Capgras for Cats and Canaries

Capgras syndrome is the delusion that a familiar person has been replaced by a nearly identical duplicate. The imposter is usually a loved one or a person otherwise close to the patient.

Originally thought to be a manifestation of schizophrenia and other psychotic illnesses, the syndrome is most often seen in individuals with dementia (Josephs, 2007). It can also result from acquired damage to a secondary (dorsal) face recognition system important for connecting the received images with an affective tone (Ellis & Young, 1990).¹ Because of this, the delusion crosses the border between psychiatry and neurology.

The porous etiology of Capgras syndrome raises the question of how phenomenologically similar delusional belief systems can be constructed from such different underlying neural malfunctions. This is not a problem for Freudian types, who promote psychodynamic explanations (e.g., psychic conflict, regression, etc.). For example, Koritar and Steiner (1988) maintain that “Capgras' Syndrome represents a nonspecific symptom of regression to an early developmental stage characterized by archaic modes of thought, resulting from a relative activation of primitive brain centres.”

The psychodynamic view was nicely dismissed by de Pauw (1994), who states:

While often ill-founded and convoluted, these formulations have, until recently, dominated many theoretical approaches to the phenomenon. Generally post hoc and teleological in nature, they postulate motives that are not introspectable and defence mechanisms that cannot be observed, measured or refuted. While psychosocial factors can and often do play a part in the development, content and course of the Capgras delusion in individual patients it remains to be proven that such factors are necessary and sufficient to account for delusional misidentification in general and the Capgras delusion in particular.

Canary Capgras

Although psychodynamic explanations were sometimes applied ² to cases of Capgras syndrome for animals,³ other clinicians report that the delusional misindentification of pets can be ameliorated by pharmacological treatment of the underlying psychotic disorder. Rösler et al. (2001) presented the case of “a socially isolated woman who felt her canary was replaced by a duplicate”:

Mrs. G., a 67-year-old woman, was admitted for the first time to a psychiatric hospital for late paraphrenia. ... She had been a widow for 11 years, had no children, and lived on her own with very few social contacts. Furthermore, she suffered from concerns that her canary was alone at home. She was delighted with the suggestion that the bird be transferred to the ward. However, during the first two days she repeatedly asserted that the canary in the cage was not her canary and reported that the bird looked exactly like her canary, but was in fact a duplicate. There were otherwise no misidentifications of persons or objects.

Earlier, Somerfield (1999) had reported a case of parrot Capgras, also in an elderly woman with a late-onset delusional disorder:

I would like to report an unusual case of a 91-year-old woman with a 10-year history of late paraphrenia (LP) and episodes of Capgras syndrome involving her parrot. She was a widow of 22 years, nulliparous, with profound deafness and a fiercely independent character.  The psychotic symptoms were usually well controlled by haloperidol 0.5 mg orally. However, she was periodically non-compliant with medication, resulting in deterioration of her mental state, refusal of food and her barricading herself in her room to stop her parrot being stolen. At times she accused others of “swapping” the parrot and said the bird was an identical imposter. There was no misidentifcation of people or objects. Her symptoms would attenuate rapidly with reinstatement of haloperidol.

Both of these patients believed their beloved pet birds had been replaced by impostors, but neither of them misidentified any human beings. Clearly, this form of Capgras syndrome is different from what can happen after acquired damage to the affective face identification system (Ellis & Young, 1990). Is there an isolated case of sudden onset Capgras for animals that does not encompass person identification as well? I couldn't find one.


A Common Explanation?

Despite these differences, Ellis and Lewis (2001) suggested that “It seems parsimonious to seek a common explanation for the delusion, regardless of its aetiology.” I'm not so sure. If that's true, then haloperidol should effectively treat all instances of Capgras syndrome, including those that arise after a stroke. And there's evidence suggesting that antipsychotics would be ineffective in such patients.

Are there systematic differences in the symptoms shown by Capgras patients with varying etiologies? Josephs (2007) reviewed 47 patient records and found no major differences between the delusions in patients with neurodegenerative vs. non-neurodegenerative disorders. In all 47 cases, the delusion involved a spouse, child, or other relative. {There were no cases involving animals or objects.}

The factors that did differ were age of onset (older in dementia patients) and other reported symptoms (e.g., visual hallucinations ⁴ in all patients with Lewy body dementia, LBD). In this series, 81% of patients had a neurodegenerative disease, and only 4% had schizophrenia [perhaps the Capgras delusion was under-reported in the context of wide-ranging delusions?]. Other cases were due to methamphetamine abuse (4%) or sudden onset brain injury, e.g. hemorrhage (11%).

