Depressed, delusional, and ‘dead’

History: Suddenly Speechless

Mr. P, age 52, is transferred to our behavioral health unit after 1 month of unsuccessful treatment at a psychiatric hospital. He is mute and disheveled with blunted affect.

Before his hospitalization, Mr. P—who is mildly retarded and has an IQ of 67—lived independently, managed his finances, held two part-time jobs, volunteered as an usher at church, and had a girlfriend. He has been medically stable with diagnoses of indolent stage-zero chronic lymphocytic leukemia (for which he took no medication), moderate obesity, and essential hypertension. For 2 years he has been taking reserpine, 0.25 mg/d, for hypertension, and weighs 200 lb at presentation (body mass index: 29 kg/m²). He has no history of mental illness.

Seven months ago, Mr. P began having trouble dressing and bathing. He also began eating considerably less—about one-third of his normal food intake—and lost 20 lbs over 6 months.

Mr. P also began standing in the street for hours at a time—calling out to passers-by that people were dying and he was causing their deaths—until family members persuaded him to return home. He was not hallucinating, but his brother—who is Mr. P’s legal guardian—said symptoms worsened after a family friend died. After Mr. P became mute, resistant to direction, and immobile, his brother got him admitted to the psychiatric hospital.

The attending physician stopped reserpine—which might cause depression—and started hydrochlorothiazide, 25 mg/d, to maintain normal blood pressure. A psychiatrist diagnosed major depressive disorder and psychosis not otherwise specified, and prescribed mirtazapine, 30 mg nightly, and quetiapine, 25 mg bid. The psychiatrist ruled out lethal catatonia, as vital signs remained stable. When Mr. P’s symptoms did not improve after 1 month, the psychiatrist recommended electroconvulsive therapy (ECT) and transferred him to our facility.

Physical examination and laboratory findings are normal except for lymphocytosis secondary to leukemia:

poll here

The authors’ observations

Mr. P. has major depression with psychotic features. His staring, catalepsy, negativism, selective mutism, and posturing indicate catatonia, and his nihilistic delusions signal Cotard’s syndrome, a delusional depressive disorder.

Catatonia consists of changes in muscle tone and activity and is accompanied by echopraxia and echolalia. Many medical conditions or medications can cause catatonia (Table 1).¹ Resultant immobility and stupor can lead to contractures, pressure ulcers, venous thrombosis, and pulmonary emboli. Refusal to eat or drink can cause malnutrition, dehydration, weight loss, and muscle wasting. Approximately 9% of psychiatric inpatients develop catatonia at some point.²

DSM-IV-TR³ describes catatonia criteria as specifiers in affective illness and requires two or more of the following features for diagnosis:

• catalepsy or stupor
  
• purposeless, excessive motor activity
  
• negativism or mutism
  
• peculiar voluntary behaviors, such as posturing, stereotypy, or mannerisms
  
• echolalia or echopraxia (Table 2).
  

No consensus exists regarding which behaviors are pathognomonic or how long they must persist to meet criteria for catatonia.

Catatonia can occur during an excited or retarded state:

• Excited catatonia—also called delirious mania or an oneiroid state—is marked by a dreamlike sensorium, rapid onset, confabulation, derealization, depersonalization, disorientation, and a mixture of catatonic features.⁴
  
• Retarded catatonia can be diagnosed using DSM-IV-TR criteria for catatonia. In mild cases or early in presentation, symptoms resemble anergy and psychomotor slowing typical of depression.
  

Lethal catatonia—a rare, extreme, potentially life-threatening form—is clinically indistinguishable from neuroleptic malignant syndrome. Its cause is often toxic or iatrogenic.⁵ Hyperthermia, hypertension, tachycardia, fever, tachypnea, leukocytosis, and serum creatine phosphokinase >500 u/L indicate lethal catatonia.

