Nature and extent of person recognition impairments associated with Capgras syndrome in Lewy body dementia

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Patients with Capgras syndrome (CS) adopt the delusional belief that persons well-known to them have been replaced by an imposter. Several current theoretical models of CS attribute such misidentification problems to deficits in covert recognition
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  ORIGINAL RESEARCH ARTICLE published: 24 September 2014doi: 10.3389/fnhum.2014.00726 Nature and extent of person recognition impairmentsassociated with Capgras syndrome in Lewy body dementia Chris M. Fiacconi  1 *, Victoria Barkley  2  , Elizabeth C. Finger   3  , Nicole Carson  2  , Devin Duke  1 ,R. Shayna Rosenbaum 2,4  , Asaf Gilboa  4,5  and  Stefan Köhler  1,4  *  1 Department of Psychology,The Brain and Mind Institute, University of Western Ontario, London, ON, Canada  2  Department of Psychology,York University,Toronto, ON, Canada  3  Department of Clinical Neurological Sciences, Schulich School of Medicine, University of Western Ontario, London, ON, Canada  4  Rotman Research Institute, Baycrest,Toronto, ON, Canada  5  Department of Psychology, University ofToronto,Toronto, ON, Canada  Edited by:  Srikantan S. Nagarajan, University of California San Francisco, USA Reviewed by:  Babu Adhimoolam, University of California San Francisco, USAGeorges Naasan, University of California San Francisco, USA *Correspondence:  Stefan Köhler and Chris M. Fiacconi,Department of Psychology,The Brainand Mind Institute, University of Western Ontario, London,ON N6A 5B7, Canada e-mail:;  PatientswithCapgrassyndrome(CS)adoptthedelusionalbeliefthatpersonswell-knowntothemhavebeenreplacedbyanimposter. SeveralcurrenttheoreticalmodelsofCSattributesuch misidentification problems to deficits in covert recognition processes related to thegeneration of appropriate affective autonomic signals.These models assume intact overtrecognition processes for the imposter and, more broadly, for other individuals. As such, ithasbeensuggestedthatCScouldreflectthe“mirror-image”ofprosopagnosia.ThepurposeofthecurrentstudywastodeterminewhetherovertpersonrecognitionabilitiesareindeedalwayssparedinCS.Furthermore, weexaminedwhetherCSmightbeassociatedwithanyimpairments in overt affective judgments of facial expressions. We pursued these goalsby studying a patient with Dementia with Lewy bodies (DLB) who showed clear signs ofCS, and by comparing him to another patient with DLB who did not experience CS, as wellas to a group of healthy control participants. Clinical magnetic resonance imaging scansrevealed medial prefrontal cortex (mPFC) atrophy that appeared to be uniquely associatedwith the presence CS.We assessed overt person recognition with three fame recognitiontasks, using faces, voices, and names as cues.We also included measures of confidenceand probed pertinent semantic knowledge. In addition, participants rated the intensity offearful facial expressions.We found that CS was associated with overt person recognitiondeficits when probed with faces and voices, but not with names. Critically, these deficitswere not present in the DLB patient without CS. In addition, CS was associated withimpairments in overt judgments of affect intensity.Taken together, our findings cast doubton the traditional view that CS is the mirror-image of prosopagnosia and that it sparesovert recognition abilities. These findings can still be accommodated by models of CSthat emphasize deficits in autonomic responding, to the extent that the potential role ofinteroceptive awareness in overt judgments is taken into account. Keywords: Capgras syndrome, Lewy body dementia, interoceptive awareness, person recognition, affectperception INTRODUCTION Misidentification syndromes are among the most fascinatingand puzzling forms of memory problems that can result frompsychiatric or neurological disease. They are monothematicdelusions that have intrigued psychologists and philosophersalike for over a century, but have only recently been broughtinto the realm of scientific investigation. Misidentification syn-dromes have been observed in relation to places, objects, andpeople, and have become known collectively as “delusions of misidentification.” Perhaps the most striking condition is Cap-gras syndrome (CS), in which individuals come to adopt thedelusional belief that persons well-known to them have beenreplaced by an impostor or a “double.” A defining characteris-tic of delusions that is also present in CS is that patients willfirmly hold on to their delusional beliefs in the presence of mounting contradictory evidence. While commonly observed inthe context of psychiatric disease, CS can also result from var-ious neurological conditions. The purpose of the current study is to shed more light on the nature of cognitive and affectivedeficits associated with CS in the context of neurodegenerativedisease. CAPGRASSYNDROME:AGENERALFRAMEWORKFORUNDERSTANDINGFUNCTIONALIMPAIRMENTS Given its close association with psychiatric illness (e.g., paranoidschizophreniaandotherpsychoses),itwasthoughtformanyyearsthat CS is the result of abnormal psychodynamic processes. How-ever, research conducted over the past 40 years has attempted toground CS symptomatology in brain-based dysfunction withinface-processing and person recognition models (Ellis etal., 1997;Ellis and Lewis, 2001). In this newer endeavor, it has beenhypothesized that patients can normally map faces onto stored Frontiers in Human Neuroscience  September 2014 | Volume 8 | Article 726 |  1  Fiacconi etal. Cognitive impairment in Capgras syndrome representations of known individuals based on computations per-formed within structures of the ventral visual pathway (Bauer,1984; Bauer and Verfaellie, 1988; Ellis and Young, 1990; Ellis etal., 1997; Ellis and Lewis, 2001). Critically, however, recogni- tion processes computed within a second pathway,which divergesafter initial structural analysis and allows for the generation of an appropriate affective signal to familiar individuals, is proposedto be impaired. This second pathway is thought to be comprisedof limbic structures, such as the amygdala, and possibly frontalregions, including the insula and anterior cingulate cortex (Breenetal., 2000). Alternatively, it has been suggested that CS couldresult from a disconnection between ventral visual structures andlimbic structures dedicated to affective processing. Evidence infavor of accounts that link CS to affective processing has comefrom a handful of case studies in patients with CS caused by avariety of etiologies,which revealed reduced autonomic responses[as measured by skin conductance responses (SCRs)] to picturesof personally known individuals and of famous people (Ellisetal., 1997; Hirstein and Ramachandran, 1997; Brighetti etal., 2007). Based on these findings, it has been hypothesized that themonothematic delusional belief that characterizes CS is a result of thepatients’attemptto“makesense”of theabsenceof anexpectedaffective signal (e.g.,Young, 2008).In functional terms, the “cognitive” and “affective” routes toface recognition described above have been suggested to underlieovert and covert aspects of face-processing, respectively (Traneland Damasio, 1985, 1988; Bauer and Verfaellie, 1988). Overt face recognition refers to the ability to make accurate explicitrecognition judgments for faces, whereas covert face recogni-tion refers to signs of an implicit differentiation between familiarand unfamiliar faces in behavior, or most pertinent in the con-text of CS, at the level of autonomic responding. Evidencein favor of this distinction has come from neuropsychologi-cal patient studies that revealed a double dissociation betweenthese two forms of face recognition (Tranel etal., 1995). Specifi- cally,bilateral lesions to ventro-medial prefrontal cortex (vmPFC)have been shown to disrupt covert face recognition, as assessedusing SCR, while leaving overt face recognition intact. By con-trast, bilateral lesions to occipito-temporal cortex resulted inimpairments in overt but not covert face recognition judg-ments (see also Bauer, 1984; Tranel and Damasio, 1985; Bauer and Verfaellie, 1988, for similar findings in other prosopag-nosic patients). The preservation of covert face recognition inprosopagnosic patients also stands in contrast to findings of impaired covert face recognition, as reflected in reduced SCR responses, in CS (Ellis etal., 1997; Hirstein and Ramachan- dran, 1997; Brighetti etal., 2007). Indeed, some researchers have endorsed the view that the face recognition deficits in CS are themirror-imageof thoseobservedinprosopagnosia(EllisandLewis,2001).According