The Delusional Misidentification
Syndromes: Strange, Fascinating,
and Instructive
George N. Christodoulou, MD, FRCPsych, Maria Margariti, MD,
Vassilis P. Kontaxakis, MD, and Nikos G. Christodoulou, MD, MSc
Corresponding author
George N. Christodoulou, MD, FRCPsych
Athens University, Hellenic Center for Mental Health and
Research, Vasilissis Sofias Avenue 52, 115 28, Athens, Greece.
E-mail: gchristodoulou@ath.forthnet.gr
Current Psychiatry Reports 2009, 11:185–189
Current Medicine Group LLC ISSN 1523-3812
Copyright © 2009 by Current Medicine Group LLC
The delusional misidentification syndromes (Capgras’
syndrome, Frégoli syndrome, intermetamorphosis
syndrome, syndrome of subjective doubles) are rare
psychopathologic phenomena that occur primarily
in the setting of schizophrenic illness, affective dis-
order, and organic illness. They are grouped together
because they often co-occur and interchange, and
their basic theme is the concept of the double (sosie).
They are distinguished as hypoidentifications (Cap-
gras’ syndrome) and hyperidentifications (the other
three syndromes). In this review, we present the basic
hypotheses that have been put forward to explain
these syndromes and propose that the appearance of
these syndromes must alert physicians to investigate
the existence of possible organic contributions.
Introduction
Recent biological experiments producing doubles, most
notably cloning, have stimulated our imagination (as
well as the imagination of television and fi lm producers)
and revived our interest in relevant psychopathologic
phenomena—the syndromes of doubles, or illusions des
sosies (according to the French clinicians of the early 20th
century). These phenomena are grouped together under
the term delusional misidentification syndromes (DMS)
because they have many similarities and very often co-
exist or interchange. The fi rst of us distinguished them
as hypoidentifications (Capgras’ syndrome) and hyperi-
dentifications (Frégoli syndrome, intermetamorphosis
syndrome, and syndrome of subjective doubles) [1].
The concept of the double is inherent in the DMS. This
concept appears very frequently in the traditions, myths,
literature, religious beliefs, and metaphysical notions of
all cultural and ethnic groups, which explains the uni-
versality of these syndromes. People have always been
thrilled by the notion of doubles. Greek mythology, from
which the notion of sosie is derived, is replete with refer-
ences to concepts of doubles, metamorphosis, and similar
phenomena; this is also the case with the Homeric poems,
Latin literature, French and Portuguese literature, Irish
myths, ancient Egyptian theology, and notions of many
primitive tribes (eg, the Nagas, Andamanese, East India
islanders, Karo Bataks, Aranda tribes of Central Austra-
lia, the Yakut in Siberia, and the Jicarilla Apache tribe of
New Mexico Indians). Modern literature is also full of
accounts (and often self-descriptions) concerning doubles.
The writings of Dostoyevsky are very characteristic, as
are those of d’ Annunzio, de Musset, de Maupassant (who
described the experience of his own double), Stevenson
(Dr. Jekyll and Mr. Hyde), and others [2].
Review of the Literature
Syndrome subtypes
Within the framework of the DMS, four basic syndrome
subtypes traditionally are included:
1. Capgras’ syndrome, described by Capgras and
Reboul-Lachaux [3], who reported a patient
believing that her family and other individuals
in her entourage had been replaced by identical
doubles. The syndrome refers to the delusional
denial of identification of familiar people and their
replacement by doubles (sosies) who are physi-
cally—but not psychologically—identical to the
misidentified people.
2. Frégoli syndrome, described by Courbon and Fail
[4] in 1927, which is characterized by false identi-
fication of a familiar person among strangers. In
this case, the patient maintains that the familiar
person (who is usually believed to be a persecutor)
differs in physical appearance from the stranger
but is the same person psychologically.
186
I Nonschizophrenic Psychotic Disorders
3. Intermetamorphosis syndrome, described by
Courbon and Tusques [5] in 1932, a variant of
Frégoli syndrome in which the patient believes that
the familiar person and the stranger have not only
psychological but also physical similarities and that
the misidentified people interchange with each other.