Table 1

Recognized causes of catatonia

Affective disorders and schizophrenia CNS injury or infection (such as encephalitis) Lupus cerebritis Medications (bupropion, disulfiram, fluoroquinolones, neuroleptics, steroids) Metabolic imbalance Porphyria Seizure disorders Substance abuse (cocaine, phencyclidine)

Table 2

Catatonia: Defining clinical characteristics

Term	Definition
Ambitendency	Indecision, hesitance, becoming stuck regarding stimuli
Analgesia to painful stimuli	Failure to feel or withdraw from pain
Catalepsy	Posturing, including facial expressions such as exaggerated lip puckering, with waxy flexibility and automatic obedience
Echolalia	Repeating words and phrases
Echopraxia	Repeating another person’s movements
Excitement	Loquacious confabulation and autonomic instability
Mannerisms	Purposeful eccentric movements, such as saluting
Negativism	Rigidity and resistance to commands
Perseveration	Continuing a response long after it is appropriate
Prosectic speech	Decreased production and volume of speech
Selective mutism	Absence of speech
Stereotypy	Persistently repeating gestures that do not appear goal-directed, such as head-banging, rocking, and twirling objects
Verbigeration	Repeating a word, phrase, or sentence

In Cotard’s syndrome (Table 3), the patient might believe that he and others around him are dead, that his body is putrefying and missing internal organs and blood, or that the world no longer exists.⁶ Some patients also have delusions of negation and damnation.⁷

Cotard’s syndrome, first described in the late 1800s by French neurologist Jules Cotard, can accompany folie à deux⁷ or lycanthropy, the delusional belief that one has been transformed into a werewolf.⁸ In rare cases, patients believe that their bodies are abnormally enlarged.⁷ Cotard’s syndrome can exist alone or as part of a psychiatric illness with nihilistic delusions.⁷

 

poll hereTable 3

Characteristics of Cotard’s syndrome

Delusional belief that one’s body parts, friends, family, money, or the world do not exist Can accompany major depression, schizophrenia, dementia, or a general medical condition Relatively rare, with unknown incidence and prevalence. More common during late middle life and among women Sudden onset with no history of psychiatric disorder Associated with nondominant parietal lobe lesions and catatonia

The authors’ observations

Mr. P.’s episode appears to have been idiopathic.

Reserpine could have caused his decompensation, though precisely how is unclear. The medication is alleged to cause depression by depleting serotonin, dopamine, and norepinephrine, but some researchers believe it exacerbates pre-existing depression.^9,10

When treating any patient with a history of depression, find out if he or she is taking reserpine. Advise the primary care physician to discontinue the drug if the patient is self-deprecating or despondent, or reports early morning insomnia, loss of appetite, or impotence.¹¹

Treatment: False Start

To address Mr. P’s catatonia, we stop quetiapine and mirtazapine and start IM lorazepam, 2 mg qid. After 4 days his condition is stable, but he still believes that he and everyone else is dead.

poll here

The authors’ observations

Parenteral benzodiazepines typically are used to treat patients with catatonia and Cotard’s syndrome while the clinician searches for a toxic or medical cause. Most patients with nonemergent catatonia respond to a benzodiazepine.¹²

Although opinion differs on starting dosages of IM lorazepam in retarded catatonia, we recommend 2 mg IM and repeat doses every 3 hours if the patient does not respond.^4,13 Lack of response after 20 mg (10 doses) warrants ECT.⁴

Consider ECT—which has shown effectiveness for treating both catatonia and Cotard’s syndrome in case reports^6-8,14,15—as first-line treatment in emergent catatonia. Do not try a first- or second-generation neuroleptic, which can worsen clinical outcome.

Treatment: a Three-Week Trial

We receive informed consent from Mr. P’s brother to try 10 ECT treatments over 3 weeks. We choose left anterior right temporal electrode placement to minimize cognitive interference,¹⁶ and give Mr. P glycopyrrolate, 0.2 mg before each treatment, to manage bradycardia resulting from enhanced vagal tone after electrical stimulation. According to ECT protocol, we administer the anesthetic methohexital, 0.75 to 1.0 mg/kg, and the muscle relaxant succinylcholine, 0.5 to 1 mg/kg, to shorten seizure duration during ECT.

Mr. P also receives forced ventilation at each treatment to counteract brief succinylcholine-induced paralysis of the diaphragm and other muscle tissue. Stimulus intensity begins at 35% and is increased to 50% as the patient’s seizure threshold increases. Each morning, Mr. P also receives extended-release venlafaxine, 225 mg, for depressive symptoms, and hydrochlorothiazide, 25 mg.

After the first ECT treatment, Mr. P’s affect starts to brighten. He speaks a few words after the third treatment and begins eating larger portions by the fifth treatment. After the last treatment, he is performing activities of daily living, talking readily and coherently, and playing basketball with peers. He shows no adverse cognitive effects or other complications from ECT.

