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Cefepime: Underrecognized Cause of NCSE
Hospitalized patients with sepsis or severe nosocomial infections are frequently treated empirically with broad‐spectrum antibiotics. Cefepime hydrochloride, a fourth‐generation cephalosporin, is a common antibiotic of first choice. Its proconvulsant properties are well described in the literature,1, 2 but its importance as a potential cause of change in mental status is probably underestimated. We report a case of change in mental status related to nonconvulsive status epilepticus (NCSE) caused by the use of cefepime in an elderly, hospitalized patient. Our goal is to raise awareness about this uncommon and still underrecognized complication.
Case Report
A 72‐year‐old woman with stage III chronic kidney disease secondary to hypertension with a stable creatinine of 1.5 mg/dL (glomerular filtration rate (GFR) estimated by the modification of diet in renal disease (MDRD) at 36 mL/minute/1.73 m2) was admitted to the hospital for worsening of her chronic back pain. She had a past medical history significant for hyperlipidemia, asthma, and peripheral vascular disease, with breast cancer in remission since 1989. She had no history of seizures or cerebrovascular disease. Her medications were ibuprofen, oxycontin, cilastazol, acetaminophen/oxycodone, and an albuterol/empratropium inhaler. Her physical examination was remarkable only for decreased strength in the right lower extremity. Magnetic resonance imaging (MRI) of the lumbosacral spine showed signs consistent with an inflammatory process at the level of L4‐L5. A computed tomography (CT)‐guided biopsy was performed and confirmed a diagnosis of osteomyelitis on biopsy. Cultures from the biopsy grew Pseudomonas aeruginosa and treatment with intravenous cefepime at a dose of 1 g every 12 hours was initiated. Over the next 3 days, the patient had a gradual worsening of her mental status, leading to pronounced somnolence with occasional episodes of agitation during which she had no focal motor deficits. Her mental status declined to the point of unresponsiveness to simple verbal commands. She had not received any new medications other than cefepime. Her creatinine level was stable throughout this time period at 1.6 mg/dL. No other abnormalities were found on laboratory evaluation or on CT and MRI scans of the brain. An electroencephalogram (EEG) was markedly abnormal due to a generalized background slowing and disorganization with frequent bilateral paroxysmal epileptiform discharges, confirming the clinical diagnosis of subclinical generalized status epilepticus. Given that there were no other intrinsic neurological or metabolic reasons for this mental status change, and given that cefepime was the only new medication added before the patient started deteriorating, cefepime was discontinued and treatment for seizures was started with intravenous benzodiazepines. Over the next 2 days, her mental status returned to normal. She was soon discharged to a rehabilitation center.
Discussion
Beta‐lactam antibiotics have been described to induce seizures due to their direct and/or indirect inhibition of the gamma‐aminobutyric acid (GABA) system.1, 3 Previous experiments have shown a dose‐dependent effect on seizures, and suggest that the cephalosporin with the most pronounced proconvulsant effect is cefazolin.1, 3
Cefepime has been associated with neurological side effects such as headache, confusion, hallucinations, agitation, myoclonus, ataxia, seizures, and coma. Another underrecognized but critical side effect is NSCE. This is defined as seizure activity for more than 30 minutes, with cognitive and behavioral changes, but without convulsive clinical manifestations. This complication has been reported in the literature, but it is probably underrecognized.3‐7 The tendency for cefepime to produce more subclinical activity than the other cephalosporins is not well understood.
Cefepime is mainly eliminated though renal excretion (85%) and displays linear pharmacokinetic properties, thus its dose needs to be adjusted according to renal function. Consequently, in the case of renal dysfunction, accumulation of the drug is proportional to the degree of renal impairment. For NSCE, the most important risk factor is renal impairment, although cases in patients with normal kidney function have been described.36 Age, preexisting central nervous system (CNS) disease, sepsis, and cardiopulmonary bypass have also been reported as possible risk factors for NCSE.1
Cefepime can accumulate in the cerebrospinal fluid (CSF) in the setting of renal dysfunction, decreased protein‐binding capacity (as is sometimes seen in the elderly), and increased blood‐brain permeability in the setting of CNS infections. Accumulation of the drug in the CSF can lead to blockade of the GABA‐A receptor through a mechanism of competitive antagonism1, 8
The onset of NSCE varies between 1 and 16 days after initiation of cefepime therapy.3‐5, 7 It is frequently confused with delirium, since hospitalized patients treated with broad‐spectrum antibiotics such as cefepime frequently have other comorbidities and risk factors for delirium.
This can delay the diagnosis of NSCE due to a lack of awareness of this critical complication in the setting of renal dysfunction. In order to quantify the likelihood that the NSCE was related to cefepime and not to other causes, we calculated a Naranjo adverse drug events probability score, which consists of 9 questions on the relationship between the adverse event and the incriminated drug.9 Each answer is scored from 1 to +2 points. This score was designed to quantify the strength of the association between any adverse event and a pharmacological agent.
In our patient, the Naranjo score was 7 points, suggesting that the diagnosis of cefepime‐induced NCSE was probable.
The diagnosis of NCSE is made through a combination of a high index of clinical suspicion, specific findings on EEG, and improvement with withdrawal of the drug. Fatal outcomes have been reported.5, 6 Early and prompt recognition of the condition is crucial for the prevention of its morbidity and mortality.
The mainstay of treatment is prompt withdrawal of antibiotics and symptomatic treatment with benzodiazepines or barbiturates. Very severe cases with refractory seizures have been treated with hemodialysis. Phenytoin should be avoided as a treatment of this condition due to its lack of GABA‐agonist activity.
Conclusion
Cefepime can cause NCSE, predominantly in patients with renal dysfunction. Its frequency is probably underestimated in hospitalized patients with multiple comorbid conditions. Hospitalists should be aware of this unusual but critical relationship, especially in patients with renal failure. A high level of clinical suspicion and an emergency EEG are essential to obtain a prompt and accurate diagnosis.
- .Antibiotic‐induced convulsions.Crit Care Clin.1997;13:741‐762.
- ,.Cefepime neurotoxicity: case report, pharmacokinetic considerations, and literature review.Pharmacotherapy.2006;26(8):1169‐1174.
- ,,,,.Relationship between structure and convulsant properties of some β‐lactams antibiotics following intracerebroventricular microinjections in rats.Antimicrob Agents Chemother.1995;39:232‐237.
- ,,,,,.Cefepime‐ and cefixime‐induced encephalopathy in a patient with normal renal function.Neurology.2005;65(11):1840.
- ,,, et al.Cefepime induced neurotoxicity: an underestimated complication of antibiotherapy in patients with acute renal failure.Intensive Care Med.2002;28:214‐217.
- ,,,.Nonconvulsive status epilepticus due to cefepime in a patient with normal renal function.Epilepsy Behav.2006;8(1):312‐314.
- ,,, et al.Nonconvulsive status epilepticus associated with cephalosporins in patients with renal failure.Am J Med.2001;111(2):115‐119.
- ,,, et al.Evidence for the involvement of GABA(A) receptor blockade in convulsions induced by cephalosporins.Neuropharmacology.2003;45(3):304‐314.
