[Delusional Misidentification Syndromes in Organic Brain Disorders].

Delusional misidentification syndromes (DMSs) are a fascinating group of disorders involving a fixed, false belief about the identity of persons, places, and objects in one's environment. DMSs include Capgras syndrome, Frégoli syndrome, intermetamorphosis, the syndrome of subjective doubles, and reduplicative paramnesia. Although DMSs have been described in patients with focal neurological lesions, they are more commonly associated with neurodegenerative diseases, specifically dementia with Lewy bodies. Lesion network mapping was used to identify brain regions functionally connected to the lesion locations in patients with lesion-induced DMSs. The left retrosplenial cortex and the right ventral frontal cortex/anterior insula were functionally connected to almost all lesion locations. In a model of Capgras symptom as a mirror of prosopagnosia, there are two routes of visual recognition; one covert and one overt. Capgras symptom represents an interruption to the covert route with an intact overt route. This model, however, does not explain other DMSs. Therefore, propose a new model where the delusional belief content in DMSs results from dysfunctional linking between externally perceived objects and appropriately retrieved internal autobiographical memories associated with an object.

A case of Capgras syndrome and folie à duex in monozygotic twins.

Both Capgras syndrome and folie à deux (insanity of two) are rare and fascinating psychopathological syndromes. Their etiology and the nosological position remain unclear. We present a case of substance-induced Capgras syndrome emerging as folie à deux (insanity of two) in monozygotic twins with strongly overlapping life histories. Then, we discuss the etiology and the nosological position of these two conditions as well as their significance for understanding the concept of psychosis.

El síndrome de Capgras: el delirio de suplantación / Capgras syndrome: the delusion of impersonation

No disponible

Capgras Syndrome and Other Delusional Misidentification Syndromes.

The delusional misidentification syndromes (DMS) are a group of disorders, characterized by patients mistaking the identity of people they know, although they recognize them physically. The term DMS is an umbrella term which may cover disorders whose definition extends to objects other than people, such as animals, places, or familiar material objects. The most common and best known DMS is Capgras syndrome. In this disorder, the misidentification leads to the delusional conviction that a close friend or relative has been replaced by an identical - or almost identical - "double," whose original has disappeared. This double is an imposter without name or identity. Most often considered as a persecutor, the double may be subjected to aggression, which may be very violent. Neuropsychological hypotheses based on cerebral dysfunctions are now commonly considered to be at the origin of the disorder. They have been elaborated from achievements in the neurosciences, particularly the facial recognition models. In return, knowledge about the normal cognitive processes involved in recognition and familiarity has benefited from the work that cognitive neuropsychiatry has invested in these disorders. The DMS are observed in various contexts of morbidity: primary psychiatric diagnosis, or secondary to various organic disorders, particularly in neurodegenerative disease; they are rarely met in isolated form. Most often, they develop in line with the associated pathology. In the absence of consensual clinical description, the epidemiology of DMS is uncertain; they may be more frequent than previously supposed. There is no specific treatment for these disorders; neuroleptics are generally used in association with treatment of the concomitant disorder. The frequent association of DMS with organic disorders which may be curable and the particularly dangerous profile of these patients are factors that underline the need for better screening.

The doxastic shear pin: delusions as errors of learning and memory.

We reconsider delusions in terms of a "doxastic shear pin", a mechanism that errs so as to prevent the destruction of the machine (brain) and permit continued function (in an attenuated capacity). Delusions may disable flexible (but energetically expensive) inference. With each recall, delusions may be reinforced further and rendered resistant to contradiction. We aim to respond to deficit accounts of delusions - that delusions are only a problem without any benefit - by considering delusion formation and maintenance in terms of predictive coding. We posit that brains conform to a simple computational principle: to minimize prediction error (the mismatch between prior top-down expectation and current bottom-up input) across hierarchies of brain regions and psychological representation. Recent data suggest that delusions may form in the absence of constraining top-down expectations. Then, once formed, they become new priors that motivate other beliefs, perceptions, and actions by providing strong (sometimes overriding) top-down expectation. We argue that delusions form when the shear-pin breaks, permitting continued engagement with an overwhelming world, and ongoing function in the face of paralyzing difficulty. This crucial role should not be ignored when we treat delusions: we need to consider how a person will function in the world without them..

A case of Capgras syndrome with one's own reflected image in a mirror.

We report the case of a 78-year-old patient admitted to the hospital for behavioral and psychological disorders consisting in impressions of presence of a stranger located behind the bathroom mirror, who strikingly shared the patient's appearance but was considered a different person, yet. We discuss how this case can be interpreted as an atypical Capgras syndrome for his mirror image and how it suggests an adjustment of the classical dual-route model that sustains face recognition between covert (or affective) and overt neural pathways.

