Cotard’s Syndrome: A Review Hans Debruyne, MD, Michael Portzky, MSc, Frédérique Van den Eynde, MD, and Kurt Audenaert, MD, PhD
Corresponding author Hans Debruyne, MD Department of Psychiatry, University Hospital Ghent, De Pintelaan 185, 9000 Ghent, Belgium. E-mail:
[email protected] Current Psychiatry Reports 2009, 11:197–202 Current Medicine Group LLC ISSN 1523-3812 Copyright © 2009 by Current Medicine Group LLC
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 DSMIV, 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.
Introduction Cotard’s syndrome is characterized by the appearance of nihilistic delusions concerning one’s own body. Whether the syndrome is a distinct disorder or a symptom of other disorders has been a subject of debate. There is growing consensus to consider Cotard’s syndrome and its typical nihilistic delusions as a symptom of an underlying disorder. The syndrome as such is not mentioned in the DSM-IV-TR. Nihilistic delusions are reported as an example of moodcongruent delusions of a depressive episode with psychotic features [1]. Although it is not a diagnostic entity in our current psychiatric practice, knowledge on Cotard’s syndrome and a specific approach to treating patients is valuable. This paper presents an overview of the historical aspects, classification, clinical characteristics, etiology, and more recent views on pathogenesis and neuroimaging of Cotard’s syndrome. A short overview of treatment options is also presented. The literature is almost completely dominated by case reports. Larger sample, prospective studies are lacking. Because Cotard’s syndrome is a rare condition, the literature as a whole is scarce and scattered (eg, a PubMed search of “Cotard’s syndrome,” with language limited to English, French, German, and Dutch, revealed only 47 hits since 1960). We aim to provide an up-to-date review of this rare psychiatric phenomenon, starting with two cases from our hospital.
Two Cases 1. An 88-year-old man with mild cognitive impairment was admitted to our hospital for treatment of a severe depressive episode. He was convinced that he was dead and felt very anxious because he was not yet buried. This delusion caused extreme suffering and made outpatient treatment impossible. Treatment with sertraline, 50 mg, and risperidone, 1 mg, resulted in complete remission of the depressive episode and nihilistic delusions. Pharmacologic treatment was continued [2]. 2. A 46-year-old woman with known rapidcycling bipolar disorder was admitted to our hospital. She presented with a depressive episode with psychotic features. Her nihilistic delusions were compatible with Cotard’s syndrome. She had the constant experience of having no identity or “self” and being only a body without content. In addition, she was convinced that her brain had vanished, her intestines had disappeared, and her whole body was translucent. She refused to take a bath or shower because she was afraid of being soluble and disappearing through the water drain. She had several admissions to different hospitals as a result of depressive or manic episodes since the age of 29 years. Laboratory fi ndings, MRI, and 99Tc-ethyl cysteinate dimer single-photon emission CT (SPECT) showed no abnormalities. Despite these fi ndings, severe right hemispheric dysfunction was found during neuropsychological testing (eg, clock drawing test, Rey complex fi gure test). The following pharmacologic treatments previously had been used to treat this patient, without consistent effect: lithium, valproate, carbamazepine, haloperidol, olanzapine, risperidone, clozapine, pimozide, sulpiride, clomipramine, sertraline, paroxetine, fl uoxetine, citalopram, mirtazapine, and venlafaxine. Electroconvulsive therapy (ECT) was also used without effect. The nihilistic delusions disappeared in this patient, but a mood switch to a hypomanic episode occurred. It seemed the disorder took its natural rapid-cycling bipolar course despite all treatments administered.
