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Hi Ayelet. Below is our final wikipedia article. We hope you enjoy it! Mark, Nick and Stuart


Overview of disorder[edit]

Capgras syndrome (also known as Capgras delusion) is a phenomenon characterised by a recurrent and sustained delusional belief that an object or person has been replaced with a double[1]. Capgras syndrome is classified as a delusional misidentification syndrome that commonly presents itself with other disorders, including schizophrenia, Alzheimer's disease, affective disorders, cerebral vascular disease and epilepsy[2] One third of cases of the delusion are documented as being a result of traumatic brain damage/lesions suggesting an underlying organic basis[3]. Research by Capgras and Reboul-Lachaux [4], from which the syndrome got its name, reported one of the first cases of the syndrome in which a woman believed that her husband, children and neighbors had been replaced by doubles. Research tends to observe that when a person is involved with the delusion, this person is someone that the patient has an emotional attachment to.[3]

Capgras syndrome is a bizarre delusion in that patients appear to recognize the face or object they are looking at but yet at the same time they deny its authenticity; putting it apart from other misidentification disorders such as prosopagnosia in which patients fail to show any overt recognition of previously familiar faces[3]. The nature of Capgras syndrome has resulted in a great deal of research into understanding its underlying causes. Many theories have arisen that try to explain the causes of Capgras, ranging from Freudian psychodynamic approaches to anatomical approaches.[5].

As well as mistaking humans as imposters, cases of Capgras syndrome have arisen where patients believe that their pets have been replaced by a double[6] Interestingly, another study[7] reported a rare case of Capgras Syndrome in which a patient believed that a number of familiar household objects had been replaced with doubles. Her delusion did not include anybody close to her.

Theory and Research: Linking emotion to (mis)recognition[edit]

History of the syndrome[edit]

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)[5] 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)[8], 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)[9] suggests a one-stage phenomenal account is inadequate to explain the causal factors underlying its onset.

Contemporary theories[edit]

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)[1] 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)[10] 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)[11], 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)[12] 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)[13] 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)[14], 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)[5] 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)[5] 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)[15] 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)[16], 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.

Investigative Methods and Findings[edit]

Case Studies[edit]

Prior to the growth of knowledge of Capgras and modern investigative techniques case studies were common place and fuelled this growth in knowledge. Capgras and Reboul-Lachaux's syndrome defining study is one such example and brought the syndrome into the scientific communities awareness [4]. See the above and below sections for more discussion on these examples.

GSR[edit]

GSR has been measured in patients on order to detect covert facial recognition in miss identification syndromes. GSR measures the conductance of the skin using electrodes (often on the hands) and can be linked with psychological events [17]. Ramachandran [3] states that when a healthy person is shown pictures of family members, the rate of sweating increases resulting in a change in the GSR, linking the measure to "emotional arousal". However when images of family members were shown to a Capgras sufferer, no GSR change was measured, suggesting a lack of emotional arousal. This lack of emotion was contrary to the fact that the patient acknowledged that those in the image shared a physical resemblance to the real family member [18]. The authors demonstrated the patients GSR did however change when they were exposed to other emotional stimuli concluding the deficit not to be caused by damage to the emotion centres of the brain (E.G. the Amygdala). It is worth noting the pattern of GSR changes demonstrated by capgras patients is different to that of sufferers of a similar syndrome. Prosopagnosia patients show GSR changes but are unable to acknowledge physical similarities resulting in a failure to recognise those they know [19]. Therefore while prosopagnosia appears to occur due to defective overt recognition, literature suggests it is covert recognition that is affected in capgras patients.

Brain Imaging[edit]

Magnetic resonance imaging (MRI) and Computerised tomography (CT) have been utilised to gain an understanding in structural brain changes that may lead to behaviours expressed by Capgras patients. However these studies are limited in number and are somewhat limited regarding the findings due to the fact that patients scanned often also have other conditions that may have associated structural changes. This presents challenges to identification of links between structural and behavioural changes.

CT[edit]

CT scans have revealed mixed and sometimes opposing . Todd, Dewhurst and Wallis (1981), [20] using CT, found general atrophy of the sulci of the frontal lobes of a capgras sufferer. However the patient presented other conditions that have been associated with cortical atrophy such as Parkinsonism and schizophrenia. A study by Forstl, Almeida, Owen, Burns and Howard (1991) [21] of multiple CT scans of Capgras patients revealed 58% had cortical atrophy, however many of these also presented symptoms of other conditions. CT has also been employed to highlight areas affected by traumatic brain injuries that have resulted in capgras delusions. Alexander, Stuss and Benson (1979) [22] found right temporal and bilateral frontal damage may have caused their patients new delusions. However the patient presented different behaviours to those in the Capgras literature such as being apathetic toward the imposter rather than feeling animosity toward them. A further CT study concluded that there were no signs of structural abnormalities of the brain of a Capgras sufferer [23] suggesting the cause could be at the molecular level.

