特別寄稿

Delusions and the Cognitive Neuroscience of False beliefs

Martin L. Albert and Joshua Berger

Key words : , False beliefs, Cognitive neuroscience, Confabulation, Brain damage

A is a false belief（ a belief not generally structural brain damage in frontotemporal areas, and, accepted by a person’s culture）, based upon an errone- in agreement with previous studies, a preponderance ous inference about external reality and maintained of these lesions to be in the right hemisphere（ Holt & despite evidence to the contrary. The relationship be- Albert, 2006）. tween abnormal brain function and delusions has been The altered perceptual processing which results a topic of interest in cognitive neuroscience for de- from structural brain damage has led some to propose cades, given its relevance to the understanding of in- that the construction of false beliefs is the result of the teractions among perception, memory, attention, and individual’s attempt to create a meaningful explanation the construction of beliefs. Notable patterns of neuro- to account for their anomalous experiences（ Maher, logical damage across varying types of delusional be- 2005）. The role of such anomalous experiences in de- liefs have been described（ Cummings, 1985）, yet the lusional beliefs is reminiscent of the anomalous expe- pathogenesis of delusions remains elusive. Delusional riences of illusions and hallucinations, yet they remain misidentification （ DMS） comprise those qualitatively different. An illusion is an erroneous per- delusions “in which a patient consistently misidentifies ception of external reality, but unlike a delusion, the il- persons, places, objects, or events”（Feinberg & lusion can be modified with reason and explanation. A Roane, 2005）. Common delusional syndromes are hallucination is a false or disordered sensory experi- listed in Table 1. Research has often found misidenti- ence involving an erroneous internal perception which fication syndromes to involve organic dysfunction does not necessarily entail an attribution about the ex- （Joseph, 1986） and a strong correlation between mis- ternal environment. In this paper we propose that the identification syndromes and right hemisphere lesions distinguishing qualities of a delusion which must be

（Forstl et al., 1991）. A meta-analysis of late-onset accounted for by any comprehensive neuro-cognitive delusions in persons over age 60 found individuals theory of false beliefs includes the following factors :

with late-onset delusions of the DMS type to exhibit （1） altered perceptual experience of external reality, （2） construction of a story that becomes a false belief, From the Department of , Harold Goodglass Aphasia Research Center and Language in the Aging Brain and（ 3） persistence of the belief. Laboratory, Boston University School of Medicine and VA Theories of delusional syndromes have encom- Boston Healthcare System, Boston, MA Supported in part by the National Institute of Deafness and passed psychological, cognitive, and neurological per- Communication Disorders, National Institute on Aging, spectives and are typically formulated based upon a and, Department of Veterans Affairs Medical Research Service vertical analysis of a single delusional . In

268 Japanese Journal of Cognitive Neuroscience Table 1. Delusional Syndromes in Neurology

Capgras Syndrome – Replacement by imposter

Cotard Syndrome – Belief that one is dead

Anton’s Syndrome – Denial of blindness

Alien Hand Syndrome – Not my hand

Reduplicative paramnesia – Substitution or duplication of person or place

Anosognosia – Denial of hemiplegia

Fregoli Syndrome – People in disguise

Othello Syndrome – Unfaithful spouse

Phantom boarder – Unwelcome guest

Lycanthropy – Animal transformation

Mirror self-misidentification – Not me in mirror this paper we review four syndromes of delusion :（a） and neurological conditions such as Alzheimer’s dis- Capgras,（ b） Cotard,（ c） Alien Hand, and（ d） Anton, ease（ Mendez, Martin, & Smyth, 1992）, Tourette’s and then employ a horizontal analysis across these syndrome （Sverd, 1995）, head trauma （Alexander, syndromes to determine the neurological and cognitive Stuss, & Benson, 1979）, cerebrovascular disease, epi- factors shared amongst them. Finally, based on this lepsy（ Forstl et al., 1991）, intoxication or with- horizontal analysis of shared attributes, we offer an drawal, infectious and inflammatory disease, endocrine explanatory model of the cognitive neuroscience of disorders, mental retardation（ Signer, 1992）, intrace- false beliefs. rebral hemorrhage（ Hayman & Abrams, 1977）, and （ MacCallum, 1973）. Characteristic features of Capgras disorder include Capgras syndrome is the most common of the delu- （a） apathy,（ b） dysfunction in facial recognition,（ c） sional misidentification syndromes. Persons with the depersonalization,（ d） confabulation,（ e） memory im- Capgras delusion persist in believing that a close ac- pairment, and（ d） executive system dysfunction. Ac- quaintance has been replaced by a double or an “im- cording to Alexander, Stuss, and Benson（ 1979）, the poster”. This syndrome was first described by Capgras syndrome was formerly considered to be primarily a and Reboul-Lachaux（ 1923） who reported the case of functional, psychiatric disorder characterized by para- a 53-year-old woman with psychotic symptoms who noid psychotic reactions（ Merrin & Silberfarb, 1976）. insisted that her “husband, children, neighbors, and However, structural brain damage has so often been others had been replaced by doubles”, and these “dou- implicated that most experts now consider this syn- bles themselves were replaced by other doubles（ 80 drome to be neurological or neuropsychiatric in origin. times, in the case of her husband）”（ Ellis & Lewis, Case reports have demonstrated a preponderance of 2001）. According to Roane et al.（1998）, Capgras damage to the right hemisphere（ Feinberg and Shap- syndrome has been reported with a range of medical iro, 1989 ; Forstl et al., 1991）. Likewise, those pa-