The authors’ observations

Although little evidence guides treatment of catatonia in the developmentally disabled,¹⁷ we support early use of ECT in those with serious refractory mental illness.¹⁸ Some clinicians hesitate to administer ECT to patients with mental retardation because they might be particularly vulnerable to adverse medication effects.¹⁹ ECT, however, has been found to cause minimal side effects in this population²⁰ and does not cause or exacerbate brain damage.²¹

If the patient is mentally incapable of consenting to ECT, obtain informed consent from his or her legal guardian.

Conclusion: Leaving the Hospital

We discharge Mr. P after 25 days. He shows no evidence of psychosis, suicidality, or intent to harm others. He continues hydrochlorothiazide and venlafaxine at the same dosages. He returns home with his brother, and 6 months later is functioning well.

Related resources

• National Mental Health Association. Electroconvulsive therapy. www.nmha.org/infoctr/factsheets/ect.cfm.
  

Drug brand names

• Bupropion • Wellbutrin
  
• Disulfiram • Antabuse
  
• Glycopyrrolate • Robinul
  
• Hydrochlorothiazide • Various
  
• Lorazepam • Ativan
  
• Methohexital • Brevital
  
• Mirtazapine • Remeron
  
• Quetiapine • Seroquel
  
• Reserpine • Serpasil
  
• Succinylcholine • Anectine
  
• Venlafaxine XR • Effexor XR
  

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

History: Suddenly Speechless

Mr. P, age 52, is transferred to our behavioral health unit after 1 month of unsuccessful treatment at a psychiatric hospital. He is mute and disheveled with blunted affect.

Before his hospitalization, Mr. P—who is mildly retarded and has an IQ of 67—lived independently, managed his finances, held two part-time jobs, volunteered as an usher at church, and had a girlfriend. He has been medically stable with diagnoses of indolent stage-zero chronic lymphocytic leukemia (for which he took no medication), moderate obesity, and essential hypertension. For 2 years he has been taking reserpine, 0.25 mg/d, for hypertension, and weighs 200 lb at presentation (body mass index: 29 kg/m²). He has no history of mental illness.

Seven months ago, Mr. P began having trouble dressing and bathing. He also began eating considerably less—about one-third of his normal food intake—and lost 20 lbs over 6 months.

Mr. P also began standing in the street for hours at a time—calling out to passers-by that people were dying and he was causing their deaths—until family members persuaded him to return home. He was not hallucinating, but his brother—who is Mr. P’s legal guardian—said symptoms worsened after a family friend died. After Mr. P became mute, resistant to direction, and immobile, his brother got him admitted to the psychiatric hospital.

The attending physician stopped reserpine—which might cause depression—and started hydrochlorothiazide, 25 mg/d, to maintain normal blood pressure. A psychiatrist diagnosed major depressive disorder and psychosis not otherwise specified, and prescribed mirtazapine, 30 mg nightly, and quetiapine, 25 mg bid. The psychiatrist ruled out lethal catatonia, as vital signs remained stable. When Mr. P’s symptoms did not improve after 1 month, the psychiatrist recommended electroconvulsive therapy (ECT) and transferred him to our facility.

Physical examination and laboratory findings are normal except for lymphocytosis secondary to leukemia:

poll here

The authors’ observations

Mr. P. has major depression with psychotic features. His staring, catalepsy, negativism, selective mutism, and posturing indicate catatonia, and his nihilistic delusions signal Cotard’s syndrome, a delusional depressive disorder.

Catatonia consists of changes in muscle tone and activity and is accompanied by echopraxia and echolalia. Many medical conditions or medications can cause catatonia (Table 1).¹ Resultant immobility and stupor can lead to contractures, pressure ulcers, venous thrombosis, and pulmonary emboli. Refusal to eat or drink can cause malnutrition, dehydration, weight loss, and muscle wasting. Approximately 9% of psychiatric inpatients develop catatonia at some point.²

DSM-IV-TR³ describes catatonia criteria as specifiers in affective illness and requires two or more of the following features for diagnosis:

• catalepsy or stupor
  
• purposeless, excessive motor activity
  
• negativism or mutism
  
• peculiar voluntary behaviors, such as posturing, stereotypy, or mannerisms
  
• echolalia or echopraxia (Table 2).
  