4. The syndrome of subjective doubles, described by
Christodoulou [6] in 1978, which is characterized by
the patient’s delusional conviction of other people’s
physical transformation into his or her own self.
The term delusional misidentification syndromes was
introduced in 1981 to emphasize the delusional nature of
the syndrome [7]. Although Capgras and Reboul-Lach-
aux [3] termed their patient’s belief in the existence of
doubles the illusion of doubles, the phenomenon is more
accurately described as a delusion. The defi ning and dis-
tinguishing feature is the central idea of doubles.
Pathogenetic hypotheses
The DMS have been explained since the fi rst descriptions
on the basis of a variety of pathogenetic hypotheses. Most
of these concern Capgras’ syndrome exclusively. The
proposed models follow the historical dichotomy in psy-
chiatry: functional versus organic.
In his original publications, Capgras considered the
syndrome to be an agnosia of identification produced by a
confl ict between sensory and mnemonic images. However,
in a later publication, probably reflecting the ideas of his
psychoanalytically oriented colleagues, he considered the
syndrome to be a defense mechanism against unconscious
prohibited desires [8].
Others, such as Todd [9], provided an explanation for
the phenomena of doubles by hypothesizing that psychotic
illness causes regression to archaic modes of thought, as
in thinking in terms of doubles. He maintained that the
concept of doubles is very prominent in mythology and
primitive religions. In 1981, Todd et al. [10] reconsidered
this hypothesis, taking into consideration that such dis-
solution of the nervous system must not be severe to be
compatible with Capgras’ syndrome because a clear sen-
sorium is the rule in patients manifesting it.
Psychological mechanisms such as “projection” and
“splitting” have been repeatedly involved as well. Enoch
[11] considered Capgras’ syndrome to be a psychologi-
cal solution to the love–hate confl ict. Love and hate for a
familiar person exist simultaneously. The patient “imag-
ines” the existence of a double who becomes the “bad”
object, while the original remains the “ideal.”
Nevertheless, as noted by Christodoulou [12], the
emotional attitude of the patient toward the principal mis-
identified person is not always negative or ambivalent. Many
cases of doubles have been reported to involve a range of
inanimate objects with which the emotional bond was
understandably weak or even absent. Indeed, psychodynamic
theories may be useful for us to understand individual cases,
but they fail to account for all different types of DMS.
Neuropsychiatric explanations
During the past few decades, along with psychopatho-
logic research, there has been a widespread trend toward
providing neuropsychiatric and cognitive neuropsychiat-
ric explanations for DMS symptoms, using a variety of
techniques. The DMS were investigated systematically by
Christodoulou [13] with all available techniques of the
1970s. This work, along with that of others, heralded the
systematic exploration of the delusion using neuropsy-
chiatric means, which later became important tools for
exploring the delusional formation.
An organic cerebral dysfunction was apparent in the
studied population and was identified as a strong patho-
genetic contributor along with the presence of a paranoid
component [13]. The role of depersonalization/dereal-
ization experiences in the development of the DMS was
also emphasized; it has been argued that under certain
conditions (presence of a paranoid element, cerebral
dysfunction, and a charged emotional relationship to the
principal misidentified person), depersonalization/dere-
alization symptoms may evolve into a full delusional
misidentification condition.
Neuropsychological, cognitive, and neuroanatomic
fi ndings converge and support the hypothesis that
DMS symptoms are produced at least in part by a dam-
aged or dysfunctional brain, predominantly in the right
hemisphere. Many case reports with neuroimaging data
support this association [14].
Cutting [15] synthesized the existing neuropsycho-
logical and clinical information and reached the conclusion
that delusional misidentifications have a specific link to
right rather than left hemisphere damage. He also proposed
that the neuropsychological deficit in delusional misiden-
tification is a disturbance in the judgment of identity or
uniqueness and is considered as a measure of individuality.