- ,,, et al.A method for estimating the probability of adverse drug reactions.Clin Pharmacol Ther.1981;30(2):239‐245.
Hospitalized patients with sepsis or severe nosocomial infections are frequently treated empirically with broad‐spectrum antibiotics. Cefepime hydrochloride, a fourth‐generation cephalosporin, is a common antibiotic of first choice. Its proconvulsant properties are well described in the literature,1, 2 but its importance as a potential cause of change in mental status is probably underestimated. We report a case of change in mental status related to nonconvulsive status epilepticus (NCSE) caused by the use of cefepime in an elderly, hospitalized patient. Our goal is to raise awareness about this uncommon and still underrecognized complication.
Case Report
A 72‐year‐old woman with stage III chronic kidney disease secondary to hypertension with a stable creatinine of 1.5 mg/dL (glomerular filtration rate (GFR) estimated by the modification of diet in renal disease (MDRD) at 36 mL/minute/1.73 m2) was admitted to the hospital for worsening of her chronic back pain. She had a past medical history significant for hyperlipidemia, asthma, and peripheral vascular disease, with breast cancer in remission since 1989. She had no history of seizures or cerebrovascular disease. Her medications were ibuprofen, oxycontin, cilastazol, acetaminophen/oxycodone, and an albuterol/empratropium inhaler. Her physical examination was remarkable only for decreased strength in the right lower extremity. Magnetic resonance imaging (MRI) of the lumbosacral spine showed signs consistent with an inflammatory process at the level of L4‐L5. A computed tomography (CT)‐guided biopsy was performed and confirmed a diagnosis of osteomyelitis on biopsy. Cultures from the biopsy grew Pseudomonas aeruginosa and treatment with intravenous cefepime at a dose of 1 g every 12 hours was initiated. Over the next 3 days, the patient had a gradual worsening of her mental status, leading to pronounced somnolence with occasional episodes of agitation during which she had no focal motor deficits. Her mental status declined to the point of unresponsiveness to simple verbal commands. She had not received any new medications other than cefepime. Her creatinine level was stable throughout this time period at 1.6 mg/dL. No other abnormalities were found on laboratory evaluation or on CT and MRI scans of the brain. An electroencephalogram (EEG) was markedly abnormal due to a generalized background slowing and disorganization with frequent bilateral paroxysmal epileptiform discharges, confirming the clinical diagnosis of subclinical generalized status epilepticus. Given that there were no other intrinsic neurological or metabolic reasons for this mental status change, and given that cefepime was the only new medication added before the patient started deteriorating, cefepime was discontinued and treatment for seizures was started with intravenous benzodiazepines. Over the next 2 days, her mental status returned to normal. She was soon discharged to a rehabilitation center.
Discussion
Beta‐lactam antibiotics have been described to induce seizures due to their direct and/or indirect inhibition of the gamma‐aminobutyric acid (GABA) system.1, 3 Previous experiments have shown a dose‐dependent effect on seizures, and suggest that the cephalosporin with the most pronounced proconvulsant effect is cefazolin.1, 3
Cefepime has been associated with neurological side effects such as headache, confusion, hallucinations, agitation, myoclonus, ataxia, seizures, and coma. Another underrecognized but critical side effect is NSCE. This is defined as seizure activity for more than 30 minutes, with cognitive and behavioral changes, but without convulsive clinical manifestations. This complication has been reported in the literature, but it is probably underrecognized.3‐7 The tendency for cefepime to produce more subclinical activity than the other cephalosporins is not well understood.
Cefepime is mainly eliminated though renal excretion (85%) and displays linear pharmacokinetic properties, thus its dose needs to be adjusted according to renal function. Consequently, in the case of renal dysfunction, accumulation of the drug is proportional to the degree of renal impairment. For NSCE, the most important risk factor is renal impairment, although cases in patients with normal kidney function have been described.36 Age, preexisting central nervous system (CNS) disease, sepsis, and cardiopulmonary bypass have also been reported as possible risk factors for NCSE.1
Cefepime can accumulate in the cerebrospinal fluid (CSF) in the setting of renal dysfunction, decreased protein‐binding capacity (as is sometimes seen in the elderly), and increased blood‐brain permeability in the setting of CNS infections. Accumulation of the drug in the CSF can lead to blockade of the GABA‐A receptor through a mechanism of competitive antagonism1, 8
The onset of NSCE varies between 1 and 16 days after initiation of cefepime therapy.3‐5, 7 It is frequently confused with delirium, since hospitalized patients treated with broad‐spectrum antibiotics such as cefepime frequently have other comorbidities and risk factors for delirium.
This can delay the diagnosis of NSCE due to a lack of awareness of this critical complication in the setting of renal dysfunction. In order to quantify the likelihood that the NSCE was related to cefepime and not to other causes, we calculated a Naranjo adverse drug events probability score, which consists of 9 questions on the relationship between the adverse event and the incriminated drug.9 Each answer is scored from 1 to +2 points. This score was designed to quantify the strength of the association between any adverse event and a pharmacological agent.
In our patient, the Naranjo score was 7 points, suggesting that the diagnosis of cefepime‐induced NCSE was probable.
The diagnosis of NCSE is made through a combination of a high index of clinical suspicion, specific findings on EEG, and improvement with withdrawal of the drug. Fatal outcomes have been reported.5, 6 Early and prompt recognition of the condition is crucial for the prevention of its morbidity and mortality.
The mainstay of treatment is prompt withdrawal of antibiotics and symptomatic treatment with benzodiazepines or barbiturates. Very severe cases with refractory seizures have been treated with hemodialysis. Phenytoin should be avoided as a treatment of this condition due to its lack of GABA‐agonist activity.
Conclusion
Cefepime can cause NCSE, predominantly in patients with renal dysfunction. Its frequency is probably underestimated in hospitalized patients with multiple comorbid conditions. Hospitalists should be aware of this unusual but critical relationship, especially in patients with renal failure. A high level of clinical suspicion and an emergency EEG are essential to obtain a prompt and accurate diagnosis.
Hospitalized patients with sepsis or severe nosocomial infections are frequently treated empirically with broad‐spectrum antibiotics. Cefepime hydrochloride, a fourth‐generation cephalosporin, is a common antibiotic of first choice. Its proconvulsant properties are well described in the literature,1, 2 but its importance as a potential cause of change in mental status is probably underestimated. We report a case of change in mental status related to nonconvulsive status epilepticus (NCSE) caused by the use of cefepime in an elderly, hospitalized patient. Our goal is to raise awareness about this uncommon and still underrecognized complication.
