Exploring the Etiology of Capgras Syndrome

The following is a paper on the Capgras Delusion written for my Neuropsychology class in the final year of my Psychology B.A.

Doctor, There’s an Impostor in My Bed! Perceptual Anomalies in the Capgras Delusion
November 2006

Imagine that you are eating lunch with your mother when you realize something about her is different. It is not a physical alteration, such as a new haircut or glasses, so much as the uneasy feeling you get while looking at her. As the weeks go by you continue to treat her with suspicion; you carefully inspect her behaviour and notice that she is responding strangely. The obvious truth finally sinks in—she is not your real mother! Though practically identical, this woman is clearly an impostor!

Welcome to the life of a Capgras syndrome patient, where anything from the people or pets to the places and objects you hold most dear may suddenly feel so unfamiliar that a delusion emerges: that of their substitution or duplication, perhaps by an actor, a robot, or simply, innocently, their identical twin figure.

The first well-documented case of this syndrome was an article by Capgras and Reboul-Lachaux (1923, as cited in Doran, 1990). Their patient was a 53-year-old woman who had the illusion that people in her life were being replaced by identical doubles; at one point, she came to believe that she herself had been duplicated. This “illusion of doubles” came to be coined ‘Capgras Syndrome’, and is now considered the prototype of various delusional anomalies categorized as misidentification syndromes.

Symptoms of Capgras tend to be monothematic and circumscribed. In other words, the impostor delusion tends to stand out against an otherwise normal belief system—“an island of irrationality within a sea of rationality” (Stone and Young, 1997). General trends within these patients, as summarized by Stone and Young, include difficulty in certain facial processing tasks, lack of interest concerning the fate of the “original” duplicated person, suspiciousness and occasional hostility (but mainly agreeableness) toward the double, and little recasting of beliefs to accommodate the delusional one. There is no evidence of overall reasoning deficits among these patients, especially considering that most feel it necessary to provide evidence for their claim.

Though Capgras typically accompanies a diagnosis of paranoid schizophrenia and is most often encountered in patients of middle or old age, over one third of cases occur in conjunction with traumatic brain lesion (Ramachandran and Blakeslee, 1998), especially injury to regions of the brain implicated in the processing of faces. As discussed in a detailed review by Stone and Young (1997), the delusions are often linked to lesions in the parieto-temporal regions of the right hemisphere.

Specifically, facial recognition is thought to be processed along two neural routes of the visual system, as proposed by Bauer (1984, as cited in Stone and Young, 1997): the ventral route for overt recognition or identification, and the dorsal route to the limbic system for affective significance. Cognitive dissonance resulting from a dysfunction in this second pathway is hypothesized to be at the root of Capgras syndrome. Brain imaging studies have provided evidence of dysfunctional connections among frontal cortex, multimodal association areas and paralimbic structures, resulting in cognitive-perceptual-affective dissonance (Papageorgiou et al., 2003); this suggestion of dissonance is consistent with the popular hypothesis that Capgras patients are able to recognize someone but not experience the appropriate affective responses. Since prosopagnosia, an inability to recognize faces, is thought to result from damage to the ventral route, these two syndromes are often considered mirror images of one another (Young and Ellis, 1990, as cited in Stone and Young, 1997). Finally, worsening of the condition is promoted by the vicious circle of confirmation bias: the patient looks for strange behaviours in others, and in response to this unusual behaviour, others act strangely toward the patient. This makes it difficult to break from a cycle of self-fulfilling prophecy.

Most reported cases of Capgras were diagnosed before modern diagnostic criteria and current neuroimaging methods; therefore, it should come as no surprise that the previously widely accepted explanation for the delusion was proposed by the psychodynamic field of psychology. It was believed that a patient created a double according to a defense mechanism due to guilt or conflicting emotions, most notably the Oedipus or Electra complex. Since a person would experience internal dissonance at discovering sexual feelings toward a parent or family member, it was proposed that they created a double in order to replace the object of their emotions and relieve this tension. However, current technology caused a shift from the psychodynamic foundation to viewing Capgras as a disorder of the central nervous system (Doran, 1990); advances in brain imaging clearly show some neurological damage in the majority of cases. Furthermore, the fact that Capgras delusions exist for pets, among other things, further weakens the psychodynamic approach.

Though psychological factors cannot be ruled out of the etiology, there seems to be an undeniable organic or physiological basis to misidentification syndromes. Stone and Young (1997) discuss two factors that partially explain the existence of Capgras delusions: a perceptual deficit and a reasoning bias. The Perceptual Deficit Account, similar to Fine, Craigie and Gold’s (2005) Explanation Account, claims that the delusion is the sufferer’s attempt to account for an anomalous perceptual experience. This account is incomplete on its own because the questions of why the impostor belief persists or that other sensory modalities do not override the faulty interpretation of the visual experience remain to be answered.

