The human brain is a complex piece of machinery allowing humans to see, read, write, think, talk, walk, and complete many other tasks. Occasionally areas of the brain get damaged and stop working properly. Generally if the occipital lobe is damaged, vision is lost. If the frontal lobe is damaged, making wise decisions is out of the question. If the parietal lobe is damaged, the senses serve no purpose. And if the temporal lobe is damaged, processing auditory information is impossible. Within these sections of the brain lie deeper structures that, if damaged, can lead to many psychological disorders. One of these is called Cotard’s syndrome, AKA Cotard delusion, or walking corpse syndrome.
Cotard’s syndrome causes individuals to have delusions of being dead, nonexistent, decaying, or losing their blood or internal organs. There are 3 classifications of Cotard’s syndrome: psychotic depression, Cotard type I, and Cotard type II. Psychotic depression causes delusions and hallucinations, and social impairment. Cotard type I causes delusions. Cotard type II causes anxiety, depression, and auditory hallucinations. The majority of patients who have Cotard’s syndrome comprise the subcategories of psychotic depression and Cotard type II.
Psychotic depression is a form of Cotard’s syndrome that causes patients to experience extreme melancholia, psychosis, delusions of being dead or rotting, paranoia, and hallucinations. “Barbara” a 46 year old female with Cotard’s syndrome described herself as “a dead plant. All the organs inside me have rotten… I haven’t slept for years… I have no blood… I have no heart, it doesn’t beat anymore… I’m not alive anymore” (Vaxevanis and Vidalis 42). She believed that because she was not living she did not have to take care of herself. Patients with psychotic depression may self mutilate, attempt suicide, or fail to take care of themselves and may experience extreme hallucinations, making them highly dangerous to themselves.
Cotard type I consists of individuals without depression or other diseases and “comprises a ‘pure’ Cotard’s syndrome whose nosology is closer to delusional disorders” (Griffiths). Patients with this form of Cotard’s syndrome are less likely to self mutilate or commit suicide and are more likely to experience extreme delusions that alter their perceptions of themselves, such as being immortal, which can be fatal.
Cotard type II is a “mixed group” that consists of individuals who have anxiety, depression, and auditory hallucinations. Similar to psychotic depression, patients are likely to self mutilate or commit suicide. Patients may also hear voices or sounds that are not actually present, which can cause them to be dangerous to others. “Michael”, a 35 year old male, claimed that “he was born ‘without a mind’, meaning that his head is empty without a brain and for this reason he is retarded”, and after he was given medication for treatment he stopped taking it and justified his decision by stating that “because I don’t have a brain, medication could not react” (Vaxevanis and Vidalis 42-43).
Delusional paralysis is another variant of Cotard’s syndrome that causes patients to believe that their body parts are paralyzed when they are not. Symptoms may include logorrhea, or excessive and often incoherent wordiness, and mourning and depressive moods. “Maria”, a 71 year old female, said “‘my feet and legs, my hands, my cervical, vertebra, head, and my back are paralysed by drugs… if the paralysis progresses, I fear my hands, feet and legs will have to be amputated.’ In striking contrast to her complaints, she was psychomotorically agitated and far from being paralysed” (Reif, Murach, and Pfuhlmann 219). Delusional paralysis is often related to psychotic depression although it is unique in the delusions that it creates.
According to studies completed in Hong Kong, 2 out of 349 patients were diagnosed with Cotard’s syndrome suggesting a prevalence of .57% that was increased to 3.2% when depressed elderly were included (Debruyne et al. 68), classifying advanced age as a risk factor. The prevalences presented in this study suggest the importance of completing further research on Cotard’s syndrome so the increasing pervasiveness of the disorder can be addressed before it gets out of hand.
Studying the brains of patients with Cotard’s syndrome has helped researchers discover causes or biological factors of the disorder. Examinations show that Cotard’s syndrome is closely linked to problems with the frontal and parietal lobes. In 1986 the first structural imaging study was performed using Computed Tomography (CT), in which Cotard’s syndrome was associated with multifocal brain shrinkage and interhemispheric enlargement (Debruyne et al. 69). One study showed that individuals with Cotard’s syndrome had more brain atrophy, particularly in the frontal lobe, compared to individuals without the syndrome (Joseph and O’Leary 518-20). An article written by Filimonova discussing the effects of Cotard’s syndrome on the brain unveils the discovery of activity in significant parts of the frontal and parietal lobes that was so low in patients with Cotard’s syndrome that it resembled a person in vegetative state, yet individuals with Cotard are able to communicate and function like normal people. Damage to certain areas of the frontal and parietal lobes of patients promotes the belief they are dead, further explained by Debruyne et al., specifying that “a lack of differential autonomic response to anything is suggested, [which] can lead to the delusion of being dead [because patients are unable] to reject the hypothesis ‘I’m dead’” (69). Psychological factors play a role in the development of Cotard’s syndrome as well.
