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Cotard's Syndrome: A Review

  • PC Gent-Sleidinge, campus Gent


Cotard's syndrome is a rare disorder in which nihilistic delusions concerning one's own body are the central feature. It is not listed as a specific disorder in the DSM-IV, as it is typically viewed as a part of other underlying disorders. However, it remains important to recognize the syndrome because specific underlying mechanisms are present, and prognostic and therapeutic consequences have to be taken into account. This review presents an up-to-date overview of Cotard's syndrome, which was initially described more than a century ago.
Cotard’s Syndrome
Hans Debruyne
, Michael Portzky
, Kathelijne Peremans
and Kurt Audenaert
Department of Psychiatry, University Hospital Ghent, Ghent, Belgium;
PC Dr. Guislain, Psychiatric Hospital, Ghent, Belgium and
Department of
Psychiatry, Zorgsaam/RGC, Terneuzen, The Netherlands
Cotard’s syndrome is characterized by nihilistic delusions focused on the individual’s body including loss of body parts, being dead, or not
existing at all. The syndrome as such is neither mentioned in
nor in
. There is growing unanimity that Cotard’s syndrome
with its typical nihilistic delusions externalizes an underlying disorder. Despite the fact that Cotard’s syndrome is not a diagnostic entity in
our current classification systems, recognition of the syndrome and a specific approach toward the patient is mandatory.
This paper overviews the historical aspects, clinical characteristics, classification, epidemiology, and etiological issues and includes recent
views on pathogenesis and neuroimaging. A short overview of treatment options will be discussed.
Keywords: Cotard’s syndrome, nihilistic delusion, misidentification syndrome, review
Correspondence: Hans Debruyne, P.C. Dr. Guislain Psychiatric Hospital Ghent, Fr. Ferrerlaan 88A, 9000 Ghent, Belgium. Tel: 32 9 216
3311; Fax: 32 9 2163312; e-mail:
Cotard’s syndrome is named after Jules Cotard (18401889),
a French neurologist who described this condition for the
first time in 1880, in a case report of a 43-year-old woman.
Mss X, affirms she has no brain, no nerves, no
chest, no stomach, no intestines; there’s only
skin and bones of a decomposing body. ...She
has no soul, God does not exist, neither the
devil. She’s nothing more than a decomposing
body, and has no need to eat for living, she
cannot die a natural death, she exists eternally if
she’s not burned, the fire will be the only
solution for her. (Translation from Cotard
Cotard formulated a new type of depression, characterized by
anxious melancholia, ideas of damnation or rejection,
insensitivity to pain, delusions of nonexistence concerning
one’s own body, and delusions of immortality. He categor-
ized this under lype
´manie, a kind of psychotic depression,
based on the analogy with five cases described in 1838 by
Later, Cotard introduced de
´lire des negations as new
terminology for the syndrome.
The eponym Cotard’s syndrome
was introduced in 1887 by Se
A few years later, Re
stated that the syndrome (he named it de
´lire de Cotard) was not
only associated with depression, but might be linked to other
psychiatric disorders as well.
Two components of the syndrome were defined by Tissot:
an affective component associated with anxiety and a cognitive
component associated with the presence of delusion.
and Martinez
made a first attempt to classify different types
of the syndrome. They described a nongeneralized de
´lire de
negation, associated with paralysis, alcoholic psychosis,
dementia, and the ‘‘real’’ Cotard’s syndrome, only found in
anxious melancholia and chronic hypochondria.
Later, in
1968, Saavedra proposed a classification into three types:
depressive,mixed,andschizophrenic. He drew a distinction
between a ‘‘genuine’’ Cotard’s syndrome occurring during
depressive states and what he described as a pseudonihilistic
or pseudo-Cotard syndrome classified as ‘‘co-anaesthetic
In 1995, for the first time, a classification was made on
evidence basis. In a retrospective factor analysis of 100 cases
in literature, Berrios and Luque subdivided Cotard’s syn-
drome into three types. A first type included a form of
psychotic depression, characterized by anxiety, melancholic
delusions of guilt, and auditory hallucinations. A second
type, described as Cotard’s syndrome type I, was associated with
hypochondriac and nihilistic delusions and absence of
depressive episodes. The third group was the Cotard’s syndrome
type II, with anxiety, depression, auditory hallucinations,
delusions of immortality, nihilistic delusions, and suicidal
behavior as characteristic features.
Cotard’s syndrome is currently not classified as a separate
disorder in DSM-IV-TR and ICD-10.InDSM-IV-TR, nihilistic
delusions are categorized as mood congruent delusions within
a depressive episode with psychotic features.
Cotard’s syndrome as a separate entity is an extremely difficult
exercise in our current diagnostic classification system.