Case Report
A 72‐year‐old woman with stage III chronic kidney disease secondary to hypertension with a stable creatinine of 1.5 mg/dL (glomerular filtration rate (GFR) estimated by the modification of diet in renal disease (MDRD) at 36 mL/minute/1.73 m2) was admitted to the hospital for worsening of her chronic back pain. She had a past medical history significant for hyperlipidemia, asthma, and peripheral vascular disease, with breast cancer in remission since 1989. She had no history of seizures or cerebrovascular disease. Her medications were ibuprofen, oxycontin, cilastazol, acetaminophen/oxycodone, and an albuterol/empratropium inhaler. Her physical examination was remarkable only for decreased strength in the right lower extremity. Magnetic resonance imaging (MRI) of the lumbosacral spine showed signs consistent with an inflammatory process at the level of L4‐L5. A computed tomography (CT)‐guided biopsy was performed and confirmed a diagnosis of osteomyelitis on biopsy. Cultures from the biopsy grew Pseudomonas aeruginosa and treatment with intravenous cefepime at a dose of 1 g every 12 hours was initiated. Over the next 3 days, the patient had a gradual worsening of her mental status, leading to pronounced somnolence with occasional episodes of agitation during which she had no focal motor deficits. Her mental status declined to the point of unresponsiveness to simple verbal commands. She had not received any new medications other than cefepime. Her creatinine level was stable throughout this time period at 1.6 mg/dL. No other abnormalities were found on laboratory evaluation or on CT and MRI scans of the brain. An electroencephalogram (EEG) was markedly abnormal due to a generalized background slowing and disorganization with frequent bilateral paroxysmal epileptiform discharges, confirming the clinical diagnosis of subclinical generalized status epilepticus. Given that there were no other intrinsic neurological or metabolic reasons for this mental status change, and given that cefepime was the only new medication added before the patient started deteriorating, cefepime was discontinued and treatment for seizures was started with intravenous benzodiazepines. Over the next 2 days, her mental status returned to normal. She was soon discharged to a rehabilitation center.
Discussion
Beta‐lactam antibiotics have been described to induce seizures due to their direct and/or indirect inhibition of the gamma‐aminobutyric acid (GABA) system.1, 3 Previous experiments have shown a dose‐dependent effect on seizures, and suggest that the cephalosporin with the most pronounced proconvulsant effect is cefazolin.1, 3
Cefepime has been associated with neurological side effects such as headache, confusion, hallucinations, agitation, myoclonus, ataxia, seizures, and coma. Another underrecognized but critical side effect is NSCE. This is defined as seizure activity for more than 30 minutes, with cognitive and behavioral changes, but without convulsive clinical manifestations. This complication has been reported in the literature, but it is probably underrecognized.3‐7 The tendency for cefepime to produce more subclinical activity than the other cephalosporins is not well understood.
Cefepime is mainly eliminated though renal excretion (85%) and displays linear pharmacokinetic properties, thus its dose needs to be adjusted according to renal function. Consequently, in the case of renal dysfunction, accumulation of the drug is proportional to the degree of renal impairment. For NSCE, the most important risk factor is renal impairment, although cases in patients with normal kidney function have been described.36 Age, preexisting central nervous system (CNS) disease, sepsis, and cardiopulmonary bypass have also been reported as possible risk factors for NCSE.1
Cefepime can accumulate in the cerebrospinal fluid (CSF) in the setting of renal dysfunction, decreased protein‐binding capacity (as is sometimes seen in the elderly), and increased blood‐brain permeability in the setting of CNS infections. Accumulation of the drug in the CSF can lead to blockade of the GABA‐A receptor through a mechanism of competitive antagonism1, 8
The onset of NSCE varies between 1 and 16 days after initiation of cefepime therapy.3‐5, 7 It is frequently confused with delirium, since hospitalized patients treated with broad‐spectrum antibiotics such as cefepime frequently have other comorbidities and risk factors for delirium.
This can delay the diagnosis of NSCE due to a lack of awareness of this critical complication in the setting of renal dysfunction. In order to quantify the likelihood that the NSCE was related to cefepime and not to other causes, we calculated a Naranjo adverse drug events probability score, which consists of 9 questions on the relationship between the adverse event and the incriminated drug.9 Each answer is scored from 1 to +2 points. This score was designed to quantify the strength of the association between any adverse event and a pharmacological agent.
In our patient, the Naranjo score was 7 points, suggesting that the diagnosis of cefepime‐induced NCSE was probable.
The diagnosis of NCSE is made through a combination of a high index of clinical suspicion, specific findings on EEG, and improvement with withdrawal of the drug. Fatal outcomes have been reported.5, 6 Early and prompt recognition of the condition is crucial for the prevention of its morbidity and mortality.
The mainstay of treatment is prompt withdrawal of antibiotics and symptomatic treatment with benzodiazepines or barbiturates. Very severe cases with refractory seizures have been treated with hemodialysis. Phenytoin should be avoided as a treatment of this condition due to its lack of GABA‐agonist activity.
Conclusion
Cefepime can cause NCSE, predominantly in patients with renal dysfunction. Its frequency is probably underestimated in hospitalized patients with multiple comorbid conditions. Hospitalists should be aware of this unusual but critical relationship, especially in patients with renal failure. A high level of clinical suspicion and an emergency EEG are essential to obtain a prompt and accurate diagnosis.
- .Antibiotic‐induced convulsions.Crit Care Clin.1997;13:741‐762.
- ,.Cefepime neurotoxicity: case report, pharmacokinetic considerations, and literature review.Pharmacotherapy.2006;26(8):1169‐1174.
- ,,,,.Relationship between structure and convulsant properties of some β‐lactams antibiotics following intracerebroventricular microinjections in rats.Antimicrob Agents Chemother.1995;39:232‐237.
- ,,,,,.Cefepime‐ and cefixime‐induced encephalopathy in a patient with normal renal function.Neurology.2005;65(11):1840.
- ,,, et al.Cefepime induced neurotoxicity: an underestimated complication of antibiotherapy in patients with acute renal failure.Intensive Care Med.2002;28:214‐217.
- ,,,.Nonconvulsive status epilepticus due to cefepime in a patient with normal renal function.Epilepsy Behav.2006;8(1):312‐314.
- ,,, et al.Nonconvulsive status epilepticus associated with cephalosporins in patients with renal failure.Am J Med.2001;111(2):115‐119.
- ,,, et al.Evidence for the involvement of GABA(A) receptor blockade in convulsions induced by cephalosporins.Neuropharmacology.2003;45(3):304‐314.
- ,,, et al.A method for estimating the probability of adverse drug reactions.Clin Pharmacol Ther.1981;30(2):239‐245.
- .Antibiotic‐induced convulsions.Crit Care Clin.1997;13:741‐762.
- ,.Cefepime neurotoxicity: case report, pharmacokinetic considerations, and literature review.Pharmacotherapy.2006;26(8):1169‐1174.
- ,,,,.Relationship between structure and convulsant properties of some β‐lactams antibiotics following intracerebroventricular microinjections in rats.Antimicrob Agents Chemother.1995;39:232‐237.
- ,,,,,.Cefepime‐ and cefixime‐induced encephalopathy in a patient with normal renal function.Neurology.2005;65(11):1840.
- ,,, et al.Cefepime induced neurotoxicity: an underestimated complication of antibiotherapy in patients with acute renal failure.Intensive Care Med.2002;28:214‐217.
- ,,,.Nonconvulsive status epilepticus due to cefepime in a patient with normal renal function.Epilepsy Behav.2006;8(1):312‐314.
- ,,, et al.Nonconvulsive status epilepticus associated with cephalosporins in patients with renal failure.Am J Med.2001;111(2):115‐119.