認知神経科学 Vol. 11 No. 3・4 2009 269 tients with unilateral hemispheric damage have shown tients may lead to a deficit in resolving mental- con Capgras to be significantly more common with right flicts and an increased level of apathy towards address- unilateral damage than with left sided damage（ see, ing such conceptual conflict. Furthermore, according Alexander, Stuss, & Benson, 1979）. to Feinberg and Roane（ 2005） the emeregence of con- Delusional misidentification has also been attributed fabulation is associated with executive system dys- to disconnection between the right and left hemi- function and memory impairment （Alexander &

spheres. The resulting disruption of inter-hemispheric Freedman, 1984 ; Deluca, 2000 ; Feinberg & Giacino, communication prevents integration of the varying 2003 ; Fischer et al., 1995 ; Johnson et al., 2002 ; representations produced by each hemisphere（ Ellis & Moscovitch & Melo, 1997 ; Ptak & Schnider, Young, 1990 ; Joseph, 1986 ;）. Joseph（ 1986） pro- 1999; Schnider & Ptak, 1999; Stuss et al., posed that each hemisphere generates separate repre- 1978 ; Vilkki, 1985）. sentations of a face which are normally combined to In summary, Capgras syndrome is associated with a construct an integrated perception of the external range of neurologic lesions, each of which may con- world, and that “depending upon which hemispheric tribute to a portion of the syndrome. The predominant connections are most impaired, the clinical syndromes lesions appear to be bifrontal, right frontal, or right of misidentification, reduplicative paramnesia, or dis- frontoparietal. The resulting executive system impair- orientation will result”. ment is correlated with confabulation, memory dys- Posterior damage to the right cerebral hemisphere function, and apathetic response. Brain damage asso- can lead to a shift in one’s “sense of familiarity”（ Al- ciated with the right posterior area correlates with exander, Stuss, & Benson 1979）. Ellis and Young depersonalization, and can impair facial processing of （1990） proposed that Capgras syndrome is the result covert affective cues in response to familiar faces. of malfunction in the visual “dorsal route” responsible Furthermore, interhemispheric dysfunction related to for covert/autonomic/affective recognition of familiar callosal disconnection can prevent the integration of faces. The “dorsal route” involves messages from the pertinent hemispheric representations. visual cortex being transmitted through the superior temporal sulcus, inferior parietal lobule, and finally the Cotard Delusion cingulate gyrus to the limbic system and amygdala. In 1880, the French physician Jules Cotard present- This visual system is in contrast to that of the ventral ed a case of a 43 year old woman who claimed that she tract of the “identification detector” which processes had ‘no brain, nerves, chest, or entrails and was just information from the visual cortex through the longitu- skin and bone – neither God nor Devil existed – she dinal fasciculus to the limbic system （Bauer, was eternal and would live forever’（ Enoch & Ball, 1984 ; Ellis & Lewis, 2001）. Ellis and Young（ 1990） 2001 ; Kudler, George, & Jaimon, 2007）. This syn- posited that damage to this ventral route is associated drome, as it became known subsequently, involves a with . dissociation of a person from his or her own body According to Merrin & Silberfarb（ 1976）, deper- parts, and then from his or her self. According to sonalization in Capgras patients has been linked to bi- Kudler, George, and Jaimon（ 2007）, the severity of lateral caudal orbital frontal damage. Alexander et al. this 'nihilistic delusion' can vary widely, from that of a （1979） proposed that frontal damage in Capgras pa- patient insisting that they and the world don’t exist to