For this article, we started from the search results for
‘‘Cotard syndrome,’’ ‘‘Cotard’s syndrome,’’ and ‘‘nihilistic
delusion(s)’’ using PubMed and Web of Science. Relevant
articles in English, French, Dutch, and German were
gathered. Since data on this topic is scarce, we looked at
every article for relevant cross references. A general Internet
search on Google was also used. From this last result, we
only included articles written in peer-reviewed journals. Using
this method, we tried to obtain all available peer-reviewed
data on this topic. This was necessary because there are no
controlled studies available. All literature is dominated by
case studies and some case series.
As described earlier, nihilistic delusions concerning the
individuals body are the central features of Cotards syn-
drome. In an analysis of 100 cases, the most prominent
symptoms in Cotards syndrome are: depressive mood (89%),
nihilistic delusions concerning ones own existence (69%),
anxiety (65%), delusions of guilt (63%), delusions of
immortality (55%), and hypochondriac delusions (58%).
Some case reports concerning delusional denial of preg-
nancy despite clear morphologic signs
and delusional
paralysis in a patient with psychomotor agitation
reported as a special form of Cotards syndrome. However,
the classification of these delusions as nihilistic delusions
concerning ones body can be debated.
A classical description of the course of Cotards syndrome is
given by Enoch and Trethowan. In its early stages, Cotards
syndrome is characterized by a vague feeling of anxiety, with a
varying time span from weeks to years. This anxious state
gradually augments and can result in nihilistic delusions
where denial of life or denial of body parts are the prominent
features. The patient looses sense of reality.
Despite the
delusion of being dead, these patients show an increased
tendency to automutilation or suicidal behavior. Additional
symptoms may include analgesia and mutism. The core
symptoms always reflect a preoccupation with guilt, despair,
and death.
Delusions can be accompanied by a de
´, a delusion of massive increase of body measures.
This has been described as the manic Cotards syndrome.
As the
syndrome often occurs in association with other psychotic
states, symptoms of these specific disorders are likely to be
present. As an example, nihilistic delusions grafted on a
depressive illness are often associated by other characteristics
of a depressive episode such as weight loss and sleeping
difficulties and the syndrome associated with organic disease
is often associated with other symptoms such as disorienta-
tion or neurological signs.
The duration of the syndrome
can vary from weeks to years depending on the underlying
In 1999, Yamada et al
made a proposal for staging
Cotards syndrome. Based on a case report, he defined three
stages: germination stage, blooming stage, and chronic
stage. The germination stage is characterized by important
hypochondria, cenesthopathy, and depressive mood. A
diagnosis of Cotards syndrome cannot be made in this
stage yet. In the blooming stage, the characteristic features of
Cotards syndrome (nihilistic delusions, delusions of im-
mortality together with anxiety and negativism) are seen. The
last stage, the chronic stage is differentiated in two forms: one
with persistent emotional disturbances (depressive type) and
a second where depressive symptoms are less prominent
(paranoid type).
This hypothesis was supported in a second
case report.
The prevalence and incidence of this rare syndrome is not
known. Only one study reported on prevalence in a selected
psychogeriatric population in Hong Kong. In 2 out of 349
patients, Cotards syndrome was diagnosed suggesting a
prevalence of .57% in this population. A prevalence of 3.2%
was reached when severely depressed elderly were included.
A recent study found .62% (n3) of patients in a Mexican
sample (screened over a 2-year period) of primary psychiatric
patients having Cotards syndrome.
Using the same
methodology they found also .11% (n1) having Cotards
syndrome in a sample of neurological patients with mental
The likelihood of developing Cotards delu-
sion appears to increase with age.
Berrios and Luque
found a mean age of 56 years in their analysis of 100 cases.
A more recent study of 138 cases reported a mean age of
47.7 years.
Women appear to be more vulnerable.
syndrome is found in different ethnic groups.
syndrome is also occasionally described in children and
Diagnosis of Cotards syndrome in people
under 25 years old was described to be associated with
bipolar disorder.
Since Cotards syndrome is conceptualized as part of an
underlying disorder, several psychiatric and somatic diseases
have been associated with the syndrome. Unipolar
or bipolar
depression are the most common
associated psychiatric disorders but also comorbid psychotic
has been reported. Some studies repor-
ted on the occurrence of Cotards syndrome with more
uncommon psychiatric syndromes (hydrophobia,
folie a deux,
Capgras delusion,
Capgras and
Fregoli delusion,
depersonalization disorder
). Also Par-
kinsonian symptoms, disappearing with successful treat-
ment, are described.
