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Clinical Psychology and Psychotherapy

Clin. Psychol. Psychother. 18, 202217 (2011)


Published online 14 July 2010 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/cpp.711

Post-Stroke Depression:
The Case for Augmented,
Individually Tailored Cognitive
Behavioural Therapy
Niall M. Broomfield,1* Ken Laidlaw,2
Emma Hickabottom,3 Marion F. Murray,4
Rachel Pendrey,3 Janice E. Whittick3 and
David C. Gillespie4
1

Department of Clinical Health Psychology, Western Infirmary General, Glasgow


and Department of Psychological Medicine, University of Glasgow, Scotland, UK
2
School of Health in Social Science, University of Edinburgh, Scotland, UK
3
Department of Clinical Psychology, Stratheden Hospital, Cupar, Scotland, UK
4
Department of Clinical Psychology, Astley Ainslie Hospital, Edinburgh,
Scotland, UK
In this review, we begin by considering why post-stroke depression
(PSD) is so prevalent. We then examine the current evidence base to
support cognitive behavioural therapy (CBT) as a treatment approach
for the condition. While there is limited evidence currently, we demonstrate that much remains to be established with regard to PSD and
the efficacy of CBT. We argue there is every reason to believe CBT
should be an effective treatment, but that clinicians must augment and
individually tailor this approach to ensure effectiveness. We set out our
rationale for a novel augmented, individually tailored CBT protocol,
and describe five key components that we believe once incorporated,
and tested using randomized controlled methods, should enhance
treatment outcome of PSD. Copyright 2010 John Wiley & Sons, Ltd.
Key Practitioner Message:
Depression is a common consequence of stroke.
Despite a lack of clear evidence, there is reason to believe cognitive behavioural therapy (CBT) for post-stroke depression should be
effective, if it is adapted and tailored to the specific needs of stroke
survivors.
Augmented and individually tailored therapy using motivational
interviewing techniques, grief resolution, selection optimization
compensation, cognitive deficits adaptations and executive skills
training is recommended.
It is important to individualize augmented CBT, based on principles
of case formulation.
Keywords: Stroke, Depression, Post-Stroke Depression, Cognitive
Behavioural Therapy
*Correspondence to: Dr Niall M. Broomfield, Consultant Clinical Psychologist and Honorary Senior Lecturer, Clinical Psychology Department, 3rd Floor, G Block, Western Infirmary, Glasgow G11 6NT, Scotland UK.
E-mail: Niall.Broomfield@ggc.scot.nhs.uk

Copyright 2010 John Wiley & Sons, Ltd.

CBT and PSD

INTRODUCTION
Stroke Prevalence and Incidence
Stroke is the single most common cause of adult
disability in the UK and the third most common
cause of death (National Audit Office, 2005).
Annually, stroke affects around 130 000 people in
the UK. Direct costs to the National Health Service
are estimated at 2.8 billion, with an additional
2.4 billion per year for informal care provided by
families (National Audit Office, 2005).
As stroke is a potentially fatal disease, reduction of mortality after the onset of the illness is an
important initial aim. However, as survival rates
following stroke continue to rise, a more pressing
aim becomes reduction of morbidity, as life after
stroke needs to be one that is worth living. An
important factor determining both quality of life
and morbidity is post-stroke depression (PSD).
Stroke usually occurs without warning. Thus,
survivors and those who care for them, have
little to no time to make adjustments to markedly
changed life circumstances, which has profound
consequences for actual and planned futures. PSD
is thus very common. One in three stroke survivors
suffer the condition in the first 12 months after
stroke onset (Hackett, Anderson, House, & Xia,
2009; Hackett, Yapa, Parag, & Anderson, 2005).
The consequences of PSD are highly significant.
PSD increases risk of subsequent mortality (House,
Knapp, Bamford, & Vail, 2001), impedes functional
recovery (Pohjasvaara, Vataja, Laeppavouri, Kaste,
& Erkinjuntti, 2001) and heightens levels of disability, as depressed stroke survivors give up prematurely on physical rehabilitation programmes due
to apathy and hopelessness.

Why are Stroke Patients Vulnerable


to Depression?
Much research has examined the potential of neuroanatomical factors, for example, lesion location,
to explain PSD (Robinson, Kubos, Starr, Rao, &
Price 1983). However, there is a lack of consensus
regarding this (Carson et al., 2000). Furthermore,
irrespective of the nature and location of any given
stroke, psychological factors pertinent to that individual are likely to play some role in the aetiology and maintenance of the emotional disturbance
(Laidlaw, 2008).
There are four key features of stroke that render
individuals vulnerable to the development of PSD,
namely: (i) stroke survivors often experience physCopyright 2010 John Wiley & Sons, Ltd.

203
ical impairments, including fatigue, that restrict
their levels of activity and participation; (ii) stroke
survivors are often elderly, have comorbid health
problems and experience a range of additional
stressors that are independent of their stroke; (iii)
the thinking of people surviving stroke can become
generally more negative and (iv) impairment of
cognitive abilities due to stroke impacts the way
stroke survivors process information. Each of these
factors may heighten vulnerability to development
of PSD, as outlined below.

(i) Physical Consequences of Stroke Reduce


Activity and Participation
It may seem an obvious point, but stroke often
results in significant physical impairment. Lawrence et al. (2001) investigated the prevalence of
physical impairments in 1259 stroke patients at
the acute stage of recovery and found that 77%
of individuals experienced upper limb weakness,
72% experienced lower limb weakness and 48%
of individuals were urine incontinent. Physical
impairments inevitably limit the range of activities an individual can undertake. Almost 65% of
participants in the Lawrence et al. (2001) study
showed moderate to severe disability scores on
the Barthel Index, a commonly used measure of
independence in day-to-day activities.
In a more recent study, 55% of stroke survivors
obtained Barthel Scale scores in the same range
when assessed three months post-stroke, with little
evidence of improvement on this instrument thereafter (Lo et al., 2008).
Fatigue is also a problem for many stroke survivors, and has been attributed to the increased
physical effort associated with neurological
deficits (Skaner, Nilsson, Sundquist, Hassler, &
Krakau, 2007). In one study, 56% of individuals
experienced significant fatigue 6 months poststroke. This too places limits on the extent to which
survivors can resume activities undertaken before
stroke onset (Winard, Sackley, Metha, & Rothwell,
2009). Stroke survivors are thus highly likely to
experience physical impairment and restricted
independence following the onset of their illness,
and the limitations they face are long-term rather
than short-term.
The consequence of physical impairment and
reduced independence is that individuals are less
able to freely, or easily, participate in activities
that were once pleasurable or meaningful. Ekstam,
Uppgard, von Koch, and Tham (2007) conducted
interviews with 27 older stroke survivors (average
age 78.8 years) to explore everyday functionClin. Psychol. Psychother. 18, 202217 (2011)
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204
ing and life satisfaction, and to identify reasons
for changes in these domains. Most participants
reported significant deterioration in everyday lifestyle activities that had been carried out in the 6
months pre-stroke (e.g., travel outings, car rides,
gardening, Do It Yourself [DIY], reading). Indeed,
the majority of the sample reported dissatisfaction
with life as a whole.
Similar results were obtained in a larger study
of 56 younger stroke survivors (average age 57.7
years). For this sample, the proportion of leisure
activities retained from pre-stroke was only 48.8%
(Hartman-Maeir, Soroker, Ring, Avni, & Katz
2007). In addition, only 39% were satisfied with
life as a whole, with activity level found to be a
significant predictor of individual satisfaction.
Predictably therefore, several investigators have
reported a relationship between post-stroke physical impairment and depression such that stroke
survivors with poorest physical functioning and
lowest life satisfaction show the highest rates of
PSD (e.g. Gayman, Turner, & Cui, 2008; Gum,
Snyder, & Duncan, 2006; Sharpe et al., 1994). These
results are consistent with behavioural theories
of depression, which suggest low mood results
from a reduction in positive reinforcement when
individuals are unable to engage in activities that
would normally bring a sense of mastery or pleasure (Westbrook, Kennerley, & Kirk 2007).