The Reasoning Bias Account claims that the original misperception is triggered by an organic process but that the delusion itself is determined by the psychology of the patient; in other words, the delusion is caused by a misinterpretation of an unusual experience. Delusional patients have abnormal reasoning processes: they tend to request less information before making a decision and jumping to conclusions (Huq et al., 1988, as cited in Stone and Young, 1997) and they have a tendency to attribute even hypothetical negative events to external causes (Candido and Romney, 1990, as cited in Stone and Young, 1997). Therefore, they are experiencing biases (rather than deficits) by using available information in a certain way through otherwise normal processes; for instance, by attributing their lack of affect to external consequences, they may be mistaking changes in the self for changes in others.

Both accounts are insufficient to determine why Capgras patients maintain these implausible beliefs despite available contradicting evidence. Stone and Young (1997) explore a philosophical model of belief formation to determine how patients might validate their decisions. Maher (1988, as cited in Stone and Young, 1997) claimed that delusional beliefs are formed the same way as normal and scientific ones: through a balance of observational adequacy and conservationism. It was proposed therefore that Capgras patients rely too heavily on observational adequacy (they have a bias toward first-hand experiences or the evidence of their senses), but maintain the integrity of their own personal beliefs by isolating this delusional belief, which is why the delusion tends to be circumscribed.

When patients feel that they must further validate their claims or beliefs, they have tended to refer to slight physical differences between the original and the impostor. Though this exploration is a step closer to resolving the dilemma of why the impostor belief is not rejected, it cannot explain the consistency of the impostor belief over other potential rationalizations. As put by Fine, Craigie, and Gold (2005):

The delusional belief is just one of several hypotheses that are observationally adequate… Many neurologic conditions result in direct perceptual abnormalities (e.g., acquired color blindness), yet we would not expect a corresponding delusion (e.g., that the world has been drained of color) as a default.

Furthermore, hypothesizing an abnormality in a patient’s belief acceptance system insinuates general patient susceptibility to any number of beliefs when an experience conflicts with prior knowledge. It is yet unknown whether Capgras patients experience subtler but similarly strange delusions.

The possibility that Capgras patients experience widespread emotional impairments, and not simply those pertaining to their loved ones, has been explored. This accompanies the suggestion that the misinterpretation of sensory evidence results from the fact that there is a larger discrepancy between, say, the affective response you should have to your mother as opposed to the delivery boy, so the missing affect toward the mother would be more noticeable. It has indeed been noted that patients often report persistent loss of affective response and generalized feelings of unfamiliarity, and they often seem to lack appropriate accompanying emotion (Christodoulou, 1977, as cited in Stone and Young, 1997). This could also explain why patients show little concern regarding the whereabouts or wellbeing of the original that was replaced.

Though this idea (that all emotions have been reduced due to some injury to the amygdale) seems intuitive, a case study by Hirstein and Ramachandran (1997, as cited in Ramachandran and Blakeslee, 1998) showed that this is not necessarily the case. Ramachandran hypothesized that his Capgras patient would not register a change in skin conductance when looking at pictures of his family intermixed with those of strangers. Control participants had a large response to their parents as expected, whereas the delusional patient showed no increased response; however, at times there would be a blip after a long delay, as if the brain were doing a double take. This showed that the patient was not responding emotionally to his parents. The experimenter kept track of the patient’s other emotions over a period of months to determine whether there was a global disturbance in emotion, but his responses were appropriate and diverse in all other situations. It was hypothesized that the large discrepancy between expected and actual emotion when the patient should have been experiencing a “warm fuzzy” feeling is the cause of the rationalization or delusion, and supports the Perceptual Deficit/Explanation Account. Ramachandran also considered that Cotard’s syndrome, where a person believes they are dead, is an exaggerated form of Capgras, where all affect is diminished or absent.

This finding is undermined by the argument that patients with similar perceptually anomalous experiences do not necessarily form Capgras syndrome; Coltheart et al. (2000, as cited in Fine, Craigie, and Gold, 2005) reported that patients with bilateral ventromedial frontal damage (an area thought to be important for integrating somatic state information) also failed to show increased autonomic responsiveness to familiar faces, though these patients did not develop delusional beliefs. Therefore, a lack of autonomic responses is itself insufficient to produce the delusion; there must be other determining factors (Ellis and Lewis, 2001).

Fine et al. (2005) also explore the Expression Account, where delusional beliefs are expressions of the content of a particular disordered experience. In other words, the disordered experience is directly that of replacement by an impostor, so the account eliminates the problem of why the impostor belief is invariably constructed. Dalgarrondo, Fijuisawa, and Banzato (2002) performed a case study on a 26-year-old blind woman with Capgras syndrome based on the sensory modalities of touch, smell, and taste. Neurological examinations, MRI, and SPECT were all normal. This case reinforces the argument that facial recognition impairment is an insufficient explanation for Capgras delusions, suggesting that psychological factors such as ambivalence and fear of losing someone may play a role. The authors believe that an anomalous perceptual process is the result of a delusional transformation of the world, rather than the cause. This is consistent with the Expression Account presented above; however, such an account must then explain how such a perceptual belief arises.

