ArticlePDF AvailableLiterature Review

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.
1. Cotard J. Du de
´lire hypocondriaque dans une forme grave de la
´lancholie anxieuse. Ann Med Psychol. 1880;4:168174.
2. Cotard J. Du de
´lire des ne
´gations. Arch Neurol. 1882;4:282428.
3. Se
´glas J. Me
´lancholie anxieuse avec de
´lire des negations. Progr Med.
4. Re
´gis E. Notre historique et clinique sur le de
´lire de negations. Gaz Med
Paris. 1893;2:6164.
5. Tissot F. De
´lire des negations termine
´par gue
´rison. Coside
´rations sur
lhypochondrie et la melancholie. Ann Med Psychol. 1921;79:321328.
6. Loudet O, Martinez DL. Sobre la psicoe
´nesis y el valor pronostico del
sindrome de Cotard. Arch Argent Neurol. 1933;1:112.
7. Saavedra V. El syndrome de Cotard. Consideraciones psicopathologicas y
nosograficas. Rev Neuropsiquiatr. 1968;11:175211.
8. Berrios GE, Luque R. Cotards syndrome: analysis of 100 cases. Acta
Psychiatr Scand. 1995;91:185188.
9. American Psychiatric Association. Diagnostic and Statistical Manual Of
Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). Washington, DC:
APA; 2000:413.
10. Walloch JE, Klauwer C, Lanczik M, Brockington IF, Kornhuber J.
Delusional denial of pregnancy as a special form of Cotards syndrome.
Psychopathology. 2007;40:6164.
11. Reif A, Murach WM, Pfuhlmann B. Delusional paralysis: an unusual
variant of Cotards syndrome. Psychopathology. 2003;36:218220.
12. Enoch D, Trethowan W. Cotards syndrome. In: Uncommon Psychiatric
Syndromes. 3rd ed. Oxford: Butterworth & Heinemann; 1991:162183.
13. Hansen ES, Bolwig TG. Cotard syndrome: an important manifestation of
melancholia. Nord J Psychiatry. 1995;36:218223.
14. Yamada K, Katsuragi S, Fujii I. A case study of Cotards syndrome: stages
and diagnosis. Acta Psychiatr Scand. 1999;100:396399.
15. Duggal HS, Jagadheesan K, Haque Nizamie S. Biological basis and
staging of Cotards syndrome. Eur Psychiatr. 2002;17:108109.
16. Chiu HFK. Cotards syndrome in psychogeriatric patients in Hong Kong.
Gen Hosp Psychiatr. 1995;17:5455.
17. Ramirez-Bermudez J, Aguilar-Venegas LC, Crail-Melendez D, Espinola-
Nadurille M, Nente F, Mendes MF. Cotard syndrome in neurological and
psychiatric patients. J Neuropsychiatry Clin Neurosci. 2010;22:409416.
18. Edelstyn NMJ, Oyebode F. A review of the phenomenology and cognitive
neuropsychological origins of the Cotard delusion. Neurol Psychiatry Brain
Res. 2006;13:914.
19. Consoli A, Soultanian C, Tanhuy M, et al. Cotards syndrome in
adolescents and young adults is associated with an increased risk of
bipolar disorder. Bipolar Disord. 2007;9:665668.
20. Allen JR, Pfefferbaum B, Hammond D, Speed L. A disturbed childs use
of a public event: Cotards syndrome in a ten-year-old. Psychiatry.
21. Butler PV. Diurnal variation in Cotards syndrome (copresent with
Capgras delusion) following traumatic brain injury. Aust N Z J Psychiatry.
22. Camarero M, Real V. Sindrome de Cotard en adolescente. Psiquiatria
Biologica. 1997;4:213214.
23. Cohen D, Cottias C. Basquin M. Cotards syndrome in a 15-year old girl.
Acta Psychiatr Scand. 1997;4:164165.
24. Dugas M, Haflon O, Badoual AM, Golse B, Huet S. Le syndrome de
Cotard chez ladolescent. Neuropsychiatr Enf. 1985;33:493498.
25. Fillastre M, Fontaine A, Depecker L, Degiovanni A. Cinq cas de syndrome
de Cotard de ladolescent et de ladulte jeune. Ence
´phale. 1992;18:6566.
