Capgras Delusions: Symptoms and Areas of the Brain Essay

A fixed, firm and false belief that people, in particular the close relatives or the spouse of a person, have been replaced by doubles or imposters is termed as a Capgras delusion (Capgras, 19232 cited in Edelstyn,1999 ). This term was first coined in the early 19^th century when Capgras and Reboul reported the case of a patient named Mme M. who presented with psychotic symptoms and a unique kind of delusion of substitution that imposters had replaced her family members (Capgras, 19232 cited in Sinkman, 2008). Ever since then, several cases presenting with similar features have been reported and extensive research in this arena has been conducted, in order to explore the underlying mechanisms and pathology of this rare and interesting presentation. Lately, Capgras delusion has been grouped under the umbrella term of Delusional Misidentification Syndromes (DMS) along with 11 other similar disorders (Joseph, 1986 cited in Edelstyn, 1999). Although Capgras delusions are considered to be a rare disorder, studies have shown that they are observed in up to 4% of patients with psychosis (Frazer and Roberts, 1994 & Kirov et al., 1994 cited in Edelstyn, 1999) and approximately 30% of patients suffering from Alzheimer’s diseases have also been shown to demonstrate this symptom (Ballard et al., 1995 cited in Edelstyn, 1999).

Symptoms associated with Capgras Delusions

Studies have shown that Capgras delusions do not occur in isolation. Rather, they are accompanied by a variety of other features which constitute the Capgras syndrome. A review of the case reports of patients with this disorder has shown that the most consistent presenting feature this disorder is the monothematic delusion of substitution of ones close relatives by a look alike or an imposter. Other abnormalities of thought which can coexist with Capgras delusions include multiple person misidentifications (Oyebode and Sargeant, 1996, Edelstyn et al., 1998a), presence of misidentification of inanimate objects (Young et al., 1994, Silva and Leong, 1995a & Edelstyn et al., 1998a), delusions of multiplicity of self, delusions of persecutions (Sinkman, 2008) and perception of morphological changes in the body (Sinkman, 2008). There have also been reports of associated hostility and aggression towards the imposters in some cases (O’Reilly, 1987)

Various presentations of Capgras delusions have been reported in literature. Lucchelli and Spinnler, reported a case of a gentleman who presented with capgras delusions in association with dementia, obsessive-compulsive symptoms and motor disturbances. During the course of the disease the patient also demonstrated the presence of the “phantom boarder” phenomenon and the “mirror sign phenomenon. In the quest to identify the etiology and pathophysiological basis of Capgras delusions, the patient was subjected to several diagnostic tests and assessment modalities. Neuroradiological investigations (CT and MRI) revealed nonspecific findings of mild enlargement of the ventricles and the brain sulci while the EEG showed bilaterally slowed cortical activity in the anterior regions. General cognitive assessment was also performed which showed global cognitive impairment which deteriorated over time. In order to assess the face and person recognition, the face assessment tools developed by Faglioni et al. and other commonly used assessment tools were employed. A modified version of Ekman and Friesen’s test was used to assess perceptual deficits with unknown faces and impairment in emotion recognition but the results were unremarkable. The patient was also tested for recognition of famous faces and autobiographical faces. The pertinent findings of these tests were that although the ability to identify faces and names were spared, patient’s familiarity judgment was significantly impaired (Lucchelli and Spinnler, 2007).

Similarly, Sinkman (2008) reported three cases of Capgras Syndrome amongst known cases of severe Schizophrenia, who in addition to Capgras delusions, demonstrated a variety of misidentity delusions including Fregoli delusions in one instance and profound identity diffusion and loss of ego boundaries. However, this theory has the limitation that it does not explain the multiplicity of delusions observed in several cases of Capgras delusions. Other similar cases of Capgras delusions have been reported by Young et al. (1993) while Hayman has reported two cases of Capgras delusions associated with pre-existing cerebral dysfunction (Hayman, 1977).

Moreover, patients with Capgras delusions have also been tested for the autonomic skin conductance response in the presence of familiar faces. Amongst normal peoples, there is an increase in this autonomic response when a familiar face is encountered. In contrast, various studies have shown that patients with Capgras delusions demonstrate a lack of differential skin conductance response in the presence of close relatives. In addition, their overall skin conduction responses are also diminished (Ellis 1997 & Hirstien, 1997).

