Cotard's Syndrome: A Review

Abstract

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.

Full text

Cotard’s Syndrome
Hans Debruyne
1,2,3
, Michael Portzky
1
, Kathelijne Peremans
1
and Kurt Audenaert
1
Affiliations:
1
Department of Psychiatry, University Hospital Ghent, Ghent, Belgium;
2
PC Dr. Guislain, Psychiatric Hospital, Ghent, Belgium and
3
Department of
Psychiatry, Zorgsaam/RGC, Terneuzen, The Netherlands
ABSTRACT
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
DSM-IV-TR
nor in
ICD-10
. 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: hans.debruyne@fracarita.org
INTRODUCTION: HISTORICAL ASPECTS AND
CLASSIFICATION
Cotard’s syndrome is named after Jules Cotard (18401889),
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
1880)
1
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
Esquirol.
1
Later, Cotard introduced de
´lire des negations as new
terminology for the syndrome.
2
The eponym Cotard’s syndrome
was introduced in 1887 by Se
´glas.
3
A few years later, Re
´gis
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.
4
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.
5
Loudet
and Martinez
6
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.
6
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
schizophrenia.’’
7
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.
8
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.
9
Classifying
Cotard’s syndrome as a separate entity is an extremely difficult
exercise in our current diagnostic classification system.
METHODS
For this article, we started from the search results for
‘‘Cotard syndrome,’’ ‘‘Cotard’s syndrome,’’ and ‘‘nihilistic
MIND & BRAIN, THE JOURNAL OF PSYCHIATRY REVIEW ARTICLE
www.slm-psychiatry.com 67 M&B 2011; 2:(1). July 2011

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.
PRESENTATION AND COURSE
As described earlier, nihilistic delusions concerning the
individual’s body are the central features of Cotard’s syn-
drome. In an analysis of 100 cases, the most prominent
symptoms in Cotard’s syndrome 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
Some case reports concerning delusional denial of preg-
nancy despite clear morphologic signs
10
and delusional
paralysis in a patient with psychomotor agitation
11
are
reported as a special form of Cotard’s syndrome. However,
the classification of these delusions as nihilistic delusions
concerning one’s body can be debated.
A classical description of the course of Cotard’s syndrome is
given by Enoch and Trethowan. In its early stages, Cotard’s
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.
12
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.
12
Delusions can be accompanied by a de
´lire
d’e
´normite
´, a delusion of massive increase of body measures.
This has been described as the manic Cotard’s syndrome.
12
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.
12
The duration of the syndrome
can vary from weeks to years depending on the underlying
disorder.
13
In 1999, Yamada et al
14
made a proposal for staging
Cotard’s 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 Cotard’s syndrome cannot be made in this
stage yet. In the blooming stage, the characteristic features of
Cotard’s 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).
14
This hypothesis was supported in a second
case report.
15
EPIDEMIOLOGY
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, Cotard’s syndrome was diagnosed suggesting a
prevalence of .57% in this population. A prevalence of 3.2%
was reached when severely depressed elderly were included.
16
A recent study found .62% (n3) of patients in a Mexican
sample (screened over a 2-year period) of primary psychiatric
patients having Cotard’s syndrome.
17
Using the same
methodology they found also .11% (n1) having Cotard’s
syndrome in a sample of neurological patients with mental
disturbances.
17
The likelihood of developing Cotard’s delu-
sion appears to increase with age.
18
Berrios and Luque
8
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.
19
Women appear to be more vulnerable.
12
The
syndrome is found in different ethnic groups.
18
Cotard’s
syndrome is also occasionally described in children and
adolescents.
1930
Diagnosis of Cotard’s syndrome in people
under 25 years old was described to be associated with
bipolar disorder.
19
Since Cotard’s syndrome is conceptualized as part of an
underlying disorder, several psychiatric and somatic diseases
have been associated with the syndrome. Unipolar
10,12,16,3144
or bipolar
12,14,15,19,25,29,4549
depression are the most common
associated psychiatric disorders but also comorbid psychotic
disorder
12,13,37,45,5053
has been reported. Some studies repor-
ted on the occurrence of Cotard’s syndrome with more
uncommon psychiatric syndromes (hydrophobia,
41
lycantro-
phy,
48
folie a deux,
54
Capgras delusion,
12,21,51,5456
Capgras and
Fregoli delusion,
30
depersonalization disorder
17
). Also Par-
kinsonian symptoms, disappearing with successful treat-
ment, are described.
17
Several organic conditions were also
associated: dementia,
13,57
major depressive episode in mild
cognitive impairment,
46
depression in frontotemporal atro-
phy,
58
severe mental retardation,
59
typhoid fever,
60
cerebral
infarction,
61
superior sagittal sinus thrombosis,
62
brain
tumors,
63
temporal lobe epilepsy,
61,64
limbic epileptic in-
sults,
64
postictal depression,
28
cerebral arteriovenous mal-
formation,
65
cerebral arteriovenous malformation and
epilepsy,
61
migraine,
66
Laurence-Moon-Bardet-Biedl syn-
drome,
67
multiple sclerosis,
65
Parkinson’s disease,
68,69
brain
injury,
7072
a noninfectious complication of heart transplan-
tation
73
as a consequence of an adverse drug reaction to
aciclovir and its prodrug valaciclovir
74
and in herpetic
77
and
nonherpetic
17
encephalitis.
Mind & Brain, the Journal of Psychiatry
M&B 2011; 2:(1). July 2011 68 www.slm-psychiatry.com