Several organic conditions were also
associated: dementia,
major depressive episode in mild
cognitive impairment,
depression in frontotemporal atro-
severe mental retardation,
typhoid fever,
superior sagittal sinus thrombosis,
temporal lobe epilepsy,
limbic epileptic in-
postictal depression,
cerebral arteriovenous mal-
cerebral arteriovenous malformation and
Laurence-Moon-Bardet-Biedl syn-
multiple sclerosis,
Parkinsons disease,
a noninfectious complication of heart transplan-
as a consequence of an adverse drug reaction to
aciclovir and its prodrug valaciclovir
and in herpetic
Mind & Brain, the Journal of Psychiatry
M&B 2011; 2:(1). July 2011 68
The first structural imaging study was performed in 1986,
using Computed Tomography (CT). An association of
Cotards syndrome with multifocal brain atrophy and inter-
hemispheric enlargement was suggested.
Others have
described an enlargement of the third and lateral ventricle,
a specific lesion to the temporoparietal areas,
and changes
in the nondominant temporoparietal areas, sometimes to-
gether with frontal damage.
In general, these studies point
to an important role for the frontotemporoparietal circuitry
in the pathophysiology of the syndrome. However, in most
cases, gross structural changes on structural brain imaging
were absent.
Several functional imaging studies in Cotards syndrome
patients were published. A dopamine D2 receptor SPECT
study with
I-iodobenzamide (IBZM), performed in one
patient, showed an asymmetric striatal D
receptor binding in
favor of the left hemisphere. These SPECT-findings persisted
after remission. In this specific patient, no perfusion altera-
tions were found with
Tc-hexamethylpropylenamide ox-
ime (HMPAO) SPECT before treatment.
Several, but not all,
case studies reported decreased perfusion in several cortical
areas measured with the same perfusion SPECT tracer. In one
patient, a left-sided hypoperfusion in temporal, parietal, and
frontal lobes was found with full recovery of the left inferior
frontal hypoperfusion and minimal remaining hypoperfusion
in the left temporal lobe after successful treatment using
electroconvulsive therapy (ECT).
A similar recovery of
perfusion was found in another patient after ECT-treatment
in the medial parietal cortex, medial and dorsolateral
prefrontal cortex, the basal ganglia, and thalamus.
ful treatment with ECT in a patient with underlying major
depressive disorder resulted in recovery of left and right
temporal hypoperfusion
and normalization of perfusion in
the frontal cortex was reported after treatment with anti-
In one patient, severe right hemispheric
dysfunction on neuropsychological tasks was not accompa-
nied by perfusion abnormalities measured with
TC Ethyl
Cysteine Dimer (ECD) SPECT.
Psychological and Neuropsychological Factors
A depersonalization phenomenon was reported as an
essential step in the development of Cotards syndrome by
´glas (1887).
Alheid elaborated depersonalization in the
Cotards syndrome context using the German terminology
‘‘Leib’’ (body for me) and ‘‘Ko¨rper’’ (body as such). Deperso-
nalization may occur when ‘‘Ko¨rper’’ prevails over ‘‘Leib’’ and
when the body is less associated with the self (Leib). However,
in depersonalization the patient feels like being dead
(indifference of affect), while in Cotards syndrome the
patient is convinced to be dead (lack of feeling).
In the development of bizarre psychiatric syndromes related
to parietal brain dysfunction, Critchley stated that the role of
premorbid personality characteristics is essential.
regard to this premorbid personality characteristic, it is
proposed that in Cotards syndrome, patients with a more
internal attributional style (which is often co-occurring with
depression) are more vulnerable to develop the syndrome.
While patients with a more external attributional style (which
is more co-occurring with paranoia) are more prone to
develop Capgrass syndrome (a delusion where familiar
persons are replaced by identical impostors).
This hypoth-
esis that Cotards patients have a more internal attribution
style was empirically tested in one case.
A significant higher
score on two attribution bias indices (internalizing bias index,
internalizing bias for negative events) calculated on the
IPSAQ (Internal, Personal, and Situational Attributions Ques-
tionnaire) was found in this patient with Cotards syndrome
compared to control subjects.
However, several authors
reported the co-occurrence of both Cotards syndrome and
Capgrass syndromes.
Vinkers suggested that a
combination of attribution styles occur in these patients, in
so far that these patients are both depressed and paranoid or
that they suffer from delusions about self-identity and about
identity of others.
Unfortunately, evidence-based proof for
this hypothesis is lacking.
The origin of both syndromes (and other delusional
misidentification syndromes) is supposed to be related to a
dysfunction of an information processing subsystem where
face and body recognition is associated with recognition of
familiarity. When a feeling of familiarity is absent, the
patients may experience a feeling of derealization and
This hypothesis is supported by several
studies for a number of misidentification syndromes and
especially for Capgrass syndrome.
Interestingly, in
studies on face recognition tasks with skin conductance as
outcome measure the differential autonomic response to
familiar faces compared to unknown faces is absent in
patients with Capgrass syndrome.
Another patient with
atypical Capgrass delusion showed impaired interpretation
of facial expressions. This leads to mistake differences in
expression for differences in identity.