(ii) Stroke Survivors Experience Comorbid


Problems that are themselves Depressogenic
The incidence of stroke increases sharply with
increasing age, with approximately three quarters
of strokes occurring in people aged over 65 years
(Myint et al., 2008). This is an important demographic fact because rates of subthreshold depressive syndromes such as dysthymia also increase
with age (e.g. Beekman, Copeland, & Prince, 1999;
Mulsant & Ganguli, 1999), and because disability
is strongly associated with depression in later life
(McDougall et al., 2007).
It is also important to note that stroke survivors
often live with other long-term conditions, for
example, hypertension, heart failure and hearing
loss. In Scotland, of those people recorded by
national statistics as having had a stroke, only
15% experienced stroke alone, that is, stroke as a
single long-term condition. Twenty-five per cent
had a stroke and one other long-term condition,
while 60% had stroke and two or more long-term
conditions (NHS National Services Scotland, 2008).
Indeed it is well known that certain illnesses that
often co-present with stroke (e.g., hypertension,
Copyright 2010 John Wiley & Sons, Ltd.

N. M. Broomfield et al.
diabetes), are themselves independently associated
with depression. In addition, the more illnesses an
individual has, the greater their risk of mood disorder (Montano, 1999). Therefore, one would expect
stroke survivors with comorbid health concerns
to be at higher risk of depression than individuals
with no history of stroke.
Stroke survivors are not only more likely to
experience additional health problems, they are
also more likely to experience stressful life events
that can negatively impact mood. Ekstam et al.
(2007) demonstrated that almost half their sample
of stroke survivors experienced new major life
events in the year after their stroke: falls in four
of 27 participants, death of a close relative in six
of 27 and change of housing in two of 27. Becker
(1993) also found that 25 of 36 participants experienced a major life event in the year following their
stroke. Taken as a whole, these data reinforce the
point that stroke survivors are quite likely to experience physical calamity (e.g., falling because of
limb weakness or poor balance), bereavement (e.g.,
spouses and friends, like themselves, are likely to
be older) and social disruption (e.g., having to
move to new accommodation because of strokeimposed limitations).

(iii) Stroke Produces Negative Cognitions about


Self, World and Future
Becks cognitive theory (Beck, 1987; Beck, Rush,
Shaw & Emery, 1979) proposes that negative automatic thoughts about self, world and future play
a role in the development and maintenance of
depression. Consistent with this, there is evidence
that negative self-referent cognitions in stroke may
be important (Thomas & Lincoln, 2006).
Several studies show that individuals with stroke
experience low self-esteem (e.g. Chang, MacKenzie, & Dhillon, 1999; Vickery, 2006). This suggests
a good proportion may hold negative beliefs about
self. In a recent study for instance, 80 individuals
with stroke in an inpatient rehabilitation setting
were individually matched to non-stroke individuals on the basis of age and education, and compared on measures of self-esteem and depression
(Vickery, Sepehri, & Evans 2008). Stroke patients
as a group reported significantly lower self-esteem
than the non-stroke group, rating themselves as
less intelligent, and also more depressed. Currently there are limited data as to whether low
self-esteem constitutes a risk factor for PSD or is
a symptom of it. This would require longitudinal investigations with large numbers of stroke
survivors.
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CBT and PSD


Negative attitudes about the world and the future
have however been investigated in a longitudinal
study by Lewis, Dennis, ORourke, and Sharpe
(2001). Three hundred and seventy-two stroke
survivors 6 months post-stroke were interviewed
regarding negative beliefs about the world (e.g., I
feel like life is hopeless) and future (e.g. I am not very
hopeful about the future) using a modified version
of the Mental Adjustment to Cancer Scale (where
the word stroke was substituted for cancer).
Although the actual number of individuals who
endorsed each belief was not provided, Lewis et al.
(2001) reported a significant relationship between
PSD and the constructs of helplessness/hopelessness and fatalism. Interestingly, these two
constructs were also significantly associated with
decreased survival at 3 and 5 years post-stroke,
even after adjustment for older age, the presence
of peripheral vascular disease and living alone.
Similarly, Paradiso, Ohkubo, and Robinson (1997)
found that helplessness was more common in individuals who were diagnosed with PSD, and this
was true at all four time points post-stroke (3, 6,
12 and 24 months). Taken together, these findings
provide some evidence that stroke survivors may
experience negative cognitions about themselves,
the world and their future following stroke.
It is of course possible that for some individuals who survive stroke, negative thinking is a
symptom of their depressed mood, rather than
representing a vulnerability factor for it. Work
published by Nicholl, Lincoln, Muncaster, and
Thomas (2002) would seem to support this. They
gave a measure of negative thinking (the Stroke
Cognitions Questionnaire) to 50 stroke patients
classified as depressed or not depressed using
the Beck Depression Inventory (BDI; Beck, Steer,
& Brown, 1996) and the Wakefield Self-Assessment
of Depression Inventory (WDI; Snaith, Ahmed,
Mehta, & Hamilton 1971). Data analysis found that
the depressed stroke patients reported significantly
more negative cognitions than non-depressed
stroke patients. Depressed stroke patients also
showed significantly fewer positive cognitions.
Arguably though, the precise directional relationship of negative cognition and low mood following stroke may not matter, at least with respect
to understanding recovery. Clinical experience
suggests negative thoughts can, and do, act as
a powerful maintaining factor for low mood via
a cognitive feedback loop: depressed affect can
promote negative thinking, which if not addressed,
can promote further low mood, and so on. In turn,
confidence, personal agency and activity levels
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205
are eroded, and stroke recovery rate slows. In our
view, regardless of whether negative thinking is a
cause or a consequence of depressed mood, what
is critical is to make sure that any psychological
intervention being used actually addresses it (cf.
Nicholl et al., 2002).

(iv) Stroke Produces Cognitive Deficits and


Information Processing Biases that may
Maintain Depression
Fifty to seventy five per cent of stroke survivors
experience cognitive impairment in the early stages
after their stroke (Tatemichi et al., 1994). Twentyfive per cent reach criteria for Dementia 3 months
after onset (Desmond et al., 2000). The range
and nature of cognitive deficits varies. Attention,
memory and executive difficulties are common
(Tatemichi et al., 1994). Strokes to the anterior circulation system and brain areas linked to frontal
and prefrontal circuitry in particular can promote
executive and problem solving deficits (Lezak,
Howieson, & Loring, 2004), which we know are
linked to depression (Mitchell & Madigan, 1984;
Seibert & Ellis, 1991). If stroke survivors struggle to
think flexibly, accurately self-monitor or problem
solve, negative interpretations may be more likely,
raising the likelihood of mood disturbance.
Research also shows impaired cognitive functioning post-stroke directly impedes functional
recovery (Galski, Bruno, Zorowitz, & Walker, 1993;
Robertson, Ridgeway, Greenfield, & Parr, 1997).
Poor functional outcome is likely to produce high
levels of frustration and distress in at least some
stroke survivors, again raising vulnerability to
depressed mood.
Cognitive deficits after stroke may also maintain
depressed mood by influencing information processing. A wealth of experimental evidence shows
anxiety is characterized by selective attention bias
for threat and vulnerability, and depression with
memory and interpretation biases for sadness, loss
and failure (Williams, Watts, Macleod, & Mathews,
1997). There is also emerging evidence of selective attention bias favouring negative material in
depression (Broomfield, Davies, McMahon, Farah,
& Cross, 2007; Mogg & Bradley, 2005). If attention processes are disrupted following stroke,
stroke survivors may be particularly subject to
such biased processing patterns, and thus more
prone to noticing, dwelling on and remembering negative information, particularly if mood is
already compromised. This hypothesis is untested,
although healthy (non-stroke) participants with
good attentional control are less likely to report
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negative affect than those with reduced attentional
control (Derryberry & Rothbart, 1988). Similarly,
following stroke, some patients struggle to inhibit
self-perspective (Samson, Apperly, Kathirgamanathan, & Humphreys, 2005), tending to over personalize events, another common cognitive feature of
depression (Woodruff-Borden, Brothers, & Lister,
2001).

