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Deconstructingtheconceptof‘schizophrenia’

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Journal of Mental Health (1993) 2, 223-238

Deconstructing the concept of ‘schizophrenia’

RICHARD P BENTALL

Department of Clinical Psychology, Whelan Building, Liverpool University PO Box 147, Liverpool L.69 3BX

Abstract In this article I challenge two assumptions that inform much of traditional research into psychosis: the assumption that psychotic disorders fall into discrete types such as schizophrenia and the assumption that psychotic experiences and behaviour have no meaning. Illustrating my argument with recent research on hallucinations and delusions carried out at Liverpool University I show how scientific progress can be made by abandoning the concept of schizophrenia and focusing on particular symptoms. In addition to the scientific advantages of this approach, it has the further advantage of linking the experiences of mentally ill people to the experiences of ordinary people.

Introduction

‘Schizophrenia’ has been described as amongst the most serious of illnesses afflict- ing modem society. Between one half and one per cent of people in the developed world can expect to be diagnosed as ‘schizophrenic’ at some time in their lives (Torrey, 1987). Yet our understanding of ‘schizophrenia’ has not kept pace with our understanding of other serious diseases like cancer or heart disease. Many different theories have been proposed to account for the disorder, implicating vari- ables as diverse as childhood trauma, early family environment, life stresses, neuropsych- ological, neurophysiological and neuroana- tomical abnormalities, diet, genetic endow- ment and even exposure to viruses (Neale & Oltmans, 1980). Indeed, it is no exaggeration to say that every variable known to influence human behaviour has, at one time or another, been identified as a potential cause of ‘schizo- phrenia’.

In this article, in which I summarise some arguments I have developed at greater length in a series of previous publications, I will suggest that it is time to abandon the concept of ‘schizophrenia’, mainly because it has outlived its usefulness. This suggestion is usually attributed to sociological, anti- psychiatric or even antiscientific attitudes. However, I will attempt tojustify my position on scientific grounds, rather than on the basis of ethical or philosophical arguments. This is not because ethical or philosophical argu- ments are irrelevant to the question of how we construe mental illness but because I want to show that it is possible to challenge the traditional approach to psychiatric disorder using the kinds of evidence which should be highly valued by psychiatric researchers. Adopting this approach, I will argue that the concept of ‘schizophrenia’ has impeded the development of adequate scientific accounts of psychotic behaviour, that there are ways of thinking about psychotic behaviour which do

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224 Richard P Bentall

not depend on the kinds of diagnostic classi- fications in wide use today, and that these ways of thinking are more consistent with recent developments in the psychological and neurobiological sciences than what might be called ‘the standard approach’ in psycho- pathology. By way of illustrating this latter point, I will describe some of the research carried out by my colleagues and myself at Liverpool University, in order to show how it is possible to do meaningful scientific re- search into psychotic behaviour without re- course to the concept of ‘schizophrenia’.

The Standard Approach to ‘Schizophrenia’

It will help to remind ourselves of the origins of the concept of ‘schizophrenia’. Most current research into severe psycho- pathology takes as its starting point an approach to psychiatric classification which has evolved from the pioneering work of Emil Kraepelii in the second half of the last century. Although he lacked the statistical methods available to modem researchers, Kraepelin was one of the first psychopa- thologists to systematically collect data on the course and outcome of psychiatric dis- orders, believing that such data were cru- cial for the development of an adequate diagnostic system(Berrios &Hauser, 1988). When thinking about how these data might be interpreted he made a number of as- sumptions which seem over-simple when judged by the standards of today, but which were reasonable for his time:

‘Judging from our experience in internal medicine it is a fair assumption that similar disease processes will produce identical symptom pictures, identical pathological anatomy andan identical aetiology. If; there- fore, we possessed a comprehensive knowl- edge of any of these three fields - pathologi-

cal anatomy, symptomatology, or aetiology - we would at once have a uniform and stand- ard classification of mental diseases. A simi- lar comprehensive knowledge of either of the other two fields would give us not just as uniform and standard classifications, but all of these classifications would exactly coin- cide. ’

(Kraepelin (1907; quoted in Reider, 1974) Applying this kind of reasoning to the data

he had collected from his patients, Kraepelin believed that he had identified two major types of psychiatric disorder. On the one hand there was dementia praecox (under which category he grouped together a number of syndromes previously described by Morel, Hecker and Kahlbaum), characterised by early onset followed by a very poor outcome, and which was later renamed ‘schizophrenia’ by Bleuler(l911). Ontheotherhand,therewere the manic depressive psychoses character- ised by a later onset and better outcome. This distinction has informed all subsequent sys- tems of psychiatric classification (see Boyle, 1990, for a historical account beginning with Kraepelin and ending with the third edition of the American Psychiatric Association’s Di- agnostic and Statistical Manual) and has been described by Kendell and Gourlay (1970) as, ‘One of the cornerstones of modem psychia- by’. It is a distinction which has become increasingly problematic over the years be- cause many patients exhibit signs and symp toms belonging to both hypothetical syn- dromes. This latter observation has led some authors to suggest there may be a third cat- egory of ‘schizo-affective’ psychoses (Kasanin, 1933).