Psychological factors of Cotard’s syndrome include the depersonalization phenomenon and premorbid personality characteristics as illustrated in the image above. Stated by Debruyne et al., the depersonalization phenomenon is an essential step in the development of Cotard’s syndrome. Depersonalization was elaborated in the Cotard’s syndrome context using the German terms ‘Leib’, meaning body for me, and ‘Korper’, meaning body as such. When ‘Korper’ prevails over ‘Leib’ and when the body is less associated with ‘Leib’, depersonalization may occur (Debruyne et al. 69), meaning that, because patients are presenting dissociation, they are able to convince themselves that they are dead. “In the development of bizarre psychiatric syndromes related to parietal brain dysfunction the role of premorbid personality characteristics is essential, [and] with regard to this premorbid personality characteristic, it is proposed that in Cotard’s syndrome, patients with a more internal attributional style are more vulnerable to develop the syndrome”(Debruyne et al. 69). Premorbid personality characteristics are factors that influence physical or cognitive health and are affected by attributional style, the way that individuals make inferences about the causes and effects of events and behavior in order to understand their experiences. Individuals who have a more internal attributional style are more vulnerable to Cotard’s syndrome because they infer that events and behaviors occur because of personal factors such as traits, abilities, or feelings; therefore, their perceptions have a more negative impact on them psychologically resulting in negative feelings and delusions towards themselves leading to depression, a symptom that is present in both psychotic depression and Cotard type II. For example, a person acquiring a more internal attributional style is likely to respond to his/her car breaking down with the conclusion that the car breaking down was his/her fault. Premorbid personality characteristics are the least likely cause of Cotard type I because Cotard type I is predominantly associated with delusions. Many theories for causes of Cotard’s syndrome have been discussed and evaluated by researchers, but there is still not enough information to create an exact treatment plan specifically designed for Cotard’s syndrome, although options do exist.
There are two main treatment options for Cotard's syndrome: pharmacotherapy and electroconvulsive therapy (ECT). In a case report of Cotard’s syndrome Ms. L was treated with a combination of olanzapine, escitalopram, and lorazepam, after which she “expressed hopefulness about her future and a desire to participate in psychiatric follow-up care” (Ruminjo and Mekinulov). Pharmacotherapy treatment is most effective in patients with Cotard type I and II. Monotherapy has been reported to be effective, but combination strategies are generally used (Debruyne et al. 70). If pharmacotherapy does not work patients are advised to complete ECT treatment, an effective method of treatment for patients with Cotard type psychotic depression as well as a variety of other severe mental illnesses. It is a safer procedure than it used to be but is still associated with short term side effects, such as headaches and muscle pain that go away shortly after each treatment, and long term side effects that impair cognition and memory (Freedman and Duckworth), making it somewhat controversial. Before ECT treatment the patient is given general anesthesia and a muscle relaxant. Electrodes are placed on the patient’s scalp and a controlled electric current is applied causing a brief seizure in the brain. Because the muscles are relaxed movement is limited. During the treatment patients are monitored carefully. Minutes later the patient wakes up with no recollection of the treatment and is momentarily confused (“Electroconvulsive Therapy”). Depending on what stage of Cotard the patient is in, treatment may not work, and severe distress may lead to suicide (Debruyne et al. 70). In most publications regarding Cotard’s syndrome prognosis is not discussed and seems to vary from patients getting remarkably better to developing severe chronic conditions. More information regarding the development of Cotard’s syndrome is essential to improving treatment and creating more predictable prognoses. In the case of Ms. L, pharmacotherapy treatment helped dramatically because it allowed her to recover enough to want to seek out psychiatric help, but other patients may not be so lucky.