- ,,, et al.Evidence for the involvement of GABA(A) receptor blockade in convulsions induced by cephalosporins.Neuropharmacology.2003;45(3):304‐314.
- ,,, et al.A method for estimating the probability of adverse drug reactions.Clin Pharmacol Ther.1981;30(2):239‐245.
When your brother becomes a ‘stranger’
History: ‘They’re making me crazy’
Ms. D, age 22, is brought to the emergency room by her older brother for psychiatric evaluation after a family argument. He tells us that his sister is out most nights, hanging out at nightclubs. When she’s home, he says, she locks herself in her room and avoids him and his younger brother, who also lives with them.
Recently, her brother says, Ms. D signed a contract to appear in pornographic videos. When he found out, he went to the studio’s producer and nullified the contract.
Ms. D, frustrated with her brother’s interference, tells us she dreams of becoming a movie star and going to college, but blames him for “holding me back” and keeping her unemployed.
Worse, she says, he and her two sisters are impostors who are “trying to hurt me” and are “making me go crazy.” She fears her “false brother” will take her house if she leaves, yet she feels unsafe at home because strangers—envious of “my beauty and intelligence”—peek into her windows and stalk her. She tells us her father is near and guards her—even though he died 4 years ago.
Ms. D, who lost her mother at age 2, began having psychotic episodes at age 19, a few months after her father’s death. At that time, she was hospitalized after insisting that her father had faked his death because of a conspiracy against him. A hospital psychiatrist diagnosed bipolar disorder and prescribed a mood stabilizer, but she did not take the medication and her psychosis has worsened.
Ms. D’s Mini-Mental State Examination score of 30 indicates that she is neither grossly confused nor has underlying dementia. However, she is emotionally labile with grossly disorganized thought processes and paranoid and grandiose delusions.
We could not locate other family members, so Ms. D’s family psychiatric history is unknown. She has casual relationships with men but does not have a boyfriend. She acknowledges that she frequents local nightclubs but denies using alcohol.
Blood work and other medical examination results are normal. Negative urine toxicology screen suggests she not abusing substances, and electrolytes and thyroid-stimulating hormone levels are normal. Negative rapid plasma reagin rules out tertiary syphilis. We do not order radiologic studies because her presentation does not suggest focal abnormality, and neurologic exam results are benign.
poll here
The authors’ observations
Patients with both paranoid delusions and manic features are challenging. Prognoses and treatment options for each group of symptoms differ substantially.
Ms. D’s grandiosity, pressured speech, tangential flight of ideas, and hypersexuality strongly suggest bipolar disorder. We could not rule out schizophrenia, however, because of her prominent hallucinations and paranoia.
Pharmacologic intoxication was not likely based on laboratory results and the longstanding, progressive course of Ms. D’s disorder. Organic pathology also was unlikely, given her normal neurologic examination and lack of other medical issues.
Treatment: Talk therapy
We tentatively diagnose Ms. D as having bipolar disorder type I with a manic episode and psychotic features. She does not meet DSM-IV-TR criteria for schizophrenia and lacks affective flattening, poverty of speech, avolition, and other negative symptoms typical of the disorder. We admit her to the inpatient psychiatric unit and prescribe lithium, 300 mg tid, and quetiapine, 50 mg bid.
An internal medicine (IM) resident visits Ms. D for 30 to 45 minutes daily during her hospitalization to check her medical status and to allow her to vent her frustration. A resident in psychiatry also interviews Ms. D for about one half-hour each day. The patient rarely interacts with other patients and speaks only with physicians and nurses.
Ms. D appears to trust the IM resident and confides in her about her brother. During their first meeting, she appears most disturbed that a man who “claims” to be her brother is sabotaging her life. She does not fear that this “impostor” will physically harm her but still distrusts him. She repeatedly reports that her late father is nearby or in the room above hers. She adds that she feels much safer in the hospital, where the “stalkers” cannot reach her.
At times, Ms. D tells the IM resident she has a twin. Other times, she believes her family is much larger than it is, and she sometimes laments that she is losing her identity. She often perseverates on Judgment Day, at which time she says her “fake” relatives will answer for their actions against her.
Ms. D’s delusions of grandiosity, tangentiality, circumferential speech, and flight of ideas persist through 4 days in the hospital. Her affect is extremely labile and occasionally inappropriate. She sometimes cries when discussing her father’s death, then stops, thinks a moment, and begins laughing. At this point, we increase lithium to 600 mg tid and quetiapine to 100 mg tid. She is suffering no side effects and infrequently requires haloperidol as a demand dose only.
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The authors’ observations
A patient such as Ms. D who lives in a minimally supportive environment and has paranoid delusions could fabricate an explanation for what she perceives as family members’ incongruent behavior. She could create a reality in which these relatives are impostors.
Although this behavior is not unusual, Ms. D’s extreme reaction toward her siblings suggests Capgras syndrome, a rare misidentification disorder (Box). The syndrome is often missed in clinical practice, and its prevalence has not been quantified.
Capgras syndrome is seen most often in patients with paranoid schizophrenia—the highest functioning and most preserved schizophrenia patients. This association may indicate that both neurologic dysfunction and psychological background are necessary to produce the syndrome.
The belief that family members are impostors could point to a conspiracy theory or paranoid delusion. Ms. D’s suspicion and distrust toward her older brother indicate a paranoid state, and her other delusions—such as her belief that others are stalking her—suggest that her Capgras symptoms are another manifestation of paranoia.
Capgras syndrome—named for Jean Marie Joseph Capgras, a French psychiatrist who first described the disorder—is characterized by paranoid delusions that close friends or relatives are impostors or “doubles” for the family member/friend or are somehow feigning their identity.
Depersonalization and derealization symptoms are common, as is inability to endorse the verity of another’s identity. Misidentifications—defined as misperceptions with delusional intensity—can also involve people who do not prompt negative or ambivalent feelings or even inanimate objects.
Capgras syndrome may be neurologically and structurally similar to prosopagnosia—which describes inability to recognize familiar faces—but may also be a variation of a paranoid delusion in which the patient seeks to explain affective experiences. The disorder’s coexistence with paranoid delusions also suggests an association with schizophrenia.
