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Cotard's syndrome
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.
... In later years, several attempts to classify different types of the syndrome were made [5]. In 1995, for the first time a classification was made based on evidence using factor analysis of published cases. ...
... Several psychiatric and somatic diseases have been asso ciated with the syndrome. Unipolar and bipolar depressions are the most common associated psy chiatric disorders, but psychotic disorder is also frequently reported [5]. In a recent review, several organic conditions were listed: dementia; major depressive episode in mild cognitive impair ment; depression in frontotemporal atrophy; severe mental retardation; typhoid fever; cerebral infarction; superior sagittal sinus thrombosis; brain tumors; temporal lobe epilepsy; limbic epi leptic insults; postictal depression; cerebral arte riovenous malformation with and without epi lepsy; migraine; Laurence-Moon-Bardet-Biedl syndrome; multiple sclerosis; Parkinson's dis ease; brain injury; noninfectious complications of heart transplantation; consequences of adverse drug reaction to acyclovir and valacyclovir; and herpetic or nonherpetic encephalitis [5]. ...
... Unipolar and bipolar depressions are the most common associated psy chiatric disorders, but psychotic disorder is also frequently reported [5]. In a recent review, several organic conditions were listed: dementia; major depressive episode in mild cognitive impair ment; depression in frontotemporal atrophy; severe mental retardation; typhoid fever; cerebral infarction; superior sagittal sinus thrombosis; brain tumors; temporal lobe epilepsy; limbic epi leptic insults; postictal depression; cerebral arte riovenous malformation with and without epi lepsy; migraine; Laurence-Moon-Bardet-Biedl syndrome; multiple sclerosis; Parkinson's dis ease; brain injury; noninfectious complications of heart transplantation; consequences of adverse drug reaction to acyclovir and valacyclovir; and herpetic or nonherpetic encephalitis [5]. More recently, case reports of Cotard's syndrome in semantic dementia [16] and tuberculosis infection in an HIV patient [17] have been published. ...
Cotard’s syndrome is a rare disorder. The central feature is a nihilistic delusion concerning one’s own body (including loss of body parts, being dead or not existing at all). The syndrome is not mentioned in DSM-IV-TR or the International Classification of Diseases-10, since there is growing consensus that the syndrome is part of an underlying disorder. Although not a separate diagnostic entity, the phenomenologic study of rare monothematic delusional disorders (such as Cotard’s syndrome) remains important to have a better understanding of the pathophysiology of delusions. In this report, historical aspects, classification, course and epidemiology are briefly reviewed, different pathophysiologic hypotheses are described and therapeutic options are discussed.
... In terms of neurobiological evidence, [1,24] many studies suggest lack of gross abnormalities in the neuroimaging. However, studies which have found neurobiological changes suggest involvement of fronto-temporo-parietal circuitry in the pathophysiology of Cotard's syndrome. ...
... However, studies which have found neurobiological changes suggest involvement of fronto-temporo-parietal circuitry in the pathophysiology of Cotard's syndrome. [1] In terms of personality attributes, studies suggest that patients with a more internal attributional style are more prone to develop Cotard's syndrome. [24,28,29] In terms of neurophysiological changes some authors suggest lack of differential autonomic response to anything and reduction of affective response to stimuli in patients with Cotard's syndrome. ...
... [24,28,29] In terms of neurophysiological changes some authors suggest lack of differential autonomic response to anything and reduction of affective response to stimuli in patients with Cotard's syndrome. [1] Role of cultural factors in shaping the psychopathology in patients with Cotard's syndrome has also been proposed. [45] In terms of treatment of Cotard's syndrome, [1,25] ECT has been reported to be useful although there are case reports of beneficial effect of antidepressant alone, antipsychotic alone or a combination of both. ...
Cotard's syndrome is a rare neuropsychiatric condition in which the patient denies existence of one's own body to the extent of delusions of immortality. One of the consequences of Cotard's syndrome is self-starvation because of negation of existence of self. Although Cotard's syndrome has been reported to be associated with various organic conditions and other forms of psychopathology, it is less often reported to be seen in patients with catatonia. In this report we present two cases of Cotard's syndrome, both of whom had associated self-starvation and nutritional deficiencies and one of whom had associated catatonia.
... Such a person insists that even he is aware that this claim is irrational (Campbell, 2001). People with this disorder very often suffer from severe depression and anxiety (Debruyne, Portzky, Peremans, & Audenaert, 2011). They also may have problems when recognizing familiar faces and perceiving emotional expressions (Kudlur, George, & Jaimon, 2007). ...
... Much research has been conducted, the aim of which was to find the neural basis of these delusions. Neuroimaging studies have provided the information that in Cotard delusion an important role is played by the fronto-temporo-parietal circuitry (Debruyne et al., 2011;Kudlur et al., 2007). Some cases have also found different kinds of impairments: dilation of the third and lateral ventricles, bilateral cerebral atrophy, sylvian and interhemispheric fissure enlargement, left parietal lobe lesions, and haemorrhagic contusion of the right temporal cortex (Kudlur et al., 2007). ...