MRI[edit]

One of the earliest MRI scans of a patient suffering from Capgras delusions revealed similar areas of damage to those presented in CT scans [24]. However this patient had lesions rather than atrophy located bilaterally in the frontal lobe and larger lesions bilaterally to the occipital lobe extending anteriorly into the parietal lobe. This area is commonly associated with spatial visual processing and not recognition tasks [25]. Mackie, Ebmeier and O'Carroll (1994) [26] used MRI to show that no focal lesions were present in their patient and rather generalised dilation (enlargement) of the ventricular system was noted. Using SPECT the authors also identified hemispherical asymmetries in the uptake of a tracer particle in the calcarine region of the occipital lobe (primary visual cortex) suggesting disrupted functioning of this area.

EEG[edit]

Electroencephalography measures the brains activity by placing electrodes on the scalp. A study of 59 patients with misidentification syndromes exclusively involving others revealed 53% as having slow background activity [21], this has been specifically located in the Occipitotemporal region [24], an area proposed to be involved in the recognition of multiple stimuli categories such as faces [27] and objects [28]

Meta-Analysis[edit]

Articles have combined findings from multiple papers and case histories in order to form a picture of co-morbidity. Meta-analysis have reported capgras to have high concordance rates with other delusional disorders. One such paper reviewed reports that out of 131 instances of Capgras or Fregoli syndrome (another misidentification syndrome), most of which were capgras cases, 52% were also diagnised with schizophrenia and 65% had paranoid psychotic symptoms [21]. Authors have also used meta-anlysis to group data using the above techniques together acquiring a more generalized view of tissue damage and abnormal brain activity that may result in or be a result of Capgras. The technique has also been used in order to compare and contrast Capgras with other misidentification syndromes aiming to develop our understanding of the visual system.

Treatments[edit]

Historically, treatments included the use of modified insulin, insulin coma therapy and Electroconvulsive Therapy (ECT) to reduce the symptoms of Capgras delusion to some success[8] . However these treatments, with the exception of ECT, have been replaced by modern forms of treatment. Some success has still been found from using ECT in modern times to treat Capgras syndrome, although this is usually used only as a last resort when other methods have failed to lead to remission of the Capgras delusion.[29]

Behavioural treatments tailored to the patient, such as Cognitive Behavioural Therapy (CBT), have been shown to be effective in the treatment of misidentification delusions [30]. In CBT the therapist tries to help the patient deal with the distress that Capgras delusion may cause and manage any challenging thoughts and behaviour that may result from the delusion[31]. Methods that are used to bring about such change include providing patients with strategies that allow them to challenge their thoughts associated with the delusion and in doing so hopefully lead to a re-evaluation of their cognitive processes linked to the individual or object at the centre of their delusion. By providing self instruction or through the use of other meta-cognitive strategies, patients may become able to redirect thoughts and any behaviours to less challenging ones. Patients are made aware of cognitive processes that may be reinforcing their delusion and therapy will work on changing these through the help of the therapist and the use of the methods mentioned above.

As well as therapeutic treatment, pharmacological treatment has also been shown to be effective with treating delusions including Capgras delusion, in particular the use of anti-psychotic drugs. Some examples of drugs being used effectively include the use of Pimozide[32], mirtazapine[33] and chlorpromazine[7]. Other research has show success rates of antipsychotics on treatment of delusions in 50% of patients[34]

Capgras and Crime[edit]

There have been a number of criminal cases committed by suffers of Capgras syndrome, those that most catch the media attention are often homicides. One of the most recent examples of Capgras delusions being used as a defence to murder occurred in 2009 when a male sufferer killed his wife whom he believed to be an imposter [35]. However, in this case the jury did not accept the defence due to concerns that the act seemed too planned out to have only been due to a delusional episode [36]. Other criminal cases reveal Capgras sufferers do not only have delusions in which another person is the impostar. Another murder defendant claimed his Capgras delusions lead him to believe others to have been replaced by aliens, clones and robots [37]. The defendant believed his step-father to have been replaced by a “malevolent robot” clone leading him to kill the impostar robot and open him up in order to find proof. Previously the defendant had threatened to kill his wife and on another occasion had threatened members of the public in a bar believing they were all clones sent by aliens to destroy humans.

