The Talking Dead: Cefepime-Induced Cotard Syndrome.

P-1235 - Effect of cultural themes on forming cotard's syndrome; reporting a case of cotard's syndrome with depersonalization and out of body experience symptoms

P-239 - Cotard's syndrome - a case report

In Cotard delusion, the subject believes that she has died or no longer exists. One explanation of the delusion proceeds from the fact that depersonalization is often reported as the experience of feeling ‘as if’ the subject no longer exists. In Cotard delusion, this depersonalization experience is coupled with a metacognitive deficit that leads the subject to endorse the experience or take it at face value. An alternative explanation treats depersonalization and Cotard delusion as products of different impairments to the avatar. Unlike depersonalization in which the avatar is largely intact, in Cotard delusion, the avatar degrades and disintegrates. The result is that the narrative ‘I’ remains as a purely verbal construct detached from an underlying sense of self as a unified persisting entity.

Back to table of contents Previous article Next article LETTERFull AccessDelusion of Cotard’s Syndrome Successfully Treated with a Dopamine AgonistTomohisa Takahashi M.D.Masashi Nibuya M.D., Ph.D.Soichiro Nomura M.D., Ph.D.,Tomohisa Takahashi M.D.Search for more papers by this authorMasashi Nibuya M.D., Ph.D.Search for more papers by this authorSoichiro Nomura M.D., Ph.D.Search for more papers by this author,Published Online:1 Apr 2010https://doi.org/10.1176/jnp.2010.22.2.247.e27AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Cotard’s syndrome, which is characterized by delusions of negation and increased anxiety accompanied by severe depressive symptoms, is reported to be resistant to antidepressants. Although delusions are treated with neuroleptics, Cotard’s syndrome responds poorly to dopamine antagonists. Several case studies have recommended that ECT most effectively ameliorates Cotard’s syndrome. 1 In this article, we describe the case of a patient with Cotard’s syndrome that was successfully treated with dopamine augmentation therapy for treatment-resistant depression. 2Case ReportA 58-year-old woman had been diagnosed with recurrent major depression and treated with antidepressants for about 25 years. No hypomanic-to-manic episode or depressive episode with psychotic features had been observed. Because of irregular oral administration of psychotropic drugs during the remission period, she experienced a relapse of depression twice in 5 years. The present episode was that of severe depression with psychotic features. Her delusional complaints were “I cannot eat any food, because my mouth does not salivate. I would never be able to get out of the hospital. I have no money to pay for my hospital stay. My mother is dead. My mind is completely blank with no thoughts, and there seems to be no brain in my head. I would have to stay bare all my life, because I have no clothes. I cannot sleep for a moment. I cannot talk because I have lost all my words.” Suicidal ideation, anxiety, loss of interest and pleasure, agitation, weight loss of 6 kg in 2 months, and depressive mood were observed. Paroxetine (up to 40 mg/day) was administered for 36 days from the time of admission, but no improvement was observed. For augmentation for treatment-resistant depression, pramipexole (up to 0.75 mg/day) was administered as a dopamine agonist in addition to paroxetine. The depressive symptoms, including appetite loss and agitation, improved 6–9 days after the augmentation, and no worsening of delusional symptoms was observed. The delusions disappeared at 14 days after the initiation of the augmentation. No relapse of delusion and depression was observed during the 8-week follow-up period. Paroxetine, 20 mg/day, and pramipexole, 0.75 mg/day, were administered at the time of discharge.Discussion This is the second case report indicating the effectiveness of dopamine agonist augmentation therapy for treating delusions of Cotard’s syndrome. Although bromocriptine was added to clomipramine in the previous study, 3 pramipexole was chosen as the dopamine agonist 4 to avoid fibrotic cardiac valvulopathy by ergot alkaloids. The effectiveness of additional neuroleptics for the treatment of psychotic depression has also been reported. 5 Few studies, however, have addressed the effectiveness of neuroleptics in the treatment of Cotard’s syndrome. For over a hundred years, Cotard’s syndrome has survived as a distinct psychopathological diagnostic entity. The present case indicated the existence of a group of patients with psychotic depression whose depression needs to be treated first, even by enhancing dopamine activities. Considering the fact that ECT is generally ineffective in treating delusions, this case indicated the importance of treating severe depression first in Cotard’s syndrome. Department of Psychiatry, National Defense Medical College, Tokorozawa, Japan

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.

