Capgras' syndrome with organic disorders

Abstract

Summary: Capgras' syndrome, one form of the delusional misidentification syndromes, is described. Three patients with the syndrome are reported. The first had a right cerebral infarction, the second had nephrotic syndrome secondary to severe pre-eclampsia in the puerperium, and the third had uncontrolled diabetes mellitus with dementia. Evidence is reviewed regarding an organic aetiology for Capgras' syndrome. We conclude that, when the syndrome is present, a thorough search for organic disorder should be made.

Can we learn from the clinically significant face processing deficits, prosopagnosia and capgras delusion?

“…Although two out of three of Capgras and colleagues' reports concerned patients with neurologic disorders, the neurologic aspect was overlooked in early studies in an attempt to provide a psychodynamic explanation for the delusion. In more recent studies, the delusion has served as the focus for an etiological debate supported by investigators who believe that the disorder has organic causes (Christodoulou, 1977;Collins et al, 1990;F6rstl, 1990;Joseph, 1986aJoseph, , 1986bJoseph et al, 1990;Luaut6 et al, 1990;Spier, 1992) and by investigators who are convinced that it is caused by psychodynamic factors (Berson, 1983;Christodoulou, 1977;Enoch and Trethowan, 1991;Koritar and Steiner, 1988;O'Reilly and Malhotra, 1987;Shraberg and Weitzel, 1979;Sinkman, 1983;Spier, 1992). McAllister (1992), Critchley (1989), Cutting (1991), Doran (1990), F6rstl (1990), and Koritar and Steiner (1988) have suggested that Capgras delusion stems from a coalescence of organic and psychodynamic factors.…”

“…A number of researchers (Alexander et al, 1979;Cutting, 1991;Ellis and Young, 1994;F6rstl et aL, 1991;Joseph, 1986a;Lewis, 1987;Spier, 1992; have opted for the organic view because Capgras delusion has opted in association with various organic illnesses, such as dementing disorders (Anderson, 1990;Burns, 1987;Crawford et al, 1986;Kumar, 1987;Kurucz and Feldmar, 1979;Luaut6 et al, 1990), epilepsy (Fishbain, 1987) schizophrenia (Christodoulou, 1977;Ellis and Young, 1994), diabetes (Collins et al, 1990), stroke head trauma (Fishbain, 1987(Fishbain, , 1989Romanik and Snow, !984), and the effects of electroconvulsive therapy (ECT; Hay, 1986). The organicity of Capgras delusion has often been supported by brain imaging techniques such as computerized tomography (CT) scans, magnetic resonance imaging (MRI), positron emission tomography (PET), single photon emission computed tomography (SPECT), brain electrical activity mapping (BEAM), and field potential techniques such as the electroencephalography (EEG) (Alexander et al, 1979;Burns, 1985;Collins et al, 1990;Feinberg and Shapiro, 1989;F6rstl, Almeida et al, 1991;F6rstl, Burns et al, 1991;Joseph et al, 1990;Lewis, 1987).…”

“…The organicity of Capgras delusion has often been supported by brain imaging techniques such as computerized tomography (CT) scans, magnetic resonance imaging (MRI), positron emission tomography (PET), single photon emission computed tomography (SPECT), brain electrical activity mapping (BEAM), and field potential techniques such as the electroencephalography (EEG) (Alexander et al, 1979;Burns, 1985;Collins et al, 1990;Feinberg and Shapiro, 1989;F6rstl, Almeida et al, 1991;F6rstl, Burns et al, 1991;Joseph et al, 1990;Lewis, 1987).…”

“…Additionally, these evaluations have revealed signs of more injury in the right cerebral hemisphere than in the left cerebral hemisphere (Alexander et aL, 1979;Christodoulou, 1977;Collins, 1990;Cutting, 1991;Ellis and Young, 1990;F6rstl et al, 1991;Kapur et al, 1988;Joseph, 1986b;Joseph et al, 1990;Lewis, 1987). Lewis (1987), in a single-case study of transient Capgras delusion, used MRI data to show bilateral occipitotemporal lesions (much like the lesions found in prosopagnosia) as well as bilateral frontal lesions, which were smaller and fewer in number than the occipltotemporal lesions.…”

“…Some studies (e.g., Collins et aL, 1990;F6rstl et al, 1991) were unable to show clear evidence of right hemisphere involvement (or a distinction between left and right hemisphere lesions) because of the presence of global or diffuse lesions. Possibly, test results in many of these studies did show such a distinction, but because that distinction was not related to the focal point of the studies, it was not noted by the investigators and was, therefore, not communicated in their publications.…”