Division of Psychiatry, University Department of Psychological Medicine, Gartnavel Royal Hospital, Glasgow, UK
Correspondence: Professor Jan Scott, Division of Psychiatry, University Department of Psychological Medicine, Gartnavel Royal Hospital, Glasgow G12 0XH, UK. Tel: +44 (0) 141 211 3937; fax: +44 (0) 141 357 4899; e-mail: jan.scott{at}clinmed.gla.ac.uk
Declaration of interest J.S. is the Principal Investigator of a multicentre trial of cognitive therapy for bipolar disorders funded by the Medical Research Council.
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ABSTRACT |
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Aims To explore current psychological models of bipolar disorder, describing the clinical rationale for using cognitive therapy and providing a brief overview of the approach.
Method Results from outcome studies are discussed.
Results Preliminary findings indicate that cognitive therapy may be beneficial for patients with bipolar disorder. The collaborative, educational style of cognitive therapy, the use of a stepwise approach and of guided discovery is particularly suitable for patients who wish to take an equal and active role in their therapy.
Conclusions Randomised, controlled trials of cognitive therapy in bipolar disorder are required to establish the short-term and long-term benefits of therapy, and whether any reported health gain exceeds that of treatment as usual.
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INTRODUCTION |
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Since the 1980s there has been a greater emphasis on stress-diathesis models. This has led to the development of new aetiological theories of severe mental disorders which emphasise psychological aspects of vulnerability and risk, and has also increased the acceptance of cognitive therapy as an adjunct to medication for individuals with treatment-resistant schizophrenia and with severe and chronic depressive disorders (Scott & Wright, 1997). Research in bipolar disorder has been limited, but there is evidence that cognitive therapy may benefit this patient group.
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IS THERE A PSYCHOLOGICAL MODEL OF BIPOLAR DISORDER? |
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Early descriptions
Beck's original cognitive model suggests that depressed mood states are
accentuated by patterns of thinking that amplify mood shifts. For example, as
people become depressed they become more negative in how they see themselves,
their world and their future (called the negative cognitive
triad). Hence they tend to jump to negative conclusions,
overgeneralise, see things in all-or-nothing terms, and personalise and
self-blame to an excessive degree (cognitive distortions). Changes in
behaviour, such as avoidance of social interaction, may be a cause or a
consequence of mood shifts and negative thinking. Cognitive vulnerability to
depression is thought to arise as a consequence of dysfunctional underlying
beliefs (e.g. I'm unlovable), which develop from early learning
experiences and drive thinking and behaviour. It is hypothesised that these
beliefs may be activated by life events that have specific meaning for that
individual (e.g. rejection by a significant other).
Beck's original model suggested that mania was a mirror image of depression and was characterised by a positive cognitive triad of self, world and future, and positive cognitive distortions. The self was seen as extremely lovable and powerful, with unlimited potential and attractiveness. The world was filled with wonderful possibilities, and experiences were viewed as overly positive. The future was one of unlimited opportunity and promise. Hyperpositive thinking (stream of consciousness) was typified by cognitive distortions, as in depression, but in the opposite direction: for example, jumping to positive conclusions (I'm a winner, I can do anything); underestimating risks (there's no danger); minimising problems (nothing can go wrong); and overvaluing immediate gratification (I will do this now). Thus, cognitive distortions provided biased confirmation of the positive cognitive triad of self, world and future. Positive experiences were selectively attended to, and it was suggested that in this way underlying beliefs and self-schemata that guide behaviours, thought and feelings were maintained and strengthened. It was also suggested that dysfunctional beliefs were likely to involve high levels of social desirability (Winters & Neale, 1985). Examples of such underlying beliefs and self-schemata include I'm special and being manic helps me to overcome my shyness.
