability factor for depression. Stability, however, doesn’t
imply that a vulnerability factor is impermeable to change. It is possible, for
example, that cognitive therapy (CT) is able to alter these negative cognitive
structures. CT is comparable in effectiveness to behavior therapy, other bona
fide psychological treatments and antidepressant medication for an acute
episode of depression, with each treatment producing superior results compared
to placebo (see Beck & Dozois, 2011). CT also carries an advantage,
relative to antidepressant medication, for the prevention of relapse (Glogcuen,
Cottraux, Cucherat, & Blackburn, 1998).
The self-schema and treatment
The precise mechanisms underlying the prophylactic power of CT are not
presently known. One possibility is that CT and antidepressant medication may
both change certain aspects of negative thinking (such as information processing,
automatic thoughts, dysfunctional attitudes) but that cognitive therapy also
alters the “deeper” cognitive structures that give rise to relapse (DeRubeis,
Webb, Tang, & Beck, 2010; Garratt, Ingram, Rand, & Sawalani, 2007).
Consistent with this idea, Segal, Gemar and Williams (1999) compared
patients who had successfully completed either CT or pharmacotherapy. After
remission, participants were administered the Dysfunctional Attitude Scale
(DAS), a self-report measure of negative beliefs and attitudes concerning self.
They were subsequently induced into a dysphoric mood state and then
administered a parallel form of the DAS. Individuals who received
antidepressant medication showed an elevation of DAS scores whereas individuals
in the CT group did not. Segal et al. (2006) showed that this activation was
predictive of subsequent relapse. Thus, it is conceivable that CT changes an
individual’s core negative structures and that this shift may be responsible
for lasting therapeutic gains.
Also consistent with this idea, are the findings from a trial which
compared the combination of cognitive therapy and pharmacotherapy (CT+PT) to
pharmacotherapy (PT) alone (Dozois et al., 2009). Patients were randomly
assigned to one of the two conditions. CT was provided for 15 individual
sessions (one hour/week) and administered according to the
empirically-supported protocol outlined by Beck and his colleagues (Beck et
al., 1979). PT involved medication plus clinical management (SSRI or SNRI plus
augmentation if needed, following the Canadian Network for Mood and Anxiety
Treatment [CANMAT] guidelines; see Kennedy et al., 2009).
There were no significant between-group differences on age, education,
marital status, ethnicity, previous depressive episodes, suicide attempts, current
medications or comorbidity. Similarly, no group differences were obtained on
depression or anxiety at initial assessment. No group differences were found
post-treatment on symptom scores. In other words, both treatments were equally
effective at treating depression.
Consistent with the hypothesis that negative thinking would improve as
depression improved, automatic thoughts changed significantly in both
groups — positive automatic thoughts increased significantly and negative
automatic thoughts decreased significantly (with no statistically significant
between-group differences). Significant changes were also evident on the
Dysfunctional Attitudes Scale — both groups showed a significant decrease
in dysfunctional attitudes from pre- to post-treatment, with no significant
between-group differences.
Individuals treated with CT+PT, however, showed significantly greater
cognitive organization of positive interpersonal content and less
well-connected negative interpersonal content than did individuals treated with
PT alone. Moreover, individuals in the CT+PT group showed significant pre-post
differences on positive and negative cognitive organization, whereas a shift in
cognitive structure was not evident in the PT group (Dozois et al., 2009).
These results are intriguing in light of previous research which has shown that
the organization of interpersonal negative content is stable despite the
remission of depressive symptoms (Dozois, 2007; Dozois & Dobson, 2001a). It
appears that cognitive therapy is able to modify these stable cognitive
structures, an effect that was unique to CT+PT.
These results suggest that, although both medication and CT improve
depressive symptoms, automatic thoughts and dysfunctional attitudes, CT may
offer more in terms of deeper structural change than medication. An important
caveat is that this study examined only CT+PT compared to PT alone. It is
possible that it was the combination of interventions rather than CT alone that
resulted in this change. As such, there is a need to replicate this study
comparing CT alone to medication alone.
Lena Quilty and her colleagues recently completed a trial that compared
cognitive behavioral therapy (CBT) to pharmacotherapy on cognitive products,
processes and structure. A sample of 104 patients were randomly assigned to CBT
(n = 54) or PT (n = 50). The dropout rate was 9 percent and 14 percent,
respectively for CBT and PT, leaving a final sample of 92. Preliminary data
analyses revealed that over the course of 16 weeks of treatment, both the CBT
and the PT groups showed a significant decrease in psychological distance for
positive content (so positive content became more interconnected over time).
There were no significant between-group differences, however, nor a significant
interaction between time and treatment group. Similarly, both groups showed a
significant increase in negative distance (i.e., there was less
interconnectedness of negative content over the course of treatment). In
contrast to the previous study, however, no group differences were found and
the interaction of time and treatment group was not significant.
Conclusion and future directions
Cognitive organization appears to be an important vulnerability factor for
depression. This variable, assessed via the Psychological Distance Scaling
Task, appears to demonstrate sensitivity, specificity and stability. Across two
independent trials, negative cognitive organization remained well
interconnected even though people improved significantly from a depressive
episode.
The impact of cognitive therapy and antidepressant medication on cognitive
organization has also been examined in two trials. In the first trial,
cognitive therapy outperformed medication in shifting cognitive organization.
However, the more recent trial found no significant differences between groups
on cognitive organization. Instead, both treatments resulted in a significant
shift — the positive content became significantly more interconnected and
the negative content less interconnected.
Why were there no differences between groups in the second trial? What may
account for the differences between studies? One argument might be that the
combination of CT+PT resulted in stronger effects on cognitive change
variables; however, in the second trial, CBT and pharmacotherapy each
independently showed a significant shift on cognitive organization. In
addition, it was the PT group in the previous trial that did not shift
significantly for negative content whereas it did in the subsequent trial. The
average severity of depression in the initial trial was somewhat higher than in
the second trial — this may have rendered CT more powerful in changing
cognitive structure in the initial trial, whereas both conditions were able to
do so in the second trial.
Another possibility is that the pharmacological treatment was superior in
the second trial. This explanation seems highly unlikely, however. In both
trials, the pharmacotherapy provided was top of the line: rigorous CANMAT
guidelines were followed closely and the psychiatrist was free to switch or
augment the medication. It is also possible that the first trial was
underpowered compared to the second trial — although effects were found
for CT+PT, there was not sufficient statistical power to detect effects in the
PT alone arm.
These more recent findings are just preliminary and should be treated as
such. Quilty and colleagues will be conducting more nuanced lagged
analyses to see if the causal pathways between psychological distance and
depression are different across treatment groups.
Regardless of the exact reason, these findings call into question the idea
that cognitive organization or structure shifts uniquely in CT. The more recent
trial suggests that pharmacotherapy may also be capable of shifting these
stable cognitive structures — however, this does not rule out the
possibility that the cognitive shift is perhaps the final common pathway.
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