26. Haflon O, Mouren-Simeoni MC, Dugas M. Le syndrome de Cotard chez
ladolescent. Ann Med Psychol. 1985;149:876879.
27. Liebowitz MC, McGrath PJ, Bush SC. Mania occurring during treatment
for depersonalisation: a report of two cases. J Clin Psychiatry. 1980;41:
28. Mendhekar DN, Gupta N. Recurrent posticatal depression with Cotard
delusion. Indian J Pediatr. 2005;72:529531.
29. Soultanian C, Perisse D, Re
´vah-Levy A, Luque R, Mazet P, Cohen D.
Cotards syndrome in adolescents and young adults: a possible onset of
bipolar disorder requiring a mood stabilizer? J Child Adolesc Psychophar-
macol. 2005;15:706711.
30. Yalin S, Varol Tas F, Gu
¨venir T. The coexistence of Capgras, Fregoli and
Cotards syndromes in an adolescent case. Arch Neuropsychiatry.
31. Christensen RC. Cotards syndrome in a homeless man. Psychiatric
Services. 2001;52:12561257.
32. De Berardis D, Serroni N, Campanella D, Marasco V, Moschetta FS, Di
Giannantonio M. A case of Cotards syndrome successfully treated with
aripiprazole monotherapy. Prog Neuro-Psychopharmacol Biol Psychiatry.
2010;37:1348. doi: 10.1016/j.pnpbp.2010.06.015
33. De Risio S, De Rossi G, Sarchiapone M, et al. A case of Cotard syndrome:
123I-IBZM SPECT imaging of striatal D2 receptor binding. Psychiatry Res.
34. Hagen S, Voss SH. Cotards syndrome in depression and maintenance
electroconvulsive therapy [abstract]. Ugeskr Leager. 2002;164:34523453.
35. Hamon JM, Ginestet D. De
´lire des ne
´gations: a
`propos de quatre
observations. Ann Med Psychol. 1994;152:425443.
36. Hashioka S, Monji A, Sasaki M, Yoshida I, Baba K, Tashiro N. A patient
with Cotard syndrome who showed an improvement in single photon
emission computed tomography findings after successful treatment with
antidepressants. Clin Neuropharmacol. 2002;25:276279.
37. Ko SM. Cotards syndrome*two case reports. Sing Med J. 1989;30:277
38. Kucia K, Delkowski RS. ECT treatment of Cotards syndrome in a patient
with combined valvular heart disease and persistent atrial fibrillation
[abstract]. Wiad Lek. 2004;57:290292.
39. Leistedt S, Coumans N, Ladha K, Linkowski P. La ne
´gation du corps: a
propos de trois observations concernant les de
´lires de Jules Cotard. Ann
Med Psychol. 2009;167:669676.
40. Lohmann T, Nishimura K, Sabri O, Klosterko¨tter J. Successful electro-
convulsive therapy of Cotard syndrome with bitemporal hypoperfusion.
Nervenartz. 1996;67:400403.
41. Nejad AG. Hydrophobia as a rare presentation of Cotards syndrome: a
case report. Acta Psychiatr Scand. 2002;106:156158.
42. Petracca G, Migliorelli R, Vazquez S, Starkstein SE. SPECT findings
before and after ECT in a patient with major depression and Cotards
syndrome. J Neuropsychiatry Clin Neurosci. 1995;7:505507.
43. Takahashi T, Nibuya M, Nomura S. Delusion of Cotards syndrome
successfully treated with a dopamine agonist. J Neuropsychiatry Clin
Neurosci. 2010;22:E27.
44. Wani ZA, Khan AW, Baba AA, Khan HA, Wani QA, Taploo R. Cotards
syndrome and delayed diagnosis in Kashmir, India. Int J Ment Health Syst.
45. Baeza I, Salva J, Bernardo M. Cotards syndrome in a young male bipolar
patient. J Neuropsychiatry Clin Neurosci. 2000;12:119120.
46. Debruyne H, Portzky M, Van den Eynde F, Audenaert K. Cotards
syndrome: a review. Curr Psychiatr Rep. 2009;11:197202.
47. Kondo S, Hayashi H, Eguchi T, Oyama T, Wada T, Otani K.
Bromocriptine augmentation in a patient with Cotards syndrome. Prog
Neuro-Psychopharmacol Biol Psychiatr. 2003;27:719721.
