Cotard delusion

Cotard delusion

The neurologist Jules Cotard (1840–89) described "The Delirium of Negation" as a mental illness of varied severity.
Classification and external resources
Specialty Psychiatry
ICD-10 F22
ICD-9-CM 297.1

The Cotard delusion (also Cotard's syndrome and walking corpse syndrome) is a rare mental illness in which an afflicted person holds the delusion that they are dead, either figuratively or literally; yet said delusion of negation is not a symptom essential to the syndrome proper.[1] Statistical analysis of a hundred-patient cohort indicates that the denial of self-existence is a symptom present in 69% of the cases of Cotard's syndrome; yet, paradoxically, 55% of the patients present delusions of immortality.[2]

In 1880, the neurologist Jules Cotard described the condition as Le délire des négations ("The Delirium of Negation"), a psychiatric syndrome of varied severity. A mild case is characterized by despair and self-loathing, and a severe case is characterized by intense delusions of negation and chronic psychiatric depression.[3][4] The case of Mademoiselle X describes a woman who denied the existence of parts of her body and of her need to eat, and said that she was condemned to eternal damnation and therefore could not die a natural death. In the course of suffering "The Delirium of Negation", Mademoiselle X died of starvation.

As a mental illness, Cotard's syndrome also includes the patient's delusion that they do not exist as a person, are putrefying, and have lost blood, internal organs, or both. The Cotard delusion is not included in the Diagnostic and Statistical Manual of Mental Disorders (DSM).[5] In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10), of the World Health Organization, code F22 identifies the Cotard delusion as a disease of human health.[6]

Signs and symptoms

The delusion of negation is the central symptom in Cotard's syndrome. The patient afflicted with this mental illness usually denies their existence, or the existence of a certain body part, or the existence of a portion of their body. Cotard's syndrome exists in three stages: (i) Germination stage—the symptoms of psychotic depression and of hypochondria appear; (ii) Blooming stage—the full development of the syndrome and the delusions of negation; and (iii) Chronic stage—continued, severe delusions and chronic psychiatric depression.[7]

The Cotard syndrome withdraws the afflicted person from other people, which includes neglecting their personal hygiene and physical health. The delusion of negation of self prevents the patient from making sense of external reality, producing a distorted view of the external world. Such a delusion of negation is usually found in the psychotic patient who also presents with schizophrenia. Although a diagnosis of Cotard's syndrome does not require the patient's having had hallucinations, the strong delusions of negation are comparable to those found in schizophrenic patients.[8]

Distorted reality

The article Betwixt Life and Death: Case Studies of the Cotard Delusion (1996) describes a contemporary case of Cotard delusion, which occurred in a Scotsman whose brain was damaged in a motorcycle accident:

[The patient's] symptoms occurred in the context of more general feelings of unreality and [of] being dead. In January 1990, after his discharge from hospital in Edinburgh, his mother took him to South Africa. He was convinced that he had been taken to Hell (which was confirmed by the heat), and that he had died of septicaemia (which had been a risk early in his recovery), or perhaps from AIDS (he had read a story in The Scotsman about someone with AIDS who died from septicaemia), or from an overdose of a yellow fever injection. He thought he had "borrowed [his] mother's spirit to show [him] around hell", and that she was asleep in Scotland.[9]

The article Recurrent Postictal Depression with Cotard Delusion (2005) describes the case of a fourteen-year-old epileptic boy whose distorted perception of reality resulted from Cotard Syndrome. His mental-health history was of a boy expressing themes of death, chronic sadness, decreased physical activity in playtime, social withdrawal, and disturbed biological functions. About twice a year, the boy suffered episodes that lasted between three weeks and three months. In the course of each episode, he said that everyone and everything was dead, including trees; described himself as a dead body; and warned that the world would be destroyed within hours. Throughout the episode, the boy showed no response to pleasurable stimuli and had no interest in social activities.[10]

Pathophysiology

Neural misfiring in the fusiform face area, in the Fusiform gyrus (orange), might be a cause of the Cotard delusion.
In the cerebrum, organic lesions in the parietal lobe might cause the Cotard delusion.

The underlying neurophysiology and psychopathology of Cotard's Syndrome might be related to problems of delusional misidentification. Neurologically, the Cotard delusion (negation of the Self) is thought to be related to the Capgras delusion (people replaced by impostors); each type of delusion is thought to result from neural misfiring in the fusiform face area of the brain (which recognizes faces) and in the amygdalae (which associate emotions to a recognized face).[11]

The neural disconnection creates in the patient a sense that the face they are observing is not the face of the person to whom it belongs; therefore, that face lacks the familiarity (recognition) normally associated with it, which results in derealization—disconnection from the environment. If the observed face is that of a person known to the patient, they experience that face as the face of an impostor (the Capgras delusion). If the patient sees their own face, they might perceive no association between the face and their own sense of Self—which results in the patient believing that they do not exist (the Cotard delusion).