270 Japanese Journal of Cognitive Neuroscience that of a somewhat milder, but nevertheless serious, some authors have argued that medial “frontoparietal distress on the part of the patient of losing one’s reason and thalamic perfusion abnormalities produce a de- and feelings. graded body schema, which in the context of depres- This ‘nihilistic delusion’ can present in pure form or sion” and internalized/depressive attributions produces manifest in conjunction with other psychiatric condi- the syndrome. tions（ Berrios & Luque, 1995）. According to Enoch It has been suggested that Cotard and Capgras syn- and Ball（ 2001）, comorbid symptoms include “anal- dromes share a common underlying neurostructural gesia, mutism, self-mutilation, suicidal ideas, illusions, deficit associated with damage to the non-dominant and in some cases hallucinations. The latter can be vi- cerebral hemisphere（ Joseph, 1986 ; Kudler, George, sual but are more typically auditory”. Also, in this & Jaimon, 2007 ; Wright, Young, & Hellawell, 1993）.

“psycho-organic syndrome” there are often “signs of McKay and Cipolotti（ 2007） suggest that Cotard and an impairment of the sensorium such as disorienta- Capgras syndromes are differentiated according to an tion, defects of grasp, attention and concentration, to- internal and external attribution style respectively, both gether with memory loss”. in response to the same underlying perceptual anoma- Anderson（ 1964） asserted that this disorder is an ly. Wright, Young, and Hellawell（ 1993） reported a outgrowth of a lifelong accumulation of tendencies case of sequential Cotard and Capgras delusions, in stemming from obsessive-compulsive disorder, which which the Cotard delusion manifested in concordance forms a fertile ground for the emergence of delusions with a depressive affect and associated internal attribu- of negation（ Enoch & Ball, 2001）. tion tendency, whereas the Capgras syndrome emerged Many cases of Cotard syndrome have been reported in the context of persecutory delusions associated with with normal CT/MRI findings, although some appear external attribution. to be associated with structural and functional brain In summary, Cotard syndrome is associated with dysfunction（ Kudlur, George, & Jaimon, 2007）. In frontal damage, leading to memory impairment and their review of the literature, Kudlur, George, and Jai- executive system dysfunction, and damage to temporal mon（ 2007） noted “abnormalities in the non-dominant and parietal regions in the non-dominant hemisphere. frontal, temporal, and occasionally parietal lobes”. Jo- Damage to the temporal and parietal regions is associ- seph & O’Leary（ 1986） showed that in comparison to ated with altered body schema which in conjunction controls, patients with Cotard delusion exhibited great- with right frontal damage has been shown to lead to er diffuse cerebral atrophy and inter-hemispheric fis- depersonalization from one’s own body, general disso- sure enlargement, related to medial atro- ciation, and deficits in facial processing similar to phy（ particularly the superior frontal gyri, paracentral those found in the Capgras syndrome. lobules, and cingulate gyrus）, and dilation of lateral ventricles. Alien Hand Syndrome In the review conducted by Kudler, George, and Jai- This syndrome is characterized by a varied set of mon（ 2007）, it is reported that SPECT studies have complex motor dysfunctions, typically found in the

“identified abnormalities in the frontal regions”, in ad- non-dominant hand, and results in a patient perceiving dition to “decreased blood flow to the medial fronto- the alien hand as having ‘a mind of its own’ or being parietal and frontal dorsolateral cortex”. Furthermore, outside of one’s control（ Biran, 2006）. Brion and Je-

認知神経科学 Vol. 11 No. 3・4 2009 271 dynak （1972） first proposed the term “la main clude “disruption of complex willed motor acts by the etrangere” to describe corpus callosotomy patients left hand”, in addition to intermanual conflict（ Scep-

who failed to recognize their left hand in the absence kowski & Cronin-Golomb, 2003）. Lesions in the pos- of visual input. Bogen（ 1979） later adopted the term terior portion of the corpus callosum, particularly in Alien Hand（ AH） to emphasize the subject’s dissoci- the ventral region, are associated with diagnostic dys- ated reaction to the alien limb. According to Scep- praxia, which is a lesser form of intermanual conflict

kowski and Cronin-Golomb（ 2003）, the hallmark of characterized by non-antagonistic intermanual move- this disorder is the “autonomous complex movements” ments（ Aboitiz et al., 2003 ; Tanaka et al., 1996）, and

