cotard's syndrome, often paired with capgras, is a neurological disorder in which a person becomes dissociated from their identity. researching cotard's is not recommended at night--- i wrote this inquiry for my cognition course, while everyone else wrote about mirror neurons and wernicke's region. bonus fact = your nostrils are asymmetrical (one is bigger than the other) so that you can smell more accurately. now, hope you never get this syndrome:
Cotard syndrome in relation to underlying conditions or severe brain trauma in which regions of the brain relevant in sensory recognition are impaired
Cotard’s syndrome is a rare neuropsychiatric disorder, in which the patient suffers varying degrees of depression and nihilistic delusions (denial of their own sense of self and the existence of the external world) due to the dissociation of outer and inner sensations/perceptions (Swamy, 2007). These delusions may include a feeling of immortality/supernatural abilities, lack of organs/body parts, belief of being dead/possessed, etc. (Berrios, 1995). Patients often experience a wide range of sensory hallucinations; McKay’s patient described persistent tactile (sensation of running water on the forearm), visual (moving walls), and auditory (disco music) hallucinations. CS generally occurs as a seeming offshoot of severe depression and seems to be more prevalent in older women (Berrios, 1995; Helen, 1995). Although also in younger age groups, the return to normalcy/degradation in insistence of delusions is much better in young patients (Berrios, 1995). There are three general stages of CS: germination (prodromal period of depressive and hypochondriacal symptoms), blooming (full blown development in which delusions begin to appear), and chronic (chronic depressive/delusional type) (Swamy, 2007). CS is similar to other neuropsychological conditions such as Bipolar disorder in that it works on a spectrum; three main types, which are paired with the stages, of CS have been culled from this spectrum: psychotic depression/germination (mostly depressive with few nihilistic delusions), Cotard type I/chronic (mostly delusions, mildly depressive), and Cotard type II/blooming (mixed depression, anxiety, and hallucinations); a patient with extreme CS is considered to be type I, while mild patients are considered to have psychotic depression (Swamy, 2007). This range of intensity lead early observers to believe CS was therefore a loose term for the diffuse, non-specific symptoms related to more concrete, definable conditions (Berrios, 1995).
CS is often paired with underlying conditions such as schizophrenia, bipolar disorder, depression, temporal lobe epilepsy, typhoid fever, and brain tumors/injuries (Duggal, 2002). This long list of common concurrent conditions for patients with CS is not surprising due to their shared symptoms (hallucinations/delusions of grandeur in schizophrenia and bipolar disorder, which could be compared with the sense of immortality extreme patients exhibit; depression; lesions of the [temporal] lobe). The problem with underlying conditions, especially these which have such particular commonalities, is their role as inevitable confounding factors, which results in a near impossibility to extricate specific attributes and origins of CS (Swamy, 2007). However, although depression is seen as a major component in CS staging, McKay’s study included a control subject with a higher test level of depression than the CS subject; the control subject did not show any signs of delusion and tested more similarly to the other control subjects. And so depression in itself obviously does not trigger delusions, but rather, as is supposed, serves as a strong context for which CS to spring from. As of yet, categorization of CS is therefore not clearly defined, which is why CS was originally thought of as a subtype of depression. CS has also been posited as a syndrome that is defined only in relation to certain conditions (may be triggered by these conditions, if the patient is predisposed) and as an independent, distinct entity in itself, although this is hard to defend with clinical case studies (Swamy, 2007; Berrios, 1995). The most rational approach to a categorization of CS is as a derivative of other, associated conditions. The development of CS in the context of other disorders and traumas would seem to be the most logical if it weren’t for another, more specific attribute of CS. 
CS is often associated with Capgras delusion, another neurological disorder, because of their possession of a certain, shared neurological quirk: an impairment of face identification (Swamy, 2007). Both are involved in different aspects of misidentification; Capgras delusion patients believe identical imposters have replaced the people around them, while CS symptoms of detachment from the self and the external world stem from the recognition of their own face in other people; patients undergo a derealization due to the resulting lack of association between their own face and self (Swamy, 2007; Berrios, 1995; Bulter, 2000). CS patients often show impairment of facial-recognition during Warrington Recognition Memory Tests (Swamy, 2007; McKay, 2006). This impairment in CS is related to a disconnect between areas that recognize faces and associate facial emotion (Swamy, 2007); the fusiform face areas in the visual cortex and limbic structures are both involved in face recognition and therefore have become important in the specific study of CS (Butler, 2000). In a study by Butler, a patient co-exhibited CS and Capgras after severe brain injury, which resulted in sustained trauma to the right thalamus and left basal ganglia, bilateral ventricular hemorrhaging, and injury to the pituitary stalk. The thalamus and basal ganglia relate to the symptoms of CS in their relay of sensory and motor signals (misinterpreted sensations and perceptions [especially visual]; moments of paralysis). Ventricular damage further exaggerates CS because of its relative position near limbic structures and general interconnectivity to regions of the brain. The pituitary stalk is interesting in the context of CS because of its connection to the hypothalamus, which, among other things, controls sensations of hunger and sleep. In multiple studies, some observed in the mid-19th century by psychiatrists Leuret, Morel, and Baillarger, even before the eponymous Cotard, CS is prefaced by depressive symptoms like poor sleep and appetite (Duggal, 2002; Berrios, 1995; Helen, 1995); the intensification of this lack of regulation leads to the delusions of supernatural status (patients no longer feel the need to eat or sleep, and usually die of starvation). It is no surprise extreme CS delusions of complete separation from the self/everything follow errors in sensory perception because of the (impaired) brain’s scramble to rationalize irrational input.