48. Nejad AG, Toofani K. Co-existence of lycantrophy and Cotards
syndrome in a single case. Acta Psychiatr Scand. 2005;111:250252.
49. Silva JA, Leong GB, Weinstock R, Gonzales CL. A case of Cotards
syndrome associated with self-starvation. J Forensic Sci. 2000;45:188190.
50. Caliyurt O, Vardar E, Tuglu C. Cotards syndrome with schizophreniform
disorder can be successfully treated with electroconvulsive therapy: case
report. Rev Psychiatr Neurosci. 2004;29:138141.
51. Joseph AB. Cotards syndrome in a patient with coexistent Capgras
syndrome in schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry.
Cotards syndrome 71 M&B 2011; 2:(1). July 2011
52. Matsukura S, Yoshimi H, Sueoka S, Chihara K, Fujita T, Tanimoto K.
b-endorphin in Cotards syndrome. Lancet. 1981;17:162163.
53. Nejad AG, Kerdegari M, Reihani-Kermani H. Self-mutilation of the nose
in a schizophrenic patient with Cotard syndrome. Arch Iranian Med.
54. Wolff G, McKenzie K. Capgras, Fregoli and Cotards syndromes and
Koro in folie a
`deux. Brit J Psychiatry. 1994;106:842.
55. Shiraishi H, Ito M, Hayashi H, Otani K. Sulpiride treatment of Cotards
syndrome in schizophrenia. Prog Neuro-Psychopharmacol Biol Psychiatry.
56. Wright S, Young AW, Hellawell DJ. Sequential Cotard and Capgras
delusions. Br J Clin Psychol. 1993;32:345349.
57. Conchiglia G, Della Rocca G, Grossi D. When the body image becomes
empty: Cotards delusion in a demented patient. Achta Neuropsychiatrica.
58. Fazzari G, Benzoni O, Sangaletti A, et al. Improvement of cognition in a
patient with Cotards delusions and frontotemporal atrophy receiving
electroconvulsive therapy (ECT) for depression. Int Psychiogeriatrics.
59. Kearns A. Cotards syndrome in a mentally handicapped man. Brit J
Psychiatr. 1987;150:112114.
60. Campbell S, Volow MR, Cavenar JO. Cotards syndrome and the
psychiatric manifestations of typhoid fever. Am J Psychiatr.
61. Drake MEJ. Cotards syndrome and temporal lobe epilepsy. Psychiatr J
Univ Ott. 1988;13:3639.
62. Hu WT, Diesing TS, Meissner I. Cotards syndrome in a patient with
superior sagittal sinus thrombosis. Biol Psychiatr. 2006;56:263S.
63. Bathia MS. Cotard syndrome in parietal lobe tumor. Indian Pediatr.
64. Greenberg DB, Hochberg FH, Murray GB. The theme of death in
complex partial seizures. Am J Psychiatr. 1984;141:15871589.
65. Gardner-Thorpe C, Pearn J. The Cotard syndrome. Report of two
patients: with a review of the extended spectrum of de
´lire des ne
Eur J Neurology. 2004;11:563566.
66. Bathia MS, Agrawal P, Malic SC. Cotards syndrome in migraine (a case
report). Indian J Med Sci. 1993;47:152153.
67. Lerner V, Bergman J, Greenberg D, Bar El Y. Laurence-Moon-Bardet-
Biedl syndrome in combination with Cotards syndrome. Case report. Isr J
Psychiatr Relat Sci. 1995;32:291294.
68. Cannas A, Spissu A, Floris GL, et al. Bipolar affective disorder and
Parkinsons disease: a rare, insidious and often unrecognised associa-
tion. Neurol Sci. 2002;23:S67S68.
69. Factor SA, Molho ES. Treating auditory hallucinations and Cotard
syndrome in Parkinson disease. Clin Neuropharmacol. 2004;27:205207.
70. Kundlur SNC, George S, Jaimon M. An overview of the neurological
correlates of Cotard syndrome. Eur J Psychiat. 2007;21:99116.
71. Paulig M, Bo¨ttger S, Sommer M, Prosiegel M. Depersonalisationssyn-
drom nach erworbener Hirnscha
¨digung. U
¨berblick anhand von 3 Fall-
beispielen und Literatur sowie Diskussion a
¨tiologischer Modelle.