Research shows Cotard’s syndrome is a serious, life threatening condition that should be examined further so individuals know more about it and get proper treatment. There are many forms of Cotard’s syndrome that affect patients in somewhat different but similar ways. Delusions and hallucinations are the main symptoms, but others such as depression and anxiety occur in most cases. There are many biological and psychological factors of Cotard’s syndrome, such as frontal lobe damage, premorbid personality characteristics, and depersonalization. Currently the only treatment options available to patients are pharmacotherapy and electroconvulsive therapy. Prognosis is unpredictable because not much is known about the causes of Cotard’s syndrome. With further research the causes of Cotard’s syndrome may become clearer, more treatment options may become available, and a more predictable, and hopefully positive, prognosis may arise.
Works Cited
Debruyne, Hans, Michael Portzky, Kathelijne Peremans, and Kurt Audenaert. "Cotard's
Syndrome." Mind & Brain, The Journal of Psychiatry 2.1 (2011): 67-72. Web. 30 Sept. 2014.
"Electroconvulsive Therapy." Cleveland Clinic. The Cleveland Clinic Foundation, n.d. Web. 21
Oct. 2014.
Filimonova, Yana. "Cotard's Syndrome: Living without the Brain." English Pravda.ru.
Pravda.Ru, 13 June 2013. Web. 30 Sept. 2014.
Freedman, Jacob L., and Ken Duckworth. "Electroconvulsive Therapy (ECT)." NAMI. N.p., July
2012. Web. 11 Oct. 2014.
Griffiths, Mark. "Dead Man Walking: A Beginner's Guide to Cotard's Syndrome."
Drmarkgriffiths. N.p., 15 June 2012. Web. 30 Sept. 2014.
Joseph, AB, and O'Leary, DH. "Brain Atrophy and Interhemispheric Fissure Enlargement in
Cotard's Syndrome." The Journal of Clinical Psychiatry 47.10 (1986): 518-20. Web. 11 Oct. 2014.
Reif, Andreas, Waldemar M. Murach, and Bruno Pfuhlmann. "Delusional Paralysis: An Unusual
Variant of Cotard's Syndrome." ResearchGate. N.p., 10 Apr. 2003. Web. 11 Oct. 2014.
Ruminjo, Anne, and Boris Mekinulov. "Dear Editor." National Center for Biotechnology
Information. U.S. National Library of Medicine, 27 Nov. 0005. Web. 24 Sept. 2014.
Vaxevanis, A., and A. Vidalis. "Cotard’s Syndrome. A Three-case Report." 9.1 (2005): 41-44.
Web. 30 Sept. 2014.
Cotard’s syndrome causes individuals to have delusions of being dead, nonexistent, decaying, or losing their blood or internal organs. There are 3 classifications of Cotard’s syndrome: psychotic depression, Cotard type I, and Cotard type II. Psychotic depression causes delusions and hallucinations, and social impairment. Cotard type I causes delusions. Cotard type II causes anxiety, depression, and auditory hallucinations. The majority of patients who have Cotard’s syndrome comprise the subcategories of psychotic depression and Cotard type II.
Psychotic depression is a form of Cotard’s syndrome that causes patients to experience extreme melancholia, psychosis, delusions of being dead or rotting, paranoia, and hallucinations. “Barbara” a 46 year old female with Cotard’s syndrome described herself as “a dead plant. All the organs inside me have rotten… I haven’t slept for years… I have no blood… I have no heart, it doesn’t beat anymore… I’m not alive anymore” (Vaxevanis and Vidalis 42). She believed that because she was not living she did not have to take care of herself. Patients with psychotic depression may self mutilate, attempt suicide, or fail to take care of themselves and may experience extreme hallucinations, making them highly dangerous to themselves.
Cotard type I consists of individuals without depression or other diseases and “comprises a ‘pure’ Cotard’s syndrome whose nosology is closer to delusional disorders” (Griffiths). Patients with this form of Cotard’s syndrome are less likely to self mutilate or commit suicide and are more likely to experience extreme delusions that alter their perceptions of themselves, such as being immortal, which can be fatal.
Cotard type II is a “mixed group” that consists of individuals who have anxiety, depression, and auditory hallucinations. Similar to psychotic depression, patients are likely to self mutilate or commit suicide. Patients may also hear voices or sounds that are not actually present, which can cause them to be dangerous to others. “Michael”, a 35 year old male, claimed that “he was born ‘without a mind’, meaning that his head is empty without a brain and for this reason he is retarded”, and after he was given medication for treatment he stopped taking it and justified his decision by stating that “because I don’t have a brain, medication could not react” (Vaxevanis and Vidalis 42-43).
