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History of the syndrome
Historically, Capgras Syndrome has been framed in psychiatric/ psychological terms. In recent decades research into the syndrome has shifted to a neurological/ neuropsychological focus. This has occurred in parallel with the growing dominance of neuroscientific methods in Psychology.

The dominant theoretical framework during the early-to-mid-twentieth century for understanding Capgras Syndrome was psychoanalysis. For example, a male patient who views his mother as an 'imposter' could be interpreted as the defensive rationalization of socially unacceptable, formally repressed, latent sexual desire for her (see Oedipus Complex). This would be prompted by some sort of psychological trauma. However, from the dominant contemporary perspective, interested in the brain-behaviour relationship, this account is largely unsatisfactory. Ramachandran (2012) for instance, illustrates this point by arguing latent sexual desire is not always applicable as an explanation. He refers to his Capgras Syndrome patient Steve, who in this case was convinced his pet poodle, Fifi, was in fact an imposter.

The above account views the appearance of the disorder as a proactive defensive process, elicited to rationalize unacceptable feelings. Capgras and Carvette (1924), for example, used such an approach to discuss comorbid presentations (appearing with other dysfunctions) of the condition (1924; as cited in Enoch, 1963), questioning whether it can achieve unique psychiatric classification or whether it should be placed on a continuum of psychosis. The debate has slowly moved in favor of a nosological description, despite the suggestion of relatively diffuse and comorbid etiology. Indeed, Young (2008) suggests a one-stage phenomenal account is inadequate to explain the causal factors underlying its onset.

Contemporary theories
The influence of neuroimaging, neuropsychological and neuropharmacological methods in the study of the epidemiology of Capgras Syndrome has increased in recent decades. Edelstyn and Oyebode (1999) suggest 25-40% of cases are associated with organic disorders in the literature, particularly right hemisphere abnormalities of the temporal and frontal regions.

McKay, Langdon and Coltheart (2005) describe two types of theorizing about delusions. The 'motivational' approach views them as defensive, palliative and potentially adaptive; reminiscent of aspects of the psychoanalytic tradition. Whereas, the 'cognitive deficit' approach adopts a pathological conceptualization; which suggests the cognitive system is functioning abnormally.

A key theory in current thinking was proposed by Ellis and Young (1990), who suggest Capgras Syndrome is a 'mirror image' of the impairments underlying prosopagnosia. That is to say, where disease has led to misrecognition of a close familiar as an imposter but recognition of their face is maintained in Capgras Syndrome, in prosopagnosia there is an opposite pathology in which recognition of a face is absent but a sense that the unique identity of the person, once recognized, belongs. Bauer (1984) used neuropsychological data in a 'guilty knowledge test' with galvanic skin response (GSR) to propose a ‘dual-route’ theory of recognition. This incorporates an 'overt' ventral visual-limbic pathway and a 'covert' dorsal visual-limbic pathway in face recognition. The former refers to a recognition pathway in the brain mediating memories for faces, their visual features and declarative knowledge (explicit and knowledge-based), whilst the latter to a pathway mediating memories for faces and their emotional salience.Young, Reid, Wright and Hellawell (1993) suggest damage to the ventral route forms the etiology (origin) of the syndrome; preventing 'emotion' information from being linked to recognition. Hence, an impoverished autonomic response (a bodily and embodied feeling) to a familiar person or object may ensue.

There is neuropsychological support for dissociating between covert and overt recognition. Hirstein and Ramachandran (1997), for instance, reported the case of DS, who had a 'modality-specific' presentation of Capgras Syndrome. Although he would look at his parents and believe them to be imposters, in conversation on the telephone, could speak to them with the conviction he was hearing the voices of his ‘real’ parents. Looking at DS’ GSR, they did not find it to be larger in magnitude for familiar faces than non-familiars, which would normally be expected within the average population. This suggests an auditory pathway remained intact. Also, when shown photographs of a model with her face in a slightly different direction each time, he referred to each as a different but 'similar looking' person. Hirstein and Ramachandran postulate this is because a lack of limbic activation leads to separate memory schemas and, therefore, a link to a common denominator of successive episodic memories cannot be discerned.

In The Tell-Tale Brain, Ramachandran (2012) proposes a different conceptualization of the dual-route explanation. In referring to several recognition pathways, he suggests that 'pathway 3' (a "so what" stream, which evokes emotions), and 'pathway 2' (a "what" stream, enabling identification), underlie the double dissociation between Capgras Syndrome and prosopagnosia. Ramachandran distinguishes these recognition routes from a linguistic/ auditory pathway, to explain the apparent ‘normal’ identification in patients such as DS, for whom the delusion does not present in conversations (e.g. telephone) minus the physical presence of the misrecognized subject.

Ramachandran and Young et al.’s theories lay out the pathology of the delusion. The neuropsychological evidence informing these theories relies on the subtractive method. This involves an inference of functionality based on the loss of function due to organic disease. This allows the brain to be split into specific functional modular components; allowing in this case the double dissociation (where different impairments between individuals show different patterns) between the covert-overt and “so what”-“what” recognition pathways. However, the existence of brain plasticity (the adoption of function by 'alternate' brain regions) makes inferences of strict and generalizable functional topography (specific areas of anatomy with a primary functional role) problematic.

Ramachandran (2012) supplements the neuroanatomical explanation by maintaining an evolutionary standpoint; in which the brain has developed to adaptively rationalize the input received. For such a disturbance of conscious processing, the brain attempts to correct for the "intolerable discrepancy" (via "recurrent experiential feedback loops"; p.290) with the rationalization characteristic of the syndrome. Here, global plasticity to input, which is normally adaptive, demonstrates an attempt to make sense of the environment.

Young (2008), on the other hand, uses a cognitive conceptualization to argue the 'mirror image' model neglects the phenomenal aspect of the condition, which was paid sole attention in early psychoanalytic explanations. He reaffirms the causal explanatory value of positing a physiological fault, but argues that a 'confirmatory bias' maintains the delusion; where a sense of estrangement is perpetuated by efforts to make sense of the experience. He terms this an 'interactionist model' to denote the bidirectional relationship between bottom-up and top-down processes.

The anatomical element of these models diminishes some of their explanatory power when the comorbidity of the delusion with other diseases is perceived. For instance, Sidoti and Lorusso (2007) describe a case of comorbid multiple sclerosis and Capgras delusion following a high dose of steroids. Although it does not refute the neurophysiological localizations of the theories, the relative rarity of 'pure' Capgras Syndrome cases makes it difficult to make inferences with any certainty, particularly with diffuse neurochemical pathologies such as schizophrenia.

Evidence from Horikawa et al. (2006), who used single photon emission computed tomography (SPECT) and event-related potentials (ERPs) to study types of delusional misidentification, including Capgras syndrome, suggests that right frontal regions implicated in inhibitory processes show abnormal readings. They suggest such syndromes can be influenced by a dysexecutive state, reducing behavioural and cognitive control. This may be suggestive of the more global processing occurring in the phenomenal aspect of the delusion.