[Capgras symptom associated parricides. 2 case reports]. / Capgras-féle tünettel összefüggo szülogyilkosságok. Két eset bemutatása.

Capgras symptom is characterized by the delusional belief that a person significant to the patient has been replaced by a 'double' or 'impostor'. Capgras symptom was discussed to be associated with violent behavior. We report here the cases of two male patients with schizophrenia paranoid type, where parricide was connected to Capgras delusion. It is important to emphasize that in our observed cases, non-adherence played an essential role in the development of violent behavior, parricide. Orv Hetil. 2019; 160(42): 1673-1676.

Review of epidemiology, clinical presentation, diagnosis, and treatment of common primary psychiatric causes of cutaneous disease.

Approximately half of all patients presenting to dermatologists exhibit signs and symptoms of psychiatric conditions that are either primary or secondary to cutaneous disease. Because patients typically resist psychiatric consult, dermatologists often are on the front line in evaluating and treating these patients. Accordingly, distinguishing the specific underlying or resulting psychiatric condition is essential for effective treatment. The etiology, epidemiology, clinical presentation, diagnosis, and first-line treatment of specific primary psychiatric causes of dermatologic conditions, including delusional infestation, Morgellons syndrome, olfactory reference syndrome, body dysmorphic disorder, excoriation disorder, trichotillomania, and dermatitis artefacta are discussed here, followed by a discussion of the recommended treatment approach with an overview of the different first-line therapies discussed in this review, specifically cognitive behavioral therapy, atypical antipsychotics, selective serotonin reuptake inhibitors, and tricyclic antidepressants. Included is a guide for dermatologists to use while prescribing these medications.

Finding the imposter: brain connectivity of lesions causing delusional misidentifications.

SEE MCKAY AND FURL DOI101093/AWW323 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Focal brain injury can sometimes lead to bizarre symptoms, such as the delusion that a family member has been replaced by an imposter (Capgras syndrome). How a single brain lesion could cause such a complex disorder is unclear, leading many to speculate that concurrent delirium, psychiatric disease, dementia, or a second lesion is required. Here we instead propose that Capgras and other delusional misidentification syndromes arise from single lesions at unique locations within the human brain connectome. This hypothesis is motivated by evidence that symptoms emerge from sites functionally connected to a lesion location, not just the lesion location itself. First, 17 cases of lesion-induced delusional misidentifications were identified and lesion locations were mapped to a common brain atlas. Second, lesion network mapping was used to identify brain regions functionally connected to the lesion locations. Third, regions involved in familiarity perception and belief evaluation, two processes thought to be abnormal in delusional misidentifications, were identified using meta-analyses of previous functional magnetic resonance imaging studies. We found that all 17 lesion locations were functionally connected to the left retrosplenial cortex, the region most activated in functional magnetic resonance imaging studies of familiarity. Similarly, 16 of 17 lesion locations were functionally connected to the right frontal cortex, the region most activated in functional magnetic resonance imaging studies of expectation violation, a component of belief evaluation. This connectivity pattern was highly specific for delusional misidentifications compared to four other lesion-induced neurological syndromes (P < 0.0001). Finally, 15 lesions causing other types of delusions were connected to expectation violation (P < 0.0001) but not familiarity regions, demonstrating specificity for delusion content. Our results provide potential neuroanatomical correlates for impaired familiarity perception and belief evaluation in patients with delusional misidentifications. More generally, we demonstrate a mechanism by which a single lesion can cause a complex neuropsychiatric syndrome based on that lesion's unique pattern of functional connectivity, without the need for pre-existing or hidden pathology.

Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families.

