Schizophrenia Research 132 (2011) 135–139

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Schizophrenia Research

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Review

Improving cognitive treatments for delusions

Daniel Freeman ⁎Department of Psychiatry, Oxford University, UK

⁎ Oxford Cognitive Approaches to Psychosis (O-CAPOxford University, Warneford Hospital, Oxford, OX3 7JX

E-mail address: daniel.freeman@psych.ox.ac.uk.

0920-9964/$ – see front matter © 2011 Elsevier B.V. Alldoi:10.1016/j.schres.2011.08.012

a b s t r a c t

a r t i c l e i n f o

Article history:Received 2 February 2011Received in revised form 6 August 2011Accepted 22 August 2011Available online 9 September 2011

Keywords:DelusionsCognitive therapySchizophrenia

A clear challenge for schizophrenia research is to improve markedly the efficacy of psychological treatmentsfor delusional beliefs. Effect sizes for the first generation of cognitive approaches are weak to moderate. Thesetherapies now lag behind the transformation over the past ten years in understanding the causes of delu-sions. This paper advocates an interventionist–causal model approach: to focus on one putative causal factorat a time, show that an intervention can change it, and examine the subsequent effects on the delusional be-liefs. A number of new studies that illustrate this approach with patients with schizophrenia spectrum disor-ders who have not responded to previous treatment are reviewed. These early stage studies show greatpromise in terms of efficacy, although remain to be subjected to methodologically rigorous evaluation. Theadvantages and difficulties of the interventionist approach applied to psychosis are considered, and futurestudies are highlighted. The importance for clinical services of cognitive approaches to psychosis will increasefurther if the theoretical advances can be translated into treatment.

S), Department of Psychiatry,, UK.

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© 2011 Elsevier B.V. All rights reserved.

1. Introduction

Thefirst generation of cognitive–behavioural treatments for psycho-sis 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 encouragingpatients not to talk about their psychotic symptoms to an appreciationthat, if done in the correctway, it can be beneficial. However, the efficacyof these first generation therapies is weak tomoderate, with effect sizesof about 0.4 (Wykes et al., 2008), though notably not dissimilar to that ofclozapine (Leucht et al., 2009). When assessed, it has not been shownthat the standard therapy changes the factors thought to cause the psy-chotic symptoms (e.g. Garety et al., 2008). The therapy lags behind thesubstantial developments in the theoretical understanding of experi-ences such as delusions and hallucinations. The situation may well beanalogous to the CBT treatment of anxiety. Initial approaches hadmod-erate outcome effect sizes thatwere then greatly increased by the devel-opment of disorder-specific and theoretically driven cognitive therapies(e.g. Clark, 2004).

2. Ideas underpinning improvement

HowcanCBT forpsychosismove forward?Theapproach recommendedhere is to follow three principles: reduce the heterogeneity of psychosis byfocussing on single symptoms; use developments in the theoretical un-derstanding to guide therapy; and show that putative causal processes

have been changed, in what has been termed an interventionist–causalmodel approach (see Kendler and Campbell, 2009).

Psychosis in typical clinical settings is complex — a truism but worthrestating. Individuals frequently present with multifaceted delusionsthat occur in the context of anomalous experiences such as hallucinationsand perceptual disturbances; with emotional disorders such as anxietyand depression; andwith long-standing social difficulties. Each can affectthe other. However, factor analysis has identified distinct types of psy-chotic experience and at least four even within the restricted categoryof positive symptoms (e.g. Vázquez-Barquero et al., 1996; Peralta andCuesta, 1999; Wigman et al., 2011). This makes clinical sense — experi-ences such as persecutory delusions, grandiose delusions, auditoryhallucinations and thought disorder present as different phenomena atclinical interview. Their co-occurrence in clinical settings is inflated byBerkson's bias (Maric et al., 2004; Bak et al., 2005). In essence,more com-plex cases will be admitted to hospital or seen by a health professional,inflating estimates of symptom associations. Therefore a sensiblestrategy for the treatment of psychosis is to focus on single psy-chotic symptoms or single factor types. At the very least thisshould ensure that techniques are tested with people with similarproblems 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 under-standing psychotic symptoms. Arguably the most significant advanceshave 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). Arange of emotional, cognitive, biological and social factors have beenidentified that, in combination, provide plausible accounts of delusion