For Ms. D, structural brain deficits probably interacted with her psychosocial milieu to create Capgras delusions, though we did not perform confirmatory brain imaging or functional neurologic testing. Whereas right cortical lesions might impair recognition while preserving familiarity, Capgras syndrome preserves recognition but deadens the emotion that makes faces seem familiar. When focal lesions are found to cause Capgras delusion, however, the right hemisphere—specifically the frontal cortex—usually is affected.2,3
Table
Proposed causes of Capgras syndrome
| Physiologic |
| Frontal lobe damage may distort visual stimuli monitoring, thus impairing facial recognition.4 |
| Disruption of neuronal connections within the right temporal lobe scrambles memories needed for facial recognition.5 |
| Neurologic |
| Disconnection between brain hemispheres lead to cognitive but not affective recognition.6 |
| Bifrontal pathology or other organic cause blurs “judgment of individuality or uniqueness,” as in prosopagnosia.3 |
| Dorsal pathway impairment alters affective response to faces.7 |
| Dissociation in the amygdala may distort affective response to faces.8 |
| Psychological* |
| In depression, misidentification develops secondary to rationalizing feelings of guilt and inferiority.9 |
| “Two-armed recognition”—one automatic and almost instantaneous, the other attentive and mnemonic—begins to falter.10 |
| Suspicion, preoccupation with details leads to “agnosia through too great attention.”11 |
| Avoidance of unconscious desires leads to recognition problems.12 |
| Patient “projects and splits” family member into two persons; directs love toward real person and hate toward imagined impostor.13 |
| In schizophrenia, world is viewed through primitive mechanisms, such as doubles and dualism.14 |
| *Dependent on psychiatric comorbidity |
The authors’ observations
When interviewing a patient with paranoid delusions, get as much detail as possible about his or her close relationships. Try to interview one or two family members or friends. The information can help determine whether Capgras symptoms underlie paranoia.
Brain imaging might uncover pertinent abnormalities, but the cost could outweigh any benefit. No evidence supports use of CT to diagnose Capgras syndrome. Some evidence supports use of brain MRI, but more research is needed.
No specific treatment exists for Capgras delusions apart from using antipsychotics to treat the psychosis based on clinical suspicion and constellation of symptoms.
Studies have shown no difference in response to atypical antipsychotics between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. In clinical practice, we have found that treating Capgras symptoms does improve schizophrenia’s course.
Adjunctive psychotherapy has not been studied in Capgras syndrome, and directed, insight-guided therapy might not resolve deeply rooted delusions for some patients. With Ms. D, however, “talk therapy” helped us build rapport and gave us insight into her strained familial relationships. Establishing a therapeutic alliance with the patient and encouraging healthy relationships with his or her family and friends can mitigate the effects of Capgras paranoia.
Continued treatment: Gradual change
Day by day Ms. D’s mania subsides gradually, though she still fears that a stranger posing as her brother is stalking her. She talks about her brother less frequently, though she is clearly holding fast to her delusional beliefs.
We discharge Ms. D after 10 days. Although her symptoms have not resolved, she is markedly less manic and less agitated than at admission. We arrange treatment with outpatient psychiatry. She does not follow up with her original psychiatrist and is lost to follow-up.
Related resources
- PsychNet-UK. Disorder information sheet: Capgras (delusion) syndrome. www.psychnet-uk.com/dsm_iv/capgras_syndrome.htm.
- Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry 2004;49:719-25. Available at: www.cpa-apc.org/Publications/Archives/CJP/2004/november/bourget.asp.
- Barton JJ. Disorders of face perception and recognition. Neurol Clin 2003;21:521-48.
- Lewis S. Brain imaging in a case of Capgras’ syndrome. Br J Psychiatry 1987;150:117-21.
- Christodoulou GN. The syndrome of Capgras. Br J Psychiatry 1977;130:556-64.
- Haloperidol • Haldol
- Lithium • Eskalith, others
- Quetiapine • Seroquel
The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Chatterjee A, Farah M. The cognitive architecture of the brain revealed through studies of face processing. Neurology 2001;57:1151-2.
2. Fleminger S, Burns A. The delusional misidentification syndromes in patients with and without evidence of organic cerebral disorder: a structured review on case reports. Biol Psychiatry 1993;33:23-32.
3. Cutting J. Delusional misidentifications and the role of the right hemisphere in the appreciation of identity. Br J Psychiatry 1991;159(Suppl 14):70-5.
4. Rapcsak S, Nielsen L, Littrell L, et al. Face memory impairments with frontal lobe damage. Neurology 2001;57:1168-75.
5. Hudson A, Grace G. Misidentification syndromes related to face specific area in the fusiform gyrus. J Neurol Neurosurg Psychiatry 2000;69:645-8.
6. Joseph A. Focal central nervous system abnormalities in patients with misidentification syndromes. Biol Psychiatry 1986;164:68-79.
7. Ellis H. The role of the right hemisphere in the Capgras delusion. Psychopathology 1994;27:177-85.
8. Breen N, Caine D, Coltheart M. Models of face recognition and delusional misidentification: a critical review. Cognit Neuropsychol 2000;17:55-71.
9. Christodoulou G. The delusional misidentification syndromes. Br J Psychiatry 1991;159:65-9.
10. Capgras J, Reboul-Lachaux J. Illusions des soises dans un delire systematize chronique. Bulletin de la Societe Clinique de Medecine Mentale 1923;2:6-16.
11. Capgras J, Lucchini P, Schiff P. Du sentiment d’etrangete a l’illusion des soises. Bulletin de la Societe Clinique de Medecine Mentale 1924;121:210-17.
12. Capgras J, Carrette P. Illusions des soises et complexe d’Oedipe. Ann Med Psychol 1924;82:48-68.
13. Enoch D. The Capgras syndrome. Acta Psychiatr Scand 1963;39:437-62.
14. Todd J. The syndrome of Capgras. Psychiatric Q 1957;31:250-65.
History: ‘They’re making me crazy’
Ms. D, age 22, is brought to the emergency room by her older brother for psychiatric evaluation after a family argument. He tells us that his sister is out most nights, hanging out at nightclubs. When she’s home, he says, she locks herself in her room and avoids him and his younger brother, who also lives with them.
Recently, her brother says, Ms. D signed a contract to appear in pornographic videos. When he found out, he went to the studio’s producer and nullified the contract.
Ms. D, frustrated with her brother’s interference, tells us she dreams of becoming a movie star and going to college, but blames him for “holding me back” and keeping her unemployed.
Worse, she says, he and her two sisters are impostors who are “trying to hurt me” and are “making me go crazy.” She fears her “false brother” will take her house if she leaves, yet she feels unsafe at home because strangers—envious of “my beauty and intelligence”—peek into her windows and stalk her. She tells us her father is near and guards her—even though he died 4 years ago.
Ms. D, who lost her mother at age 2, began having psychotic episodes at age 19, a few months after her father’s death. At that time, she was hospitalized after insisting that her father had faked his death because of a conspiracy against him. A hospital psychiatrist diagnosed bipolar disorder and prescribed a mood stabilizer, but she did not take the medication and her psychosis has worsened.
Ms. D’s Mini-Mental State Examination score of 30 indicates that she is neither grossly confused nor has underlying dementia. However, she is emotionally labile with grossly disorganized thought processes and paranoid and grandiose delusions.
We could not locate other family members, so Ms. D’s family psychiatric history is unknown. She has casual relationships with men but does not have a boyfriend. She acknowledges that she frequents local nightclubs but denies using alcohol.
Blood work and other medical examination results are normal. Negative urine toxicology screen suggests she not abusing substances, and electrolytes and thyroid-stimulating hormone levels are normal. Negative rapid plasma reagin rules out tertiary syphilis. We do not order radiologic studies because her presentation does not suggest focal abnormality, and neurologic exam results are benign.
poll here
The authors’ observations
Patients with both paranoid delusions and manic features are challenging. Prognoses and treatment options for each group of symptoms differ substantially.