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Historical Aspects and Classification
Epidemiology
Cotard’s syndrome is named for Jules Cotard (1840– 1889), a French neurologist who described this condition for the fi rst time in 1880. He formulated it as a new type of depression characterized by the following symptoms: anxious melancholia, ideas of damnation or rejection, insensitivity to pain, delusions of nonexistence concerning one’s own body, and delusions of immortality. In the classification system of that period, Cotard categorized it as lypémanie, a kind of psychotic depression described by Esquirol (as detailed by Berrios and Luque [3]). In 1882, Cotard introduced délire des négations as new terminology for the syndrome. Régis (1893) fi rst used the term délire de Cotard. He also stated that the syndrome is not only associated with depression but can be linked to other psychiatric disorders. The current name, Cotard’s syndrome, was fi rst used by Séglas (1887) in his book Le Délire de Négation [4]. Tissot (1921) extracted two components from Cotard’s syndrome: an affective component associated with anxiety and a cognitive component associated with the presence of a delusion. Loudet and Martinez (1933) tried to clarify the heterogeneity by defi ning different types. They fi rst described a nongeneralized délire de négation associated with paralysis, alcoholic psychosis, or dementia. However, they described the “real” Cotard’s syndrome as being only found in anxious melancholia and chronic hypochondria [4,5]. In 1968, Saavedra described 10 cases of Cotard’s syndrome and classified them into three types: depressive, mixed, and schizophrenic. He drew a distinction between “genuine” Cotard’s syndrome, occurring during depressive states, and what he described as a pseudonihilistic or pseudo–Cotard syndrome. He also termed the latter coenaesthetic schizophrenia [5]. The fi rst evidence-based classification was made by Berrios and Luque [6] in 1995. They conducted a retrospective factor analysis of 100 cases in the literature and described three types of Cotard’s syndrome. The fi rst is a form of psychotic depression in which anxiety, melancholia, delusions of guilt, and auditory hallucinations are the more prominent features. Second, they described Cotard’s syndrome type I, which is associated with hypochondriac and nihilistic delusions and absence of a depressive episode. The third is Cotard’s syndrome type II, in which anxiety, depression, auditory hallucinations, delusions of immortality, nihilistic delusions, and suicidal behavior are characteristic features [6]. In the DSM-IV-TR, Cotard’s syndrome is not classified as such. Nihilistic delusions are mentioned as an example of mood-congruent delusions when a depressive episode with psychotic features is diagnosed [1]. This reflects the current status of Cotard’s syndrome, which is conceptualized as part of an underlying disorder (mostly a depressive episode). Classifying Cotard’s syndrome as an isolated state is an extremely difficult exercise in our current diagnostic classification system.
No quality data are available on the prevalence and incidence of Cotard’s syndrome. The only prevalence study was performed in a selected psychogeriatric setting in Hong Kong. Cotard’s syndrome was diagnosed in 2 of 349 patients, suggesting a prevalence of 0.57% in this population [7]. Taking into account only severely depressed older adult patients, a prevalence rate of 3.2% was determined [7]. Berrios and Luque [6] found in their 100-case review that the mean age of patients was 52 years, but Cotard’s syndrome is also occasionally described in children and adolescents. Diagnosis of Cotard’s syndrome in people less than 25 years of age is associated with bipolar disorder [8•]. The disorder is more common in women [5]. Cotard’s syndrome has been diagnosed as part of several psychiatric and somatic diseases, with unipolar depression [5,7,9–15] and bipolar depression [5,8•,11,16–18] being the most common associated psychiatric disorders. Psychotic disorder is also associated with Cotard’s syndrome [4,5,19]. One report notes voluntary starvation as an associated condition [20]. Some reports described the co-occurrence of Cotard’s syndrome with other rare psychiatric syndromes (hydrophobia [21], lycanthropy [17], and folie à deux [22]). Several organic conditions were also associated with it: dementia [4,23], severe mental retardation [24], typhoid fever [25], cerebral infarction [26], superior sagittal sinus thrombosis [27], brain tumors [28], temporal lobe epilepsy [26,29], limbic epileptic insults [29], postictal depression [30], cerebral arteriovenous malformation [31], cerebral arteriovenous malformation and epilepsy [26], migraine [32], Laurence-Moon/Bardet-Biedl syndrome [33], multiple sclerosis [31], Parkinson’s disease [34,35], and brain injury [36–38,39••].
Symptoms and Course In his fi rst description, Cotard described hypochondriac ideas that varied from the spontaneous destruction of different organs, the entire body, or soul to the complete denial of one’s own existence as the most important characteristic elements of the syndrome. As a result, some patients become convinced they have no need to eat anymore or have the delusion of being dead. The most prominent symptoms of Cotard’s syndrome are depressive mood (89%), nihilistic delusions concerning one’s own body (86%), nihilistic delusions concerning one’s own existence (69%), anxiety (65%), delusions of guilt (63%), delusions of immortality (55%), and hypochondriac delusions (58%) [6]. Self-mutilation of the nose was mentioned in association with Cotard’s syndrome in one recent case report [40]. Some delusions present as special forms of Cotard’s syndrome (eg, delusional denial of one’s pregnancy despite clear morphologic signs [41] and delusional paralysis in a patient with psychomotor agitation [42]). In its early course, Cotard’s syndrome is characterized by a vague feeling of anxiety lasting from weeks to years. This anxious state gradually increases and can result in the
Cotard’s Syndrome: A Review
origin of nihilistic delusions in which denial of body parts or life is the prominent feature. The patient then further loses touch with reality [5]. With the delusion of being dead, patients show an increased tendency toward self-mutilation or suicidal behavior. Accompanying symptoms may include analgesia and mutism. The content always reflects a preoccupation with guilt, despair, and death [5]. Delusions also sometimes go together with a délire d’énormité—a delusion of a massive increase of body measures. This is sometimes called manic Cotard’s syndrome [5]. As the syndrome often occurs in association with other psychotic states, symptoms of these other disorders also are likely to be present. For example, nihilistic delusions grafted on a depressive illness are often associated with other characteristics of depression, and the syndrome associated with organic disease is often associated with other symptoms (eg, disorientation or neurologic signs) [5]. The duration of Cotard’s syndrome can vary from days to years, depending on the underlying disorder [4]. A proposal for the staging of Cotard’s syndrome was made by Yamada et al. [43] in 1999. Working with one patient, three stages were defined: germination stage, blooming stage, and chronic stage. The germination stage is characterized by important hypochondria, cenesthopathy, and depressive mood. Cotard’s syndrome cannot be diagnosed during this stage. In the blooming stage, the characteristic features of Cotard’s syndrome (nihilistic delusions, delusions of immortality together with anxiety and negativism) are seen. In the chronic stage, differentiation into two forms is made: one with persistent emotional disturbances (depressive type) and a second in which depressive symptoms are more in the background (paranoid type) [43].