Background: Cotard syndrome is a rare condition whose main feature is a nihilistic delusion ranging from the denial of body parts to that of the existence of one’s own life or even the entire universe.Objectives: The aim of this article is to review the nosological significance of Cotard syndrome and to explore the disorder among patients with dementia.Methods: Medline and Google Scholar searches were conducted for relevant articles, chapters and books published before 2018. Search terms used included Cotard delusion, Cotard syndrome and dementia, nihilistic delusion. Publications found through this indexed search were reviewed for further relevant references.Results and conclusion: In this narrative review we emphasise the fact that cases of Cotard syndrome involving patients with dementia are reported quite infrequently. Published studies are limited to very short series or isolated cases. Clinicians are obliged to treat the disorder. They should be alert to the potential high risk inherent in this condition.KeypointsCotard syndrome is a rare condition characterised by nihilistic delusions that may range from negation of existence of parts of the body to delusion of being dead.The prevalence and incidence of this rare syndrome are not known.Since Cotard’s syndrome is conceptualised as part of an underlying disorder, several psychiatric and somatic diseases have been associated with the syndrome.The syndrome may occur in patients suffering from dementia.

Depersonalization is an essential step in the development of the Cotard delusion. Based on Philip Gerrans’ account (this collection), which is an integration of the appraisal theory, the simulation theory, and the predictive coding framework, this commentary aims to argue that the role of memory systems is to update the knowledge of prior probability required for successful predictions. This view of memory systems under the predictive coding framework provides an explanation of how experience is related to the construction of mental autobiographies, how anomalous experience can lead to delusions, and thus how the Cotard delusion arises from depersonalization.

The initial cause of Cotard delusion is pervasive dyshomeostasis (dysregulation of basic bodily function).This explanation draws on interoceptive active inference account of self‐representation. In this framework, the self is an hierarchical predictive model made by the brain to facilitate homeostatic regulation. The account I provide is an alternative to two factor accounts of the Cotard delusion that treat depersonalisation experience as the first factor in genesis of the Cotard delusion. I argue that depersonalisation experience and the Cotard delusion are produced by different breakdowns in the process of self‐modelling.

The sociocultural context of psychiatric patients shapes symptoms experience and expression, as well as how patients deal with a disorder and how society appraises its symptoms. Specifically, the context may influence the social appraisal of a behavior as normal or pathological. Therefore, markedly pathological symptoms may not be accordingly recognized by peers when they are in consonance with the sociocultural context. Per "Dead" Ohlin was a Swedish musician who was a member of the Norwegian black metal band Mayhem from 1988 until his suicide in 1991, at age 22. Black metal is a musical movement characterized by death worshiping and anti-Christianism, and is also associated with church arsons and murders during the 1990s. Even among peculiar personalities such as black metal musicians, Ohlin was considered the personification of the movement ideals due to his eccentric and unparalleled beliefs and behaviors, claiming, for instance, that he was already dead. In this article, we propose that Ohlin's eccentric beliefs and behaviors were symptoms of an unrecognized psychiatric condition, Cotard's syndrome, and discuss the diagnostic dilemma presented by Ohlin's artistic persona and singular context. The compatibility between his symptoms and the sociocultural context of black metal may have obscured his mental disorder. If so, Ohlin's unique case may shed light upon one of the effects of context in a psychopathological process: concealing a psychiatric disorder and reinforcing symptoms that fit a particular environment.