The role of diagnostic investigations in Capgras delusions is limited. Cerceo et al. suggested that although brain imaging may play a role in revealing underlying abnormalities, the cost of imaging outweighs the benefits since results of brain imaging do not contribute significantly towards the treatment. No evidence has been found which supports use of CT to diagnose Capgras syndrome while some evidence supports use of brain MRI, however, but more research is required (Cerceo, 2006)

Areas of the brain associated with Capgras Delusions

Originally, this disorder was thought to be exclusively psychiatric in origin, since Capgras delusions have been found to be associated with certain psychiatric conditions including Schizophrenia especially the paranoid type, schizoaffective disorders and less commonly, affective disorders (Edelstyn, 1999). Over time, it has been increasingly observed that this delusion can also result from organic brain lesions that have resulted either due to trauma, hypoxia, toxins, neoplasms (Lucchelli and Spinnler, 2007).

Capgras delusions are also commonly observed in association with degenerative diseases such as Alzheimer ’s disease and dementia. Josephs (2007) in their study of 38 patients with Capgras delusions reported that 81% of the patients had concomitant neurodegenerative disease, the most common one being Lewy body disease. There was also coexistence of Visual hallucinations. They also reported that in the absence of neurodegenerative disease, the age of onset of Capgras delusion is lower and it is most commonly associated with psychiatric illnesses, substance abuse and cerebrovascular diseases (Josephs, 2007).

Cerebral dysfunction leading to Capgras delusions can involve different regions of the brain. The role of right hemispheric involvement in misidentification syndromes was first proposed by Wienstien et al. and later supported by many studies (Breen, 2001). Although some contradictory views exist, which have propose limbic system dysfunction and basal ganglia lesions as the primary factors involved in the development of capgras delusions while cortical involvement plays a secondary role in modifying the characteristics, content and form of the delusions(Cummings, 1997). A review of the identified cases of Capgras from 1968- 1999, revealed that most patients with this disorder demonstrate global atrophy and lateralization of the lesions to the right hemisphere is more common as compared to the left (Breen, 2001). The areas of the brain most commonly seen involved are the frontal and the temporal lobes (Edelstyn, 1999). Keeping in view the transient nature of the disorder as observed in certain cases, it has been postulated that instead of there being structural involvement of the brain tissues, dopaminergic or serotonergic overactivity and reduced activity if platelet monoamine oxidase, contribute towards the development of this condition (Daniel et al., 1987, Canagasabey and Katona, 1991 & Lehmann, 1988 cited in Edelstyn, 1999)

Models of Face Recognition and Capgras Delusions

The ability to recognize different faces, acknowledge, remember and recall them is a complex phenomenon. The first model which was thought to be involved in facial recognition was the modal model, which proposed that the transfer of information related to the identity of a particular face is takes place via a single route which is parallel to those for dealing with the expression of the face and picture codes of the image. (Hay and Young, 1982). Later on, Bauers introduced a two route model of face recognition according to which facial recognition occurs via two distinct and independent routes. Facial recognition can be classified as either covert (which occurs via the ventral route, which involves the longitudinal fasciculus between visual cortex and limbic system) or overt (which involves the use of the dorsal route which passes from visual cortex via the superior temporal sulcus, inferior parietal lobe and cingulate gyrus and finally gets relayed to the parts of the limbic system, especially the amygdala) (Bauer, 1984). Based on this two route model of face recognition, Ellis and Young hypothesized that patients experiencing Capgras delusions have intact covert facial recognition but a compromised dorsal route which leads to the impairment of affect associated with recognition of familiar faces and subsequent loss of familiarity (Ellis, 1990). This loss of proven by demonstration of decreased skin conduction response in the presence of familiar faces as shown by different studies (Ellis 1997 & Hirstien, 1997).

The cognitive model of face recognition introduced by Bruce and Young (1986) proposed that a single sequential pathway is involved in face recognition. When a person encounters a new face, its details are encoded using viewer centered descriptions in the Face Recognitiom Units (FRU) of the persons memory. There are separate descriptions about the person which are integrated in the memory regarding the person’s expression, speech, and demographic information (e.g.: sex, age, and race). When the same face is encountered again, the information stored in the FRU is retrieved and leads to activation of the Person Identity Node (PIN), which resembles a database containing stored semantic and biographical information for previously encountered persons. The PINs can be accessed by other input modalities including voice and gait. When all this information is retrieved, then the person’s name is recalled via a different pathway. This constitutes the cognitive model of face recognition (Young, 1986)

More recently, however, Breen e al. have postulated a modified dual route model of face recognition according to which delusions occur when the Face Recognition Units (FRUs) are intact but there is a disturbance in either in the connection between FRUs and the affective response or in the generation of an affective response itself (Breen, 2001).Similarly Luchelli and Spinnler have hypothesized that Capgras delusions constitute a cross modal disorder of familiar people processing in which the Personal Identity Nodes (PINs), involved in storing knowledge about familiar faces, are functioning normally and thus an encounter with a familiar face leads to addressing of the proper the Exemplar Semantics archives and normal Gestalt guessing. There is, however, a disturbance at the level of analytical checking which leads to the origination of a conflict and subsequent delusions (Lucchelli and Spinnler, 2007). Other proposed theories derived from observation of patients with frontal lobe damage include, the inability to form successive modification and integration to pre-existing memories if a person, on repetitive encounters with the same person which leads to formation of new memories of the same person every time that person is encountered (Hirstien, 1997) and a possible conflict between previous memories and actual experience (Alexander, 1979).

