Original Paper
Psychopathology 2001;34:299–304

The Delusions of Capgras and
Intermetamorphosis in a Patient with
Right-Hemisphere White-Matter Pathology
Nicola M.J. Edelstyn a Femi Oyebode b Ken Barrett c
a University of Keele, b Queen Elizabeth Psychiatric Hospital, Birmingham, and c Haywood Hospital,
Stoke on Trent, UK

Abstract
Previous neuropsychological studies have demonstrated an association between person misidentification
and right-hemisphere dysfunction. In the study reported
here, we explore the contribution of facial and visual recognition impairments in a patient with right-hemisphere
subcortical white-matter pathology in the frontal and
parietal lobes and a diagnosis of vascular cognitive
impairment. The patient displayed false recognition of
unfamiliar faces and deficient retrieval of key biographic
detail for famous faces. These results are discussed in
the context of the contribution of deficiencies in the
visual system and subcortical white-matter lesions to the
development of Capgras delusion.
Copyright © 2002 S. Karger AG, Basel

Introduction

Disorders of face memory and face perception have
been the focus of much neuropsychological investigation
over the past 50 years. The most extensively studied of

ABC

© 2002 S. Karger AG, Basel
0254–4962/01/0346–0299$17.50/0

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these is prosopagnosia – a condition characterised by the
inability to identify all familiar faces, including famous
persons, friends, family and even the prosopagnosic’s own
face [1]. The critical lesion sites in prosopagnosia involve
right ventromedial occipitotemporal regions which include the inferior temporal cortex and medial temporal
lobe limbic areas [2].
Although less well documented, areas of the prefrontal
cortex are also involved in facial processing: projections
from the face-processing areas in the right ventromedial
occipitotemporal regions to the ventromedial prefrontal
cortex via the uncinate fasciculus as well as limbothalamic pathways are well established [3]; single cell recordings have identified face-sensitive neurons in the inferior
frontal convexity region of non-human primates [4], and
neuropsychological studies have documented an association between false facial recognition and right frontal lobe
dysfunction [5]. These frontal patients, in striking contrast to the lack of conscious facial recognition described
in prosopagnosics, mistakenly believe that unfamiliar
faces are familiar [6, 7].
In a small subset of psychotic patients, false recognition can lead to frank misidentification which can reach
delusional proportions [5, 8–10] – as in the case of Frégoli
delusion (FD) [11]. The hallmark of FD is the recognition
of a familiar other in a stranger. The patient believes that
the familiar other is able to take on different physical

Dr. N. Edelstyn
Psychology Department, University of Keele
Keele, Staffordshire ST5 5BG (UK)
Tel. +44 1782 584318, Fax +44 1782 583387
E-Mail n.edelstyn@psy.keele.ac.uk

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Key Words
Capgras delusion W Right hemisphere W White-matter
pathology W Face processing

Case Report
Background
V.J. was a 64-year-old right-handed man, with a 20-year history
of hypertension. He was married with 1 grown-up son. V.J. worked as
an instrument maker before retiring, aged 59. His hobbies included

