Dream experience and a revisionist account of delusions of misidentification

Consciousness and Cognition xxx (2012) xxx–xxx

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Consciousness and Cognition

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Dream experience and a revisionist account of delusionsof misidentification

Philip Gerrans ⇑Department of Philosophy, University of Adelaide, Adelaide, SA 5005, Australia

a r t i c l e i n f o a b s t r a c t

Article history:Received 3 May 2011Available online xxxx

Keywords:Delusions of misidentificationAbductive inferenceDreamingFeature bindingDéjà vuJamais vu

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Please cite this article in press as: Gerrans, P.and Cognition (2012), doi:10.1016/j.concog.20

Standard accounts of delusion explain them as responses to experience. Cognitive modelsof feature binding in the face recognition systems explain how experiences of mismatchbetween feelings of ‘‘familiarity’’ and faces can arise. Similar mismatches arise in phenom-ena such as déjà and jamais vu in which places and scenes are mismatched to feelings offamiliarity. These cognitive models also explain similarities between the phenomenologyof these delusions and some dream states which involve mismatch between faces, feelingsof familiarity and identities. Given these similarities it makes sense to retain that aspect ofthe standard account in the face of revisionist arguments that feature binding anomalieswhich lead to delusions of misidentification are not consciously experienced.

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1. Introduction

John Nash said of his delusions ‘‘Its kind of like a dream. In a dream it’s typical not to be rational’’. His words express acommon idea that dreams and delusions are both states characterised by absent or compromised ‘‘reality testing’’ (Bentall,2004). This intuition is now supported by a research program which compares neural activity, cognitive processing and phe-nomenology in dreaming and waking (A. Hobson, 1999; J. Hobson, 1999).

This program depends on the fact that the basic cognitive architecture of the mind does not change during dreams. Whatchanges in dreams are the patterns of neural activation, driven by brainstem neuroregulation, which drive processing in thiscognitive architecture. Some cognitive processes, such as late states of perceptual processing, remain relatively intact indreams, producing the characteristic stream of imagery. Others, such as logical argumentation, volitional control and plan-ning are absent or reduced. Thus in REM dreams we experience cognitive fragments such as images and sensations juxta-posed incongruously in vignettes and scenarios rather than coherently organised in narratives or explanations (Braunet al., 1997, 1998; Desseilles et al., 2011; Domhoff, 2003; A. Hobson, 1999; J. Hobson, 1999; Manni, 2005; Roehrenbach &Landis, 1995; Schwartz, 2002; Schwartz & Maquet, 2002; Solms, 2007).

This phenomenon reflects an important cognitive distinction between feature binding (the construction of a integratedperceptual or quasi-perceptual representation, Ashby et al., 1996) and contextual binding (the ability to organise such rep-resentations into a coherent metacognitive structure such as a narrative or theoretical explanation. See Revonsuo and Tarkko(2002)). Feature binding is a relatively modular process implemented in localised neural circuits whose processing proper-ties are fairly rigid (Ashby et al., 1996; Coltheart, 1999; David, 1994). Context binding is a more flexible cognitive processdependent on the maintenance of coordinated activity in widely distributed circuitry. Consequently context binding is morevulnerable to disintegration when resources required to stabilise and synchronise the necessary distributed activation pat-terns are withdrawn (Cleeremans, 2003; Maia & Cleeremans, 2005).

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Dream experience and a revisionist account of delusions of misidentification. Consciousness11.11.003

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In this paper I apply some of these ideas to help explain the phenomenon of delusional misidentification. In these delu-sions people report seeing ‘‘doubles’’, imposters, people in disguise, people changing appearance and identity (Breen et al.,2000; Ellis, 1991; Ellis, Luautè, et al., 1994; Ellis, Whitley, et al., 1994; Luaute & Bidault, 1994; Tzavaras et al., 1986). Thephenomenology of these delusions can be explained in terms of abnormalities of feature binding, combined with abnormal-ities in context binding. The abnormality of feature binding produces a representation in which elements normally boundtogether such as face, name, autonomic response to a familiar person, and identity may dissociate (Noreika et al., 2010; Kahn& Hobson, 2003, 2005; Kahn et al., 2002). For example if a representation of a feature such as the face of a spouse is notbound to information which drives autonomic response to a familiar person the result will be an incongruity: the patientsees a person who appears familiar but the patient does not have a characteristic autonomic reaction to that person. Thisincongruity, produced by the failure to bind the familiar face to a signal initiating autonomic response, then leads to delu-sional context binding: ‘‘my wife has been replaced by an imposter’’. The delusion binds the incongruous representation intoa larger explanatory context which accounts for the fact that perception of the familiar person does not produce the ‘‘famil-iar’’ autonomic response (Ellis & de Pauw, 1994; Ellis & Lewis, 2001; Spier, 1992; Young et al., 1993).

2. The standard account

This way of putting things accords with an explanation of the Capgras delusion (of imposters or doubles) which has be-come standard within cognitive neuropsychiatry. This standard explanation decomposes the causal structure of delusioninto two main components or ‘‘factors’’ which map onto the distinction between feature and context binding (Bayne &Pacherie, 2004; Breen et al., 2000; Coltheart, 2007; Davies et al., 2001; Langdon & Coltheart, 2000). The consensus is thatthe architecture of delusion formation includes cognitive processes which identity faces and higher order cognitive processeswhich explain abnormalities or incongruities produced by the face recognition system. The neural substrate of the former isthe face recognition system, centred on the fusiform facial area. The neural substrate of higher order context binding involvesprefrontal regions, especially, it is now hypothesised, right dorsolateral prefrontal cortex (A. Hobson, 1999; Coltheart, 2007;J. Hobson, 1999; Kahn et al., 2002; Wood & Grafman, 2003).