... Some cases have also found different kinds of impairments: dilation of the third and lateral ventricles, bilateral cerebral atrophy, sylvian and interhemispheric fissure enlargement, left parietal lobe lesions, and haemorrhagic contusion of the right temporal cortex (Kudlur et al., 2007). On the other hand, in most cases there were no structural brain changes (Debruyne et al., 2011;Kudlur et al., 2007). ...
The text concerns the role of emotions in delusion formation. Provided are definitions from DSM-V and DSM-IV-R and the problems found in those definitions. One of them, the problem of delusion formation, is described when providing cognitive theories of delusions. The core of the paper is a presentation of the emotional and affective disorders in delusions, especially Capgras delusion and Cotard delusion. The author provides a comparison of the kinds of delusions and the conclusions taken from neuroimaging studies. As a result of the fact that an explanation of delusion formation focusing on emotional problems turns out to be insufficient, the author provides examples of the reasoning impairments which coexist with them. At the end of the article, some hypotheses are proposed concerning the role of emotions and reasoning in delusion formation and the relation between belief disorders and emotional disorders.
... Initially, Cotard formulated that the condition would be a new kind of depression characterized by anxious melancholy, condemnation of ideas, insensitivity to pain, negation delusion of the organs, and immortality delusion. Sometime later, he created the term negation delusion to denominate the syndrome [6,7]. ...
... From the neurobiological point of view, there are some reports with PET scan studies which suggest a hypometabolism of the frontal-parietal-temporal cortex associative circuit [6,26,27] and a hypermetabolism in the basal ganglia [26,27] and cerebellum [26]. However, it was not possible to proceed neuroimaging studies for the reported patient due to the lack of availability of these examinations in our region through the public health system. ...
Cotard’s Syndrome (CS) is a rare clinical event described for the first time in 1880 by the neurologist and psychiatrist Jules Cotard and characterized by negation delusions (or nihilists). Immortality and hypochondriac delusions are also typical. Nowadays, it is known that CS can be associated with many neuropsychiatric conditions. In this article, we describe the case of a patient that believed not having more organs and having the body deformed and whose CS was associated with a bigger depressive disorder. Although the electroconvulsive therapy is the most described treatment modality in the literature, the reported case had therapeutic success with association of imipramine and risperidone.
... These estimates were consistent with data published for patients with schizophrenia with depressive symptoms [71]. PET studies suggested hypometabolism in the fronto-temporo-parietal cortex [104][105][106] and hypermetabolism in the basal ganglia [105,106] and the cerebellum [105]. ...
... Oszacowania te są zgodne z danymi opublikowanymi dla pacjentów z schizofrenią z objawami depresyjnymi [71]. Badania PET sugerują hipometabolizm kory czołowo-skroniowo-ciemieniowej [104][105][106] i hipertabolizm w zwojach podstawowych [105,106] i móżdżku [105]. ...
Introduction: The development of biological sciences, as well as cultural and civilizational changes have led to the emergence of practice within the medicine of science, called psychiatry. Already at the turn of the 19th and the beginning of the 20th century, Karl Jaspers - a German scholar - father of psychopathology - in the work “Allgemeine Psychopathologie” crystallized his intuitions in the field of psychopathology, which classifies and describes states that are deviations from the physiological mental state of a human being.
Material and method: his paper reviews available literature to approximate the symptoms of the most interesting psychopathological syndromes in psychiatry such as: Clerambault syndrome, Otheller syndrome, Cotard syndrome, Ekboma syndrome and Folie à deux.
Results: A multitude of psychopathological syndromes results from the wealth of survival of psychiatric patients. They represent the delusions of different contents that develop in a primitive way or as a consequence of other types of disorders. Psychopathological teams have been inspiring the poets and directors for centuries. The relationship between psychiatry and culture, film and literature undoubtedly testifies to its interdisciplinary nature.
Discussion: Despite the passage of time, the descriptions of these syndromes with a rich historical description, symptomatology and criteria have not lost their relevance and are still a clinical reality.
... Uważa się, że zespół Cotarda może występować wtórnie do innych schorzeń, takich jak schizofrenia, ChAD, udar mózgu, stwardnienie rozsiane, uszkodzenia płata ciemieniowego, zespół czołowy, atrofia mózgu, AIDS, demencja, choroba Parkinsona, epizod depresji z łagodnymi zaburzeniami funkcji poznawczych, ciężkie upośledzenie umysłowe, depresja w atrofii czołowo-skroniowej, niezakażone powikłanie przeszczepu serca, depresje pooperacyjne czy krwiak podtwardówkowy, oraz do rzadkich stanów chorobowych: hydrofobii, likantropii, paranoi indukowanej (Debruyne et al., 2009(Debruyne et al., , 2011Dieguez, 2018;Gonçalves i Tosoni, 2016;Joseph i O'Leary, 1986;Sahoo i Josephs, 2018). Ponieważ infekcje zwiększają ryzyko rozwoju schizofrenii, wolno przypuszczać, że pośrednio mogą także mieć wpływ na indukowanie zespołu Cotarda (Wiciński et al., 2014). ...
