by Devavrat Joshi, Md; Sharad Koirala, MD; Sachin Lamichhane, MD; Anubha Paladugu, MD; Rupinder Johal, MD; and Steven Lippmann, MD
Drs. Joshi, Koirala, and Lamichhane are from the Mental Hospital in Lagankhel, Lalitpur, Nepal. Drs. Paladugu, Johal, and Lippmann are from University of Louisville, School of Medicine, Department of Psychiatry and Behavioral Sciences, Louisville, Kentucky.

Psychiatry (Edgemont) 2010;7(3):37-39

Funding: There was no funding for the development and writing of this article.

Financial disclosure: The authors have no conflicts of interest relevant to the content of this article.

Key Words: Capgras syndrome, delusion, epilepsy, anticonvulsant medication, postictal, delirium


A 34-year-old man with a seizure disorder had not been taking anticonvulsant medications regularly. A previous pattern of recurrent seizures resolved after restarting anticonvulsant drugs. Recent seizure episodes were followed by delirium and presentation of Capgras syndrome. A variety of functional and organic etiologies for Capgras syndrome are known. This syndrome has been documented in cases of postictal delirium. These symptoms along with delirium ended with seizure control once back on anticonvulsant medicines.


Capgras syndrome is defined as a delusional condition in which a patient falsely believes that someone, usually a close relative or friend, has been replaced by an imposter.[1] This presentation can be part of a functional illness, psychiatric disorders, organic diseases, drug usage, and rarely as an independent phenomenon.[2] Capgras syndrome, associated with organic etiologies, usually resolves following resolution of the primary pathology.[3,4]

Clinical Vignette

A 34-year-old man was diagnosed with epilepsy and had been taking phenytoin and phenobarbital orally for the last 12 years. He did not have a history of high-grade fever, head injury, substance abuse, or any psychiatric disorder prior to the seizure onset. In the past, erratic adherence with medicine resulted in recurrent episodes of generalized tonic-clonic convulsions. His wife reported that, during these episodes, he was confused, disoriented, and frequently misrecognized people after each seizure episode. Over a two-day period following the last ictal event, the patient became fearful and suspicious about somebody trying to attack him. Seizures and these symptoms decreased three days after restarting anticonvulsant medication.

The present illness episode began after the patient stopped taking his seizure medicines at the advice of a faith healer. He was apparently well for a few days; but then over a 24-hour period exhibited 8 to 9 episodes of generalized tonic-clonic convulsions, each lasting for less than five minutes. An electroencephalogram (EEG) at that time evidenced wave patterns suggestive of generalized seizure activity. The following day, after seizure control was reestablished, the patient was transferred from the general hospital to a psychiatric facility because of bizarre behavior and thinking. No abnormal neurological findings were detected in the physical examination. Routine blood and urine investigations were within normal limits.

On mental status examination, the patient was unkempt and restless. He was disoriented, anxious, muttering, uncooperative, and tried to grasp objects in his vicinity; he became assaultive without provocation. Incontinence of urine was noted. The patient said that he could hear voices arising within a thick smoke in the room. He also claimed that his wife, relatives, and neighbors were “duplicates.” His belief did not change despite logic to the contrary. He even refused food from his wife.

The patient began oral valproic acid 1,000mg/day, risperidone 2mg/day, and lorazepam 2mg at night. He slept well that night and became more cooperative the next day. On the second day of the admission to psychiatry, he revealed Capgras symptoms, persecutory delusions, visual hallucinations, and remained disoriented. His recent memory, judgment, and insight were impaired. Scores of 20 out of 30 on the Mini Mental Status Examination (MMSE) suggested cognitive dysfunction in a presentation of delirium.

A computerized tomogram (CT) of the head and an EEG were obtained on the fourth psychiatric hospital day. The CT scan was unremarkable. This second EEG revealed no focal changes or epileptiform discharges during this recording. By the fifth day, he became oriented and the MMSE scores improved to 27 out of 30. He was no longer fearful; the persecutory delusions and visual hallucinations disappeared. However, he still claimed that his wife had been replaced by someone else.
Valproic acid was continued, but risperidone and lorazepam were discontinued. He gradually improved by hospital Day 10 and was fully oriented without delusional symptoms. Valproic acid remained as the single pharmacotherapy.

The neurological diagnosis remained primary generalized epilepsy, without a known history of aura, focal symptoms, or documented focal neurological deficits before or after seizures; the same characterized past episodes and on this occasion. Previous EEGs were consistently symmetrical in wave forms. There was no evidence for an identifiable brain lesion.


Approximately 7 to 10 percent of patients with epilepsy suffer from psychoses, sometimes resembling a schizophreniform disorder.[5] Psychotic symptoms in the form of Capgras syndrome or similar delusional misidentifications have been less commonly described in cases of epilepsy.[6]

Capgras syndrome usually has been observed in cases of functional psychoses, psychiatric diseases, such as schizophrenia (paranoid) and other delusional disorders.[7] This phenomenon has also been documented in organic conditions, including systemic infections, nutritional deficiencies (e.g., folate deficiency), head injuries, basilar migraines, dementias, myxedema, cerebrovascular accidents, metabolic encephalopathies, and delirium secondary to epilepsy.[2,8–11] Psychotic conditions, such as Capgras syndrome, are occasionally observed after a convulsion, more commonly following complex partial seizures and in some cases after generalized tonic-clonic convulsions.3 It has also been described after electroconvulsive therapy.[10,12] Thorough evaluation for organic pathology is recommended in all cases of delusional misidentification.[13] Capgras syndrome associated with organic diseases usually remits with improvement of the primary illness.[4]

These delusions may result from postictal disinhibition of the dominant hemisphere involved in recognition or from dysfunction of nondominant hemisphere centers involved in perceptual integration.[12,14,15] Most of the peri-ictal or postictal psychotic symptoms resolve after regaining seizure control without antipsychotic drugs being necessary. In the above case, the patient had delusions during delirium following generalized tonic-clonic convulsions. The symptoms subsided after a few days of establishing seizure control. Anticonvulsant medication was the primary pharmacotherapy.


Any patient having Capgras syndrome or other delusional misidentification disorders mandates a thorough evaluation for organic etiologies. Capgras syndrome was observed during a delirium following repeated generalized tonic-clonic convulsions. The delusions were evident even in the presence of a normal follow-up EEG. The resolution of delirium followed seizure control and led to complete disappearance of the Capgras syndrome.


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