Given that dreams are characterised by activity in face recognition circuitry in the ventral visual processing stream, com-bined within reduced or absent activity in dorsolateral circuitry required for metacognitive context binding, some similarityin the phenomenology of both delusions of misidentification and dreams is not surprising. Equally, given that activity in theface recognition systems is evoked differently in delusions and dreams (by perceptual inputs in one case and subcorticalafferents in the other) some differences are also to be expected. Similarly, dorsolateral inactivity in dreams has a differentcausal origin and cognitive signature to the hypoactivity or absence characteristic of delusions. So, while we might expectsome similarities, we should not expect the consequent phenomenology to be identical.

Nonetheless examining similarities and differences between the two conditions might shed light on the nature of pro-cesses by which delusional beliefs arise as a consequence of activity in the face-recognition circuitry.

3. The revisionist account

In this paper I focus on a particular theory about the genesis of these delusions to which the phenomenology of dreamingis (I claim) especially relevant. That theory recently advanced by Coltheart and collaborators has two aspects. The first is thatdelusions are produced by processes of abductive inference: that is the production of an hypothesis which if it were truewould explain a datum. In the case of delusions of misidentification the datum is the representation produced by unusualfeature binding in the face recognition system (Coltheart et al., 2010).

This way of putting things is entirely compatible with the framework advocated above. The abductive inference is a formof contextual binding which explains anomalous feature binding in the face processing system.

My aim in this paper is not to dispute the conceptualisation of the second factor as an abductive inference. However thereis another controversial aspect of the revisionist account which rejects one of the foundational ideas shared on all sides of thedebate about the nature of delusion formation. That foundational idea is that these delusions are explanations of experiences.Coltheart et al. agree with the basic structure of the standard account but on their, revisionist, view the abnormality of faceprocessing and the generation of the hypothesis which explains it occur prior to conscious awareness.

[U]nconscious processes of abductive inference are invoked to seek a hypothesis which, if true, would explain that abnor-mality, and a hypothesis is found which is judged satisfactory by these unconscious inferential processes. After all of thatunconscious processing has been completed, the hypothesis is accepted as a (delusional) belief, and enters consciousness.(Coltheart et al., 2010, pp. 264–65) My italics.Everything that preceded the occurrence of that belief and was responsible for the belief having come about; the stroke,the neuropsychological disconnection, the absence of an autonomic response when the wife is next seen, the invocationof a process of abductive inference to explain this and the successful generation of such an hypothesis. All of these pro-cesses are unconscious. (Coltheart et al., 2010, p. 264)

To recapitulate: on the standard account the first factor in delusion formation is anomalous feature binding in the facerecognition system: for example a familiar face is not bound to activity in systems which initiate the autonomic responseto familiar faces. This anomaly of feature binding produces an anomalous experience. Crudely put, something feels amiss

Please cite this article in press as: Gerrans, P. Dream experience and a revisionist account of delusions of misidentification. Consciousnessand Cognition (2012), doi:10.1016/j.concog.2011.11.003


P. Gerrans / Consciousness and Cognition xxx (2012) xxx–xxx 3

when the patient looks at the familiar person. The basic idea that propelled research in the area was that a delusion repre-sented an attempt by the subject to make sense of her experience. Theorists differed in the account they gave of the content ofthe experience and the nature of ‘‘making sense’’. However a foundational premise shared on all sides is that an anomalousexperience is the first stage or factor in delusion formation.

‘‘these experiences demand explanation which the patient develops though the same cognitive mechanisms that are foundin the normal and scientific theory-building’’, (Maher, 1974, p. 111)‘‘We are proposing then that the Capgras delusion is the sufferer’s attempt to account for anomalous perceptual experi-ence’’. (Stone & Young, 1997)

The revisionist view is so radical precisely because it calls this premise into question. The revisionist view does not deny arole for anomalous perceptual processing in the genesis of delusion. However the delusion is generated as a response to thatanomaly prior to conscious awareness. Thus for the revisionist experience plays no causal role in the formation of delusions ofmisidentification. This is claim is not necessarily counterintuitive. There are many instances where early, quite complex, per-ceptual and doxastic processing takes place below the threshold of conscious awareness. The intuitive judgements belovedof cognitive psychologists are examples (Kahneman et al., 1982; Stanovich, 1999). It could well be the case that the processesthat lead to the delusions of misidentification are similar in nature. And, as we shall see below, models of face processinginvoked to explain the DMS are consistent with this hypothesis.

