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Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.

Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)

Capgras Syndrome and Other Delusional


Misidentification Syndromes
Alain Barrelle a · J.-P. Luauté b
a
Service de psychiatrie, Centre Jacques Arnaud, FSEF, Bouffémont, and bNeuropsychiatrist, Romans, France

Abstract
The delusional misidentification syndromes (DMS) are a group of disorders, characterized by patients
mistaking the identity of people they know, although they recognize them physically. The term DMS
is an umbrella term which may cover disorders whose definition extends to objects other than peo-
ple, such as animals, places, or familiar material objects. The most common and best known DMS is
Capgras syndrome. In this disorder, the misidentification leads to the delusional conviction that a
close friend or relative has been replaced by an identical – or almost identical – “double,” whose
original has disappeared. This double is an imposter without name or identity. Most often considered
as a persecutor, the double may be subjected to aggression, which may be very violent. Neuropsy-
chological hypotheses based on cerebral dysfunctions are now commonly considered to be at the
origin of the disorder. They have been elaborated from achievements in the neurosciences, particu-
larly the facial recognition models. In return, knowledge about the normal cognitive processes in-
volved in recognition and familiarity has benefited from the work that cognitive neuropsychiatry has
invested in these disorders. The DMS are observed in various contexts of morbidity: primary psychi-
atric diagnosis, or secondary to various organic disorders, particularly in neurodegenerative disease;
they are rarely met in isolated form. Most often, they develop in line with the associated pathology.
In the absence of consensual clinical description, the epidemiology of DMS is uncertain; they may
be more frequent than previously supposed. There is no specific treatment for these disorders; neu-
roleptics are generally used in association with treatment of the concomitant disorder. The frequent
association of DMS with organic disorders which may be curable and the particularly dangerous
profile of these patients are factors that underline the need for better screening.
© 2018 S. Karger AG, Basel

Introduction

If we consider recognition as the judgment of the known or unknown character of


an object (a living being or thing) and identification the process of attributing to
the  recognized object a specifically related set of information – name, expected
behavior, history etc., the Capgras syndrome (CS) and other related delusions: the
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University of Groningen
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Capgras Syndrome Fregoli Syndrome

"In short, everywhere Mme de Rio Branco "Several individuals bearing no resemblance are
perceives resemblance and everywhere she taken to be the incarnation of another whom
fails to recognize true identities of the people"* they do not resemble either"*

Patient
Patient

Metamorphosis Syndrome Subjective Doubles Syndrome

"A delusion whereby different individuals “An 18-year-old female suffering who believed
embody themselves, physically and psycho- that her next door neighbor had transformed
logically, into the body of the same individual"* her physical self into the patient's double"**

Patient
Patient

Fig. 1. The main types of Delusional Identification of People. Clear circles represent the person(s)
present; dark circles the person(s) identified. * Ratcliffe [2]; ** Christodoulou [4].

delusional misidentification syndromes (DMS) represent a group of disorders char-


acterized by the mistaken and delusional identification of one or more people despite
the process of recognition operating in an apparently correct manner. In the usual
cases, the misidentified object is a person, hence justifying the title of Delusional
Identification of People [1]. The group of DMS is comprised of 4 main sub-types: CS,
Fregoli syndrome, intermetamorphosis syndrome, and subjective doubles syndrome
(Fig. 1) [3, 4], each of which may involve a distinct sort of alteration of the mecha-
nisms through which an object is identified. With no consensual clinical criteria for
the various entities of this group, it is usual to refer to their original description in
portraying them. Since its identification, CS, and to a lesser extent, the other DMS,
have aroused the interest of numerous neuroscientists, and even philosophers [2]:
considered as “failures” of the normal process of recognition/identification, they may
open the way to theoretical elaborations of the neuro psychobiological basis of this
process.
CS is named after the French psychiatrist Joseph Capgras who first described it
[5]. It is the most common and the best studied of all the DMS. In this disorder,
patients have the delusional conviction that one or more close friends or family