No consensus exists regarding which behaviors are pathognomonic or how long they must persist to meet criteria for catatonia.

Catatonia can occur during an excited or retarded state:

• Excited catatonia—also called delirious mania or an oneiroid state—is marked by a dreamlike sensorium, rapid onset, confabulation, derealization, depersonalization, disorientation, and a mixture of catatonic features.⁴
  
• Retarded catatonia can be diagnosed using DSM-IV-TR criteria for catatonia. In mild cases or early in presentation, symptoms resemble anergy and psychomotor slowing typical of depression.
  

Lethal catatonia—a rare, extreme, potentially life-threatening form—is clinically indistinguishable from neuroleptic malignant syndrome. Its cause is often toxic or iatrogenic.⁵ Hyperthermia, hypertension, tachycardia, fever, tachypnea, leukocytosis, and serum creatine phosphokinase >500 u/L indicate lethal catatonia.

Table 1

Recognized causes of catatonia

Affective disorders and schizophrenia CNS injury or infection (such as encephalitis) Lupus cerebritis Medications (bupropion, disulfiram, fluoroquinolones, neuroleptics, steroids) Metabolic imbalance Porphyria Seizure disorders Substance abuse (cocaine, phencyclidine)

Table 2

Catatonia: Defining clinical characteristics

Term	Definition
Ambitendency	Indecision, hesitance, becoming stuck regarding stimuli
Analgesia to painful stimuli	Failure to feel or withdraw from pain
Catalepsy	Posturing, including facial expressions such as exaggerated lip puckering, with waxy flexibility and automatic obedience
Echolalia	Repeating words and phrases
Echopraxia	Repeating another person’s movements
Excitement	Loquacious confabulation and autonomic instability
Mannerisms	Purposeful eccentric movements, such as saluting
Negativism	Rigidity and resistance to commands
Perseveration	Continuing a response long after it is appropriate
Prosectic speech	Decreased production and volume of speech
Selective mutism	Absence of speech
Stereotypy	Persistently repeating gestures that do not appear goal-directed, such as head-banging, rocking, and twirling objects
Verbigeration	Repeating a word, phrase, or sentence

In Cotard’s syndrome (Table 3), the patient might believe that he and others around him are dead, that his body is putrefying and missing internal organs and blood, or that the world no longer exists.⁶ Some patients also have delusions of negation and damnation.⁷

Cotard’s syndrome, first described in the late 1800s by French neurologist Jules Cotard, can accompany folie à deux⁷ or lycanthropy, the delusional belief that one has been transformed into a werewolf.⁸ In rare cases, patients believe that their bodies are abnormally enlarged.⁷ Cotard’s syndrome can exist alone or as part of a psychiatric illness with nihilistic delusions.⁷

 

poll hereTable 3

Characteristics of Cotard’s syndrome

Delusional belief that one’s body parts, friends, family, money, or the world do not exist Can accompany major depression, schizophrenia, dementia, or a general medical condition Relatively rare, with unknown incidence and prevalence. More common during late middle life and among women Sudden onset with no history of psychiatric disorder Associated with nondominant parietal lobe lesions and catatonia

The authors’ observations

Mr. P.’s episode appears to have been idiopathic.

Reserpine could have caused his decompensation, though precisely how is unclear. The medication is alleged to cause depression by depleting serotonin, dopamine, and norepinephrine, but some researchers believe it exacerbates pre-existing depression.^9,10

When treating any patient with a history of depression, find out if he or she is taking reserpine. Advise the primary care physician to discontinue the drug if the patient is self-deprecating or despondent, or reports early morning insomnia, loss of appetite, or impotence.¹¹

Treatment: False Start

To address Mr. P’s catatonia, we stop quetiapine and mirtazapine and start IM lorazepam, 2 mg qid. After 4 days his condition is stable, but he still believes that he and everyone else is dead.

poll here

The authors’ observations

Parenteral benzodiazepines typically are used to treat patients with catatonia and Cotard’s syndrome while the clinician searches for a toxic or medical cause. Most patients with nonemergent catatonia respond to a benzodiazepine.¹²

Although opinion differs on starting dosages of IM lorazepam in retarded catatonia, we recommend 2 mg IM and repeat doses every 3 hours if the patient does not respond.^4,13 Lack of response after 20 mg (10 doses) warrants ECT.⁴

Consider ECT—which has shown effectiveness for treating both catatonia and Cotard’s syndrome in case reports^6-8,14,15—as first-line treatment in emergent catatonia. Do not try a first- or second-generation neuroleptic, which can worsen clinical outcome.