However it is also true that we are aware in consciousness of the outputs of perceptual processes, including abnormalitiesof feature binding. People with blurry vision or scotoma have characteristic experiences even though they are unaware of theprocess by which the defective percept is assembled. So to assess the revisionist hypothesis requires us to determine at whatpoint in the processing stream (if at all) the misbinding between representation of a familiar face and autonomic response isconsciously available. A difficulty with these cases, as with many others in the field of delusions, is that the precise phenom-enology is elusive. For example what is the phenomenology (if anything) of seeing a familiar person but not responding auto-nomically? It can’t be quite like seeing a stranger, even thought the lack of autonomic response is similar that produced byseeing a stranger, because otherwise a delusion would not be generated. As Brighetti et al. put it in their thorough discussionof a case of Capgras delusion ‘‘identity recognition of familiar faces [is] associated with a lack of SCR’’. (Brighetti, Bonifacci,et al., 2007). The idea that the delusion rationalises this incongruity is an inference to the best explanation which imputes adistinctive phenomenology to the patient according to the particular theory which anchors the explanation. On the standardaccount the incongruity is experienced. On the revisionist account the incongruity is not experienced: but that lack, associ-ated with perceiving the familiar, must also have a phenomenology. It must feel like something. It certainly cannot feel likeseeing the familiar. Nor can it feel quite like seeing a stranger. The revisionist of course acknowledges this but denies that theexperience, whatever it is, is causally primary in the genesis of the delusion. For the revisionist the incongruity is detected andexplained below the threshold of conscious awareness.

4. Dreams and the argument against revisionism

My argument against the revisionist view depends on the idea that the first stage of these delusions is generated by pro-cesses similar to those which occur in dreams. And in dreams we experience the outputs of those processes. Although thedelusional mind is not the same as the dreaming mind I argue that the cognitive profiles of both states are sufficiently similarto suggest that these anomalies of feature binding are experienced in both cases. More accurately.

1. Some dream episodes involve abnormal feature binding in face recognition circuitry in the ventral visual processingstream.

2. These abnormalities are experienced.3. The first stage in formation of delusions of delusions of misidentification is abnormal feature binding in face recognition

circuitry in the ventral visual processing stream similar to that involved in dreams.4. Similar patterns of neural activation produce similar experiences.

Conclusion: the first stage of delusions of misidentification is an experience, similar to dream experience produced by acti-vation in the face recognition circuitry.

Clearly this argument is not deductive. Each step relies on an inference about the relationship between experience andneural activity in the face processing systems. However 1 and 2, suitably qualified, are not especially controversial. Evenso the conclusion requires considerable defence. After all it is open to a defender of the revisionist view to deny 3 and/or4. Perhaps patterns of activation in the face processing systems and the circuits to which it is connected are not sufficientlysimilar in delusions and dreaming to license any conclusion about similarities in the phenomenology of each condition. Analternative might be to accept 3 but deny 4. The revisionist could argue that patterns of neural activity are similar in bothconditions but are experienced in one condition (dreaming) but not the other (delusion). This could occur in virtue of differ-ences in the way the face recognition system is linked to other systems in both conditions. Neither of these responses is apriori wrong.




I will argue that however that dreams and delusions of misidentification both involve similar abnormalities of featurebinding in the face recognition system. I will then argue that those abnormalities are experienced in dreams and in delusions.

The first stage is to examine the role abnormalities of face processing play in the standard account of delusions of mis-identification, particularly the Capgras delusion. The next stage is to examine the relationship between face processing indreams, delusions, normal and pathological cognition. Here the Fregoli delusion assumes centre stage. Changing the focusof the discussion from Capgras to Fregoli delusion is not ideal but, as we shall see, there is far more evidence for occurrenceof Fregoli-like phenomenology in dreams. In any case it is an explicit commitment of the revisionist account that it extendsto the other delusions of misidentification including Fregoli (‘‘we consider that this form of analysis holds true for manyforms of delusion, not just for the Capgras delusion. . . after all the unconscious processing has been generated the hypothesisis accepted as a (delusional) belief and enters consciousness’’ (Coltheart et al., 2010, p. 264). Finally we examine the revision-ist argument that anomalous face processing is part of the causal chain leading to delusion, but that the anomaly is notexperienced.

5. The cognitive architecture of face processing

The standard account depends essentially on cognitive theories of prosopagnosia, the inability to recognise faces conse-quent on damage to the face processing circuitry in the right fusiform area. Prosopagnosia comes in different forms but therelevant one for us is one in which a subject can recognise a face qua face and recognise facial features but is unable to deter-mine whether a seen face is familiar to her. Such patients will produce identical responses when presented with both noveland previously seen faces (Bauer, 1984, 1986; Bruyer, 1991; Ellis et al., 1993; Landis et al., 1986; Sergent & Signoret, 1992;Shraberg & Weitzel, 1979; Young et al., 1993).

In associative prosopagnosia the subject has no explicit (overt as it is called in the face recognition literature) awarenessthat she has seen a face before. Nonetheless in some cases lack of explicit recognition is accompanied by preserved implicitrecognition (called covert recognition in the face recognition literature). Covert recognition comes in two forms: the first Iwill call behavioural covert recognition (BCR). The second is skin conductance response (SCR). These covert forms usuallyco-occur but it is useful to distinguish them.