to the two-factor framework of delusions, deficitsin affective reactivity in face recognition may not provide a fullaccount of CS (Coltheart, 2010; Coltheart etal., 2011). Coltheart (2010) has argued that such deficits in isolation cannot explainwhy CS patients typically remain firmly wedded to their delu-sional beliefs,even when strong counter-evidence (e.g.,a weddingband with engraving) is presented. To explain these observations,Coltheart(2010)proposedthatCSinvolvesanadditionaldeficitinexecutive control processes that are necessary for monitoring thecontents of memory retrieval, as well as the critical evaluation of hypotheses. Evidence in support of this idea comes from observa-tions that many cases of CS,and other delusions,have been foundto be associated with right prefrontal cortical damage (Alexanderetal., 1979; Staff etal., 1999; Corlett etal., 2007; Devinsky, 2009; Ismail etal., 2012; Thiel etal., 2014). Regardless of whether a sec- ond factor is required to explain CS (see Corlett etal., 2010, for critique), the two-factor model as well as previous single-factormodels (e.g., Breen etal., 2000; Ellis and Lewis, 2001) emphasize the presence of a deficit in covert familiarity responses that leavesovert person recognition judgments intact. Here we examine thiscentral notion in the literature on CS more closely. NATUREANDEXTENTOFPERSONRECOGNITIONDEFICITSINCAPGRASSYNDROME When thinking about the functional impairments that charac-terize CS, perhaps the most critical issue is the extent to whichperson recognition is affected. What appears puzzling, at least atfirst glance, is that the delusion appears to be restricted to oneor a small number of individuals who typically have close emo-tional bonds to the patient. However, it would seem premature toconclude solely based on the scope of the delusion and anecdotalreportsfromrelativesthatabnormalitiesinpersonrecognitionareindeed restricted to loved ones. Rather, this issue requires system-atic investigation of person recognition abilities with controlledexperimental tasks.Recent psychophysiological research in healthy individuals hasdemonstrated that exposure to faces of loved ones is associ-ated with a larger autonomic response than exposure to otherwell-known people as reflected in SCR, heart rate, and other psy-chophysiological measures (Vico etal., 2010; Guerra etal., 2011, 2012).However,thegenerationofautonomicarousalisnotuniqueto exposure to loved ones in person recognition. In fact, severalstudieshaverevealedincreasedautonomicarousalforfamouspeo-ple as compared to unfamiliar people as well (Tranel etal., 1985;Bauer and Verfaellie, 1988; Stone etal., 2001), and there are anec- dotal reports that even a single exposure to a new face in thestudyphaseofanexperimentalrecognitionmemoryparadigmcanlead to differential SCR responses during subsequent recognition judgments (Morris etal., 2008). Findings from experimental research with affective primingparadigms in healthy individuals suggest that autonomic arousalresponses may even play a role in overt recognition judgments forthe identity of faces (Goldinger and Hansen, 2005; Duke etal., 2014). For example, Goldinger and Hansen (2005) found that presenting a subtle vibrating tactile stimulus (a “buzz”) simul-taneously with test items during a recognition memory test ledto an increased endorsement of new faces as “old.” Followinga similar rationale, Duke etal. (2014) demonstrated that thesubliminal presentation of affective information (i.e., a happy face) prior to a test probe (i.e., an emotionally neutral face)increased the likelihood that participants judged the probe facesas familiar. These behavioral findings suggest that feelings of familiarity and corresponding overt recognition responses canbe influenced by arousal. Such evidence is consistent with many  Frontiers in Human Neuroscience  September 2014 | Volume 8 | Article 726 |  2  Fiacconi etal. Cognitive impairment in Capgras syndrome other lines of evidence from the cognitive neuroscience litera-ture at large, revealing that some internal bodily changes can beconsciously experienced or “felt” (through interoceptive aware-ness), and influence conscious decision making (Critchley andHarrison, 2013). To the extent that abnormalities in autonomicarousal have been proposed to be a core feature of CS, thefindings