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renovating classic motor bikes, building computers and following the
stock market. There was no personal or family history of psychiatric
disorder, alcohol or drug abuse. For the preceding 12 months, V.J.
had experienced a gradual deterioration in his memory, ability to
work previously familiar gadgets, problems with writing and understanding written material. Medication included propranolol (80 mg
daily), trazodone (50 mg nocte) and oxypertine (20 mg daily).
An MRI scan showed abnormal areas of high T2-weighted signal
in the brain stem and basal ganglia bilaterally, primarily involving
the globus pallidus. In the white matter of the right hemisphere, 3
small ischaemic lesions were identified in the frontal (postfrontal cortex and just below the superior frontal gyrus) and anterior parietal
lobes (fig. 1: upper, middle and lower images, respectively). The
reported abnormalities were consistent with a diagnosis of cerebrovascular disease. Corrected visual acuity was 6/6 for both eyes, near
vision was N5.
The reported study was carried out over a 7-month period.
Informed consent was obtained, and patient initials have been
changed. During mental state examination, V.J. was well oriented for
time and place, although concentration (attention and calculation
0/5) and immediate recall (0/3) were poor. There were no apparent
perceptual problems and he was able to follow verbal commands. A
summary of V.J.’s cognitive neuropsychological assessment follows –
a full report is available on request.
Episodes of Misidentification
Over the 7-month period of contact, V.J. exhibited episodes of
CD and ID. Episodes of CD for his wife were experienced on a recurrent basis. He claimed that there were several ‘Jeans’ in the house, the
‘Jean in the kitchen’ was different from the ‘Jean’ he had been chatting to in the living room. Occasionally, these episodes took a more
ominous turn – V.J. believed that the ‘Jean-impostor’ was a spy sent
by the Inland Revenue who was out to trap him. He described the
impostor as looking like Jean but that the ‘real Jean’ had gone away:
‘I care a lot about Jean, but I don’t like you at all.’
Instances of ID occurred less frequently, one centred around the
delusional belief that his wife had been transformed (physically and
psychologically) into his (deceased) mother-in-law. Recognition of
his grown-up son and elderly mother, whom he saw on a weekly basis,
was preserved.
The periods of misidentification were selective (focused on his
wife), occurred on average a couple of times a day, were transient
(seconds to minutes) and appeared to be exacerbated by feelings of
anxiety (e.g. an out-patient visit), changes in the appearance of his
wife (e.g. leaving the room and returning in a coat), fatigue and disorientation (episodes occurred more frequently in the evening, or
when waking from a nap). These episodes were frequently accompanied by verbally aggressive behaviour, which has been quite a shock
for his wife, who described him as a quiet, easygoing man who rarely
raised his voice.
V.J. did not always regard his wife as an impostor, and during
these lucid periods he would acknowledge her as ‘the real Jean’. No
other psychotic features were evident, and he was not depressed.
Cognitive Neuropsychological Assessment
His current levels of functioning (table 1) were placed in the mentally deficient range [20], which was well below his premorbid levels
of functioning based on his former employment and hobbies.
There was clear evidence of both ideomotor and constructional
apraxia, which is consistent with his reported problems in using gad-

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forms and adopt another’s appearance. It has been suggested that FD develops when spurious feelings of familiarity evoked by novel faces are combined with the retrieval of incorrect biographic detail [5]. A related phenomenon – the delusion of intermetamorphosis (ID) [12] – is
marked by the false belief that a person has been transformed, physically and psychologically, into another. Patients report the presence of physical similarities between
the original and misidentified individuals, and a dynamic
transformation occurring between the two. Finally, the
Capgras delusion (CD) [13], a subtly different form of
misidentification from FD and ID, is characterised by the
delusional belief that a significant other has been replaced
by an impostor who bears a close physical resemblance to
the original [14]. Again, small misperceived differences,
for instance in physical appearance and behaviour, are
frequently used to distinguish the impostor from the
loved one.
Neuroanatomical evidence suggests that CD is commonly associated with right-hemisphere abnormalities,
particularly in the region of the temporal and/or parietal
lobes coupled with right or bilateral frontal pathology [15,
16]. It has been suggested that CD results from a disconnection between the face-processing areas in the inferior
temporal lobe, responsible for the conscious recognition
of the face and recall of associated biographic information, and key limbic structures which mediate the feelings
of familiarity which accompany overt recognition [17,
18]. A loss of the normal skin conductance response to
familiar faces has been demonstrated in a small number
of CD patients [18, 19].
In this study, we explore facial and visual recognition
in a patient with CD and ID arising in the context of cognitive impairment. This case is of interest on two counts:
firstly, the neuro-anatomical evidence of combined whitematter lesions in right prefrontal and parietal regions –
previous reports of pathology have been largely restricted
to the grey matter. Secondly, the transient co-existence of
ID and CD raises questions as to the role played by transient (functional changes in terms of neurotransmission
and/or neurophysiology) as well as stable (i.e. organic) factors in the development of these symptoms of delusional
misidentification.