Treatment: a Three-Week Trial

We receive informed consent from Mr. P’s brother to try 10 ECT treatments over 3 weeks. We choose left anterior right temporal electrode placement to minimize cognitive interference,¹⁶ and give Mr. P glycopyrrolate, 0.2 mg before each treatment, to manage bradycardia resulting from enhanced vagal tone after electrical stimulation. According to ECT protocol, we administer the anesthetic methohexital, 0.75 to 1.0 mg/kg, and the muscle relaxant succinylcholine, 0.5 to 1 mg/kg, to shorten seizure duration during ECT.

Mr. P also receives forced ventilation at each treatment to counteract brief succinylcholine-induced paralysis of the diaphragm and other muscle tissue. Stimulus intensity begins at 35% and is increased to 50% as the patient’s seizure threshold increases. Each morning, Mr. P also receives extended-release venlafaxine, 225 mg, for depressive symptoms, and hydrochlorothiazide, 25 mg.

After the first ECT treatment, Mr. P’s affect starts to brighten. He speaks a few words after the third treatment and begins eating larger portions by the fifth treatment. After the last treatment, he is performing activities of daily living, talking readily and coherently, and playing basketball with peers. He shows no adverse cognitive effects or other complications from ECT.

The authors’ observations

Although little evidence guides treatment of catatonia in the developmentally disabled,¹⁷ we support early use of ECT in those with serious refractory mental illness.¹⁸ Some clinicians hesitate to administer ECT to patients with mental retardation because they might be particularly vulnerable to adverse medication effects.¹⁹ ECT, however, has been found to cause minimal side effects in this population²⁰ and does not cause or exacerbate brain damage.²¹

If the patient is mentally incapable of consenting to ECT, obtain informed consent from his or her legal guardian.

Conclusion: Leaving the Hospital

We discharge Mr. P after 25 days. He shows no evidence of psychosis, suicidality, or intent to harm others. He continues hydrochlorothiazide and venlafaxine at the same dosages. He returns home with his brother, and 6 months later is functioning well.

Related resources

• National Mental Health Association. Electroconvulsive therapy. www.nmha.org/infoctr/factsheets/ect.cfm.
  

Drug brand names

• Bupropion • Wellbutrin
  
• Disulfiram • Antabuse
  
• Glycopyrrolate • Robinul
  
• Hydrochlorothiazide • Various
  
• Lorazepam • Ativan
  
• Methohexital • Brevital
  
• Mirtazapine • Remeron
  
• Quetiapine • Seroquel
  
• Reserpine • Serpasil
  
• Succinylcholine • Anectine
  
• Venlafaxine XR • Effexor XR
  

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

History: Suddenly Speechless

Mr. P, age 52, is transferred to our behavioral health unit after 1 month of unsuccessful treatment at a psychiatric hospital. He is mute and disheveled with blunted affect.

Before his hospitalization, Mr. P—who is mildly retarded and has an IQ of 67—lived independently, managed his finances, held two part-time jobs, volunteered as an usher at church, and had a girlfriend. He has been medically stable with diagnoses of indolent stage-zero chronic lymphocytic leukemia (for which he took no medication), moderate obesity, and essential hypertension. For 2 years he has been taking reserpine, 0.25 mg/d, for hypertension, and weighs 200 lb at presentation (body mass index: 29 kg/m²). He has no history of mental illness.

Seven months ago, Mr. P began having trouble dressing and bathing. He also began eating considerably less—about one-third of his normal food intake—and lost 20 lbs over 6 months.

Mr. P also began standing in the street for hours at a time—calling out to passers-by that people were dying and he was causing their deaths—until family members persuaded him to return home. He was not hallucinating, but his brother—who is Mr. P’s legal guardian—said symptoms worsened after a family friend died. After Mr. P became mute, resistant to direction, and immobile, his brother got him admitted to the psychiatric hospital.

