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With the growing interest in the role of cognitions in PTSD, this prospective study
examined the course and bi-directional relationship between post-trauma cognitions and symptoms of PTSD. A sample of Israeli combat veterans, including
former prisoners of war, was assessed in 1991, and later followed up in 2003 and
2008. PTSD symptoms were measured at three time points. Cognitions concerning the self and the world were measured twice. Applying Autoregressive CrossLagged (ARCL) modeling strategy, initial PTSD symptoms predicted subsequent
negative cognitions but not vice versa. In addition, repeated measures design revealed that individuals with chronic PTSD symptoms had relatively negative cognitions that further amplified with time. More specifically, increasingly negative
cognitions were documented among ex-prisoners of war. The main findings suggest that negative cognitions are fueled by PTSD and that in chronic PTSD there
is an amplification of pathogenic outcomes over time. Discussion of the findings
is in the context of current cognitive models of PTSD.
Sharon Dekel, Ph.D., is affiliated with the PTSD Research Laboratory, Massachusetts General Hospital-East,
Charlestown, Massachusetts. Zahava Solomon, Ph.D., is affiliated with the Bob Shapell School of Social Work, Tel
Aviv University, Tel-Aviv, Israel. Tamar Peleg, Ph.D., is with the Department of Social Work, Ben Gurion University
of the Negev, Israel.
This study was supported by the Young Investigator Grant of the Brain and Behavior Research Foundation sponsored by Dr. Dylan Tauber, which was awarded to Sharon Dekel.
Address correspondence to Sharon Dekel, PTSD Research Laboratory, Massachusetts General Hospital-East, 120
Second Ave., Charlestown, MA 02129. E-mail: dekel.sharon@gmail.com
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The popular view advocates that maladaptive post-trauma (and pre-trauma) cognitions are an imperative catalyst of PTSD.
With their rigid nature, they impede the
processing of corrective information, rendering the individual vulnerable to developing and maintaining PTSD. In accord with
emotional processing theory (EPT) (e.g.,
Foa & Rothbaum, 1998), survivors who
come to view the world as extremely dangerous and the self as inept may be reluctant
to engage in daily behaviors that disconfirm
these views, systematically avoiding traumarelated thoughts and activities. This way, a
pathological memory fear structure entailing
numerous danger stimulus-responses is
maintained and chronic PTSD develops.
In accord with the cognitive processing theory (Resick, & Schnicke, 1992),
drawn on information-processing models,
survivors who eventually develop PTSD experience a conflict between their pre-trauma
beliefs about the self and world (e.g., the belief that nothing bad will happen to me) and
post-trauma information (e.g., the trauma as
evidence that the world is not a safe place).
These conflicts, so-called stuck points, interfere with the emotional processing of the
event and the recovery.
At the same time, others have postulated that PTSD may trigger negative posttrauma cognitions. As Power and Dalgleish
(Dagleish & Power, 2004; Power & Dagleish, 1999) originally postulated, the relation
of cognitive schemas to emotional disorders,
including PTSD, is bi-directional. In their
multi-level model, post-trauma negative automatic thoughts related to the trauma may
result in shattered schematic representation
(higher order ideation of extreme belief in
vulnerability), which then generate symptoms and accompanied emotions. Once these
elements are active, a top-down process begins, suggesting that symptoms of PTSD may
fire back and amplify negative cognitions.
More specifically, PTSD is coined a
pervasive disorder and its debilitating symptoms may therefore penetrate the traumatized inner psychological world. In fact,
symptoms of PTSD were previously found
to have a pathogenic effect on survivors attachment orientation (Solomon, Dekel, &
Mikulincer, 2008), which is underlined by a
relational cognitive schema. It follows that
PTSD symptoms and accompanied behaviors may lead to impairments in the traumatized core cognitions. For example, maladaptive social functioning entailing outbursts of
uncontrolled anger and violence along with
an enduring sense of loneliness, often seen in
PTSD (Solomon & Dekel, 2008), may give
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Descriptive Statistics
Initially, we conducted a series of Pearson correlations assessing the magnitude of
associations between post-trauma cognitions
and PTSD (Table 1). Significant cross-sectional and longitudinal relations were found
between cognition and PTSD symptom levels. Individuals with more PTSD symptoms
had relatively negative cognitions in both T1
and T3. Likewise, individuals who tended to
have more PTSD symptoms in T2 their cognitions were relatively negative in T1 and T3.
-. 13
41.25(7.33)
.43***
.01
.26**
-. 15**
-. 15*
-. 14
33.24(6.19)
WA-1, T3
WA-2, T3
WA-3, T3
PTSD, T1
PTSD, T2
PTSD, T3
Mean (SD)
.36***
WA-3, T1
51.17(6.88)
-.04
-.08
-.11*
.26**
.08
.08
31.07(6.94)
-.41***
-.33***
-.03
-.52***
-.24***
40.86(7.91)
-.16*
-.20*
-.04
.27***
50.53(8.84)
-.40***
-.31***
-.05
1.76(3.36)
.24***
.37***
6.37(5.74)
.80***
6.63(5.79)
Note. WA-1 = benevolence of the world, WA-2 = meaningfulness of the world, WA-3 = self-worth. PTSD refers to PTSD symptom count, T1, T2, and T3 = measurement in 1991, 2003, and
2008. N = 240. *p < .05.**p < .01. ***p < .001.
-. 06
.11*
.14
.37*
.27*
.13*
.21***
WA-2, T1
WA-1, T1
TABLE 1. Means, Standard Deviations, and Intercorrelations Between Main Study Measures
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FIGURE 1. ARCL Model for Assessing the Bidirectional Association Between PTSD and Cognitions
Across Three Time Points, 1991, 2003, and 2008.
able distribution. Recommended NNFI cutoffs vary between .80 (Hooper, Coughlan,
& Mullen, 2008) and .95 (Bollen & Curran,
2006). While RMSEA values .05 are considered a good fit, values between .08 and
.10 are still acceptable, representing a mediocre fit (Browne & Cudeck, 1993).
The stability of cognitions and PTSD
over time ranged from moderate to high.
Participants with high cognition or PTSD
symptom levels in T1 had high cognition
and PTSD symptom levels, respectively, in
T3. More importantly, higher PTSD symptom levels in T2 predicted subsequent more
negative cognitions levels in T3, above and
beyond cognition stability. However, initial
cognition levels in T1 did not predict later
PTSD symptom levels in T2 and T3.
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