AimThis report aims to illustrate the possibility of an acute onset of psychosis after COVID‐19 infection in a patient without previous history of psychiatric disorders and to highlight the need for early screening and intervention in such cases.MethodsClinical presentation of a case, followed by clinical discussion and literature review of the effect of the new coronavirus SARS‐CoV‐2 and its impact on mental health in terms of neuropsychiatric conditions.ResultsWe present a case of acute and transient psychotic disorder following complete recovery of COVID‐19 bilateral pneumonia. The patient has no prior psychiatric history and presents with acute onset, disorganized behaviour, Cotard's delusion and a potentially high risk of psychotic homicide and suicide.ConclusionEarly intervention and treatment with antipsychotic medication are of crucial importance for the effective treatment and complete recovery of these patients.

BackgroundCotard's delusion/Cotard's syndrome is a series of delusions ranging from a false, fixed, unshakeable belief that one has lost their soul, blood, organs, and body parts to the belief that one is dead. The syndrome was initially thought to be associated with only mood disorders but later was found in other psychiatric illnesses as well.AimThe study aimed to find an association between Cotard's delusion and the psychopathology of different psychiatric diagnoses.MethodThe clinical study comprised seven patients presenting with symptoms of Cotard syndrome with different presentations, diagnoses, and onset and meeting inclusion criteria. The study was carried out in the Department of Psychiatry, Assam Medical College and Hospital. The patients were hospitalized and, after a detailed history, mental status examination, and laboratory investigations, were treated with pharmacological and non-pharmacological methods. A descriptive statistical analysis was done.ResultsDenial of the existence of body organs was the most similar complaint encountered in the cases. The duration of illness onset ranged from weeks to months. The symptoms were found to be present in different psychiatric illnesses like schizophrenia, delusional disorder, depression, and intellectual disability. The patient had responded well to pharmacological agents with the exception of three patients who were treated with electroconvulsive therapy.ConclusionThe study highlights the different subtypes of Cotard’s syndrome and its associated symptoms, which provides a better understanding of the condition. The case series presents a finding of a higher proportion of male patients and adolescent cases than in previous reports. The study also provides valuable insights into its heterogeneity in the diagnosis and treatment of Cotard’s syndrome, which may help in the early recognition and management of this rare condition.

On what I will call a rationalist approach to delusion, delusion is a matter of top-down disturbance in some fundamental beliefs of the subject, which may consequently affect experiences and actions. On an empiricist approach, in contrast, delusion is a rational response to highly unusual experiences that the subject has, perhaps as a result of organic damage. Ellis and Young (1990) recently provided an empiricist analysis of the Capgras and Cotard delusions. I want to begin with some remarks on just why it is important to the empiricist approach that it should acknowledge the rationality of the subject's delusional responses to unusual stimuli. We will see that when the rationale for the rationality constraint is fully set out, it is questionable whether Ellis and Young's approach actually succeeds in giving its place to the rationality constraint. In conclusion, I will look briefly at the prospects for a rationalist approach and at what other approaches might be possible.

Research suggests that clinical symptom dimensions may be more useful in delineating the genetics of bipolar disorder (BD) than standard diagnostic models. To date, no study has applied this concept to data from genome-wide association studies (GWAS). We performed a GWAS of factor dimensions in 927 clinically well-characterized BD patients of German ancestry. Rs9875793, which is located in an intergenic region of 3q26.1 and in the vicinity of the solute carrier family 2 (facilitated glucose transporter), member 2 gene (SLC2A2), was significantly associated with the factor analysis-derived dimension ‘negative mood delusions' (n=927; P=4.65 × 10−8, odds ratio (OR)=2.66). This dimension was comprised of the symptoms delusions of poverty, delusions of guilt and nihilistic delusions. In case–control analyses, significant association with the G allele of rs9875793 was only observed in the subgroup of BD patients who displayed symptoms of ‘negative mood delusions' (allelic χ2 model: PG=0.0001, OR=1.92; item present, n=89). Further support for the hypothesis that rs9875793 is associated with BD in patients displaying ‘negative mood delusions' symptom, such as delusions of guilt, was obtained from an European American sample (GAIN/TGEN), which included 1247 BD patients and 1434 controls (PEA=0.028, OR=1.27).