The DMS also have been seen as disconnection syn-
dromes. Joseph [16] suggested that organic causes may
produce disconnection between right and left cortical areas
that decode afferent sensory information. The result of this
would be lack of integrated representation of the outside
world and adoption of two separate, physically identical
objects. Thus, the patient would be aware of two separate,
physically identical people, places, etc. Experimental data,
however, do not support this interesting hypothesis [17].
DMS have been reported in cases of brain injury or
other brain organic disorder, and it also has been reported
that they are closely connected to reduplicative phenom-
ena [18,19]. Reduplicative paramnesia has been described
in patients suffering from central nervous system disease
[20]. In many cases, it also appears to co-occur with
reduplication for places, time, or events, while in the neu-
rologic literature, reduplicative paramnesia patients also
demonstrate reduplication for people [21].
The neuropsychiatric aspects of the DMS appear with
increasing frequency in the DMS literature, as neuropsy-
chiatry encompasses symptoms that lie in the gray zone
between neurology and psychiatry [22]. Researchers have
 The Delusional Misidentification Syndromes
attempted to link psychopathology with measurable brain
deficits. These attempts raise some basic questions:
• Does a phenomenon of doubles that arises in
the context of a neuropsychiatric/neurologic or
organic disease have the same origin as one that
arises in the context of psychiatric illness?
• Can the DMS be explained in terms of brain
lesions only?
• Can neuropathologic fi ndings alone elucidate the
delusion etiologically and pathogenetically?
Worth noting in this context is that although misiden-
tification syndromes have been reported in neurologic
patients and in patients with organic brain disease [23],
most instances occur in psychiatric illness. Addition-
ally, in psychiatric illness, patients have no insight into
their misidentifications; hence, the misidentifications
are termed delusional (although in some cases, there is a
kind of implicit insight).
Many of the neuropsychiatric findings presented in the
literature concern the primary psychiatric disorder rather
than the delusional misidentifications per se. For example,
the right hemisphere is implicated in the background ill-
ness, schizophrenia [24–26], and the DMS, and a search
for differential neuropsychological evidence in DMS has
not led to undisputed conclusions [27,28]. There is evidence
that DMS are associated specifically with organic lesions
affecting limbic structures and also involving the frontal
and parietal lobes [29•]. Right-sided lesions predominate
in the etiology and, as pointed out by Oyebode [29•], the
common link between schizophrenia, schizophrenia-like
psychosis of epilepsy, and DMS appears to be involvement
of the limbic structures in their pathophysiology.
Research on the DMS has hit several barriers. Among
the obstacles for the differential investigation remain the
limited number of patients and the absence of a direct
relationship between cognitive or mental phenomena and
brain regions or neural circuits. Neuropsychiatric investi-
gation offers mostly relational answers in its aim to link
the syndromes to biological correlates. It does not provide
us with the “meaning” of the delusional misidentification
phenomena or answers as to why and how the mind cre-
ates doubles. During the past decade, the DMS (especially
Capgras’ syndrome) became the ideal ground for cognitive
neuropsychiatrists to test models on delusion formation.
Cognitive neuropsychiatry aspects
Cognitive neuropsychiatry brings together cognitive
and neurobiological research to improve understand-
ing of mental disorders [30,31]. By drawing inspiration
from cognitive neuroscience, it aims to explain psychi-
atric and neuropsychiatric symptoms within normal
models of cognitive function and uses the study of
psychopathology to update existing models. It attempts
to link such functional explanations to relevant brain
structures and their pathology. More specifi cally, Ellis
and Young [32] suggested that DMS may result from
I Christodoulou et al.
I 187
defects at different stages of an information-processing
model put forth by Bruce and Young [33].
In specifically explaining Capgras’ syndrome, the
authors use the model created by Bauer and Verfaellie [34]
for visual recognition of faces. This model was supported
by the case of a prosopagnostic patient (agnosia of faces
of significant others) who could not recognize faces but
displayed skin conductance response conductivity (auto-
nomic response) to known faces.