performed by the alien hand against the patient’s will is typically found in early post-operative corpus cal- （Biran & Chatterjee, 2004 ; Biran et al., 2006 ; Bo- losotomy patients（ Aboitiz et al., 2003）. Intermanual gen, 1979 ; Brion & Jedynak, 1972 ; Cooney & Gaz- conflict involves antagonistic unimodal movements of

zaniga, 2003 ; Feinberg, 1997 ; Fisher, 2000 ; Gas- the alien hand which performs actions at cross-purpos- quione, 1993 ; Kertesz, 2000 ; Marchetti & Della es to the dominant hand's intentional actions, such as Sala, 1998 ; Trojano et al., 1993）. the right hand putting on clothes while the left hand

There has been considerable nosological confusion takes them off （Scepkowski & Cronin-Golomb, in attempting to classify the various behavioral symp- 2003 ; Tanaka et al., 1996）. toms associated with AH syndrome （Aboitiz et al, According to Feinberg et al. （ 1992）, the second 2003 ; Chan & Ross, 1997）. This problem has form of AH is associated with lesions to the medial stemmed, in part, from the difficulty in classifying the frontal area, including the premotor area, supplemen-

nuanced set of symptoms related to higher-level motor tary motor areas, and the anterior cingulate gyrus

processing. Biran & Chatterjee（ 2004） proposed a （Scepkowski & Cronin-Golomb, 2003）. Most cases

three-fold classification to account for the symptoms involve damage to the frontal region and anterior two- of AH ; diagnostic dyspraxia, anarchic hand, and auto- thirds of the callosal region as a result of unilateral or criticism. Furthermore, Biran et al. （ 2006） added, bilateral infarction of the anterior cerebral artery（ Gas- that in addition to these motor/sensory dysfunctions, a quoine, 1993 ; Giroud & Dumas, 1995 ; Scepkowski

patient must have adequate awareness of the alien & Cronin-Golomb, 2003）. According to Skepkowski

limb’s actions in order to perceive its ‘alien’ quality. & Cronin-Golomb（ 2003）, the behavioral symptoms In all cases, the alien limb is perceived as foreign and associated with this form of AH include “grasp reflex, outside of voluntary control, however, this may or may impulsive groping, and compulsive tool manipulation” not lead to persistent abject denial of ownership. Pa- （e.g. anarchic hand）. It has been posited that this pat- tients who do deny ownership, may personify the alien tern of behavior is indicative of heightened environ- limb, and adopt names, such as “monster” or “cheeky”, mentally driven（ exogenous） determinants of response which in turn reflects their negative affect towards this with a corresponding reduction in intention driven

body part（ Scepkowski & Cronin-Golomb, 2003）. （endogenous） executive control factors（ Biran et al., Feinberg, Schindler, Flanagan, & Haber （1992） 2006 ; Giovanetti et al., 2005）. These impulsive suggested that the two major subtypes of the syndrome movements increase in time of fatigue, anxiety, and correspond to callosal lesions and damage to the fron- executive processing load （Giovannetti et al., tal lobes. Symptoms associated with ‘callosal AH’ in- 2005 ; Goldberg & Bloom, 1990） suggesting that the

