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Improving cognitive treatments for delusions
Schizophrenia Research 132 (2011) 135–139
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Review
Improving cognitive treatments for delusions Daniel Freeman ⁎ Department of Psychiatry, Oxford University, UK
a r t i c l e
i n f o
Article history: Received 2 February 2011 Received in revised form 6 August 2011 Accepted 22 August 2011 Available online 9 September 2011 Keywords: Delusions Cognitive therapy Schizophrenia
a b s t r a c t A clear challenge for schizophrenia research is to improve markedly the efficacy of psychological treatments for delusional beliefs. Effect sizes for the first generation of cognitive approaches are weak to moderate. These therapies now lag behind the transformation over the past ten years in understanding the causes of delusions. This paper advocates an interventionist–causal model approach: to focus on one putative causal factor at a time, show that an intervention can change it, and examine the subsequent effects on the delusional beliefs. A number of new studies that illustrate this approach with patients with schizophrenia spectrum disorders who have not responded to previous treatment are reviewed. These early stage studies show great promise in terms of efficacy, although remain to be subjected to methodologically rigorous evaluation. The advantages and difficulties of the interventionist approach applied to psychosis are considered, and future studies are highlighted. The importance for clinical services of cognitive approaches to psychosis will increase further if the theoretical advances can be translated into treatment. © 2011 Elsevier B.V. All rights reserved.
1. Introduction The first generation of cognitive–behavioural treatments for psychosis have demonstrated efficacy for treating delusions and hallucinations (see meta-analyses by Gould et al., 2004; Zimmermann et al., 2005; Wykes et al., 2008; NICE, 2009). A shift has occurred from encouraging patients not to talk about their psychotic symptoms to an appreciation that, if done in the correct way, it can be beneficial. However, the efficacy of these first generation therapies is weak to moderate, with effect sizes of about 0.4 (Wykes et al., 2008), though notably not dissimilar to that of clozapine (Leucht et al., 2009). When assessed, it has not been shown that the standard therapy changes the factors thought to cause the psychotic symptoms (e.g. Garety et al., 2008). The therapy lags behind the substantial developments in the theoretical understanding of experiences such as delusions and hallucinations. The situation may well be analogous to the CBT treatment of anxiety. Initial approaches had moderate outcome effect sizes that were then greatly increased by the development of disorder-specific and theoretically driven cognitive therapies (e.g. Clark, 2004). 2. Ideas underpinning improvement How can CBT for psychosis move forward? The approach recommended here is to follow three principles: reduce the heterogeneity of psychosis by focussing on single symptoms; use developments in the theoretical understanding to guide therapy; and show that putative causal processes ⁎ Oxford Cognitive Approaches to Psychosis (O-CAPS), Department of Psychiatry, Oxford University, Warneford Hospital, Oxford, OX3 7JX, UK. E-mail address: [email protected]. 0920-9964/$ – see front matter © 2011 Elsevier B.V. All rights reserved. doi:10.1016/j.schres.2011.08.012
have been changed, in what has been termed an interventionist–causal model approach (see Kendler and Campbell, 2009). Psychosis in typical clinical settings is complex — a truism but worth restating. Individuals frequently present with multifaceted delusions that occur in the context of anomalous experiences such as hallucinations and perceptual disturbances; with emotional disorders such as anxiety and depression; and with long-standing social difficulties. Each can affect the other. However, factor analysis has identified distinct types of psychotic experience and at least four even within the restricted category of positive symptoms (e.g. Vázquez-Barquero et al., 1996; Peralta and Cuesta, 1999; Wigman et al., 2011). This makes clinical sense — experiences such as persecutory delusions, grandiose delusions, auditory hallucinations and thought disorder present as different phenomena at clinical interview. Their co-occurrence in clinical settings is inflated by Berkson's bias (Maric et al., 2004; Bak et al., 2005). In essence, more complex cases will be admitted to hospital or seen by a health professional, inflating estimates of symptom associations. Therefore a sensible strategy for the treatment of psychosis is to focus on single psychotic symptoms or single factor types. At the very least this should ensure that techniques are tested with people with similar problems and that there is a similar outcome target, but it will also, of course, enable the application of detailed theoretical models. The task becomes more specified. The last ten years have seen an undoubted transformation in understanding psychotic symptoms. Arguably the most significant advances have come in delusion research (see reviews by Bentall et al., 2001; van der Gaag, 2006; Freeman, 2007; Garety et al., 2007; Beck et al., 2008; Langdon et al., 2008; Howes and Kapur, 2009; Murray, 2011). A range of emotional, cognitive, biological and social factors have been identified that, in combination, provide plausible accounts of delusion