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development andmaintenance. In the rare instances that these types offactors have been assessed in randomised controlled trials pre- andpost-CBT, which is the only way that treatment-specific effects can bedefinitively determined, they have not been shown to change withtherapy (Garety et al., 2008). Reasoning biases, skewed views of theself and others (frequently based on adverse life experiences), rumina-tion, interpersonal sensitivity, catastrophic appraisals, and avoidancebehaviours have all been plausibly linked to delusions, but it has notbeen shown that CBT alters them in patients with psychosis. The argu-ment is that we need to go back to basics and show that we can alterthe 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 tothe topic of mental health, for the need to illuminate causal inferenceby use of an ‘interventionist–causal model’ approach (see Table 1).Causation is substantiated by examining the effect of intervening onor manipulating the putative causal factor. As Kendler and Campbell(2009) put it: ‘The interventionist model says that questions aboutwhether X causes Y are questions about what would happen to Y ifthere were an intervention on X.’ In turn this provides interventiontechniques. If you change the causal factor and there are reductionsin the psychotic experience then your manipulation method has thepotential to prove a treatment technique. However, there are caveats.Most causes are ‘inus conditions’ — ‘an insufficient but non-redundantpart of an unnecessary but sufficient condition’ (Mackie, 1974). Mosteffects result from a combination of causes and each cause generallyonly increases the probability of an effect occurring. Further, whilst con-vincing andmost likely sufficient for clinical purposes, thismethod doesnot of itself necessarily demonstrate themechanisms throughwhich thecausal relationship holds (Shadish et al., 2002)— thiswould still requirea furthermediational analysis (see Emsley et al. (2010) for a descriptionof new statistical methods).

3. New treatment studies of delusions

This process of improving treatments for delusions has begun, anda number of examples by the author and colleagues will be noted.One of the most convincing early demonstrations has concerned theuse of worry reduction techniques. Research has shown that levelsof worry in individuals with persecutory delusions are often compa-rable to those in generalised anxiety disorder, that the tendency toworry is a predictor of the occurrence of paranoid thinking, that levelsof worry predict the persistence of persecutory delusions and thatworry makes the delusional ideas more distressing (Freeman andGarety, 1999; Morrison andWells, 2007; Startup et al., 2007; Freemanet al., 2008b; Bassett et al., 2009). A worry cognitive style brings

Table 1The interventionist–causal approach.

‘The paradigmatic assertion in causal relationships is that manipulation of a causewill result in the manipulation of an effect’ Cook and Campbell (1979).‘The very essence of causation is the ability to predict the consequences of newmanipulations. Viewing causality this way explains why scientists pursuecausal explanations with such zeal and why it is accompanied by a sense ofgaining deep understanding and being in control.’ Pearl (2009).

‘The distinguishing feature of causal explanations is that they are explanations thatfurnish information that is potentially relevant to manipulation and control’Woodward (2003).

‘It [the interventionist–causal approach] connects causation with the practicalinterests of psychiatry, defining causation in terms of what would happenunder interventions, a question of key interest to those of us whose interest isultimately 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 developexperiments in which the cognitive abnormalities and maintaining processesspecified in the models are manipulated in order to see whether they have thepredicted effects on symptoms. The experiments, when successful, have oftenbecome incorporated into the full treatment programmes.’ Clark (2004).

implausible ideas to mind, keeps them there, and makes the experi-ence more distressing. In a recent pilot randomised controlled trial,involving 24 patients with persistent persecutory delusions andworry in the context of a psychotic disorder, the effects of a cognitivebehavioural worry reduction intervention were evaluated (Foster etal., 2010). The worry reduction intervention was brief, comprisingjust four one-hour sessions over four weeks, and did not address thecontent of paranoid fears. The main techniques were psychoeducationabout worry, reviewing positive and negative beliefs about worry, in-creasing awareness of the start of a worry episode and identificationof individual triggers, learning to ‘let go’ of worry, use of worry periods,substituting problem-solving for worry, and relaxation exercises. Halfthe patients were randomised to the intervention in addition to theirstandard psychiatric care and half were randomised to the controlgroup (standard psychiatric care). Assessments were carried out atbaseline, end of treatment (one month), and at follow-up (twomonths). The intervention led to a large reduction in worry (effectsize=1.05) and also in persecutory delusions (effect size=1.35) (ef-fect sizes calculated for the treatment group's change in scores relativeto the control group). These reductions were maintained at follow-up.One in three patients showed a 25% or greater reduction in worry anddelusions. Changes in worry were associated with changes in persecu-tory delusions. The studywas successful in changing the putative causalfactor, leading to a reduction in delusions. A larger and more rigorousevaluation of this intervention is starting at the end of 2011 (Freemanet al., 2011a).