272 Japanese Journal of Cognitive Neuroscience residual frontal processing, perhaps in the ipsilateral lobe（ Wolpert et al., 1998）-and mapped onto internal hemisphere, can still maintain some control. Accord- templates of the body to generate expected sensory ing to Biran et al. （ 2006）, although these movements outcomes （McGonigle et al., 2002）. An efference consist of stereotypic motor fragments （Luria, copy is also sent to the motor areas—particularly the 1966 ; Sandson & Albert, 1984） – for which there is premotor cortex—in preparation for rapid corrective evidence that they may be generated in the parietal adjustment of movements when errors between the ex- lobe（ Colby, 1998 ; Denny-Brown, 1958, ; Milner, & pected and actual sensory outcomes are detected Goodale, 1995）― these motor fragments are stimu- （Helmholtz, 1995 ; Lewis, 2006）. The perception of lus bound and retain the perception of purposeful ac- a limb moving in space is largely based on a “feedfor- tion. Yet they are not properly coordinated into inte- ward model” of where the limb should be in space grated goal directed behavior due to a lack of executive （Leube et al., 2003）. Damage to this feed forward- processing（ see Giovannetti et al., 2005）. feedback network can result in alien hand movement The manifestation of anarchic hand was discussed which is not perceived as intentional, resulting in an by Denny-Brown（ 1958） who described the presence anomalous experience, usually characterized by “per- of magnetic and repellant apraxias as corresponding to ceptual repulsion”. This “perceptual repulsion” is the anterior and posterior damage respectively. According equivalent of the “dissociation between events that ei- to this theory, the parietal lobe contains the networks ther do or do not produce self-attribution”（ Giummar- for approach behavior whereas the frontal lobe con- ra, 2008 ; Tsakiris & Haggard, 2005）. trols avoidance behavior. Damage to the frontal lobe These behavioral elements may take place within releases pronounced stimulus bound motor primitive the context of frontal lobe damage resulting in ‘utiliza- responses related to parietal lobe function（ e.g. mag- tion behavior’（ Biran & Chatterjee, 2004 ; Boccardi netic apraxia ; anarchic hand） whereas damage to the et al., 2002 ; Lhermitte, 1983;） wherein little insight posterior cortex results in disorders of motor control, is present. Although, patients with frontal damage called repellant apraxia（ Biran & Chatterjee, 2004）. may refer to their arms in the third person due to the Impaired sensory feedback from the posterior regions anomalous motor experience, they remain capable of has been implicated as a underlying factor in repellant recognizing that it is indeed their arm in a physical apraxia（ Marey-Lopez et al., 2002 ; Scepcowski & sense. However, this anomalous experience lays the Golomb, 2003）. groundwork for the confabulation of denying owner-

The frontal lobes have dense interconnections with ship, as described in the ‘two-deficit’ model of delu- regions of the parietal lobe where high level multi- sion formation（ Davies, Coltheart, Langdon, & Breen, modal sensory integration takes place （Giummarra 2001）. 2008）. The frontal area has been posited as the feed- In summary, alien hand syndrome consists of a fail- forward action planning area, whereas the posterior re- ure to recognize the non-dominant hand in the absence gion acts as a feedback system to these feedforward of visual input, leading to disruption of control of representations, resulting in coordinated movement. complex voluntary motor movements of the non-dom- Giummarra（ 2008） explains that upon generation of a inant hand. These motor control abnormalities, in con- movement an efference copy of the movement is sent junction with the executive system dysfunction and to the parietal cortex-particularly the superior parietal memory impairment resulting from frontal damage,

認知神経科学 Vol. 11 No. 3・4 2009 273 can lead to confabulation and depersonalization of the Anton’s syndrome is also associated with confu- ‘alien limb’. sional states and memory loss （Hecean & Albert, 1978）. Heilman（ 1991）, cites that this dysfunction

Anton’s Syndrome can result from damage to the inferior-medial tempo- G. Anton（ 1899） described a patient who claimed ral areas caused by posterior circulation insufficiency

that he could see despite documented blindness. This （Caplan & Hedley-White, 1974）. At the same time, condition, in which patients deny loss of vision despite memory disorders within the context of confusional blindness, has come to be known as Anton’s syndrome. states or bifrontal damage have been shown to contrib- A subject exhibits denial of blindness with confabula- ute to confabulation （Berlyne, 1972 ; Kapur & tion, such as, “there’s insufficient light to （see” Al- Coughlan, 1980 ; Kopelman, 1987 ; McDaniel & drich et al., 1987 ; Abutelaebi et al., 2007） or “No, I McDaniel, 1991 ; Shapiro et al., 1981 ; Stuss et al., can see it, I just have a headache...”（ McDaniel & Mc- 1978;）. Confusional states have been found in pa- Daniel, 1991）. Furthermore, these patients can exhibit tients with Anton’s syndrome, and have been associat-

full-blown confabulated descriptions of what they pur- ed with damage to the left fusiform and lingual gyri, portedly see, when in fact no such thing is present, as also caused by insufficient output from the posterior when a patient described a book in detail, when an un- cerebral artery（ see Heilman, 1991）. This confusional related object, and not a book, is placed in front of element could potentially contribute towards the de- them and they are asked to describe it（ Goldenberg, velopment of , but confusional states and Mullbacher, & Nowak, 1995）. In a detailed review of memory loss have been dissociated from anosognosia two typical cases, Brockman and Hagen（ 1946） con- and Anton’s syndrome in the research literature（ see tended that patients exhibit “…considerable intellectu- Heilman, 1991）. Suzuki et al. （ 1997） presented a pa- al deterioration, impairment of memory, disorientation, tient with denial of left hemiplegia and blindness who