Fig. 1. An MRI scan showing abnormal

areas of high T2-weighted signal in the white
matter of the right hemisphere. Three small
ischaemic lesions were identified in the postfrontal cortex, just below the superior frontal
gyrus and the anterior parietal lobe (arrows
in upper, middle and lower images, respectively).

Psychopathology 2001;34:299–304

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Capgras Delusion and Right-Hemisphere
White-Matter Pathology

Table 1. V.J.’s profile on the Wechsler Adult Intelligence Scales –

Revised
Verbal
Information
Digit span
Vocabulary
Arithmetic
Comprehension
Similarities
Verbal IQ
Full-scale IQ

Performance
6
2
7
3
1
3
68
67

Picture completion
Picture arrangement
Block design
Object assembly
Digit symbol

5
1
4
2
2

Performance IQ

68

Deficiencies in ability to access stored knowledge from vision
were also evident using animate and inanimate stimuli (table 2). V.J.
performed poorly on an object decision task [22] which involved discriminating real (animate or inaminate exemplars) from unreal items
(i.e. constructed by replacing one feature of a real item with a feature
from another item, e.g. a tortoise’s head and snake’s body). A visual
test of object constancy [22] which involved matching line drawings
of the objects presented from different viewpoints was performed
within normal limits. Ability to identify 10 inanimate objects taken
from V.J.’s home (work tools, clothing, household items) from a set
of matched unfamiliar ones was flawless.
A group of 11 age- and education-matched normal controls is
reported for the sorting and facial recognition tasks. V.J.’s wife was
the control for the 3 odd-one-out tasks. All of the controls were righthanded, and none reported a neurological or psychiatric history.

Table 2. Facial and visual processing

Discussion
Face sorting (max. 25)
Familiar face hits
Novel face rejections
Familiar face recognition (max. 25)
Profession
Name
Minimal features (max. 25)
Object decision (max. 32)
Odd-one-out (max. 10)
Visual
Spoken
Written

Score

Normal range

25
17

23–25
21–25

22
10
22
21

22–25
17–25
19–25
22–32

1
3
6

10
10
10

gets around the home. Assessment of language function revealed
preservation of repetition, ability to name pictures, read high-frequency and high-imageability words. However, difficulties were evident on tests of comprehension, writing and reading nonwords, lowfrequency and low-imageability words. Both apraxia and comprehension deficits have been reported following damage to the dominant basal ganglia [21].
Assessment of facial recognition revealed abnormalities in familiarity judgements and accessing stored knowledge from vision (table 2). A face familiarity task, which involved sorting photographs of
famous from unfamiliar faces, revealed an elevated false recognition
rate for unfamiliar faces but a normal hit rate for famous faces. However, retrieval of stored information (profession and name) was poor.
This was confirmed in a second task which required identification of
the odd-one-out from a set of three photographs on the basis of profession (e.g. John Major, Margaret Thatcher, Michael Aspel). Interestingly, when this odd-one-out task was repeated using spoken or
written names (matched for profession and notoriety), V.J.’s performance showed improvement – particularly in the written version.
His poor performance on the visual version of the odd-one-out task
was not attributable to a generalised naming problem as evidenced
by his ability to correctly name a set of 30 line drawings of animate
and inanimate items.