A Case of Capgras Syndrome Related to Hypothyroidism.

Hypothyroidism is commonly associated with a variety of psychiatric conditions, most commonly depression and cognitive impairment, but up to 5% to 15% of symptomatically hypothyroid patients may develop a nonaffective psychosis, classically referred to as "myxedema madness." We report the case of a woman who developed Capgras syndrome in the context of hypothyroidism, and whose psychosis rapidly resolved with levothyroxine supplementation. To date, very few cases of Capgras syndrome related to hypothyroidism have been reported. The pathophysiology of this condition remains unclear but it may be related to global cerebral hypometabolism or possibly to increased cerebral dopamine. Given the robust response of "myxedema madness" to thyroid replacement, psychiatrists should remain vigilant for covert hypothyroidism in patients with psychosis and atypical histories or presentations.

Brain Metabolic Dysfunction in Capgras Delusion During Alzheimer's Disease: A Positron Emission Tomography Study.

Capgras delusion is characterized by the misidentification of people and by the delusional belief that the misidentified persons have been replaced by impostors, generally perceived as persecutors. Since little is known regarding the neural correlates of Capgras syndrome, the cerebral metabolic pattern of a patient with probable Alzheimer's disease (AD) and Capgras syndrome was compared with those of 24-healthy elderly participants and 26 patients with AD without delusional syndrome. Comparing the healthy group with the AD group, the patient with AD had significant hypometabolism in frontal and posterior midline structures. In the light of current neural models of face perception, our patients with Capgras syndrome may be related to impaired recognition of a familiar face, subserved by the posterior cingulate/precuneus cortex, and impaired reflection about personally relevant knowledge related to a face, subserved by the dorsomedial prefrontal cortex.

Los delirios en la anorexia nerviosa: una hipótesis neurobiológica (Segunda Parte) / The deliriums of nervous anorexia: a neurobiological hypothesis (second part)

La anorexia nerviosa (AN) es una enfermedad muy grave. Tiene un curso crónico y una morbi-mortalidad entre las más altas de las patologías psiquiátricas. Se caracteriza por una firme negativa a aumentar o recuperar peso, un miedo intenso a engordar y distorsiones de la imagen corporal. Estas ideas extrañas, exageradas en muchas ocasiones sorprenden por la firmeza con que son defendidas por las pacientes. "En algunos casos la desnutrición autoprovodada está asociada con creencias sobre la alimentación y la forma del cuerpo que son tan extremas que los psiquiatras las describen como delirantes o cuasi delirantes". De hecho, las características de la enfermedad la hacen comparable con algunos tipos de psicosis. De acuerdo con Bruch existe como un rasgo propio de la enfermedad la "negación delirante de la delgadez". A lo largo del trabajo se revisa una posible fisiopatología de estas ideas delirantes. Y se las compara con las ideas delirantes presentes en otras patologías. Para ello en la primera parte del trabajo se ha decripto la AN, su clínica y su fisopatología. En esta segunda parte se detalla la fisiopatología del síntoma delirio. Se concluye con una descripción de los delirios del tipo que se presentan en la anorexia nerviosa.

Nervous Anorexia (NA) is a very serious disease. It is a chronic condition and its morbidity is among the highest of psychiatric pathologies. It is characterized by a strong unwillingness to put on or regain weight, a deep fear to grow fat, and by distortions of the body image. These strange ideas, which in many circumstance are exaggerated, are striking in the sense that they are strongly held by the patients. At times, self-induced malnutrition is associated with beliefs about diet and silhouette, which are so extreme that Psychiatrists describe them as delirious or quasi-delirious. In fact, the characteristics of the disease make it possible to compare it with some types of psychosis. According to Bruch, there is a feature which is characteristic of the disease, namely, "the delirious denial of thinness". In this article, the author does a review of a possible physiopathology of these delirious ideas and compares them with the delirious ideas existing in other pathologies. In this second part the auhtor specifies the physiopathology of the delirium symptom and concludes with a description of the types of deliriums that manifest in nervous anorexia.

When a loved one feels unfamiliar: a case study on the neural basis of Capgras delusion.

Perception of familiar faces depends on a core system analysing visual appearance and an extended system dealing with inference of mental states and emotional responses. Damage to the core system impairs face perception as seen in prosopagnosia. In contrast, patients with Capgras delusion show intact face perception but believe that closely related persons are impostors. It has been suggested that two deficits are necessary for the delusion, an aberrant perceptual or affective experience that leads to a bizarre belief as well as an impaired ability to evaluate beliefs. Using functional magnetic resonance imaging, we compared neural activity to familiar and unfamiliar faces in a patient with Capgras delusion and an age matched control group. We provide evidence that Capgras delusion is related to dysfunctional activity in the extended face processing system. The patient, who developed the delusion for the partner after a large right prefrontal lesion sparing the ventromedial and medial orbitofrontal cortex, lacked neural activity to the partner's face in left posterior cingulate cortex and left posterior superior temporal sulcus. Further, we found impaired functional connectivity of the latter region with the left superior frontal gyrus and to a lesser extent with the right superior frontal sulcus/middle frontal gyrus. The findings of this case study suggest that the first factor in Capgras delusion may be reduced neural activity in the extended face processing system that deals with inference of mental states while the second factor may be due to a lesion in the right middle frontal gyrus.