The treatment of worry in patients with delusions has recentlybeen approached from a different angle, inspired by work on writ-ten emotional disclosure (e.g. Gortner et al., 2006). One route bywhich worry may cause more delusion-related distress is by imped-ing emotional processing of upsetting paranoid experiences. Facili-tating emotional processing should therefore reduce levels ofworry and paranoia distress. Hence a new brief treatment – Emo-tional Processing and Metacognitive Awareness (EPMA) – was eval-uated with twelve patients with persistent persecutory delusions(Hepworth et al., 2011). The intervention focussed on patients re-telling recent paranoid experiences in an experiential manner (i.e.simply describing and fully experiencing their thoughts, sensationsand feelings at the time) rather than a ruminative/evaluative fash-ion. This approximates written emotional expression interventions.But patients were also encouraged to gain distance from their men-tal experiences, by, for example, discriminating between thoughts,feelings and memories, and writing down particularly troublingwords on pieces of paper and scrunching them up and throwingthem away. This metacognitive aspect of the intervention overlapswith recent mindfulness and ACT approaches to psychosis (e.g.Chadwick et al., 2009; Gaudiano et al., 2010). All participants re-ceived the three session intervention and the delusions wereassessed during a baseline period, post intervention, and at a onemonth follow-up. Levels of worry were reduced (effect size=0.6),and it was also found that EPMA particularly reduced levels of delu-sion distress (effect size=1.03), outcomes that were maintained atfollow-up. Nine of the patients reported a greater than 25% reduc-tion in paranoia distress. These preliminary data indicate that sim-ply 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 thedevelopment of delusional thinking. Clinical insomnia is present in ahigh proportion of individuals with persecutory delusions; there aresubstantial associations between difficulties sleeping and persecutoryideation; and insomnia raises the risk of both the development andpersistence of paranoid thinking (Freeman et al., 2009, 2010, 2011b,in press). The link is highly plausible, since earlier work shows thatinsomnia 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 inter-vention in its own right, and well-evaluated cognitive–behaviouralinterventions are available (see Morin et al., 1999; Smith et al.,2005; Espie, 2006; Freeman and Freeman, 2010). However, from theinterventionist–causal model approach the prediction is that treatingthe insomnia will also lead to a reduction in delusions. This is exactlywhat was found in a case series of 15 patients with persistent perse-cutory delusions (Myers et al., 2011). Following a four-session sleepintervention, significant reductions were found in levels of insomnia(effect size=2.64) and the persecutory delusions (effectsize=1.07). At least two thirds of participants made substantial im-provements in insomnia and approximately half showed substantialreductions in the persecutory delusions. This was an uncontrolledtest, but at the very least it indicates that standard CBT for insomniais appropriate for people with psychosis, and may well bring signifi-cant additional benefits.

Reasoning processes are inherently implicated in delusional beliefs.The most replicated finding has been that individuals with delusionstend 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 lesswillingnessto consider alternative explanations for events (belief inflexibility) andto higher levels of conviction in the belief (Freeman et al., 2004; Garetyet al., 2005; Freeman et al., 2008c). Therefore jumping to conclusionsand belief inflexibility have now been targeted. Ross et al. (2011) useda very brief reasoning programme, presented on a computer and featur-ing only abstract materials. (Two parts of the programme were adaptedfrom themeta-cognitive training programme ofMoritz et al. (2011), whotake a rather different approach. Over eightweeks they provide educationabout a large number of psychological biases to a group of patients withschizophrenia.) The effects of the 45-minute programme evaluated byRoss et al. (2011), with 34 patients with delusions randomised to eitherthe reasoning programme or an attention control condition, weremodest. Reasoning training significantly improved data-gathering, and asmall number of participants experienced changes in delusionalconviction. Lincoln et al. (2010b) have also shown that the reasoningbias can be directly manipulated. Arising from this work the MaudsleyReview Training Programme has now been developed. The originalprogramme used by Ross et al. (2011) has been substantially alteredand extended, specifically by adding new sections, delusion relevantmaterial, interactive components and video clips, and handoutssummarising key points. The length of the training has doubled. Itsefficacy has been initially evaluated with 13 patients with persistentpersecutory delusions in an ABA design (Waller et al., 2011). Therewere improvements in JTC (effect size=0.30), belief flexibility (effectsize=0.82) and delusional conviction (effect size=1.06) between pre-and post-intervention measures. This brief intervention, enhancing rea-soning skills and setting the scene for directly addressing the contentsof a delusion, is likely best followed by other intervention techniques(e.g. behavioural tests).