Various psychodynamic models have also been proposed to explain these delusions including the theories of Oedipal and Electra complex and the concept of personality disintegration leading to a regression to elementary modes of functioning (Edelstyn, 1999). Another psychodynamic model postulates that Capgras delusion are mechanisms adopted by patients in order deal with ambivalent feelings and unresolved conflicts towards a close relative. Since unacceptable feelings such as anger, hatred, etc are inadequately repressed and since they cannot be directed at the close relative, the patient justifies those feelings by targeting them towards the perceived imposter (Sinkman, 2008).

Sinkman (20008) has proposed a different model for the multitude of delusions seen in schizophrenics with Capgras syndrome. According to this model, the underlying disorder contributing to all delusions is the breakdown of the patient’s ability to evoke and employ the preformed mental representations of both self and other people which leads to mental fragmentation and disorganization. This is overcome and rationalized in the form of delusions (Sinkman, 2008). It has also been postulated that the loss of ego boundaries observed in schizophrenia is due to frontal lobe damage.

Treatment for Capgras Delusions

As discussed above Capgras delusions can occur with a variety of psychiatric and neurological disorders. The treatment of Capgras delusions therefore cannot occur in isolation. It has to be integrated with the treatment of the underlying disorder. Also, till date no definitive treatment for Capgras delusions has been discovered, the treatment options available help to ameliorate the symptoms but do not completely treat the condition. Two modalities can be used for the treatment of Capgras delusions viz. psychological treatment and pharmacological treatment. As with most other delusions, psychological treatment is the mainstay of therapy for Capgras Delusions. It has to be kept in mind that therapy has to be tailored on individual basis keeping in mind the patient’s delusions and the spectrum of thought disorders that a patient might be present concomitantly.

The role of Cognitive Behavioral Therapy in treating delusions in schizophrenic patients is well established. Keeping in view the cognitive and psychoanalytical models proposed in the pathophysiology of Capgras delusions, Cognitive Behavioral Therapy (CBT) has been proposed to be an effective treatment for Capgras delusions. Over time, various theories have been proposed to explain the causative factors for delusions. Maher (1992) defined delusions as ‘hypotheses generated by normal reasoning processes to explain abnormal sensory input’ (Maher, 1992 cited in Brakoulias, 2008:149). On the other hand, Coltheart et al. have proposed a two model theory for delusions which states that an abberent experience leads to an abnormal belief evaluation. For this abnormal belef to progress to a delusion, concomitant impairment in perception or affect must be present (Coltheart, 2005 cited in Brakoulias, 2008:149). Extensive research has shown three main reasoning anomalies in delusional patients viz. ‘anomalies on probabilistic reasoning, theory of mind (ToM) tasks, and attributional biases’ as summarized by Brakoulias (Brakoulias, 2008:149). Keeping this background in view, CBT is proposed to be effective in the treatment of Capgras delusion. It is thought to work by modifying the patients perceptions regarding different condition and thus reduces delusional conviction. However, the limitation of CBT is that it does not modify the general reasoning styles of the person which are thought to be the main anomaly in delusional patients (Brakoulias, 2008:149). An important factor while considering psychotherapy, in particular CBT, for delusions is persistence in establishing a therapeutic empathy. The physician/therapist should refrain from both validating the person’s delusions, even inadvertently, and overtly confronting the system. In addition, cognitive techniques that include reality testing and reframing can be used (Capgras Delusion/Syndrome, 2003).

In the pharmacological treatment, no single drug has been shown to be particularly effective in treating Capgras delusions. Trials of an antipsychotics or SSRI at starting doses can be given (Cerceo, 2006). Drugs which are indicated in the treatment of Capgras delusions include Pimozide, Risperidone and Clozapine (Capgras Delusion/Syndrome, 2003). Moreover, no difference in response to atypical antipsychotics has been shown by comparative studies done between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. However, treatment of Capggras delusions leads to concomitant improvement in the symptoms of schizophrenia (Cerceo, 2006).

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