It is hard to overemphasise the impact of Kraepelin’s model on the research method- ologies which have been employed when investigating psychotic disorders. One im- plication of Kraepelin’s categorical approach to psychiatric classification is that patients

Deconstructing schizophrenia 225

should be studied according to their diag- noses. Not surprisingly, therefore, the most common paradigm for studying the psycho- ses involves comparing patients with a diag- nosis of ‘schizophrenia’ with individuals di- agnosed as ‘normal’ (or perhaps as suffering from some other kind of disorder), on the assumption that those suffering from ‘schizo- phrenia’ will have something in common (hopefully of aetiological significance) which will be absent in the case of those not suffer- ing from the disorder. This approach is almost as dominant in clinical psychology as it is in psychiatry. Sarbin and Mancuso (1980) surveyed The Journal of Abnormal and Social Psychology (later renamed The Jouml of Abnormal Psychology) between the years 1959 and 1978, finding that 374 papers totalling 15.3 percent of the journal space used the presence or absence of a diagnosis of ‘schizophrenia’ as an independ- ent variable in this way and there is no sign that psychologists’ enthusiasm for this kind of research has diminished in the years fol- lowing their report. Of course, if ‘schizo- phrenics’ do not, in fact, have something uniquely in common which is of aetiological significance then this strategy is doomed to yield weak and inconsistant findings.

When looking for variables on which to compare ‘schizophrenic’ and ‘nonschizo- phrenic’ individuals, most psychological re- searchers have assumed that ‘schizophrenia’ is a disorder which reflects dysfunctions in the biological systems that sustain core cog- nitive processes. This assumption reflects Bleuler’s (191 1) belief that ‘schizophrenic’ symptoms are products of an underlying dis- order of association and also Jaspers’ (1963) later assertion that true psychosis is ‘ununderstandable’ and hence inexplicable in terms of a patient’s personality or life experiences. The popularity of this approach in recent years to some extent reflects a

prevailing scientific Zeitgeist in which it is widely assumed that, ‘There is no such thing as apsychiatry which is too biological’ (Guze, 1989) and in which many clinicians believe that the model form of psychiatric treatment is by means of drugs prescribed following a psychiatric interview lasting approximately fifteen minutes (Andreasen, 1984).

An important but not often articulated dis- tinction which merits attention in this context is that between cognitive deficits and cogni- tive biases. Deficits concern what the patient cannot do and are typically studied using emotionally neutral tests, such as traditional memory and attention tasks. Biases, on the other hand, concern the way in which the processing of information is affected by its content, and are typically studied by requir- ing the individual to memorise or think about emotionally significant material. It is impor- tant to study cognitive deficits because they provide evidence about the role of neuro- psychological impairment in psychiatric dis- orders. Indeed, it is natural to look for dys- functions in the biological mechanisms sus- taining cognition when gross deficits in the ability to attend, memorise and reason are observed. On the other hand, it is also impor- tant to study cognitive biases because human mental life has the property described by philosophers as ‘intentionality’, which is to say that it is a feature of all mental states (thoughts, desires, beliefs, as well as what in ordinary language are known as intentions) that they are always about something (Tallis, 1991). This human ability to mentally repre- sent the world and behave in response to that representation depends in turn on the ability to process information according to its con- tent. When individuals show evidence of abnormal cognitive biases in the absence of cognitive deficits it is natural to assume that these biases reflect past learning and unusual life experiences.

226 Richard P Bentall

There is good evidence that cognitive defi- cits can be found in patients diagnosed as ‘schizophrenic’ and some creative accounts of these deficits have been proposed in recent years (e.g. Frith & Done, 1987; Gray et al., 199 1; Hemsley, 1992). However, the possi- bility that cognitive biases may also be impli- cated in the behaviours and experiences of psychotic patients, and that these behaviours and experiences may be in some sense ‘mean- ingful’, has been almost entirely ignored by contemporary researchers (Bentall, 1992a). despite the fact that such biases have been fruitfully studied in the context of other kinds of psychiatric disorder, notably anxiety and depression.