Nervenartzt. 1998;69:11001106.
72. Young AW, Robertson IH, Hellawell DJ. Cotard delusion after brain
injury. Psychol Med. 1992;22:799804.
73. Munoz P, Valerio M, Palomo J, et al. Infections and non-infectious
neurologic complications in heart transplantations recipients. Medicine.
74. Hellde
´n A, Odar-Cederlo¨f I, Larsson K, Fehrman-Ekholm I, Linde
Death delusion. BMJ. 2007;335:1305.
75. Joseph AB, OLeary DH. Brain atrophy and interhemispheric fissure
enlargement in Cotards syndrome. J Clin Psychiatr. 1986;47:518520.
76. Gerrans P. Refining the explanation of Cotards delusion. Mind Lang.
77. McKay R, Cipolotti L. Attributional style in a case of Cotard delusion.
Conscious Cogn. 2007;16:349359.
78. Vinkers DJ. Reactie op Het syndroom van Cotard. Een overzicht.Tijdschr
Psychiatr. 2008;50:391392.
79. Young AW, Leafhead KM. Betwixt life and death: case studies of Cotard
delusion. In: Halligan PW, Marshall JC, eds. Method in Madness: Case Studies
in Cognitive Neuropsychiatry. Hove, East Sussex: Taylor & Francis;
80. Ellis HD, Young AW, Quayle AH, de Pauw KW. Reduced automatic
responses to faces in Capgras delusion. Proc Biol Sci. 1997;264:10851092.
81. Hirstein W, Ramachandran VS. Capgras syndrome: a novel probe for
understanding the neutral representation of the identity and familiarity of
persons. Proc Biol Sci. 1997;264:437444.
82. Breen N, Caine D, Coltheart M. The role of affect and reasoning in a
patient with a delusion of misidentification. Cognitive Neuropsychiatry.
83. Davis M, Coltheart M, Langdon R, Breen N. Monothematic delusions:
towards a two-factor account. Philosophy. Psychiatry Psychol. 2001;8:133
84. Coltheart M. The 33rd Sir Frederick Barlett Lecture: cognitive neurop-
sychiatry and delusional belief. Q J Exp Psychol. 2007;60:10411062.
85. Coltheart M, Langdon R, McKay R. Schizophrenia and monothematic
delusions. Schizophr Bull. 2007;33:642647.
86. Coltheart M. The neuropsychology of delusions. Ann N Y Acad Sci.
87. Corlett PR, Aitken MR, Dickinson A, et al. Prediction error during
retrospective evaluation of causal associations in humans: fMRI evidence
in favor of an associative model of learning. Neuron. 2004;44:877888.
88. Fletcher PC, Anderson JM, Shanks DR, et al. Responses of human frontal
cortex to surprising events are predicted by formal associative learning
theory. Nat Neurosci. 2001;10:10431048.
89. Turner DC, Aitken MR, Shanks DR, et al. The role of the lateral frontal
cortex in causal associative learning: exploring preventative and super-
learning. Cereb Cortex. 2004;14:872880.
90. Gerrans P. Delusions as performance failures. Cognitive Neuropsychiatry.
91. Kozian R. Duloxetin bei Cotard Syndrom. Psychiatr Prax. 2005;32:412413.
92. Jitsuiki H, Sasaki T, Wada K, Takaishi Y, Mifune Y. Two cases of senile
mood disorders successfully treated with olanzapine. Intl Clin Psycho-
pharmacol. 2006;24:A6.
93. Madani Y, Sabbe BGC. Het Cotardsyndroom. Differentie
¨le behandling
volgens subclassificatie. Tijdschr Psychiatr. 2007;49:4953.
94. Chan JH, Chen CH, Robson D. Case report: effective treatment of
Cotards syndrome: quetiapine in combination with venlafaxine. Psychia-
try Clin Neurosci. 2009;63:125126.
95. Ruminjo A, Mekinulov B. A case report of Cotards syndrome. Psychiatry
(Edgmont). 2008;5(6):2829.
96. Bourgeois M. Le syndrome de Cotard aujourdhui. Ann Med Psychol.
97. Mahgoub NA, Hossain A. Cotards syndrome and electroconvulsive
therapy. Psychiatr Serv. 2004;55:1319.