Strong familial aggregation of schizophrenia has been reported but there is uncertainty concerning the degree of genetic contribution to the phenotypic variance of the disease. This study aimed to examine the familial aggregation and heritability of schizophrenia, and the relative risks (RRs) of other psychiatric diseases, in relatives of people with schizophrenia using the Taiwan National Health Insurance Database. The study population included individuals with affected first-degree or second-degree relatives identified from all beneficiaries (n = 23 422 955) registered in 2013. Diagnoses of schizophrenia made by psychiatrists were ascertained between January 1, 1996 and December 31, 2013. Having an affected co-twin, first-degree relative, second-degree relative, or spouse was associated with an adjusted RR (95% CI) of 37.86 (30.55-46.92), 6.30 (6.09-6.53), 2.44 (1.91-3.12), and 1.88 (1.64-2.15), respectively. Compared with the general population, individuals with one affected first-degree relative had a RR (95% CI) of 6.00 (5.79-6.22) and those with 2 or more had a RR (95% CI) of 14.66 (13.00-16.53) for schizophrenia. The accountability for the phenotypic variance of schizophrenia was 47.3% for genetic factors, 15.5% for shared environmental factors, and 37.2% for non-shared environmental factors. The RR (95% CI) in individuals with a first-degree relative with schizophrenia was 3.49 (3.34-3.64) for mood disorders and 3.91 (3.35-4.57) for delusional disorders. A family history of schizophrenia is therefore associated with a higher risk of developing schizophrenia, mood disorders, and delusional disorders. Heritability and environmental factors each account for half of the phenotypic variance of schizophrenia.

[Schizophrenia or a group of endogenous diseases? The past and the present].

A critical analysis of the main concepts of schizophrenia (from the Kraepelin paradigm to the current studies attempted to «destruct¼ schizophrenia as nosologically independent disease) is presented. In author's opinion, the elimination of schizophrenia may lead to negative consequences as in aspect of clinical practice (the diagnosis of schizophrenia provides information about disease course, clinical and social outcomes) as well as in aspect of denial of autochthonous (endogenous) origin of mental disorders that fall under this definition. Based on the current level of knowledge, manifestation of these disorders can't be well explained by the adverse effects of situational, psychogenic or somatogenic factors. The restriction of the definition of schizophrenia («process¼ schizophrenia) should be brought about by the elimination of a group of schizophrenia spectrum disorders (schizotypal disorder, schizoaffective disorder, delusional psychosis).

Paranoid delusional disorder follows social anxiety disorder in a long-term case series: evolutionary perspective.

Social anxiety disorder (SAD) patients may have self-referential ideas and share other cognitive processes with paranoid delusional disorder (PDD) patients. From an evolutionary perspective, SAD may derive from biologically instinctive social hierarchy ranking, thus causing an assumption of inferior social rank, and thus prompting concerns about mistreatment from those of perceived higher rank. This naturalistic longitudinal study followed four patients with initial SAD and later onset of PDD. These four patients show the same sequence of diagnosed SAD followed by diagnosed PDD, as is often retrospectively described by other PDD patients. Although antipsychotic medication improved psychotic symptoms in all patients, those who also had adjunctive serotonin-specific reuptake inhibitors for SAD had much more improvement in both psychosis and social functioning. From an evolutionary perspective, it can be conjectured that when conscious modulation of the SAD social rank instinct is diminished due to hypofrontality (common to many psychotic disorders), then unmodulated SAD can lead to paranoid delusional disorder, with prominent ideas of reference. Non-psychotic SAD may be prodromal or causal for PDD.

How do people with persecutory delusions evaluate threat in a controlled social environment? A qualitative study using virtual reality.