In the behavioural case, covert recognition is evidenced by things like Stroop-type interference effects, response timepriming and by a paradigm called true face name relearning. Interference effects were shown in a task in which a prospag-nosic patient was asked to classify names presented in a list (e.g. politician or actor). His performance was affected by the

Fig. 1. Basic architecture of the face processing system: from perception to identification.




presentation of a distractor face from the wrong semantic category (e.g. George Clooney presented alongside David Cam-eron) (De Haan, Young, & New Combe, 1987). The point of these interference cases is that the distractor face could only inter-fere with performance if identified. In response time priming prosopagnosic patients are asked to judge familiarity of names,which typically presents no problem (their problem is with faces not names). However their response time is faster if theyhave previously been presented with the named face. This should not be the case if they are genuinely unable to recognisefaces. In true face relearning patients are presented with pairs of faces and names. In half the cases the names are incorrect.The patients are then re-presented with the pairs after an interval and asked to name the face. The fact that their perfor-mance is better in the ‘‘true’’ case is evidence of covert or implicit recognition (Bruyer, 1991; Schweinberger & Burton,2003; Sperber and Spinnler, 2003; Bruyer, 1991).

An example of covert SCR was provided by Bauer who tested the galvanic skin responses of an overtly prosopagnosicpatient, LF, to photos of familiar and unfamiliar faces. LF could not spontaneously name a single face and guessed namesat chance level from a list of five, but covertly responded to more than 60% of familiar faces (Bauer, 1984, 1986).

It is possible that SCR is simply a way of testing for BCR, that is to say that it is another indication of activation in the sameneural system responsible for true face name relearning and response time priming. In fact this is one way to interpretBauer’s early work in the area.

However, there is some evidence to suggest that for the processing of faces, SCR and BCR depend on processing in distinctpathways. BCR is indicative of early stages of processing in the pathways culminating in face recognition. SCR is indicative ofthe subject’s autonomic response to the face consequent on ‘‘early’’ activation in this pathway.

Consequently as Young puts it, ‘‘it is inadequate to think of it [prosopagnosia] as simply involving loss of recognitionalmechanisms. Instead, at least some degree of recognition does take place. What has been lost is awareness of recognition.’’(quoted by Schweinberger and Burton (2003), p. 284. My italics).

A model which explains how this can be the case is now a basis for standard two factor accounts (see Fig. 1).The standard account of delusions of misidentification is that the correct stranger/familiar autonomic response is inverted

in these delusions. In each case autonomic response is ‘‘mismatched’’ to a seen face. In Capgras delusion the autonomicresponse to a familiar is absent. This makes Capgras delusion in effect a double dissociation with prosopagnosia withpreserved SCR. This is shown in the figure above by the locations of the relevant lesions. In Capgras the lesion is to pathwaysconnecting the face recognition units and the amygdala. In prosopagnosia the lesion is to pathways leading from the FRU tolater more explicit forms of recognition (Bauer, 1984, 1986; Bruyer, 1991; Ellis et al., 1993; Schweinberger & Burton, 2003;Sergent & Signoret, 1992; Shraberg & Weitzel, 1979; Young et al., 1993).

The same model can also explain the Fregoli delusion as the result of anomalous feature binding. One hypothesis here isthat the delusion arises when perception of strangers evokes an autonomic response characteristic of familiars. This could bedue to hyperactivity in connections between the FRU and amygdala, leading to experience of familiarity for a face that is notfamiliar. The subject is then confronted with the converse of the Capgras delusion: a feeling of familiarity combined with theinability to recognise the face.

A theoretically economical explanation of the relationship between Fregoli and Capgras in terms of mismatch between aseen face and a felling of familiarity for that face would equate them to pathological instances of déjà and jamais vu for facesinstead of places. Déjà vu for place involves a feeling of familiarity for a place that is not recognised as familiar. ‘‘For déjà vu,an inappropriate feeling of familiarity is experienced (alongside the awareness that it is inappropriate’’ (O’Connor & Moulin,2010 p165). Jamais vu is the reverse: A feeling of unfamiliarity simultaneous with recognition that the place is in fact famil-iar. Of course in normal déjà vu experiences the feeling is fleeting and background knowledge overrides any tendency to forma consequent belief. The analogy with Fregoli would require that the experience be pathologically sustained and that thedelusional belief formed as an attempt to explain it. This analogy has been explicitly drawn a number of times (Ellis, Whitley,et al., 1994; Malloy & Richardson, 1994; O’Connor & Moulin, 2010).

6. Character identification in dreams

Feelings of ‘‘hyperfamiliarity’’ are relatively frequent in dreams, and in seeking to explain them, dream theorists haveused the model of face recognition described above. In so doing they equate this type of dream experience to the ‘‘first factor’’in the Fregoli delusion: an experience of familiarity for a face which is not in fact recognised.

Revonsuo and Tarkko (2002) analysed 592 dream reports which contained bizarre dream characters (people who appearin dreams). They divide bizarreness into two types which correspond to relational (e.g. ‘‘lives in UK’’) and intrinsic (facialappearance, familiarity and identity) properties of the character. Among the latter, which they hypothesise is essentially aconsequence of feature-binding in the face recognition system, they include ‘‘the emotional component signalling the famil-iarity or unfamiliarity of the person’’. Interestingly, and in accordance with the hypothesis that the modularity of the cogni-tive process that produces it corresponds to the degree of representational disintegration in dreams, relational bizarrenesswas more frequent than intrinsic. Thus characters encountered in unusual or impossible settings or behaving uncharacter-istically are more frequently reported than characters with unusual appearance. The latter account for only 2.2% of bizarrereports while the former account for more than 50%. Bizarreness of familiarity accounts for 5.7%.

