ARTICLE IN PRESS

Journal of Behavior Therapy

and Experimental Psychiatry 35 (2004) 307–318
www.elsevier.com/locate/jbtep

Metacognitive therapy for PTSD: a preliminary

investigation of a new brief treatment
Adrian Wellsa,, Sundeep Sembib
a
Department of Clinical Psychology, University of Manchester, Rawnsley Building, MRI, Oxford Road,
Manchester, M13 9WL, UK
b
University of Liverpool, UK
Received 12 September 2003; received in revised form 21 June 2004; accepted 9 July 2004

Abstract

The effectiveness of a new treatment for post traumatic stress disorder (PTSD) is addressed.
Treatment was based on a metacognitive theory of mechanisms by which natural traumatic
processing is enabled or hindered by coping strategies. It suggests that elimination of worry/
rumination, of maladaptive attention strategies, and enhancing metacognitive flexibility, will
permit natural processing and a return to normal cognition. An A-B direct replication series
(n ¼ 6) with follow-up assessments at 3, 6, and 18–41 months was implemented. Treatment
commenced 3–10 months post-trauma. All patients showed large and statistically significant
improvements in general emotion and specific PTSD measures. Gains were maintained at
follow-up. Two further consecutively referred patients were treated at 8 and 12 months post-
trauma to add to sample size (n ¼ 8). Overall Post treatment effect sizes were large, ranging
from 3.0 to 5.0. Further evaluations are clearly warranted.
r 2004 Elsevier Ltd. All rights reserved.

Keywords: Cognitive therapy; Metacognition; PTSD; Worry; Attention

Corresponding author. Tel.: +44-161-276-5399; fax: +44-161-273-2135.

E-mail address: adrian.wells@man.ac.uk (A. Wells).

0005-7916/$ - see front matter r 2004 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jbtep.2004.07.001
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308 A. Wells, S. Sembi / J. Behav. Ther. & Exp. Psychiat. 35 (2004) 307–318

1. Introduction

Primary psychological treatments for post traumatic stress disorder (PTSD)

consist of prolonged imaginal exposure to traumatic memories (Foa & Kozak, 1986;
Cooper & Clum, 1989; Richards, Lovell, & Marks, 1994), and cognitive
restructuring of appraisals and beliefs emerging from trauma experiences (Marks,
Lovell, Noshirvani, Livanou, & Thrasher, 1998; Tarrier et al., 1999). Meta-analyses
show that patients improve with these treatments, however a significant proportion
of patients fail to respond, discontinue treatment or show only partial improvement
(Sherman, 1998; van Etten & Taylor, 1998). Debriefing has been advocated for
routine use following trauma with the aim of reducing complicated emotional
reactions later. However, evidence suggests it may not be particularly helpful in some
circumstances and some individuals appear to get worse as a result of debriefing
(Bisson, Jenkins, Alexander, & Bannister, 1997). A need has been identified for the
development of brief and effective treatments that do not involve high degrees of
specialist involvement like that which is required for typical cognitive-behavioral
interventions (Kilic, 2001).
Most cognitive approaches to understanding PTSD emphasise the need to
effectively process trauma in order to avoid or treat PTSD. However, views on what
constitutes effective processing differs between theories. One way forward in
developing new interventions is to base treatment on a model of the mechanisms that
block natural emotional processing. The metacognitive model and treatment of
PTSD (Wells, 2000) is one such approach. It proposes that effective emotional
processing consists of two basic elements: (1) the strengthening of a cognitive
configuration or plan that can guide thinking and behaviour in future potential
encounters with trauma, and (2) flexible control over processing so that low level
trauma-related processing can be reduced and cognition re-tuned to the normal
threat-free environment.
The metacognitive theory describes the mechanisms by which natural and
adaptive traumatic processing (i.e., strengthening of a plan), and flexible control
occurs or is hindered by coping strategies. Re-experiencing, intrusions and orienting
reactions following trauma act as motivationally significant interrupts that prompt
the running of mental simulations of dealing with stressful experience and introduce
programmed biases in cognition that are part of forming a new plan. Intrusions and
orienting responses normally lead to shaping of a plan by changes in knowledge,
strengthening of some processing operations/biases and coping strategies and the
weakening of others.
This normal Reflexive Adaptation Process (RAP) of plan development is initiated
by lower-level processing activity, it is disrupted by several factors, and as a result
stress symptoms persist culminating in PTSD. Internal disrupting factors are: (1) the
occurrence of worry/rumination styles of thinking following trauma; (2) attentional
strategies of threat monitoring; (both 1 and 2 are linked to the persons metacognitive
beliefs about the utility of these strategies for coping); (3) beliefs that lead to the
negative interpretation of symptoms; (4) coping through cognitive, emotional or
situational avoidance. External factors also contribute to these processes such as
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A. Wells, S. Sembi / J. Behav. Ther. & Exp. Psychiat. 35 (2004) 307–318 309

