Delusional Misidentification Disorders: Part 1 - Capgras Syndrome
isa misidentification syndrome where a person holds a delusion or belief that an acquaintance, typically a close family member, has been replaced by an identical looking imposter. This syndrome can be transient, developing very quickly after a brain injury, or can take a chronic form where the delusion is long standing. The syndrome is named after Joseph Capgras lived 1873-1950 French psychiatrist who first described the disorder in a 1923 paper and used the term ‘illusion of doubles’ to describe a case of woman who had various doubles that had taken the place of people she knew. For some people with Capgras syndrome, even inanimate objects such as chairs and animals can be imposters. Often patients are so disturbed with seeing their doubles that they remove all mirrors from house. In some cases, if the Capgras sufferer can be convinced that one person is not an imposter, they will develop a Capgras delusion with someone else. (Sinkman, 2008).
Many patients suffering from Capgras Syndrome have already been diagnosed with schizophrenia. However, Capgras Syndrome can also be co-morbid with other mental health problems including; Alzheimer’s Disease, Cotard’s Syndrome, epilepsy, Farh’s Disease, Fregoli Syndrome, Hashimoto’s Hypothyroidism, Incubus Syndrome, Neurodegenerative Disease, Diogenes Syndrome, Parkison’s Disease (Bourget & Whitehurst, 2004; Ceylan et al., 2010; Chiu, 2009; Donnelly et al., 2008; Fischer et al., 2009; Josephs, 2007; Mishra, Prakesh, Mishra, Praharaj, & Sinha, 2009; Pande, 1981; Rodríguez, Madoz-Gúrpide, & Ustárroz, 2011; Yalin, Taş, & Güvenir, 2008). Capras has also been associated with the administration of morphine and ketamine (Bekelman & Hallenbeck, 2006; Corlett, D’Souza, & Krystal, 2010).
Since the time Capgras Syndrome was first described (and even a bit before) a number of theoretical explanations have been put forth as to its origins. As might be expected many of these theories were psychoanalytically based in the early days. De Pauw (Sinkman, 2008) has written a comprehensive account of these early conceptualizations of Capgras. In this article de Pauw notes that many of the psychoanalytic explanations are mutually incompatible. These psychoanalytic theories include; defense against unconscious homosexuality, a regression to the early stage of primary narcissism, which some writers believe was due to anxiety, and a novel resolution to the Oedipal and especially the Electra complexes. Psychodynamic explanations seemed to make sense because the people being replaced by imposters were almost always close family members. However, on closer scrutiny of the literature this argument falls apart as other people or things are often found to also be imposters, from doctors and nurses to entire buildings and other inanimate objects. In general, according to de Pauw psychoanalytic explanations tend to be “generally post hoc and teleological in nature, postulating motives that are not introspectable and defense mechanisms that cannot be observed, measured, or refuted” (p. 158). He concludes that while the presence of brain injury also does not fully explain Capgras Syndrome it may be due to a breakdown in the manner in which sensory information is brought into the brain and the way it is stored (and presumably retrieved).
Another issue in the published case literature about Capgras Syndrome is the focus on the delusion of the imposter to the exclusion of other aspects of the syndrome. Closer scrutiny often demonstrates other DMS and psychotic/schizophrenic symptoms in Capgras cases. Many patients suffer from a sort of expanded Capgras Syndrome where there are many other delusions present. Some of these delusions may be somatic in nature with the patient experiencing bizarre changes to their bodies, with their seeming strange and alien. Even the patient’s sense of self is changed and subject to delusion. These symptoms are reminiscent of schizophrenia and it is no surprise that many cases of Capgras have a co-morbid diagnosis of schizophrenia, usually of the paranoid variety. Upon closer examination it can become difficult to make a differential diagnosis between Capgras and schizophrenia in many sufferers, and the Capgras symptoms may be another aspect of the schizophrenic illness. In fact, studies have shown that misidentification symptoms occur in a large number of cases of schizophrenia, maybe even as high as 40% (Sinkman, 2008).
Modern clinicians and researchers now believe that Capgras has an organic basis, which is specifically related to cerebral dysfunction. Neuroimaging studies have shown that lesions in the right hemisphere of the brain are common among Capgras sufferers. Some studies have demonstrated bilateral damage to the hemispheres in Capgras patients (Bourget & Whitehurst, 2004). In one small study 81% of Capgras sufferers also had neurodegenerative disease, usually involving the Lewy body. As would be expected, these Capgras sufferers were older than Capgras patients without neurodegenerative disease, who were more likely to also suffer from paranoid schizophrenia, schizoaffective disorder, methamphetamine abuse, or other cerebrovascular problems. 100% of patients with Capgras and Lewy body disease experienced visual hallucinations (Josephs, 2007).
Capgras patients are prone to acts of violence, especially against people they have misidentified (Bourget & Whitehurst, 2004). Given the relation of Capgras to paranoid schizophrenia this makes sense.
There is evidence to support the idea that an emotional processing module in the brain, especially as it related to feelings of familiarity and unfamiliarity, and its connection to facial recognition is flawed in Capgras sufferers (Pacherie, 2009). This flaw in emotional processing can be demonstrated via facial recognition tasks and eye movement patterns (Brighetti, Bonifacci, Borlimi, & Ottaviani, 2007; Grignon & Trottier, 2005; Walther et al., 2010). Similar differences in audio perceptions related to working memory have also been reported for Capgras sufferers (Papageorgiou, Lykouras, Ventouras, Uzunoglu, & Christodoulou, 2002). In one dramatic case a Capgras patient had sexual relations with his wife, thinking she was a ‘double’. He had no feelings of familiarity with his wife whatsoever and essentially felt as if he were having sex with a different woman; so much so that he even changed his sexual behavior. The authors (Thomas Antérion, Convers, Desmales, Borg, & Laurent, 2008) note that this may be the only known documentation of a patient who was able to make his wife into his mistress!
As might be expected the typical treatment for Capgras Syndrome is anti-psychotic medications. However, when anti-psychotic medication is only partially or not effective the use of electroconvulsive therapy has been shown to be helpful. This is especially the case when Capras is co-morbid with Parkinson’s Disease (Chiu, 2009).
[Next - Fregoli Delusion]
Bekelman, D. B., & Hallenbeck, J. (2006). Capgras Syndrome Associated with Morphine Treatment. Journal of Palliative Medicine, 9(3), 810–813. doi:10.1089/jpm.2006.9.810
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Rodríguez, R. H., Madoz-Gúrpide, A., & Ustárroz, J. T. (2011). Propuesta de una batería neuropsicológica para la exploración del síndrome de Capgras. Revista Española de Geriatría y Gerontología, 46(5), 275–280. doi:10.1016/j.regg.2011.06.001
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Thomas Antérion, C., Convers, P., Desmales, S., Borg, C., & Laurent, B. (2008). An odd manifestation of the Capgras syndrome: Loss of familiarity even with the sexual partner. Neurophysiologie Clinique/Clinical Neurophysiology, 38(3), 177–182. doi:10.1016/j.neucli.2008.04.003
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