This is consistent with the standard model in which face perception and recognition is highly modular (FRU in thediagram above) but the link between a face and semantic knowledge about a person is not. Thus mismatches between face




and semantic knowledge are quite possible if the relevant circuits are not linked by perceptually-driven synchronisation ofactivity. The link between face recognition and autonomic response (FRU to amygdala and downstream) is less modularisedthan face recognition per se, but far more modular than the linking of semantic knowledge and familiar faces. Consequently,as the authors note, inappropriate feelings of familiarity are one of the most common reports of internal bizarreness. ‘‘[W]emay interpret the abundance of pseudo-familiar persons in dreams as over-activation of face recognition units: they fireeven when the face precept does not correspond to any of the descriptions in the store. This creates the inappropriate feelingof familiarity’’ (Revonsuo & Tarkko, 2002).

The authors explain erroneous familiarity terms of the relationship between the face recognition unit and the autonomicresponse. If an unfamiliar face is mistakenly represented as familiar an autonomic response is generated. A similar effectcould be produced by endogenous activation of subcortical structures that generate autonomic response. Since limbic sys-tems are active in dreams but not driven by perceptual inputs this is another possible cause of inappropriate feelings offamiliarity. In either case the subject could have an autonomic response to a face that is not in fact familiar. Schwartzand Maquet (2002) note in their discussion of dream experience that it includes many other instances of anomalous featurebinding characteristic of neuropsychological disorder such as achromatopsia, polyopsia and microtopsia. All these cases canbe explained in terms of abnormal patterns of activity produced when later processing in the ventral visual processingstream is driven by sub cortical afferents rather than its usual inputs from early vision.

Slighly different Fregoli-like phenomena have been remarked on by Schwartz and Maquet (Roehrenbach & Landis, 1995;Schwartz & Maquet, 2002). They use the following examples.‘‘ I had a talk with your colleague but she looked differently,much younger, like someone I went to school with, perhaps a 13 year old girl’’. In another case a subject reported ‘‘I recogniseA’s sister. I am surprised by her beard. She looks much more like a man, with a beard and a big nose’’ Schwarz and Maquetdescribe these as ‘‘Fregoli-like’’ phenomenona generated by activation in the facial fusiform area. Once again it is plausible tosee these cases as candidates for delusional rationalisation: if the sister was disguised as a man it would explain her mas-culine appearance. Of course in dreams no such rationalisations are produced.

An interesting feature of this type of Fregoli-like report is that the mismatch here is between facial appearance and iden-tity (‘‘your sister’’) rather than facial appearance and autonomic response. In this sense the phenomenon perhaps resemblesthe phenomenon described by Revonsuo and Tarkko as appearing infrequently in dreams ‘‘cases of imposter relatives; per-son we have never met in the real world but who we accept as our ‘sisters’ ‘brothers’ or ‘cousins’ or ‘uncles’ in the dream.’’(Revonsuo & Tarkko, 2002, p. 16)

Such cases are in some ways the converse of the Capgras delusion in which a familiar person is identified as an imposter.Very interestingly there are almost no reports of Capgras-like phenomena in dreams. This suggests to dream theorists thatthe patterns of activity in the facial fusiform area which produce the Capgras delusion do not arise in dreams: ‘‘thus weshould expect the pattern of brain activity to be different in normal REM sleep and Capgras patients’’ Revonsuo & Tarkko,2002, p. 18).

This sentence makes explicit the hypothesis of dream theorists about these phenomena of hyperfamiliarity and/or mis-match between appearance, familiarity and identify in dreams. They depend on similarities between patterns of brain activ-ity in REM sleep and the delusional waking state. Precisely why Fregoli-like phenomena but not Capgras phenomena arisemust depend on the nuances of circuitry and physiology.

The point I wish to emphasise is that these Fregoli-like phenomena are experienced in dreams. This would of course bepredicted by standard accounts in which the face recognition system computes the identity of a seen person and producesan experience as output. The standard account predicts that subjects can experience mismatches between appearance, famil-iarity and identity if feature binding in this circuitry misfires. This patient seems to have experienced a mismatch betweenappearance and identity.

An important point to note is that these experiences seem unmediated or uninterpreted by higher-level cognitive pro-cesses. In the case described by Schwartz and Maquet the subject ‘‘saw’’ A’s sister with a drastically changed appearance(beard and big nose). He did not infer that A’s sister was in disguise or had changed identity. He simply experienced theanomaly of feature binding. Of course it could be the case that in cases such as this the subject is making some kind of infer-ence as to the identity of the character. Perhaps, but Maquet and Schwarz note that these types of experiences do not havethe quality of explanations. Their subject did not report for example that the 13-year-old girl was impersonating the col-league. The reason is ‘‘the absence of supervisory control functions normally exerted by the frontal lobe (markedly hypoac-tive during REM sleep) would then prevent the detection of mismatch between face identity and face appearance, hencefavouring the delusive quality of Fregoli-like representations in dreams, usually accepted without much surprise by the drea-mer’’ (Schwartz & Maquet, 2002). This is quite consistent with theories of dreaming which explain the phenomenology interms of the deactivation of prefrontal systems, particularly dorsolateral, involved in higher-level cognition.