WHAT IS THE EVIDENCE TO SUPPORT


COGNITIVE BEHAVIOURAL THERAPY
EFFICACY FOR PSD?
Cognitive behavioural therapy (CBT) has established efficacy as a treatment for depressed
younger (Blackburn, 1995; Williams, 1992) and
older adults (Pinquart, Duberstein, & Lyness,
2006; Scogin & McElreath, 1994; Wilson, Mottram,
& Vassilas, 2008). CBT interventions are based on
the simple premise that behaviour can change, and
in working with individuals who have survived a
stroke it is important to conceptualize the nature
of an individuals problem within a behavioural
frame of reference (Laidlaw, 2008). CBT also has
utility in the overall rehabilitation of an individual
after a stroke as it provides a means of reducing
PSD that can be very important for the individuals
post-stroke recovery generally (Hibbard, Grober,
Stein, & Gordon, 1992).
Focusing specifically on the evidence regarding efficacy of CBT for PSD, there are three main
studies of note. The first by Lincoln and colleagues
(Lincoln, Flannaghan, Sutcliffe, & Rother, 1997)
was a small pilot study where treatment was
delivered to 19 participants out of a possible 155
identified as depressed from hospital records. All
participants in this study were diagnosed with
major depression. Each participant acted as their
own control during baseline and within-treatment
assessments as treatment was delivered using
standard AB design methods. All participants
were assessed using the BDI (Beck et al., 1996), the
Hospital Anxiety and Depression scale (Zigmond
& Snaith, 1983) and clinical interview.
In this study, CBT involved a combination of
distraction methods, cognitive restructuring,
behavioural activation and psychoeducation. A
4-week baseline preceded a 16-week treatment
phase, with the number of treatment sessions
determined by therapist and participant, up to a
maximum of 10 sessions. The primary outcome
variable was weekly BDI scores. As a group, participants showed significantly reduced BDI scores
Copyright 2010 John Wiley & Sons, Ltd.

N. M. Broomfield et al.
over time. Four participants showing consistent
benefit of CBT, six showed some benefits and
nine showed no benefits. Lincoln et al. (1997) concluded that CBT for PSD may be effective for some
patients, and argued for larger scale evaluation.
Overall, while there are many merits of this study,
there are a number of limitations such as the small
number of participants receiving CBT out of those
identified. In addition there was a lack of experience in the delivery of CBT and it is unclear as
to whether the treatment was provided according
to a specific CBT manual and whether individual
therapists were receiving supervision and support
from experienced CBT practitioners.
Similar to Lincoln et al. (1997), Rasquin, Van De
Sande, Praamstra, and Van Heugten (2009) delivered CBT to five first-episode depressed stroke
survivors using a single-subject quasi-experimental AB design. Following a 4-week baseline,
participants completed eight (weekly) 1-hour
treatment sessions of CBT for PSD with a psychologist. Patients received an intervention book
adapted for stroke patients. Structure was clear
with easy to understand information, accounting for participants cognitive difficulties. Initial
treatment sessions covered mood monitoring and
relaxation (sessions two, three, four), then cognitive restructuring (sessions five, six) and activity
planning (sessions seven, eight). Homework exercises were frequent. Visual analogue measures
(VAS) were employed thrice weekly, with repeat
of baseline assessments at treatment end, 1 month
and 3 months follow-up. Results were mixed,
consistent with Lincoln et al. (1997). All patients
were positive about the intervention. Four out of
the five participants showed improved mood on
VAS at treatment end, relative to baseline scores.
Three of five participants showed significant mood
improvement at 1 month and 3 months follow-up.
However, not all participants showed consistent
improvements and some continued to complain
of depressogenic symptoms. Rasquin et al. (2009)
conclude that CBT may have had impact, but that
larger scale, longer term evaluation including a
control group will be required in order to clarify
how efficacious this intervention can be.
Lincoln and Flannaghan (2003) followed-up the
earlier work by Lincoln et al. (1997) and carried
out the first ever randomized controlled trial (RCT)
of CBT for PSD. In this pioneering study, participants were randomly allocated to receive one of
three options: 10 sessions of CBT, 10 sessions
of attention control interviews with no therapeutic
intervention or usual care (no treatment). In this
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CBT and PSD


trial, attention placebo comprised supportive discussions regarding the physical effects of stroke.
In total, 123 participants were recruited into this
study, 1, 3 and 6 months after experiencing a stroke.
Participants were assessed as depressed on the
BDI (Beck et al., 1996) and the WDI (Snaith et al.,
1971) and Schedules for Clinical Assessment of
Neuropsychiatry clinical interview (SCAN; Wing
et al., 1990). Only 60 participants met diagnostic
criteria for depression although all participants
scored above cut-off for depressive symptoms on
the BDI. Manualized CBT was consistent with that
provided by Lincoln et al. (1997). Outcomes were
assessed blind by an Assistant Psychologist at 3
and 6 months. The results were disappointing in
that there were no differences between the three
conditions.
Despite the lack of a clear benefit for CBT for
PSD, the study by Lincoln and Flannaghan (2003)
should not be dismissed entirely. The study, the
first of its kind to examine CBT for PSD using randomized controlled methods, was both pioneering and well conducted. Such treatment research
involving brain-injured populations is always difficult to organize and deliver, which likely accounts
for the lack of previous attempts.
Several methodological limitations may account
for the null effect. Sample sizes at 6 months were
small (N = 34, 41, 36 for CBT, attention control
and wait list respectively), and therefore analyses may have been underpowered. Potential participants were not referred by a third party, but
were selected from the stroke register, based on
BDI, WDS and SCAN data. Thus, no a priori judgments were made by referrers regarding patient
suitability and motivation for change. As patient
suitability for CBT was not assessed ahead of inclusion, no detailed assessment of cognitive deficits
was made. Also, participants randomized to CBT
received a mean of only 10 sessions, much less than
is usual in comparable trials (e.g. Koder, Brodaty,
& Anstey, 1996). Moreover, patients were recruited
early in the pathway, at just 1 month post-stroke.
Arguably, this may have increased the likelihood
of spontaneous recovery effects.
In addition, as Lincoln and Flannaghan (2003)
themselves note, CBT was of short duration and
low intensity. These aspects may also account for
the lack of a treatment effect. Moreover, the one
trial therapist used was not only inexperienced
(a research nurse, not a CBT therapist), but also
delivered both active conditions (CBT and attention placebo). It seems somewhat questionable
whether any one individual within the context of a
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207
research trial could switch from delivering CBT to
delivering supportive discussion, without error or
at the very least contamination between treatment
modes. Finally, no formal evaluation of the quality
of CBT delivered was attempted. Thus, while
the neutral outcomes observed by Lincoln and
Flannaghan (2003) are disappointing, it is arguable that a definitive trial has not been conducted
to measure the impact of CBT on PSD.

SHOULD CBT BE EFFECTIVE FOR PSD?


CBT for PSD has yet to establish a solid case,
although outcome-research remains at an early
stage. Many issues are unresolved and currently
the evidence is insufficient (Anderson, Hackett, &
House, 2004; Hackett, Anderson, & House, 2004).
While the case for CBT as a treatment for PSD
is not yet established, the characteristics of CBT
seem to suggest it ought to be an especially good
fit to meet the needs of people who have become
depressed after a stroke. CBT is designed to help
patients better regulate emotion, increase activity
towards optimal levels of functioning and maintain realistic (but optimistic) thinking. By contrast,
poor emotion management, inactivity and negative thinking, is exactly what we suspect maintains
PSD. Although direct (stroke specific) evidence is
limited, depressed stroke survivors endorse significantly more negative cognitions than nondepressed stroke survivors (Nicholl et al., 2002;
Vickery et al., 2008). And there is good evidence
that remaining active, expressing emotion and
finding positive meaning ensures good psychological adjustment in other chronic physical
illnesses (e.g. De Ridder, Geenen, Kuitjer, & Van
Middenhorp, 2008).
The here and now orientation of CBT perfectly
matches the immediate nature of stroke survivors
concerns. CBT adopts a skills enhancing, problemsolving focus that fits with the aims and needs of
people who have survived a stroke when learning
to manage the personal consequences of their new
situation. CBT monitors and evaluates the cognitions of stroke survivors, many of whom have
objectively made a good recovery but whose subjective appraisal is to see only failure. Finally, the
primary aim of CBT is symptom reduction, with
an emphasis on reducing symptoms of depression such as apathy, hopelessness and low mood.
These symptoms of depression are likely to result
in excess disability, that is, the impact of a stroke
is magnified by depressive symptoms, resulting in
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208
decreased levels of functioning. For these reasons,
CBT for PSD ought to be the first choice psychotherapy treatment option and would be if a stronger
case could be made for its efficacy (Laidlaw, 2008).
One theme common to all existing studies of CBT
for PSD, concerns the intervention itself. Psychotherapy models are not usually designed to take
account of physical comorbidity in depression and
this is usually reserved as an area requiring great
experience and skill on the parts of therapists. Yet
the CBT interventions offered by both Lincoln
et al. (1997) and Lincoln and Flannaghan (2003)
employed traditional non-modified CBT. Although
Rasquin et al. (2009) did employ an intervention
book to account for cognitive deficits, their CBT
intervention still focused on examining the impact
of activity scheduling and cognitive restructuring
on mood. Perhaps the lack of consistent treatment
effects observed thus far in the nascent literature
relates not just to the methodological limitations
of previous studies, but also to what CBT actually
comprised in these trials. In order for CBT to be
shown efficacious with this population, consideration may also need to be given to the elements of
CBT itself. We turn to this now.