Delusional paralysis is another variant of Cotard’s syndrome that causes patients to believe that their body parts are paralyzed when they are not. Symptoms may include logorrhea, or excessive and often incoherent wordiness, and mourning and depressive moods. “Maria”, a 71 year old female, said “‘my feet and legs, my hands, my cervical, vertebra, head, and my back are paralysed by drugs… if the paralysis progresses, I fear my hands, feet and legs will have to be amputated.’ In striking contrast to her complaints, she was psychomotorically agitated and far from being paralysed” (Reif, Murach, and Pfuhlmann 219). Delusional paralysis is often related to psychotic depression although it is unique in the delusions that it creates.
According to studies completed in Hong Kong, 2 out of 349 patients were diagnosed with Cotard’s syndrome suggesting a prevalence of .57% that was increased to 3.2% when depressed elderly were included (Debruyne et al. 68), classifying advanced age as a risk factor. The prevalences presented in this study suggest the importance of completing further research on Cotard’s syndrome so the increasing pervasiveness of the disorder can be addressed before it gets out of hand.
Studying the brains of patients with Cotard’s syndrome has helped researchers discover causes or biological factors of the disorder. Examinations show that Cotard’s syndrome is closely linked to problems with the frontal and parietal lobes. In 1986 the first structural imaging study was performed using Computed Tomography (CT), in which Cotard’s syndrome was associated with multifocal brain shrinkage and interhemispheric enlargement (Debruyne et al. 69). One study showed that individuals with Cotard’s syndrome had more brain atrophy, particularly in the frontal lobe, compared to individuals without the syndrome (Joseph and O’Leary 518-20). An article written by Filimonova discussing the effects of Cotard’s syndrome on the brain unveils the discovery of activity in significant parts of the frontal and parietal lobes that was so low in patients with Cotard’s syndrome that it resembled a person in vegetative state, yet individuals with Cotard are able to communicate and function like normal people. Damage to certain areas of the frontal and parietal lobes of patients promotes the belief they are dead, further explained by Debruyne et al., specifying that “a lack of differential autonomic response to anything is suggested, [which] can lead to the delusion of being dead [because patients are unable] to reject the hypothesis ‘I’m dead’” (69). Psychological factors play a role in the development of Cotard’s syndrome as well.
Psychological factors of Cotard’s syndrome include the depersonalization phenomenon and premorbid personality characteristics as illustrated in the image above. Stated by Debruyne et al., the depersonalization phenomenon is an essential step in the development of Cotard’s syndrome. Depersonalization was elaborated in the Cotard’s syndrome context using the German terms ‘Leib’, meaning body for me, and ‘Korper’, meaning body as such. When ‘Korper’ prevails over ‘Leib’ and when the body is less associated with ‘Leib’, depersonalization may occur (Debruyne et al. 69), meaning that, because patients are presenting dissociation, they are able to convince themselves that they are dead. “In the development of bizarre psychiatric syndromes related to parietal brain dysfunction the role of premorbid personality characteristics is essential, [and] with regard to this premorbid personality characteristic, it is proposed that in Cotard’s syndrome, patients with a more internal attributional style are more vulnerable to develop the syndrome”(Debruyne et al. 69). Premorbid personality characteristics are factors that influence physical or cognitive health and are affected by attributional style, the way that individuals make inferences about the causes and effects of events and behavior in order to understand their experiences. Individuals who have a more internal attributional style are more vulnerable to Cotard’s syndrome because they infer that events and behaviors occur because of personal factors such as traits, abilities, or feelings; therefore, their perceptions have a more negative impact on them psychologically resulting in negative feelings and delusions towards themselves leading to depression, a symptom that is present in both psychotic depression and Cotard type II. For example, a person acquiring a more internal attributional style is likely to respond to his/her car breaking down with the conclusion that the car breaking down was his/her fault. Premorbid personality characteristics are the least likely cause of Cotard type I because Cotard type I is predominantly associated with delusions. Many theories for causes of Cotard’s syndrome have been discussed and evaluated by researchers, but there is still not enough information to create an exact treatment plan specifically designed for Cotard’s syndrome, although options do exist.