confabulation, and complete blindness…”. had sustained damage to the “right fronto-parietal Anton’s syndrome has traditionally been associated area, left lateral frontal area, and bilateral occipital ar- with bilateral lesions to the occipital area, commonly eas”. The patient confabulated frequently, was disori- due to bilateral occipital cortex ischemia due to insuf- ented to time and place, and exhibited short term ficient circulation in the posterior cerebral arteries memory loss in addition to unilateral spatial neglect of （Aldrich et al., 1987 ; Abutelabi et al., 2007 ; Mc- the left side. Daniel & McDaniel, 1991）. According to McDaniel However, not all patients with cortical blindness & McDaniel（ 1991）, there have also been cases in- deny their deficit, yet both anosognosia and cortical volving damage to pregeniculate areas, and these cases blindness are associated with damage to the right are typically associated with diffuse brain damage hemisphere and deafferentation of the right thalamic （Redlich & Dorsey, 1945 ; Geschwind, 1965 ; Swartz, area from the parietal and visual association areas（ see 1984）. Geschwind （1965） suggested that Anton’s McDaniel & McDaniel, 1991）. Some authors have

syndrome resulting from damage to anterior visual ar- suggested that non-recognition of deficit in cortical eas is more dependent on a diffuse dysfunction of cog- blindness is the result of damage to higher order visual nition relative to those with damage to the primary vi- association areas（ BA 18 and 19）（ Cusumano, Fletcher, sual association areas in the occipital cortex. & Patel, 1981 ; McDaniel & McDaniel, 1991）. An-

274 Japanese Journal of Cognitive Neuroscience Table 2. Neuropsychological and neuroanatomical correlates of delusional syndromes

Syndrome Neuropsychology Neuroanatomy

Capgras Delusion Apathy Bifrontal Sometimes a disorder in face recog- Right frontal nition Right frontoparietal Depersonalization Interhemispheric disconnection Confabulation Executive system impairment Memory Impairment

Cotard Delusion Sometimes deficit in face processing Right frontal （as in Capgras syndrome） Right fronto-temporal Depersonalization Right fronto-parietal Confabulation Interhemispheric fissure enlarge- Executive system impairment ment Memory impairment Dissociation

Alien Hand Syndrome Disruption of complex voluntary Callosal lesions motor movement in non-dominant Frontal lesions hand Fronto-parietal lesions Intermanual conflict Failure to recognize left hand in the absence of visual input Grasp reflex, impulsive groping with right hand Depersonalization Confabulation Executive system dysfunction Memory impairment

Anton’s Syndrome Often（ not always） with confusion- Blindness may be due to lesion any- al state where from posterior orbital region Confabulation to calcarine cortex Executive system dysfunction Bilateral occipital cortex Memory impairment Systematic hypoxia with border zone lesions frontal, parietal, and occipital Right frontoparietal Bifrontal/orbitofrontal/optic nerve Corpus callosum Deafferentation of right thalamus to right parietal cortex and visual asso- ciation cortex