... Objawy są wówczas związane z wysokim poziomem CMMG (9-karboksymetoksymetyloguaniny), metabolitu acyklowiru. Podejrzewa się, że stosowanie amantadyny i kortykosteroidów również może się przyczynić do wystąpienia CS, podobnie jak hiponatremia wynikająca z odwodnienia (Debruyne et al., 2011;Sahoo i Josephs, 2018). Odpowiedzialne za rozwój zespołu Cotarda mogą być zaburzenia w obrębie kory wyspy (Morgado et al., 2015), na jego skutek może natomiast dojść do zaniku płata czołowego mózgu (Joseph i O'Leary, 1986 (Consoli et al., 2007). ...
Zespół Cotarda, w 1880 roku opisany przez francuskiego lekarza Jules’a Cotarda jako le délire des négations (złudzenie negacji),
to choroba, w której pacjent doświadcza urojeń nihilistycznych i przeświadczenia o własnej śmierci, a następnie – nieśmiertelności.
Ta niezwykle rzadka jednostka współwystępuje często z depresją, schizofrenią czy innymi chorobami charakteryzującymi się
zaburzeniem identyfikacji: zespołem Capgrasa i zespołem Fregolego. Do dziś dyskutuje się, czy zespół Cotarda powinien zostać uznany
za samodzielną jednostkę chorobową; ze względu na niespotykane w żadnym innym zespole objawy i zmiany w strukturach mózgu
rozwiązanie to zyskuje coraz liczniejszych zwolenników. Z uwagi jednak na rzadkość występowania omawianego zespołu nie
uwzględniają go ani Diagnostic and Statistical Manual of Mental Disorders (DSM-V), ani Międzynarodowa Statystyczna Klasyfikacja
Chorób i Problemów Zdrowotnych (ICD-10). Obecnie leczenie ma charakter przyczynowy, czyli skupia się na terapii choroby, która
najprawdopodobniej powoduje zespół Cotarda (depresja, schizofrenia, krwiak podtwardówkowy, ale również AIDS, choroba
Parkinsona, hydrofobia). Wśród skutecznych substancji wymienia się leki przeciwdepresyjne i przeciwpsychotyczne. Mimo istnienia
wielu podziałów najbardziej znana jest klasyfikacja Berriosa i Luque’a z 1995 roku. Badacze ci wyróżnili trzy postacie choroby: postać
z depresją i halucynacjami, zespół Cotarda I(bez depresji, z zaburzeniami hipochondrycznymi) i zespół Cotarda II (z depresją).
... Cotard's syndrome Delusional belief that one is dead or no longer exists. Debruyne et al., 2011 (World Health Organization [WHO], 1992), depersonalization and in Cotard's syndrome. Whereas under dissociation and depersonalization, the patient still possesses an intact, nonpsychotic self-representation, but experiences this representation as detached, alien or unreal (Hunter et al., 2004;Ataria, 2015), in Cotard's syndrome the patient does not identify with his self-representation anymore, but instead completely denies his or her own ontological existence (Debruyne et al., 2011). ...
... Debruyne et al., 2011 (World Health Organization [WHO], 1992), depersonalization and in Cotard's syndrome. Whereas under dissociation and depersonalization, the patient still possesses an intact, nonpsychotic self-representation, but experiences this representation as detached, alien or unreal (Hunter et al., 2004;Ataria, 2015), in Cotard's syndrome the patient does not identify with his self-representation anymore, but instead completely denies his or her own ontological existence (Debruyne et al., 2011). A third example, exclusively relating to SoA, would be delusions of control (Frith, 2004) where the patient is convinced that someone or something else (e.g., a supernatural power) controls his or her whole actions. ...
Usually, we do not question that we possess a body and act upon the world. This pre-reflective awareness of being a bodily and agentive self can, however, be disrupted by different clinical conditions. Whereas sense of ownership (SoO) describes the feeling of mineness toward one’s own body parts, feelings or thoughts, sense of agency (SoA) refers to the experience of initiating and controlling an action. Although SoA and SoO naturally coincide, both experiences can also be made in isolation. By using many different experimental paradigms, both experiences have been extensively studied over the last years. This review introduces both concepts, with a special focus also onto their interplay. First, current experimental paradigms, results and neurocognitive theories about both concepts will be presented and then their clinical and therapeutic relevance is discussed.
... Thirdly, Cotard's syndrome type II, with anxiety, depression, auditory hallucinations, delusion of immortality, nihilistic delusions, and suicidal behaviour as characteristic features. [15] Sound epidemiological data regarding Cotard's syndrome is lacking, with no reports from India. A Hong Kong-based prevalence study in a selected psychogeriatric population reported Cotard's syndrome in two out of 349 patients. ...