BACKGROUND: Environmental factors have been associated with psychosis but there is little qualitative research looking at how the ongoing interaction between individual and environment maintains psychotic symptoms. AIMS: The current study investigates how people with persecutory delusions interpret events in a virtual neutral social environment using qualitative methodology. METHOD: 20 participants with persecutory delusions and 20 controls entered a virtual underground train containing neutral characters. Under these circumstances, people with persecutory delusions reported similar levels of paranoia as non-clinical participants. The transcripts of a post-virtual reality interview of the first 10 participants in each group were analysed. RESULTS: Thematic analyses of interviews focusing on the decision making process associated with attributing intentions of computer-generated characters revealed 11 themes grouped in 3 main categories (evidence in favour of paranoid appraisals, evidence against paranoid appraisals, other behaviour). CONCLUSIONS: People with current persecutory delusions are able to use a range of similar strategies to healthy volunteers when making judgements about potential threat in a neutral environment that does not elicit anxiety, but they are less likely than controls to engage in active hypothesis-testing and instead favour experiencing "affect" as evidence of persecutory intention.

Clinico-Epidemiological Comparison of Delusion-Prominent and Hallucination-Prominent Clinical Subgroups of Paranoid Schizophrenia.

BACKGROUND: Though hallucinations and delusions are prominent basic impairments in schizophrenia, reports of the relationship between hallucinatory and delusional symptoms among schizophrenia patients are scant. AIMS: To examine the epidemiological and clinical differences between mainly hallucinatory and mainly delusional subgroups of paranoid schizophrenia patients. METHODS: One hundred schizophrenia patients, paranoid type, were recruited. In a cross-sectional study, participants were divided into Mainly Hallucinatory (H) and Mainly Delusional (D) subgroups. Demographic variables were compared and clinical characteristics were evaluated using the Scale for the Assessment of Positive Symptoms, the Scale for the Assessment of Negative Symptoms, and the Clinical Global Impression Scale. The Quality-of-Life Enjoyment and Satisfaction Questionnaire-18 was used to assess quality of life. RESULTS: Clinically, the H group was more heterogeneous as expressed by the broader range of scores that described the clinical picture of patients in that subgroup (in 43 of 78 variables, 55.13%) and similar ranges of scores (31 of 78 variables, 39.74%) for patients in the D group. Duration of hospitalization was significantly longer in group H than in group D (p=0.047). There was no statistically significant difference between the H and D subgroups in demographic characteristics. CONCLUSIONS: There are distinct epidemiological and clinical differences between the H and D subgroups, with more severe positive and negative symptoms and greater functional impairment in the H group. Paranoid schizophrenia patients with prominent hallucinations have poorer prognosis and need intensive therapeutic rehabilitation beginning with onset-of-illness. Further genetic studies and comparisons of fMRI and/or PET findings are warranted to investigate additional distinctive characteristics of these subgroups.

Source-based morphometry reveals distinct patterns of aberrant brain volume in delusional infestation.

Little is known about the neural correlates of delusional infestation (DI), the delusional belief to be infested with pathogens. So far, evidence comes mainly from case reports and case series. We investigated brain morphology in 16 DI patients and 16 healthy controls using structural magnetic resonance imaging and a multivariate data analysis technique, i.e. source-based morphometry (SBM). In addition, we explored differences in brain structure in patient subgroups based on disease aetiology. SBM revealed two patterns exhibiting significantly (p<0.05, Bonferroni-corrected) lower grey and higher white matter volume in DI patients compared to controls. Lower grey matter volume was found in medial prefrontal cortex, anterior cingulate cortex, medial temporal lobe structures (parahippocampus and hippocampus), sensorimotor cortices, bilateral insula and thalamus and inferior parietal regions. Higher white matter volume was found in medial and middle frontal and temporal cortices, left insula and lentiform nucleus. Grey matter volume was abnormal in both "psychiatric" (primary DI and DI associated with an affective disorder) and "organic" DI (DI due to a medical condition). In contrast, aberrant white matter volume was only confirmed for the "organic" DI patient subgroup. These results suggest prefrontal, temporal, parietal, insular, thalamic and striatal dysfunction underlying DI. Moreover, the data suggest that aetiologically distinct presentations of DI share similar patterns of abnormal grey matter volume, whereas aberrant white matter volume appears to be restricted to organic cases.

[The Capgras syndrome].