認知神経科学 Vol. 11 No. 3・4 2009 275 ton’s syndrome and anosognosia have been attributed less, if we conduct a horizontal analysis of these four to interhemispheric disconnection （Abutalebi et al., syndromes, we can extract the general patterns of neu- 2007 ; Heilman, Barret, & Adair, 1998） implicating rological damage and neuropsychological deficits the possible role of disconnection between the visual shared amongst them. （ Please refer to Table 2）. It is association areas and the language area in the left our contention that a tentative model for the cogni- hemisphere as a precipitating factor in confabulation tive neuroscience of false beliefs can reasonably be denying blindness（ Heilman, 1991）. developed by looking at shared factors across multiple McDaniel and McDaniel（ 1991）, reported a patient syndromes rather than by limiting analyses to one syn- with Anton’s syndrome whose confabulation resolved drome alone. The three stages of delusion formation along with improvement in memory and vision. Con- which we will attempt to account for through this fabulation has been associated with “frontal lobe dys- method of horizontal analysis are （ 1） misidentifica- function manifesting as perseveration, lack of verbal tion, or, altered perceptual experience of external reali- inhibition, and poor self-monitoring”. The authors ty,（ 2） construction of a story that becomes a false be- concluded that a failure to self-monitor due to frontal lief, and（ 3） persistence of the belief. dysfunction in conjunction with a memory deficit to- Firstly, misidentification, or, altered perceptual ex- gether with severe vision impairment was sufficient to perience of external reality. The predominance of le- produce the patient’s Anton’s syndrome. sion localization for all four syndromes reviewed in In summary, Anton’s syndrome is oftentimes associ- this paper is right frontal or right frontoparietal. Per- ated with a confused mental state and tendencies to- ceptual misidentification results from damage in these ward confabulation, in conjunction with executive sys- areas. Four aspects of misidentification are important tem dysfunction and memory impairment, as well as in the construction of a neurological theory of delu- visual system impairment. Many patients have sus- sions, including（ a） perceptual problems leading to al- tained bilateral damage to the occipital cortex, but tered experience,（ b） lack of attribution alternatives, blindness in Anton’s syndrome may be due to lesions （c） deficit in cognitive synthesis（ impaired executive anywhere from the posterioir orbital region to the cal- function）, and（ d） impairment of feed-forward/feed- carine cortex. Occipital damage often results from back interaction between parietal and frontal associa- systemic hypoxia which can also lead to border zone tion areas, thereby preventing the altered experience lesions in the frontal and parietal areas. Cases have from being placed in its proper cognitive context. presented with damage to the right frontoparietal re- At their core, all four of these syndromes involve gion, bifrontal and orbitofrontal areas, callosal dam- either sensory（ Capgras, Anton’s, and Cotard） or mo- age, and deafferentation of the right thalamus to the tor（ Alien Hand） dysfunction leading to a perceptuo- right parietal cortex and visual association area. motor alteration, supporting the theory that anomalous experience is a basic building block in the develop- Towards a Neurological Theory of Delusional ment of delusional beliefs. Furthermore, damage to

Misidentification Syndromes the temporo-parietal regions disrupts cortico-limbic Not one of the syndromes of delusion reviewed in interactions, resulting in altered emotional processing this paper emerges from available case reports with a in addition to the altered perceptual experience（ see single, defining clinicoanatomical profile. Neverthe- Cummings, 1985）. Although anomalous experience

276 Japanese Journal of Cognitive Neuroscience may be a necessary factor, it is not sufficient to - ac regard for information which contradicts the individu- count for the fully developed delusion, since the al’s false belief. For example, in Capgras syndrome anomalous experience does not account for volitional the individual does not take due credence of the fact

influences, symbolic, and conscious executive- func that the so-called ‘imposter’ both acts and speaks like tions, including attribution tendencies （Langdon & the real person. The inability to appropriately incorpo- Coltheart, 2000）, which interact with perceptual expe- rate countervailing information in cognition is indica- rience to produce a fixed belief . tive of a lack of generated alternatives in conjunction

Garety and Hemsley（ 1994） and Stone and Young with a dysfunction in self-monitoring and error detec- （1997） proposed that deluded individuals exhibit an tion. According to Lieberman et al. （ 2002）, error de- attribution bias. These individuals are prone to expla- tection is associated with the anterior cingulate region, nations derived from the immediate experience of their which shares connections with the "amygdala, basal senses over explanations that incorporate past regulari- ganglia, lateral temporal cortex, hippocampus, pre- ties and general knowledge. This is because first per- frontal cortex, and regions associated with somatic and son sensory information is naturally more salient than visceral sensations" ; whereas processing exceptions the other modes of knowledge, and in deluded invidu- to rules and generating alternative hypothesis has been als there is evidence of a pronounced lack of ability in shown to be associated with the prefrontal cortex and suspending this natural bias in order to properly pro- working memory. The prefrontal cortex has also been cess incoming information which in turn leads to a shown to be involved in ongoing reality monitoring, lack of generated alternatives（ see Langdon and Col- and lesions to this area leads to spontaneous confabu- theart, 2000）. There is evidence to suggest that auto- lation（ Schnider, 2001）. matic attribution construction processes are associated The frontal lobes have dense interconnections with with the inferotemporal cortex （Boucart et al., regions of the parietal lobe where high level multi- 2000 ; Gerlach et al., 2000 ; Hoffman & Haxby, modal sensory integration takes place（ see Giummarra