threats that are difficult to bring under personal control and social factors that
contribute to worry/rumination and to negative appraisal of one’s coping or
responses during or after trauma. In summary, worry/rumination thinking styles,
threat monitoring and avoidant coping (e.g., thought suppression), lead to a fixed
pattern of repetitive processing that does not lead low-level processing activity to
decrease and return to normal. We have coined the term ‘‘trauma-lock’’ as a
shorthand label for this state.
The problem with worry/rumination, which is predominantly a negative verbal
activity, is that it anchors attention on threat and it uses up executive processing
resources so that individuals have difficulty using flexible control and returning
thinking to its normal threat-free status. Moreover, this dominance of verbal activity
reduces the resources available for running imaginal simulations, which normally
present an effective way of strengthening plans. Imaginal mental simulation is a good
vehicle for plan development, because it presents complex cause-effect and stimulus-
action sequences over a time course. Imagery is capable of combining information
with behaviour (i.e., motor control programs), which are the basis of plans for
cognition and action. The problem with attentional strategies such as threat
monitoring is that they fix attention on threat-related information leading to a sense
of recurrent threat, thereby maintaining activation of the anxiety program and
strengthening metacognitive strategies of threat detection. The individual becomes a
skilled ‘‘threat-detector’’ tuning in to unlikely threat and failing to re-tune to the
normal threat-free environment. Problems with avoidant strategies such as
attempting to suppress thoughts are that this prevents the running of simulations
and interferes with the biasing and tuning of cognition by intrusions. Moreover, it
may inadvertently activate a new threat-monitoring plan in which thoughts
themselves become the source of threat and they are more likely to be detected.
This theoretical approach implies that it may not be necessary to modify patients’
cognitions about the trauma, memories of trauma, or facilitate habituation to
trauma memories. It suggests that it will be helpful to enable the patient to activate a
more adaptive style of thinking and behaving in response to intrusive symptoms that
‘‘unlocks’’ barriers to natural in-built adaptation processes (the RAP). This can be
achieved by implementing strategies for dealing with intrusive symptoms that enable
patients to break free of the constraints and problems of locked-in self-processing in
the form of worry, threat monitoring, and maladaptive self-control.
A central novel aspect of this model is its emphasis on the role of thinking styles
that are linked to metacognitive beliefs. A prediction of this approach is that worry/
rumination disrupts adaptation following stress and contributes to the development
of PTSD symptoms. Empirical studies support this prediction. Two studies of the
manipulation of thinking styles show that in non-patients, worrying following
exposure to stress is associated with an incubation of intrusive images related to the
stressor over the next three days (Butler, Wells, & Dewick, 1995; Wells &
Papageorgiou, 1995). In a prospective study of the development of PTSD following
road traffic accidents, Holeva, Tarrier and Wells (2001) demonstrated that a
tendency to use worry as a means of controlling thoughts, and lack of social support
both independently predicted the presence of PTSD approximately 3 months later.
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Warda and Bryant (1998) found that following road accidents individuals with acute
stress disorder used more worry and punishment based thought control strategies
than those without acute stress disorder. In a different line of research on thinking
styles, rumination has been shown to be linked to subsequent negative psychological
outcomes in the form of depressive symptoms following negative life events such as
an earthquake (Nolen-Hoeksema & Morrow, 1991) and bereavement (Nolen-
Hoeksema, Parker, & Larson, 1994).
This paper reports a preliminary evaluation of a new treatment based on the
metacognitive model of PTSD. The most basic or ‘‘core’’ components of the
treatment were used in order to reduce overlaps with exposure and cognitive-
challenging of thoughts. The goal of the core treatment is to allow patients to
develop flexible metacognitive awareness and control, and break-free of processing
in the form of worry/rumination, and threat monitoring.