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development and maintenance. In the rare instances that these types of factors have been assessed in randomised controlled trials pre- and post-CBT, which is the only way that treatment-specific effects can be definitively determined, they have not been shown to change with therapy (Garety et al., 2008). Reasoning biases, skewed views of the self and others (frequently based on adverse life experiences), rumination, interpersonal sensitivity, catastrophic appraisals, and avoidance behaviours have all been plausibly linked to delusions, but it has not been shown that CBT alters them in patients with psychosis. The argument is that we need to go back to basics and show that we can alter the key processes. To paraphrase, good theory can be very practical. This ties in with calls by statisticians and philosophers of science, and now a number of psychologists and psychiatrists in relation to the topic of mental health, for the need to illuminate causal inference by use of an ‘interventionist–causal model’ approach (see Table 1). Causation is substantiated by examining the effect of intervening on or manipulating the putative causal factor. As Kendler and Campbell (2009) put it: ‘The interventionist model says that questions about whether X causes Y are questions about what would happen to Y if there were an intervention on X.’ In turn this provides intervention techniques. If you change the causal factor and there are reductions in the psychotic experience then your manipulation method has the potential to prove a treatment technique. However, there are caveats. Most causes are ‘inus conditions’ — ‘an insufficient but non-redundant part of an unnecessary but sufficient condition’ (Mackie, 1974). Most effects result from a combination of causes and each cause generally only increases the probability of an effect occurring. Further, whilst convincing and most likely sufficient for clinical purposes, this method does not of itself necessarily demonstrate the mechanisms through which the causal relationship holds (Shadish et al., 2002) — this would still require a further mediational analysis (see Emsley et al. (2010) for a description of new statistical methods). 3. New treatment studies of delusions This process of improving treatments for delusions has begun, and a number of examples by the author and colleagues will be noted. One of the most convincing early demonstrations has concerned the use of worry reduction techniques. Research has shown that levels of worry in individuals with persecutory delusions are often comparable to those in generalised anxiety disorder, that the tendency to worry is a predictor of the occurrence of paranoid thinking, that levels of worry predict the persistence of persecutory delusions and that worry makes the delusional ideas more distressing (Freeman and Garety, 1999; Morrison and Wells, 2007; Startup et al., 2007; Freeman et al., 2008b; Bassett et al., 2009). A worry cognitive style brings Table 1 The interventionist–causal approach. ‘The paradigmatic assertion in causal relationships is that manipulation of a cause will result in the manipulation of an effect’ Cook and Campbell (1979). ‘The very essence of causation is the ability to predict the consequences of new manipulations. Viewing causality this way explains why scientists pursue causal explanations with such zeal and why it is accompanied by a sense of gaining deep understanding and being in control.’ Pearl (2009). ‘The distinguishing feature of causal explanations is that they are explanations that furnish information that is potentially relevant to manipulation and control’ Woodward (2003). ‘It [the interventionist–causal approach] connects causation with the practical interests of psychiatry, defining causation in terms of what would happen under interventions, a question of key interest to those of us whose interest is ultimately in intervening to prevent and treat illness’ Kendler and Campbell (2009). ‘In order to test our cognitive models of anxiety disorders, we have had to develop experiments in which the cognitive abnormalities and maintaining processes specified in the models are manipulated in order to see whether they have the predicted effects on symptoms. The experiments, when successful, have often become incorporated into the full treatment programmes.’ Clark (2004).
implausible ideas to mind, keeps them there, and makes the experience more distressing. In a recent pilot randomised controlled trial, involving 24 patients with persistent persecutory delusions and worry in the context of a psychotic disorder, the effects of a cognitive behavioural worry reduction intervention were evaluated (Foster et al., 2010). The worry reduction intervention was brief, comprising just four one-hour sessions over four weeks, and did not address the content of paranoid fears. The main techniques were psychoeducation about worry, reviewing positive and negative beliefs about worry, increasing awareness of the start of a worry episode and identification of individual triggers, learning to ‘let go’ of worry, use of worry periods, substituting problem-solving for worry, and relaxation exercises. Half the patients were randomised to the intervention in addition to their standard psychiatric care and half were randomised to the control group (standard psychiatric care). Assessments were carried out at baseline, end of treatment (one month), and at follow-up (two months). The intervention led to a large reduction in worry (effect size= 1.05) and also in persecutory delusions (effect size= 1.35) (effect sizes calculated for the treatment group's change in scores relative to the control group). These reductions were maintained at follow-up. One in three patients showed a 25% or greater reduction in worry and delusions. Changes in worry were associated with changes in persecutory delusions. The study was successful in changing the putative causal factor, leading to a reduction in delusions. A larger and more rigorous evaluation of this intervention is starting at the end of 2011 (Freeman et al., 2011a). The treatment of worry in patients with delusions has recently been approached from a different angle, inspired by work on written emotional disclosure (e.g. Gortner et al., 2006). One route by which worry may cause more delusion-related distress is by impeding emotional processing of upsetting paranoid experiences. Facilitating emotional processing should therefore reduce levels of worry and paranoia distress. Hence a new brief treatment – Emotional Processing and Metacognitive Awareness (EPMA) – was evaluated with twelve patients with persistent persecutory delusions (Hepworth et al., 2011). The intervention focussed on patients retelling recent paranoid experiences in an experiential manner (i.e. simply describing and fully experiencing their thoughts, sensations and feelings at the time) rather than a ruminative/evaluative fashion. This approximates written emotional expression interventions. But patients were also encouraged to gain distance from their mental experiences, by, for example, discriminating between