According to this model, there are two routes to face
recognition: a ventral route that is responsible for con-
scious recognition and runs from the visual cortex to the
temporal lobes via the inferior longitudinal fasciculus, and
a dorsal route that is responsible for covert unconscious
recognition and runs between the visual cortex and the
limbic system via the inferior parietal lobule. When the
former route is damaged, prosopagnosia occurs. When
the latter route is damaged, a possible result is Capgras’
syndrome. The patient receives the appropriate semantic
information but lacks the affective confi rmation of this
information. As a result, he or she makes some sort of
rationalization and creates a double to explain the dis-
crepancy between absence of emotional familiarity and
recognition without familiarity.
There are some objections to the hypothesis that
considers DMS to be a disorder of face processing:
• It does not explain the co-occurrence of the subtypes
(on many occasions, the misidentification involves
objects, places, and events together with misidentifi-
cation of people in different subtype variations) [35].
• The patient recognizes the person he or she misiden-
tifies and does not mistake the person. The patient
knows the name and, for example, the role of this
person but does not identify the person properly [36].
• The hypotheses that are based solely on face
recognition models do not explain a frequently
met feature of the DMS: the presence of multiple
doubles of the misidentified person [37,38,39•]. If
a patient creates a double to explain the discrep-
ancy between absence of emotional familiarity and
recognition without familiarity, it is difficult to
fi nd a logical reason for a patient to create multiple
doubles, as one double should be enough.
Other approaches
Taking into consideration these limitations, a different
explanation for the DMS has been proposed [39•]. This
hypothesis suggests that the disturbance occurs at a stage
responsible for attributing identity to objects, people, or
places rather than simply at the level of face recognition.
Thus, DMS are regarded mainly as identification disorders.
Identity encompasses the notion of uniqueness by definition.
The hypothesis proposed assumes that in DMS patients,
there is a total breakdown of the identification process and
an inability to attribute uniqueness to specific surrounding
objects or even to the self. In particular, it is proposed that
188
I Nonschizophrenic Psychotic Disorders
perceptual, personal, and affective information regard-
ing surrounding objects is implemented on the ground of
uniqueness, the role of which is to compensate for a certain
degree of discrepancy between recent and stored informa-
tion, serving identification constantly and successfully. A
disorder at that level is believed to result in a breakdown of
the identification process by allowing even a slight discrep-
ant input, as in the case of psychotic perceptual or emotional
experiences, to misdirect identification through a denial of
the true identity and reidentification as a double.
Coltheart et al. [40] suggested a two-factor model for
DMS. According to this theory, for monothematic delusions
such as Capgras’ syndrome and the rest of the DMS to occur,
two abnormalities must be present. The first abnormality
initially prompts the delusional belief and is responsible
for the content of the delusion (in the case of Capgras’ syn-
drome, Coltheart et al. [40] consider it to be the failure of
autonomic responsivity to familiar faces). This abnormality
is considered to be different for each type of monothematic
delusion. The second abnormality prevents the person from
rejecting the belief in the light of the very strong evidence
against it. This abnormality is hypothesized to be common
in all varieties of monothematic delusions and is speculated
to arise as a consequence of damage to a belief evaluation
system associated with the right frontal cortex.
Young [41] recently advocated an interactionist model
while endorsing the two-stage model to explain Capgras’
syndrome. Young [41] argues that the delusional belief
constitutes an attempt on the part of the patient to explain
his/her initially odd and somewhat disturbed phenomenal
content and that the delusion then structures the patient’s
experience in such a way that what he/she perceives is an
impostor. According to the author, this explains the resis-
tance to revision of the delusional belief.
Conclusions
Through their enigmatic etiology and the peculiarity of
their content, the DMS have attracted considerable atten-
tion and revived research in psychopathologic constructs.
These colorful syndromes are presently considered not
only psychopathologic oddities but also a most promis-
ing ground for testing theories and models concerning the
nature of delusions and their formation process.