The attending physician stopped reserpine—which might cause depression—and started hydrochlorothiazide, 25 mg/d, to maintain normal blood pressure. A psychiatrist diagnosed major depressive disorder and psychosis not otherwise specified, and prescribed mirtazapine, 30 mg nightly, and quetiapine, 25 mg bid. The psychiatrist ruled out lethal catatonia, as vital signs remained stable. When Mr. P’s symptoms did not improve after 1 month, the psychiatrist recommended electroconvulsive therapy (ECT) and transferred him to our facility.

Physical examination and laboratory findings are normal except for lymphocytosis secondary to leukemia:

poll here

The authors’ observations

Mr. P. has major depression with psychotic features. His staring, catalepsy, negativism, selective mutism, and posturing indicate catatonia, and his nihilistic delusions signal Cotard’s syndrome, a delusional depressive disorder.

Catatonia consists of changes in muscle tone and activity and is accompanied by echopraxia and echolalia. Many medical conditions or medications can cause catatonia (Table 1).¹ Resultant immobility and stupor can lead to contractures, pressure ulcers, venous thrombosis, and pulmonary emboli. Refusal to eat or drink can cause malnutrition, dehydration, weight loss, and muscle wasting. Approximately 9% of psychiatric inpatients develop catatonia at some point.²

DSM-IV-TR³ describes catatonia criteria as specifiers in affective illness and requires two or more of the following features for diagnosis:

• catalepsy or stupor
  
• purposeless, excessive motor activity
  
• negativism or mutism
  
• peculiar voluntary behaviors, such as posturing, stereotypy, or mannerisms
  
• echolalia or echopraxia (Table 2).
  

No consensus exists regarding which behaviors are pathognomonic or how long they must persist to meet criteria for catatonia.

Catatonia can occur during an excited or retarded state:

• Excited catatonia—also called delirious mania or an oneiroid state—is marked by a dreamlike sensorium, rapid onset, confabulation, derealization, depersonalization, disorientation, and a mixture of catatonic features.⁴
  
• Retarded catatonia can be diagnosed using DSM-IV-TR criteria for catatonia. In mild cases or early in presentation, symptoms resemble anergy and psychomotor slowing typical of depression.
  

Lethal catatonia—a rare, extreme, potentially life-threatening form—is clinically indistinguishable from neuroleptic malignant syndrome. Its cause is often toxic or iatrogenic.⁵ Hyperthermia, hypertension, tachycardia, fever, tachypnea, leukocytosis, and serum creatine phosphokinase >500 u/L indicate lethal catatonia.

Table 1

Recognized causes of catatonia

Affective disorders and schizophrenia CNS injury or infection (such as encephalitis) Lupus cerebritis Medications (bupropion, disulfiram, fluoroquinolones, neuroleptics, steroids) Metabolic imbalance Porphyria Seizure disorders Substance abuse (cocaine, phencyclidine)

Table 2

Catatonia: Defining clinical characteristics

Term	Definition
Ambitendency	Indecision, hesitance, becoming stuck regarding stimuli
Analgesia to painful stimuli	Failure to feel or withdraw from pain
Catalepsy	Posturing, including facial expressions such as exaggerated lip puckering, with waxy flexibility and automatic obedience
Echolalia	Repeating words and phrases
Echopraxia	Repeating another person’s movements
Excitement	Loquacious confabulation and autonomic instability
Mannerisms	Purposeful eccentric movements, such as saluting
Negativism	Rigidity and resistance to commands
Perseveration	Continuing a response long after it is appropriate
Prosectic speech	Decreased production and volume of speech
Selective mutism	Absence of speech
Stereotypy	Persistently repeating gestures that do not appear goal-directed, such as head-banging, rocking, and twirling objects
Verbigeration	Repeating a word, phrase, or sentence

In Cotard’s syndrome (Table 3), the patient might believe that he and others around him are dead, that his body is putrefying and missing internal organs and blood, or that the world no longer exists.⁶ Some patients also have delusions of negation and damnation.⁷

Cotard’s syndrome, first described in the late 1800s by French neurologist Jules Cotard, can accompany folie à deux⁷ or lycanthropy, the delusional belief that one has been transformed into a werewolf.⁸ In rare cases, patients believe that their bodies are abnormally enlarged.⁷ Cotard’s syndrome can exist alone or as part of a psychiatric illness with nihilistic delusions.⁷

 

poll hereTable 3

Characteristics of Cotard’s syndrome

Delusional belief that one’s body parts, friends, family, money, or the world do not exist Can accompany major depression, schizophrenia, dementia, or a general medical condition Relatively rare, with unknown incidence and prevalence. More common during late middle life and among women Sudden onset with no history of psychiatric disorder Associated with nondominant parietal lobe lesions and catatonia

The authors’ observations

Mr. P.’s episode appears to have been idiopathic.