36 Barrelle · Luauté

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
members have been replaced by a “double,” identical in every way – or almost – to
the original, considered as an imposter, void of both identity and name. Certain au-
thors extend the disorder to material objects, pets, places, or to emotion-laden
events [6].
CS is a “hypo-identification”, distinguishing it from other DMS where a mistaken
identity is attributed by “hyper-identification” of an otherwise named object. This
distinction between hyper- and hypo-identification is used as the basis for the most
widely used classification of the DMS [1]. Other phenomena of hyper-identification
and duplication of persons have been described in recent years. They only justify in-
clusion in the DMS group if they take place in the presence of the misidentified object
(a necessary characteristic owing to the description of the original case by Capgras),
which excludes entities where duplication is the result of various delusional, imagina-
tive, or hallucinatory mechanisms.
CS, like other DMS, can be encountered in very varied contexts of morbidity, in
primary psychiatric diagnosis (particularly in schizophrenia and mood disorders) –
where an organic element may exist in about a third of all cases [7] – or secondary to
organic disorders or medication-induced, through to overt organic brain damage,
particularly in neurodegenerative disease.
It sometimes occurs isolated, hence justifying its autonomy as a “delusion”. It may
be transitory; developing along with the associated pathology as if fixed to it or may
persist after the associated disorder has disappeared.
The DMS were initially described in purely psychiatric contexts and viewed in the
light of psychodynamic theories. Beginning in the 1970s, consideration of cases in-
volving new medical specialties allowed different neuropsychological hypotheses to
be put forward, on the basis of cerebral dysfunction. Empirical research carried out
through advances in the neurosciences – particularly in the field of face recogni-
tion – resulted in the first models of the box-and-arrow type, explaining the DMS in
terms of deficient cognitive processes [8]. These models evolved progressively, tak-
ing clinical observations and new experimental evidence into account. The trans-
modal character of disorders involving senses other than vision (auditory, olfactory,
tactile) was thus incorporated [9]. Taking into account the delusional character of
the disorder, some dual-factor models have been proposed, where the primary per-
ception anomaly – loss of emotional familiarity – is associated with a secondary de-
fect in one or several processes of the information treatment chain [10, 11]. Thus,
studies of the DMS have been the basis for a better understanding of normal cogni-
tion (e.g., [12]).
These disorders have a practical interest for clinicians as much as an epistemolog-
ical interest. Violent behavior has often been reported in patients suffering from a
DMS: the hostility manifested towards “imposters” ranges from verbal or physical ag-
gression to homicide, with some cases of parricide and infanticide [13].
Furthermore, the frequency of a – sometimes curable – underlying organic disor-
der means that the DMS require exhaustive screening.

CS and Other DMSs 37

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
Epidemiology

The absence of consensual clinical criteria renders the epidemiological data uncertain.
In the earliest studies, the prevalence of DMS in psychiatric populations was less
than 1%. It is around 3% for patients in psychiatric hospitals and 4% if only hospital-
ized psychotic patients are taken into account [14]. In a recent prospective study of
patients hospitalized for a first psychotic episode, CS was diagnosed in 14% of patients
(73/517). The prevalence was maximal among patients presenting a schizophreni-
form disorder (50%), a brief psychotic disorder (35%), or an unspecified psychosis
(24%); it was moderate for a major depressive episode (15%), schizophrenia (11%), or
delusional disorders (11%) [15].
Identification disorders are very frequent in neurodegenerative diseases. The prev-
alence of CS in Lewy body dementia may be as high as 25% [16] and 10% in Alzheim-
er-type dementia [17]. DMS are much rarer in other types of dementia, particularly
those associated with Parkinson’s disease.
CS is more frequent in women than men, with a sex-ratio of around 2: 1 [18],
though this result was not found across all studies [15].

Disease Pathogenesis

From a psychodynamic point of view, CS has been conceptualized without empirical


evidence as a psychotic response to an unbearable ambivalence or regression to either
an archaic way of functioning or to an earlier stage of development [19].
First of all, Ellis and Young, drawing on the work done on face recognition [20],
attempted to explain the disorder through a change in the normal affective response
upon seeing familiar faces [8]. This hypothesis was confirmed experimentally using
measurements of skin conductance response: CS patients showed a reduced auto-
nomic response on seeing familiar faces (e.g., [21]). This dissociation between im-
paired emotional response and exact recognition was integrated into a dual lane mod-
el, where one lane – covered path – involving the limbic system – is attributed to the
affective response while the second lane – the open path – involving the ventral vi-
sual structures, enables recognition and leads to semantic and biographical informa-
tion related to the person and the name. This model was then generalized to include
other sensory modalities, such as the sound of the voice [9] (Fig. 2). In this model, CS
results from the patient’s attempt to give meaning to the experience of absent emo-
tional response in the presence of a significant other.
Nonetheless, the dual lane hypothesis alone does not seem able to explain the de-
lusional nature of the disorder, as the absence of emotional response is not necessar-
ily associated with CS [22]. A second factor has been postulated to take into account
the delusional character of CS: failure of the “system of evaluation of convictions”
[11], anomalies in salience [23], or in abductive inference processes [10].