There is no convincing evidence of a schizophrenia syndrome

I have outlined two assumptions which I believe inform most contemporary efforts to understand psychosis: the assumption that psychosis falls into discrete categories such as ‘schizophrenia’ and the assumption that the symptoms experienced by psychotic pa- tients lack meaning and invariably reflect underlying cognitive deficits. I now want to outline some evidence that gives cause for questioning the first of these assumptions. Because I have reviewed this evidence else- where (Bentall, Jackson & Pilgrim, 1988; Bentall, 1992b,c) the account given here will be relatively brief.

To begin with, it will be helpful to remem- ber that the concept of ‘schizophrenia’ has been used to denote a strikingly wide range of behaviours and experiences, including hallu- cinations, delusions, passivity experiences, cognitive disorganization, disordered and impoverished speech, anhedonia, flat affect and social disabilities. These behaviours and experiences are rarely al l present in the same individual. As a consequence ‘schizophre-

nia’ is a disjunctive concept, such that two people may receive the diagnosis while hav- ing little if anything in common (Bannister, 1968). Over the years different ‘schizophre- nia’ researchers have highlighted different symptoms as important when determining whether the diagnosis should be applied to particular individuals (Koehler, 1979).

Two criteria are important when we con- sider the scientific usefulness of any diagnos- tic system, namely the reliability and validity of the diagnostic classifications it yields. Reliability refers to the extent to which dif- ferent observers can agree about the applica- tion of a particular diagnosis. Validity is a more complex criterion and refers to the extent to which a diagnosis is meaningful in terms of its internal consistency and covariation with a range of scientifically in- teresting variables. It is worth noting that a diagnosis can be reliable without being valid, as in the case of the fictitious ‘Bentall’s Disease’ which has the following ‘first rank‘ symptoms: long fingernails (greater than on9 inch on average), red hair (natural, not dyed) and a preference for the music of Pink Floyd (ownership of at least four albums). Al- though this syndrome could be diagnosed with a high degree of reliability (it would be a relatively simple matter to measure the length of fingernails, determine hair colour and count Pink Floyd albums) applications for research grants to study Bentall’s Disease are not likely to be well received.

Because early studies of the reliability of psychiatric diagnoses yielded disappointing results, a number of investigators have devel- oped structured psychiatric interviews, for example, The Present State Examination (Wing, Cooper & Sartorius, 1974), for reli- ably eliciting symptom data from patients, and have proposed operational criteria for awarding diagnoses such as ‘schizophrenia’. Perhaps the most widely used operational

Deconstructing schizophrenia 22 7

criteria are those in DSM-ILI-R (American Psychiatric Association, 1987), but many others have been proposed. Unfortunately, different operational criteria do not always diagnose the same patients as ‘schizophrenic’ (Brockington, Kendell & Leff, 1978; McGuffin, Farmer & Harvey, 1992). As a consequence, disagreements between clini- cians about who meritsthe diagnosis of schizo- phrenia have been replaced by, “A babble of precise but differing formulations of the same concept” (Brackington et a]., 1978).

A number of tests can be evoked to address the validity of the ‘schizophrenia’ diagnosis. For example, the concept of ‘schizophrenia’ should map on to a cluster of symptoms which tend to occur together in real life. Research in which multivariate statistical methods have been applied to symptoms data collected from large groups of patients have generally failed toreveal such acluster(S1ade & Cooper, 1979; Blashfield, 1984). Indeed, some authors have argued that the available evidence from these kinds of studies points to two (Crow, 1980) or even three (Liddle, 1987) independent ‘schizophrenia’ syn- dromes.

A quite different way of addressing the validity of a psychiatric diagnosis involves determining whether it predicts course, out- come or response to treatment. Ordinary people, when consulting a physician, gener- ally hope that the doctor’s diagnosis will allow predictions about what is likely to happen in the future and about which kinds of treatment are likely to be useful. In the case of psychotic disorders, however, the course of illness is extremely variable and is better predicted by social variables than by symp- toms (Ciompi, 1984; Sartorius et al., 1987). Moreover, although neuroleptic drugs are usually regarded as the treatment of choice for patients diagnosed as ‘schizophrenic’, many ‘schizophrenic’ patients consistently

fail to respond toneuroleptics (Warner, 1985; Brown & Hertz, 1989) and some respond to other drugs such as lithium (Delva & Letemendia, 1982) or benzodiazapines (Lingjaerde, 1982). Interestingly, in those few trials in which drugs have been assigned to patients irrespective of diagnosis, response to neuroleptics seems to have been better predicted by particular symptoms rather than by broad diagnostic classifications (Kendell, 1989).