Delusional misidentification syndromes and dementia: a border zone between neurology and psychiatry.

The delusional misidentification syndromes (DMSs) are psychopathologic phenomena in which a patient consistently misidentifies persons, places, objects, or events. Although often described in relation to psychotic states including schzofrenia, it is, nevertheless, widely considered that these syndromes have an anatomical basis because of their frequent association with organic brain disease; studies have pointed to the presence of identifiable lesions, especially in the right frontal lobe and adjacent regions, in a considerable proportion of patients. The purpose of this article is to examine the phenomenon in people with dementia. We searched the electronic databases for original research and review articles on DMS in patients with dementia using the search terms "Delusional Misidentification Syndrome, Capgras syndrome, Fregoli syndrome, reduplicative paramnesia, and dementia." The DMSs are a frequent problem in dementia. The violence and dangerousness in patients with dementia having these syndromes are well documented, and forensic aspects are highlighted. Pathogenetic viewpoint and management are considered.

Aparición de delirio de Capgras tras afección por hemorragia subaracnoidea en paciente con trastorno mental grave / Emergence of Capgras delusion after a subarachnoid hemorrhage in a patient with severe mental disorder

Se presenta el caso de una paciente con trastorno mental grave que tras sufrir una hemorragia subaracnoidea comienza a manifestar la idea delirante consistente en que unos dobles usurpan la identidad de personas allegadas a ella (delirio de Capgras). Se observa a la paciente durante proceso rehabilitador en unidad de media estancia dos años después del episodio HSA, donde ingresa por empeoramiento y viraje psicopatológico. Las distintas teorías o modelos que por sí solos han intentado dar cuenta de la etiopatogenia del delirio de Capgras no consiguen explicarlo de forma satisfactoria. Aunque algunos enfatizan su origen orgánico la realidad es que no hay localización de un daño común para todos los casos, y no siempre es posible determinarlo. El interés del caso que aquí se estudia estriba en la coexistencia de diversos factores implicados, orgánicos y no orgánicos, así como en la propia resolución del delirio. Utilizando un enfoque etiopatogénico multifactorial se hipotetizará acerca de la particular formación del delirio de Capgras en la paciente, atendiendo a las propuestas teóricas existentes e introduciendo cuestiones idiosincrásicas pertinentes, factores personales y ambientales que no deben obviarse. Tras el análisis del caso y en base a algunos resultados hallados se discute finalmente acerca de cuestiones tales como la unicidad del fenómeno y sus posibles implicaciones terapéuticas (AU)

It presents a case of a patient with severe mental disorder who after suffering a subarachnoid hemorrhage starts manifiestar the delusion that some doubles are usurping the identity of people close to her (Capgras delusion). It observes the patient during the rehabilitation process in medium-stay unit two years after the episode HSA, where entered for worsening and the psychopathology evolution. The various theories or models alone that have tried to explain the etiology of Capgras delusion fail to explain successfully. Although some emphasize an organic origin, the reality is that no damage on a common location for all cases and not always possible to determine it. The interest of the case studied here lies in the coexistence of different factors involved, organics and not organics, and particular resolution of the delirium. Using a multivariate approach it has hypothesized about the Capgras delusion singular formation in the patient, taking into account the existing theoretical proposals and introducing relevant issues idiosyncratic, personal and environmental factors, that should not be ignored. After analyzing the case and based on some results finally it has found out, it discussed about issues such as the oneness of the phenomenon and its possible therapeutic implications (AU)

[The measurement of electrodermal activity]. / La mesure de la réaction électrodermale.

