Fregoli Delusion

History

The delusion was first described by Courbon and Fail in 1927 and was named after Leopoldo Fregoli, an actor at the time who was famous for his disguises on stage. The authors described a 27-year-old woman who believed she was being persecuted by two actors whom she often saw at the theater. The woman believed the actors pursued her closely, taking the form of people she knew or met.

The Fregoli Delusion: Nosology

The delusion has been categorized as one of the four main and classical delusional misidentification syndromes, the other three being the following:

• a.
  Capgras syndrome (in which the patients believe that a person, usually a relative, has been replaced by a double)
• b.
  Intermetamorphosis (in which the patients believe that persons in their environment change places with one another)
• c.
  The syndrome of subjective doubles (in which the patients believe that other persons have been transformed into themselves)

The four syndromes are grouped together since they often co-occur and interchange in the same patient as well as because they present the same basic themes—namely, the negation of true identity and the belief in doubles (sosies).

In the classic form of the Fregoli delusion, patients were thought to make a “hyperidentification.” Although they recognize the forms of the strangers, they identify those people as other people, specific persecutors. In contrast, patients with the Capgras delusion are thought to “hypoidentify” their relative by denying his or her identity. Delusional misidentifications have also been reported to concern misidentifications of objects or places and therefore are thought to be linked to another delusional belief sometimes found in neurological patients, reduplicative paramnesia (a delusional belief that a place or a location exists simultaneously in two different places or that it has been relocated to another site).

Etiological Hypotheses

Fregoli delusion as a symptom usually occurs in psychotic illnesses and especially in schizophrenic illness, schizophrenia-like psychosis, and schizoaffective and affective disorders, though it has been reported to occur as a manifestation of various organic brain disorders, such as head trauma, ischemic brain damage (i.e., from a stroke), Alzheimer's disease, Parkinson's disease, epilepsy, or metabolic diseases. Delusions of misidentification in general appear to be associated especially with organic lesions affecting mostly limbic structures and, to a lesser extent, both the frontal and parietal lobes. Contemporary accumulated evidence suggests that right hemisphere lesions predominate in the etiology of delusional misidentifications.

Fregoli delusion, for example, was reported in a patient following abruptly after ischemic brain damage that involved the right fusiform gyrus and face specific area; furthermore it is estimated that up to a third of all patients with Alzheimer's disease display the phenomenon at some point during the course of their illness. Delusional misidentification syndromes therefore have been used as an exemplar pathological phenomenon for the study of delusion formation. However, despite the accumulated evidence for the importance of organic factors in the etiology of these syndromes, physiological data alone, according to present knowledge, cannot explain the “delusional” nature of the belief, and therefore, the pathogenesis of the delusion remains unclear.

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