... [13] Successful pharmacotherapeutic approaches have also been published, mostly with antidepressants, antipsychotics, or a combination of both. [15] Bipolar disorder should be considered in patients under the age of 25 years. [19] Adding bromocriptine to clomipramine and lithium had a beneficial effect in a patient with bipolar disorder type I. [19] Special measures may be needed due to an important risk of suicide. ...
Cotard’s syndrome has always borne a historical construct, being linked to pure psychosis, affective disorders as well as organic disorders like Parkinson’s, temporal lobe epilepsy, migraine, and cerebral infarction. Emphasis has remained on the psychopathology, involving beliefs of negation, damnation, guilt, and denouncing of body organs. Treatment aspects has been focused on less frequently; moreover, sparsely from India. We present a case of bipolar affective disorder, current episode severe depression with psychotic symptoms (Cotard’s syndrome) with special focus on treatment.
... CS was first identified by James Cotard in 1880 as a new form of depression composed of anxious melancholia, ideas of damnation or rejection, insensitivity to pain, delusions of nonexistence concerning one's own body, and delusions of immortality. There is insufficient data about the prevalence and incidence of the syndrome (14). CS is described as a cluster of symptoms as part of an underlying disorder, mostly depressive and bipolar (15)(16)(17)(18). ...
... The first two stages were present in our case. Prognosis and treatment is based on the underlying disorder, and monotherapy, combination therapy, or ECT can be used as a treatment option (14). Thus, we both prescribed anti-psychotics and planned to imply ECT in the course of our treatment. ...
Neuroleptic malignant syndrome (NMS) is an uncommon but potentially fatal idiosyncratic reaction to neuroleptics and characterized by a distinctive clinical syndrome of mental status change, rigidity, fever, and dysautonomia. Cotard’s syndrome is characterized by the appearance of nihilistic delusions concerning one’s own body or life. By presenting this case, we aim to discuss the differential diagnosis and treatment plan of a patient with catatonia and Cotard’s syndrome, which were noted after NMS, in light of the literature.
... This syndrome differs from depressive disorders in the sense that, depressed patients ostend the intention of committing suicide however in CS, patients are already under the impression of being dead or having lost body parts. [3] ...
Cotard syndrome is a queer mental illness where the subject has delusional assumptions such that, they are dead, or have lost their limbs or internal organs or are imperishable. The patient ultimately suffers from nihilistic delusions that they no longer exist. Though the syndrome was first recognized in the 17 th century, it is neither classified under DSM-IV-TR nor ICD-10. One of the main consequences of this syndrome is self-starvation, refusal to consume medication and negligence to counseling. Though Cotard syndrome have been reported in association with many other affective disorders, it is less often found in patients with catatonia. In this article we are studying a 45-year-old patient, adamant about being dead and claiming that his abdomen was rotting.
... 6 W przeciwieństwie do urojenia Capgrasa, przy urojeniu Cotarda pacjent szuka przyczyny zmiany afektu w samym sobie. W tym przypadku występuje globalna zmiana afektu (jego spłycenie, które może być skutkiem silnej depresji) (Debruyne, Portzky, Peremans, Audenaert 2011). Ponieważ zmiana doznań pacjenta ma charakter stały -nie dotyczy jedynie reakcji na konkretne osoby -dochodzi on do wniosku, że przyczyną tej zmiany jest on sam. ...
Przedmiotem artykułu jest problematyka formalnego aspektu urojeń-rozumowania i wnioskowania. Autorka poddaje krytycznej analizie wybrane kognitywne teorie urojeń, skupiając uwagę na teoriach odgórnych (top-down) (dotyczących zmiany twierdzeń ramowych, zaburzenia Tła, mechanizmów atrybucyjnych, funkcjonowania wy-obraźni i mechanizmów wnioskowania, braku harmonii między zasadami konserwatyzmu i obserwacyjnej adekwatności, problemami związanymi z odpornością urojeń na rewizje oraz z niespójnością przekonań i działań). Uwzględniając różne koncepcje urojeń, stawia pytanie o racjonalność osób z urojeniami. Słowa kluczowe: urojenia, rozumowanie, racjonalność, kognitywne teorie urojeń Urojenia i halucynacje są podstawowymi symptomami zaburzeń psychicznych. W odróżnieniu od halucynacji-zaburzeń percepcji-urojenia dotyczą myślenia i sfery przekonań. We współczesnej filozofii umysłu o przekonaniu (P) osoby A możemy mówić, gdy uznaje ona P za prawdę i zgodnie z tym działa (jest to jedna z definicji, którą warto przyjąć w kontekście definicji urojeń). Przekonania można ujmować albo jako postawy albo jako reprezentacje umysłowe (Schwitzgebel 2014). Wydaje się, że definicja urojeń bliższa jest temu drugiemu podejściu. Natomiast w DSM-IV urojenie definiowane jest jako: Fałszywe przekonanie oparte na niewłaściwym wnioskowaniu o zewnętrznej rzeczywisto-ści, silnie podtrzymywane pomimo tego, w co wierzy prawie każdy i pomimo ustanowienia bezspornych i oczywistych dowodów lub faktów przeciwnych (DSM-IV 2000). Powstaje pytanie, co odróżnia przekonania urojeniowe od innego rodzaju przekonań-czy różnica tkwi tylko w treści, czy też formie (sposobie rozumowania)? Wybrane kognitywne teorie urojeń posłużą do analizy problematyki związanej z formalnym aspektem urojeń-rozumowania i wnioskowania.