Beck's model of depression is well tested, with reliable and valid questionnaires applied in research settings. The model of mania, in contrast, is largely derivative, based on careful observation of patients in a manic state. Interestingly, a recent study of patients with bipolar disorder demonstrated that, between episodes of illness, patients show patterns of cognitive vulnerability similar to those of individuals with major depressive disorder (Scott et al, 2000). In comparison with healthy control subjects, patients with bipolar disorder had more fragile, unstable levels of self-esteem, higher levels of dysfunctional attitudes (particularly related to need for social approval and perfectionism), over-general memory and poorer problem-solving skills. Scott et al (2000) argued that even though it was not possible to determine whether these cognitive dysfunctions are a cause or a consequence of bipolar disorder, it was noteworthy that the difficulties persisted between episodes in patients who adhered to their prophylactic medication regimen. Furthermore, the beliefs identified (e.g. I'm different) are potentially dysfunctional when a positive or negative valence is applied to them.
Recent reformulations
Although Beck's earlier description (now termed the Linear Schematic
Processing Model) has clinical validity, it fails to take into account the
well-recognised biological aspects of vulnerability to bipolar disorder. Beck
(1996) has now concluded that a
more complex model of cognitive processing (the Integrative Model) is needed
to replace the original theory. Beck's reformulation includes two key
additions: the concepts of modes and charges, and
further refinements about precipitants of shifts in mood and thinking. Modes
are an integrated network of subsystems (cognitive, affective, motivational
and behavioural schemata) which can act in synchrony to produce goal-directed
strategies. Charges (energy levels) explain activation of the modes, and
account for shifts from quiescent states (normal) to activated states
(abnormal). Importantly for the cognitive theory of bipolar disorder, modes
can be activated by external and internal events, and when this occurs
congruent memories are also activated. An orienting schema, described by Beck
as a kind of algorithm, sets the conditions necessary for
activating the mode. It rapidly assigns a preliminary meaning to a situation
and activation is spread across the network as the relevant mode is activated.
In turn, this mode activates the schema. When a person is in a depressed or
hypomanic/manic mode state the orienting schema requires less evidence to make
the match.
The Integrative Model offers a possible explanation of the development of depression, mixed states or hypomania. It also argues that belief in the meaning of distorted thoughts leads to dysfunctional mood states. The goal of cognitive therapy is therefore to change dysfunctional interpretations as well as underlying dysfunctional beliefs (thus changing construct accessibility). Beck writes that therapy for dysfunctional modes involves deactivation, modification or neutralisation by the construction of an adaptive mode. This is achieved through interventions such as restructuring absolute and conditional rules (core schemata) that shape interpretations, or by learning new skills, which can be applied in adverse circumstances and inhibit the action of dysfunctional beliefs.
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IS THERE A CLINICAL RATIONALE FOR USING COGNITIVE THERAPY? |
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The approach outlined in Fig. 1 (adapted from Basco & Rush, 1995) is particularly useful when working with individuals with bipolar disorder as it allows the therapist to emphasise a stress-diathesis model that may also include biological factors as precipitants of symptom shift. In order to use this approach, the therapist should first ask about the patient's own views on the causes of the disorder and the associated problems. The patient's aetiological theory is then incorporated within the framework of the model. Links between the individual's cognitions, behaviour, mood and other symptoms (particularly sleep disturbance) and the interaction between these and the environment (stressful events or experiences that are a cause or a consequence of other shifts) are emphasised. This rationale is used to engage the patient in cognitive therapy through monitoring and linking changes in thoughts, behaviours, feelings and the biological symptoms of bipolar disorder. The model also acknowledges that sleep disturbance may be a useful predictor of biological and/or psychosocial disruption and may act as an early-warning sign of shifts from euthymic to abnormal mood states (Wehr et al, 1987). When the connections between the biological and other aspects of their experience are exposed, patients are able to understand the reasons for using cognitive therapy as well as medication. This establishes the rationale for cognitive and behavioural interventions, and also provides a starting point to explore attitudes towards the use of, and adherence to, medication.