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CD, FD and ID are highly correlated with facial processing impairments. Abnormalities are evident at the
level of discriminating between pairs of familiar and
unfamiliar faces on the basis of same/different judgements [23], recognition memory for unfamiliar faces [24]
and retrieval of biographic data from photographs of
famous faces [23]. In this study, we have demonstrated a
discrepancy in V.J.’s ability to access stored biographic
knowledge – increased levels of preservation are apparent
when this is done verbally, i.e. spoken or written name as
compared to a visual image. These findings extend work
which documented a discrepancy in recognition memory
for words (which was good) and faces (which was poor) by
showing that the verbal/visual disparity is also evident at
the level of access to stored knowledge – i.e. retrieval of
biographic data is facilitated tapped from the verbal
domain. Studies of recognition memory in psychotic patients who do not exhibit any evidence of CD, FD or ID
have reported poor recognition memory for faces and
words, which suggests that delusional misidentification
syndromes like CD, FD and ID emerge when right-hemisphere dysfunction is substantial relative to left-hemisphere preservation [24].
Recently, Ramachandran and Blakeslee [25] described
a patient with CD who misidentified his father when in
his company, but not when speaking to him on the phone.
This report seems to indicate the important role of accessing stored knowledge from vision in the aetiology of CD.
However, CD has also been reported in a number of blind
patients which suggests that it cannot have an exclusively
visual basis [26, 27]. In the study of Reid et al. [26], their
patient believed her cat had been replaced by an impostor
because its miaow was different. Testing of her auditory

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Test

recognition revealed abnormalities in her ability to recognise familiar voices.
Posterior coupled with anterior right-hemisphere dysfunction has been implicated in the emergence of CD
[16]. The neuro-imaging evidence reported for V.J. is consistent with this – however, his pathology is at the level of
white rather than grey matter. The authors are aware of
only one other case which reports delusional person misidentification arising in the context of white-matter pathology, which – as in the present case – was also located
mainly in the frontal and parietal lobes [28].
The rich reciprocal afferent-efferent connections between the prefrontal cortex with limbic structures and
cortical association areas make it a highly complex site for
the integration of perceptual, cognitive and affective data
[29, 30]. Pathological lesions in subfrontal white matter
have been reported in the context of metachromatic leukodystrophy, a rare inherited demyelinating disorder of
the central and peripheral nervous systems, which is
accompanied by psychiatric symptoms including complex auditory hallucinations and bizarre delusions. The
presence of subfrontal white-matter lesions suggest that
psychosis [31, 32] and CD in particular [28, 33] may
result from disruption of corticocortical and corticosubcortical connections especially involving the frontal lobes.
It has been suggested that CD results from the disconnection of the face-processing areas in the inferior temporal
lobe from structures in the limbic system, particularly the
amygdala, which is crucial in assigning an emotional valence to familiar faces [17, 19]. Although V.J.’s sMRI
failed to reveal any evidence of an amygdala lesion, the
presence of functional abnormalities arising from the

remote effects of lesions on corticolimbic networks cannot
be ruled out.
However, anatomical disconnection models fail to adequately account for the transient nature of the misidentification episodes. It has been suggested that CD may be
associated with the ‘kindling of subcortical structures’
[33]. Kindling refers to repeated subthreshold stimuli
which may result in psychomotor outbursts or overt seizure activity [34]. According to Kim [33], the effects of
psychomotor outbursts may interfere with the integration
of perceptual, cognitive and affective processing in the
prefrontal cortex, by altering interlobar signal transmission through subcortical tracts. Psychomotor outbursts of
limited duration may be responsible for the transient
nature of the delusional experiences, whilst subtle changes
in foci may account for impaired processing at different
stages in the facial recognition system which, in turn,
would have an impact on the particular form of misidentification experienced. On this basis, the cognitive impairments represent stable or mediating vulnerability factors,
rather than transient indicators of dysfunction. Inherent
weaknesses within the face-processing system remain hidden during non-psychotic periods but may be artificially
exposed during formal cognitive neuropsychological testing by challenging the processing system with the particular stimuli and tasks found most difficult. Such deficits in
visual processing, when combined with other factors such
as changes in mental state (paranoia or anxiety) and
impaired cognitive reasoning, operate in a complex interaction to produce symptoms of delusional misidentification [23].

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