... Here, we report a patient with Cotard's syndrome in the context of schizophrenia, showing brain metabolism abnormalities in 18 F-PDG PET scan and treated with ECT successfully. This report provides new insights regarding possible structural and functional brain abnormalities related to Cotard's syndrome (Debruyne et al., 2011): hypometabolism in the frontalparietal-temporal association cortex and hypermetabolism in the basal ganglia might be related to the pathophysiology of the illness and ECT could be first-line treatment in Cotard's syndrome. ...
Nihilistic delusions, also known as délires de négation, are specific psychopathological entities characterized by the delusional belief of being dead, decomposed or annihilated, having lost one's own internal organs or even not existing entirely as a human being. The world may be perceived as catastrophic, about to collapse or nonexistent at all. According to Jaspers (1959) "Nihilistic delusions in melancholia give us the prototype. The world does not exist anymore, the patient himself does not exist; he only appears to live and he must live like this forever. He has no feelings and he cares for nothing." 1 In the following report we present the clinical case of a schizophrenic patient with remarkable nihilistic delusions and ideations of immortality, successfully treated with haloperidol 15 mg, promazine 10 mg, valproate 1500 mg, diazepam 20 mg during an involuntary psychiatric treatment in our psychiatric ward.
Misidentification delusions involve an incorrect belief about the identity of other people, oneself, animals, objects, or places. Examples include Capgras delusion (the belief that a person or animal has been replaced by a visually similar impostor), the delusion of inanimate doubles (the belief that objects have been replaced by replicas), and reduplicative paramnesia (the belief that a person or place has been duplicated). Although encompassing a wide range of different beliefs, misidentification delusions share two common elements: 1) a misidentified entity, and 2) an incorrect belief about the identity of that entity. Misidentification delusions can occur in many different clinical conditions. These include, for example, schizophrenia, dementia, affective disorders, stroke, and traumatic brain injury. This chapter reviews different types of misidentification delusions, examining the etiology and prevalence of misidentification delusions and offering a theoretical explanation based on Langdon and Coltheart's two-factor theory of delusions.
The authors describe the frequency and characteristics of Cotard syndrome among neurological and psychiatric inpatients at a tertiary referral center. All inpatients from the National Institute of Neurology of Mexico (March 2007-May 2009) requiring neuropsychiatric consultation were reviewed. Among 1,321 inpatient consultations, 63.7% had neurological disease and one (0.11%) had viral encephalitis and Cotard syndrome. Of inpatients, 36.2% had pure psychiatric disorders and three (0.62%) had Cotard syndrome, associated with psychotic depression, depersonalization, and penile retraction (koro syndrome). This review discusses potential mechanisms for Cotard syndrome, including the role of a perceptual-emotional dissociation in self-misattribution in the deliré des negations.
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.
A 69-year-old man presented with Cotard's delusions, insomnia, profound depression, amnesia, difficulty concentrating, and cognitive deficit after two different surgical interventions. Brain imaging showed frontotemporal-subcortical atrophy and lateral ventricular enlargement. He responded poorly to a combination of sertraline, amisulpride and mirtazapine, with modest benefit on insomnia, and developed hypotension. After 18 days he was switched to olanzapine and venlafaxine, but his cognition worsened. He underwent bilateral electroconvulsive therapy (ECT). His mood improved, cognitive performance increased and anxiety symptoms remitted. This improvement persisted through the one-month post-discharge follow-up and depression eventually remitted.
Laurence-Moon-Bardet-Biedl (LMBB) syndrome is a symptom complex that usually presents with retinitis pigmentosa, poly- or syndactyly, mental retardation, obesity and hypogenitalism. Cotard's syndrome is a state in which the central symptom is a delusion of negation. The case reported here is a combination of these two rare conditions.
Patients with Capgras syndrome regard people whom they know well such as their parents or siblings as imposters. Here we describe a case (DS) of this syndrome who presents several novel features. DS was unusual in that his delusion was modality-specific: he claimed that his parents were imposters when he was looking at them but not when speaking to them on the telephone. Unlike normals, DS's skin conductance responses to photographs of familiar people, including his parents, were not larger in magnitude than his responses to photographs of unfamiliar people. We suggest that in this patient connections from face-processing areas in the temporal lobe to the limbic system have been damaged, a loss which may explain why he calls his parents imposters. In addition, DS was very poor at judging gaze direction. Finally, when presented with a sequence of photographs of the same model's face looking in different directions, DS asserted that they were "different women who looked just like each other'. In the absence of limbic activation, DS creates separate memory "files' of the same person, apparently because he is unable to extract and link the common denominator of successive episodic memories. Thus, far from being a medical curiosity. Capgras syndrome may help us to explore the formation of new memories caught in flagrante delicto.