38 Barrelle · Luauté

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
Facial Face Face Voice
expression code code code

Facial
speech FRU FRUs VRUs

(1) (2)
PIN PINs Affective
response

Name generation Name retrevial


SCR
a b

Right hemisphere Left hemisphere

Face Voice (Name) (Face) (Voice) Name

FRUs VRUs NRUs FRUs VRUs NRUs

PINs PINs

c Sensory semantics Verbal semantics

Fig. 2. Simplified models of person identification. a Functional recognition model of Bruce and
Young (1986) [20]; after the structural encoding step, the information is compared with information
stored in the Face Recognition Unit (FRU) corresponding to faces already seen before enabling re-
trieval of information from the Personal Identity Node (PIN) and of the name. b The Lewis and Ellis
model (2001) incorporates voice recognition; CS is linked to an interruption of lane 1 and/or 2 [9].
c The Gainotti model (2014) proposes a hemispherical specialization for treatment of information
enabling recognition and identification [12].

The lesions particular to CS were found largely in the temporal and frontal lobes
(mainly in the right hemisphere; for review [24]); patients with DMS after focal neu-
rological injuries had right hemisphere (92%) injuries, specifically right frontal inju-
ries (63%) [25, 26].

Diagnosis

CS is characterized by the delusional negation of identity of a significant other and the


belief that they have been replaced by a “double:” (a) the person is recognized, the pa-
tient affirms the resemblance of the double to the misidentified significant other; (b)
no identity is attributed to the double, who has neither name nor existence; (c) the
double is an imposter, pretending to be the original they are replacing; (d) the original
has disappeared, his/her absence remaining unquestioned. The phenomenon can the-

CS and Other DMSs 39

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
oretically affect the subject faced with his/her own image [1]. It may concern other
emotionally laden familiar objects: places, animals, material objects. Nonspecific, de-
realization-depersonalization experiences are frequent, especially in schizophrenia,
and are considered a core symptom of CS [6, 7].
Usually, but not systematically, the patients support their conviction with a reveal-
ing detail [1]. This sign may be material – a physical particularity – or not, such as a
habit or a personality trait; it may vary over time [27]. Vision is the usual modality of
CS, though other senses may be involved, such as hearing, for example the voice over
the telephone or through the door [9]. CS is distinguished by its delusional mecha-
nism: it is neither a hallucination – the object is present – nor an illusion: the object
is correctly recognized in its appearance. CS is not a memory disorder: the person is
correctly recognized; people are memorized.
The patient’s experience may be envisaged as something missing – something ab-
sent from the experience: familiarity, or the feeling of missing something, the feeling
of unfamiliarity [2, 28]; it is also the recognition, passing from ignorance to knowl-
edge, of the real nature of the misidentified person – an anagnorisis which is both
cognitive and affective [27].
CS may be associated with other DMS and these frequently evolve from one an-
other [6]. Common to all DMS is the delusional negation of identity of objects having
affective importance for the patient, and these objects are limited in number [29]. Se-
lectivity for familiar persons is essential, though sometimes relative, and the syn-
drome can extend to persons who are simply known or famous. The double is most
often seen as a persecutor and this may help in detecting the disorder in a patient lack-
ing sufficient discursive capacities and indicating the presence of a stranger while be-
coming aggressive with a significant other.
If the actual presence of the misidentified object excludes from these disorders du-
plications without imposter and substitution, in clinical practice several varieties of
double – DMS or otherwise – may co-exist or succeed one another [27]. These doubles
then form part of a broader paranoid delusion where the symptoms seem to nurture
between them a relationship which is not solely contingent.
CS may vary according to the neurological or psychiatric context. In patients with
organic brain disease, it may be associated with little or no affective manifestations,
such as hostility, and not with paranoid elements [30].
In DMS leading to homicide, as a general rule, there are several types of misidenti-
fied objects and a past history of violence against other misidentified objects [9].

Treatment and Management

There are no guidelines to help clinicians care for patients presenting with a DMS,
be it in the choice of complementary examinations to be carried out or that of treat-
ment.

40 Barrelle · Luauté

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
As a general rule, the DMS are known to develop similar to the comorbid disorder
that they accompany, disappearing after remission and reappearing during relapses,
even though it is not unusual for them to persist after disappearance of the comorbid
disorder. The DMS component is considered to be one of the most persistent psy-
chotic symptom in schizophrenic patients – remissions of CS associated with curable
neurological pathologies being more common [31].
There have been no prospective studies on the efficacy of drug therapy in CS, either
during the acute episode or in preventing relapses. It is generally accepted that the
reference drug therapy for CS is the treatment with neuroleptics [30]. Atypical neu-
roleptics are the most used pharmacological class due to their tolerance profile, but
there is no evidence to suggest that they are more effective than older drugs. Among
the older agents, pimozide has been associated with a particular efficacy (e.g., [32]).
No studies have been carried out to distinguish which of the atypical neuroleptics
may be more effective.
Therapies other than neuroleptics – such as mirtazapine – have been used success-
fully in certain isolated cases [33].
Very little has been published on other treatments for CS. ECT has been used suc-
cessfully in particularly resistant cases [34].
The proposed use of a cognitive behavioral type of treatment on the basis of the
dual-factor neurocognitive model of CS remains theoretical, as does that of hypnosis.
To our knowledge, no results have been published on the use of these treatment types
for this indication.

