COTARD'S SYNDROME (COTARD'S DELUSION) - TYPES, CAUSE , SYMPTOMS, TREATMENT , CASES, AND A DETAILED OVERVIEW
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| Figure 1 |
- History:
- What the disease is?
Cotard's syndrome is a rare neuropsychiatric condition characterized by anxious melancholia, delusions of non-existence concerning one's own body to the extent of delusions of immortality. It has been most commonly seen in patients with severe depression. However, now it is thought to be less common possibly due to early institution of treatment in patients with severe depression with psychotic symptoms.
- Alternative names
👉Cotard’s delusion; Cotard’s syndrome (described 1880; attributed 1893)
👉 Le délire des négations
👉 nihilistic delusional disorder
👉 Walking corpse syndrome
- Three types of Cotard’s syndrome (CS) exist and each type may need to be treated differently and has different therapeutic implications.
1) The psychotic depression type: includes individuals with melancholia and a few nihilistic delusions.
2) The Cotard type I: includes individuals with no depression or other disease and comprises a “pure” CS whose nosology (the branch of medical science dealing with the classification of diseases.) is closer to delusional disorders.
3) The Cotard type II: includes individuals with anxiety, depression and auditory hallucinations and comprise a mixed group.
- The core concept of Cotard’s syndrome is a delusion of negation and classically progresses through three stages:
1. Germination Stage – symptoms of psychotic depression and hypochondria
2. Blooming Stage – full development of the syndrome and the appearance of the delusions of negation
3. Chronic Stage – severe delusions with chronic depressive symptoms
It is most common in patients with underlying schizophrenia and psychosis and patients often withdraw from society and the outside world. Partly because of the delusions and partly due to personal neglect of appearance and hygiene. There is no DSM-V (Diagnostic and Statistical Manual of Mental Disorders, DSM–5) diagnosis for Cotard’s syndrome, so it falls under the category of somatic delusions.
- Symptoms
People with this syndrome often become much less social. Sometimes, they may stop speaking at all. Some hear voices that tell them they're dead or dying.
Others may refuse to eat (because, among other reasons, they see no point since they're "dead"). Some may try to harm themselves.
In one well-documented case of Cotard's syndrome reported in 2008, a 53-year-old woman was admitted to the hospital after her family called 911. They said the woman believed that she was dead and smelled like rotting fish. She also asked to be taken to a morgue because she wanted to be with dead people.
- Causes
It's not clear what causes Cotard's syndrome. We do know that it's often a symptom of a deeper medical problem that affects the brain, such as:
👉 Dementia
👉 Encephalopathy (a disease where a virus or toxin affects how your brain works)
👉 Epilepsy
👉 Migraine
👉 Multiple sclerosis
👉 Parkinson’s disease
👉 Stroke
👉 Bleeding that happens outside the brain because of a severe brain injury (your doctor may call it subdural bleeding)
Some experts think Cotard's syndrome results from two types of brain damage. The first changes the way people view themselves. The second makes them continue to believe this false view, even when they’re shown it’s not true. Not everyone agrees with this idea, though.
- Who Gets It?
Cotard's syndrome can happen at almost any age, though it strikes many people in their early 50s. Many people who have it also have a history of mental health problems, especially:
👉Depression
👉Anxiety
👉 Schizophrenia
👉 Substance abuse
Most have some kind of brain damage that shows up on imaging tests. The harm may come from:
👉 A stroke
👉 A tumor
👉 A blood clot
👉 An injury
Additionally, Cotard's syndrome may cause bipolar disorder in teens and young adults.
- Pathophysiology
The underlying neurophysiology and psychopathology of Cotard syndrome might be related to problems of delusional misidentification. Neurologically, Cotard's delusion (negation of the Self) is thought to be related to 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.
The theoretical explanations to the delusions in this syndrome vary (Figure 1) and can be divided into two groups:
(a) a “one-stage” or experimental model, where delusions may be normal reasoning in response to an abnormal perception and
(b) a “two-stage” or inferential model, where delusions are caused by abnormal reasoning in response to an abnormal perception defend the two-stage model.