Taking all this evidence together, it is dif- ficult to see why modem researchers con- tinue to take the concept of ‘schizophrenia’ seriously. Indeed, we are inevitably drawn to an important conclusion: ‘schizophrenia’ appears to be a disease which has no particu- lar symptoms, which has no particular course and which responds to no particular treat- ment. It is therefore not surprising that aetiological research has revealed that it has no particular cause (Bentall et al., 1988). One obvious implication of this account is that, if we wish to make progress in the understanding of serious psychiatric disor- der, the concept of ‘schizophrenia’ will have to be abandoned. In this regard the concept of ‘schizophrenia’ is similar to a number of other concepts; for example ‘phlogiston’ and ‘the luminiferous ether’, which were widely employed by scientists for a time but which turned out to be scientifically misleading in the long term.

Perhaps one reason why the concept of ‘schizophrenia’ has continued to beemployed, despite its poor validity, is because it is widely believed that to abandon it would amount to rejecting science and falling down some kind of Langian abyss. It will, therefore, be useful to anticipate a common objection to the argu- ments I have just outlined, which is neatly encapsulated in Kety’s (1974) famous re- mark that, ‘If schizophrenia is a myth it is a myth with a strong genetic component’. This

228 Richard P Bentall

objection has recently resurfaced in reviews of Mary Boyle’s (1990) historical deconstruction of the ‘schizophrenia’ con- cept which, in many ways, parallels the argu- ments sketched out here. Farmer (1991), for example, takes Boyle to task for failing to acknowledge recent developments in genet- ics and the neurosciences which, she main- tains, point to the existence of a wide range of biological abnormalities in ‘schizophrenic’ patients.

In response to this kind of objection it might be argued that the achievements of biological psychiatry have been overstated (see, for example, Marshall’s 1990 review of research on the genetics of ‘schizophrenia’), a point which is conceded at times even by biological scientists (Charlton, 1990). How- ever, this response does little to answer the widely held conviction that the identification of biological abnormalities - any biological abnormalities - in patients diagnosed as ‘schizophrenic’ givessubstance tothe ‘schizo- phrenia’ concept. In fact, the real problem faced by those who would wish to defend the concept of ‘schizophrenia’ on such grounds is an embarrassment of riches. Indeed, the genetic (Read, Potter & Gurling, 1992), neuropsychological and neurochemical (Seidman, 1984; Jackson, 1990) abnormali- ties found in association with the diagnosis of ‘schizophrenia’ are so diverse and yet also so nonspecific that they provide further evi- dence against the existence of a single, dis- crete ‘schizophrenia’ disease entity.

Recent biological findings, then, give us few grounds for retaining the concept of ‘schizophrenia’ but, on the contrary, should encourage us to abandon it. On this view there is little point in carrying out further research in which patients diagnosed as ‘schizophrenic’ are compared to individuals diagnosed as normal or as suffering from some other kind of disorder. Clearly, if we

are to abandon this kind of research and at the same time continue to inquire into the causes of psychotic disorders new research strate- gies are required. One obvious possibility would be to try and develop a new system of psychiatric classification, perhaps by divid- ing the disorders now subsumed by the term ‘schizophrenia’ into subtypes such as those described by Liddle (1987). In my view, any such new typology would have to be dimen- sional rather than categorical, given that sub- stantial researchnow shows that ‘schizotypal’ characteristics (and even sometimes full- blown ‘symptoms’ such as hallucinations or paranoid ideas) are present in a substantial minority of individuals who have not re- ceived psychiatric treatment and who are, in all other respects, quite normal (see Claridge, 1987,1990 for detailed reviews of th is litera- ture).

A more radical alternative strategy would be to abandon the attempt to classify psy- chotic experiences andbehaviours altogether. As Bannister (1968) suggested some time ago, instead of trying to study ‘schizophre- nia’ we could make what we observe in the psychiatric clinic the subject of ourinvestiga- tions. After all, patients rarely complain of ‘schizophrenia’; they complain about spe- cific ‘symptoms’ such as hearing voices or feeling persecuted. The fact that each symp- tom of ‘schizophrenia’ can occur in the ab- sence of any others suggest that each may be associated with a particular profile of cogni- tive abnormalities. It should therefore be possible to identify those abnormalities im- plicated in each symptom in the hope that this will eventually allow us to construct symp- tom-specific aetiological models.