2. Method

Six consecutive patients, five female and one male, who had been referred for
treatment of Post Traumatic Stress Disorder following varied violent assaults, sexual
assaults or robbery were included in this case series. Patients were general
practitioner or psychiatrist referrals to a clinical psychology outpatient service. All
patients fulfilled DSM IV (American Psychiatric Association, 1994) criteria for
PTSD as assessed by section F25-30 of the Structured Clinical Interview for DSM
IV—Patient edition (First, Spitzer, Gibbon, & Williams, 1997). All patients also met
criteria for major depressive disorder, which had developed following the trauma.
Patients were included in the study if no significant head injury was sustained,
there were no co-morbid alcohol/drug dependency problems, and patients had not
received any previous cognitive-behavioural treatment. Based on earlier treatment
development work a minimum of 8 treatment sessions were offered and treatment
was terminated when patients reported that they were no longer distressed by their
symptoms. The first three sessions were of 60 min duration but after this sessions
were of 30 min duration. A range of 2–9 months had elapsed following the trauma
before patients entered a four-week baseline monitoring period. Therefore, a range
of 3–10 months had elapsed since the trauma and prior to commencement of
treatment.

2.1. Participants

Patient 1: A 38-year-old married mother of two, with no premorbid psychiatric

history. She worked as an assistant manager in a jewellery store and within the space
of two months she was a victim of two armed robberies. Over the course of her
treatment and follow-up there were several more incidents of theft from her place of
employment. Treatment commenced 6 months after the trauma.
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Patient 2: A 19 year-old single woman with no premorbid psychiatric history. She

worked in a mobile telephone shop and she was held at knifepoint whilst the shop
was burgled. Treatment commenced 10 months after the trauma.
Patient 3: A 35-year-old married mother of two children with no premorbid
psychiatric history. She worked with two others in a wine store, where she was the
victim of an armed robbery. Treatment commenced 8 months after the trauma.
Patient 4: A 50-year-old unmarried woman in a long-term relationship. She did
not have a formal psychiatric history although had been involved in a past physically
abusive relationship with an alcoholic. While out one evening walking her dog she
was the victim of an assault and attempted rape. Treatment commenced 5 months
after the trauma.
Patient 5: A 36 year-old married father of two who worked as a food vendor. He
had no premorbid psychiatric history. He was the victim of a violent assault and
robbery in which his assailant poured petrol over him and threatened to set him on
fire. Treatment commenced 3 months after the trauma.
Patient 6: A 33-year-old unemployed mother of four, with no pre-morbid
psychiatric history. She was attacked and raped whilst returning home from a
nightclub. Treatment commenced 5 months after the trauma.

2.2. Experimental design

The six consecutive patients in the case series participated in a brief treatment
evaluation using a single case A-B design with follow-up. Follow-up was conducted
at three and six months post-treatment, and at a longer term of 18–41 months.
Replication across 6 patients constitutes a ‘‘direct replication’’ (Barlow & Hersen,
1984; Sidman, 1960), which can establish the generality of treatment effects across
different PTSD patients. This type of design can produce data on the generality of
findings that surpasses that of the treatment versus no-treatment group design
(Barlow & Hersen, 1984), and offers a strategy for assessing if a more ambitious
study is warranted.
All patients initially entered a four-week baseline period during which they met
with the therapist (SS) and completed a number of standardised psychometric
measures at each session. The therapist did not provide any treatment during
baseline but merely reviewed briefly the self-report measures. In all cases follow-up
was at three and six months post treatment, and individual longer-term follow-ups
varied from 18–41 months (this is because we decided to examine longer follow-up
intervals only after the last patient had completed the 6 month follow-up).