The above cases illustrate the threat that can be posed to the general public as well as those emotionally connected to those suffering Capgras delusions. They also highlight the fact that imposters are not always believed to be human and therefore mental illness associated with these delusions appears to cross into schizophrenia type delusions. In many criminal cases the defendant has not only been diagnosed as suffering Capgras delusions but also meet the criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders for Schizophrenia or bi-polar disorder [37]. This suggests that Capgras delusions alone may not result in violence while the presence of other disorders along with Capgras may increase the likelihood of the sufferer to act out violently. However whether this is true is not currently answered by the literature on Capgras. Such cases have however helped fuel the debate as to whether Capgras is merely an element of schizophrenia or can arise independently.

References[edit]

  1. ^ a b Edelstyn, N. M. J. & Oyebode, F. (1999). A review of the phenomenology and cognitive neuropsychological origins of the Capgras Syndrome. International Journal of Geriatric Psychiatry, 14, 48-59. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1099-1166(199901)14:1%3C48::AID-GPS891%3E3.0.CO;2-0/pdf
  2. ^ 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. 49,719-725
  3. ^ a b c d Ramachandran, V.S. (1998). Consciousness and body image: lessons from phantom limbs, Capgras syndrome and pain asymbolia. Philosophical Transactions of the Royal Society of London. Series B. Biological Sciences. 353, 1851-1859. Cite error: The named reference "three" was defined multiple times with different content (see the help page).
  4. ^ a b Capgras, J., Reboul-Lachaux, J. (1923). Illusions des sosies dans un délire systématisé chronique. Bull. Soc. Clin. Méd. Ment. 11, 6–16.
  5. ^ a b c d Ramachandran, V. S. (2012). The Tell-Tale Brain, London, England, Windmill Books
  6. ^ Wright, B., Mindham, R.,Burn, W. (1994). Canine Capgras. Irish Journal of Psychological Medicine, 11, 31–3.
  7. ^ a b Abed, R.T., Fewtrell, W.D. (1990) Delusional misidentification of familiar inanimate objects: A rare variant of Capgras Syndrome. British Journal of Psychiatry 157, 915-917
  8. ^ a b Enoch, M. D. (1963) The Capgras Syndrome. Acta Psychiatrica Scandinavica, 39, 437-462. DOI: 10.1111/j.1600-0447.1963.tb07475.x
  9. ^ Young, G. (2008). Capgras delusion: An interactionist model. Consciousness and Cognition, 17, 863-876. doi:10.1016/j.concog.2008.01.006
  10. ^ McKay, R., Langdon, R. & Coltheart, M. (2005). "Sleights of mind": Delusions, defences, and self-deception. Cognitive Neuropsychiatry, 10, 305-326. Doi: 10.1080/13546800444000074
  11. ^ Ellis, H. H. & Young, A. W. (1990). Accounting for delusional misidenifications. British Journal of Psychology, 157, 239-248. DOI: 10.1192/bjp.157.2.239
  12. ^ Bauer, R. M. (1984). Autonomic recognition of names and faces in prosopagnosia: A neuropsychological application of the guilty knowledge test. Neuropsychologia, 22, 457-469. http://dx.doi.org/10.1016/0028-3932(84)90040-X
  13. ^ Young, A. W., Reid, I., Wright, S. & Hellawell, D. J. (1993). Face-processing impairments and the Capgras delusion. British Journal of Psychology, 162, 685-689. DOI: 10.1192/bjp.162.5.695
  14. ^ Hirstein, W. & Ramachandran, V. S. (1997). Capgras syndrome: a novel probe for understanding the neural representation of the identity and familiarity of persons. Proceedings of The Royal Society, 264, 437-444. doi: 10.1098/rspb.1997.0062
  15. ^ Sidoti, V. & Lorusso, L. (2007). Multiple sclerosis and Capgras' syndrome. Clinical Neurology and Neurosurgery, 109, 786-787. doi:10.1016/j.clineuro.2007.05.022
  16. ^ Horikawa, H., Monji, A., Sasaki, M., Maekawa, T., Onitsuka, T., Nitazaka, Y., Hirano, Y., Hirano, S., Hashioka, S., Kato, T., Yoshida, I. & Kanba, S. (2006). Different SPECT findings before and after Capgras' syndrome in interictal psychosis. Epilepsy and Behaviour, 9, 189-192. doi:10.1016/j.yebeh.2006.04.016