98. Montgomery JH, Vasu D. The use of electroconvulsive therapy in
a typical psychotic presentations: a case review. Psychiatry (Edgmont).
99. Malone K, Malone JP. Remarkable resolution of an uncommon
psychosyndrome*epilepsy-induced remission of Cotards syndrome. Ir
J Psychological Med. 1992;9:5354.
Mind & Brain, the Journal of Psychiatry
M&B 2011; 2:(1). July 2011 72
... Nihilistic delusions are reported as an example of mood congruent delusions of a depressive episode with psychotic features. 8 The duration of syndrome can vary from weeks to years depending on the underlying disorder. 7 One of the consequences of this syndrome is self -starvation because of negation of existence of self. 4 Patients are mostly found in advanced state, in severe psychomotor retardation with impairment in biological functions, requiring electroconvulsive therapy. ...
... 2,10 Studies found that the most prominent symptoms are depressive mood (89%), nihilistic delusions concerning one's own existence (69%), anxiety (65%), delusions of guilt (63%), delusions of immortality (55%) and hypochondriac delusions (58%). 8 No quality data are available on the prevalence and incidence of Cotard's syndrome. Studies suggest a prevalence of 0.57% -3.2%. ...
... Studies suggest a prevalence of 0.57% -3.2%. 8 The first evidence -based classification was made by Berrios and Luque in 1995. 8 They described three types of Cotard's syndrome: Psychotic depression (patients with melancholia and nihilistic delusions), Cotard type 1 included the pure forms of nihilistic delusions without affective symptoms and Cotard type 2 with a mixed group of symptoms of anxiety, depression and auditory hallucinations. ...
Full-text available
A síndrome de Cotard é uma condição neuropsiquiátrica rara. É uma síndrome que se caracteriza pela presença de delírios niilistas congruentes com o humor. O objetivo do presente trabalho é rever as evidências da literatura sobre a síndrome de Cotard e descrever um caso clínico identificado no nosso serviço. Os dados foram obtidos a partir do processo clínico de um paciente e através de pesquisa bibliográfica no PubMed. Apresenta‐se o caso de uma mulher de 68 anos, com síndrome de Cotard, no contexto de um transtorno depressivo, para ilustrar como este quadro pode ser prejudicial e desafiante e, de que modo a terapia individualizada e eficaz pode melhorar o quadro. Em relação ao tratamento, a combinação de antipsicóticos e antidepressivos é frequentemente utilizada, mas se não houver melhoria, sugere‐se a eletroconvulsivoterapia. É necessária uma maior consciencialização desta síndrome, que garanta uma melhor e mais rápida identificação e tratamento dos pacientes.
... There are studies where patients have benefitted from monotherapy of an antidepressant or an antipsychotic alone or in combination of both [20]. In this series of cases, three patients had improvement in symptoms with a second-generation antipsychotic alone. ...
Full-text available
Background Cotard's delusion/Cotard's syndrome is a series of delusions ranging from a false, fixed, unshakeable belief that one has lost their soul, blood, organs, and body parts to the belief that one is dead. The syndrome was initially thought to be associated with only mood disorders but later was found in other psychiatric illnesses as well. Aim The study aimed to find an association between Cotard's delusion and the psychopathology of different psychiatric diagnoses. Method The clinical study comprised seven patients presenting with symptoms of Cotard syndrome with different presentations, diagnoses, and onset and meeting inclusion criteria. The study was carried out in the Department of Psychiatry, Assam Medical College and Hospital. The patients were hospitalized and, after a detailed history, mental status examination, and laboratory investigations, were treated with pharmacological and non-pharmacological methods. A descriptive statistical analysis was done. Results Denial of the existence of body organs was the most similar complaint encountered in the cases. The duration of illness onset ranged from weeks to months. The symptoms were found to be present in different psychiatric illnesses like schizophrenia, delusional disorder, depression, and intellectual disability. The patient had responded well to pharmacological agents with the exception of three patients who were treated with electroconvulsive therapy. Conclusion The study highlights the different subtypes of Cotard’s syndrome and its associated symptoms, which provides a better understanding of the condition. The case series presents a finding of a higher proportion of male patients and adolescent cases than in previous reports. The study also provides valuable insights into its heterogeneity in the diagnosis and treatment of Cotard’s syndrome, which may help in the early recognition and management of this rare condition.