The techniques presented in these studies that have explicitlyadopted an interventionist–causal model approach must be scrutinisedwith greater methodological rigour. But the effect sizes in these studiesare very promising, especially when it is considered how long the pa-tients have held their delusions despite attempts at other treatmentsand the brevity of the interventions. Importantly, these techniquesseem to encourage higher levels of engagement because they work onproblems that have been agreedwith the patient and that do not directlydispute the validity of delusional beliefs. It is easier to get agreement toreduce, for example, insomnia then to evaluate the correctness of a belief.Explaining the intervention is simply easier (e.g. ‘You aren’t sleepingwell? Then we can work on improving your sleep and it should putyou in a better state to tackle your other difficulties’). It is likely thatthe sorts of techniques covered will improve affect and improveflexibility in thinking, thus enablingmore effective application of stan-dard cognitive techniques that review the delusional belief and

alternative explanations and allow behavioural testing of ideas. It isalso of note that these briefmodular treatmentsmay bemore easily dis-seminated to other professionals.

4. Difficulties

There are difficulties in this work. Not every causal factor is rele-vant to every individual with delusions. For example, interventionsfor worry or insomnia are clearly not warranted for individuals with-out such difficulties. Perhaps only the reasoning intervention, whichworks on the problem of high conviction inherent in delusionalideas, is relevant to all. Therefore there will need to be a range of inter-vention techniques sufficient to capture the variety of causal factors inpsychosis. And we will need measures of these causal processes thatare sensitive to change. Further, whilst the focus on delusional beliefsreduces the heterogeneity of psychosis to an extent, outcome targetsoften vary: for example, reducing distress, reducing levels of conviction,or improving social functioning (e.g. Harrow et al., 2004; Birchwoodand Trower, 2006; Fowler et al., 2009; Ben-Zeev et al., 2011). In clinicalsettings it should not be forgotten that the presence of multiple prob-lems tends to be the rule, and therefore it would be useful to also exam-ine the effect of other symptoms on the success of therapy. Moreover,fine judgements must be made on the length of interventions — whatis optimal for producing long-term change? Treatment must be devel-oped and refined from experimental manipulation to clinical interven-tion. When building a full intervention, there are also questionsconcerning the best order of therapeutic techniques. Finally, we shouldnot lose sight of the fact that patients derive benefit simply from beinglistened to, from their distress being taken seriously, and from the clini-cian not being shocked, blaming, or rejecting.

5. Future work

It is clear that delusions arise not from one or two factors, but frommany. Therefore interventions must be developed and tested forother 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 andMorrison, 2006), emotion regulation (e.g. Myin-Germeys and vanOs, 2007), attributional biases (e.g. Bentall et al., 2009), illicit sub-stance use (e.g. Morrison et al., 2009), coping strategies (e.g. Lincolnet al., 2010a) and safety behaviours (e.g. Freeman et al., 2001). Tack-ling appraisals of psychotic experiences is also likely to prove benefi-cial (Lobban et al., 2004; Watson et al., 2006). There is also a need forinterventions focussed on specific situations, for example helping pa-tients cope with being outside in a crowded shopping street (Ellett etal., 2008) or in social relationships (Combs et al., 2007). Andmodifica-tions may be needed for particular types of delusions (e.g. persecutoryversus grandiose) and the presence of other psychotic symptoms. Thiswill need to be informed bywork determining the number of distinct de-lusion types. Current assessments vary in the items included and evensometimes whether the item is classified as a delusion or anomalous ex-perience (e.g. delusion of control vs replacement of will experience). Fac-tor analytic studies to date indicate at least two key general types ofdelusions: 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 intothe interventionist–causal approach. Preliminary evidence has beenobtained for belief flexibility and prefrontal cortex activity as treatmentspecific moderators for standard CBT for psychosis (Garety et al., 1997;Kumari et al., 2009). Information gained about moderators, which maybe 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 re-quires careful scrutiny is the interaction between psychological andpharmacological treatments (e.g. Kingdon et al., 2007; Christodoulideset al., 2008). Technologies such as virtual reality could also be intro-duced into treatment, allowing a safer environment for patients to trybehavioural experiments and practise new coping strategies (Freeman,2008). It is likely to prove beneficial to include individuals' own ac-counts of how they helped themselves (e.g. Chapman, 2002; Adam,2011; see website www.paranoidthoughts.com). Testing of self-helpmethods based upon the new understanding of delusions will also bevaluable (Freeman et al., 2008a; Morrison et al., 2008). Examination ofhow 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 numberof the areas requiring attention in the development of better treatmentsfor individuals with delusions. Certainly it is no longer considered pref-erable to discourage discussion of delusions; we are instead entering anexciting period of finding out how best to address them directly.

Role of funding sourceThe paper was not reviewed by the funder.

ContributorsThe paper was written by Daniel Freeman.

Conflict of interestNone.

AcknowledgmentDaniel Freeman is supported by a Medical Research Council (MRC) Senior Clinical

Fellowship.

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