thoughts, feelings and memories, and writing down particularly troubling words on pieces of paper and scrunching them up and throwing them away. This metacognitive aspect of the intervention overlaps with recent mindfulness and ACT approaches to psychosis (e.g. Chadwick et al., 2009; Gaudiano et al., 2010). All participants received the three session intervention and the delusions were assessed during a baseline period, post intervention, and at a one month follow-up. Levels of worry were reduced (effect size = 0.6), and it was also found that EPMA particularly reduced levels of delusion distress (effect size = 1.03), outcomes that were maintained at follow-up. Nine of the patients reported a greater than 25% reduction in paranoia distress. These preliminary data indicate that simply allowing individuals to talk about their delusional experiences, in the right way, can be strikingly helpful in itself. The latest empirical research has directly linked insomnia to the development of delusional thinking. Clinical insomnia is present in a high proportion of individuals with persecutory delusions; there are substantial associations between difficulties sleeping and persecutory ideation; and insomnia raises the risk of both the development and persistence of paranoid thinking (Freeman et al., 2009, 2010, 2011b, in press). The link is highly plausible, since earlier work shows that insomnia leads to anxiety, depression and anomalies of experience (e.g. Luby et al., 1960; Breslau et al., 1996; Morphy et al., 2007), each of which are risk factors for paranoid thinking. Of course, if
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patients are reporting insomnia then this should be a target for intervention in its own right, and well-evaluated cognitive–behavioural interventions are available (see Morin et al., 1999; Smith et al., 2005; Espie, 2006; Freeman and Freeman, 2010). However, from the interventionist–causal model approach the prediction is that treating the insomnia will also lead to a reduction in delusions. This is exactly what was found in a case series of 15 patients with persistent persecutory delusions (Myers et al., 2011). Following a four-session sleep intervention, significant reductions were found in levels of insomnia (effect size = 2.64) and the persecutory delusions (effect size = 1.07). At least two thirds of participants made substantial improvements in insomnia and approximately half showed substantial reductions in the persecutory delusions. This was an uncontrolled test, but at the very least it indicates that standard CBT for insomnia is appropriate for people with psychosis, and may well bring significant additional benefits. Reasoning processes are inherently implicated in delusional beliefs. The most replicated finding has been that individuals with delusions tend to gather less evidence before making a decision, a process termed ‘jumping to conclusions’ (see reviews by Fine et al., 2007; Freeman, 2007; Garety and Freeman, 1999). This seems to lead to less willingness to consider alternative explanations for events (belief inflexibility) and to higher levels of conviction in the belief (Freeman et al., 2004; Garety et al., 2005; Freeman et al., 2008c). Therefore jumping to conclusions and belief inflexibility have now been targeted. Ross et al. (2011) used a very brief reasoning programme, presented on a computer and featuring only abstract materials. (Two parts of the programme were adapted from the meta-cognitive training programme of Moritz et al. (2011), who take a rather different approach. Over eight weeks they provide education about a large number of psychological biases to a group of patients with schizophrenia.) The effects of the 45-minute programme evaluated by Ross et al. (2011), with 34 patients with delusions randomised to either the reasoning programme or an attention control condition, were modest. Reasoning training significantly improved data-gathering, and a small number of participants experienced changes in delusional conviction. Lincoln et al. (2010b) have also shown that the reasoning bias can be directly manipulated. Arising from this work the Maudsley Review Training Programme has now been developed. The original programme used by Ross et al. (2011) has been substantially altered and extended, specifically by adding new sections, delusion relevant material, interactive components and video clips, and handouts summarising key points. The length of the training has doubled. Its efficacy has been initially evaluated with 13 patients with persistent persecutory delusions in an ABA design (Waller et al., 2011). There were improvements in JTC (effect size=0.30), belief flexibility (effect size=0.82) and delusional conviction (effect size=1.06) between preand post-intervention measures. This brief intervention, enhancing reasoning skills and setting the scene for directly addressing the contents of a delusion, is likely best followed by other intervention techniques (e.g. behavioural tests). The techniques presented in these studies that have explicitly adopted an interventionist–causal model approach must be scrutinised with greater methodological rigour. But the effect sizes in these studies are very promising, especially when it is considered how long the patients have held their delusions despite attempts at other treatments and the brevity of the interventions. Importantly, these techniques seem to encourage higher levels of engagement because they work on problems that have been agreed with the patient and that do not directly dispute the validity of delusional beliefs. It is easier to get agreement to reduce, for example, insomnia then to evaluate the correctness of a belief. Explaining the intervention is simply easier (e.g. ‘You aren’t sleeping well? Then we can work on improving your sleep and it should put you in a better state to tackle your other difficulties’). It is likely that the sorts of techniques covered will improve affect and improve flexibility in thinking, thus enabling more effective application of standard cognitive techniques that review the delusional belief and
