What is Delusional Misidentification Syndrome?


Delusional misidentification syndrome is an umbrella term, introduced by Christodoulou (in his book The Delusional Misidentification Syndromes, Karger, Basel, 1986) for a group of delusional disorders that occur in the context of mental and neurological illness.

They all involve a belief that the identity of a person, object, or place has somehow changed or has been altered. As these delusions typically only concern one particular topic, they also fall under the category called monothematic delusions.


This psychopathological syndrome is usually considered to include four main variants:

  • The Capgras delusion is the belief that (usually) a close relative or spouse has been replaced by an identical-looking impostor.
  • The Fregoli delusion is the belief that various people the believer meets are actually the same person in disguise.
  • Intermetamorphosis is the belief that an individual has the ability to take the form of another person in both external appearance and internal personality.
  • Subjective doubles, described by Christodoulou in 1978 (American Journal of Psychiatry 135, 249, 1978), is the belief that there is a doppelgänger or double of themselves carrying out independent actions.

However, similar delusional beliefs, often singularly or more rarely reported, are sometimes also considered to be part of the delusional misidentification syndrome. For example:

  • Mirrored-self misidentification is the belief that one’s reflection in a mirror is some other person.
  • Reduplicative paramnesia is the belief that a familiar person, place, object, or body part has been duplicated. For example, a person may believe that they are in fact not in the hospital to which they were admitted, but an identical-looking hospital in a different part of the country, despite this being obviously false.
  • Cotard’s syndrome is a rare disorder in which people hold a delusional belief that they are dead (either figuratively or literally), do not exist, are putrefying, or have lost their blood or internal organs. In rare instances, it can include delusions of immortality.
  • Syndrome of delusional companions is the belief that objects (such as soft toys) are sentient beings.
  • Clonal pluralisation of the self, where a person believes there are multiple copies of themselves, identical both physically and psychologically, but physically separate and distinct.
  • Clinical lycanthropy is the belief that one is turning or has turned into an animal.

There is considerable evidence that disorders such as the Capgras or Fregoli syndromes are associated with disorders of face perception and recognition. However, it has been suggested that all misidentification problems exist on a continuum of anomalies of familiarity, from déjà vu at one end to the formation of delusional beliefs at the other.

What is Cognitive Neuropsychiatry?


Cognitive neuropsychiatry is a growing multidisciplinary field arising out of cognitive psychology and neuropsychiatry that aims to understand mental illness and psychopathology in terms of models of normal psychological function.


A concern with the neural substrates of impaired cognitive mechanisms links cognitive neuropsychiatry to the basic neuroscience. Alternatively, CNP provides a way of uncovering normal psychological processes by studying the effects of their change or impairment.

The term “cognitive neuropsychiatry” was coined by Prof Hadyn Ellis (Cardiff University ) in a paper “The cognitive neuropsychiatric origins of the Capgras delusion”, presented at the International Symposium on the Neuropsychology of Schizophrenia, Institute of Psychiatry, London (Coltheart, 2007).

Although clinically useful, current syndrome classifications (e.g. DSM-IV; ICD-10) have no empirical basis as models of normal cognitive processes. No neuropsychological accounts of how the brain ‘works’ would ever be complete without a cognitive level of analysis. CNP moves beyond diagnosis and classification to offer a cognitive explanation for established psychiatric behaviours, regardless of whether the symptoms are due to recognised brain pathology or to dysfunction in brain areas or networks without structural lesions.

CNP has been influential, not least because of its early success in explaining some previously bizarre psychiatric delusions, most notably the Capgras delusion, Fregoli delusion and other delusional misidentification syndromes. The Capgras delusion is “explained as the interruption in the covert route to face recognition, namely affective responses to familiar stimuli, localised in the dorsal route of vision from striate cortex to limbic system. According to standard molecular hypotheses, acute delusions are the result of a dysregulated activity of some neuromodulators.”

Additionally, the study of cognitive neuropsychiatry has shown to intersect with the study of philosophy. This intersection revolves around a reconsideration of the mind-body relationship and the contemplation of moral issues that can arise by fields such as neuropsychopathology. For example, it has been under consideration whether or not Parkinson’s patients should be held morally accountable for their physical actions. This discussion and study has taken place due to the discovery that under certain circumstances, Parkinson’s patients can initiate and control their own movement. Examples such as this are cause for difficult judgement calls, i.e. “about who is mad and who is bad” (Stein 1999). Cognitive neuropsychiatry has also explored the difference between implicit and explicit cognition, especially in catatonic patients. For more information on the bridge between neuropsychiatry and philosophy see (e.g. Stein, 1999).


Coltheart, M. (2007) The 33rd Sir Frederick Bartlett Lecture Cognitive Neuropsychiatry and Delusional Belief. Quarterly Journal of Experimental Psychology. https://doi.org/10.1080/17470210701338071.

Stein, D. (1999) Philosophy, Psychiatry, & Psychology 6.3, pp.217-221. https://www.researchgate.net/publication/236774712_Philosophy_and_Cognitive_Neuropsychiatry.