The contribution of organic factors to the pathogene-
sis of these disorders has been stressed by various authors,
and this organicity does not seem to be specific, although
in many cases, a dysrhythmic component in the right side
of the brain has been detected. Brain dichotomy theories,
regression theories, and psychodynamic splitting formula-
tions are fascinating and aid in our understanding of these
phenomena, but in practical terms, they provide little help
to clinicians. Face recognition theories and identification
explanations are promising, but further research and
elaboration is necessary. In practical terms, the appear-
ance of DMS in a setting of a “functional” disorder calls
for attention to a possibly coexisting organic contributor.
Disclosure
No potential confl icts of interest relevant to this article
were reported.
References and Recommended Reading
Papers of particular interest, published recently,
have been highlighted as:
• Of importance
•• Of major importance
1. Christodoulou GN, ed: The Delusional Misidentifi cation
Syndromes. Basel, Switzerland: Karger; 1986.
2. Christodoulou GN: The origin of the concept of doubles.
In The Delusional Misidentifi cation Syndromes. Edited by
Christodoulou GN. Basel, Switzerland: Karger; 1986:1–8.
3. Capgras J, Reboul-Lachaux J: L’illusion des socies dans un
delire systematise chronique [in French]. Bull Soc Clin Med
Ment 1923, 11:6–16.
4. Courbon P, Fail G: Illusion de Fregoli [in French]. Bull Soc
Clin Med Ment 1927, 15:121–124.
5. Courbon P, Tusques J: Illusions d’intermetamorfose et
de la charme [in French]. Ann Med Psychol (Paris) 1932,
90I:401–406.
6. Christodoulou GN: Syndrome of subjective doubles. Am J
Psychiatry 1978, 135:249–251.
7. Christodoulou GN, Malliara-Loulakaki S: Delusional
misidentification syndromes and cerebral ‘dysrhythmia.’
Psychiatr Clin (Basel) 1981, 14:245–251.
8. Luauté JP: Joseph Capgras and his syndrome. In The
Delusional Misidentifi cation Syndromes. Edited by
Christodoulou GN. Basel, Switzerland: Karger; 1986:9–22.
9. Todd J: The syndrome of Capgras. Psychiatr Q 1957, 31:250.
10. Todd J, Dewhurst K, Wallis G: The syndrome of Capgras.
Br J Psychiatry 1981, 139:319–327.
11. Enoch MD: The Capgras syndrome. Acta Psychiatr Scand
1963, 39:437–462.
12. Christodoulou GN: Role of depersonalisation-derealization
phenomena in the delusional misidentification syndromes.
In The Delusional Misidentification Syndromes. Edited by
Christodoulou GN. Basel, Switzerland: Karger; 1986:99–104.
13. Christodoulou GN: The delusional misidentification
syndromes. Br J Psychiatry Suppl 1991, 14:65–69.
14. Forstl H, Almeida OP, Owen AM, et al.: Psychiatric, neuro-
logical and medical aspects of misidentification syndromes:
a review of 260 cases. Psychol Med 1991, 21:905–910.
15. Cutting J: Delusional misidentification and the role of
the right hemisphere in the appreciation of identity. Br J
Psychiatry 1991, 159(Suppl 14):70–75.
16. Joseph AB: Focal central nervous system abnormalities
in patients with misidentification syndromes. In The
Delusional Misidentifi cation Syndromes. Edited by Christ-
odoulou GN. Basel, Switzerland: Karger; 1986:68–79.
17. Ellis HD, de Pauw KW, Christodoulou GN, et al.:
Responses to facial and non-facial stimuli presented tachis-
toscopically in either or both visual fields by patients with
the Capgras delusion and paranoid schizophrenics. J Neurol
Neurosurg Psychiatry 1993, 56:215–219.
18. Alexander MP, Stuss DT, Benson DF: Capgras syndrome: a
reduplicative phenomenon. Neurology 1979, 29:334–339.
19. Weinstein EA, Burnham DL: Reduplication and the
syndrome of Capgras. Psychiatry 1991, 54:78–88.
20. Benson DF, Gardner H, Meadows JC: Reduplicative
paramnesia. Neurology 1976, 26:147–151.