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alternative explanations and allow behavioural testing of ideas. It is also of note that these brief modular treatments may be more easily disseminated to other professionals. 4. Difficulties There are difficulties in this work. Not every causal factor is relevant to every individual with delusions. For example, interventions for worry or insomnia are clearly not warranted for individuals without such difficulties. Perhaps only the reasoning intervention, which works on the problem of high conviction inherent in delusional ideas, is relevant to all. Therefore there will need to be a range of intervention techniques sufficient to capture the variety of causal factors in psychosis. And we will need measures of these causal processes that are sensitive to change. Further, whilst the focus on delusional beliefs reduces the heterogeneity of psychosis to an extent, outcome targets often vary: for example, reducing distress, reducing levels of conviction, or improving social functioning (e.g. Harrow et al., 2004; Birchwood and Trower, 2006; Fowler et al., 2009; Ben-Zeev et al., 2011). In clinical settings it should not be forgotten that the presence of multiple problems tends to be the rule, and therefore it would be useful to also examine the effect of other symptoms on the success of therapy. Moreover, fine judgements must be made on the length of interventions — what is optimal for producing long-term change? Treatment must be developed and refined from experimental manipulation to clinical intervention. When building a full intervention, there are also questions concerning the best order of therapeutic techniques. Finally, we should not lose sight of the fact that patients derive benefit simply from being listened to, from their distress being taken seriously, and from the clinician not being shocked, blaming, or rejecting. 5. Future work It is clear that delusions arise not from one or two factors, but from many. Therefore interventions must be developed and tested for other targets: for example, negative views of the self and others (e.g. Barrowclough et al., 2003; Hall and Tarrier, 2003; Fowler et al., 2006), anomalies of experience including perceptual disturbances, hallucinations, and dopamine-related salience (e.g. Maher, 1988; van Os, 2009; Smeets et al., 2010), interpersonal sensitivity (e.g. Freeman et al., 2008b), post-traumatic stress (e.g. Larkin and Morrison, 2006), emotion regulation (e.g. Myin-Germeys and van Os, 2007), attributional biases (e.g. Bentall et al., 2009), illicit substance use (e.g. Morrison et al., 2009), coping strategies (e.g. Lincoln et al., 2010a) and safety behaviours (e.g. Freeman et al., 2001). Tackling appraisals of psychotic experiences is also likely to prove beneficial (Lobban et al., 2004; Watson et al., 2006). There is also a need for interventions focussed on specific situations, for example helping patients cope with being outside in a crowded shopping street (Ellett et al., 2008) or in social relationships (Combs et al., 2007). And modifications may be needed for particular types of delusions (e.g. persecutory versus grandiose) and the presence of other psychotic symptoms. This will need to be informed by work determining the number of distinct delusion types. Current assessments vary in the items included and even sometimes whether the item is classified as a delusion or anomalous experience (e.g. delusion of control vs replacement of will experience). Factor analytic studies to date indicate at least two key general types of delusions: paranoid (reference/persecutory) and grandiose/bizarre (e.g. Vázquez-Barquero et al., 1996; Peralta and Cuesta, 1999; Kimhy et al., 2005; Yung et al., 2009; Wigman et al., 2011). The study of moderators of treatment outcome can also be built into the interventionist–causal approach. Preliminary evidence has been obtained for belief flexibility and prefrontal cortex activity as treatment specific moderators for standard CBT for psychosis (Garety et al., 1997; Kumari et al., 2009). Information gained about moderators, which may be specific to a particular form and type of intervention, can then be
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used to refine and improve the techniques. Another key issue that requires careful scrutiny is the interaction between psychological and pharmacological treatments (e.g. Kingdon et al., 2007; Christodoulides et al., 2008). Technologies such as virtual reality could also be introduced into treatment, allowing a safer environment for patients to try behavioural experiments and practise new coping strategies (Freeman, 2008). It is likely to prove beneficial to include individuals' own accounts of how they helped themselves (e.g. Chapman, 2002; Adam, 2011; see website www.paranoidthoughts.com). Testing of self-help methods based upon the new understanding of delusions will also be valuable (Freeman et al., 2008a; Morrison et al., 2008). Examination of how best to disseminate the new work into services will be needed (e.g. Granholm et al., 2010; Rathod et al., 2010). These are just a number of the areas requiring attention in the development of better treatments for individuals with delusions. Certainly it is no longer considered preferable to discourage discussion of delusions; we are instead entering an exciting period of finding out how best to address them directly. Role of funding source The paper was not reviewed by the funder. Contributors The paper was written by Daniel Freeman. Conflict of interest None. Acknowledgment Daniel Freeman is supported by a Medical Research Council (MRC) Senior Clinical Fellowship.