reviewed raise the possibility that overt judgments of person recognition may also be affected by these abnormalitiesin CS.Most research and theoretical commentary on CS has focusedon person recognition in the visual modality (i.e., face recogni-tion).However,thegenerationofdifferentialautonomicresponsesto famous individuals is not limited to faces but has also beenshown to accompany voice recognition (Lewis etal., 2001). Lewis etal. (2001) reported larger SCRs for famous relative to non-famous voices, which were of comparable magnitude to the SCR response observed for famous versus non-famous faces in healthy individuals. Incontrasttothesefindingswithface-andvoicecues,there is evidence to suggest that recognition of famous peoplebased on their names is not accompanied by a differential auto-nomicresponse(Ellisetal.,1999). Fromthisperspective,potential impairments in overt recognition of famous people in patientswith CS, although perhaps not limited to faces, may still show some cue specificity.Existingexperimentalevidencethatspeakstotheextentofovertpersonrecognitionimpairmentswithinandacrossmodalitiesandcues in CS is currently limited. Several studies that have addressedthis question by using faces of famous individuals have revealedsome impairment (Young etal.,1993; Ellis etal.,1997; Breen etal., 2002; Lucchelli and Spinnler, 2008; Thiel etal., 2014). For exam- ple, Ellis etal. (1997) reported that two of four patients testedwere impaired at judging whether a presented face was famousin a yes/no recognition task, and these same two patients alsodemonstrated deficits in identifying the occupation of the famousface in question. Particularly relevant to the current investigation,Lucchelli and Spinnler (2008) used a forced-choice recognitiontask to probe fame recognition in a patient with CS in asso-ciation with an unspecified neurodegenerative condition; theseauthors observed a noticeable impairment in judging which of four faces was famous. It should be noted, however, that all of the aforementioned studies tested person recognition using facesonly. Overt recognition of famous voices has only been exam-ined in two individuals with CS in prior work (Reid etal., 1993;Lewis etal., 2001), with impairments observed in both cases. Atpresent, it is unclear whether these impairments can be observedtogether, and whether they occur against a background of normalname recognition. Moreover, given that none of these prior stud-ies compared performance of CS patients with that of patients of matched etiology, but no indication of CS symptomatology, it isalso unclear whether the instances of impairment in overt personrecognition that have previously been reported are in fact specificto CS.A final question regarding the scope of person recognitionimpairments in CS is whether any such impairments extendbeyond person identity and include deficits in overt recognitionof facial affect, i.e., facial emotional expressions. Given the pro-posed role for abnormal autonomic responses in CS (Ellis etal.,1997; Hirstein and Ramachandran, 1997), it is conceivable that overt recognition of affect in others might also be impaired inCS patients. In fact, several researchers have suggested a potentiallink between the recognition of affect and the experience of affec-tive states – a link that has been referred to as affective mimicry (e.g., Dimberg etal., 2000; Oberman etal., 2007; Heberlein etal., 2008; Stel and van Knippenberg, 2008). The limited research on recognitionof emotionalfacialexpressionsinpatientswithCShasprovidedmixedresultswithrespecttothisissue.Whilesomestud-ies revealed no such deficit (Hirstein and Ramachandran, 1997), there are also reports of a modest deficit in identifying partic-ular emotions such as fear or disgust (Breen etal., 2002). Prior studies typically required participants to discriminate betweendifferent types of emotions as opposed to detecting any sign of affect or judging the degree of emotional intensity. This is animportant distinction to make, given that recent neuropsycho-logical research in patients with focal lesions (but without any reported indication of CS) has shown that some prefrontal lesionscan produce deficits that are only noticeable when fine-graineddiscrimination between subtle changes in facial expression withina given emotion category are required (Heberlein