AUGMENTING AND
INDIVIDUALIZING CBT FOR PSD:
USING PSYCHOLOGICAL MODELS
AS VEHICLES FOR CHANGE
We believe the next generation of CBT treatment
research in PSD should not only learn from the
design limitations of prior work, but also examine
the efficacy and feasibility of an augmented CBT
intervention. The need for an augmented CBT
model is analogous to the situation in CBT for
anxiety disorders. To refine the effectiveness of
interventions and enhance outcome, there is more
than one model of CBT for the anxiety disorders.
For instance, a CBT treatment plan based upon
the CBT model for panic disorder may have some
relevance when working with someone who has a
simple phobia but for a better treatment outcome,
the use of a more specific treatment model is necessary. It is a better fit and results in better treatment. Thus, what is proposed here is simply that
for CBT to be a better fit for the needs of stroke
survivors, there should be a specific model for its
use, one which takes account of the trauma, acute
onset and loss elements of stroke, including physical and psychological loss and the consequences to
that individual.
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N. M. Broomfield et al.
No existing model of CBT currently exists that
is an optimal fit for PSD and therefore an adequate test of CBT as a treatment for PSD has not
yet been executed. Grant and Casey (1995) have
similarly argued that when using CBT with frail
older people, the therapist needs to be creative
in individualizing therapeutic interventions.
Increasingly, researchers are looking at how to
enhance psychotherapy outcome by addressing age specific issues (Knight & Laidlaw, 2009)
and the cognitive deficits of acquired brain
injury (Gracey, Evans, & Malley, 2009). While the
ability to individualize CBT is a hallmark of this
therapy, for clinicians inexperienced in working
with stroke survivors there is a need for guidance
about candidate elements for augmentation and
individualization.
Due to the nature of stroke, strict manualized
traditional CBT may be missing out important aspects of therapeutic work. Kneebone and
Dunmore (2000) have highlighted that PSD is a
heterogeneous phenomenon. Therefore traditional
therapies may require specific adaptations, at
least in the context of applying CBT for depression after stroke. Dewar and Gracey (2007), for
example, state that loss of identity emerges as
a key theme in psychotherapeutic interventions
addressing adjustment to acquired brain injury.
They outline an intervention using CBT techniques
but with greater emphasis on behavioural experiments, which may be a particularly effective means
of modifying the meaning of current situations to
patients, thus helping create a more positive sense
of self.
In a similar vein, Laidlaw and colleagues
(Laidlaw, 2008; Laidlaw, Thompson, Dick-Siskin,
& Gallagher-Thompson, 2003) propose a specific
cognitive error associated with stroke that an augmented CBT programme should include. Baseline
distortions occur when stroke survivors compare
their current level of functioning with that prior
to the onset of their stroke. Individuals become so
focused on wanting to make a full recovery from
stroke, they catastrophize about what they cannot
do now, compared with what they could achieve
pre-stroke, unhelpfully contrasting their current
level of functioning to how they were the day before
their stroke, rather than the days after. By doing so,
stroke survivors focus on deficits and can become
demoralized as they appraise their progress as
inadequate, with a consequent increase in anxiety,
hopelessness, apathy and frustration. This difference in appraisal can be most usefully illustrated
to patients with a graph (see Figure 1).
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209

100%

75%

10%
Day
before
CVA

Day
after
CVA

Time after a stroke

Figure 1. Baseline distortion in stroke


Source. Laidlaw, 2008.

Clinically, identification of such stroke-specific


cognitive errors can be highly useful. A more realistic and helpful comparison is to consider current
level of functioning, with functioning 1 day after
stroke onset.
We believe it will be important for the next
generation of researchers, to test out the importance of these and other behavioural and cognitive adaptations in CBT studies of PSD. We would
further suggest there are five psychological components, to date not considered within the PSD
literature, which we believe may provide the key
to developing an effective augmented CBT for PSD
protocol. These are (i) motivational interviewing
(MI; Arkowitz, Westra, Miller, & Rollnick 2008),
(ii) grief resolution (Worden, 2001), (iii) selection
optimization with compensation (Baltes, 1997),
(iv) cognitive deficits adaptations and (v) executive skills training (Mohlman & Gorman, 2005).
We consider these additional components are necessary to augment the effectiveness and relevance
of CBT for survivors of stroke, so as to be assistive
at an individual level in successfully adjusting to
acutely changed circumstances. We examine each
of these components in more detail now.

MOTIVATIONAL INTERVIEWING and PSD


There has been growing interest in the use of MI
procedures to treat different psychological disorders, including depression (e.g. Arkowitz et al.,
2008). MI has a beneficial effect on mood when provided early after stroke onset (Watkins et al., 2007).
The central goal of MI is to increase an individuals
internal motivation to change, rather than to bring
about change by external means such as persuasion or attempts to cajole. Watkins and colleagues
Copyright 2010 John Wiley & Sons, Ltd.

increased stroke survivors internal motivation by


helping them to identify personally meaningful
goals, and assisting them to brainstorm potential
blocks to achieving these goals. Participants were
thereby allowed to work through any ambivalence
they had to change, and to experience feelings of
optimism and self-efficacy.
MI is therefore potentially useful when individuals are requiredas is true of depressed stroke
patients undergoing rehabilitationto make behavioural changes, such as increasing activity levels. A
significant proportion of stroke patients experience
organically-based disorders of motivation or drive
(Bains, Powell, & Lorenc 2007; Habib, 2000; Oddy,
Cattran, & Wood 2008), and in addition, PSD itself
has been associated with symptoms of anergia and
low motivation (e.g., Paradiso et al., 1997). Therapists should therefore not be surprised to find that
many depressed stroke patients struggle to maintain interest in talking-based therapies, or find
themselves unwilling or unmotivated to carry out
the types of homework exercises and behavioural
experiments employed in CBT. Over 10% of participants allocated to CBT intervention in Lincoln and
Flannaghans 2003 study dropped out by 6 months
(compared with 5% receiving no intervention and
2% receiving an attention placebo control), and
these were individuals who, by meeting the studys
inclusion criteria and agreeing to participate, presumably already had demonstrated some level of
motivation. Clearly, any talking-based treatment in
this patient group needs to take the issue of motivation to change very seriously.
Fortunately there is reason for optimism. One
would expect MIs emphasis on enhancing individuals motivation for change to be especially
useful when treating depressed individuals who
have had a stroke. We therefore propose that our
augmented CBT for PSD includes MI as a fixedsession pre-treatment to enhance the effectiveness
of the overall therapeutic work. MI has already
been used as an effective pre-treatment in CBT
for anxiety disorders (Westra & Dozois, 2006) and
meta-analysis and systematic review have confirmed MIs usefulness in treating disorders where
behaviour change is an important therapeutic goal
(e.g. Burke, Arkowitz, & Menchola, 2003; Hettema,
Steele, & Miller, 2005).

Grief-Resolution in PSD
Stroke often results in multiple losses and a subsequent reaction of grief towards these losses. Unless
Clin. Psychol. Psychother. 18, 202217 (2011)
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210
resolved, rehabilitation efforts can be affected
(Coetzer, 2004). For at least the first 612 months
after a stroke, patients often go through a period
of loss and grief for their former self and therefore
CBT may need to employ strategies associated with
bereavement work. Although most rough approximations of care suggest that psychotherapy after a
stroke should take place about 6 months after the
initial onset this is a matter of opinion rather than
any scientific study. If an individual is in distress
and medications have not worked, it may be useful
to employ CBT in an explorative manner, earlier. At
any stage however, working with stroke survivors
can usefully employ the conception that the loss
experienced through a stroke leaves the individual
grieving for their lost pre-stroke self. Supporting
the individual through this process and educating them about the phases of grief (Kubler-Ross
& Kessler, 2005; Worden, 2001) should be a useful
addition to a package of CBT care at this time.
An example of the initial stage of denial can be
seen in the common wish of stroke survivors to
make an immediate and full recovery to the extent
that they often deny the reality of their situation
and the demands required to make a substantial recovery. This stage of anger is often seen in
stroke survivors irritation and fury at either their
lack of perceived progress or an ultimately futile
attempt to beat this stroke, rather than have it beat
me. The notion that a transition is taking place
in stages similar to bereavement has a lot of relevance to people who are attempting to achieve
a new resolution of an acutely intense and frightening situation. Similarly, as people can become
emotionally labile during recovery from stroke,
it is reassuring and normalizing to help people
think of bereavement where often difficult and
intense emotions are experienced. As many older
people will already have experienced bereavement
after a loss, this concept carries high validity for
them. It is important to bear in mind that after
a stroke, loss is not just of physical mobility but
also a loss of an anticipated future. These are significant and distressing experiences for individuals
to try to resolve. Thus, existing stage theories of
bereavement intuitively and clinically make sense
in working with stroke survivors. In support of
this, Hibbard et al., (1992) outline a single case
study design involving CBT for PSD modified to
consider grief and loss issues, alongside problems
of insight and cognitive deficit. Treatment duration
comprised 52 sessions, including some additional
sessions with the clients spouse. Both patient
and spouse completed outcome measures. After
Copyright 2010 John Wiley & Sons, Ltd.