Interestingly, Josephs puts forth dopamine dysfunction as a unifying theme, in line with Ellis and Lewis's general suggestion of a common explanation. The pathology in dementia with Lewy bodies includes degeneration of neurons containing dopamine and acetylcholine. The cognitive/behavioral symptoms of LBD overlap with those seen in Parkinson's dementia, which also involves degeneration of dopaminergic neurons. But dopamine-blocking antipsychotics like haloperidol should not be used in treating LBD. So from a circuit perspective, using “dopamine dysregulation” as a parsimonious explanation isn't really an explanation. And this conception doesn't fit with the neuropsychological model (shown at the bottom of the page).

I'm not a fan of parsimony in matters of brain function and dysfunction. We don't know why one person thinks her canary has been replaced by an impostor, another thinks her husband has been replaced by a woman, while a third is convinced there are six copies of his wife floating around.⁵ I don't expect there to be a unifying explanation. The BRAIN Initiative and the Human Brain Project will teach us absolutely nothing about the content of delusions. Ultimately, the study of Capgras and other delusional misidentification syndromes present a challenging puzzle for those of us seeking neural explanations of thought and behavior.


Footnotes

¹ From Ellis and Young (1990). Also see figure below.

Bauer (1984, 1986) advanced the view that there are two routes to facial recognition. The main route runs from visual cortex to temporal lobes via the inferior longitudinal fasciculus....the 'vental route' corresponds to the system responsible for overt or conscious recognition, and it is the route which typically is damaged in cases of prosopagnosia. The other, described as the 'dorsal route', runs between the visual cortex and the limbic system, via the inferior parietal lobule, and is sometimes intact in prosopagnosic patients. It is this latter route which ... gives the face its emotional significance and hence, when the ventral route is selectively damaged, can give rise to covert recognition (i.e. recognition at an unconscious level).

² Canine Capgras:

Reports 2 separate cases (a 76-yr-old woman and a 57-yr-old woman) in which the S believed that her pet dog had been replaced by an identical double. The psychodynamic issues that these cases raise are discussed. [NOTE: I don't have access to this article, sorry I can't say more.] In the Capgras delusion the double is usually a key figure in the life of the patient.

³ Capgras for animals was dubbed zoocentric Capgras syndrome by Ehrt (1999). He presented the “case of a 23-year old women who had the delusional belief that her cat had been replaced by the cat of her former boy-friend.”

⁴ There are a number of interesting hypotheses on why visual hallucinations are so common in Lewy body dementias.

⁵ Unless he's a character in Orphan Black... But really, why six copies instead of three? What I mean here is an explanation beyond the trivial: one person lives alone with a canary, while the other two live with a spouse.


References

de Pauw KW. (1994). Psychodynamic approaches to the Capgras delusion: a critical historical review. Psychopathology 27(3-5):154-60.

Ellis HD, Lewis MB. (2001). Capgras delusion: a window on face recognition. Trends Cogn Sci. 5(4):149-156.

Ellis, H., & Young, A. (1990). Accounting for delusional misidentifications. The British Journal of Psychiatry, 157 (2), 239-248 DOI: 10.1192/bjp.157.2.239

Josephs, K. (2007). Capgras Syndrome and Its Relationship to Neurodegenerative Disease. Archives of Neurology, 64 (12) DOI: 10.1001/archneur.64.12.1762

Koritar E, Steiner W. (1988). Capgras' syndrome: a synthesis of various viewpoints. Can J Psychiatry 33(1):62-6.

Rösler, A., Holder, G., & Seifritz, E. (2001). Canary Capgras. The Journal of Neuropsychiatry and Clinical Neurosciences, 13 (3), 429-429 DOI: 10.1176/jnp.13.3.429

Somerfield D. (1999). Capgras syndrome and animals. Int J Geriatr Psychiatry 14(10):893-4.

 from Ellis & Lewis (2001)