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Delusions and the Cognitive Neuroscience of False Beliefs

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Delusions and the Cognitive Neuroscience of False Beliefs 特別寄稿 Delusions and the Cognitive Neuroscience of False beliefs Martin L. Albert and Joshua Berger Key words : Delusions, False beliefs, Cognitive neuroscience, Confabulation, Brain damage A delusion 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 syndromes（ 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 Neurology, 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 syndrome. 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）, drug 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 migraine（ MacCallum, 1973）. Capgras Delusion 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 prosopagnosia. 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
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