Capgras Syndrome
Overview
Capgras Syndrome (CS), frequently dubbed “delusion of doubles,” is a delusional misidentification syndrome where the patient falsely believes that an identical duplicate has replaced someone very familiar to them. CS is known to be the most prevalent delusional misidentification syndrome, stemming from structural issues in the brain leading to neuroanatomical damage. Previously regarded as a psychiatric disorder, like schizophrenia, CS is now referred to as a psychiatric and neurological disorder since the delusion emerges from organic brain degeneration.[1] CS was initially thought to only affect women, but it is now known to affect both sexes.[2] Structural changes in the brain that can lead to CS include atrophies, lesions, dysfunctions and injuries.[3] Its rarity also renders the condition difficult to study, so information on CS is commonly gathered from studying trends in individual patient case reports.
Causes
Typically, CS is most common in patients with other brain conditions, (e.g., Parkinson’s disease, schizophrenia, bipolar disorder) or if they have had a stroke or other traumatic brain injury.[4] The disorder has been correlated with damage to the right hemisphere of the brian, leading to problems with visual recognition, and damage to the frontal lobe of the brain, leading to problems with familiarity. Another delusional misidentification syndrome, reduplicative paramnesia (where one strongly believes that a location has been relocated) is thought to be linked to CS since they affect the same regions of the brain. Common underlying psychiatric diagnoses in CS are schizophrenia, schizoaffective disorder, and bipolar affective disorder. Brain imaging studies have supported hypotheses that familiar faces (visual stimuli) are inducing inappropriate emotional responses, likely due to a disconnect between the temporal lobe and limbic system, and the ability to effectively reject delusional beliefs.[5] It is also more common amongst people with other neurodegenerative conditions such as Lewy body dementia and Alzheimer’s. Risk factors and potential underlying disorders include: brain tumors, various neurodegenerative disorders, brain injuries and trauma, infectious diseases, metabolic issues, endocrinopathies, vitamin B12 deficiency, drug and toxin abuse and epilepsies.[6]
Signs and Symptoms
CS has revealed that the doubles/imposters are typically people with strong affective ties to the patient (e.g., a close family or friend). Patients claim to not recognize a familiar person, misidentify them as a stranger and/or perceive them as a threat. Sometimes, the familiar subject being misidentified could also be a pet or object instead of a person.[7] It is also common for the patient to act aggressive or violent towards the one they are misidentifying. Depending on the underlying cause of the for each individual patient, they may also experience other symptoms of the contributing condition. Individuals with CS often exhibit:[8]
Poor social relationships
Being prone to self-harm/violence
Lack of ability to retain jobs
Feelings of strangeness
Ambivalence issues
Pathological splitting of internalized object representations
Oedipal issues
Potential psychotic regression to a paranoid state
Primitive thinking or indecisiveness.
Depersonalization or derealization.[9]
Diagnosis
This condition is organic and complex, and due to its rare nature, it has not been addressed under the Diagnostic and Statistical Manual of Mental Disorders (DSM) classification. Its rarity and complexity is also why no single underlying cause has been identified. CS is clinically diagnosed through a psychiatric evaluation, clinical assessment of symptoms, and sometimes brain imaging to examine for damage to the bifrontal, right limbic and temporal regions.[10]
Treatments
Therapy and antipsychotic medications are common treatments, along with medications that target the underlying cause of an individual patient’s CS. It is crucial to identify and treat the comorbid psychiatric disorders that a patient may have as well, to indirectly treat the CS. It may sometimes be necessary to hospitalize the patient if they are acting violently towards themselves or someone they are misidentifying. Psychodynamic therapy intervention is crucial to manage a patient’s delusions. If the CS coincides with psychosis, symptoms may appear and reappear along with psychotic conditions. For many CS patients, there is no treatment that can completely cure their delusions. However, with proper treatment and care, patients can live healthier, more fulfilling lives.[11]
Case Studies