For Cotards syn-
drome, a lack of differential autonomic response to anything
is suggested. This can lead to the delusion of being dead,
where in Capgrass delusion there is only lack of familiarity to
familiar faces, leading to the delusion of familiar persons
being replaced by identical impostors. In this hypothesis, the
psychopathology in Cotards syndrome is more severe and
more generalized.
On the other hand, the lack of feeling
of familiarity cannot completely explain the pathophysiology
of delusional misidentification syndromes. Patients with
brain damage of the ventromedial region of the frontal cortex
also demonstrate absence of differential autonomic respon-
sivity to familiar faces, despite the absence of delusions. The
same is seen in patients suffering from pure autonomic
failure. There a lack of differential autonomic responsivity to
anything is seen despite the absence of delusions. Therefore,
to explain delusions a second factor is needed. This factor is
responsible for the failure to reject the hypothesis (eg, Im
dead as a explanation for the lack of feeling of familiarity to
anything) despite the presence of (often overwhelming)
Cotard’s syndrome 69 M&B 2011; 2:(1). July 2011
evidence against it.
Hence, for Cotards syndrome, a two-
factor hypothesis is proposed. Here, the first factor con-
tributes to the total lack of autonomic response to anything
(as in pure autonomic failure), the second to not being able to
reject the hypothesis ‘‘Im dead.’’
In this hypothesis the
loss of affect (first factor) is more pronounced and general-
ized than in Capgras patients.
On the other hand, the
difference in attributional style could also be an explanation
for the different hypothesis formation in the first factor.
The importance of the right dorsolateral prefrontal cortex
(RDLPFC) for hypothesis evaluating was demonstrated with
It has also been observed that right frontal damage
is commonly occurring in cases of delusional misidentifica-
tions (including Cotards syndrome).
Complete recovery may occur as spontaneously and as
suddenly as its onset, even in the most severe cases.
and Trethowan
link the prognosis to the underlying
If the nihilistic delusions are related to an acute
psycho-organic syndrome, the prognosis is
good and the condition tends to resolve. If,
however, it is associated with a depressive
illness, it may well persist even when the other
symptoms of the depressive illness have
cleared. Under this circumstance, and where
the condition becomes chronic, the delusional
state of negation usually waxes and wanes in
intensity, depending on the periodic fluctua-
tions of the depressive disorder. When the
phenomenology is part of a schizophrenic
illness, it usually improves when the other
symptoms respond to therapy, but it can also
persist for years as part of a chronic schizo-
phrenic condition.
In general, no further statements can be made about
prognosis from the available literature. In most publications,
prognosis is not discussed. It seems prognosis can widely
vary from spontaneous recovery to a very severe chronic
condition. An important exclusion for this is when Cotards
syndrome is diagnosed under the age of 25 years. In these
cases, there seems to be an association with bipolar
Diagnostic work-up of the underlying disorders should
therefore be a guide for treatment. Several reports are
published about successful treatments. Pharmacological
monotherapy such as amitriptyline,
has been reported as effective. However, usually
combination strategies are used (clomipramine/
risperidone citalopram,
and olanzapine/escitalopram/lora-
Adding bromocriptine to clomipramine and
lithium had a beneficial effect in a patient with bipolar
disorder type I.
The most reported treatment strategy for Cotards syndrome
is electroconvulsive therapy (ECT).
Based on the classification of Berrios and
a suggestion was made that ECT is indicated in
patients with Cotards syndrome and psychotic depression,
while antipsychotics exert better effects in Cotards syndrome
type I.
In one patient, spontaneous recovery after two grand
mal seizures was reported illustrating the usefulness of
seizure activity in the treatment of Cotards syndrome.
Treatment should initially follow current treatment guidelines
of the underlying conditions, since no randomized studies are
performed on this Cotards syndrome. In depressive disorder
with psychotic features, ECT (often in combination with
farmacotherapy) seems to be the most supported strategy.
Enoch and Trethowan rightly argue that apart from these
treatments, special measures can be needed. The severe
distress may lead to important suicide risk, especially in
patients suffering from major depressive disorder. This may
be in contrast with the delusion of being already dead. During
recovery this risk may even become more pronounced when
the patient becomes more active.
They also mention the
importance of therapeutic support for these patients. They
indeed suffer from severe fright and despair, making contact
with caring professionals essential.
Despite that Cotards syndrome was first described more
than a century ago, literature on this topic remains restricted
to case reports. Although the syndrome is rare, more larger
scale research is needed to further clarify the pathophysiolo-
gic underpinnings of the disease and its relation to other
delusions of misidentification such as Capgras syndrome.