... Item 24 assesses time shrinking as previous statistical analyses found that it was specifically correlated to bodily detachment (see Table 5 in Caputo, 2019) and also indicated by diagnostic criteria of depersonalization (DSM-5: 300-6-A-1; APA, 2013). In addition to this 7-item scale for detachment of bodily face, there are items 18 for dead-like face (i.e., an Out-of-Life or non-living face, which can be akin to an experimentally-induced Cotard's syndrome, i.e. the delusion that one's own body is dead; Debruyne et al., 2009) and 20 for face-body detachment. It should be noted that bodily feelings (which are usually difficult to articulate verbally) can be tied to visual perception, as the participant's feeling can often be seen in the mirror as a multisensory integration (vs., conversely, a bodily detachment) between the interoceptively felt face and the visual perception of the reflected body image. ...
Full-text available
Anomalous strange-face illusions (SFIs) are produced when mirror gazing under a low level of face illumination. In contrast to past studies in which an observer's task was to pay attention to the reflected face and to perceive potential facial changes, the present research used a mirror gazing task (MGT) that instructed participants to fixate their gaze on a 4-mm hole in a glass mirror. The participants' eye-blink rates were thus measured without priming any facial changes. Twenty-one healthy young individuals participated in the MGT and a control panel-fixation task (staring at a hole in a gray non-reflective panel). The Revised Strange-Face Questionnaire (SFQ-R) indexed derealization (deformations of facial features; FD), depersonalization (bodily face detachment; BD), and dissociative identity (new or unknown identities; DI) scales. Mirror-fixation increased FD, BD, and DI scores compared to panel-fixation. In mirror-fixation, FD scores revealed fading specific to facial features, distinct from "classical" Troxler- and Brewster-fading. In mirror-fixation, eye-blink rates correlated negatively with FD scores. Panel-fixation produced low BD scores, and, in a few participants, face pareidolias as detected on FD scores. Females were more prone to early derealization and males to compartmentalization of a dissociative identity. SFQ-R may be a valuable instrument for measuring face-specific dissociation (FD, BD, DI) produced by MGT. Use of MGT and panel-fixation task for differential diagnoses between schizophrenia and dissociative identity disorder is discussed.
... Therefore, in the model, we indicate two patterns of behavior: a passive coping strategy and an active strategy centered on manipulation. The first pattern is the feigned death reflex activity, which will appear with a range of manifestations including motor arrest, catatonia, Cotard, and Ganser Syndromes (205,206). ...
Full-text available
In recent years, some neurologists reconsidered their approach to Medically Unexplained Symptoms and proposed Functional Neurologic Disorders (FND) as a new entity, claiming that neurology could offer alternative treatment options to the psychotherapies provided in psychiatry settings. FNDs, for this purpose, should include only the disorders listed as Conversion from the Somatic Symptom and Related Disorders (SSRD) group. The present review analyzes the rationale of this position and challenges the arguments provided for its support. The review also discusses the systematization of these disorders as provided by public health systems. It outlines risks stemming from economic support and public funding uncertainty, given their negligible epidemiological dimensions resulting from the parcellation of SSRD. The review underlines the unresolved issue of Factitious Disorders, which are in the same SSRD category of the international classification but are, nonetheless, overlooked by the theoretical proponents of the FND entity. Comorbidity with other psychiatric disorders is also analyzed. We propose a model that supports the continuum between different SSRD conditions, including Factitious Disorders. The model is based on the emergence of feigned death reflex and deception from frontal lobe dysfunction. Finally, the paper summarizes the wealth of historical psychiatric and psychodynamic approaches and critical reviews. The study also puts in context the categorization and interpretation efforts provided by the most eminent researchers of the past century.
... Pacjenci mogą być przekonani, że umarli, nigdy nie istnieli, są nieśmiertelni lub nie posiadają niektórych narządów wewnętrznych (Dieguez, 2018). Z uwagi na rzadkość występowania omawianego zespołu (dotychczas opisano mniej niż 200 przypadków) nie uwzględniają go ani Diagnostic and Statistical Manual (Enoch i Trethowan, 1991;Chiu, 1995;Consoli et al., 2007;Debruyne et al., 2009;Moschopoulos, 2016). Pacjenci z zespołem Cotarda zwykle izolują się od otoczenia, wykazują też skłonności do samookaleczania, głodzenia się oraz prób samobójczych. ...