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.
We report the case of a middle-aged woman with Cotard's syndrome in whom clinical course was evaluated according to stages. Longitudinally this syndrome seems to have three stages, namely germination, blooming and chronic (depressive type/paranoid type) stages. In this patient, the chronic stage, primarily characterized by delusions, was observed without raising suspicion of affective disorder. She did not respond to any pharmacotherapies, but improved dramatically after ECT performed during the chronic stage. Although symptoms change according to the stage, most cases of Cotard's syndrome may belong to the affective spectrum and are probably best treated with ECT, as documented here. In evaluation of the mode of separation between emotion and cognition during follow-up it is important to consider stage and diagnosis.
Recent work in cognitive neuropsychiatry explains the Capgras and Cotard delusions as alternative explanations of unusual qualitative states caused by dam-age to an affective component of the face recognition system. The difference between the delusions results from differences in attributional style. Cotard patients typically exhibit a style of internal attribution associated with depression, while Capgras patients exhibit the external attribution style more typical of paranoia. Thus the Cotard patient attributes her condition to drastic changes in herself and the Capgras patient attributes the same changes to alterations in the environment. I suggest three modifications to this explanation. Firstly, the nature of the affective deficit in Cotard cases may be more global than in Capgras cases, resulting from the diffuse effects of the neurochemical substrate of depression. Secondly, this explanation gives us additional insight into the content of the delusion. It is unsurprising that persons whose global affective responses were suppressed would explain their lack of response by saying that they had no bodily existence. Finally I suggest that in Cotard cases the delusion is produced by a reasoning deficit, rather than attributional style.
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.
Depersonalisation nach Hirnschädigung ist ein bislang selten beschriebenes und wenig verstandenes Phänomen. Wir berichten über 3 Patienten im Alter zwischen 21 und 25 Jahren, die ein Depersonalisations- bzw. Derealisationserleben über einen Zeitraum von 6 Wochen bis zu 4 Monaten erfuhren. Zwei hatten ein Schädel-Hirn-Trauma erlitten, eine Patientin war an einem Pineozytom operiert und bestrahlt worden. Die Patienten glaubten, sich in einem Alptraum zu befinden; sie dachten über die Möglichkeit nach, sich zu suizidieren um aufzuwachen. Einer der Patienten entwickelte zusätzlich Symptome, die dem Cotard-Syndrom zugerechnet werden. Neuroanatomische, psychodynamische und anthropologische Aspekte werden unter Berücksichtigung der Literatur diskutiert. Frontale und temporale Läsionen scheinen allenfalls eine fazilitierende Rolle zu spielen, nicht aber eine notwendige Bedingung zu sein. Es ergeben sich jedoch Hinweise auf einen zusätzlichen Einfluß psychologischer und prämorbider persönlichlichkeitsnaher Faktoren. Nach Zusammenschau des derzeitigen Informationsstandes betrachten wir Depersonalisation mit z.B. traumartigem oder todesähnlichem Erleben als eine heuristische Reaktion auf die Hirnschädigung. Ähnliche Modelle werden bereits bei neuropsychologischen Syndromen wie reduplikative Paramnesien, Neglekt und Anosognosie diskutiert.
Neurologic complications are important causes of morbidity and mortality in heart transplant (HT) recipients. New immunomodulating agents have improved survival rates, although some have been associated with a high rate of neurologic complications (infectious and non-infectious). We conducted this study to analyze the frequency of these complications, before and after the use of daclizumab induction therapy. We reviewed all neurologic complications in our HT cohort, comparing infectious with non-infectious complications over 2 periods of time in which different induction therapies were used (316 patients with OKT3 or antithymocyte globulin from 1988 to 2002, and 68 patients with daclizumab from 2003 to 2006). Neurologic complications were found in 75/384 patients (19.5%) with a total of 78 episodes. Non-infectious complications accounted for 68% of the 78 episodes of neurologic complications. A total of 51 patients and 53 episodes were detailed as follows: 25 episodes of stroke (25 of 78 total episodes, 32%; 19 ischemic, 6 hemorrhagic); 7 neuropathies; 6 seizures; 4 episodes of transient ischemic attack (TIA); 3 anoxic encephalopathy; 2 each brachial plexus palsy and metabolic encephalopathy; and 1 each myoclonia, central nervous system (CNS) lymphoma, subdural hematoma, and Cotard syndrome. Mean time to presentation of stroke, TIA, and encephalopathy was 1 day (range, 1-19 d) posttransplant. Mortality rate among non-infectious complications was 12/53 (22.6%). Infectious complications accounted for 32% of the 78 total episodes. We found 25 episodes in 24 patients: 17 herpes zoster (median, 268 d after HT), 3 CNS aspergillosis (median, 90 d after HT), 1 CNS toxoplasmosis and tuberculosis (51 d after HT), 1 pneumococcal meningitis (402 d after HT), and 2 Listeria meningitis (median, 108 d after HT). The 3 patients with CNS aspergillosis died. The mortality rate among patients with infectious neurologic complications was 12% (42.8% if the CNS was involved). When we compared the OKT3-ATG and daclizumab groups, we found that the incidence of non-infectious complications was 15.1% vs. 7.3%, respectively, and the incidence of infectious complications was 7.5% vs. 1.4%, respectively. All but 1 opportunistic infection occurred in the OKT3-ATG time period. In conclusion, a wide variety of neurologic complications affected 19.5% of HT recipients. Non-infectious causes clearly predominated, but infections still accounted for 32% of the episodes. New monoclonal induction therapies have contributed to diminished CNS opportunistic infections in our program.