Promising hypotheses have been formulated but evidence-
based support is lacking. To elucidate uncertainties regarding
epidemiology, course, associated diseases, treatment options,
and prognosis, a careful registration of all cases could be of
great value. In this regard, recognition of this condition is
essential. The restriction of publications to case reports is a
potential pitfall. Sometimes general conclusions on course,
pathophysiology, or treatment are made, based on one or a
few cases. On this topic, the literature has to be read
The syndrome as such is not catalogued in our current
classification system. It has to be diagnosed as part of an
underlying disorder. Also treatment is guided by this
diagnosis. Although Cotards syndrome is more like a
symptom of its underlying condition, in our opinion
recognition of this phenomenological entity remains impor-
tant. Its very specific presentation, in spite of the extensive list
of etiologies indicating a shared pathological pathway, is
intriguing. In the management of these patients, a better
Mind & Brain, the Journal of Psychiatry
M&B 2011; 2:(1). July 2011 70
understanding of the psychopathology and its neuropsycho-
logic mechanisms can be of great value. Specific safety
measures can also be required due to the dramatic sympto-
Disclosures: The author declares no conflict of interest.
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Mind & Brain, the Journal of Psychiatry
M&B 2011; 2:(1). July 2011 72
... Cotard's syndrome is a rare psychiatric disorder characterised by nihilistic delusions concerning one's own body. 1 Described in 1880 by Jules Cotard, a French psychiatrist, patients typically believe they are dead or their bodily organs and limbs are rotting and disintegrating. 2 In accordance with the Mental Health Act (MHA) legislation, for a patient who is detained under section 3 of the MHA 2007 and does not consent to treatment, where the responsible consultant considers treatment necessary, the Mental Health Act Commission must be contacted and the advice of a Second Opinion Appointed Doctor (SOAD) must be sought. ...
... Treatment of Cotard's syndrome secondary to an underlying mood disorder with ECT has been observed to be extremely effective. 1 We report the case of a female patient who has a long history of somatisation presenting with depression and Cotard's phenomenon; highlighting an ethical dilemma of treatment with ECT within the United Kingdom's MHA. ...
... This case demonstrates that Cotard's phenomenon occurs in severe depression and while the role of ECT in Cotard's syndrome is already well established, maintenance ECT has a role in the management of Cotard's syndrome. 1 The case also highlights that a capacitated but non-consenting patient cannot be given ECT, even if the patient is detained under the MHA 2007, which is an amendment of the MHA 1983. Furthermore, this is in keeping with the Mental Capacity Act 2005; but there are some ethical dilemmas for the treating doctor. ...
Full-text available
Treatment of Cotard's syndrome with electroconvulsive therapy (ECT) has been seen to be an effective treatment option when pharmacological options are not successful. Recent changes in the Mental Health Act 2007 used within the United Kingdom has resulted in clinicians unable to prescribe treatment for patients who have capacity but are not providing consent for treatment. We report a case of a patient in the UK with Cotard's phenomenon and severe depression, where the only effective treatment of ECT was restricted due to changes in mental health law. The role of maintenance ECT as well as the ethical dilemma faced is discussed.
... Treatment depends on the cause of the condition. ECT is the treatment of choice for cotard syndrome caused by psychotic depression (6). In addition, antidepressant and antipsychotic medications have a place in the management (6). ...
... ECT is the treatment of choice for cotard syndrome caused by psychotic depression (6). In addition, antidepressant and antipsychotic medications have a place in the management (6). ...
Full-text available
Coatard syndrome is an uncommon disorder where elderly patients present with severe depression and nihilistic delusions. Author of this study illustrates a case of a 66 year old female presented with predominant nihilism and depression. The patient was managed with ECT, antidepressants and antipsychotics.
... Lesions of the non- dominant hemisphere have been implicated specifically, thus to indicate that the findings related to nondominant hemisphere changes may be indeed significant (McKay & Cipolotti, 2007). Nevertheless, in most cases, gross structural changes on structural brain imaging were absent (Debruyne et al., 2009). Among neuro- biological theories, some authors have linked CS with lesions of the temporoparietal junction, an important multimodal area that incorporates inputs from the tactile, proprioceptive, visual and vestibular systems. ...
... In organic disease, either management of the underlying condi- tion or use of psychotropic medication can lead to an improve- ment. Several reports about successful pharmacological treatments have been published, both monotherapies with anti- depressants, antipsychotics or lithium, and by antidepressant and antipsychotic combination treatments including aripiprazole (De Berardis et al., 2010), paliperidone (Morgado, Ribeiro, & Cerqueira, 2015), amitriptyline (Soultanian et al., 2005), duloxetine (Kozian, 2005), fluoxetine (Chiu, 1995), venlafaxine (Ruiz-Doblado, RuedaVillar, & Casillas-Lara, 2009), combination therapy of clozapine, flu- voxamine, and imipramine ( Risio et al., 2004), combination ther- apy of fluoxetine and risperidone ( Chou et al., 2011), risperidone and sertraline (Debruyne et al., 2009), venlafaxine and zuclopen- tixolo (Vaxevanis & Vidalis, 2005), haloperidol and mitazapin ( Wani et al., 2008), haloperidol and clomipramine (Soultanian et al., 2005), risperidone and citalopram (Walloch, Klauwer, Lanczik, Brockington, & Kornhuber, 2007), pimozide and amitriptyline (Soultanian et al., 2005), combined use of imipramine and risperi- done ( Machado et al., 2013), quetiapine in combination with ven- lafaxine (Chan, Chen, Robson, & Tan, 2009). The electroconvulsive therapy (ECT) has been the preferred treatment form for CS in several case reports (Kobayashi et al., 2012;Mahgoub & Hossain, 2004;Weiss et al., 2013). ...