As promised at the outset, in what remains of this article I will illustrate the value of this approach by describing some recent research which my colleagues and I have carried out into hallucinations and persecutory delusions.

Deconstructing schizophrenia 229

In discussing this work I will attempt to challenge the second assumption underlying much contemporary research into psychosis which I identifiedearlier: the assumption that psychotic disorders are meaningless and thus reflect the exclusive influence of cognitive deficits rather than biases. Again, because of limitations of space the following treatments will be relatively brief.

Hallucinations

It will be helpful to begin our discussion of hallucinations with a few observations. Al- though usually regarded as pathological, hal- lucinatory experiences are highly valued in some societies (Bourguignon, 1970) and are reported by a substantial minority of other- wise normal individuals in the developed world (Slade & Bentall, 1988; R o m e & Escher, 1989). There is considerable cross- cultural variation in the extent to which hal- lucinations are reported by ordinary people, and in the kinds of hallucinations reported to psychiatrists, with visual hallucinations be- ing much more commonly recorded in unde- veloped countries than in the West (Al-Issa, 1978; Sartorius et al., 1986).

Research has shownthat hallucinations tend to occur under conditions of stress (Slade, 1973) and are accompanied by stress-related changes in the autonomic nervous system (Cooklin, Sturgeon & Leff, 1983). Auditory hallucinations are also most likely to occur under particular environmental circum- stances, particularly when the individual is exposed to restricted or unpatterned stimula- tion (Margo, Hemsley & Slade, 1980; Gallagher, Dinin & Baker, in press). There is some indication that these kinds of hallucina- tions are accompanied by ‘subvocalisation’ or small movements of the speech muscles (McGuigan, 1966; Inouye & Shimizu, 1970) although some of the relevant data is equivo-

cal (Green & Kinsbourne, 1990). Consistent with the idea that auditory hallucinations are associated with speech activity, remote telemetered EEG data indicates that the left frontal areas of the brain are activated when patients hear their ‘voices’ (Stevens & Livermore, 1982). Moreover, voices tend to be suppressed when patients engage in verbal tasks such as humming or naming objects (Margo et al., 1980; James, 1983).

The simplest way of accounting for these findings is to suppose that hallucinations occur when internal, mental processes are misattributed to an external source. Various versions of this theory have been proposed in recent times. For example, Hoffman ( I 986) has suggested that auditory hallucinations reflect a speech-planning disorder, so that voices are heard when the individual experi- ences unintended speech acts. Frith and Done (1987), on the other hand, have argued that the misattribution of speech acts to an exter- nal source may reflect a failure in a neuropsychological mechanism responsible for monitoring actions. In my own version of this theory (Bentall, 1990), I have suggested that the hallucinator’s misattribution of an internal event to an external source may re- flect both a failure to accurately discriminate between internal and external events and ‘top-down’ influences: beliefs and expecta- tions of the sort which normally guide our interpretation of perceptions.

Investigating the way in which hallucinat- ing and nonhallucinating people discrimi- nate between self-generated and external events has proved quite difficult, and at Liv- erpool we have tried to address this problem using avariety of strategies. In ourfmt study, using signal detection theory, we compared hallucinating and nonhallucinating patients on the one hand, and students who scored high or low on a hallucination questionnaire on the other (Bentall & Slade, 1985). Sub-

230 Richard P Bentall

jects were asked to listen to a series of pas- sages of white noise, half of which contained a voice quietly speaking a single word. By observing subjects’ judgements about when they thought they had heard the voice it was possible to calculate two values: perceptual sensitivity (roughly, how well the individu- al’s hearing is functioning) and perceptual bias (roughly, the individual’s willingness to believe that a stimulus has been presented in conditions of uncertainty). Hallucinating pa- tients and hallucinating students showed a greater bias towards detecting stimuli than their respective controls but no differences were observed on the measure of perceptual sensitivity.

In a more recent study (Bentall, Baker & Havers, 1991) we have employed a ‘reality monitoring’ paradigmin which subjects were asked to discriminate between memories of their own thoughts and memories of informa- tion they had heard. The subjects - hallucinat- ing psychiatric patients, nonhallucinating psychiatric patients and normal controls - had to answer simple clues which varied in diffi- culty (e.g. ‘Think of a vehicle beginning with C’; ‘Think of a vegetable beginning with 0’) and also listened to a list of easy and difficult paired associates (eg. ‘Footwear-shoe’; ‘Country-Norway’). One weeklater they were given a list of words which included the answers they had given to the clues, words from the list of paired associates and new words. Hallucinators did not perform worse than the psychiatric controls in terms of over- all accuracy. However, they were modestly but significantly more likely than the psychi- ahic controls to mistake their own answers to the difficult clues for words that they had heard.