What is Capgras Delusion?


Capgras delusion, also known as Capgras syndrome. is a psychiatric disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical impostor.

It is named after Joseph Capgras (1873-1950), a French psychiatrist.

The Capgras delusion is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects. It can occur in acute, transient, or chronic forms. Cases in which patients hold the belief that time has been “warped” or “substituted” have also been reported.

The delusion most commonly occurs in individuals diagnosed with:

  • Paranoid schizophrenia, but has also been seen in;
  • Brain injury;
  • Dementia with Lewy bodies; and
  • Other dementia.

It presents often in individuals with a neurodegenerative disease, particularly at an older age. It has also been reported as occurring in association with diabetes, hypothyroidism, and migraine attacks.

In one isolated case, the Capgras delusion was temporarily induced in a healthy subject by the drug ketamine.

It occurs more frequently in females, with a female to male ratio of approximately 3 to 2.

Brief History

Capgras syndrome is named after Joseph Capgras, a French psychiatrist who first described the disorder in 1923 in his paper co-authored by Jean Reboul-Lachaux, on the case of a French woman, “Madame Macabre,” who complained that corresponding “doubles” had taken the places of her husband and other people she knew. Capgras and Reboul-Lachaux first called the syndrome “l’illusion des sosies”, which can be translated literally as “the illusion of look-alikes.”

The syndrome was initially considered a purely psychiatric disorder, the delusion of a double seen as symptomatic of schizophrenia, and purely a female disorder (though this is now known not to be the case) often noted as a symptom of hysteria. Most of the proposed explanations initially following that of Capgras and Reboul-Lachaux were psychoanalytical in nature. It was not until the 1980s that attention was turned to the usually co-existing organic brain lesions originally thought to be essentially unrelated or accidental. Today, the Capgras syndrome is understood as a neurological disorder, in which the delusion primarily results from organic brain lesions or degeneration.

Signs and Symptoms

The following two case reports are examples of the Capgras delusion in a psychiatric setting:

Mrs. D, a 74-year-old married housewife, recently discharged from a local hospital after her first psychiatric admission, presented to our facility for a second opinion. At the time of her admission earlier in the year, she had received the diagnosis of atypical psychosis because of her belief that her husband had been replaced by another unrelated man. She refused to sleep with the impostor, locked her bedroom and door at night, asked her son for a gun, and finally fought with the police when attempts were made to hospitalise her. At times she believed her husband was her long deceased father. She easily recognised other family members and would misidentify her husband only. )Passer and Warnock, 1991).

Diane was a 28-year-old single woman who was seen for an evaluation at a day hospital program in preparation for discharge from a psychiatric hospital. This was her third psychiatric admission in the past five years. Always shy and reclusive, Diane first became psychotic at age 23. Following an examination by her physician, she began to worry that the doctor had damaged her internally and that she might never be able to become pregnant. The patient’s condition improved with neuroleptic treatment but deteriorated after discharge because she refused medication. When she was admitted eight months later, she presented with delusions that a man was making exact copies of people – “screens” – and that there were two screens of her, one evil and one good. The diagnosis was schizophrenia with Capgras delusion. She was disheveled and had a bald spot on her scalp from self-mutilation. (Sinkman, 2008).

The following case is an instance of the Capgras delusion resulting from a neurodegenerative disease:

Fred, a 59-year-old man with a high school qualification, was referred for neurological and neuropsychological evaluation because of cognitive and behavioural disturbances. He had worked as the head of a small unit devoted to energy research until a few months before. His past medical and psychiatric history was uneventful. […] Fred’s wife reported that about 15 months from onset he began to see her as a “double” (her words). The first episode occurred one day when, after coming home, Fred asked her where Wilma was. On her surprised answer that she was right there, he firmly denied that she was his wife Wilma, whom he “knew very well as his sons’ mother”, and went on plainly commenting that Wilma had probably gone out and would come back later. […] Fred presented progressive cognitive deterioration characterised both by severity and fast decline. Apart from [Capgras disorder], his neuropsychological presentation was hallmarked by language disturbances suggestive of frontal-executive dysfunction. His cognitive impairment ended up in a severe, all-encompassing frontal syndrome. (Lucchelli and Spinnler, 2007).


It is generally agreed[14] that the Capgras delusion has a complex and organic basis (caused by structural damage to organs) and can be better understood by examining neuroanatomical damage associated with the syndrome.

In one of the first papers to consider the cerebral basis of the Capgras delusion, Alexander, Stuss and Benson pointed out in 1979 that the disorder might be related to a combination of frontal lobe damage causing problems with familiarity and right hemisphere damage causing problems with visual recognition.

Further clues to the possible causes of the Capgras delusion were suggested by the study of brain-injured patients who had developed prosopagnosia. In this condition, patients are unable to recognize faces consciously, despite being able to recognize other types of visual objects. However, a 1984 study by Bauer showed that even though conscious face recognition was impaired, patients with the condition showed autonomic arousal (measured by a galvanic skin response measure) to familiar faces, suggesting that there are two pathways to face recognition – one conscious and one unconscious.