Full-text available
Background: Cotard syndrome is a rare condition whose main feature is a nihilistic delusion ranging from the denial of body parts to that of the existence of one’s own life or even the entire universe. Objectives: The aim of this article is to review the nosological significance of Cotard syndrome and to explore the disorder among patients with dementia. Methods: Medline and Google Scholar searches were conducted for relevant articles, chapters and books published before 2018. Search terms used included Cotard delusion, Cotard syndrome and dementia, nihilistic delusion. Publications found through this indexed search were reviewed for further relevant references. Results and conclusion: In this narrative review we emphasise the fact that cases of Cotard syndrome involving patients with dementia are reported quite infrequently. Published studies are limited to very short series or isolated cases. Clinicians are obliged to treat the disorder. They should be alert to the potential high risk inherent in this condition. • Keypoints • Cotard syndrome is a rare condition characterised by nihilistic delusions that may range from negation of existence of parts of the body to delusion of being dead. • The prevalence and incidence of this rare syndrome are not known. • Since Cotard’s syndrome is conceptualised as part of an underlying disorder, several psychiatric and somatic diseases have been associated with the syndrome. • The syndrome may occur in patients suffering from dementia.
... The psychotic features of PsyMDD are dominated by delusions, particularly involving guilt, worthlessness and being deserving of punishment (Ohayon and Schatzberg, 2002;Parker et al., 2017;Picardi et al., 2018;Sourey et al., 2011;Vargas et al., 2019), and thus mood congruent. Mood incongruent delusional themes can, however, occur in PsyMDD and include beliefs of persecution, Scheiderian first-rank delusions (Picardi et al., 2018;Soares-Weiser et al., 2015), nihilistic delusions (Cotard's syndrome) (Debruyne et al., 2009) and somatic delusions (particularly related to the gastrointestinal tract) (Gournellis et al., 2011;Parker et al., 1991;Parker and Manicavasagar, 2005). Constipation is a common complaint and over-represented in those with PsyMDD, even in the absence of constipating medications, particularly in the elderly (Agüera-Ortiz et al., 2020;Parker et al., 1991;Parker et al., 2017). ...
Psychotic episodes occur in a substantial proportion of patients suffering from major mood disorders (both unipolar and bipolar) at some point in their lives. The nature of these episodes is less well understood than the more common, non-psychotic periods of illness and hence their management is also less sophisticated. This is a concern because the risk of suicide is particularly high in this subtype of mood disorder and comorbidity is far more common. In some cases psychotic symptoms may be signs of a comorbid illness but the relationship of psychotic mood to other forms of psychosis and in particular its interactions with schizophrenia is poorly understood. Therefore, our targeted review draws upon extant research and our combined experience to provide clinical context and a framework for the management of these disorders in real-world practice – taking into consideration both biological and psychological interventions.
... Cotard syndrome was first described by Jules Cotard in 1880, and one of the characteristics is the nihilistic delusions that are related to denying the existence of oneself or the world. Capgras syndrome was described in 1923 by Capgras and Reboul-Lachaux and is characterized by the delusion that the individual or family members have been replaced by substitutes [1]. We report the case of a patient with treatment-resistant schizophrenia who had symptoms of both syndromes. ...
Full-text available
The presentation of both Cotard and Capgras syndromes is uncommon in schizophrenia. We present a case of a 23-year-old male with the diagnosis of schizophrenia with Cotard syndrome who later developed Capgras syndrome. By persisting significant symptoms despite the use of two antipsychotics, he was given the diagnosis of treatment-resistant schizophrenia, and his symptoms improved with clozapine. This is one of the few cases of Cotard and Capgras syndromes in a patient with schizophrenia.
... For instance, macrosomatognosia can concern the entire body in patients with Alice in Wonderland syndrome, who have an erroneous perception of their whole body size with respect to the external environment. 32 Similarly, extreme forms of depersonalization in which patients claim to be nonexistent or dead (i.e., Cotard's syndrome) 33 can be considered as an equivalent of the feeling of amputation described earlier, but concerning the whole body. ...