2.3. Measures

Following referral all patients initially underwent an assessment consisting of: an

unstructured clinical interview, Structured clinical interview using Section F25–30
of the SCID and psychometric assessment. The measures used are briefly
outlined below.
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Posttraumatic stress diagnostic scale (Foa, 1995). A 49 item self-report instrument

designed to aid in the diagnosis of PTSD. The structure and content of the PDS
mirror the diagnostic criteria for PTSD set out in DSM IV (APA, 1994). The PDS
assesses symptoms across the six criteria (Criteria A-F) necessary for a diagnosis of
PTSD according to DSM IV.
Beck depression inventory (BDI) (Beck, Ward, Mendelson, Mock, & Erbaugh,
1961). A 21-item scale designed to assess an individual’s current level of depression
and provide an estimate of clinical severity. Each Item of the BDI is rated on a 4-
point scale, ranging from 0 to 3 with the total score, out of a maximum of 63 giving
an indication of clinical severity.
Beck anxiety inventory (BAI) (Beck, Epstein, Brown, & Steer, 1988). A 21-item
scale that measures the severity of an individual’s current level of anxiety. Each Item
of the BAI is rated on a 4-point scale, ranging from 0 to 3 with the total score, out of
a maximum of 63, giving an indication of clinical severity.
Penn inventory for PTSD (Hammarberg, 1992). A 26 item self-report measure
used to assess the severity of PTSD. Each item is scored on a 0–3 scale with a total
cut-off score of 35 indicating PTSD.
Impact of events scale (Horowitz, Wilner, & Alvarez, 1979). A measure of current
emotional distress related to a specific event that has been used extensively with
PTSD. It is a 15-item measure consisting of two sub scales intrusion (7 items) and
avoidance (8 items). Subjects are required to respond to each question on a four
point scale ranging from ‘not at all’ to ‘often,’ with scoring by assigning the values 0,
1, 3, 5, to each of the frequency categories. The maximum possible total score for the
IES is therefore 75, with the maximum for avoidance being 40 and for intrusion
being 35.
Davidson trauma scale. (DTS) (Davidson, 1996). A 17-item self-rating scale
designed to evaluate symptoms of PTSD in individuals with a history of trauma. The
seventeen items in the scale reflect the symptoms of PTSD across the three symptom
clusters of Intrusions, Avoidance and Hyperarousal, as defined in DSM-IV. Each
Item of the DTS is rated on a 5-point scale, ranging from 0 to 4. Patients are required
to provide an estimate of frequency and severity for each of the symptoms assessed.
The cumulative score, out of a maximum of 136, giving an indication of clinical
severity.
Procedure. Patients were asked to complete the DTS, IES, BAI, and BDI at each
baseline and treatment session and at follow-up. The Penn Inventory was
administered at the first baseline session and at post treatment and three and six-
month follow-up. The PDS was administered at assessment, post treatment and
follow-up as a means of checking DSM-IV criteria.
Following the assessment and baseline periods patients entered the treatment
phase. Treatment consisted of enabling patients to shift to a metacognitive mode of
processing, discontinue worry/rumination strategies, discontinue threat monitoring,
and establish a strategy of ‘‘detached mindfulness’’ (cf Wells & Matthews, 1994) in
dealing with symptoms. These techniques form the basis of the treatment evaluated
in the present study. It should be noted that other strategies have also been outlined
as part of the metacognitive treatment approach, namely running mental simulations
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of coping with trauma, and direct challenging of dysfunctional metacognitive beliefs

about symptoms. We did not include these strategies in the present study since we
aimed to evaluate the effects of an intervention containing process-oriented
metacognitive strategies while minimising overlaps with imaginal exposure and
cognitive restructuring. We refer to the collection of treatment components used in
this study as the ‘‘core treatment’’ which is described in detail in a core treatment
manual (Wells & Sembi, 2001). The treatment consisted of homework practise.
In the first treatment session an idiosyncratic formulation of the patients problem
was presented based on the metacognitive model. The unhelpful effects of
perseverative thinking (rumination/worry) and attentional strategies of threat
monitoring in maintaining symptoms were explored and emphasised. Patients were
instructed that by removing these unhelpful styles of thinking they would be able to
free up their cognitive system to process traumatic information and therefore ‘‘Exit’’
the PTSD cycle. As their cognitive system ‘‘Exited’’, symptoms would reduce in
frequency and severity.
Next patients undertook an advantages/disadvantages analysis of worry/rumina-
tion. This was used to demonstrate that engaging in rumination served no purpose
and ‘‘locked’’ the individual into merely replaying negative aspects of the traumatic
event or their dissatisfaction with their own coping responses in the situation. This
analysis was also later applied to the patients’ use of threat-monitoring strategies.
Patients were then trained to respond to their symptoms using the method of
‘‘Detached Mindfulness’’ (Wells & Matthews, 1994; Wells, 2000), which aims to
enhance metacognitive awareness and increase flexible control of responses. They
were asked to respond in a particular way when they experienced intrusive thoughts,
flashbacks and nightmares. First, to acknowledge to themselves that these symptoms
were occurring, and to remind themselves that engaging with these symptoms was
unhelpful. Engagement with these symptoms included, questioning the meaning of
the symptoms, trying to work out what had happened to them, ruminating about
why it should have happened, worrying about the significance of symptoms,
suppressing thoughts or avoiding symptoms. Patients therefore needed to acknowl-
edge them but not engage with them in any way. Several analogies and experiential
exercises were used to illustrate detached mindfulness.
To further enhance metacognitive awareness and disengagement of daily worry/
rumination, ‘‘postponed worry exercises’’ were introduced. Patients were instructed
that whenever they experienced intrusive phenomena, they needed to acknowledge
that the thought/flashback/nightmare had occurred and then tell themselves that
they were not going to worry about it or ruminate about the trauma now, but they
would think about it later. Patients were therefore instructed to acknowledge the
thought and to make a mental note of it’s content, tell themselves they would think
about the thought later, and to then let the thought fade away in its own time.
Patients were asked to allot half an hour each evening as their designated worry time.
Finally, attention modification was used. Patients were asked to become aware of
when they were paying attention to internal and/or external sources of threat when
in situations that reminded them of the trauma or in which they felt vulnerable.
Internal forms of attention consisted of focusing on bodily symptoms, and fragments
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of trauma related-memories. External forms of attention to threat were factors such