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of developing Capgras’ syndrome (a delusion in which familiar people are replaced by identical impostors) [45]. It is thought that the origins of both bizarre syndromes are related to a dysfunction in an information-processing subsystem in which face and body recognition are associated with an affect of familiarity. When the normal feeling of familiarity is absent, patients may experience an unusual feeling of derealization and depersonalization [46]. Whereas for Capgras’ syndrome, this hypothesis was confi rmed by several groups using skin conductance response as an outcome measure [47,48], empiric research on this disturbance in information processing is lacking for Cotard’s syndrome. The mechanism is supposed to be the same for both Cotard’s syndrome and Capgras’ syndrome, but the way in which patients cope is related to their attributional style [46,49]. The hypothesis that patients with Cotard’s syndrome have an internal attribution style was recently empirically tested in one case. McKay and Cipolotti [50••] showed a significantly higher score on two attribution bias indices (internalizing bias index, internalizing bias for negative events) calculated on the Internal, Personal and Situational Attributions Questionnaire (IPSAQ) in their patient with Cotard’s syndrome compared with those of a group of 10 controls. In addition, several authors wrote about the co-occurrence of Cotard’s and Capgras’ syndromes [22,38,51–53]. It is suggested that in these cases, a combination of attribution styles exists, and patients are depressed and paranoid or have delusions about the identity of self and others [54]. Again, empiric data are lacking.
Neuroimaging, electrophysiology, and neuropsychology
Etiology and Pathogenesis Psychological factors Séglas (1887) cited the depersonalization phenomenon as an essential step in the development of Cotard’s syndrome. Alheid (1968) elaborated on depersonalization in Cotard’s syndrome using the German terminology leib (“body for me”) and körper (“body as such”). As körper becomes more prominent than leib and the body becomes less associated with the self (leib), depersonalization can occur. However, in depersonalization, the patient feels as if he or she is dead (indifference of affect), whereas in Cotard’s syndrome, the patient is convinced that he or she is dead (lack of feeling) [5]. Critchley [44] presented an overview of bizarre psychiatric syndromes that were related to parietal brain dysfunction. In this framework, the role of premorbid personality characteristics in these bizarre syndromes was crucial [5,44]. On one hand, for Cotard’s syndrome, patients with a more internal attribution style, which often co-occurs with depression, are more likely to develop the syndrome. On the other hand, patients with a more external attribution style, which more often co-occurs with paranoia, should have a better chance
The fi rst imaging study on Cotard’s syndrome was performed by Joseph and O’Leary [55] in 1986. Using CT, they suggested that Cotard’s syndrome was associated with multifocal brain atrophy and interhemispheric fissure enlargement [55]. Others have described an enlargement of the third and lateral ventricles [19], a specific focal lesion to the temporoparietal areas [31], and changes in the nondominant temporoparietal areas that are sometimes seen together with frontal damage [36]. In general, there seems to be an important role for the frontotemporoparietal circuitry in the pathophysiology of Cotard’s syndrome. Nevertheless, in most cases, gross structural changes on structural brain imaging were absent [39••]. In addition, functional imaging studies of patients with Cotard’s syndrome were published. Asymmetric striatal D2 receptor binding favoring the left side was shown in one case using 123I-iodobenzamide SPECT. These SPECT fi ndings persisted after remission. Before treatment, no perfusion abnormalities were found with 99m Tc-hexamethylpropyleneamine oxime (HMPAO) SPECT [12]. These fi ndings are consistent with data published for schizophrenic patients with depressive symptoms [12]. In one Cotard’s syndrome patient diagnosed with a schizophreniform disorder, a left-sided