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The above approach is generally well received, particularly in the early stages of cognitive therapy, when the patient is trying to make sense of the disorder and the proposed treatment. Virtually all aetiological theories can be incorporated in the model outlined, giving the patient confidence that the therapist is listening to these ideas and is trying to help make sense of them.
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OVERVIEW OF COGNITIVE THERAPY |
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Socialisation into the cognitive therapy model and development of an
individualised formulation and treatment goals
Therapy begins with an exploration of the patient's understanding of
bipolar disorder and a detailed discussion of previous episodes, focusing on
identification of prodromal signs, events or stressors associated with onset
of previous episodes, typical cognitive and behavioural concomitants of both
manic and depressive episodes, and an exploration of interpersonal functioning
(e.g. family interactions). Early sessions include development of an
understanding of key issues identified in the life chart, education about the
disorder, facilitation of adjustment to the disorder by identifying and
challenging negative automatic thoughts, and developing behavioural
experiments particularly focused on ideas about stigmatisation and fragile
self-esteem. Other sessions are dedicated to collating accurate information
and enhancing understanding about the epidemiology, treatment approaches and
prognosis of the disorder, and the development of an individualised
formulation of the patient's problems which takes into account underlying
maladaptive beliefs.
Cognitive and behavioural approaches to symptom management and
dysfunctional automatic thoughts
With the aid of information gathered previously, sessions are used to help
the patient learn self-monitoring and self-regulation techniques, which
enhance self-management of depressive and hypomanic symptoms, and to explore
skills for coping with depression and mania. This involves establishing
regular activity patterns, daily routines, regular sleep patterns, developing
coping skills, time management, use of support, and recognising and tackling
dysfunctional automatic thoughts about self, world and future using
automatic thought diaries.
Dealing with cognitive and behavioural barriers to treatment
adherence and modifying maladaptive beliefs
Problems with adherence to medication and other aspects of treatment are
tackled, for example through exploration of barriers (challenging automatic
thoughts about drugs; beliefs about bipolar disorder and self-reliance; or
exploring attitudes to autonomy and control) and by using behavioural and
cognitive techniques to enhance treatment adherence
(Scott, 1999). This and data
from previous sessions are used to help the patient identify maladaptive
assumptions and underlying core beliefs, and to commence work on modifying
these beliefs.
Anti-relapse techniques and belief modification
Further work is undertaken on recognising early signs of relapse and
developing coping techniques in fortnightly sessions. Examples include
self-monitoring of symptoms, identifying possible prodromal features (the
relapse signature), developing a list of at-risk
situations (e.g. situations that activate specific personal beliefs),
high-risk behaviours (e.g. increased alcohol intake), combined with a
hierarchy of coping strategies for each; identifying strategies for managing
medication intake and obtaining advice regarding it; and planning how to cope
and self-manage problems after discharge from therapy. Sessions also include
typical cognitive therapy approaches to the modification of maladaptive
beliefs, which might otherwise increase vulnerability to relapse.
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DOES COGNITIVE THERAPY IMPROVE OUTCOME? |
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The aim of Cochran's study was to apply cognitive therapy to enhance adherence to prescribed lithium treatment. It compared 28 patients randomly assigned to either six sessions of group cognitive therapy or standard clinic care (Cochran, 1984). Following treatment, enhanced lithium adherence was reported in the therapy group, where only three patients (21%) discontinued medication, compared with the standard clinic care group, where eight patients (57%) discontinued medication. There were fewer hospitalisations in the group receiving cognitive therapy.
In an exploratory study by Palmer et al (1995), six patients with bipolar disorder were offered cognitive therapy in a group format. The focus of the programme was psychoeducational, recognising the process of change, strategies for coping and interpersonal problems. Overall findings indicated that group therapy combined with mood-stabilising medications was effective for some of the participants. Improvements were found in symptomatology and in overall social adjustment. All participants improved on one or more measures, although the pattern of change varied across individuals. A more recent study by Palmer et al (presented at the annual meeting of the British Association of Behavioural and Cognitive Psychotherapists, Durham, UK, 1998; further details available from J.S. upon request) included a larger number of participants receiving group cognitive therapy (n=25) and a comparison group (n=12) receiving only treatment as usual. The results showed that there was no difference in mood state between groups, but, in comparison with the control group, cognitive therapy reduced non-specific symptomatology and increased social adjustment.