There are two main treatment options for Cotard's syndrome: pharmacotherapy and electroconvulsive therapy (ECT). In a case report of Cotard’s syndrome Ms. L was treated with a combination of olanzapine, escitalopram, and lorazepam, after which she “expressed hopefulness about her future and a desire to participate in psychiatric follow-up care” (Ruminjo and Mekinulov). Pharmacotherapy treatment is most effective in patients with Cotard type I and II. Monotherapy has been reported to be effective, but combination strategies are generally used (Debruyne et al. 70). If pharmacotherapy does not work patients are advised to complete ECT treatment, an effective method of treatment for patients with Cotard type psychotic depression as well as a variety of other severe mental illnesses. It is a safer procedure than it used to be but is still associated with short term side effects, such as headaches and muscle pain that go away shortly after each treatment, and long term side effects that impair cognition and memory (Freedman and Duckworth), making it somewhat controversial. Before ECT treatment the patient is given general anesthesia and a muscle relaxant. Electrodes are placed on the patient’s scalp and a controlled electric current is applied causing a brief seizure in the brain. Because the muscles are relaxed movement is limited. During the treatment patients are monitored carefully. Minutes later the patient wakes up with no recollection of the treatment and is momentarily confused (“Electroconvulsive Therapy”). Depending on what stage of Cotard the patient is in, treatment may not work, and severe distress may lead to suicide (Debruyne et al. 70). In most publications regarding Cotard’s syndrome prognosis is not discussed and seems to vary from patients getting remarkably better to developing severe chronic conditions. More information regarding the development of Cotard’s syndrome is essential to improving treatment and creating more predictable prognoses. In the case of Ms. L, pharmacotherapy treatment helped dramatically because it allowed her to recover enough to want to seek out psychiatric help, but other patients may not be so lucky.
Research shows Cotard’s syndrome is a serious, life threatening condition that should be examined further so individuals know more about it and get proper treatment. There are many forms of Cotard’s syndrome that affect patients in somewhat different but similar ways. Delusions and hallucinations are the main symptoms, but others such as depression and anxiety occur in most cases. There are many biological and psychological factors of Cotard’s syndrome, such as frontal lobe damage, premorbid personality characteristics, and depersonalization. Currently the only treatment options available to patients are pharmacotherapy and electroconvulsive therapy. Prognosis is unpredictable because not much is known about the causes of Cotard’s syndrome. With further research the causes of Cotard’s syndrome may become clearer, more treatment options may become available, and a more predictable, and hopefully positive, prognosis may arise.
Works Cited
Debruyne, Hans, Michael Portzky, Kathelijne Peremans, and Kurt Audenaert. "Cotard's
Syndrome." Mind & Brain, The Journal of Psychiatry 2.1 (2011): 67-72. Web. 30 Sept. 2014.
"Electroconvulsive Therapy." Cleveland Clinic. The Cleveland Clinic Foundation, n.d. Web. 21
Oct. 2014.
Filimonova, Yana. "Cotard's Syndrome: Living without the Brain." English Pravda.ru.
Pravda.Ru, 13 June 2013. Web. 30 Sept. 2014.
Freedman, Jacob L., and Ken Duckworth. "Electroconvulsive Therapy (ECT)." NAMI. N.p., July
2012. Web. 11 Oct. 2014.
Griffiths, Mark. "Dead Man Walking: A Beginner's Guide to Cotard's Syndrome."
Drmarkgriffiths. N.p., 15 June 2012. Web. 30 Sept. 2014.
Joseph, AB, and O'Leary, DH. "Brain Atrophy and Interhemispheric Fissure Enlargement in
Cotard's Syndrome." The Journal of Clinical Psychiatry 47.10 (1986): 518-20. Web. 11 Oct. 2014.
Reif, Andreas, Waldemar M. Murach, and Bruno Pfuhlmann. "Delusional Paralysis: An Unusual
Variant of Cotard's Syndrome." ResearchGate. N.p., 10 Apr. 2003. Web. 11 Oct. 2014.
Ruminjo, Anne, and Boris Mekinulov. "Dear Editor." National Center for Biotechnology
Information. U.S. National Library of Medicine, 27 Nov. 0005. Web. 24 Sept. 2014.
Vaxevanis, A., and A. Vidalis. "Cotard’s Syndrome. A Three-case Report." 9.1 (2005): 41-44.
Web. 30 Sept. 2014.