Convulsive therapy and its progeny, electroconvulsive therapy (ECT), were originally used for the treatment of catatonic schizophrenia, and there is little doubt that ECT remains an effective intervention for the treatment of schizophrenia. However, current practice tends to favor the use of ECT in severe or treatment refractory affective disorders, and its use in schizophrenia and other nonaffective (atypical) psychotic disorders has become controversial.CASE REPORTS HAVE SUGGESTED A ROLE FOR ECT IN TWO SPECIFIC ATYPICAL PSYCHOTIC DISORDERS: Cotard's syndrome and cycloid psychosis. In this article, we review the atypical psychotic disorders and report a series of five case examples that signify the role of ECT in atypical psychotic presentations, particularly when the symptoms resemble those found in Cotard's syndrome and cycloid psychosis.
Work in the field of cognitive neuropsychiatry over the past 20 years has made it plain that various forms of delusional belief are scientifically understandable in the sense that plausible neuropsychological explanations of their nature and genesis have been formulated. A two-factor theory of delusional belief has emerged from this work. According to this theory, explaining the presence of a delusion requires (a) the presence a neuropsychological impairment that initially prompts the delusional belief and (b) the presence of a second neuropsychological impairment that interferes with processes of belief evaluation that would otherwise cause the delusional belief to be rejected. A very similar account of delusion has recently emerged from research on hypothesis evaluation using the associative-learning paradigm with healthy control subjects and people with psychosis. Neuroimaging studies in this context suggest that the region of the brain specifically involved in hypothesis evaluation (and therefore, according to the two-factor theory, impaired in people with delusions) is the right lateral prefrontal cortex.
A 14 year old adolescent girl who was diagnosed with Capgras, Fregoli and Cotard's syndromes was described. Her clinical presentation contained the signs of all three disorders of delusional misidentification syndrome. Coexistence of the signs of all three disorders is very rare in adolescents. In addition to rarity, lack of information and experience about the etiology and treatment of these situations challenge the clinicians. (Archives of Neuropsychiatry 2008; 45: 149-51)
Synopsis
A right-handed young man with contusions affecting temporo-parietal areas of the right cerebral hemisphere and some bilateral frontal lobe damage became convinced that he was dead (the Cotard delusion), and experienced difficulties in recognizing familiar faces, buildings and places, as well as feelings of derealization. Neuropsychological investigation while these symptoms were resolving revealed impairment on face processing tests. We suggest that these impairments contributed to his Cotard delusion by heightening feelings of unreality, and that the underlying pathophysiology and neuropsychology of the Cotard delusion may be related to other problems involving delusional misidentification.
Two cases of Cotard's Syndrome are described--one in a 33-year-old housewife suffering from paranoid schizophrenia and another in a 43-year-old housewife with acute psychotic depression. This rare syndrome is characterized by an extreme form of nihilistic delusion in which the patient, more frequently a woman, denies her own existence and that of the external world. Its onset is often sudden with no previous psychiatric history. Treatment of the condition depends on the underlying psychiatric illness. Both cases responded well to treatment.
A mentally handicapped man with Cotard's syndrome is described, and the usefulness of electroconvulsive therapy in his management discussed. Even the more uncommon psychiatric syndromes such as this can be found in people with lower intellectual functioning, with clinical features little modified.
The hallmark of Cotard's syndrome is the delusion of being dead. The literature indicates that it is often associated with parietal lobe lesions. This association was investigated by blindly comparing the computed tomographic scans of eight patients who had Cotard's syndrome (one of whom is described) with those of eight controls matched as closely as possible for age, sex, race, and principal psychiatric diagnosis. Two trends emerged. Compared with controls, patients with Cotard's syndrome had more brain atrophy in general and more median frontal lobe atrophy in particular. Parietal disease did not discriminate between the index and control groups. Cotard's syndrome may be associated with multifocal brain atrophy and medial frontal lobe disease.
The theme of death highlighted the depersonalization phenomena of four patients with complex partial seizures. These patients became preoccupied with death in association with psychomotor seizures, visual hallucinations, and altered perception of time and reality. The episodic sense of being dead or of having an appointment with death is a clue to the diagnosis of recurrent complex partial seizures even without overt motor stigmata of seizures. The syndrome differs from fear of death, steroid psychosis, the "near death syndrome," and Cotard's syndrome. Adjustment of antiseizure medication is an important therapeutic maneuver.