The Life Goals programme developed by Bauer & McBride (1997) is a structured, manual-based intervention which seeks to improve patients' management skills and their social and occupational functioning. Although outcome data are not yet available, an analysis of data on process goals showed that the manual could be used by therapists inexperienced in treating bipolar disorder. Furthermore, the programme was effective in terms of knowledge gained and goals achieved by patients (Bauer & McBride, 1997).
Perry et al (1999) undertook the largest study so far (n=68), using cognitive and behavioural techniques to help people identify and manage early-warning signs of relapse in a group of patients at high risk of further episodes of bipolar disorder. In comparison with the control group, the intervention group had significantly fewer manic relapses, significantly fewer days in hospital, higher levels of social functioning and better work performance. However, the intervention did not have a significant impact on depression, and the researchers suggested that more formal cognitive therapy might be important to produce significant changes in this area.
A pilot study by Scott et al (2001) examined the effect of 20 sessions of cognitive therapy in 42 patients with bipolar disorder. Patients were randomly allocated to this therapy in addition to treatment as usual, or to a waiting-list control condition of treatment as usual for 6 months followed by cognitive therapy plus treatment as usual. Preliminary results show cognitive therapy plus treatment as usual may offer some benefit to about 70% of these patients and is a highly acceptable treatment intervention (90% of subjects endorsed this approach). The results also suggest that cognitive therapy plus treatment as usual v. treatment as usual alone may lead to fewer relapses, as well as reducing levels of both depression and mania, and improving self-esteem and self-reported adherence to medication. An out-patient study of similar size (n=25) and design demonstrated comparable results, with additional significant improvements in social adjustment (Lam et al, 2001).
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CONCLUSION |
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On the evidence available, it appears that cognitive therapy has particular characteristics that may benefit patients with bipolar disorder. Its collaborative, educational style, and the use of a stepwise approach and of guided discovery, make it acceptable to individuals who wish to take an equal and active role in their therapy (Beck et al, 1979; Scott, 1995b). This is important as many individuals with this disorder resist and challenge a didactic approach to treatment (Miklowitz & Goldstein, 1990). However, cognitive therapy is not the only short-term therapy that can be used: psychotherapies of proven effectiveness in major depressive disorder, such as interpersonal and family therapies, are also being piloted in bipolar disorder.
Finally, larger-scale treatment intervention studies will be needed to establish the effectiveness of cognitive therapy and to differentiate between the specific and non-specific benefits of therapy. Ultimately, it is important for clinicians and researchers to know not only whether the use of this form of therapy is indicated, but also whether it helps the individual with bipolar disorder because it enhances medication adherence, changes cognitive representations of the disorder, leads to the development of compensatory skills, or reduces vulnerability to relapse through schema change. Such research will also allow for the further exploration of the complex interplay between psychological, social and biological factors.
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Clinical Implications and Limitations |
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LIMITATIONS
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REFERENCES |
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Bauer, M. & McBride, R. (1997) Structured Group Psychotherapy for Bipolar Disorder The Life Goals Program. New York: Springer.
Beck, A. T. (1996) Beyond belief: a theory of modes, personality and psychopathology. In Frontiers of Cognitive Therapy (ed. P. Salkovskis). New York: Guilford Press.
Beck, A. T., Rush, A. J., Shaw, B., et al (1979) Cognitive Therapy of Depression. New York: Wiley.
Chor, P., Mercier, M. & Halper, I. (1980) Use of cognitive therapy for treatment of a patient suffering from a bipolar affective disorder. Journal of Cognitive Psychotherapy, 2, 51 -58.
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