Examining individual cases of CS or groups of correlated cases has allowed researchers to uncover more information about the causes and symptoms of the syndrome. One particular case described a 57-year-old female patient diagnosed with posterior cortical atrophy (PCA), who was then diagnosed with CS eight years after her first symptoms of PCA. The patient did not recognize her husband and viewed him as a threat. Multimodal neuroimaging was used to specifically identify atrophied changes that could relate to the development of CS, and imaging revealed a progressive decrease in gray matter volume in the occipital and temporoparietal regions. It was concluded that the appearance of CS in this patient was related to atrophy in the right posterior cingulate gyrus/precuneus and frontal gyrus/frontal eye field. This finding supports the idea that the right frontal areas of the brain are pertinent in regards to Capgras syndrome.[12]
In another study conducted in 1999, brain imaging and electroencephalographic examinations (EEG) were used to analyze nine ethnic Chinese Taiwanese patients with clinical CS admitted into an acute psychiatric ward between November 1994 and October 1995. Results showed that four of the nine patients with CS had clearly abnormal anatomical lesions, and the other 5 showed major physical illness, consistent with organic factors involved in the development of CS. The crude prevalence of 2.5% of CS in the entire psychiatric ward (of 364 patients) is also consistent with the rarity of CS, with organic mental disorder and schizophrenia being the two major psychiatric underlying illnesses in these CS patients.[13]
Another study on four cases assessing the potential for physical violence towards the misidentified person in CS patients using neurophysiological and clinical factors found that the victims of CS patient violence were close family members living with the patient. Also, the four CS patients exhibiting interpersonal violence were men with a previous history of aggressive behavior and long-standing delusions. The violence was also usually planned beforehand by the CS patient, with hostility and anger previously demonstrated towards the misidentified person. After the violent event, each of the four men were diagnosed with some form of psychosis, including schizophrenia. The results of this study are consistent with the modest relationship between interpersonal violence and delusional disorders found in epidemiologic studies.[14]
Conversely, a research study performed on 34 cases of CS from Camden and Islington NHS Foundation Trust (a major London provider of mental health services), seven cases were found to have the patient’s misidentified subject be a non-family member or non-partner. This is inconsistent with the common misidentified subject of most patients with CS, which is usually a close family member or friend. However, this finding does reflect the findings of a few other studies which also have shown a significant minority of cases to have the subject be a non-family member or non-partner.[15]
Contributed by: Ananya Udyaver
Editor: Jennifer (Ghahari) Smith, Ph.D.
References
1 Shah, K., Jain, S. B., & Wadhwa, R. (2022), Capgras syndrome - StatPearls - NCBI Bookshelf - National Center for ... National Library of Medicine. https://www.ncbi.nlm.nih.gov/books/NBK570557/
2 Huang, T. L., Liu, C. Y., & Yang, Y. Y. (1999). Capgras syndrome: Analysis of nine cases. Psychiatry and Clinical Neurosciences, 53(4), 455–460. https://doi.org/10.1046/j.1440-1819.1999.00582.x
3 Currell, E.A., Werbeloff, N., Hayes, J. F., Bell V. (2019), Cognitive neuropsychiatric analysis of an additional large Capgras delusion case series. CognitiveNeuropsychiatry. 24(355): 1-12. https://doi.org/10.1080/13546805.2019.1584098
4 Ibid.
5 Ibid.
6 Lilly, B., Maynard, E., Melvin, K., & Holroyd, S. (2018). "Capgras" Delusions Involving Belongings, Not People, and Evolving Visual Hallucinations Associated with Occipital Lobe Seizures. Case reports in psychiatry, 2018, 1459869. https://doi.org/10.1155/2018/1459869
7 Ibid.
8 Ibid.
9 Ibid.
10 Ibid.
11 Ibid.
12 Schroeter, M. L., Albrecht, F., Ballarini, T., Leuthold, D., Legler, A., Hartwig, S., Tiepolt, S., & Villringer, A. (2020, April 21). Capgras delusion in posterior cortical atrophy–a quantitative multimodal imaging single case study. Frontiers. https://www.frontiersin.org/articles/10.3389/fnagi.2020.00133/full
13 Huang et al., (1999)
14 Bourget, D., Whitehurst, L. (2004), Capgras Syndrome: A Review of the Neurophysiological Correlates and Presenting Clinical Features in Cases Involving Physical Violence. The Canadian Journal of Psychiatry. 49(11): 719-725. https://doi.org/10.1177/070674370404901102
15 Currell et. al., (2019)