In a 1990 paper published in the British Journal of Psychiatry, psychologists Hadyn Ellis and Andy Young hypothesised that patients with Capgras delusion may have a “mirror image” or double dissociation of prosopagnosia, in that their conscious ability to recognise faces was intact, but they might have damage to the system that produces the automatic emotional arousal to familiar faces. This might lead to the experience of recognising someone while feeling something was not “quite right” about them. In 1997, Ellis and his colleagues published a study of five patients with Capgras delusion (all diagnosed with schizophrenia) and confirmed that although they could consciously recognise the faces, they did not show the normal automatic emotional arousal response. The same low level of autonomic response was shown in the presence of strangers. Young (2008) has theorised that this means that patients with the disease experience a “loss” of familiarity, not a “lack” of it. Further evidence for this explanation comes from other studies measuring galvanic skin responses (GSR) to faces. A patient with Capgras delusion showed reduced GSRs to faces in spite of normal face recognition. This theory for the causes of Capgras delusion was summarised in Trends in Cognitive Sciences in 2001.

William Hirstein and Vilayanur S. Ramachandran reported similar findings in a paper published on a single case of a patient with Capgras delusion after brain injury. Ramachandran portrayed this case in his book Phantoms in the Brain and gave a talk about it at TED 2007. Since the patient was capable of feeling emotions and recognising faces but could not feel emotions when recognising familiar faces, Ramachandran hypothesises that the origin of Capgras syndrome is a disconnection between the temporal cortex, where faces are usually recognized (see temporal lobe), and the limbic system, involved in emotions. More specifically, he emphasises the disconnection between the amygdala and the inferotemporal cortex.

In 2010, Hirstein revised this theory to explain why a person with Capgras syndrome would have the particular reaction of not recognising a familiar person.

Furthermore, Ramachandran suggests a relationship between the Capgras syndrome and a more general difficulty in linking successive episodic memories because of the crucial role emotion plays in creating memories. Since the patient could not put together memories and feelings, he believed objects in a photograph were new on every viewing, even though they normally should have evoked feelings (e.g., a person close to him, a familiar object, or even himself). Others like Merrin and Silberfarb (1976) have also proposed links between the Capgras syndrome and deficits in aspects of memory. They suggest that an important and familiar person (the usual subject of the delusion) has many layers of visual, auditory, tactile, and experiential memories associated with them, so the Capgras delusion can be understood as a failure of object constancy at a high perceptual level.

Most likely, more than just an impairment of the automatic emotional arousal response is necessary to form the Capgras delusion, as the same pattern has been reported in patients showing no signs of delusions. Ellis suggested that a second factor explains why this unusual experience is transformed into a delusional belief; this second factor is thought to be an impairment in reasoning, although no definitive impairment has been found to explain all cases. Many have argued for the inclusion of the role of patient phenomenology in explanatory models of the Capgras syndrome in order to better understand the mechanisms that enable the creation and maintenance of delusional beliefs.

Capgras syndrome has also been linked to reduplicative paramnesia, another delusional misidentification syndrome in which a person believes a location has been duplicated or relocated. Since these two syndromes are highly associated, it has been proposed that they affect similar areas of the brain and therefore have similar neurological implications. Reduplicative paramnesia is understood to affect the frontal lobe, and thus it is believed that Capgras syndrome is also associated with the frontal lobe. Even if the damage is not directly to the frontal lobe, an interruption of signals between other lobes and the frontal lobe could result in Capgras syndrome.


Because it is a rare and poorly understood condition, there is no definitive way to diagnose the Capgras delusion. Diagnosis is primarily made on a psychiatric evaluation of the patient, who is most likely brought to a psychiatrist’s attention by a family member or friend believed to be an imposter by the person under the delusion.


Treatment has not been well studied and so there is no evidence-based approach. Treatment is generally therapy, often with support of antipsychotic medication.

Cultural References

In the Memoirs Found in a Bathtub novel by the Polish writer Stanisław Lem, first published in 1961 the narrator inhabits a paranoid dystopia where nothing is as it seems, chaos seems to rule all events, and everyone is deeply suspicious of everyone. In the end, it is revealed that the world is filled by phantom body doubles.

A central character in Richard Powers’s 2006 novel The Echo Maker suffers from Capgras Delusion subsequent to traumatic brain injury.

The protagonist in the movie Synecdoche, New York, who is named Caden Cotard (played by Philip Seymour Hoffman), goes to see his ex-wife at her apartment, and, as he enters the building, one of the resident call boxes is taped with the name “Capgras”. He is then misidentified as his ex-wife’s cleaning lady, Ellen Bascomb, as he tries to enter the apartment, and, later in the film, he actually comes to play the role of Ellen Bascomb in his own play. Throughout the film, Cotard enlists actor-doubles to play actors, and, as the film progresses, the actor-doubles are in turn then given actors-doubles.