This chapter provides a review of the main clinical alterations of body representation in neurological and psychiatric diseases. First, we describe instances of altered body representations in neurological conditions, either constrained to a specific body part (e.g., personal neglect, somatoparaphenia, phantom limbs) or impacting the whole body (autoscopic phenomena, feeling of a presence). In the second part of this chapter, we present body representation disorders associated with chronic pain and psychiatric conditions including anorexia nervosa, schizophrenia, and gender dysphoria. Beyond their clinical relevance, these conditions provide valuable insights into understanding the way our body is normally represented, and the way it is consciously experienced.
... For instance, macrosomatognosia can concern the entire body in patients with Alice in Wonderland syndrome, who have an erroneous perception of their whole body size with respect to the external environment. 32 Similarly, extreme forms of depersonalization in which patients claim to be nonexistent or dead (i.e., Cotard's syndrome) 33 can be considered as an equivalent of the feeling of amputation described earlier, but concerning the whole body. ...
... Notwithstanding, its neural bases remain to be clarified (Chatterjee & Mitra, 2015;Mendez & Ramírez-Bermúdez, 2011;Swamy, Sanju, & Jaimon, 2007). Neuroanatomical and neurofunctional analyses of Cotard syndrome have produced insufficient results, as many cases are described in psychiatric patients without evidence of focal lesions (Debruyne, Portzky, Van den Eynde, & Audenaert, 2009). Joseph and O'Leary (1986) studied eight Cotard patients and eight controls with computerized axial tomography: bilateral cerebral atrophy, particularly in parietal and temporal lobes, was more frequent in Cotard patients (Joseph & O'Leary, 1986). ...
Introduction: Cotard syndrome is a neuropsychiatric entity recognised by the presence of nihilistic delusions. Although different models have been proposed for the development of monothematic delusions, including Cotard syndrome, functional neuroanatomical models are lacking. Methods: A case report of a 19-year old male with autoimmune encephalitis and Cotard syndrome, in whom Positron Emission Tomography (¹⁸F-FDG-PET) scans were performed before and after successful treatment with electroconvulsive therapy (ECT), is presented. Literature review on brain imaging is provided to discuss a functional neuroanatomical model of Cotard syndrome, in accordance with the two-factor theory of delusions. Results: The patient’s ¹⁸F-FDG-PET showed marked insular and prefrontal metabolic abnormalities. Except for insular hypometabolism, metabolic abnormalities improved after ECT. Previously reported structural neuroimaging studies in Cotard syndrome showed a predominance of right hemisphere lesions, in which frontal lobes were more frequently involved, followed by parietal and temporal lesions. Functional neuroimaging studies reported abnormalities in frontoparietal circuits as well as midline structures included in the “default mode network”. Conclusions: Abnormalities in the functioning of the insular cortex and the prefrontal cortex could be related to the development of nihilistic delusions when a two-factor theory of delusions is considered.
... Cotard's syndrome is a rare and uncommon syndrome, which is characterized by various symptoms such as nihilistic delusions, hypochondriacal delusions, delusions of immortality, depression, and anxiety (22). Other forms such as delusions of missing organs, "walking corpse" syndrome, denial of existence and ideas of damnation might be part of the same spectrum, with some authors blaming diverse neurological conditions for this unusual psychopathology (23). ...
In this review, we have collected the latest data on Kotar syndrome. The question of its nosological affiliation is considered, etiological theories and epidemiological indicators are presented. The options for the development of the clinical picture are described, data on the results of neuroimaging diagnostic studies are presented.
Cotard's delusion is characterised by a series of bizarre beliefs ranging from loss of one's organs, blood, body parts to believing that one's soul is lost or dead, even that one does not exist at all. Lying at the core of these nihilistic delusions are themes of negativism and self-accusatory depressive delusions and the paradox that, although they believe that they are dead (in extreme cases), or that they can never die, they still try to destroy themselves. Our paper reviews the epidemiology and aetiology of Cotard's delusion. The primary focus, however, is on explanatory theories, in which psychodynamic, cerebral lesion/ dysfunction and cognitive neuropsychological accounts are presented. This is a selective review in which the following key terms: Cotard's syndrome, Cotard's delusion, nihilistic delusions were used to search PsycInfo and Medline databases.
A case of Cotard's syndrome which resolved following two grand mal seizures is described. This case illustrates how organic factors can be aetiologically significant in psychiatric disease. It also illustrates the usefulness of convulsive therapy, whether prescribed or occurring via nature, in this rare disorder.
Associative learning theory assumes that prediction error is a driving force in learning. A competing view, probabilistic contrast (PC) theory, is that learning and prediction error are unrelated. We tested a learning phenomenon that has proved troublesome for associative theory - retrospective revaluation - to evaluate these two models. We previously showed that activation in right lateral prefrontal cortex (PFC) provides a reliable signature for the presence of prediction error. Thus, if the associative view is correct, retrospective revaluation should be accompanied by right lateral PFC activation. PC theory would be supported by the absence of this activation. Right PFC and ventral striatal activation occurred during retrospective revaluation, supporting the associative account. Activations appeared to reflect the degree of revaluation, predicting later brain responses to revalued cues. Our results support a modified associative account of retrospective revaluation and demonstrate the potential of functional neuroimaging as a tool for evaluating competing learning models.