N. M. Broomfield et al.
6 months of treatment and 1-year follow up, the
diagnosis was not depressed.
Making sense of loss may be an important part
of the adjustment process and result in less distress
(Davis, Nolen-Hoeksema & Larson, 1998). Thus, it
appears sensible for the therapist to actively focus
on loss when working with stroke survivors, promoting acceptance of and adaptation to the reality
of the situation, and those issues that are personally
relevant and meaningful for them. To that end, we
suggest that an explicit grief-resolution approach
is adopted as a legitimate target for CBT for PSD.
Making sense of the individuals attributions of loss
is entirely consistent with the CBT philosophy, but
has rarely been mentioned in regard to treatment
interventions in PSD. Support for this idea also
comes from Torges, Stewart, and Nolen-Hoeksema
(2008) who showed that older adults who were
more skilled at regret-resolution were more likely
to make better adjustments to loss, and therefore,
achieve improved outcome for depression.

Selective Optimization with Compensation


and PSD
The theory of selective optimization with compensation (SOC: Baltes 1997; Freund & Baltes, 1998)
focuses on maintaining functioning in later life in
the face of challenges experienced when aging. The
SOC model has three main components that aim to
promote successful adaptation to challenges associated with aging (Baltes, 1997). Selection ensures
that highly valued roles and goals are maintained in
some form despite loss of functioning or reserves.
In order to maintain investments in valued roles,
the individual may need to select alternative
strategies to achieve this. When working with
stroke survivors, compensation will involve adopting a loss-based selection frame of reference where
the individual modifies goal attainment, given
their reduced resources (Freund & Baltes, 1998).
Optimization in stroke is more effective if done in
an intentional manner. Individuals are helped to
focus resources on achieving goals by practicing or
re-learning activities, to improve functioning. For
stroke, the most challenging aspect of SOC is often
compensation since this requires that an individual
intentionally engages in alternative methods of
achieving goals.
The utility of SOC in CBT is that it takes account
of the reality of a persons capacity and physical
integrity. Characterized in this way, this problemfocused theory-driven method to understand the
Clin. Psychol. Psychother. 18, 202217 (2011)
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CBT and PSD


realistic challenges of ageing is entirely consistent
with the philosophy of CBT. People cope with
restricted capacity by compensating, using optimization and selection (Baltes, 1997; Freund & Baltes,
1998). In SOC, stroke survivors can be encouraged
to identify particular problems and to reduce their
repertoire of a larger set of possibilities (selection).
Optimization then helps them to increase skills in
the acquisition of a desired outcome or the more
successful completion of a predetermined activity.
Compensation results in the modification of activities in order to permit the individual to maintain
activities at an optimal level, in the face of challenges to levels of functioning.
When applied to CBT for PSD, the therapist must
establish what was important and meaningful for
the individual prior to their stroke and look at ways
of promoting the individuals participation and
involvement in roles and activities that make life
meaningful. Crucially, in order for the individual
to achieve this, they must engage in activities in an
adapted way, often using compensatory strategies.
Laidlaw et al. (2003), and Laidlaw (2008), provide
examples of the application of SOC in CBT for
PSD.
Often patients are unable to do many of the
things they used to enjoy prior to their stroke and
these are often things that have a key role in that
individuals identity. Through adopting the principles of SOC, individuals can re-introduce these
activities in an adapted, modified, and hence, more
manageable way, therefore reconstructing their
post-stroke identity closer to that of their pre-stroke
self. We propose that, by incorporating elements of
SOC into a traditional CBT framework, the therapy
will be more focused, relevant and meaningful for
stroke survivors.

Cognitive Deficits Adaptations In PSD


Cognitive deficits after stroke are a common
feature (e.g. Desmond et al., 2000; Tatemichi et al.,
1994). Hibbard and colleagues advocate several
process changes for CBT, to take account of
post-stroke cognitive deficits. These include psychoeducation to raise patient (and family) awareness of stroke related cognitive damage, shorter
session length with frequent use of therapy breaks,
and patient rehearsal of key therapy dialogue to
ensure understanding. Homework can be repeated
over time and across situations to enhance generalization, notebooks or tape recordings can be
used to enhance recall, and therapists can rely on
Copyright 2010 John Wiley & Sons, Ltd.

211
the patients least deficient mode of attention to
enhance concentration (Hibbard, Grober, Gordon,
Alette, & Freeman, 1990).
Gracey and colleagues (e.g. Gracey, Oldham, &
Kritzinger, 2007; Gracey et al., 2009) use similar
process adaptations in their neuropsychological rehabilitation work with acquired brain injury
(ABI) patients. Furthermore, in CBT single casework, they demonstrate the particular clinical
benefit of behavioural experiments to treat adjustment and identity problems after ABI (Dewar
& Gracey, 2007). Behavioural experiments can
provide a powerful vehicle for new learning and
belief appraisal by operating at implicational levels
of processing (Teasedale, 1999).
In keeping with the above, and the small number
of controlled trials that show CBT for emotion disturbance following ABI can be effective if adapted
for cognitive deficits (e.g. Bradbury et al., 2008;
Tiersky et al., 2005), we would advocate that CBT
for PSD will require adaptations to take account of
an individuals cognitive weaknesses.

Executive Skills Training In PSD


Within the stroke context, executive functioning is
a particularly important cognitive deficit to consider when using CBT. Attention and executive
deficits often occur following stroke (Tatemichi et
al., 1994), and individuals with executive dysfunction and clinical risk factors for cerebrovascular
disease have been shown to be at increased risk for
developing depression (Mast, Yochim, MacNeill, &
Lichtenberg, 2004).
Executive functioning abilities are inter-related
sets of abilities that allow an individual to initiate,
plan, sequence and coordinate a series of actions.
They involve the abilities of response-inhibition,
attention-allocation, concept-formation and selfmonitoring. Deficient executive skills can very
often limit patient ability to engage with and
benefit from CBT, if not addressed.
Interestingly, in a pilot evaluation of CBT for late
life anxiety, Mohlman and Gorman (2005) demonstrated that outcome for CBT anxiety disorder was
poor in older adults with low levels of executive
functioning abilities, but increased for those initially
classified as having low levels of executive functioning, but whose executive functioning was subsequently improved using attention-training and
enhanced self-monitoring (Mohlman & Gorman,
2005). The results were somewhat mixed in that
even though the executive dysfunction group
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212
patients completed the most homework assignments, the quality of completion of homework
was judged to be poorer than those without executive dysfunction. However, this preliminary study
shows great promise in that it suggests people with
executive impairments can be supported to engage
in therapies such as CBT. For people who may have
neurological impairments after stroke and who also
develop a mood disorder, this study holds out the
promise of potential benefits if the adjustments to
CBT can be delivered in an individually tailored
way.
Mohlman et al. (2008) present a single case
evaluation of CBT for an individual with executive-dysfunction, supportive of this. Their CBT
treatment intervention was augmented with a
packet of measures designed to enhance skills in
attention, memory and executive functioning. In
the programme, the executive skills component
was completed at the start of each CBT session,
and organized to become progressively more challenging. The CBT sessions were augmented with a
standardized executive training package used in
the rehabilitation of individuals with frontal lobe
injuries (see Mohlman et al., 2008 for more details).
The interventions were very clearly structured into
three parts, consisting of executive function training, CBT and homework assignment. At the end
of treatment, there were substantial improvements
evident not only in mood, but also in neuropsychological functioning.
While the work of Mohlman et al. (2008) is intriguing, we are not arguing here that sessions for CBT
for PSD include a package of executive dysfunction
training as that is too prescriptive and is inconsistent with the collaborative individualized nature
of good CBT. Rather what is advocated here is
that CBT can be augmented using a range of ideas
so as to improve access to clients who may ordinarily be denied treatment for depression using
psychological methods. Augmenting CBT may
mean taking steps to help people with cognitive
impairment engage with therapy, and this may
consist of some training and some more structured
support around aspects of treatment such as homework completion, and by these means more people
will have access to help that may reduce mood
disorder.
It is an intriguing prospect that outcome of CBT
for PSD might be enhanced if the intervention
is specifically augmented to improve an individuals executive functioning. When applying CBT
with stroke survivors for instance, early sessions
could incorporate attention-control strategies with
Copyright 2010 John Wiley & Sons, Ltd.