It is believe that delusions in Cotard’s and Capgras syndromes are related due to their neurological and psychological similarities in reported cases. Neurophysiologists propose that delusions in Cotard’s and Capgras syndromes reflect an interaction of failures at two levels: i) abnormal perceptual experiences and an incorrect interpretation of these. The authors suggest that delusions in Capgras syndrome are due to damage to the neuroanatomical pathways responsible for proper emotional response to familiar visual stimuli. A similar process could be responsible for the delusions of Cotard’s syndrome, in which patients say that they “feel nothing inside,” so the essential difference between these delusions would not be the experience, but the wrong forms in which they are rationalized, being in Capgras an external attributional style (“He is an impostor”), while in Cotard an internal attributional style (“I’m dead”). On the contrary, Gerrans, a scientist, defends the one-stage model; he argues that delusions can only be explained in terms of an abnormal experience and that the apparently abnormal reasoning shown in the two-stage model describes normal reasoning processes. He also criticizes the proposal of Young et al.
(that Cotard’s and Capgras delusions would be intimately related). Gerrans cites Ramachandran and Blakeslee, for whom both these delusional experiences are fundamentally different due to their lack of affective response in several areas. In Cotard’s syndrome the absence of a global affective response would happen due to a disconnection of all sensitive areas of the limbic system, resulting in a complete lack of emotional contact with the world. In Capgras syndrome however this would be restricted to facial recognition.
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| Figure: 2 Theoretical explanations of Cotard and Capgras delusions. Source: Case Report Cotard’s Syndrome in a Patient with Schizophrenia: Case Report and Review of the Literature Jeff Huarcaya-Victoria,1,2 Mario Ledesma-Gastañadui,2 and Maria Huete-Cordova Volume 2016, Article ID 6968409, 7 pages http://dx.doi.org/10.1155/2016/6968409 |
- Treatment
Doctors have many ways to treat Cotard's syndrome. The usual approach is to treat the medical problem that's causing it.
Most people do best with a combination of medication and a form of talk therapy, like cognitive behavioral therapy (CBT) or psychotherapy. Both of these provide a safe place for people to talk about how they feel and help them find healthier ways to think and act.
Medicines used to treat Cotard's syndrome include:
👉Antipsychotics
👉Antianxiety drugs
👉Antidepressants
Most people need more than one type.
If medicines and talk therapy don't help, electroconvulsive therapy (ECT) is an option. It sends small electric currents through the brain. This changes the brain’s chemistry and may clear some mental health symptoms.
ECT can cause side effects like memory loss and confusion. So it’s often a last resort.
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| Figure: 3 Axial Brain Scans Highlighting Areas of Large Vascular Lesions in Three Patients With Cotard Delusions |
The image shows large vascular lesions in three patients with Cotard delusion, including a chronic right-middle cerebral artery territory infarction with frontal-temporal lobe encephalomalacia and gliosis in patient (A), a chronic right corona radiata lacunar infarct with associated hemosiderin in patient (B), and bilateral cerebral hemisphere infarcts involving both frontal lobes anteriorly and both occipital lobes in patient (C). L=Left side of the image.
- Case studies:
Since it is such a rare syndrome there are few case reports, but I managed to find a few to make a clearer image on this syndrome.
1) Cotard’s Syndrome after motorcycle accident
A well known (and it can be found on Wikipedia) case study is the one that describes a patient who suffered brain injury after an accident. He is taken by his mother in South Africa where he believes that he has died of septicemia (he reads a story about a person with AIDS who died of septicemia) or an overdose of a yellow fever injection and went to hell. His explication for his mother’s presence is the fact that he had “borrowed my mother's spirit to show me round hell".
2) Homeless Man presenting Cotard’s syndrome
A 44-a year old man became homeless because he couldn’t find a job. He developed depression in jail and because he was unable to pay for psychiatric services the symptoms worsened in six weeks.