The Capgras syndrome is one of delusional-like misidentification syndrome in which a person holds a delusion that one or several his/her friends or relatives have been replaced by an identical-looking impostor. As any other delusional disorder, the Capgras syndrome is characterized by stability despite the indisputable arguments against fault views. Initially, this syndrome was considered as a presentation of schizophrenia but later it has been described in brain organic disorders, primarily in elderly patients with dementia.

Diagnosis, assessment and management of delusional jealousy in Parkinson's disease with and without dementia.

Patients with Parkinson's disease (PD) may present delusional jealousy (DJ). In a previous cross-sectional prevalence study we identified 15 cognitively preserved and five demented PD patients with DJ. The current study aimed at evaluating their clinical (motor and non-motor) characteristics and the pharmacological treatments associated with DJ, and its subsequent pharmacological management. Patients were assessed by neurologists and psychiatrists using the Hoehn and Yahr scale, the Unified Parkinson's Disease Rating Scale, the Brief Psychiatric Rating Scale, the Beck Depression Inventory, the Hamilton Anxiety Scale and the Neuropsychiatric Inventory. Efficacy of DJ management was evaluated in follow-up visits. All patients were in therapy with dopamine agonists. A subgroup of five cognitively preserved patients developed DJ after a short period of treatment of therapy with dopamine agonists, while other patients developed DJ after a longer period of dopaminergic treatment. Psychiatric comorbidities were common in cognitively preserved and in demented patients. The pharmacological management included the interruption of dopamine agonists in two patients and the reduction of dopamine agonist dose plus the use of antipsychotics in other patients. These clinical data suggest that the management of medicated PD patients should include investigation for the presence of DJ and the evaluation of clinical characteristics potentially relevant to the prevention or the early recognition of delusions.

Schizophrenia-like psychosis associated with right lacunar thalamic infarct.

Thalamic dysfunction has been associated with schizophrenia and other psychotic disorders. We describe an adult patient with a lacunar infarct in the posterior region of the right thalamus exhibiting a paranoid schizophrenia-like psychosis as the only clinical manifestation. Neuropsychological assessment showed alterations in visuospatial memory and executive functions at follow up. This case highlights the role of information processing by the thalamus in the development of delusions. We suggest that dysfunction of the right mediodorsal and pulvinar thalamic nuclei disrupts both thalamic sensory processing and thalamo-prefrontal circuits mediating belief evaluation, leading to delusional beliefs.

Fronto-thalamic volumetry markers of somatic delusions and hallucinations in schizophrenia.

Although the psychotic phenomena of schizophrenia have been extensively investigated, somatic delusions and hallucinations have seldom been reported and their mechanisms are substantially unexplored. Here, we aimed to identify the brain structural correlates of somatic psychotic phenomena using combined volumetry and diffusivity structural neuroimaging techniques. Seventy-five individuals with a DSM-IV-TR diagnosis of schizophrenia and 75 healthy controls (HC) underwent a comprehensive clinical assessment, a high-resolution T1-weighted magnetic resonance imaging and a diffusion tensor imaging protocol using a 3T MRI scanner. Voxel-based volumetry and mean diffusivity (MD) of gray matter (GM) and fractional anisotropy (FA) of white matter (WM) of the whole brain were calculated for each subject. Reduced left fronto-insular GM volume was found in patients with somatic delusions compared with patients without somatic delusions and HC. Increased GM volume was found in the bilateral thalami, primarily in the right ventral-anterior thalamic nucleus projecting to the prefrontal-temporal cortices and the bilateral pars triangularis of the inferior frontal lobe, of patients with somatic hallucinations and HC compared with patients without somatic hallucinations. No differences emerged in GM MD and in WM FA between patients with and without psychotic somatic phenomena (i.e. delusions or hallucinations). These findings provide the first evidence that a frontal-thalamic structural perturbation mediates somatic psychotic phenomena in schizophrenia.