Conclusions

The DMS have long been considered medical curiosities. The lack of consensual
clinical criteria to define them, along with their absence from the international
classifications, is without doubt among the reasons that they often go unnoticed by
clinicians. Their frequency is nonetheless far from negligible and the unique profile
of these patients, in particular the frequent association with an (sometimes cur-
able) organic disorder and their high-risk profile, make the case for improved
screening.
While the potential risk of these patients to close friends and family members is
well known, the risk factors culminating in actual assault still remain unexplored. Un-
til now the task has drawn largely on retrospective studies of cases where data on the
diagnosis or on the patient history are lacking. Prospective studies would be particu-
larly useful, especially in cases of homicides involving close family and friends.
Recognition, identification, and the feeling of familiarity are essential aspects of
our relationships with others and with the rest of the world. They involve multiple
cognitive mechanisms which are not yet fully understood. Studies of the DMS in cog-
nitive neuropsychiatry have shown their efficiency not only in supplying psychiatrists

CS and Other DMSs 41

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
with solid pathogenic hypotheses, but also in allowing the neurosciences to develop
new models for a better understanding of normal cognition.
This search is far from over.
Does the sensation of familiarity arise in each and every sensory modality – or is it
modeless? Are there any associated lesions that we could recognize? Does an altered
perception of familiarity play a specific role in schizophrenia?
These are some of the questions that we can ask about the “curious little syndrome”
of Capgras.

Further Reading

Bauer RM: Autonomic recognition of names and faces in prosopagnosia: a neuropsychological ap-
plication of the Guilty Knowledge Test. Neuropsychologia 1984;22:457–469.
Breen N, Caine D, Coltheart M: Models of face recognition and delusional misidentification: a
critical review. Cogn Neuropsychol 2000;17:55–71.
Christodoulou GN, Margariti M, Kontaxakis VP, Christodoulou NG: The delusional misiden-
tification syndromes: strange, fascinating, and instructive. Curr Psychiatry Rep 2009;11:185–189.
Cipriani G, Vedovello M, Ulivi M, Lucetti C, Di Fiorino A, Nuti A. Delusional misidentification
syndromes and dementia: a border zone between neurology and psychiatry. Am J Alzheimers Dis
Other Demen 2013;28:671–678.
Coleman SM: Misidentification and non-recognition. Br J Psychiatry 1933;79:42–51.
Courbon P: Syndrome d’illusion de Fregoli et Schizophrenie. Bull Soc Clin Med Ment
1927;15:121–125.
Courbon P, Tusques J: Illusion d’intermétamorphose et de Charme. Ann Med Psychol 1932;90:4.
Ellis HD, Luauté J-P, Retterstøl N: Delusional misidentification syndromes. Psychopathology
1994;27:117–120.
Henriet K, Haouzir S, Petit M: L’illusion des sosies de Capgras: une interprétation délirante d’un
trouble spécifique de la reconnaissance affective des visages. Revue de la littérature et proposition
d’un modèle séquentiel. Annales Médico-Psychologiques, Revue Psychiatrique 2008;166:147–156.
Hirstein W: The misidentification syndromes as mindreading disorders. Cogn Neuropsychiatry
2010;15:233–260.
Pick A: Clinical studies. Brain 1903;26:242–267.
Thibierge S, Morin C: Identification, recognition and misidentification syndromes: a psycho-
analytical perspective. Front Psychol 2013;4:835.
Young AW, Leafhead KM, Szulecka TK: The Capgras and Cotard delusions. Psychopathology
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Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)
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Alain Barrelle, MD
Centre Jacques Arnaud
5 rue Pasteur
FR–95570 Bouffémont (France)
E-Mail alain.barrelle@gmail.com

CS and Other DMSs 43

Bogousslavsky J (ed): Neurologic-Psychiatric Syndromes in Focus. Part II – From Psychiatry to Neurology.


Front Neurol Neurosci. Basel, Karger, 2018, vol 42, pp 35–43 (DOI: 10.1159/000475680)