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National Institute for Health and Clinical Excellence, 2009. Schizophrenia: Core Interventions in the Treatment and Management of Schizophrenia in Primary and Secondary Care (Update). NICE, London. Pearl, J., 2009. Causality: Models, Reasoning and Inference. Cambridge University Press, New York. Peralta, V., Cuesta, M.J., 1999. Dimensional structure of psychotic symptoms: an itemlevel analysis of SAPS and SANS symptoms in psychotic disorders. Schizophr. Res. 38, 13–26. Rathod, S., Kingdon, D., Phiri, P., Gobbi, M., 2010. Developing culturally sensitive cognitive behaviour therapy for psychosis for ethnic minority patients by exploration and incorporation of service users' and health professionals' views and opinions. Behav. Cogn. Psychother. 38, 511–533. Ross, K., Freeman, D., Dunn, G., Garety, P., 2011. Can jumping to conclusions be reduced in people with delusions? An experimental investigation of a brief reasoning training module. Schizophr. Bull. 37, 324–333. Shadish, W.R., Cook, T.D., Campbell, D.T., 2002. Experimental and Quasi- Experimental Designs for Generalised Causal Inference. Houghton Mifflin, Boston, MA. Smeets, F., Lataster, T., Dominguez, M., Hommes, J., Lieb, R., Wittchen, H., van Os, J., 2010. Evidence that onset of psychosis in the population reflects early hallucinatory experiences that through environmental risks and affective dysregulation become complicated by delusions. Schizophr. Bull. doi:10.1093/schbul/sbq117. Smith, M.T., Huang, M.I., Manber, R., 2005. Cognitive behaviour therapy for chronic insomnia occurring within the context of medical and psychiatric disorders. Clin. Psychol. Rev. 25, 559–592. Startup, H., Freeman, D., Garety, P.A., 2007. Persecutory delusions and catastrophic worry in psychosis: developing the understanding of delusion distress and persistence. Behav. Res. Ther. 45, 523–537. Vázquez-Barquero, J.L., Lastra, I., Nuñez, M.J.C., Castanedo, S.H., Dunn, G., 1996. Patterns of positive and negative symptoms in first episode schizophrenia. Br. J. Psychiatry 168, 693–701. van der Gaag, M., 2006. A neuropsychiatric model of biological and psychological processes in the remission of delusions and auditory hallucinations. Schizophr. Bull. 32, s113–s122. Van Os, J., 2009. A salience dysregulation syndrome. Br. J. Psychiatry 194, 101–103. Waller, W., Freeman, D., Jolley, S., Dunn, G., Garety, P., 2011. Targeting reasoning biases in delusions. J. Behav. Ther. Exp. Psychiatry 42, 414–421. Watson, P.W.B., Garety, P.A., Weinman, J., Dunn, G., Bebbington, P.E., Fowler, D., Freeman, D., Kuipers, E., 2006. Emotional dysfunction in schizophrenia spectrum psychosis: the role of illness perceptions. Psychol. Med. 36, 761–770. Wigman, J.T.W., Vollebergh, W.A.M., Raaijmakers, Q.A.W., Iedema, J., van Dorsselaer, S., Ormel, J., Verhulst, F.C., van Os, J., 2011. The structure of the extended psychosis phenotype in early adolescence — a cross-sample replication. Schizophr. Bull. 37, 850–860. Woodward, J., 2003. Making Things Happen: A Theory of Causal Explanation. Oxford University Press, New York. Wykes, T., Steel, C., Everitt, B., Tarrier, N., 2008. Cognitive behaviour therapy for schizophrenia: effect sizes, clinical models, and methodological rigor. Schizophr. Bull. 34, 523–537. Yung, A.R., Nelson, B., Baker, K., Buckby, J.A., Baksheev, G., Cosgrave, E.M., 2009. Psychotic-like experiences in a community sample of adolescents. Aust. N. Z. J. Psychiatry 43, 118–128. Zimmermann, G., Favrod, J., Trieu, V.H., Pomini, V., 2005. The effect of cognitive behavioural treatment on the positive symptoms of schizophrenia spectrum disorders: a meta-analysis. Schizophr. Res. 77, 1–9.
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Schizophrenia Research journal homepage: www.elsevier.com/locate/schres
Review
Improving cognitive treatments for delusions Daniel Freeman ⁎ Department of Psychiatry, Oxford University, UK
a r t i c l e
i n f o
Article history: Received 2 February 2011 Received in revised form 6 August 2011 Accepted 22 August 2011 Available online 9 September 2011 Keywords: Delusions Cognitive therapy Schizophrenia
a b s t r a c t A clear challenge for schizophrenia research is to improve markedly the efficacy of psychological treatments for delusional beliefs. Effect sizes for the first generation of cognitive approaches are weak to moderate. These therapies now lag behind the transformation over the past ten years in understanding the causes of delusions. This paper advocates an interventionist–causal model approach: to focus on one putative causal factor at a time, show that an intervention can change it, and examine the subsequent effects on the delusional beliefs. A number of new studies that illustrate this approach with patients with schizophrenia spectrum disorders who have not responded to previous treatment are reviewed. These early stage studies show great promise in terms of efficacy, although remain to be subjected to methodologically rigorous evaluation. The advantages and difficulties of the interventionist approach applied to psychosis are considered, and future studies are highlighted. The importance for clinical services of cognitive approaches to psychosis will increase further if the theoretical advances can be translated into treatment. © 2011 Elsevier B.V. All rights reserved.
1. Introduction The first generation of cognitive–behavioural treatments for psychosis have demonstrated efficacy for treating delusions and hallucinations (see meta-analyses by Gould et al., 2004; Zimmermann et al., 2005; Wykes et al., 2008; NICE, 2009). A shift has occurred from encouraging patients not to talk about their psychotic symptoms to an appreciation that, if done in the correct way, it can be beneficial. However, the efficacy of these first generation therapies is weak to moderate, with effect sizes of about 0.4 (Wykes et al., 2008), though notably not dissimilar to that of clozapine (Leucht et al., 2009). When assessed, it has not been shown that the standard therapy changes the factors thought to cause the psychotic symptoms (e.g. Garety et al., 2008). The therapy lags behind the substantial developments in the theoretical understanding of experiences such as delusions and hallucinations. The situation may well be analogous to the CBT treatment of anxiety. Initial approaches had moderate outcome effect sizes that were then greatly increased by the development of disorder-specific and theoretically driven cognitive therapies (e.g. Clark, 2004). 2. Ideas underpinning improvement How can CBT for psychosis move forward? The approach recommended here is to follow three principles: reduce the heterogeneity of psychosis by focussing on single symptoms; use developments in the theoretical understanding to guide therapy; and show that putative causal processes ⁎ Oxford Cognitive Approaches to Psychosis (O-CAPS), Department of Psychiatry, Oxford University, Warneford Hospital, Oxford, OX3 7JX, UK. E-mail address: [email protected]. 0920-9964/$ – see front matter © 2011 Elsevier B.V. All rights reserved. doi:10.1016/j.schres.2011.08.012