A case study by Dietl et al. (2003) presents another anomaly to the current hypotheses of Capgras delusions. A 59-year-old woman with paranoid psychosis developed Capgras regarding her daughter and a close friend. A few days on antipsychotic treatment with haloperidol resolved it concerning her daughter but the delusion regarding her friend persisted. A year later, she began experiencing delusions of plans for self-substitution, but did not expect this person to be physically similar to herself. Her delusions about her daughter returned and she eventually reached the conclusion that this girl may not be her real daughter but was a pleasant person nonetheless, so did not confront her with suspicions any longer. Several inconsistencies with current hypotheses include the fact that the woman did not expect that her substitute would physically resemble her, and that a delusion regarding her daughter’s substitute occurred in that person’s absence. Therefore, this patient was not simply experiencing a face processing problem. Furthermore, the patient did not develop Capgras delusions for her husband, but rather reported that his facial features were altered; this suggests that additional cognitive processes were malfunctioning.

One insight that this case study presents is the idea that Capgras syndrome can be maintained without current visual input, which suggests that a reduced feeling of familiarity can become more general and independent; this is consistent with reports of blind patients with Capgras. It is therefore illustrated that additional factors must be integrated into the current model of Capgras etiology. Caution must be used when interpreting these results, however, due to the fact that the patient suffered from a paranoid disorder.

There are no conclusive treatments currently available for Capgras syndrome. Sometimes remission occurs naturally and sometimes the disorder persists; in many cases antipsychotic medication or neuroleptic therapy is provided. When remission does occur, it is frequently due to the removal or modification of a concomitant neurological condition; MacCallum (1973, as cited in Doran, 1990) hypothesized that organic conditions cause a change in a patient’s affects and perceptions, thus presenting Capgras syndrome.

In conclusion, no existing account or theory of Capgras syndrome is sufficiently explanatory of the phenomenon. The most credible and supported position to date is summarized neatly by Stone and Young (1997):

People voicing [the Capgras] delusion suffer an impairment that leads to faces being perceived as drained of their normal affective significance, and an additional reasoning bias that leads them to put greater weight on forming beliefs that are observationally adequate rather than beliefs that are a conservative extension of their existing stock.

Scientific evaluation of the processes in Capgras syndrome has many implications for our understanding of normal object- and face-recognition processes and the nature of beliefs, teaching us important principles about brain function. For instance, the fact that objects can be duplicated shows that items with which we are familiar or are particularly fond of may enjoy special cognitive status; also, we can deem our perceptions to be governed by comparisons between states of an object rather than absolute values (Ellis and Lewis, 2001).

The fact that Capgras patients do not recognize a loved one due to their impairments suggests that affective responses could be a key part of the ability to recognize a face; perhaps “affect and cognition are under the control of separate and partially independent systems” (Zajonc, 1980, as cited in Stone and Young, 1997). The fact that scientific studies have supported the dissociation hypothesis makes it no longer possible to interpret face recognition as proceeding in a strictly sequential fashion, but rather as a feeding process into an integrative device. Future studies should look into this possible attribution process, as this knowledge is critical for further understanding of Capgras syndrome.

References

Dalgalarrondo, P., Fujisawa, G., & Banzato, C.E.M. (2002). Capgras syndrome and blindness: Against the prosopagnosia hypothesis. Canadian Journal of Psychiatry, 47(4), 387-388.

Dietl, T., Herr, A., Brunner, H., & Friess, E. (2003). Capgras syndrome – out of sight, out of mind? Acta Psychiatry Scandinavica, 108, 460-463.

Doran, J.M. (1990). The Capgras syndrome: Neurological/neuropsychological perspectives. Neuropsychology, 4, 29-42.

Ellis, H.D., & Lewis, M.B. (2001). Capgras delusion: A window on face recognition. TRENDS in Cognitive Sciences, 5(4), 149-156.

Fine, C., Craigie, J., & Gold, I. (2005). Damned if you do; Damned if you don’t: The impasse in cognitive accounts of the Capgras delusion. PPP, 12(2), 143-151.

Papageorgiou, C., Ventouras, E., Lykouras, L., Uzunoglu, N., & Christodoulou, G.N. (2003). Psychophysiological evidence for altered information processing in delusional misidentification syndromes. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 27, 365-372.

Ramachandan, V.S., & BlakeBlakeslee, S. (1998). Phantoms in the Brain. New York: HarperCollins.

Stone, T., & Young, A.W. (1997). Delusions and brain injury: The philosophy and psychology of belief. Mind & Language, 12(3/4), 327-364.