as scanning and monitoring for certain kinds of people in the environment or
generally maintaining a sense of ‘‘readiness’’. They were instructed to consciously
acknowledge the nature of their attentional focus and to stop threat monitoring. In
order to apply this technique, patients were encouraged to practise in situations in
which they felt vulnerable. However, this differed from traditional exposure
homework because it was not systematic, directed or prolonged, but practised on
an ad-hoc short term-basis. We had also intended to modify threat-monitoring
strategies by instructing patients to redirect attention away from threat and onto
different non-threatening aspects of the external environment, but we found that it
was not necessary to use this additional phase with the patients in this study.

3. Results

The distribution of baseline1 and 4 scores, mean baseline, end of treatment, and
follow up scores was not markedly skewed and therefore correlated t-tests were used
for data analysis to supplement visual analysis of the single case graphs.
All patients met diagnostic criteria for major depressive disorder during baseline,
and they reported significant levels of depression on the BDI (range=10–37), all
patients met PDS criteria for PTSD, and all could be classified as suffering from
moderate to severe PTSD (DTS total scores=48–132).
By examining Fig. 1 it is possible to determine the effectiveness of the
metacognitive intervention. In each case baseline scores show either stable or
increasing trends. Correlated t-tests demonstrated that there were no significant
differences between baseline 1 and 4 on any of the outcome measures. This stability
of the baselines suggests that any effects occurring during treatment are unlikely to
be due to spontaneous recovery from PTSD, the results of self-monitoring, due to
therapist contact, or natural variation in scores. Fig. 1 clearly suggests that the
treatment was effective in each case. T-statistics computed using the mean baseline
scores and the post treatment scores showed significant improvements in all
measures (DTS, t ¼ 9:1; po0:0005; IES, t ¼ 10:5; po0:0005; Penn, t ¼
8:8; po0:0005; BDI, t ¼ 7:8; p ¼ 0:001; BAI, t ¼ 8:1; po0:0005).
Fig. 1 shows that treatment was associated with large reductions in specific
measures of PTSD (DTS and IES total scores), and reductions in general measures
of anxiety (BAI) and depression (BDI). At post treatment, total scores on the DTS
ranged from 0 to 36, indicating that none of the patients met conventional levels for
PTSD. Post treatment scores for patient 6 account for the highest symptom scores
and are confounded by the fact that this patient underwent surgery for suspected
cancer at the sessions 9–10 phase of the intervention. Thus, distress and trauma
measures may be reflecting these background stress-related issues. Despite this, the
measures still show clear improvement in PTSD symptoms, anxiety and mood. The
PDS showed that at post-treatment none of the patients met criteria for PTSD.
Mean percentage improvement at post treatment on the IES was 83.5%. This
figure compares favourably with reports of effects from exposure, cognitive therapy,
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Fig. 1. PTSD symptom severity, and general depression and anxiety scores for patients during baseline,
treatment, and at follow-up.
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and combination treatments of 60%, 50%, and 58% respectively (Marks et al.,
1998). However, caution is required in direct comparisons here because of differences
in the chronicity of PTSD across studies. The degree of improvement in PTSD
symptoms as measured by the IES is paralleled in the percentage improvement
obtained in DTS score in the present study of 84.6%. Mean scores on the Penn
Inventory (which was not given on a sessional basis) were as follows: pre=48.17,
post=14.83, 3 month=16.20, and 6 month=14.50. The percentage improvement in
Penn scores at post treatment was 69.21%.
Visual inspection of follow-up data in Fig. 1 shows that treatment gains on all of
the measures were maintained across the follow-up period. T-tests showed that there
were no significant differences between post treatment scores and scores at each
follow-up interval on any of the outcome measures. None of the patients met criteria
for PTSD assessed by the PDS at 3, 6 and longer term follow-up.
Effect sizes. In addition to the above single case series we extended our evaluation
of the new treatment to include a further two cases as a basis for computing post
treatment effect sizes. These patients were the next two consecutive PTSD patients
referred for treatment. These patients were both male victims of assault, aged 54 and
17 years of age. Both patients fulfilled DSM-IV criteria for PTSD as measured by
section F24–25 of the SCID. These patients were seen at 8 months and 12 months
post assault, entered treatment immediately, and they received 5 and 6 treatment
sessions, respectively. Effect sizes (Cohen’s d) were calculated by determining the
mean change in individual test scores (pre-post treatment), and dividing this by the
pooled standard deviation of scale scores. The pooled standard deviation was
computed as SD’=sqrt[(SDpre2+SDpost2)/2] as set out by Cohen (1977, p. 44). The
post-treatment effect sizes were as follows: DTS=3.5; IES=5.0; Penn=4.0;
BDI=3.0; BAI=3.5.