have been changed, in what has been termed an interventionist–causal model approach (see Kendler and Campbell, 2009). Psychosis in typical clinical settings is complex — a truism but worth restating. Individuals frequently present with multifaceted delusions that occur in the context of anomalous experiences such as hallucinations and perceptual disturbances; with emotional disorders such as anxiety and depression; and with long-standing social difficulties. Each can affect the other. However, factor analysis has identified distinct types of psychotic experience and at least four even within the restricted category of positive symptoms (e.g. Vázquez-Barquero et al., 1996; Peralta and Cuesta, 1999; Wigman et al., 2011). This makes clinical sense — experiences such as persecutory delusions, grandiose delusions, auditory hallucinations and thought disorder present as different phenomena at clinical interview. Their co-occurrence in clinical settings is inflated by Berkson's bias (Maric et al., 2004; Bak et al., 2005). In essence, more complex cases will be admitted to hospital or seen by a health professional, inflating estimates of symptom associations. Therefore a sensible strategy for the treatment of psychosis is to focus on single psychotic symptoms or single factor types. At the very least this should ensure that techniques are tested with people with similar problems and that there is a similar outcome target, but it will also, of course, enable the application of detailed theoretical models. The task becomes more specified. The last ten years have seen an undoubted transformation in understanding psychotic symptoms. Arguably the most significant advances have come in delusion research (see reviews by Bentall et al., 2001; van der Gaag, 2006; Freeman, 2007; Garety et al., 2007; Beck et al., 2008; Langdon et al., 2008; Howes and Kapur, 2009; Murray, 2011). A range of emotional, cognitive, biological and social factors have been identified that, in combination, provide plausible accounts of delusion
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development and maintenance. In the rare instances that these types of factors have been assessed in randomised controlled trials pre- and post-CBT, which is the only way that treatment-specific effects can be definitively determined, they have not been shown to change with therapy (Garety et al., 2008). Reasoning biases, skewed views of the self and others (frequently based on adverse life experiences), rumination, interpersonal sensitivity, catastrophic appraisals, and avoidance behaviours have all been plausibly linked to delusions, but it has not been shown that CBT alters them in patients with psychosis. The argument is that we need to go back to basics and show that we can alter the key processes. To paraphrase, good theory can be very practical. This ties in with calls by statisticians and philosophers of science, and now a number of psychologists and psychiatrists in relation to the topic of mental health, for the need to illuminate causal inference by use of an ‘interventionist–causal model’ approach (see Table 1). Causation is substantiated by examining the effect of intervening on or manipulating the putative causal factor. As Kendler and Campbell (2009) put it: ‘The interventionist model says that questions about whether X causes Y are questions about what would happen to Y if there were an intervention on X.’ In turn this provides intervention techniques. If you change the causal factor and there are reductions in the psychotic experience then your manipulation method has the potential to prove a treatment technique. However, there are caveats. Most causes are ‘inus conditions’ — ‘an insufficient but non-redundant part of an unnecessary but sufficient condition’ (Mackie, 1974). Most effects result from a combination of causes and each cause generally only increases the probability of an effect occurring. Further, whilst convincing and most likely sufficient for clinical purposes, this method does not of itself necessarily demonstrate the mechanisms through which the causal relationship holds (Shadish et al., 2002) — this would still require a further mediational analysis (see Emsley et al. (2010) for a description of new statistical methods). 3. New treatment studies of delusions This process of improving treatments for delusions has begun, and a number of examples by the author and colleagues will be noted. One of the most convincing early demonstrations has concerned the use of worry reduction techniques. Research has shown that levels of worry in individuals with persecutory delusions are often comparable to those in generalised anxiety disorder, that the tendency to worry is a predictor of the occurrence of paranoid thinking, that levels of worry predict the persistence of persecutory delusions and that worry makes the delusional ideas more distressing (Freeman and Garety, 1999; Morrison and Wells, 2007; Startup et al., 2007; Freeman et al., 2008b; Bassett et al., 2009). A worry cognitive style brings Table 1 The interventionist–causal approach. ‘The paradigmatic assertion in causal relationships is that manipulation of a cause will result in the manipulation of an effect’ Cook and Campbell (1979). ‘The very essence of causation is the ability to predict the consequences of new manipulations. Viewing causality this way explains why scientists pursue causal explanations with such zeal and why it is accompanied by a sense of gaining deep understanding and being in control.’ Pearl (2009). ‘The distinguishing feature of causal explanations is that they are explanations that furnish information that is potentially relevant to manipulation and control’ Woodward (2003). ‘It [the interventionist–causal approach] connects causation with the practical interests of psychiatry, defining causation in terms of what would happen under interventions, a question of key interest to those of us whose interest is ultimately in intervening to prevent and treat illness’ Kendler and Campbell (2009). ‘In order to test our cognitive models of anxiety disorders, we have had to develop experiments in which the cognitive abnormalities and maintaining processes specified in the models are manipulated in order to see whether they have the predicted effects on symptoms. The experiments, when successful, have often become incorporated into the full treatment programmes.’ Clark (2004).