While the mild phase of his illness was characterized by poor sleep, loss of appetite, and anergia, when things got worse he felt like he “melted away” and he was dead. He was then diagnosed with schizophrenia and treated with oral and depot haloperidol; in another few weeks his condition worsened again. He now believed that his “brain rotted away” and his internal organs were gone but he had no suicidal ideation. Although electroconvulsive therapy is efficacious in the treatment of this illness, he did not receive this treatment as he was unable to pay for such services.
He managed to continue his treatment with haloperidol and valproic acid doses tapered, 40 mg of fluoxetine, and 3 mg of risperidone a day. He made slow progress and was discharged with no recurrence of his delusions.
3) Bipolar Disorder patient with Cotard’s Syndrome
20 year old male diagnosed with bipolar disorder due to three manic episodes but without any depressive episodes (also had family history of bipolar disorder). His treatment consisted in lithium carbonate, 800mg/day. However, his condition worsened in only two weeks; he became isolated and entered a depression phased characterized by loss of appetite and psychomotor retardation. Nihilistic delusions appeared shortly: “my liver and stomach are being destroyed”, “my heart doesn’t beat”, “I don’t have muscles”, “I am dead”.
There was no pathology in the brain CT, laboratory assessment was within normal levels, physical examination was normal and he was admitted with bipolar disorder, severe depressive episode with psychotic symptoms. His treatment was changed and 225 mg of imipramine was added. However, this made his condition even worse: he became mute, refused to eat or drink and presented psychomotor inhibition and catatonic stupor. ECT (electroconvulsive therapy) was administered and the patient’s condition improved; however, the family stopped the sessions.
After discontinuing ECT, the patient’s condition worsened again, this time presenting the following symptoms: slowness in movement and speech and hypochondriacal delusions. The delusions consisted in: he belied that his tonsils were deteriorating, his heart was smaller and his muscles were degenerating.
The author states that after adding haloperidol 8mg/day, biperiden 4mg/day the symptoms began to improve and the patient was discharged 14 days later with almost full remission.
4) Ms. L, a 53-year-old Filipino woman, was admitted to the psychiatric unit when her family called 911 because the patient was complaining that she was dead, smelled like rotting flesh, and wanted to be taken to a morgue so that she could be with dead people. Upon interview in the hospital, the patient expressed fear that “paramedics” were trying to burn down the house where she was living with her cousin and her brother. She also admitted to hopelessness, low energy, decreased appetite, and somnolence.
Ms. L reported that she had been on antidepressants while in the Philippines (where she had resided for the last 18 years, having moved to the US only a month ago), but could not recall the name or dosage of the medication.
After organic causes were ruled out, treatment with quetiapine and bupropione SR was started. The patient was initially reluctant to take medication or eat. She subsequently developed an electrolyte imbalance (hypokalemia and hyponatremia), which necessitated intravenous electrolyte repletion. The patient was also isolative, spending much of the day in bed and neglecting her personal hygiene and grooming.
With her family’s support, the decision was made to take the patient to court for treatment over objection. Subsequently, the patient’s medication regimen was bupropion SR and olanzapine (intramuscular if she refused the oral form). A few days later, the patient had a questionable syncopal versus seizure episode, necessitating transfer to a medical unit.
After three days, she returned to the psychiatry floor where her medication regimen included olanzapine, escitalopram (because of the questionable seizure on bupropion), and lorazepam (for agitation).
Ms. L showed improvement in symptoms over one month on olanzapine 25mg daily, escitalopram 20mg daily, and lorazepam 2mg daily. At discharge she denied nihilistic or paranoid delusions and hallucinations and expressed hopefulness about her future and a desire to participate in psychiatric follow-up care.
- References:
1. https://doi.org/10.1176/appi.neuropsych.17010018
2. http://downloads.hindawi.com/journals/crips/2016/6968409.pdf
3. https://www.journalofneuropsychiatry.cl/docs/3/17.pdf
4. https://www.webmd.com/schizophrenia/cotards-syndrome#2
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