Clearly, much more work needs to be car- ried out to determine why hallucinators mis- take their thoughts for voices. However, the failure to identify group differences in per-

ceptual sensitivity on the signal detection task, together with the failure to identify group differences in overall accuracy on the reality monitoring task, might be construed as evidence that core cognitive deficits are not solely responsible for the hallucinator’s difficulties. and that ‘topdown’ or concep tual processes must therefore be implicated. This hypothesis is consistent with the ob- served cultural differences in the experience of hallucinations - if one is brought up to expect to see dead ancestors then imagined dead ancestors are likely to be classified as ‘real’ - and with the differences in perceptual bias observed between hallucinators and nonhallucinators on the signal detection task. Of course, it would be helpful to have direct evidence that beliefs and expectations influ- ence the hallucinator’s judgement about whether a perceived event is self-generated or originating from an external source. In fact, at least two studies (Mintz & Alpert, 1972; Young et al.. 1987) have shown that hallucinators respond more readily than con- trols to suggestions to see or hear particular kinds of events.

This observation raises the question of whether or not it might be possible to educate hallucinating patients to reamibute their ap- parently alien thoughts to themselves. In our latest work, we have attempted to develop just such a therapeutic strategy, which a p pears to hold some promise for some patients (Bentall, Haddock & Slade, in press; Had- dock, Bentall & Slade, in press) although it is too soon to say whether this approach will be generally effective.

Delusions

In contrast to research on hallucinations, the investigation of cognitive processes in- volved in delusions has proved to be more straightforward. In Liverpool, we have fo-

Deconstructing schizophrenia 23 I

cused our research on delusions of persecu- tion. Although diagnostic manuals such as DSM-III-R describe such beliefs as sympto- matic of psychosis and qualitatively different from nondelusional beliefs, they clearly lie on a continuum with ordinary beliefs and attitudes (Strauss, 1969; Harrow, Rattenbury, & Stoll, 1988). Indeed, Fenigsten & Vanable (1992) have recently published a question- naire which seems to validly detect subclinical paranoid traits in otherwise ordinary indi- viduals.

It seems likely that the abnormal beliefs of psychiatric patients reflect a variety of fac- tors. For example, it is entirely possible that beliefs of persecution sometimes reflect genu- inepersecutory experiences (Kaffman, 1983; Mirowski & Ross, 1983). Maher (1974) has argued that perceptual processes are also involved and that many abnormal beliefs are best seen as rational attempts to make sense of anomalous experiences. Although Maher was been unable to provide specific evidence in favour of his hypothesis, and although it is clear that abnormal beliefs often emerge in the absence of anomalous perceptions (Chapman & Chapman, 1988), it is equally clear that some delusions are indeed percep- tion-driven. This seems to be especially true of delusional misidentifications in which a loved one is believed to have been replaced by a robot or impostor. Patients with these particular delusions seem to suffer from neuropsychological impairments of facial recognition which rob them of the feeling of familiarity usually experienced when en- countering a well-known person (Ellis & Young, 1990).

In our own research we have focussed primarily on those cognitive biases which are usually regarded as reflecting motivational factors. In one of our fmt studies, we em- ployed Peterson et al.’s (1983) Attributional Style Questionnaire (ASQ to compare the

ways in which deluded and depressed pa- tients reason about success and failure expe- riences. We were able to show that, whereas depressed patients, relative to normal con- trols, tended to attribute failure to themselves and success to external causes (consistent with the theory of cognitive processes in depression suggested by Abramson, Seligman and Teasdale, 1978), our deluded subjects showed a relative tendency to blame others for failure experiences and themselves for success (Kaney & Bentall, 1988). This find- ing, which was substantially replicated by Candido and Romney (1990), can be ex- plained by hypothesising that persecutory delusions have a protective function, allow- ing the individual to maintain a fragile sense of self-esteem (Bentall, Kinderman & Kaney, in press). In fact, research with normal sub- jects has consistently indicated that ordinary people have a ‘self-serving bias’ towards blaming others for failure and themselves for success, especially in situations where there is a personal threat (Taylor, 1989). The ab- normal cognitive style of paranoid patients can therefore be thought of as an exaggera- tion of a normal defensive process.