  17. ^ Montagu, J. D., & Coles E. M. (1966). Mechanism and measurement of the galvanic skin response. Psychological Bulletin, 65(5), 261-279
  18. ^ Hirstein, W., & Ramachandran, V. S. (1997) Capgras syndrome: a novel probe for understanding the neural representation of the identity and familiarity of persons. Proceedings of the Royal Society B: Biological Sciences. 264(138), 437-444. Retrieved from http://rspb.royalsocietypublishing.org/content/264/1380/437.short
  19. ^ Bauer, R. M. (1984). Autonomic recognition of names and faces in prosopagnosia: A neuropsychological application of the Guilty Knowledge Test. Neuropsychologia. 22(4). 457-469. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/6483172
  20. ^ Todd, J., Dewhurst, K., & Wallis, G. (1981). The syndrome of capgras. The British Journal of Psychiatry. 139(4),319-327. doi 10.1192/bjp.139.4.319
  21. ^ a b c Forstl, H., Almeida, O. P., Owen, A. M., Burns, A., & Howard, R. (1991). Psychological , neurological and medical aspects of misidentification syndroms: A review of 260 cases. Psychological Medicine. 21, 905-910
  22. ^ Alexander, M. P., Stuss, D. T., & Benson, D. F. (1979). Capgras syndrome: A redupulicative phenomenom. Neurology. 29(2), 334-339. Retrieved from http://psycnet.apa.org/psycinfo/1980-23394-001
  23. ^ Thompson M. I., Silk, K. R., & Hover, G. L. (1980). Misidentification of a city: Delimiting criteria for Capgras syndrome. 137(10), 1270-1272. Retrieved from http://0-ajp.psychiatryonline.org.unicat.bangor.ac.uk/article.aspx?articleid=158559
  24. ^ a b Lewis, S. W. (1987). Brain imaging in a case of capgras' syndrome. British Journal of Psychiatry. 150(1), 117-121. doi: 10.1192/bjp.150.1.117
  25. ^ Mishkin, M., Ungerleider, L. G., & Macko, K. A. (1983). Object vision and spatial vision: Two cortical pathways. Trends in Neurosciences, 6, 414-417
  26. ^ Mackie, J., Ebmeier, K. P., & O'Carroll, R. E. (1994). An MRI, SPECT and neuropsychological study of a patient presenting with Capgras syndrome. Behavioural Neurology, 7(3-4), 211-215
  27. ^ Kanwisher, N, McDermott, J., & Chun, M. M. (1997). The fusiform face area: A module in human extrastriate cortex specialised for face perception. The journal of Neuroscience, 17(11), 4302-4311.
  28. ^ Grill-Spector, K., Kourtzi, Z., & Kanwisher, N. (2001). The lateral occipital complex and its role in object recognition. Vision Research, 10-11, 1409-1422.
  29. ^ Chiu, N.M. (2009). Repeated electroconvulsive therapy for a patient with Capgras syndrome and Parkinsonism. Progress in Neuro-Psychopharmacology and Biological Psychiatry 6, 1084-1085
  30. ^ Butler, A.C., Chapman, J.E., Forman, E.M, Beck A.T. (2006) The empirical status of cognitive-behavioural therapy: A review of meta-analyses. Clinical Psychology Review. 26, 17–31.
  31. ^ Tarriet, N.(Ed.)(2006). Case Formulation in Cognitive Behavioural Therapy: The Treatment of Challenging and Complex Cases. London: Routledge
  32. ^ Tueth, M.J., Cheong, J.A. (1992): Successful treatment with pimozide of Capgras syndrome in an elderly male. Journal of Geriatric Psychiatry and Neurology 5, 217-219
  33. ^ Khouzam, H.R. (2002). Capgras syndrome responding to the antidepressant mirtazapine. Comprehensive Therapy 28:238–40.
  34. ^ Manschreck, T.C., Khan, N.L. (2006). Recent advances in the treatment of Delusional Disorder. The Canadian Journal of Psychiatry 51:114-119
  35. ^ Murder in New York thought wife was 'imposter'. (2010, April 2) The New Zealand Herald. Retrieved from http://www.nzherald.co.nz/nz/news/article.cfm?c_id=1&objectid=10635940
  36. ^ Blazej Kot, Cornell doctoral student convicted of killing wife, sentenced to 25 years to life in prison. (2010, June 16). The Huffington Post. Retrieved from http://www.huffingtonpost.com/2010/06/16/blazej-kot-cornell-doctor_n_614004.html
  37. ^ a b Silva, J. A., Leong, G. B., Weinstock, R., & Boyer, C. L. (1989). Capgras syndrome and dangerousness. The Bulletin of the American Academy of Psychiatry and the Law, 17(1), 5-14. Retrieved from http://www.jaapl.org/content/17/1/5.full.pdf+html
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