21. Staton RD, Brumback RA, Wilson H: Reduplicative
paramnesia: a disconnection syndrome of memory.
Cortex 1982, 18:23–35.
22. Yudofsky SC, Hales EH: Neuropsychiatry and the future
of psychiatry and neurology. Am J Psychiatry 2002,
159:1261–1264.
 The Delusional Misidentification Syndromes
23. Edelstyn NMJ, Oyebode F: A review of the phenomenology
and cognitive neuropsychological origins of the Capgras
syndrome. Int J Geriatr Psychiatry 1999, 14:48–59.
24. Cutting J: The role of right hemisphere dysfunction in
psychiatric disorders. Br J Psychiatry 1992, 160:583–588.
25. Barnett KJ, Kirk IJ, Corballis MC: The right hemisphere
dysfunction in schizophrenia. Laterality 2005, 10:29–35.
26. Murphy D, Cutting J: Prosodic comprehension and expres-
sion in schizophrenia. J Neurol Neurosurg Psychiatry 1990,
53:727–730.
27. Lykouras L, Typaldou M, Mourtzouchou P, et al.: Neu-
ropsychological relationships in paranoid schizophrenia
with and without delusional misidentification syndromes.
A comparative study. Prog Neuropsychopharmacol Biol
Psychiatry 2008, 32:1445–1448.
28. Papageorgiou C, Lykouras L, Alevizos B, et al.: Psychophys-
iological differences in schizophrenics with and without
delusional misidentification syndromes: a P300 study. Prog
Neuropsychopharmacol Biol Psychiatry 2005, 29:593–601.
29.• Oyebode F: The neurology of psychosis. Med Princ Pract
2008, 17:263–269.
The author outlined and systematized the evidence linking
schizophrenia, schizophrenia-like psychosis in epilepsy, and DMS.
Previous authors (eg, Papageorgiou et al. [28]) have also presented
evidence pointing to this association.
30. Halligan PW, David AS: Cognitive neuropsychiatry:
towards a scientific psychopathology. Nat Rev Neurosci
2001, 2:209–215.
31. David AS, Halligan PW: Cognitive neuropsychiatry:
potential for progress. J Neuropsychiatry Clin Neurosci
2000, 12:506–510.
I Christodoulou et al.
I 189
32. Ellis H, Young A: Accounting for delusional misidentifications.
Br J Psychiatry 1990, 157:239–248.
33. Bruce V, Young A: Understanding face recognition. Br J
Psychol 1986, 77:305–327.
34. Bauer RM, Verfaellie M: Electrodermal discrimination of
familiar but not unfamiliar faces in prosopagnosia. Brain
Cogn 1988, 8:240–252.
35. Lykouras L, Typaldou M, Gournellis R, et al.: Coexistence
of Capgras and Fregoli syndromes in a single patient.
Clinical, neuroimaging and neuropsychological fi ndings.
Eur Psychiatry 2002, 17:234–235.
36. Weinstein E: The classification of delusional misidentification
syndromes. Psychopathology 1994, 27:130–135.
37. Murai T, Toichi M, Yamagishi H, Sengiku A: What is
meant by “misidentification” in delusional misidentification
syndromes? Psychopathology 1998, 31:313–317.
38. Voros V, Tenyi T, Simon M, Trixler M: “Clonal pluraliza-
tion of the self”: a new form of delusional misidentification
syndrome. Psychopathology 2003, 36:46–48.
39.• Margariti M, Kontaxakis V: Approaching delusional
misidentification disorders as a disorder of the sense of
uniqueness. Psychopathology 2006, 39:261–268.
The authors have put forth a new theory that emphasizes the
sense of uniqueness as being of major importance in the causation
of these syndromes.
40. Coltheart M, Langdon R, McKay R: Schizophrenia and
monothematic delusions. Schizophr Bull 2007, 33:642–647.
41. Young G: Capgras delusion: an interactionist model.
Conscious Cogn 2008, 17:863–876.