Cotard's syndrome is usually encountered in people afflicted with a psychosis (e.g., schizophrenia), neurological illness, mental illness, clinical depression, derealization, and with migraine headache.[11] The medical literature indicate that the occurrence of Cotard's delusion is associated with lesions in the parietal lobe. As such, the Cotard-delusion patient presents a greater incidence of brain atrophy—especially of the median frontal lobe—than do the people in the control groups.[12]

The Cotard delusion also has resulted from a patient's adverse physiological response to a drug (e.g., aciclovir) and to its prodrug precursor (e.g., valaciclovir). The occurrence of Cotard delusion symptoms was associated with a high serum-concentration of 9-Carboxymethoxymethylguanine (CMMG), the principal metabolite of the drug aciclovir. As such, the patient with weak kidneys (impaired renal function) continued risking the occurrence of delusional symptoms, despite the reduction of the dose of aciclovir. Hemodialysis resolved the patient's delusions (of negating the Self) within hours of treatment, which suggests that the occurrence of Cotard-delusion symptoms might not always be cause for psychiatric hospitalization of the patient.[13]

Treatment

The article Cotard's syndrome: A Review (2010) reports successful pharmacological treatments (mono-therapeutic and multi-therapeutic) using antidepressant, antipsychotic, and mood stabilizing drugs; likewise, with the depressed patient, electroconvulsive therapy (ECT) is more effective than pharmacotherapy.[14] Cotard syndrome resulting from an adverse drug reaction to valacyclovir is attributed to elevated serum concentration of one of valacyclovir's metabolites, 9-carboxymethoxymethylguanine (CMMG). Successful treatment warrants cessation of the drug, valacyclovir. Hemodialysis was associated with timely clearance of CMMG and resolution of symptoms.

See also

References

  1. ↑ Berrios G.E. and Luque R. (1995) Cotard's delusion or syndrome?. Comprehensive Psychiatry 36: 218–223
  2. ↑ Berrios G.E. and Luque R. (1995) Cotard Syndrome: Clinical Analysis of 100 Cases. Acta Psychiatrica Scandinavica 91:185–188
  3. ↑ Cotard's syndrome at Who Named It?
  4. ↑ Berrios G.E. & Luque R. (1999) Cotard's 'On Hypochondriacal Delusions in a Severe form of Anxious Melancholia. History of Psychiatry 10:269–278.
  5. ↑ Debruyne H., et al., "Cotard's syndrome: a review", Curr Psychiatry Rep. 2009 Jun;11(3):197–202; http://www.ncbi.nlm.nih.gov/pubmed/19470281
  6. ↑ Hans Debruyne, et al., "Cotard's Syndrome", Mind & Brain 2011; 2:(1). July 2011
  7. ↑ Yarnada, K.; Katsuragi, S.; Fujii, I. (13 November 2007). "A Case Study of Cotard's syndrome: Stages and Diagnosis". Acta Psychiatrica Scandinavica 100 (5): 396–398. doi:10.1111/j.1600-0447.1999.tb10884.x.
  8. ↑ Young, A.W., Robertson, I.H., Hellawell, D.J., de, P.K.W., & Pentland, B. (January 01, 1992). Cotard delusion after Brain Injury. Psychological Medicine, 22, 3, 799–804.
  9. ↑ Young, A.W.; Leafhead, K.M. (1996). "Betwixt Life and Death: Case Studies of the Cotard Delusion". In Halligan, P.W.; Marshall, J.C. Method in Madness: Case studies in Cognitive Neuropsychiatry. Hove: Psychology Press. p. 155.
  10. ↑ Mendhekar, D. N., & Gupta, N. (January 01, 2005). "Recurrent Postictal Depression with Cotard delusion." Indian Journal of Pediatrics, 72, 6, 529–31.
  11. 1 2 Pearn, J.; Gardner-Thorpe, C (May 14, 2002). "Jules Cotard (1840–1889) His Life and the Unique Syndrome that bears his Name". Neurology (abstract) 58 (9): 1400–3. doi:10.1212/wnl.58.9.1400. PMID 12011289.
  12. ↑ Joseph, AB; O'Leary, DH (Oct 1986). "Brain Atrophy and Interhemispheric fissure Enlargement in Cotard's syndrome.". The Journal of Clinical Psychiatry 47 (10): 518–20. PMID 3759917.
  13. ↑ Anders Helldén, Ingegerd Odar-Cederlöf, Kajsa Larsson, Ingela Fehrman-Ekholm, Thomas Lindén (December 2007). "Death Delusion" (Journal Article). BMJ 335 (7633): 1305–1305. doi:10.1136/bmj.39408.393137.BE. PMC 2151143. PMID 18156240.
  14. ↑ Debruyne H., Portzky M., Van den Eynde F., Audenaert K. (June 2010). "Cotard's syndrome: A Review". Current Psychiatric Reports (review article) 11 (3): 197–202. doi:10.1007/s11920-009-0031-z. PMID 19470281.
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