2000 ; Lieberman et al., 2002）. et al., 2008）. Overall, the feed-forward/feed-back in- “Disorders of the self”, such as may be found in teractions between parietal and frontal areas, particu- Capgras and Cotard syndromes, have typically been larly in the right hemisphere, are impaired in delusion

associated with damage to the right-frontal formation. Deficits of perception due to parietal dam- regions ; and in these dirorders there is evidence of a age and impaired cognitive synthesis due to frontal

significant right-hemispheric bias across the frontal, damage result in misidentification due to an inability temporal, and parietal lobes, in addition to a preva- to process the altered experiences into an appropriate

lence of bi-frontal damage（ see Feinberg & Roane, cognitive context. 2005）. All of the syndromes reviewed here exhibited Second, construction of a story that becomes a false bifrontal or frontal damage. Damage to the frontal re- belief. Ordinarily, when we build a meaningful narra- gion is associated with difficulty in taking account of tive, we perceive the world correctly and connect this the anomalous experience, poor monitoring of the re- accurately perceived experience with intact systems sulting attributions, and inability to change/alter/adapt. for semantic categorization. A person with a delusion- A deficit in cognitive synthesis among these four al misidentification syndrome also attempts to create a clinical syndromes is apparent in the pathological dis- meaningful narrative, but, as we have seen, this narra-

認知神経科学 Vol. 11 No. 3・4 2009 277 tive is built upon an anomalous experience. In the four 1987）. Perseverative phenomena are not limited to syndromes reviewed in this paper, we find evidence actions or utterences, but can also include ideas, be- for impaired callosal transfer of information from the liefs, and emotions. In the four delusional misidentifi- right to the left hemisphere. Interhemispheric fissure cation syndromes under consideration, we have found enlargement and/or callosal disconnection are present right frontal and/or right frontoparietal lesions, which

to some degree in all. Deficits in interhemispheric can result in a combination of continuous and stuck-

processing disrupt interactions between the semantic in-set perseveration, thereby accounting for the persis- systems of the left hemisphere and spatial/perceptual tence of the false beliefs. networks of the right hemisphere（ Gazzaniga, 1970 ; In summary, we propose this tentative model for Sperry, Gazzaniga, & Bogen, 1969）. Undamaged por- the cognitive neuroscience of false beliefs : 1） right tions of the right hemisphere receive inputs, process frontoparietal network disruption causes not only

them, and create a story without the normal, inter- anomalous experience, or misidentification, but also hemispheric supervisory guidance of the semantic sys- difficulty taking account of the anomalous experience tem. In order to understand ourselves and our bodies, due to impaired monitoring of experience and inability and to experience ourselves and our bodies in relation to change/alter/adapt. 2） Callosal lesions cause dis- to the world, we must have not only a healthy percep- connection of the anomalous experience from the se- tual organization of our bodies（ a sense of ourselves）, mantic system. Consequently, the person creates a but also a healthy connection between this sense of personal and unique story with regard to his or her ourselves and our knowledge of the world via the se- anomalous experience, that is, the person provides a

mantic system（ Ross, 1981 ; Bear, 1983 ; Cummings, post-hoc explanation of the anomalous experience 1985）. If, as a consequence of right frontoparietal based on impaired semantic categorization and devoid brain damage, a person sustains an anomalous experi- of ordinary semantic knowledge（ a left hemisphere/ ence, and if, subsequently, the anomalous experience right hemisphere disconnection）. The story may satis- is inadequately connected to the semantic systems of fy this person, but cannot be appreciated by others the left hemisphere because of impaired callosal trans- who do not share the anomalous experience. They fer, the story this person creates might well be mean- will see this story as incorrect or false. 3） Persistence ingful for that person, but would not, and could not, be of these incorrect stories（ false beliefs） results from shared by others. The story then would be considered damage to right frontoparietal systems producing a

incorrect or false by others. Thus, a false belief is cre- combination of stuck-in-set and continuous persevera- ated. tion, accounting for the resistance to reason found Third, persistence of the belief. Persistence of the amongst those with delusional beliefs. false belief is a perseverative phenomenon. At least three types of perseveration have been described :（a） References : recurrent perseveration（ following damage to left tem- Aboitiz F, Carrasco X, Schroeter C, Zaidel D, Zaidel E, La- poroparietal regions）, （b） continuous perseveration vados M（. 2003） The alien hand syndrome : Classifi- cation of forms reported and discussion of a new condi- （following damage to right temporoparietal regions）, tion. Neurological Science 24, 252-257. Abutalebi J, Arcari C, Rocca MA, Rossi P, Comola M, Comi and（ c） stuck-in-set perseveration（ following damage GC, Rovaris M, Filippi M.（ 2007） Anton’s syndrome to left or right frontal regions）（ Sandson & Albert, following callosal disconnection. Behavioral Neurol-

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