INTRODUCTION: Electrodermal activity (EDA) is an early physiological index and the subject of constant interest, in spite of the bad reputation attached to "lie detectors". This interest is expected to increase in the future, following the development of research related to the neurobiological aspect of emotions of which it is an index. Recent data provided by functional cerebral imaging has added to the significance of this index and should result in further interest. AIM: The authors thus re-examined the various notions related to measuring EDA, and its practical aspect as well as its mechanisms. EDA should be useful both for authors wishing to use this variable and for readers wishing to form their own critical point of view. LITERATURE FINDINGS: The article first defines the various terms used to qualify EDA. Then, it analyses the mechanisms occurring at the sweat glands' level, showing that a distinct innervation of the sweat glands causes sweat to be released in the excretory channels, thereby allowing the recording of a negative surface potential in parallel to the lowering of skin conductance. Arguments are then pointed out to illustrate that the potential's positive phase following this first answer occurs in the case of high intensity stimulations. The study of the central command of sudation demonstrates that, several areas are involved and that different functions such as thermal regulation and motricity may interfere with emotive reactions. Difficulties regarding the mode of measurement of these answers as to their number and amplitude are also brought to light. DISCUSSION: A particular interest of measuring EDA is its ability to highlight individual characteristic and unconscious emotional reactivity. Subjects who constitutionally present many spontaneous and therefore habitual EDA can indeed be opposed to subjects whose EDA reflexes are very few and hardly habitual. A theory suggests that for the first category, whose subjects are named labiles, emotional control may be at the origin of EDA. This characteristic brings to mind the case of antisocial subjects whose rate of EDA is also reduced, although for the latter a primitive drop in behavioral inhibition is involved. The production of EDA in response to non-conscious emotive stimulations can be objectified in the rare cases of prosopagnosia. These subjects who are unable to recognize familiar faces can produce EDA when presented faces with an emotional load. These cases contrast with the delusional denial of the Capgras syndrome where subjects do not present EDA, suggesting that the dysfunction of visual analysis occurs at a different level. There are other rare cases represented by cortical blindness where EDA shows that an unconscious emotional analysis is preserved. These subjects are known however to be capable of unconscious visual discriminations, which are possibly accompanied by EDA. This possibility of a "blind vision" is experimentally studied via subliminal vision testing (backward masking tests). These demonstrate that a rudimentary visual analysis is carried out in the subcortical circuits while taking into account the affective aspect of stimulations. CONCLUSION: Present or future data should allow a greater comprehension of electrodermal signals, making it possible to overcome the difficulties related to their interpretation and facilitate their applications.

Abductive inference and delusional belief.

Delusional beliefs have sometimes been considered as rational inferences from abnormal experiences. We explore this idea in more detail, making the following points. First, the abnormalities of cognition that initially prompt the entertaining of a delusional belief are not always conscious and since we prefer to restrict the term "experience" to consciousness we refer to "abnormal data" rather than "abnormal experience". Second, we argue that in relation to many delusions (we consider seven) one can clearly identify what the abnormal cognitive data are which prompted the delusion and what the neuropsychological impairment is which is responsible for the occurrence of these data; but one can equally clearly point to cases where this impairment is present but delusion is not. So the impairment is not sufficient for delusion to occur: a second cognitive impairment, one that affects the ability to evaluate beliefs, must also be present. Third (and this is the main thrust of our paper), we consider in detail what the nature of the inference is that leads from the abnormal data to the belief. This is not deductive inference and it is not inference by enumerative induction; it is abductive inference. We offer a Bayesian account of abductive inference and apply it to the explanation of delusional belief.

The misidentification syndromes as mindreading disorders.

The patient with Capgras' syndrome claims that people very familiar to him have been replaced by impostors. I argue that this disorder is due to the destruction of a representation that the patient has of the mind of the familiar person. This creates the appearance of a familiar body and face, but without the familiar personality, beliefs, and thoughts. The posterior site of damage in Capgras' is often reported to be the temporoparietal junction, an area that has a role in the mindreading system, a connected system of cortical areas that allow us to attribute mental states to others. Just as the Capgras' patient claims that that man is not his father, the patient with asomatognosia claims that his arm is not really his. A similar account applies here, in that a nearby brain area, the supramarginal gyrus, is damaged. This area works in concert with the temporoparietal junction and other areas to produce a large representation of a mind inside a body situated in an environment. Damage to the mind-representing part of this system (coupled with damage to executive processes in the prefrontal lobes) causes Capgras' syndrome, whereas damage to the body-representing part of this system (also coupled with executive damage) causes asomatognosia.

In what sense 'familiar'? Examining experiential differences within pathologies of facial recognition.

Explanations of Capgras delusion and prosopagnosia typically incorporate a dual-route approach to facial recognition in which a deficit in overt or covert processing in one condition is mirror-reversed in the other. Despite this double dissociation, experiences of either patient-group are often reported in the same way--as lacking a sense of familiarity toward familiar faces. In this paper, deficits in the facial processing of these patients are compared to other facial recognition pathologies, and their experiential characteristics mapped onto the dual-route model in order to provide a less ambiguous link between facial processing and experiential content. The paper concludes that the experiential states of Capgras delusion, prosopagnosia, and related facial pathologies are quite distinct, and that this descriptive distinctiveness finds explanatory equivalence at the level of anatomical and functional disruption within the face recognition system. The role of skin conductance response (SCR) as a measure of 'familiarity' is also clarified.