Capgras syndrome can be triggered by systemic infections, thyroid dysfunction, concussion, or intoxication. It is seen with head injury, toxic encephalopathy, and dementia.5
Joseph Capgras first described this syndrome in 1923. He discovered it by studying brain-injured patients who had prosopagnosia—the inability to recognize familiar faces. Patients with prosopagnosia are not delusional and understand that their inability to recognize faces is an impairment. Brain-injured patients with prosopagnosia had an autonomic arousal (measured by galvanic skin response) with familiar faces and thus unconscious face recognition was intact.5
Ellis et al6 described Capgras syndrome as being a “reverse” of prosopagnosia. They felt that in patients with Capgras, the conscious ability to recognize a face is intact, but the patient cannot produce an emotional response that usually occurs when seeing a familiar face. Thus, patients can recognize a person but feel that something is “off” or “wrong” and believe that the person must be an “imposter.” This hypothesis was supported by a 1997 study of 5 patients with schizophrenia who had Capgras.7
Breen2 reviewed 69 case reports of Capgras that had brain imaging results. Twenty-seven had normal brain imaging, 31 had global atrophy or bilateral brain damage, 2 had global atrophy and a right focal lesion, and 6 had a right hemispheric lesion. Thus, Capgras can occur in patients with normal or abnormal brain imaging.
Young9 developed an interactionist model of Capgras syndrome, in which a patient’s delusional belief allows the patient to explain his or her confusion and give the experience meaning. The experience then validates the belief, which makes the belief resistant to revision.
The main treatment of Capgras syndrome is pharmacotherapy with antipsychotics and cognitive-behavioral therapy (CBT) to help with fixed delusions.
Capgras syndrome: Recognition without emotion
Patients with Capgras syndrome believe people whom they know well have been replaced by identical imposters. One of the intriguing aspects of Capgras is that the patient to some extent must recognize a person’s face to be able to identify the person as an imposter.
A Capgras patient’s conscious ability to recognize a face is intact; however, the patient cannot produce the emotional response that usually occurs when seeing a familiar face. There is a disconnect between the areas in the brain that are responsible for facial recognition and those involved in emotions and memory. In patients with neurologic damage, this disconnect is believed to occur by:
- damage to the ventromedial frontal cortex, which causes impairment of automatic arousal responses and
- damage to the right frontal lobe, which causes inability to evaluate beliefs and impairs reasoning.
To rationalize the strange feeling produced by the inability to recognize a face, the patient develops a delusion that the loved one is an imposter.
TREATMENT: Pharmacotherapy
At admission, Mrs. P was taking only lithium for mood stabilization because she refused to take antipsychotics. During her stay, she reluctantly agrees to start haloperidol, which is titrated up to 20 mg bid. She experiences delusions related to the Devil attacking her via the haloperidol and thus is switched to fluphenazine, titrated up to 20 mg bid. She feels that liquid fluphenazine agrees with her the most, so she is stabilized and eventually discharged with this formulation. Switching to a depot formulation would have improved compliance, but Mrs. P adamantly resists this.
As her psychotic symptoms begin to resolve, Mrs. P begins to feel she is getting her body parts back. For example, she feels her face is her own but her nose is still not hers. During Mrs. P’s hospitalization, these bodily delusions lessen and eventually clear.