Capgras syndrome - an overview


 Abi Skraga is a year 13 student who has applied to study cognitive neuropsychology at university. Abi has written an excellent article about CAPGRAS SYNDROME. I am sure that you will agree it is very informative. Please have a read.

My personal interest by Abi Skraga

 In studying psychology and biology at A-level and developing a keen interest in the subjects, I have explored many research areas and have become primarily interested in behavioural neuroscience.

I came across Capgras syndrome while reading Ramachandran’s ‘phantoms in the brain’, ultimately amazed at the fragility of the structure and function of the human neural system and the impact of any changes to it. This is particularly the case in psychopathologies which not only have drastic effects on the patient, but their peers too. 

I find Ramachandran’s neural explanation of this condition particularly interesting, linking to topics in A-level psychology such as localisation of function and plasticity within the brain. Having extensively researched the syndrome and its causes, I now have a greater understanding of neural mechanisms and have been inspired to further question similar topics. What would happen if the connections in the brain were not only damaged, but reorganised such that emotions may be misattributed to an individual? Could it be a possible explanation for apparent ‘random’ crime, where a spouse may hurt their loved one as a result of a rewiring in the brain which evokes an emotional response anger and violence instead of love and care?

I will continue to investigate such debates, and progress in my learning of the extensive discipline that is psychology.  


Named after Joseph Capgras, the French psychiatrist who first described it, Capgras syndrome is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects. It is therefore characterised as the irrational belief that a familiar person or place has been replaced with an exact duplicate, an imposter (Ellis, 2001; Hirstein and Ramachandran, 1997) and hence concerns  the absence of differential autonomic activity to familiar faces compared with unknown faces (Ellis and Lewis, 2001). This is in contrast to patients with prosopagnosia, who cannot consciously recognise previously familiar faces but display autonomic or covert recognition in response to them.

This delusion is sometimes seen in and so is thought to be linked to people who have dementia (Förstl et al, 1991), hallucinatory schizophrenia (Christodoulou, 1997) or bipolar disorder (Silva et al, 1989), or where there has been some type of brain injury or disease (Weston and Whitlock, 1971).



From the psychodynamic perspective, the Capgras delusion is generally characterised by marked feelings of ambivalence with a misidentification delusion toward family members or friends (Berson, 1983). The feelings of ambivalence are suggested to be as a result of the Oedipus and Electra complexes in individuals, and hence are motivated by sexual jealousy towards the opposite sex parent. The misidentification delusion is therefore the primitive ego defence mechanisms providing a way to cope with the conscious/unconscious hostile impulses directed toward their loved ones, by minimising the guilt experienced with anger and aggression (Silva et al, 1987). However, there are issues with this explanation such that the oedipal impulses suggested cannot adequately explain all cases of this disorder, markedly those in which the emotional detachment is directed at a family pet or non-human creature (Hirstein and Ramachandran,1997).

With this explanation having largely been discredited, it is now generally agreed that the Capgras delusion has a more organic basis (Young et al, 1993).  It was hypothesised that patients might have damage to the system that produces the automatic emotional arousal to familiar faces (Ellis and Young, 1990; Ellis et al, 1997), hence a double dissociation of prosopagnosia. Evidence for this explanation comes from other studies measuring galvanic skin responses (GSR) to faces- a patient with Capgras delusion shows reduced GSRs to faces in spite of normal face recognition (Hadyn et al, 2000).

Similarly, it is also suggested that the origin of the disorder is as a result of damage to the connections between the brain area where faces are recognised, and the area involved in emotions. More specifically, the disconnection between the amygdala and the inferotemporal cortex (Ramachandran, 1998). The latter two examples can be used to explain the presence of the condition in sufferers of brain injury and neurodegenerative diseases, suggesting perhaps a physical aetiology.


Limited research and conclusiveness into the syndrome itself limits the availability of treatment specifically for Capgras, however there are treatments which aim to address underlying causes, and the conditions for which Capgras syndrome is most commonly associated with.

For example,  dementia behaviour management  can be used to reduce symptoms of the syndrome. This specifically includes Habilitation Therapy, the compressive behavioural approach to Alzheimer's disease and related dementias (ADRD) that the Alzheimer’s Association finds to be a best practice (Alzheimer’s Association, 2001, n.d.). Similarly, in dementia sufferers, medications like cholinesterase inhibitors, which boost neurotransmitters involved in memory and judgment, may be used.