In arecent study (Kaney & Bentall. 1992), we have studied this bias using another kind of task. Subjects were asked to play two computer games, one preprogrammed to yield a successful outcome and one preprogrammed to yield a failure outcome. After each game, our subjects were asked to estimate the extent to which they believed that they had control- led the outcome. Consistent with previous research by Alloy and Abramson (1979) the depressed subjects in this study were ‘sadder but wiser’, and returned low estimates of control after each game. The normal subjects showed the expected self-serving bias to- wards claiming more control in the ‘win’ condition than the ‘lose’ condition. As pre- dicted by our account of paranoid thinking,

232 Richard P Bentall

th is bias was present to a significantly greater degree in patients suffering from persecutory delusions.

We have explored other kinds of reasoning biases in deluded patients, for example in their attributions for the behaviour of others (Bentall, Kaney & Dewey, 1991). However, in our most recent studies we have tried to find direct evidence of the defensive function of delusional ideas. One way in which we have tackled this problem is by looking again at what happens when an individual attributes an event to a particular cause. Peterson et al.’ s ASQ requires subjects to think of a likely cause for events such as ‘winning a prize’ or ‘going on adate which turns out badly’. Once they have thought of a likely cause and then written it down the subjects then have to self- rate the cause on a seven-point internality scale (caused by self versus caused by other people or circumstances). By comparing our subjects’ self-ratings with internality ratings of their causes provided by independent judges we were able to show that it was the ratings more than the actual causes generated which discriminatedbetween the groups (Kinderman et al., 1993). Indeed, the deluded subjects often generated causes for negative events which they self rated as unequivocally exter- nal (to do with other people or circumstances) but which the judges rated as unequivocally internal.

What kind of attributions would be made, then, by deluded patients on an attributional style measure which did not require an effortful consideration of blame of the sort required when completing self-ratings on the ASQ? In order to answer this question we employed a ‘pragmatic inference task’ de- signed by Winters and Neale (1985). In th is test subjects listen to stones describing them- selves involved in endeavours which have either positive or negative outcomes. After each story, the subjects are required to com-

plete multiple-choice questions, some of which concern factual elements of the story. For each story, however, one question re- quires subjects to choose between two possi- ble causes of the described outcome, one internal and one external, which are equally implied in the text (for example, in one story about setting up a successful business, sub- jects are asked to say whether success was due to hard work or lack of competition). On this task, our depressed subjects chose inter- nal causes more often for negative than for positive outcomes, consistent with their per- formance on more conventional attributional style measures. However, the deluded sub- jects, in direct contrast to their performance on the ASQ, also attributed failure to them- selves more often than they attributed suc- cess to themselves (Lyon, Kaney & Bentall, in press).

This finding is strong evidence that persecutory delusions reflect cognitive bi- ases which have a motivational function. Moreover, they indicate that, underlying persecutory delusions, there lies a cognitive organization, particularly with respect to the self, which is in many ways similar to that of depressed patients. While the aetiology of this cognitive organization must remain, at present, a matter of speculation, it is difficult to see how a purely biological account of delusions can be offered, although biological factors may be involved to some degree (Bentall, Kinderman & Kaney, in press).

The account of persecutory delusions that emerges as a consequence of looking at mo- tivational factors may well have implications for therapy. In particular, it seems that di- rectly challenging a patient’s delusional sys- tem is no more liiely to be fruitful than challenging the core religious or political beliefs of ordinary people, which also reflect strong motivational factors. Interestingly, there are reports of successful cognitive-be-

Deconstrucring schizophrenia 233

havioural treatments for delusions (Watts, Powell & Austin, 1973; Chadwick & Lowe, 1990) and, consistent with the account I have just outlined, these treatments avoid chal- lenging patients’ beliefs head-on.

Qualifications

In this article I have, first, suggested that there are good scientific grounds for aban- doning the concept of ‘schizophrenia’ and, second, tried to show how the strategy of focusing our studies on the specific difficul- ties and experiences of psychotic patients can yield important findings. Aside from the ob- vious scientific benefits of such an approach, I hope that readers will agree that it has the effect of making psychotic behaviour more comprehensible and thus more obviously re- lated to ordinary behaviours and experiences than might have otherwise been supposed. I would like to finish by considering some further implications of this approach.

First, it is worth restating that a symptom- orientated approach to psychopathology is not antibiological as is sometimes supposed. There is absolutely no reason why biological investigators should not study particular classes of psychotic experience and behav- iour in the way I have advocated in this article. Indeed, some authors (e.g. Bomstein et al., 1989) have argued that neuropsych- ological data on psychosis can be best under- stood in relation to symptoms rather than broad classifications. An important caveat to this recommendation is that biological re- search should always go hand-in-hand with social and psychological research. One im- plication of the intentionality of psychotic symptoms is that explanations in terms of gross neurobiological dysfunction will never provide a complete account of the causal pathways which lead to particular psychotic experiences. Indeed, data on the association

between biological abnormalities and psy- chopathology is intrinsically incomplete with- out an understanding of the cognitive func- tions implemented by the relevant biological systems.