Cotard's delusion refers to the dissociation between normal representation/perception of one's own body and a lack of perception and sensations coming from 'inside one's own body'. We report a case of Cotard's syndrome in a woman affected by a probable Alzheimer's disease, whose body image was investigated as well as her capacity to perceive her internal body signs.
Background and objectives: Considerable etiologic ambiguity surrounds Cotard syndrome and a range of psychodynamic, existential and biological theories have been proposed to explain its etiopathogenesis. Despite the often-noted neurological abnormalities on examination and assessment in Cotard syndrome, an in-depth evaluation is lacking. In this paper, we provide an overview of the neurological (neurostructural, neurophysiological and neuropsychological) correlates of Cotard syndrome and discuss the implications of our findings from an etiological and clinical perspective. Methods: We searched electronic databases and key journals using the appropriate search terms. All reported cases of Cotard syndrome with neurological investigations published in English were included in the review. The two authors independently reviewed the full text of over 100 papers and selected the papers for inclusion in the final review. Results: Various organic conditions such as typhoid fever, temporal lobe epilepsy, brain tumours and brain injuries have been reported in association with Cotard syndrome. The most commonly reported neurological abnormalities in these patients include structural brain changes (bilateral cerebral atrophy, dilated lateral ventricles), functional brain changes (hypoperfusion in the frontal and parietal cortices) and neuropsychological abnormalities (impaired face recognition). Conclusions: In summary, although not all, some cases of Cotard syndrome are associated with structural and functional brain dysfunction. From a clinical perspective, it is crucial to maintain a low threshold for suspicion of organicity in cases of this uncommon psychiatric syndrome, and thereafter to consider appropriate neurological investigations.
En 1880, le médecin français Jules Cotard présente un tableau clinique de délire de négation en rapport avec le corps et survenant dans un contexte de dépression mélancoliforme sévère. Dans sa description clinique classique, le syndrome de Cotard se caractérise par une triade séméiologique : négation d’organe, délires d’immortalité, d’énormité et idées de damnation, de possession. Les cas de trois patients souffrant d’un syndrome de Cotard apparaissent dans cet article au travers de leur histoire personnelle, de l’évolution de leur maladie et de leur trajectoire psychiatrique. Une partie importante de la description des observations est centrée sur l’analyse séméiologique fine des présentations du syndrome chez chacun des patients. Dans un second temps, une revue de la littérature est présentée dans le but de fournir ainsi une étude psychopathologique de nos trois observations. L’analyse psychopathologique illustre bien la très grande hétérogénéité du syndrome, tant dans son mode d’apparition et sa présentation clinique que dans son évolution sous traitement. À travers ces trois observations, les auteurs montrent que le syndrome de Cotard est toujours bien présent sur la scène clinique psychiatrique, non plus comme il y a 100 ans, mais dans « une forme modifiée et incomplète ». De plus, l’apparition de nouvelles techniques d’exploration, en particulier l’imagerie cérébrale fonctionnelle, constitue une voie encourageante qui devrait permettre d’étudier plus avant ce syndrome particulier. En effet, actuellement le syndrome de Cotard reste peu compris dans ses mécanismes physiopathologiques et ses aspects phénoménologiques.
We provide a battery of examples of delusions against which theoretical accounts can be tested. Then we identify neuropsychological anomalies that could produce the unusual experiences that may lead, in turn, to the delusions in our battery. However, we argue against Maher's view that delusions are false beliefs that arise as normal responses to anomalous experiences. We propose, instead, that a second factor is required to account for the transition from unusual experience to delusional belief. The second factor in the etiology of delusions can be described superficially as a loss of the ability to reject a candidate for belief on the grounds of its implausibility and its inconsistency with everything else that the patient knows, but we point out some problems that confront any attempt to say more about the nature of this second factor.
In 1880 Cotard described a syndrome, the hallmark of which is the delusion of being dead. Since then the debate has centred on whether it is a distinct psychiatric entity or an extreme form of depression. The syndrome has been observed in schizophrenia, confusional states, epilepsy, and senile and presenile conditions. We report five cases of Cotard delusion in patients in whom the differential diagnosis was difficult, immediately pointing to organic or paranoid psychosis being the primary cause of illness. On the basis of the clinical decision that the nihilistic ideation was the prominent feature of a psychotic depression, the patients underwent a series of electroconvulsive therapy (ECT) with striking effect, both on the delusional and on concomitant symptoms. The psychopathology and therapy of delusional depression are discussed. The case histories show the importance of considering depressive illness in patients with nihilistic delusional symptoms with or without depressed mood, and the therapeutic efficacy of ECT in depression with severe psychotic manifestations.