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hypoperfusion in the temporal, parietal, and frontal lobes with recovery of inferior frontal and left hypoperfusion and a minimal remaining hypoperfusion at the left temporal lobe after successful ECT treatment was measured with 99mTc-HMPAO SPECT [19]. Successful treatment with antidepressants resulted in a recovered perfusion in the frontal cortex using 99mTc-HMPAO SPECT [56]. Recovery of bitemporal hypoperfusion also measured with 99mTc-HMPAO SPECT was reported in patients with an underlying major depressive disorder [57]. Nevertheless, absence of abnormalities in cerebral perfusion or metabolism patterns was also shown in Cotard’s syndrome (case 2) [12]. For the most part, there are no electroencephalogram abnormalities revealed in Cotard’s syndrome, although nonspecific abnormalities and abnormalities suggestive of the underlying organic condition have been mentioned in some cases [39••]. Only a few reports mention detailed neuropsychological examination. Most research is performed using face recognition tasks. General impairment of all aspects of face processing with no evidence that face recognition impairment could be attributed to loss of knowledge of familiar people is suggested. Normal recognition of emotional facial expressions is typically observed [39••]. As mentioned previously, damage to an affective component of the face recognition system is proposed [45,46]. Despite the normal regional brain perfusion, severe neuropsychological right hemisphere abnormalities were discovered in one case of Cotard’s syndrome in our hospital (case 2).
Prognosis and Treatment Complete recovery may occur as spontaneously and suddenly as onset of Cotard’s syndrome, even in the most severe cases [5]. Enoch and Trethowan [5] link prognosis to the underlying disorder, as follows: 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 fluctuations 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 schizophrenic condition.
Therefore, treatment should follow a thorough diagnostic work-up of the underlying disorder. There are several reports of successful pharmacologic treatment of Cotard’s syndrome. Monotherapy
with agents such as amitriptyline [18], duloxetine [58], fluoxetine [7], paroxetine [18], olanzapine [38], sulpiride [53], or lithium [18] has been reported to be effective. However, combination strategies often are used (clomipramine/amitriptyline [5], pimozide/amitriptyline [18], haloperidol/clomipramine [18], cyamemazine/ paroxetine [18], risperidone/fluoxetine [59], haloperidol/ mirtazapine [14], risperidone/sertraline [2], risperidone/ citalopram [41], clozapine/fluvoxamine/imipramine [12]). Adding bromocriptine to clomipramine and lithium had a benefi cial effect in one patient with bipolar disorder type I [11]. ECT is also an important treatment option in Cotard’s syndrome. Based on the classification of Berrios and Luque [6], Madani and Sabbe [13] suggested that ECT is an important option for patients with Cotard’s syndrome with psychotic depression, while antipsychotics should produce better effects in Cotard’s syndrome type I [13]. Especially with an underlying mood disorder, ECT was reported as a very useful technique in many case reports [4,5,7,10,13,16–19,21,24,40,42,43, 60,61]. In most reports, ECT was followed by a pharmacologic maintenance treatment, usually combination strategies (zuclopenthixol/oxcarbazepine [4], olanzapine/mirtazapine [42], trimipramine/perphenazine [21], mianserine/amisulpride [16], lithium/amisulpride [18], imipramine/haloperidol with addition of biperiden due to oculogyric crisis [60]), but monotherapy also has been reported (nomifensine [24], imipramine [5], isocarboxazide [4], lithium [18,43], risperidone [40], and olanzapine [19]). One report of spontaneous recovery after two grand mal seizures was also reported, illustrating the usefulness of the effect of seizures [62]. In young patients, use of mood stabilizers should be considered because Cotard’s syndrome in this population is often part of a bipolar disorder [8•,18]. The overall prognosis seems to be determined mostly by the treatment options and prognosis for the underlying disorder [25].
Conclusions Although Cotard’s syndrome was first described more than a century ago, the literature remains scarce and is dominated by case reports. Although the syndrome is relatively rare, more larger-scale research is needed to clarify the pathophysiologic mechanisms that underpin this condition, as well as its relationship to other delusions of misidentification, such as Capgras’ syndrome. The currently available literature suggests that a publication bias is a potential pitfall. Careful registration of the whole spectrum of cases could help to answer many questions about the epidemiology, course, associated disease, and prognosis.
Disclosure No potential confl icts of interest relevant to this article were reported.
Cotard’s Syndrome: A Review
References and Recommended Reading Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance 1.
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