Second, the generalizability of the strategy I have outlined to other types of psychopa- thology is worth considering. A number of authors have argued for the abandonment of categorical classifications of the neuroses on the basis of very similar arguments to those given here. For example, depression andanxi- ety, although usually regarded as separate kinds of disorders, covary considerably in practice and the effects of antidepressants and minor tranquillisers do not seem to be diagnosis-specific (Tyrer, 1990; Goldberg & Huxley, 1992). If we look in more detail at the concept of ‘depression’ we see that it appar- ently denotes a variety of behaviours and experiences - for example low self-esteem, guilt, dysphoria, apathy, fatigue and loss of appetite - which have defied subclassification into types (Craighead, 1980). The apparent contradictions which exist between different theories of ‘depression’ (for example, theo- ries implicating self-deprecating cognitive biases, cf. Abramson, Alloy & Metalsky (1988) and those implicating circadian disor- ders, cf. Healy & Williams (1988)) begin to dissolve if we assume that different abnor- malities are associated with different symp- toms (for example, that circadian dysrhythmia is implicated in fatigue whereas self-depre- cating cognitive biases are associated with low self-esteem).

Third, although I have argued that no con- sistent pattern of association is observed be- tween different kinds of psychotic symp- toms, it must be acknowledged that many patients experience more than one symptom. Any adequate theory of psychopathology will, therefore, have to explain why several differ- ent symptoms are often present in the same

234 Richard P Bentall

person. The solution to this problem is not to suppose, as psychiatric writers have tradi- tionally done, that covariation of symptoms in one person inevitably indicates a single underlying cause, but to recognise the rich and varied ways in which symptoms can be functionally interconnected. Taking an ex- ample from the depression literature, low self-esteem, if it leads to inactivity in the face of threatening life events, may precipitate circadian dysrhythmia and hence fatigue. On the other hand, in other patients fatigue caused by circadian dysrhythmia may be interpreted as evidence of personal inadequacy, with low self-esteem following as a consequence (Healy & Williams, 1988). In the psychotic domain it is clear that the delusions of some patients are driven by anomalous perceptions (Maher, 1974) but it is equally clear that, in other cases, hallucinatory experiences are driven by abnormal beliefs (Bentall, 1990).

Finally, I wish to return to the ethical as- pects of psychopathology which I have pur- posefully avoided until this point. Although arguments against the concept of ‘schizo- phrenia’ areoftendismissedasantipsychiatric or even antiscientific, the contribution of values to psychiatric decision-making can- not be avoided. As Szasz (1961) has so force- fully demonstrated, the attribution of ‘ill- ness’ inevitably involves a value judgement, although he was wrong to suppose that this was the case only in the field of psychiatric medicine (Bentall & Pilgrim, 1993). Recog- nition of the fact that values influence psychi- atric decision-making need not delay scien- tific research into the causes of psychosis; precisely the same strategy to that outlined here could be used to investigate the causes of positively valuedand hence ‘nonpathological’ experiences such as ‘happiness’ (Bentall, 1992d). In our pursuit of the causes of insan- ity, however, we need to be sensitive to the values and experiences of those individuals

who are the subject of our inquiries. Indeed, our years of studying ‘schizophrenic’ experi- ences at Liverpool has taught us that this kind of work is best conducted in active partner- ship with those who have first-hand knowl- edge of psychotic states.

Itisinthis way thatwhatmightbecalledthe ‘gung-ho’ biological approach which typi- fies much current psychiatric thinking so conspicuously fails users of psychiatric serv- ices: not because biological factors are unim- portant but because the biological approach, when taken to extremes, encourages an us- and-them distinction between the ‘mad‘ and the ‘sane’. In reality, of course, madness and sanity are but points on a continuum along which we are all inclined to move during difficult moments in our lives.

Acknowledgement Much of the research summarised in this

paper has been supported by grants from the Medical Research Council (to Richard Bentall and Peter Slade for the study of cognitive- behavioural interventions for patients suffer- ing from auditory hallucinations) and the Wellcome Trust (to Richard Bentall for the study of cognitive processes involved in de- lusions and hallucinations).

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Reprints from Dr Richard B e n d , Department of Clinical Psychology, Whelan Building. Liver- pool University. PO Box 147, Liverpool L69 3BX.