Ms. D’s grandiosity, pressured speech, tangential flight of ideas, and hypersexuality strongly suggest bipolar disorder. We could not rule out schizophrenia, however, because of her prominent hallucinations and paranoia.
Pharmacologic intoxication was not likely based on laboratory results and the longstanding, progressive course of Ms. D’s disorder. Organic pathology also was unlikely, given her normal neurologic examination and lack of other medical issues.
Treatment: Talk therapy
We tentatively diagnose Ms. D as having bipolar disorder type I with a manic episode and psychotic features. She does not meet DSM-IV-TR criteria for schizophrenia and lacks affective flattening, poverty of speech, avolition, and other negative symptoms typical of the disorder. We admit her to the inpatient psychiatric unit and prescribe lithium, 300 mg tid, and quetiapine, 50 mg bid.
An internal medicine (IM) resident visits Ms. D for 30 to 45 minutes daily during her hospitalization to check her medical status and to allow her to vent her frustration. A resident in psychiatry also interviews Ms. D for about one half-hour each day. The patient rarely interacts with other patients and speaks only with physicians and nurses.
Ms. D appears to trust the IM resident and confides in her about her brother. During their first meeting, she appears most disturbed that a man who “claims” to be her brother is sabotaging her life. She does not fear that this “impostor” will physically harm her but still distrusts him. She repeatedly reports that her late father is nearby or in the room above hers. She adds that she feels much safer in the hospital, where the “stalkers” cannot reach her.
At times, Ms. D tells the IM resident she has a twin. Other times, she believes her family is much larger than it is, and she sometimes laments that she is losing her identity. She often perseverates on Judgment Day, at which time she says her “fake” relatives will answer for their actions against her.
Ms. D’s delusions of grandiosity, tangentiality, circumferential speech, and flight of ideas persist through 4 days in the hospital. Her affect is extremely labile and occasionally inappropriate. She sometimes cries when discussing her father’s death, then stops, thinks a moment, and begins laughing. At this point, we increase lithium to 600 mg tid and quetiapine to 100 mg tid. She is suffering no side effects and infrequently requires haloperidol as a demand dose only.
poll here
The authors’ observations
A patient such as Ms. D who lives in a minimally supportive environment and has paranoid delusions could fabricate an explanation for what she perceives as family members’ incongruent behavior. She could create a reality in which these relatives are impostors.
Although this behavior is not unusual, Ms. D’s extreme reaction toward her siblings suggests Capgras syndrome, a rare misidentification disorder (Box). The syndrome is often missed in clinical practice, and its prevalence has not been quantified.
Capgras syndrome is seen most often in patients with paranoid schizophrenia—the highest functioning and most preserved schizophrenia patients. This association may indicate that both neurologic dysfunction and psychological background are necessary to produce the syndrome.
The belief that family members are impostors could point to a conspiracy theory or paranoid delusion. Ms. D’s suspicion and distrust toward her older brother indicate a paranoid state, and her other delusions—such as her belief that others are stalking her—suggest that her Capgras symptoms are another manifestation of paranoia.
Capgras syndrome—named for Jean Marie Joseph Capgras, a French psychiatrist who first described the disorder—is characterized by paranoid delusions that close friends or relatives are impostors or “doubles” for the family member/friend or are somehow feigning their identity.
Depersonalization and derealization symptoms are common, as is inability to endorse the verity of another’s identity. Misidentifications—defined as misperceptions with delusional intensity—can also involve people who do not prompt negative or ambivalent feelings or even inanimate objects.
Capgras syndrome may be neurologically and structurally similar to prosopagnosia—which describes inability to recognize familiar faces—but may also be a variation of a paranoid delusion in which the patient seeks to explain affective experiences. The disorder’s coexistence with paranoid delusions also suggests an association with schizophrenia.
For Ms. D, structural brain deficits probably interacted with her psychosocial milieu to create Capgras delusions, though we did not perform confirmatory brain imaging or functional neurologic testing. Whereas right cortical lesions might impair recognition while preserving familiarity, Capgras syndrome preserves recognition but deadens the emotion that makes faces seem familiar. When focal lesions are found to cause Capgras delusion, however, the right hemisphere—specifically the frontal cortex—usually is affected.2,3
Table
Proposed causes of Capgras syndrome
| Physiologic |
| Frontal lobe damage may distort visual stimuli monitoring, thus impairing facial recognition.4 |
| Disruption of neuronal connections within the right temporal lobe scrambles memories needed for facial recognition.5 |
| Neurologic |
| Disconnection between brain hemispheres lead to cognitive but not affective recognition.6 |
| Bifrontal pathology or other organic cause blurs “judgment of individuality or uniqueness,” as in prosopagnosia.3 |
| Dorsal pathway impairment alters affective response to faces.7 |
| Dissociation in the amygdala may distort affective response to faces.8 |
| Psychological* |
| In depression, misidentification develops secondary to rationalizing feelings of guilt and inferiority.9 |
| “Two-armed recognition”—one automatic and almost instantaneous, the other attentive and mnemonic—begins to falter.10 |
| Suspicion, preoccupation with details leads to “agnosia through too great attention.”11 |
| Avoidance of unconscious desires leads to recognition problems.12 |
| Patient “projects and splits” family member into two persons; directs love toward real person and hate toward imagined impostor.13 |
| In schizophrenia, world is viewed through primitive mechanisms, such as doubles and dualism.14 |
| *Dependent on psychiatric comorbidity |
The authors’ observations
When interviewing a patient with paranoid delusions, get as much detail as possible about his or her close relationships. Try to interview one or two family members or friends. The information can help determine whether Capgras symptoms underlie paranoia.
Brain imaging might uncover pertinent abnormalities, but the cost could outweigh any benefit. No evidence supports use of CT to diagnose Capgras syndrome. Some evidence supports use of brain MRI, but more research is needed.
No specific treatment exists for Capgras delusions apart from using antipsychotics to treat the psychosis based on clinical suspicion and constellation of symptoms.
Studies have shown no difference in response to atypical antipsychotics between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. In clinical practice, we have found that treating Capgras symptoms does improve schizophrenia’s course.
Adjunctive psychotherapy has not been studied in Capgras syndrome, and directed, insight-guided therapy might not resolve deeply rooted delusions for some patients. With Ms. D, however, “talk therapy” helped us build rapport and gave us insight into her strained familial relationships. Establishing a therapeutic alliance with the patient and encouraging healthy relationships with his or her family and friends can mitigate the effects of Capgras paranoia.
Continued treatment: Gradual change
Day by day Ms. D’s mania subsides gradually, though she still fears that a stranger posing as her brother is stalking her. She talks about her brother less frequently, though she is clearly holding fast to her delusional beliefs.
We discharge Ms. D after 10 days. Although her symptoms have not resolved, she is markedly less manic and less agitated than at admission. We arrange treatment with outpatient psychiatry. She does not follow up with her original psychiatrist and is lost to follow-up.
Related resources
- PsychNet-UK. Disorder information sheet: Capgras (delusion) syndrome. www.psychnet-uk.com/dsm_iv/capgras_syndrome.htm.
- Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry 2004;49:719-25. Available at: www.cpa-apc.org/Publications/Archives/CJP/2004/november/bourget.asp.
- Barton JJ. Disorders of face perception and recognition. Neurol Clin 2003;21:521-48.
- Lewis S. Brain imaging in a case of Capgras’ syndrome. Br J Psychiatry 1987;150:117-21.
- Christodoulou GN. The syndrome of Capgras. Br J Psychiatry 1977;130:556-64.
- Haloperidol • Haldol
- Lithium • Eskalith, others
- Quetiapine • Seroquel
The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
History: ‘They’re making me crazy’
Ms. D, age 22, is brought to the emergency room by her older brother for psychiatric evaluation after a family argument. He tells us that his sister is out most nights, hanging out at nightclubs. When she’s home, he says, she locks herself in her room and avoids him and his younger brother, who also lives with them.
Recently, her brother says, Ms. D signed a contract to appear in pornographic videos. When he found out, he went to the studio’s producer and nullified the contract.
Ms. D, frustrated with her brother’s interference, tells us she dreams of becoming a movie star and going to college, but blames him for “holding me back” and keeping her unemployed.
Worse, she says, he and her two sisters are impostors who are “trying to hurt me” and are “making me go crazy.” She fears her “false brother” will take her house if she leaves, yet she feels unsafe at home because strangers—envious of “my beauty and intelligence”—peek into her windows and stalk her. She tells us her father is near and guards her—even though he died 4 years ago.
Ms. D, who lost her mother at age 2, began having psychotic episodes at age 19, a few months after her father’s death. At that time, she was hospitalized after insisting that her father had faked his death because of a conspiracy against him. A hospital psychiatrist diagnosed bipolar disorder and prescribed a mood stabilizer, but she did not take the medication and her psychosis has worsened.
Ms. D’s Mini-Mental State Examination score of 30 indicates that she is neither grossly confused nor has underlying dementia. However, she is emotionally labile with grossly disorganized thought processes and paranoid and grandiose delusions.
We could not locate other family members, so Ms. D’s family psychiatric history is unknown. She has casual relationships with men but does not have a boyfriend. She acknowledges that she frequents local nightclubs but denies using alcohol.
Blood work and other medical examination results are normal. Negative urine toxicology screen suggests she not abusing substances, and electrolytes and thyroid-stimulating hormone levels are normal. Negative rapid plasma reagin rules out tertiary syphilis. We do not order radiologic studies because her presentation does not suggest focal abnormality, and neurologic exam results are benign.
poll here
The authors’ observations
Patients with both paranoid delusions and manic features are challenging. Prognoses and treatment options for each group of symptoms differ substantially.
Ms. D’s grandiosity, pressured speech, tangential flight of ideas, and hypersexuality strongly suggest bipolar disorder. We could not rule out schizophrenia, however, because of her prominent hallucinations and paranoia.
Pharmacologic intoxication was not likely based on laboratory results and the longstanding, progressive course of Ms. D’s disorder. Organic pathology also was unlikely, given her normal neurologic examination and lack of other medical issues.
Treatment: Talk therapy
We tentatively diagnose Ms. D as having bipolar disorder type I with a manic episode and psychotic features. She does not meet DSM-IV-TR criteria for schizophrenia and lacks affective flattening, poverty of speech, avolition, and other negative symptoms typical of the disorder. We admit her to the inpatient psychiatric unit and prescribe lithium, 300 mg tid, and quetiapine, 50 mg bid.
An internal medicine (IM) resident visits Ms. D for 30 to 45 minutes daily during her hospitalization to check her medical status and to allow her to vent her frustration. A resident in psychiatry also interviews Ms. D for about one half-hour each day. The patient rarely interacts with other patients and speaks only with physicians and nurses.
Ms. D appears to trust the IM resident and confides in her about her brother. During their first meeting, she appears most disturbed that a man who “claims” to be her brother is sabotaging her life. She does not fear that this “impostor” will physically harm her but still distrusts him. She repeatedly reports that her late father is nearby or in the room above hers. She adds that she feels much safer in the hospital, where the “stalkers” cannot reach her.
At times, Ms. D tells the IM resident she has a twin. Other times, she believes her family is much larger than it is, and she sometimes laments that she is losing her identity. She often perseverates on Judgment Day, at which time she says her “fake” relatives will answer for their actions against her.
Ms. D’s delusions of grandiosity, tangentiality, circumferential speech, and flight of ideas persist through 4 days in the hospital. Her affect is extremely labile and occasionally inappropriate. She sometimes cries when discussing her father’s death, then stops, thinks a moment, and begins laughing. At this point, we increase lithium to 600 mg tid and quetiapine to 100 mg tid. She is suffering no side effects and infrequently requires haloperidol as a demand dose only.
poll here
The authors’ observations
A patient such as Ms. D who lives in a minimally supportive environment and has paranoid delusions could fabricate an explanation for what she perceives as family members’ incongruent behavior. She could create a reality in which these relatives are impostors.
Although this behavior is not unusual, Ms. D’s extreme reaction toward her siblings suggests Capgras syndrome, a rare misidentification disorder (Box). The syndrome is often missed in clinical practice, and its prevalence has not been quantified.
Capgras syndrome is seen most often in patients with paranoid schizophrenia—the highest functioning and most preserved schizophrenia patients. This association may indicate that both neurologic dysfunction and psychological background are necessary to produce the syndrome.
The belief that family members are impostors could point to a conspiracy theory or paranoid delusion. Ms. D’s suspicion and distrust toward her older brother indicate a paranoid state, and her other delusions—such as her belief that others are stalking her—suggest that her Capgras symptoms are another manifestation of paranoia.
Capgras syndrome—named for Jean Marie Joseph Capgras, a French psychiatrist who first described the disorder—is characterized by paranoid delusions that close friends or relatives are impostors or “doubles” for the family member/friend or are somehow feigning their identity.
Depersonalization and derealization symptoms are common, as is inability to endorse the verity of another’s identity. Misidentifications—defined as misperceptions with delusional intensity—can also involve people who do not prompt negative or ambivalent feelings or even inanimate objects.
Capgras syndrome may be neurologically and structurally similar to prosopagnosia—which describes inability to recognize familiar faces—but may also be a variation of a paranoid delusion in which the patient seeks to explain affective experiences. The disorder’s coexistence with paranoid delusions also suggests an association with schizophrenia.