N. M. Broomfield et al.
explicit focus on homework exercises that increase
self-monitoring abilities.
For example, Mohlman and Gorman (2005)
state that prior to ending the session, the therapist
worked with the client to complete one part of the
homework assignment to ensure that the nature
of the task was understood. In addition, Mohlman
and Gorman (2005) also note that the last 5 minutes
of a therapy session were devoted to a review of
the topics and tasks completed in the session. This
type of work seeks to enhance the engagement
of individuals with cognitive impairment in CBT
and is consistent with the ethos of CBT in that
it is skills-enhancing and non-pathologizing in its
attempts to ensure treatment is collaborative and
individual (Zeiss & Steffen, 1996).
Thus, the multi-modal work suggested by the
mantra, say it, show it, do it, formulated by Zeiss
and Steffen (1996), should be emphasized in work
with people with stroke. More specifically prior to
a patient leaving the session, the therapist should
explain what is required in the homework task (say
it), encourage the completion by modeling what is
required (show it) and then ensure that no obstacles are left for the completion of the task (do it).

The Need for an Individually Tailored


Approach to Augmented CBT
We have outlined five key psychological components, which we believe provide the key to augmenting CBT for PSD, to enhance outcome. We
would also emphasize the importance of maintaining an individually tailored treatment approach
for each patient. Figure 2 summarizes the types of
choices that clinicians may wish to consider when
augmenting CBT for PSD.
In our view, CBT for PSD needs to be augmented
to be effective, but it must also be designed and
delivered based on individual patient need. Careful
assessment leading to a detailed case formulation,
which identifies predisposing, precipitating, perpetuating and protective factors for that person,
will best determine in what individual way(s)
CBT should be augmented, for that patient, at that
time. Failure to do so will result in a much poorer
treatment outcome. This last point is not particularly radical as this is a standard feature of CBT.
Any clinician working with a specific client group
needs to consider how to ensure that the therapy
provided is an optimal fit for the individual and
not the other way around (Laidlaw & Pachana,
2009).
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CBT and PSD

213

Key

Factors important in PSD:


Indicates optional
therapeutic
strategies

Predisposing

Indicates expected
therapeutic
strategies

Perpetuating

Assessment

Precipitants

Protective

Consider need for


motivational
interviewing session

Socializing to the CBT model,


translating problems into
goals, cognitive adaptations
following stroke introduced

CBT Phase 1
Sessions 1-3

CBT interventions to challenge


illness representations and to
develop individualized problemfocussed goal optimization
strategies

Cognitive
interventions

CBT Phase 2
Sessions 4-12

Behavioural
interventions

Grief work

SOC

SOC

Executive
skills training

Relapse prevention and generalization of treatment


gains prior to discharge. Reduced depression and
improved well-being and appropriate goal-setting
achieved as outcomes for therapy.

Figure 2. Illustrating augmented, individually tailored CBT for PSD


PSD = post-stroke depression. CBT = cognitive behavioural therapy. SOC = selective optimization with compensation.

SUMMARY AND CONCLUSIONS


Stroke is the single most common cause of adult
disability and the third most common cause of
death. Depression occurs in one third of stroke
survivors, and can pose a significant problem both
for subsequent mortality rates, functional recovery and engagement with physical rehabilitation
programmes.
In this review, we began by outlining key reasons
for why PSD may be so prevalent. Proposed
explanatory factors included physical impairment,
Copyright 2010 John Wiley & Sons, Ltd.

comorbid health problems, stressful life events,


negative self referent thinking, cognitive deficits
and processing biases.
We then critically appraised the existing evidence base regarding CBT for PSD. As is evident,
there have been few controlled evaluations of CBT
for PSD, and only one RCT (Lincoln & Flannaghan,
2003). Unfortunately, Lincolns seminal and pioneering study provided only neutral findings. All
that can therefore be concluded is that CBT should
work, rather than CBT does work (Laidlaw, 2008).
We believe CBT should prove most effective, if an
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214
augmented, individually tailored treatment approach
is employed. Any such augmented CBT approach
must, in our view, take account of the trauma,
acute onset and loss elements of stroke, including
the physical and psychological consequences to
the individual, and integrate a combination of five
key components: motivational interviewing, griefresolution, selection optimization compensation,
cognitive adaptations and executive skills training. We believe it is only by incorporating these
components into a novel therapy protocol, and by
testing this augmented treatment approach, tailored to individual patient need, that CBT for PSD
can ultimately be refined and treatment outcome
enhanced.

REFERENCES
Anderson, C.S., Hackett, M.L., & House, A.O. (2004).
Interventions for preventing depression after stroke.
Cochrane Database of Systematic Reviews, Issue 2. Art.
No.: CD003689. doi:10.1002/14651858.CD003689.pub2
Arkowitz, H., Westra, H.A., Miller, W.R., & Rollnick,
S. (2008). Motivational interviewing in the treatment of
psychological problems. New York: Guilford.
Bains, B., Powell, T., & Lorenc, L. (2007). An exploratory
study of mental representations for rehabilitation
based on the theory of planned behaviour. Neuropsychological Rehabilitation, 17, 174191.
Baltes, P.B. (1997). On the incomplete architecture of
human ontogeny: Selection, optimization, and compensation as foundation of developmental theory.
American Psychologist, 52, 366380.
Beck, A.T. (1987). Cognitive models of depression. Journal
of Cognitive Psychotherapy, 1, 537.
Beck, A.T., Rush, A.J., Shaw, B.F., & Emery, G. (1979).
Cognitive therapy of depression. New York: Guildford
Press.
Beck, A.T., Steer, R.A., & Brown, G.K. (1996). Beck
Depression Inventory. New York: The Psychological
Corporation.
Becker, G. (1993). Continuity after a stroke: Implications
of life-course disruptions in old age. The Gerontologist,
33, 148158.
Beekman, A.T., Copeland, J.R., & Prince, M.J. (1999).
Review of community prevalence of depression in late
life. British Journal of Psychiatry, 174, 307311.
Blackburn, IM. (1995). The relationship between drug
and psychotherapy effects. In M. Aveline, & D.A.
Shapiro (Eds.), Research foundations for psychotherapy
practice (pp. 231245). London: John Wiley.
Bradbury, C.L., Christensen, B.K., Lau, M.A., Ruttan,
L.A., Arundine, A.L., & Green, R.E. (2008). The efficacy of cognitive behaviour therapy in the treatment of
emotional distress after acquired brain injury. Archives
of Physical Medicine Rehabilitation, 89, S61S67.
Broomfield, N.M., Davies, R., MacMahon, K.M.A., Farah,
A., & Cross S. (2007). Further evidence of attention

Copyright 2010 John Wiley & Sons, Ltd.