Dreams are characterised by deactivation of the dorsolateral prefrontal cortex, a structure that helps regulate memory,attention and higher level cognition. The deactivation of the dorsolateral prefrontal cortex explains why the bizarre repre-sentations characteristic of dreams to not seem to produce any search for explanation or interpretation. The fact that thescenarios and images that occur in dreams are inconsistent with pre-existing beliefs does not lead to activity in higher levelprocessing systems which would attempt to interpret or explain them. ‘‘REM sleep may constitute a state of generalizedbrain activity with the specific exclusion of executive systems that normally participate in the highest order analysis andintegration of neural information’’ (Braun, 1997, p. 1190) This is consistent with view of dorsolateral prefrontal circuitrywhich interprets it, inter alia, as a system which is activated when new information comes to light which challenges an




existing belief, mobilising and coordinating other circuits which store and process information relevant to evaluating andresponding to the epistemic challenge.

As two well known dream theorists explain the phenomemenon:

much of wake-learned knowledge is not accessible or even applicable to the largely self contained dream narrative. Thisalleged inability to exchange information is buttressed by experiments which have shown that there is a decrease inDLPFC with orbital prefrontal exchange specifically during rapid eye movement (REM) stage when dreaming ispronounced and, a decrease in information exchange of DLPFC with parts of the occipital, parietal and temporal lobes.(Kahn & Hobson, 2003)

Kahn et al. make a similar point:

When the DLPFC is in poor communication with these areas as in REM sleep, the ability to perform logical inference, torecall accurately and to discern whether a premise is fact or fiction may very well be compromised (Kahn et al., 2002).

Thus we might predict unusual feature binding in dreams, should it occur, would not lead to any attempt to at explana-tion or interpretation. Dreamers would tend to accept incongruities without question. Another way to put this might be tosay that dreamers do not reflect on, interpret or explain their experience in any sustained of coherent way because the nec-essary cognitive resources are not available. Dreamers have experiences but they do not really form any beliefs about theirexperiences. At one point in his discussion of dreaming Alan Hobson says that the ventromedial prefrontal cortex vainly triesto ‘‘impose a plot’’ on the flux of experience but is doomed to fail because it is not in communication with other structuressuch as DLPFC which coordinate the retrieval and manipulation of information required to provide coherence andconsistency.

As a consequence in dreams we are hostage to experience. Thus at least for the Fregoli delusion 1 and 2, are plausiblehypotheses. Namely in dreams we have experiences of familiarity for people who are not recognised. Those experiencesare similar to those which lead to delusion of misidentification in a waking mind. The explanation of in both cases is anom-alous feature binding in the face recognition circuitry.

7. The first factor in delusion?

The crucial question now arises: how similar is the first factor in delusion to the dream experiences described above? Ofcourse feature binding in both conditions cannot be identical. Activity in the relevant circuitry is initiated and modulateddifferently in either condition. However, even if not identical, it does seem to produce abnormalities of feature binding inboth conditions, and those abnormalities seem candidates for the first stage of both the Fregoli delusion and the Fregoli-likedream experiences.

It is worth pointing out that the same point applies to perceptual phenomenology in general. Perceptual systems are dif-ferentially activated and modulated by connections with other circuits in dreams and waking, and, we might add, memoryand imagination. Nonetheless dream theorists explain dream experiences in terms of similarities in activation patterns be-tween the conditions. A visual image of Mt. Fuji or Nicolas Sarkozy which arises in a dream is similar to that produced inother conditions because, despite the different causal pathways, the circuitry which implements that visual representationis similarly (not identically) activated. As Braun puts it visual impairments in dreaming have parallel waking deficits, whichsuggests that the network has close relationships with at least some aspects of waking mental imagery. Once again, the neu-roimaging findings are very consistent with the neuropsychological findings, because the visual association cortex-and theauditory association cortex as well-are reactivated during REM (Braun et al., 1998).

Clearly dream theorists take the activity in the face recognition circuitry to be extremely similar in delusion and dream-ing. They draw on neuropsychological studies of delusions of misidentification and cognitive models produced by neuropsy-chiatrists to explain dream experience in terms of abnormal feature binding in the face recognition system.

I think it is also clear that a standard two-factor theorist would regard the two conditions as similar, at least for the Fregolidelusion. That is because the two-factor theorist regards an experience produced by abnormal feature binding as the firstfactor.

When we turn from activity intrinsic to the face recognition circuitry to the global cognitive context in which featurebinding occurs there are clearly many differences between the two conditions. Limbic and paralimbic systems are activateddifferently in dreams and the dopaminergic system, though active is not functioning to make information salient within acontext of goal directed waking cognition.

However there are also some very important global similarities between delusions and dreaming states that are relevantto the way outputs of the feature binding system are processed. The most important of these is the deactivation of the DLPFC.A basic mechanism here is changes in the balance of cholinergic and aminergic regulation of the brain, with aminergic sys-tems which tonically activate prefrontal areas shut off during REM sleep (A. Hobson, 1999; J. Hobson, 1999; Solms, 2007).

Clearly the causal route to reduced DLPFC activity is different in the dreaming and delusional case but a common factor isthe reduction or absence of DLPFC activity. For example there is now a large body of evidence to show that schizophrenicdelusional subjects show absent or reduced anticorrelation between DLPFC and ventromedial prefrontal cortex (VMPFC)for tasks which require high level executive functioning such as logical inference and abstract working memory. The basic




idea here is that neurotypical subjects shut down the ventromedial areas and activate the DLPFC for these tasks but that be-cause of ‘‘hyperactivity and hyperconnectivity’’ of the VMPFC the delusional patients in these experiments could not activatethe DLPFC (Buckner et al., 2008; Garrity et al., 2007; Gusnard et al., 2001; Pomarol-Clotet et al., 2008; Whitfield-Gabrieliet al., 2009).