Full-text available
Background Cotard’s Syndrome (CS) is a rare clinical entity where patients can report nihilistic, delusional beliefs that they are already dead. Curiously, while weight loss, dehydration, and metabolic derangements have been described as discussed above, a review of the literature revealed neither a single case of a severely underweight patient nor a serious metabolic complication such as Diabetic Ketoacidosis. Further, a search on PubMed revealed no articles discussing the co-occurrence of Cotard’s Delusion and eating disorders or comorbid metabolic illnesses such as diabetes mellitus. In order to better examine the association between Cotard’s Delusion and comorbid eating disorders and metabolic illness, we will present and discuss a case where Cotard’s delusion led to a severe metabolic outcome of DKA and a BMI of 15. Case presentation Mr. B is a 19 year old transgender man admitted to the hospital due to diabetic ketoacidosis secondary to Type 1 Diabetes Mellitus. Mr. B had a history of Obsessive–Compulsive Disorder, Major Depressive Disorder, and Post-Traumatic Stress Disorder. The primary pediatric team discovered that Mr. B had not been using his insulin appropriately and was severely underweight, and they believed this could be due to his underlying mental illness. The psychiatric consultation/liaison service found that Mr. B was suffering from Cotard’s delusion leading him to be noncompliant with his insulin due to a belief that he was already dead. Cotard’s delusion had in this case led to a severe metabolic outcome of DKA and a BMI of 15. Conclusions This case provides clinical insight into the interactions of eating disorders and Cotard’s delusion as well as the potential medical complications when Cotard’s delusion is co-morbid with medical conditions such as Diabetes Mellitus. We recommend that clinicians routinely screen patients for Cotard’s delusion and assess whether the presence of which could exacerbate any underlying medical illness. This includes clinicians taking special care in assessing patient’s caloric and fluid intake as well as their adherence to medications both psychiatric and medical. Further research could be conducted to explore the potential overlap of Cotard’s delusion and eating disorder phenomenology.
W artykule omówiono wpływ zaburzeń nastroju na niezdolność osoby do podjęcia istotnych obowiązków małżeńskich. Najpierw autor przedstawia dwa podstawowe typy omawianego zjawiska: typ depresyjny i typ maniakalny. Następnie aplikuje omówione zjawisko do kanonicznego prawa małżeńskiego, dotyczącego procesów o stwierdzenie nieważności małżeństwa.
Background and objective: Cotard's syndrome is a rare neuropsychiatric disorder in which the patient holds nihilistic delusions concerning his/her own existence, including the conviction of being dead or having lost parts of the body. There are occasional reports of Cotard's syndrome being accompanied by nutritional deficiencies or self-starvation. Methods: The authors describe the peculiar case of a 40-year-old man who developed severe malnutrition within a few months. At first, a diagnosis of anorexia nervosa was made. The man was admitted to the hospital where other significant psychopathological symptoms emerged. Results: One of the consequences of Cotard's syndrome is self-starvation because of negation of existence of self. The presented case points out that, although Cotard's syndrome has been reported to be associated with various organic conditions and other forms of psychopathology, loss of appetite and nutritional deficits can erroneously lead to mistake this diagnosis for anorexia nervosa, thus underestimating the high risk of these patients of committing suicide following hospital discharge. Conclusion: Taking into account its rarity and possible subdiagnosis, as a distinct clinical entity the aim of this case report is to emphasize that these patients may initially be addressed to general practitioners, due to the dysmetabolic consequences of malnutrition, rather than to psychiatrists. An early recognition of signs indicative of Cotard's syndrome can be vital to prevent the situation from worsening. In fact, missed diagnoses can put these patients at an higher risk of suicidal behaviour.
The initial cause of Cotard delusion is pervasive dyshomeostasis (dysregulation of basic bodily function).This explanation draws on interoceptive active inference account of self‐representation. In this framework, the self is an hierarchical predictive model made by the brain to facilitate homeostatic regulation. The account I provide is an alternative to two factor accounts of the Cotard delusion that treat depersonalisation experience as the first factor in genesis of the Cotard delusion. I argue that depersonalisation experience and the Cotard delusion are produced by different breakdowns in the process of self‐modelling.
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.