Patients with Cotard's syndrome generally suffer from the delusion that they have died or that they do not exist. This case report describes a man whose typhoid fever eventually manifested itself as Cotard's syndrome.
Severe depersonalization at times constitutes a chronic and disabling syndrome for which there is no generally established etiology or treatment. Two cases in which young female patients with severe depersonalization became floridly manic in response to stimulant and antidepressant drug treatment are reported, and the clinical and theoretical implications of these phenomena are discussed.
In 1880, Jules Cotard reported a clinical state he believed was a new type of agitated melancholia. A statistical analysis has been carried out of 100 cases of Cotard's syndrome to determine how this clinical concept has fared since its inception. In terms of clinical profile, no difference was found between men and women or between underlying diagnostic categories; age seemed to increase the likelihood of developing délire des négations. Depression was reported in 89% of subjects; the most common nihilistic delusions concerned the body (86%) and existence (69%). Anxiety (65%) and guilt (63%) were also common, followed by hypochondriacal delusions (58%) and delusions of immortality (55). An exploratory factor analysis extracted 3 factors: psychotic depression, Cotard type I and Cotard type II. The psychotic depression factor included patients with melancholia and few nihilistic delusions. Cotard type 1 patients, on the other hand, showed no loadings for depression or other disease and are likely to constitute a pure Cotard syndrome whose nosology may be closer to the delusional than the affective disorders. Type II patients showed anxiety, depression and auditory hallucinations and constitute a mixed group. This new grouping cuts across the more traditional view and may have therapeutic implications. Authors, in general, have considered délire des négations as a syndrome rather than a new disease and do not seem to support the view that the completeness of the syndrome is a function of presence or severity of depression. The view that délire des négations refers only to the delusion of being dead has also carried little favour as its likely to waste information.
Cotard's syndrome is characterized by the presence of nihilistic delusions. A retrospective case note study of 349 Chinese psychogeriatric patients in Hong Kong showed a prevalence of 0.57% of the syndrome. The two patients identified were both females with major depression. Case vignettes of these patients were presented and the similarity of the clinical features to those described in the Western literature was discussed.
Capgras, Fregoli and Cotard's syndromes and Koro in folie à deux - Volume 165 Issue 6 - Geoffrey Wolff, Kwame McKenzie
We report sequential Cotard and Capgras delusions in the same patient, KH, and offer a simple hypothesis to account for this link. The Cotard delusion occurred when KH was depressed and the Capgras delusion arose in the context of persecutory delusions. We suggest that the Cotard and Capgras delusions reflect different interpretations of similar anomalous experiences, and that the persecutory delusions and suspiciousness that are often noted in Capgras cases contribute to the patients' mistaking a change in themselves for a change in others ('they are impostors'), whereas people who are depressed exaggerate the negative effects of the same change whilst correctly attributing it to themselves ('I am dead'). This explains why there might be an underlying similarity between delusions which are phenomenally distinct.
A patient's major depression and Cotard's syndrome (the delusion of being dead) both resolved completely after 12 ECT treatments. A SPECT study 1 week before ECT showed reduced blood flow in the frontoparietal medial and dorsolateral frontal cortex, basal ganglia, and thalamus; SPECT 1 month after ECT showed perfusion increments in those regions. This case study demonstrates that Cotard's syndrome in the context of major depression may be successfully treated with ECT and suggests that the psychiatric improvement was accompanied by increased blood flow in specific brain areas.
A case study is presented to illustrate a rare condition described by Cotard as "délire de négation". The central symptom is a nihilistic delusion with denial of one's own existence of oneself and that of the external world. In the present case, the syndrome became manifest as an escalation of a recurrent depressive disorder late in life. After initial resistance to therapy, the syndrome was successfully treated with electroconvulsive therapy. For the first time, we report the regional cerebral blood flow measured by 99mTc-HMPAO-SPECT before and after therapy. Before treatment, significant bitemporal hypoperfusion relative to the cerebellum was found, which was no longer demonstrable on remission.
We here describe a case of Cotard's syndrome in a 15-year-old girl who exhibited a short period of malignant catatonia, and the positive effect of electroconvulsive therapy (ECT) on her disorder. A psychopathological hypothesis is proposed.
People experiencing the Capgras delusion claim that others, usually those quite close emotionally, have been replaced by near-identical impostors. Ellis & Young suggested in 1990 that the Capgras delusion results from damage to a neurological system involved in orienting responses to seen faces based on their personal significance. This hypothesis predicts that people suffering the Capgras delusion will be hyporesponsive to familiar faces. We tested this prediction in five people with Capgras delusion. Comparison data were obtained from five middle-aged members of the general public, and a psychiatric control group of five patients taking similar anti-psychotic medication. Capgras delusion patients did not reveal autonomic discrimination between familiar and unfamiliar faces, but orienting responses to auditory tones were normal in magnitude and rate of initial habituation, showing that the hyporesponsiveness is circumscribed.