An even more dramatic example of the association between reduced DLPFC activity and delusion especially relevant tothe cases discussed here is provided by cases of lesion to the DLPFC associated with delusions of misidentification. Papageor-giou et al. studied nine patients with delusions of misidentification (Capgras, Fregoli, Intermetamorphosis) with somepatients suffering more than one of these delusions (Papageorgiou, Lykouras, et al., 2005; Papageorgiou, Ventouras, et al.,2003). The 2005 study was an event related potential (ERP) focusing on the P300 ERP component. The delusional patientgroup showed significant reductions in P300 amplitude in the right frontal hemisphere compared to controls. If we acceptthe standard hypothesis that abnormal feature binding in the face recognition system is part of the causal chain leading todelusions of misidentification then these cases are instances of abnormal feature binding occurring in a mind with reducedDLPFC function.

The conclusion that hypoactivity of the right hemisphere is involved in delusion is consistent other neuropsychologicalstudies. For example in a group of 33 patients with Alzheimer’s disease, of whom 18 had a content specific delusion concern-ing place person or object, Single Positron Emission Topography revealed hypoperfusion in the right frontal hemisphere inthe delusional groups compared to the 15 nondelusional sufferers (Coltheart, 2007).

So although activity across the brain is different in the two cases two important similarities are anomalous feature bind-ing in the face recognition system and reduced or absent activity in the DLPFC.

These facts accord with the hypothesis advanced by dream theorists that the absence of higher order functioning indreams is produced by reduced activity of the DLPFC. All two factor theorists, whether standard or revisionist, advert toreduced DLPFC function to explain why the incongruity generated by abnormal feature binding leads to delusion rather thanthe far more likely hypothesis that something is wrong with the patient’s perceptual systems.

The obvious differences between delusional and dreaming states are not sufficient to dislodge the idea held by dreamtheorists that the first stage of delusions and dream experience involve similar anomalies of feature binding.

8. The revisionist account

The question then remains, does anomalous feature binding in delusion (the first stage) generate an experience whichplays a causal role in delusion formation? In explaining delusions this way the standard account agrees with Brendan Maherand before him William James and John Locke, that delusions are explanations of experiences. For example someone whoexperiences intense itching might form a delusion of infestation by invisible parasites. The standard account uses modelsof feature binding processes to explain how the relevant experience arises in delusions of misidentification.

I would suggest that the burden of proof here is on the revisionist. It seems that anomalous feature binding in dreamsleads to characteristic experiences. Not only that, but most theorists have started from the premise that delusions of misi-dentification are rationalisations of the experience of anomalous feature binding in the face recognition circuitry.

The revisionist who rejects this explanatory structure has several options. The first is to deny that dreams involve expe-rience. Although some theorists influenced by behaviourism or functionalism have adopted versions of this view (Malcolm,1956, 1959; Dennett, 1976) the majority of research in the area is conducted on the basis that dreams are experiences (see,e.g. Revonsuo (2006) for a discussion). Thus this option seems untenable. The second is to argue that similar feature bindinganomalies are experienced in dreams but not in delusions. This also seems untenable. A third is to acknowledge that theexperiences are similar in both cases but are not causally relevant to the genesis of delusion. This would be to say in effectthat the anomaly of feature binding leads to both a characteristic experience and a delusional belief but the former is notrelevant to the latter. Experience becomes epiphenomenal to the experience of delusion.

The revisionist, in Lakatosian spirit defends the boldest hypothesis. Namely to deny that the anomaly is experienced at all.‘‘What’s conscious is only the outcome that this chain of processes generated: the conscious belief ...This person isn’ t my wife.’’(Coltheart, Menzies et al. p. 264)

The reason is that

people are not conscious of the operation of their autonomic system and so a man would not be conscious of the failure ofhis autonomic system to respond when he encountered his wife. Hence what happens here is not an abnormal experi-ence, because it is not an experience. (p. 264)

While it is clearly true that people are not conscious of the activity in circuits which initiate activity in the autonomicsystem it is also true that autonomic activity is sensed, often faintly, sometimes floridly, as an accompaniment to many epi-sodes of perception. It is true that we have no access to the tacit processes which cause those feelings, but this is true formost cognitive processes. Nonetheless there are many conditions in which we can experience the results of tacit processing.Such experiences are often fleeting aspects of fringe consciousness as it is known but they exist nonetheless. Tip of the ton-gue phenomena (baptised ‘‘feeling of knowing’’ for obvious reasons) are an obvious case (Maylor, 1990) as are proprioceptivefeelings generated in non-standard situations. Trying to descend a staircase in the pitch dark is an example. The sensation,while hard to verbalise, is produced by activity in tacit systems which match proprioceptive and sensory feedback. Because




visual feedback is unavailable the matching systems centred on the inferior parietal lobule work extra hard, amplifying pro-prioceptive signals and generating sensations which are not usually sustained or amplified sufficiently to dominate aware-ness (Lafargue & Franck, 2009).

The feeling of ‘‘familiarity’’ produced by autonomic arousal is similar. The processes which produce this feeling are notavailable to consciousness, but we can become conscious of the results of those processes. Everyday experience acquaintsus with it fleetingly in the form of déjà vu for both people and places. Surely the phenomenon of déjà vu is experienced.Déjà vu is quite a normal phenomenon but also has pathological counterparts in which it is inappropriately generatedand sustained.