Important in injuries to the brain is their relation to
dysfunction of identification; CS sufferers’ negation of certain body parts and
organs especially points towards parietal and temporal lobe impairment (Duggal,
2002; Joseph, 1986; Young, 1992). Lesions of the parietal lobe would lead to
neuropsychological abnormalities due to this lobe’s role in spatial relations;
the patient would no longer be able to locate himself and familiar objects in
relation to his old self and therefore no longer feel grounded in reality
(Joseph, 1986). The temporal lobe’s role can especially be seen in relation to
auditory hallucinations (prevalent in type II) and face and familiar object
recognition by the fusiform face area; The limbic system, and especially the
amygdala, too seems to be essential for overall recognition abnormalities
because CS patients seem to have total disruption of all sensory input, which
causes the total lack of the self’s relation to reality (McKay, 2006). When
given CT scans, CS patients, in comparison to controls, show noted differences,
the most common abnormalities being bilateral cerebral atrophy,
sylvian/interhemispheric fissure enlargement, and dilation of lateral ventricles
(Joseph, 1986). However, CT/MRI scans and EEGs of CS patients more often read
as normal, which further muddles the search for clear distinctions between CS
and other, underlying organic/neurological conditions (Gardner-Thorpe, 2004;
Swamy, 2007).
A patient, normal according to CT scans,
experienced temporary instances of delusion over a period of 20 years; she
would awake at night, afraid her flesh was falling off her body, but then feel
normal again in the morning (Gardner-Thorpe, 2004). The intermittent
recurrences of CS symptoms for this patient are interesting in that she does
not experience delusions full-blown, 24/7; she has moments of irrational
thinking, but then reverts back to a normal sense of self and surrounding
reality. This patient was also actually aware of her abnormal thoughts, as
compared to Butler’s, whom was unable to encode or recall any delusions due to
his CS or Capgras (which, Butler proposes, is why he was able to return to a
sense of reality). Many CS patients described have unrelenting symptoms, which
eventually attenuate due to pharmacological and/or monotherapeutic strategies,
but this woman continued to experience random moments of CS despite treatment
(Gardner-Thorpe, 2004). The trigger of her symptoms and especially why they
seem to be prevalent at night are intriguing for further study, but as CS is
such a rare phenomenon, another patient like Gardner-Thorpe’s is unlikely to
appear again for comparative study. The fact too, that this patient was also an
older female leads one to wonder why this is the prevalent demographic amongst
CS patients; why across geographic/cultural/religious distinctions (Helen’s
study of patients in Hong Kong showed great similarities to Western patients
despite following Taoist philosophy) the CS delusions and (usual) attenuation
of said delusions are similar. The similarity of experiences in CS patients is
doubly confounding because of the seemingly diffuse locations of
disruption/impairment in the brain. The search for specific areas that may cause
CS, whether with underlying neurological/organic conditions or with sustained
brain trauma, may in fact be fruitless because it may be a derivative symptom
rather than independent entity.
- Berrios GE, Luque R. 1995. Cotard’s delusion or syndrome?: a conceptual history. Comprehensive Psychiatry 36(3): 218-223
- Butler PV. 2000. Diurnal variation in Cotard’s syndrome (copresent with Capgras delusion) following traumatic brain injury. Australian and New Zealand Journal of Psychiatry 34: 684-687.
- Duggal HS, Jagadheesan K, Haque Nizamie S. 2002. Biological basis and staging of Cotard’s syndrome. Eur Psychiatry 17: 108-109
- Gardner-Thorpe C, Pearn J. 2004. The Cotard syndrome. Report of two patients: with a review of the extended spectrum of ‘délire des négations’. European Journal of Neurology 11: 563-566.
- Helen FK, Chiu MRC. 1995. Cotard’s syndrome in psychogeriatric patients in Hong Kong. General Hospital Psychiatry 17: 54-55.
- Joseph AB, O’Leary DH. 1986. Brain Atrophy and Interhemispheric Fissure Enlargement in Cotard’s Syndrome. J Clin Psychiatry 47(10): 518-520
- McKay R, Cipolotti L. 2006. Attributional style in a case of Cotard delusion. Consciousness and Cognition 16: 349-359.
- Swamy NCK, Sanju G, Jaimon M. 2007. An overview of the neurological correlates of Cotard syndrome. Eur. J. Psychiat. 21(2): 99-116.
- Young AW, Robertson IH, Hellawell DJ, De Pauw KW, Pentland B. 1992. Cotard delusion after brain injury. Psychological Medicine 22: 799-804.
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