implausible ideas to mind, keeps them there, and makes the experience more distressing. In a recent pilot randomised controlled trial, involving 24 patients with persistent persecutory delusions and worry in the context of a psychotic disorder, the effects of a cognitive behavioural worry reduction intervention were evaluated (Foster et al., 2010). The worry reduction intervention was brief, comprising just four one-hour sessions over four weeks, and did not address the content of paranoid fears. The main techniques were psychoeducation about worry, reviewing positive and negative beliefs about worry, increasing awareness of the start of a worry episode and identification of individual triggers, learning to ‘let go’ of worry, use of worry periods, substituting problem-solving for worry, and relaxation exercises. Half the patients were randomised to the intervention in addition to their standard psychiatric care and half were randomised to the control group (standard psychiatric care). Assessments were carried out at baseline, end of treatment (one month), and at follow-up (two months). The intervention led to a large reduction in worry (effect size= 1.05) and also in persecutory delusions (effect size= 1.35) (effect sizes calculated for the treatment group's change in scores relative to the control group). These reductions were maintained at follow-up. One in three patients showed a 25% or greater reduction in worry and delusions. Changes in worry were associated with changes in persecutory delusions. The study was successful in changing the putative causal factor, leading to a reduction in delusions. A larger and more rigorous evaluation of this intervention is starting at the end of 2011 (Freeman et al., 2011a). The treatment of worry in patients with delusions has recently been approached from a different angle, inspired by work on written emotional disclosure (e.g. Gortner et al., 2006). One route by which worry may cause more delusion-related distress is by impeding emotional processing of upsetting paranoid experiences. Facilitating emotional processing should therefore reduce levels of worry and paranoia distress. Hence a new brief treatment – Emotional Processing and Metacognitive Awareness (EPMA) – was evaluated with twelve patients with persistent persecutory delusions (Hepworth et al., 2011). The intervention focussed on patients retelling recent paranoid experiences in an experiential manner (i.e. simply describing and fully experiencing their thoughts, sensations and feelings at the time) rather than a ruminative/evaluative fashion. This approximates written emotional expression interventions. But patients were also encouraged to gain distance from their mental experiences, by, for example, discriminating between thoughts, feelings and memories, and writing down particularly troubling words on pieces of paper and scrunching them up and throwing them away. This metacognitive aspect of the intervention overlaps with recent mindfulness and ACT approaches to psychosis (e.g. Chadwick et al., 2009; Gaudiano et al., 2010). All participants received the three session intervention and the delusions were assessed during a baseline period, post intervention, and at a one month follow-up. Levels of worry were reduced (effect size = 0.6), and it was also found that EPMA particularly reduced levels of delusion distress (effect size = 1.03), outcomes that were maintained at follow-up. Nine of the patients reported a greater than 25% reduction in paranoia distress. These preliminary data indicate that simply allowing individuals to talk about their delusional experiences, in the right way, can be strikingly helpful in itself. The latest empirical research has directly linked insomnia to the development of delusional thinking. Clinical insomnia is present in a high proportion of individuals with persecutory delusions; there are substantial associations between difficulties sleeping and persecutory ideation; and insomnia raises the risk of both the development and persistence of paranoid thinking (Freeman et al., 2009, 2010, 2011b, in press). The link is highly plausible, since earlier work shows that insomnia leads to anxiety, depression and anomalies of experience (e.g. Luby et al., 1960; Breslau et al., 1996; Morphy et al., 2007), each of which are risk factors for paranoid thinking. Of course, if
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patients are reporting insomnia then this should be a target for intervention in its own right, and well-evaluated cognitive–behavioural interventions are available (see Morin et al., 1999; Smith et al., 2005; Espie, 2006; Freeman and Freeman, 2010). However, from the interventionist–causal model approach the prediction is that treating the insomnia will also lead to a reduction in delusions. This is exactly what was found in a case series of 15 patients with persistent persecutory delusions (Myers et al., 2011). Following a four-session sleep intervention, significant reductions were found in levels of insomnia (effect size = 2.64) and the persecutory delusions (effect size = 1.07). At least two thirds of participants made substantial improvements in insomnia and approximately half showed substantial reductions in the persecutory delusions. This was an uncontrolled test, but at the very least it indicates that standard CBT for insomnia is appropriate for people with psychosis, and may well bring significant additional benefits. Reasoning processes are inherently implicated in delusional beliefs. The most replicated finding has been that individuals with delusions tend to gather less evidence before making a decision, a process termed ‘jumping to conclusions’ (see reviews by Fine et al., 2007; Freeman, 2007; Garety and Freeman, 1999). This seems to lead to less willingness to consider alternative explanations for events (belief inflexibility) and to higher levels of conviction in the belief (Freeman et al., 2004; Garety et al., 2005; Freeman et al., 2008c). Therefore jumping to conclusions and belief inflexibility have now been targeted. Ross et al. (2011) used a very brief reasoning programme, presented on a computer and featuring only abstract materials. (Two parts of the programme were adapted from the meta-cognitive training programme of Moritz et al. (2011), who take a rather different approach. Over eight weeks they provide education about a large number of psychological biases to a group of patients with schizophrenia.) The effects of the 45-minute programme evaluated by Ross et al. (2011), with 34 patients with delusions randomised to either the reasoning programme or an attention control condition, were modest. Reasoning training significantly improved data-gathering, and a small number of participants experienced changes in delusional conviction. Lincoln et al. (2010b) have also shown that the reasoning bias can be directly manipulated. Arising from this work the Maudsley Review Training Programme has now been developed. The original programme used by Ross et al. (2011) has been substantially altered and extended, specifically by adding new sections, delusion relevant material, interactive components and video clips, and handouts summarising key points. The length of the training has doubled. Its efficacy has been initially evaluated with 13 