N. M. Broomfield et al.
bias for negative information in late life depression.
International Journal of Geriatric Psychiatry, 22, 175180.
Burke, B., Arkowitz, H., & Menchola, M. (2003). The efficacy of motivational interviewing: A meta-analysis of
controlled clinical trials. Journal of Consulting and Clinical Psychology, 71, 843861.
Carson, A., MacHale, S, Allen, K., Lawrie, S., Dennis,
M., House, A., et al. (2000). Depression after stroke
and lesion location: A systematic review. Lancet, 356,
122126.
Chang, A.M., MacKenzie, A.E., & Dhillon, Y. (1999).
The psychosocial impact of stroke. Journal of Clinical
Nursing, 8, 477478.
Coetzer B.R. (2004). Grief, self-awareness and psychotherapy following brain injury. IIllness, Crisis and Loss,
12(2), 171186.
Davis, C.G., Nolen-Hoeksema, S., & Larson, J. (1998).
Making sense of loss and benefiting from the experience: Two construals of meaning. Journal of Personality
and Social Psychology, 75, 561574.
De Ridder D., Geenen R., Kuitjer, R., & Van Middenhorp,
H. (2008). Psychological adjustment to chronic disease.
Lancet, 372, 246255.
Derryberry, D., & Rothbart, M.K. (1988). Arousal, affect,
and attention as components of temperament. Journal
of Personality and Social Psychology, 55, 958966.
Desmond, D.W., Moroney, J.T., Paik, M.C., Sano, M.,
Mohr, J.P., Aboumatar, S., et al. (2000). Frequency
and clinical determinants of dementia after ischemic
stroke. Neurology, 54, 11241131.
Dewar, B.K., & Gracey F. (2007). Am not was: Cognitive-behavioural therapy for adjustment and identity
change following herpes simplex encephalitis. Neuropsychological Rehabilitation, 17(4/5), 602620.
Ekstam, L., Uppgard, B., von Koch, L., & Tham, K. (2007).
Functioning in everyday life after stroke: A longitudinal study of elderly people receiving rehabilitation
at home. Scandinavian Journal of Caring Science, 21,
434446.
Freund, A.M., & Baltes, P.B. (1998). Selection, optimization, and compensation as strategies of life management: Correlations with subjective indicators of
successful aging. Psychology and Aging, 13, 531543.
Galski, T., Bruno, R.L., Zorowitz, R., & Walker, J. (1993).
Predicting length of stay, functional outcome and
aftercare in the rehabilitation of stroke patients: The
dominant role of higher order cognition. Stroke, 24,
17941800.
Gayman, M.D., Turner, J. & Cui, M. (2008). Physical
limitations and depressive symptoms: Exploring the
nature of the association. Journal of Gerontology Series
B., 63, S219S228.
Gracey, F., Evans, J.J., & Malley, D. (2009). Capturing process and outcome in complex rehabilitation
interventions: A Y-shaped model. Neuropsychological
Rehabilitation, 19, 867890.
Gracey, F., Oldham, P., & Kritzinger, R. (2007). Finding
out if The me will shut down: Successful cognitive-behavioural-therapy of seizure related panic
symptoms following subarachmoid haemorrhage: A
single case report. Neuropsychological Rehabilitation, 17,
106119.

Clin. Psychol. Psychother. 18, 202217 (2011)


DOI: 10.1002/cpp

CBT and PSD


Grant, R.W., & Casey, D.A. (1995). Adapting cognitive
behavioral therapy for the frail elderly. International
Psychogeriatrics, 7, 561571.
Gum, A., Snyder, C.R., & Duncan, P.W. (2006). Hopeful
thinking, participation, and depressive symptoms
three months after stroke. Psychology and Health, 21,
319334.
Habib, M. (2000). Disorders of motivation. In J. Cummings, & J. Bogousslavsky (Eds.), Behavior and mood
disorders with focal brain lesions. Cambridge: Cambridge
University Press.
Hackett, M.L., Anderson, C.S., & House, A.O. (2004).
Interventions for treating depression after stroke.
Cochrane Database of Systematic Reviews, Issue 3. Art.
No.: CD003437. doi:10.1002/14651858.CD003437.pub2
Hackett, M.L., Anderson, C.S., House, A.O., & Xia, J.
(2009). Interventions for treating depression after
stroke. Cochrane Database of Systematic Reviews 2008,
Issue 4. Art. No.: CD003437. DOI 10.1002/14651858.
CD003437.pub3
Hackett, M.L., Yapa, C., Parag, V., & Anderson, C.S.
(2005). Frequency of depression after stroke: A systematic review of observational studies. Stroke, 36,
13301340
Hartman-Maeir, A., Soroker, N., Ring, H., Avni, N., &
Katz, N. (2007). Activities, participation and satisfaction one-year post-stroke. Disability and Rehabilitation,
29, 559566.
Hettema, J., Steele, J., & Miller, W.R. (2005). Motivational
interviewing. Annual Review of Clinical Psychology, 1,
91111.
Hibbard, M.R., Grober, S.E., Gordon, W.A., Aletta, E.G.,
& Freeman, A. (1990). Cognitive therapy and the treatment of poststroke depression. Topics in Geriatric Rehabilitation, 5, 4355.
Hibbard, M.R., Grober, S.E., Stein, P.N., & Gordon, W.A.
(1992). Post-stroke depression. In A. Freeman, & F.M.
Dattilio (Eds.), Chapter 32: Comprehensive casebook of
cognitive therapy (pp. 303310). New York, New York:
Plenum Press.
House, A., Knapp, P., Bamford, J., & Vail, A. (2001).
Mortality at 12 and 24 months after stroke may be associated with depressive symptoms at 1 month. Stroke,
32, 696701.
Koder, D.A., Brodaty, H., & Anstey, K.J. (1996). Cognitive therapy for depression in the elderly. International
Journal of Geriatric Psychiatry, 11, 97107.
Kneebone, I.H., & Dunmore, E. (2000). Psychological
management of post-stroke depression. British Journal
of Clinical Psychology, 39, 5365.
Knight, B.G., & Laidlaw, K. (2009). Translational theory:
A wisdom-based model for psychological interventions to enhance well-being in later life. In V. Bengston, M. Silverstein, N.M. Putney, & D. Gans (Eds.),
Handbook of theories of aging (2nd ed.). New York:
Springer.
Kubler-Ross, E., & Kessler, D. (2005). On grief and grieving: Finding the meaning of grief through the five stages of
loss. New York: Simon & Schuster Ltd.
Laidlaw, K. (2008). Using CBT with older people with
post-stroke depression. In D. Gallagher-Thompson, A.
Steffen, & L.W. Thompson (Eds.), Handbook of behav-

Copyright 2010 John Wiley & Sons, Ltd.

215
ioral and cognitive therapies with older adults. New York:
John Wiley & Sons Inc.
Laidlaw, K., & Pachana, N. (2009). Aging, mental health
and demographic change: Psychotherapist challenges.
Professional Psychology: Research and Practice, 40, 601
608.
Laidlaw, K., Thompson, L.W., Dick-Siskin, L., & Gallagher-Thompson, D. (2003). Cognitive behaviour therapy
with older people. Chichester: John Wiley & Sons Ltd.
Lawrence, E.S., Coshall, C., Dundas, R., Stewart, J., Rudd,
A.G., Howard, R., et al. (2001). Estimates of the prevalence of acute stroke impairments and disability in a
multiethnic population. Stroke, 32, 12791284.
Lewis, S.C., Dennis, M.D., ORourke, S.J., & Sharpe, M.
(2001). Negative attitudes among short-term stroke
survivors predict worse long-term survival. Stroke, 32,
16401645.
Lezak, M.D., Howieson, D.B., & Loring, D.W. (2004).
Neuropsychological assessment. Oxford: Oxford University Press.
Lincoln, N.B., & Flanagan, T. (2003). Cognitive behavioral psychotherapy for depression following stroke: A
randomized controlled trial. Stroke, 34, 111115.
Lincoln, N.B., Flannaghan, T., Sutcliffe, L., & Rother, L.
(1997). Evaluation of cognitive behavioral treatment
for depression after stroke: A pilot study. Clinical Rehabilitation, 11, 114122.
Lo, R.S.K., Cheng, J.O.Y., Wong, E.M.C., Kwong Tang,
W., Wong, L.K.S., Woo, J., et al. (2008). Handicap and
its determinants of change in stroke survivors. Stroke,
39, 148153.
Mast, B.T., Yochim, B., MacNeill, S.E., & Lichtenberg,
P.A. (2004). Risk factors for geriatric depression: The
importance of executive functioning within the vascular depression hypothesis. Journals of Gerontology:
Series A: Biological Sciences and Medical Sciences, 59,
12901294.
McDougall, F.A., Kvaal, K., Matthews, F.E., Paykel, E.,
Jones, P.B., Dewy, M.E., & Brayne, C. (2007). Prevalence of depression in older people in England and
Wales: The MRC CFA study. Psychological Medicine,
37, 17871795
Mitchell, J.E., & Madigan, R.J. (1984). The effects of
induced elation and depression on interpersonal
problem solving. Cognitive Therapy and Research, 8,
277285.
Mogg, K., & Bradley, B.P. (2005). Attentional bias in generalized anxiety disorder versus depressive disorder.
Cognitive Therapy and Research, 29, 2945.
Mohlman, J., Cedeno, L.A., Price, R.B., Hekler, E.B.,
Yan, G.W., & Frishman, D.B. (2008). Deconstructing
demons: The case of Geoffrey. Pragmatic Case Studies
in Psychotherapy, 4, 139.
Mohlman, J., & Gorman, J.M. (2005). The role of executive
functioning in CBT: A pilot study with anxious older
adults. Behaviour Research and Therapy, 43, 447465.
Montano, B. (1999). Primary care issues related to the
treatment of depression in elderly patients. Journal of
Clinical Psychiatry, 60, 4551.
Mulsant, B.H., and Ganguli, M. (1999). Epidemiology
and diagnosis of depression in late-life. Journal of Clinical Psychiatry, 60, 915.