etal., 2008;Tsuchida and Fellows, 2012). At present, it is unknown whetherCS may be associated with deficits in affect recognition of thisnature. GOALOFTHEPRESENTSTUDY The goal of the current study was to shed more light on the natureand extent of overt impairments in person recognition uniquely associated with CS, focusing on the specific issues describedabove. We had a unique opportunity to pursue this goal by studying a patient with Dementia with Lewy bodies (DLB) whoshowed clear signs of CS and comparing him to another patientwith DLB who did not experience CS, as well as to a groupof healthy control participants. Although the majority of CScases reported in the literature have been associated with psy-chiatric illness, affective disorders, focal lesions, or traumaticbrain injury,recent epidemiological evidence suggests that CS andother related misidentification problems are also often seen aspart of neurodegenerative disease, with a particularly large num-ber of cases associated with DLB (for review, see Josephs, 2007;Harciarek and Kertesz, 2008; Devinsky,2009; Thaipisuttikul etal., 2013). To address the extent of overt recognition impairment inthe two DLB patients in our investigation, we administered fame- judgments for faces, voices, and names that involved assessmentof familiarity as well as recovery of pertinent semantic knowledge.In addition, we sought to examine whether any deficits in personrecognition would include problems in recognizing facial expres-sionsof affect. Toprobethisability,participantswereaskedtoratethe intensity of fearful expression on a series of faces that variedin their intensity. MATERIALSANDMETHODS PARTICIPANTS DLB patients   JH (DLB w/Capgras).  JH is a 79 year old male who met diagnos-tic criteria of DLB (McKeith etal., 2005; Ferman etal., 2011) at the time of testing. Specifically, this diagnosis was made on the Frontiers in Human Neuroscience  September 2014 | Volume 8 | Article 726 |  3  Fiacconi etal. Cognitive impairment in Capgras syndrome basis of documented cognitive deficits in conjunction with thepresence of well-formed visual hallucinations, spontaneous signsof Parkinsonism (masked facies), REM sleep behavior disorder,and neuroleptic sensitivity. Testing in the current study took place ∼ 1 year after the first report of cognitive difficulties. The patienthad 9 years of formal education and additional vocational train-ing. He primarily worked as a real estate sales agent prior to hisretirement in 2003. The patient’s spouse of 28 years first notedsigns of visual misperceptions about 1 year prior to testing. Forexample, JH reportedly saw a raging dog, and at another time awoman’s face, in the chandelier of their living room. Visual mis-perceptions also included hallucinations such as seeing a crack in the wall that required fixing. More recently he also reportedsigns of auditory hallucinations, such as a buzz that he thoughtwas coming from an insect he could not see. First signs of CSwere noticed by JH’s spouse  ∼ 3 months prior to testing, andhave reoccurred with considerable frequency across this period.These misidentifications always pertain to his spouse and fol-low the classic description of the Capgras delusion. Specifically,these incidents are characterized by the expressed belief that hisspouse is not the person she claims to be but only looks simi-lar to her (i.e., an imposter). When in an acute delusional state,JH is resistant to any change in his belief and is not receptiveto rational counter-arguments or factual counter-evidence, suchas the wedding band or a wedding photograph. When his sonwas present in one of the earliest instances of an acute Cap-gras delusion, JH even asked his son how he could be so surethat this was indeed his mother. The delusion is typically associ-ated with some agitation and changed behavior, including activeattempts to find his“true”spouse. It has led to many instances of marital conflict. Although the fully expressed delusion most fre-quently occurs in sleep-wake transitions and was not present atthe time of testing, JH expressed in an interview that accompa-nied the testing session that his spouse never “feels the same” tohim the way she used to. We take this phenomenological impres-sion as a sign of a lasting cognitive deficit that is reflected inthe experimental findings described here. JH has also