For Ms. D, structural brain deficits probably interacted with her psychosocial milieu to create Capgras delusions, though we did not perform confirmatory brain imaging or functional neurologic testing. Whereas right cortical lesions might impair recognition while preserving familiarity, Capgras syndrome preserves recognition but deadens the emotion that makes faces seem familiar. When focal lesions are found to cause Capgras delusion, however, the right hemisphere—specifically the frontal cortex—usually is affected.2,3
Table
Proposed causes of Capgras syndrome
| Physiologic |
| Frontal lobe damage may distort visual stimuli monitoring, thus impairing facial recognition.4 |
| Disruption of neuronal connections within the right temporal lobe scrambles memories needed for facial recognition.5 |
| Neurologic |
| Disconnection between brain hemispheres lead to cognitive but not affective recognition.6 |
| Bifrontal pathology or other organic cause blurs “judgment of individuality or uniqueness,” as in prosopagnosia.3 |
| Dorsal pathway impairment alters affective response to faces.7 |
| Dissociation in the amygdala may distort affective response to faces.8 |
| Psychological* |
| In depression, misidentification develops secondary to rationalizing feelings of guilt and inferiority.9 |
| “Two-armed recognition”—one automatic and almost instantaneous, the other attentive and mnemonic—begins to falter.10 |
| Suspicion, preoccupation with details leads to “agnosia through too great attention.”11 |
| Avoidance of unconscious desires leads to recognition problems.12 |
| Patient “projects and splits” family member into two persons; directs love toward real person and hate toward imagined impostor.13 |
| In schizophrenia, world is viewed through primitive mechanisms, such as doubles and dualism.14 |
| *Dependent on psychiatric comorbidity |
The authors’ observations
When interviewing a patient with paranoid delusions, get as much detail as possible about his or her close relationships. Try to interview one or two family members or friends. The information can help determine whether Capgras symptoms underlie paranoia.
Brain imaging might uncover pertinent abnormalities, but the cost could outweigh any benefit. No evidence supports use of CT to diagnose Capgras syndrome. Some evidence supports use of brain MRI, but more research is needed.
No specific treatment exists for Capgras delusions apart from using antipsychotics to treat the psychosis based on clinical suspicion and constellation of symptoms.
Studies have shown no difference in response to atypical antipsychotics between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. In clinical practice, we have found that treating Capgras symptoms does improve schizophrenia’s course.
Adjunctive psychotherapy has not been studied in Capgras syndrome, and directed, insight-guided therapy might not resolve deeply rooted delusions for some patients. With Ms. D, however, “talk therapy” helped us build rapport and gave us insight into her strained familial relationships. Establishing a therapeutic alliance with the patient and encouraging healthy relationships with his or her family and friends can mitigate the effects of Capgras paranoia.
Continued treatment: Gradual change
Day by day Ms. D’s mania subsides gradually, though she still fears that a stranger posing as her brother is stalking her. She talks about her brother less frequently, though she is clearly holding fast to her delusional beliefs.
We discharge Ms. D after 10 days. Although her symptoms have not resolved, she is markedly less manic and less agitated than at admission. We arrange treatment with outpatient psychiatry. She does not follow up with her original psychiatrist and is lost to follow-up.
Related resources
- PsychNet-UK. Disorder information sheet: Capgras (delusion) syndrome. www.psychnet-uk.com/dsm_iv/capgras_syndrome.htm.
- Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry 2004;49:719-25. Available at: www.cpa-apc.org/Publications/Archives/CJP/2004/november/bourget.asp.
- Barton JJ. Disorders of face perception and recognition. Neurol Clin 2003;21:521-48.
- Lewis S. Brain imaging in a case of Capgras’ syndrome. Br J Psychiatry 1987;150:117-21.
- Christodoulou GN. The syndrome of Capgras. Br J Psychiatry 1977;130:556-64.
- Haloperidol • Haldol
- Lithium • Eskalith, others
- Quetiapine • Seroquel
The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Chatterjee A, Farah M. The cognitive architecture of the brain revealed through studies of face processing. Neurology 2001;57:1151-2.
2. Fleminger S, Burns A. The delusional misidentification syndromes in patients with and without evidence of organic cerebral disorder: a structured review on case reports. Biol Psychiatry 1993;33:23-32.
3. Cutting J. Delusional misidentifications and the role of the right hemisphere in the appreciation of identity. Br J Psychiatry 1991;159(Suppl 14):70-5.
4. Rapcsak S, Nielsen L, Littrell L, et al. Face memory impairments with frontal lobe damage. Neurology 2001;57:1168-75.
5. Hudson A, Grace G. Misidentification syndromes related to face specific area in the fusiform gyrus. J Neurol Neurosurg Psychiatry 2000;69:645-8.
6. Joseph A. Focal central nervous system abnormalities in patients with misidentification syndromes. Biol Psychiatry 1986;164:68-79.
7. Ellis H. The role of the right hemisphere in the Capgras delusion. Psychopathology 1994;27:177-85.
8. Breen N, Caine D, Coltheart M. Models of face recognition and delusional misidentification: a critical review. Cognit Neuropsychol 2000;17:55-71.
9. Christodoulou G. The delusional misidentification syndromes. Br J Psychiatry 1991;159:65-9.
10. Capgras J, Reboul-Lachaux J. Illusions des soises dans un delire systematize chronique. Bulletin de la Societe Clinique de Medecine Mentale 1923;2:6-16.
11. Capgras J, Lucchini P, Schiff P. Du sentiment d’etrangete a l’illusion des soises. Bulletin de la Societe Clinique de Medecine Mentale 1924;121:210-17.
12. Capgras J, Carrette P. Illusions des soises et complexe d’Oedipe. Ann Med Psychol 1924;82:48-68.
13. Enoch D. The Capgras syndrome. Acta Psychiatr Scand 1963;39:437-62.
14. Todd J. The syndrome of Capgras. Psychiatric Q 1957;31:250-65.
1. Chatterjee A, Farah M. The cognitive architecture of the brain revealed through studies of face processing. Neurology 2001;57:1151-2.
2. Fleminger S, Burns A. The delusional misidentification syndromes in patients with and without evidence of organic cerebral disorder: a structured review on case reports. Biol Psychiatry 1993;33:23-32.
3. Cutting J. Delusional misidentifications and the role of the right hemisphere in the appreciation of identity. Br J Psychiatry 1991;159(Suppl 14):70-5.
4. Rapcsak S, Nielsen L, Littrell L, et al. Face memory impairments with frontal lobe damage. Neurology 2001;57:1168-75.
5. Hudson A, Grace G. Misidentification syndromes related to face specific area in the fusiform gyrus. J Neurol Neurosurg Psychiatry 2000;69:645-8.
6. Joseph A. Focal central nervous system abnormalities in patients with misidentification syndromes. Biol Psychiatry 1986;164:68-79.
7. Ellis H. The role of the right hemisphere in the Capgras delusion. Psychopathology 1994;27:177-85.
8. Breen N, Caine D, Coltheart M. Models of face recognition and delusional misidentification: a critical review. Cognit Neuropsychol 2000;17:55-71.
9. Christodoulou G. The delusional misidentification syndromes. Br J Psychiatry 1991;159:65-9.
10. Capgras J, Reboul-Lachaux J. Illusions des soises dans un delire systematize chronique. Bulletin de la Societe Clinique de Medecine Mentale 1923;2:6-16.
11. Capgras J, Lucchini P, Schiff P. Du sentiment d’etrangete a l’illusion des soises. Bulletin de la Societe Clinique de Medecine Mentale 1924;121:210-17.
12. Capgras J, Carrette P. Illusions des soises et complexe d’Oedipe. Ann Med Psychol 1924;82:48-68.
13. Enoch D. The Capgras syndrome. Acta Psychiatr Scand 1963;39:437-62.
14. Todd J. The syndrome of Capgras. Psychiatric Q 1957;31:250-65.