ETIOLOGY AND PATHOGENESIS
Neuroimaging
The first structural imaging study was performed in 1986,
using Computed Tomography (CT). An association of
Cotard’s syndrome with multifocal brain atrophy and inter-
hemispheric enlargement was suggested.
75
Others have
described an enlargement of the third and lateral ventricle,
50
a specific lesion to the temporoparietal areas,
65
and changes
in the nondominant temporoparietal areas, sometimes to-
gether with frontal damage.
72
In general, these studies point
to an important role for the frontotemporoparietal circuitry
in the pathophysiology of the syndrome. However, in most
cases, gross structural changes on structural brain imaging
were absent.
70
Several functional imaging studies in Cotard’s syndrome
patients were published. A dopamine D2 receptor SPECT
study with
123
I-iodobenzamide (IBZM), performed in one
patient, showed an asymmetric striatal D
2
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
99m
Tc-hexamethylpropylenamide ox-
ime (HMPAO) SPECT before treatment.
33
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).
50
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.
42
Success-
ful treatment with ECT in a patient with underlying major
depressive disorder resulted in recovery of left and right
temporal hypoperfusion
40
and normalization of perfusion in
the frontal cortex was reported after treatment with anti-
depressants.
36
In one patient, severe right hemispheric
dysfunction on neuropsychological tasks was not accompa-
nied by perfusion abnormalities measured with
99m
TC Ethyl
Cysteine Dimer (ECD) SPECT.
46
Psychological and Neuropsychological Factors
A depersonalization phenomenon was reported as an
essential step in the development of Cotard’s syndrome by
Se
´glas (1887).
3
Alheid elaborated depersonalization in the
Cotard’s 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 Cotard’s syndrome the
patient is convinced to be dead (lack of feeling).
7,12
In the development of bizarre psychiatric syndromes related
to parietal brain dysfunction, Critchley stated that the role of
premorbid personality characteristics is essential.
12
With
regard to this premorbid personality characteristic, it is
proposed that in Cotard’s 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 Capgras’s syndrome (a delusion where familiar
persons are replaced by identical impostors).
76
This hypoth-
esis that Cotard’s patients have a more internal attribution
style was empirically tested in one case.
77
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 Cotard’s syndrome
compared to control subjects.
77
However, several authors
reported the co-occurrence of both Cotard’s syndrome and
Capgras’s syndromes.
12,21,51,5456
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.
78
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
depersonalization.
79
This hypothesis is supported by several
studies for a number of misidentification syndromes and
especially for Capgras’s syndrome.
8082
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 Capgras’s syndrome.
80,81
Another patient with
atypical Capgras’s delusion showed impaired interpretation
of facial expressions. This leads to mistake differences in
expression for differences in identity.
82
For Cotard’s syn-
drome, a lack of differential autonomic response to anything
is suggested. This can lead to the delusion of being dead,
where in Capgras’s 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 Cotard’s syndrome is more severe and
more generalized.
84,86
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, I’m
dead as a explanation for the lack of feeling of familiarity to
anything) despite the presence of (often overwhelming)
Cotard’s syndrome
www.slm-psychiatry.com 69 M&B 2011; 2:(1). July 2011

evidence against it.
8287
Hence, for Cotard’s 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 ‘‘I’m dead.’’
84,86
In this hypothesis the
loss of affect (first factor) is more pronounced and general-
ized than in Capgras patients.
90
On the other hand, the
difference in attributional style could also be an explanation
for the different hypothesis formation in the first factor.
17
The importance of the right dorsolateral prefrontal cortex
(RDLPFC) for hypothesis evaluating was demonstrated with
fMRI.
8789
It has also been observed that right frontal damage
is commonly occurring in cases of delusional misidentifica-
tions (including Cotard’s syndrome).
84
PROGNOSIS AND TREATMENT
Complete recovery may occur as spontaneously and as
suddenly as its onset, even in the most severe cases.
12
Enoch
and Trethowan
12
link the prognosis to the underlying
disorder.
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.
12
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 Cotard’s
syndrome is diagnosed under the age of 25 years. In these
cases, there seems to be an association with bipolar
disorder.
19
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,
27
aripiprazole,
32
dulox-
etine,
91
fluoxetine,
17
olanzapine,
21,92
sulpiride,
55
and
lithium
26,27
has been reported as effective. However, usually
combination strategies are used (clomipramine/
amitriptyline,
12
pimozide/amitriptyline,
24
haloperidol/clomi-
pramine,
22
cyamemazine/paroxetine,
29
risperidone/fluoxe-
tine,
36
haloperidol/mirtazapine,
44
risperidone/sertraline,
46
risperidone citalopram,
10
amisulpiride/clozapine,
93
cloza-
pine/fluvoxamine/imipramine,
33
paroxetine/pramipexole,
43
quetiapine/venlafacine,
94
and olanzapine/escitalopram/lora-
zepam.
95
Adding bromocriptine to clomipramine and
lithium had a beneficial effect in a patient with bipolar
disorder type I.
47
The most reported treatment strategy for Cotard’s syndrome
is electroconvulsive therapy (ECT).
1116,2325,29,31,34,3742,45,
48,50,58,59,93,9698
Based on the classification of Berrios and
Luque,
8
a suggestion was made that ECT is indicated in
patients with Cotard’s syndrome and psychotic depression,
while antipsychotics exert better effects in Cotard’s syndrome
type I.
93
In one patient, spontaneous recovery after two grand
mal seizures was reported illustrating the usefulness of
seizure activity in the treatment of Cotard’s syndrome.
99
Treatment should initially follow current treatment guidelines
of the underlying conditions, since no randomized studies are
performed on this Cotard’s 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.
12
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.
12
DISCUSSION
Despite that Cotard’s 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
carefully.
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 Cotard’s 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 www.slm-psychiatry.com

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-
matology.
Disclosures: The author declares no conflict of interest.
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