reportedmisidentifications of place, specifically his home, at various timesin combination with the Capgras delusion. Curiously, even whenprobed with specific cues provided by his spouse, he does notappear to recollect any episodes in which the Capgras delusionwas acutely present. Visual inspection of a clinical magnetic reso-nance imaging (MRI) scan (see  Figure 1 ) by a trained radiologistwho was blind to the specific behavioral profile of this patientrevealed mild atrophy of the medial frontal lobes and Sylvianfissures, with normal appearing posterior occipital and parietalregions. With respect to medication, JH was initially placed ona cholinesterase inhibitor (rivastigmine), and quetiapine (whichwas subsequently tapered off prior to testing) to help mitigate hisdelusions.  DF (DLB w/o Capgras).  DF is a 73 year old male who met diag-nostic criteria of DLB (McKeith etal., 2005; Ferman etal., 2011) at the time of testing,which took place ∼ 1 month after his formaldiagnosis of DLB, and 6 years after the onset of mild cognitivedifficulties,as reported by his wife. He had 21 years of formal edu-cation, having completed a Bachelor’s degree as well as a Masters FIGURE 1 | Clinical MRI images in sagittal plane for patients JH(above) and DF (below). There is visible atrophy in the dorsal aspects ofmPFC for JH but not DF. of Divinity and a Doctor of Divinity. He retired from his postas Pastor and community leader in 2008, after his spouse notedthat he had been starting to forget things. Around this time, healso began to experience a variety of clinical symptoms includ-ing visuo-spatial difficulties, left hand tremor, rigidity, disturbedbalance, REM sleep disturbances, and autonomic dysfunction,includingorthostatichypotensionandurinaryurgency/frequency.Based on a semi-structured interview conducted with his spouse,he reported experiencing hallucinations in 2012, in which heclaimed to see and hear people and animals not currently present.Often he would act on these hallucinations, sometimes talkingto the individuals he claimed to see. While he also experiencedsome paranoid beliefs, specifically sensing “someone followinghim,”these episodes were infrequent, and quickly resolved withina minute or so. His spouse also noted isolated incidents of visualmisperceptions in DF that included, for example, mistaking theirdog for a pair of shoes. Person recognition among family mem-berswasreportedtobenormal,althoughhesometimesapparently failedtorecognizeindividualshewouldhaveonlybeenintroducedto recently. His spouse also mentioned that he had experienceddisorientation, and had reported difficulties with following direc-tions. Furthermore, she noted changes in personality. In her view,he had turned from a very selfless and compassionate person intoa somewhat selfish man who complains often. In social situations,he seemed to be unwilling to initiate or engage in any conversa-tion unless it pertained to his immediate area of interest. Visualinspection of a clinical MRI scan (see  Figure 1 ) by a trainedradiologist revealed mild to moderate generalized atrophy, withslight predominance in temporal lobes. Similar to JH,DF was alsoprescribedacholinesteraseinhibitor(galantamine),andwasaddi-tionallyplacedondopamine(sinemet)andserotonin(citalopram)agonists to help alleviate Parkinsonism and depressive symptoms,respectively. Frontiers in Human Neuroscience  September 2014 | Volume 8 | Article 726 |  4  Fiacconi etal. Cognitive impairment in Capgras syndrome Neuropsychological profile  The results of several clinical neuropsychological tests of cognitivefunctioning for both patients are presented in  Table 1 . In termsof overall cognitive status as assessed using the Montreal Cogni-tive Assessment (MoCA; Nasreddine etal., 2005), both patients obtained scores in the range of mild cognitive impairment, withJH scoring slightly worse than DF. Both individuals showed clearsigns of anterograde impairment in episodic memory, with themost pronounced deficits on non-verbal (visual) tasks. While JHperformed numerically worse than DF on tests of recognitionmemory (Warrington word recognition; Warrington face recog-nition),DF obtained a lower score on the Benton face recognitiontest. Both patients were also impaired on perceptual tasks involv-ing visual object processing, with particularly poor performanceon the Embedded