Reserpine could have caused his decompensation, though precisely how is unclear. The medication is alleged to cause depression by depleting serotonin, dopamine, and norepinephrine, but some researchers believe it exacerbates pre-existing depression.^9,10

When treating any patient with a history of depression, find out if he or she is taking reserpine. Advise the primary care physician to discontinue the drug if the patient is self-deprecating or despondent, or reports early morning insomnia, loss of appetite, or impotence.¹¹

Treatment: False Start

To address Mr. P’s catatonia, we stop quetiapine and mirtazapine and start IM lorazepam, 2 mg qid. After 4 days his condition is stable, but he still believes that he and everyone else is dead.

poll here

The authors’ observations

Parenteral benzodiazepines typically are used to treat patients with catatonia and Cotard’s syndrome while the clinician searches for a toxic or medical cause. Most patients with nonemergent catatonia respond to a benzodiazepine.¹²

Although opinion differs on starting dosages of IM lorazepam in retarded catatonia, we recommend 2 mg IM and repeat doses every 3 hours if the patient does not respond.^4,13 Lack of response after 20 mg (10 doses) warrants ECT.⁴

Consider ECT—which has shown effectiveness for treating both catatonia and Cotard’s syndrome in case reports^6-8,14,15—as first-line treatment in emergent catatonia. Do not try a first- or second-generation neuroleptic, which can worsen clinical outcome.

Treatment: a Three-Week Trial

We receive informed consent from Mr. P’s brother to try 10 ECT treatments over 3 weeks. We choose left anterior right temporal electrode placement to minimize cognitive interference,¹⁶ and give Mr. P glycopyrrolate, 0.2 mg before each treatment, to manage bradycardia resulting from enhanced vagal tone after electrical stimulation. According to ECT protocol, we administer the anesthetic methohexital, 0.75 to 1.0 mg/kg, and the muscle relaxant succinylcholine, 0.5 to 1 mg/kg, to shorten seizure duration during ECT.

Mr. P also receives forced ventilation at each treatment to counteract brief succinylcholine-induced paralysis of the diaphragm and other muscle tissue. Stimulus intensity begins at 35% and is increased to 50% as the patient’s seizure threshold increases. Each morning, Mr. P also receives extended-release venlafaxine, 225 mg, for depressive symptoms, and hydrochlorothiazide, 25 mg.

After the first ECT treatment, Mr. P’s affect starts to brighten. He speaks a few words after the third treatment and begins eating larger portions by the fifth treatment. After the last treatment, he is performing activities of daily living, talking readily and coherently, and playing basketball with peers. He shows no adverse cognitive effects or other complications from ECT.

The authors’ observations

Although little evidence guides treatment of catatonia in the developmentally disabled,¹⁷ we support early use of ECT in those with serious refractory mental illness.¹⁸ Some clinicians hesitate to administer ECT to patients with mental retardation because they might be particularly vulnerable to adverse medication effects.¹⁹ ECT, however, has been found to cause minimal side effects in this population²⁰ and does not cause or exacerbate brain damage.²¹

If the patient is mentally incapable of consenting to ECT, obtain informed consent from his or her legal guardian.

Conclusion: Leaving the Hospital

We discharge Mr. P after 25 days. He shows no evidence of psychosis, suicidality, or intent to harm others. He continues hydrochlorothiazide and venlafaxine at the same dosages. He returns home with his brother, and 6 months later is functioning well.

Related resources

• National Mental Health Association. Electroconvulsive therapy. www.nmha.org/infoctr/factsheets/ect.cfm.
  

Drug brand names

• Bupropion • Wellbutrin
  
• Disulfiram • Antabuse
  
• Glycopyrrolate • Robinul
  
• Hydrochlorothiazide • Various
  
• Lorazepam • Ativan
  
• Methohexital • Brevital
  
• Mirtazapine • Remeron
  
• Quetiapine • Seroquel
  
• Reserpine • Serpasil
  
• Succinylcholine • Anectine
  
• Venlafaxine XR • Effexor XR
  

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.