patients with persistent persecutory delusions in an ABA design (Waller et al., 2011). There were improvements in JTC (effect size=0.30), belief flexibility (effect size=0.82) and delusional conviction (effect size=1.06) between preand post-intervention measures. This brief intervention, enhancing reasoning skills and setting the scene for directly addressing the contents of a delusion, is likely best followed by other intervention techniques (e.g. behavioural tests). The techniques presented in these studies that have explicitly adopted an interventionist–causal model approach must be scrutinised with greater methodological rigour. But the effect sizes in these studies are very promising, especially when it is considered how long the patients have held their delusions despite attempts at other treatments and the brevity of the interventions. Importantly, these techniques seem to encourage higher levels of engagement because they work on problems that have been agreed with the patient and that do not directly dispute the validity of delusional beliefs. It is easier to get agreement to reduce, for example, insomnia then to evaluate the correctness of a belief. Explaining the intervention is simply easier (e.g. ‘You aren’t sleeping well? Then we can work on improving your sleep and it should put you in a better state to tackle your other difficulties’). It is likely that the sorts of techniques covered will improve affect and improve flexibility in thinking, thus enabling more effective application of standard cognitive techniques that review the delusional belief and
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alternative explanations and allow behavioural testing of ideas. It is also of note that these brief modular treatments may be more easily disseminated to other professionals. 4. Difficulties There are difficulties in this work. Not every causal factor is relevant to every individual with delusions. For example, interventions for worry or insomnia are clearly not warranted for individuals without such difficulties. Perhaps only the reasoning intervention, which works on the problem of high conviction inherent in delusional ideas, is relevant to all. Therefore there will need to be a range of intervention techniques sufficient to capture the variety of causal factors in psychosis. And we will need measures of these causal processes that are sensitive to change. Further, whilst the focus on delusional beliefs reduces the heterogeneity of psychosis to an extent, outcome targets often vary: for example, reducing distress, reducing levels of conviction, or improving social functioning (e.g. Harrow et al., 2004; Birchwood and Trower, 2006; Fowler et al., 2009; Ben-Zeev et al., 2011). In clinical settings it should not be forgotten that the presence of multiple problems tends to be the rule, and therefore it would be useful to also examine the effect of other symptoms on the success of therapy. Moreover, fine judgements must be made on the length of interventions — what is optimal for producing long-term change? Treatment must be developed and refined from experimental manipulation to clinical intervention. When building a full intervention, there are also questions concerning the best order of therapeutic techniques. Finally, we should not lose sight of the fact that patients derive benefit simply from being listened to, from their distress being taken seriously, and from the clinician not being shocked, blaming, or rejecting. 5. Future work It is clear that delusions arise not from one or two factors, but from many. Therefore interventions must be developed and tested for other targets: for example, negative views of the self and others (e.g. Barrowclough et al., 2003; Hall and Tarrier, 2003; Fowler et al., 2006), anomalies of experience including perceptual disturbances, hallucinations, and dopamine-related salience (e.g. Maher, 1988; van Os, 2009; Smeets et al., 2010), interpersonal sensitivity (e.g. Freeman et al., 2008b), post-traumatic stress (e.g. Larkin and Morrison, 2006), emotion regulation (e.g. Myin-Germeys and van Os, 2007), attributional biases (e.g. Bentall et al., 2009), illicit substance use (e.g. Morrison et al., 2009), coping strategies (e.g. Lincoln et al., 2010a) and safety behaviours (e.g. Freeman et al., 2001). Tackling appraisals of psychotic experiences is also likely to prove beneficial (Lobban et al., 2004; Watson et al., 2006). There is also a need for interventions focussed on specific situations, for example helping patients cope with being outside in a crowded shopping street (Ellett et al., 2008) or in social relationships (Combs et al., 2007). And modifications may be needed for particular types of delusions (e.g. persecutory versus grandiose) and the presence of other psychotic symptoms. This will need to be informed by work determining the number of distinct delusion types. Current assessments vary in the items included and even sometimes whether the item is classified as a delusion or anomalous experience (e.g. delusion of control vs replacement of will experience). Factor analytic studies to date indicate at least two key general types of delusions: paranoid (reference/persecutory) and grandiose/bizarre (e.g. Vázquez-Barquero et al., 1996; Peralta and Cuesta, 1999; Kimhy et al., 2005; Yung et al., 2009; Wigman et al., 2011). The study of moderators of treatment outcome can also be built into the interventionist–causal approach. Preliminary evidence has been obtained for belief flexibility and prefrontal cortex activity as treatment specific moderators for standard CBT for psychosis (Garety et al., 1997; Kumari et al., 2009). Information gained about moderators, which may be specific to a particular form and type of intervention, can then be
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used to refine and improve the techniques. Another key issue that requires careful scrutiny is the interaction between psychological and pharmacological treatments (e.g. Kingdon et al., 2007; Christodoulides et al., 2008). Technologies such as virtual reality could also be introduced into treatment, allowing a safer environment for patients to try behavioural experiments and practise new coping strategies (Freeman, 2008). It is likely to prove beneficial to include individuals' own accounts of how they helped themselves (e.g. Chapman, 2002; Adam, 2011; see website www.paranoidthoughts.com). Testing of self-help methods based upon the new understanding of delusions will also be valuable (Freeman et al., 2008a; Morrison et al., 2008). Examination of how best to disseminate the new work into services will be needed (e.g. Granholm et al., 2010; Rathod et al., 2010). These are just a number of the areas requiring attention in the development of better treatments for individuals with delusions. Certainly it is no longer considered preferable to discourage discussion of delusions; we are instead entering an exciting period of finding out how best to address them directly. Role of funding source The paper was not reviewed by the funder. Contributors The paper was written by Daniel Freeman. Conflict of interest None. Acknowledgment Daniel Freeman is supported by a Medical Research Council (MRC) Senior Clinical Fellowship.
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