4. Discussion

The results of this preliminary evaluation suggest that the metacognitive-focused

intervention was effective in the treatment of moderate-severe PTSD. These results
are particularly interesting because of the concurrent depression seen in the sample.
Patients appeared to tolerate the treatment well and were able to comply with their
homework.
The presence of stable baselines, the varying amounts of time that had elapsed
since the trauma, the presence of marked effects following introduction of treatment,
and replication across cases makes it unlikely that the effects observed can be
attributable to natural remittance or extraneous factors. In addition, the six cases
provide a naturally occurring multiple baseline (Hayes & Leonhard, 1991). More
specifically, since the duration of PTSD varied substantially across cases before the
introduction of treatment, an explanation of all treatment effects in terms of
treatment coinciding with spontaneous recovery is not plausible. However, we
cannot partial-out the possible contribution of spontaneous improvement from the
percentage improvement observed in symptoms that might be due to treatment.
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Whilst this remains a limitation of the study it should be borne in mind that when
PTSD symptoms persist beyond 3 months, as with all cases here, people have a
greater probability of becoming chronic (McFarlane, 1988).
The present effects are intriguing because the intervention did not involve
conventional strategies of cognitive restructuring or imaginal reliving. The
metacognitive treatment is intended to ‘‘unlock’’ barriers to normal traumatic
processing. It may do this, at least in part, by facilitating habituation by promoting
greater exposure to naturally occurring intrusions. If this is the case then we would
conclude that the amount of exposure actually required to promote recovery is small,
so long as conscious cognitive operations exert the appropriate control over
processing to allow adaptation to run its own course.
The clinical implications of the present findings are that treatment for PTSD
focusing on disrupting maladaptive thinking styles may be promising as an
intervention. The metacognitive treatment avoids the distress associated with
procedures such as prolonged imaginal reliving of trauma. Metacognitive ‘‘core’’
treatment may provide a first-line low intensity early intervention approach that can
be applied in a cost-effective way since application of the techniques will not rely on
extensive training in cognitive-behaviour therapy.
The results of this study must be interpreted cautiously. The study relied solely on
self-report measures of symptoms, and therefore a role of demand effects on
outcome cannot be ruled out. The study was based on a small sample of patients,
who may not be fully representative of all PTSD cases. The lack of a treatment
placebo condition means that we cannot assess the impact of non-specific treatment
factors on outcome. Nevertheless, the present results suggest that continuing
evaluations of this new treatment approach are warranted.

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