In this article we report the first series of Turkish inpatients with late-onset psychosis, and describe our 9-year experience at the only inpatient geriatric psychiatry department in Turkey. Among 420 patients hospitalized between 1993 and 2002, 27 were psychotic. In this group, eight patients were diagnosed as having late-onset schizophrenia (LOS) and six very-late-onset schizophrenia-like psychosis (VLOSLP). Five patients had early-onset schizophrenia and eight had delusional disorder. Females were more frequently seen in the group with LOS and the group with VLOSLP. Except for one patient with LOS, all patients with VLOSLP and LOS had paranoid psychosis. Nihilistic delusions, delusions of poverty or guilt, thought withdrawal, thought insertion, and thought broadcasting were not seen in any of the patients. Additionally, none of the LOS or VLOSLP patients showed erotomanic delusions. Grandiose and mystic delusions were not seen in those with VLOSLP. Treatment results and antipsychotic dosages at discharge were similar to those in previous reports from other cultures.

W HEN ONE examines most textbooks on child psychiatry, he finds little or no mention of depressions in childhood. As an example, in the third edition of Child Psychiatry (1957) by Leo Kanner, the word "depression" is neither listed in the table of contents nor in the index of this otherwise excellent text. This is surprising since all psychiatrists have seen depressed children. As a matter of fact, with growing experience and awareness of this condition, such a diagnosis is being made more often. In this paper, I will explore the concepts of depression in childhood and adolescence and, through the use of clinical examples, develop means for a more effective diagnosis of this condition with the hope that early identification can lead to the prevention of some of the disabling depressions of adults. Let us first recall what the classical clinical picture of depression in adults is. Dr. Hans Lehmann 1 describes it very well: "Fortunately there has always been agreement about the phenomena that characterize the psychiatric condition which we call depression or melancholia. The characteristic symptoms are a sad or despairing mood, decrease of mental productivity and a reduction of drive, retardation or agitation in the field of expressive motor responses. These might be called the primary symptoms of depression. The group of secondary symptoms comprises feelings of hopelessness, hypochondriacal preoccupation, feelings of depersonalization, obsessive and compulsive behavior, ideas of self-accusation, nihilistic delusions, paranoid delusions, hallucinations, suicidal rumination and tendencies. Insomnia, anorexia and weight loss are usually associated with depressive states. . . The sad, despairing emotional state and depressive mood seem to constitute the real core of all depressions..." The foregoing excellent clinical description of depression is rarely seen in childhood; if we were to diagnose depressive illness in children using Dr. Lehmann's definition, we would be talking about very few children. Perhaps this accounts for the paucity of interest in depression shown by the writers of texts on child psychiatry. Yet, there is a growing awareness that depression in children does exist much more commonly than heretofore expressed. In 1959, at Cambridge, England, a symposium on depression 2 was held. I have selected a few quotations concerning children and adolescents. Dr. Glennie z said: "I think depressions in children occur quite frequently in the illnesses of children though it is hard to find straightforward evidence of the single symptom of depression. The picture in children is usually less clear-cut; anxiety seems to play a more obvious part." Later in this symposium Dr. Glennie state#: "I think I see depressive states in children though I cannot at present correlate them with what is seen in adults or understand them in isolation, that is, without considering the attitudes of the children towards their parents or vice versa." Dr. Burns, in the same conference, statesS: "Depressions in small children are more common than previously thought because they can present themselves in many different ways. An intelligent boy of ten, for example, began to fail in school, but I had no doubt he was depressed... In looking back I can think of many other cases in which children