Figures task. On tests of executive functioning,specifically the Hayling and Brixton tests, both patients exhibitedcomparable levels of impairment. Healthy control participants  Ten control participants [all male; mean age = 78.1 years(SD  =  3.28); mean education  =  11.7 years (SD  =  2.83)] wererecruited to participate in various aspects of the current study.They were selected to match the patient with CS symptomatology  Table 1 | Neuropsychological profile of each patient.Patient JH Patient DF MoCA 21/30 24/30Warrington face recognition(%ile) < 5th 10thWarrington wordrecognition (%ile)6–10th 50thDoors and people (%ile)People test (immediate) 84th 75thDoors test 25th 10thShapes test (immediate) 2nd 5thNames test 50th 50thVerbal memory 75th 75th(people + names)Visual memory 5th  < 5th(doors + shapes)Benton face recognition 47 (normal) 37 (moderateimpairment)Hooper visual organizationtest68 (normed score) 77 (normed score)Embedded figures 1st quartile 1st quartileHayling sentencecomprehension (scaledscore)3 (poor) 4 (low average)Brixton spatial anticipationtest (scaled score)1 (impaired) 1 (impaired) (i.e., JH) in sex, age, and years of education as closely as pos-sible. Of these 10 participants, nine individuals completed thefamous faces (Experiment 1A) and famous names (Experiment1C) tasks, with eight participants completing the famous voices(Experiment 1B) task as well. All ten participants completed thefear rating task (Experiment 2). Controls were screened to ensurethe absence of current or past neurological or significant psy-chiatric disorders. This research project was conducted with theapproval of the Health Sciences Research Ethics Board (HSREB)at Western University, and all participants gave written informedconsent. EXPERIMENTALPROCEDURES Experiment 1A: famous face recognition  We created a list of 64 famous faces and 64 faces of non-famousindividuals. Famous individuals were sampled broadly so as toincrease the likelihood that they would indeed be known to study participants.Eachfamouspersonbelongedtooneof threediscretehistorical eras (1950 to 1969,1970 to 1989,and 1990 to 2009) andto one of four occupation categories (politicians, movies actors,television actors/personalities, and athletes), with roughly equalnumbers of famous faces in each era and category. Images of famous faces from a front view were retrieved through a GoogleImage search and the Life magazine image archive 1 . Each famousface was yoked with a non-famous face that was found via aGoogle Image search. Non-famous faces were matched to thefamous individuals’ sex, approximate apparent age, and era. Inorder to ensure a lack of fame for the non-famous faces, imagesof anonymous models from advertisements and images fromout-of-country real estate brokerages, barristers, and genealog-ical websites were used. If a name was displayed by the searchengine, we also checked that it did not point to a famous per-son. All color images were transferred to grayscale and all imageswere standardized in size to be 380 pixels in height and between204 and 302 pixels in width. For each image, we superimposed awhiteovalframearoundthefacetooccludescenebackgroundandclothing.The experiment was presented on a laptop computer usingE-prime 1.1 programming software. Participants provided theexperimenter with oral responses to each screen prompt, and theexperimenter entered numeric responses by keyboard press andrecorded any knowledge generated by participants. Trials werepresented in random order. For each trial, participants viewedone famous face and its non-famous yoke on the screen, side by side (see  Figure 2 ). For 50% of all trials, the famous face wason the left side. While the image pairs were on screen, partici-pants verbally indicated which of the two faces they knew fromthe media. Both faces remained on the screen as participantswere asked to rate their confidence in their choice on a scaleof one to three, corresponding to “I am guessing,” “I think Iknow, but I am not sure,” and “I am certain that I have seenthis person in the media,” respectively. Following this response,the face selected as famous remained on the screen, and the par-ticipant was asked to provide information (if any) they could 1 Frontiers in Human Neuroscience  September 2014 | Volume 8 | Article 726 |  5
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