Clin. Psychol. Psychother. 18, 202217 (2011)


DOI: 10.1002/cpp

216
Myint, P.K., Sinha, S., Luben, R.N., Bingham, S.A.,
Wareham, N.J., & Khaw, K.T. (2008). Risk factors for
first-ever stroke in the EPIC-Norfolk prospective population-based study. European Journal of Cardiovascular
Prevention and Rehabilitation, 15, 663669.
National Audit Office. (2005). Reducing brain damage:
Faster access to better stroke care. Report by the Comptroller and Auditor General, Department of Health
(UK) HC 452.
NHS National Services Scotland. (2008). Measuring long-term conditions in Scotland. Retrieved
June 4, 2010, from Information Services Division
Website: http://www.isdscotland.org/isd/servlet/
FileBuffer?namedFile=2008_08_14_LTC_full_report.
pdf&pContentDispositionType=inline
Nicholl, C.R., Lincoln, N.B., Muncaster, K., & Thomas, S.
(2002). Cognitions and post-stroke depression. British
Journal of Clinical Psychology, 41, 221231.
Oddy, M., Cattran, C., & Wood, R. (2008). The development of a measure of motivational changes following
acquired brain injury. Journal of Clinical and Experimental Neuropsychology, 30, 568575.
Paradiso, S., Ohkubo, T., & Robinson, R.G. (1997). Vegetative and psychological symptoms associated with
depressed mood over the first two years after stroke.
International Journal of Psychiatry in Medicine, 27, 137157.
Pinquart, M., Duberstein, P.R., & Lyness, J.M. (2006).
Treatments for later-life depressive conditions: A
meta-analytic comparison of pharmacotherapy and
psychotherapy. American Journal of Psychiatry, 163,
14931501.
Pohjasvaara, T., Vataja, R., Laeppavouri, A., Kaste, M.,
& Erkinjuntti, T. (2001). Depression is an independent
predictor of poor long-term functional outcome poststroke. European Journal of Neurology, 8, 315319.
Rasquin, S.M.C., Van De Sande, P., Praamstra, A.J., &
Van Heugten, C.M.(2009). Cognitive-behavioural
intervention for depression after stroke: Five single
case studies on effects and feasibility. Neuropsychological Rehabilitation, 19, 208222.
Robertson, I.H., Ridgeway, V., Greenfield, E., & Parr, A.
(1997). Motor recovery after stroke depends on intact
sustained attention: A 2 year follow-up study. Neuropsychology, 11, 290295.
Robinson, R.G., Kubos, K.L., Starr, L.B., Rao, K., & Price,
T.R. (1983). Mood changes in stroke patients: relationship to lesion location. Comprehensive Psychiatry, 24,
556566.
Samson, D., Apperly, I.A., Kathirgamanathan, U., &
Humphreys, G.W. (2005). Seeing it my way: A case of
a selective deficit in inhibiting self-perspective. Brain,
128, 11021111.
Scogin, F., & McElreath, L. (1994). Efficacy of psychosocial treatments for geriatric depression: A quantitative
review. Journal of Consulting and Clinical Psychology,
62, 6974.
Seibert, P.S., & Ellis, H.C. (1991). Irrelevant thoughts,
emotional mood states and cognitive task performance. Memory and Cognition. 19: 507513.
Sharpe M., Hawton, K., Seagroatt, V., Bamford, J., House,
A., Molyneux, A., et al. (1994). Depressive disorders in
long-term survivors of stroke. Associations with demo-

Copyright 2010 John Wiley & Sons, Ltd.

N. M. Broomfield et al.
graphic and social factors, functional status, and brain
lesion volume. British Journal of Psychiatry, 164, 380386.
Skaner, Y., Nilsson, G.H., Sundquist, K., Hassler, E.,
& Krakau, I. (2007). Self-rated health, symptoms of
depression and general symptoms at 3 and 12 months
after a first-ever stroke: A municipality-based study in
Sweden. BMC Family Practice, 8, 61.
Snaith, R.P., Ahmed, S.N., Mehta, S., & Hamilton, M.
(1971). Assessment of severity of primary depressive
illness: Wakefield self-assessment depression inventory. Psychological Medicine, 1, 143149.
Tatemichi, T.K., Desmond, D.W., Stern, Y., Paik, M.,
Sano, M., & Bagiella, E. (1994). Cognitive impairment
after stroke: Frequency, patterns and relationship to
functional abilities. Journal of Neurology, Neurosurgery,
and Psychiatry, 57, 202207.
Teasedale, J.D. (1999). Emotional processing, three modes
of mind and the prevention of relapse in depression.
Behaviour Research and Therapy, 18, 5160.
Tiersky, L.A., Anselmi, V., Johnston, M.V., Kurtyka,
J., Roosen, E., Scwartz, T., et al. (2005). A trial of
neuropsychological rehabilitation in mild spectrum
traumatic brain injury. Archives of Physical Medicine
Rehabilitation, 86, 15651574.
Thomas, S.A., & Lincoln, N.B. (2006). Factors relating to
depression after stroke. British Journal of Clinical Psychology, 45, 4961.
Torges, C.M., Stewart, A., & Nolen-Hoeksema, S. (2008).
Regret resolution, aging and adapting to loss. Psychology and Aging, 232, 169180.
Vickery, C.D. (2006). Assessment and correlates of
self-esteem following stroke using a pictorial measure.
Clinical Rehabilitation, 20, 10751084.
Vickery, C.D., Sepehri, A., & Evans, C.C. (2008). Selfesteem in an acute stroke rehabilitation sample: A
control group comparison. Clinical Rehabilitation, 22,
179187.
Watkins, C.L., Auton, M.F., Deans, C.F., Dickinson, H.A.,
Jack, C.I.A., Lightbody, C.E., et al. (2007). Motivational
interviewing early after acute stroke. A randomized
controlled trial. Stroke, 38, 10041008.
Westbrook, D., Kennerley, H., & Kirk, J. (2007). An introduction to cognitive behaviour therapy: Skills and applications. Sage. London.
Westra, H.A., & Dozois, D.J.A. (2006). Preparing clients
for cognitive behavioural therapy: A randomized pilot
study of motivational interviewing for anxiety. Cognitive Therapy and Research, 30, 481498.
Williams, J.M.G. (1992). The psychological treatment of
depression. Routledge: London.
Williams, J.M.G., Watts, F.N., Macleod, C., & Mathews,
A. (1997). Cognitive psychology and emotional disorders.
Chichester: John Wiley.
Wilson, K., Mottram, P.G., & Vassilas, CA. (2008). Psychotherapeutic treatments for older depressed people.
Cochrane Database of Systematic Reviews 2008, Issue 1.
Art. No.: CD004853. doi:10.1002/14651858.CD0044853.
pub2
Winard, C., Sackley, C., Metha, Z., & Rothwell, P.M.
(2009). A population-based study of the prevalence
of fatigue after transient ischaemic attack and minor
stroke. Stroke, 40, 757761.

Clin. Psychol. Psychother. 18, 202217 (2011)


DOI: 10.1002/cpp

CBT and PSD


Wing, J.K., Babor, T., Brugha, T., Burke, J., Cooper, J.E.,
Giel, R., et al. (1990). SCAN: Schedules for clinical
assessment in neuropsychiatry. Archives of General
Psychiatry, 47, 589593.
Woodruff-Borden, J., Brothers, A.J., & Lister, S.C. (2001).
Self-focussed attention: Commonalities across psychopathologies and predictors. Behavioural and Cognitive
Psychotherapy, 29, 169178.

Copyright 2010 John Wiley & Sons, Ltd.

217
Worden, J.W. (2001). Grief counselling and grief therapy.
New York: Brunner Routledge.
Zeiss, A.M., & Steffen, A. (1996). Treatment issues with
elderly clients. Cognitive and Behavioral Practice, 3,
371389.
Zigmond, A.S., & Snaith, R.P. (1983). The hospital anxiety
and depression scale. Acta Psychiatrica Scandinavica, 67,
361370.

Clin. Psychol. Psychother. 18, 202217 (2011)


DOI: 10.1002/cpp

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