As we noted one explanation of the Fregoli delusion postulates the association of such erroneous feelings of familiaritywith perception of stranger’s faces. And as we saw such experiences of hyperfamiliarity are relatively common dream phe-nomena. No doubt Fregoli delusion is not straightforwardly matter of déjà vu for faces instead of places, but the similaritieshave been noted and explained in virtue of similarities in cognitive architecture. Indeed Feinberg and Roane say that patientswho misidentify an unfamiliar place such as a hospital room for a personally significant place such as home are bestdescribed as having ‘‘ Fregoli delusion for place’’ (Feinberg & Roane, 2005. p668). The points to emphasise are (i) feelingsof familiarity can be experienced and (ii) such feelings are invoked as first factors in the Fregoli delusion.

However the main focus of the revisionist paper is the Capgras delusion in which the autonomic signal, and any conse-quent feeling of familiarity, is absent. So it might be correct to suggest that the absence of an autonomic signal which nor-mally occurs is not experienced. And there are many neuropsychological phenomena in which people do seem unawareof even quite serious deficits leading to loss of experience. Visual agnosias and neglect cases are classic examples. In thesecases people lose conscious access to part of the visual field and behave accordingly, but they are not aware of the loss. Often,too, such people will confabulate about their deficit and in such cases it seems correct to say that all the processing whichissues in the confabulation is not consciously available. However most theorists prefer to distinguish these types of precon-scious confabulation from delusion, assimilating confabulation and delusion only in cases where experience plays a primarycausal role.

underlying both incorrigible spontaneous confabulation and other in-stances of received non mnemonic delusions is acompromised ability to inhibit the prepotent tendency to upload and maintain experience be it perceptual or mnemonic intobelief. (Langdon, 2009)

Similarly in their discussion of delusions of misidentification Feinberg and Roane conclude that ‘‘delusional misidentifi-cation and reduplication can be distinguished both clinically and neuroanatomically from confabulation (Feinberg & Roane,2005, p. 675).

Hypoactivity in the systems which generate familiarity is experienced in the form of jamais vu for places or objects. In suchcases we experience a feeling of unfamiliarity associated with recognition of the familiar place. If this is the correct analysis ofjamais vu (once again acknowledging the unreliability of self report and the absence of conclusive neuropsychological evi-dence) then it is reminiscent of the description of Capgras given by Brighetti: ‘‘identity recognition of familiar faces [is] asso-ciated with a lack of SCR’’. Brighetti of course remains neutral about the actual phenomenology, describing only theprocessing.

None of these considerations are decisive in themselves. But nor, I suggest is the revisionist argument that because wehave no access to processes linking face recognition to autonomic processing that the consequences are not experienced.

It pays then to look at the argument in favour of the revisionist view in more detail. It is presented as a dilemma for theunderstanding of the Capgras case, which applies to other delusions of misidentification. The authors say that if we allowthat the anomalous hypoactivity in the autonomic system is experienced then either

(a) we must allow that experiences can be unconscious (which we don’t want to do), or(b) we must conclude that the James-Maher explanation of delusional belief fails to account for the Capgras delusion

(which we also don’t want to do) (p. 264).

Regarding (a) however it does not follow that because we are not aware of tacit cognitive processes (the signal whichinitiates autonomic response) we are not aware of the outputs. We do experience the outputs/results of tacit cognitive pro-cesses including those which generate autonomic responses. It is however hard to verbalise them or make them the focus ofexplicit awareness since attention tends to be monopolised by explicit representations such as percepts and inner speechrather than subtle physiological sensations which accompany them. However these type of feelings are detectable if not ver-balisable, as jamais and déjà vu remind us. A recent review of neuropsychological studies of these phemomena noted. ‘‘Fordéjà vu, an inappropriate feeling of familiarity is experienced (alongside the awareness that it is inappropriate)’’ (O’Connor &Moulin, 2010, p. 167).

Regarding (b) the James-Maher theory referred to is the standard one that delusions are hypotheses which, if true, wouldexplain experience. We certainly would have to abandon that theory if the lack of autonomic response generated no expe-rience. However the main argument for that view is the fact that signals initiating autonomic activation take place below thethreshold of conscious experience. As the cases of déjà and jamais vu remind us, however the consequences of such processesare experienced.




And indeed there are cases of delusions (of reduplication) in which people report ‘‘imposter’’ houses and places whichappear similar or identical to the originals but are not felt to be the original (Roehrenbach & Landis, 1995). The most plau-sible explanation here is that the delusion is a response to a jamais vu type experience. A revisionist explanation of thesedelusions might be that the relevant processing is not experienced, the first output of which the subject is aware is the delu-sional belief. But this does seem implausible given that jamais vu without delusion is experienced.

9. Conclusion

Standard accounts of delusion explain them as responses to experience. Cognitive models of feature binding in the facerecognition systems explain how experiences characteristic of delusions of misidentification can occur. These models alsoexplain similarities between the phenomenology of these delusions and some dream states. Given these similarities it makessense to retain that aspect of the standard account in the face of revisionist arguments that feature binding anomalies whichlead to delusion are not experienced.

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Dream experience and a revisionist account of delusions of misidentification

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