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When two or more individuals share delusions and hallucinations, psychotic material has often been transferred to, or induced in, one of the sufferers. A guide to the terminology, aetiology, diagnosis and treatment of induced psychoses is given, together with a description of two cases of folie à deux.
Double suicides are regarded as uncommon phenomena. In particular, homosexuals are very rarely involved. It is reported on the unusual motivation of a dual suicide by hanging among two 20-year-old lesbian women. Due to abnormal psychic development and mutual induced reaction the thought of dying together and being reborn jointly in one person (a contemporary actor) arose. These ideas were influenced by spiritism and metempsychosis. The case is well-documented by diary records and will be discussed under phenomenological and psychodynamic aspects. Typical and atypical criteria of double suicides are featured.
In dyadic deaths, a second victim acts in consort with, is associated with, or is killed by a person who, contemporaneous with the first death, then suicides. Dyadic deaths thus include both homicide-suicides and suicide pacts. This paper describes, suggests organizing dynamics of, and illustrates distinct types of dyadic deaths. The proposed typology varies by levels of dominance, dependence-enmeshment, and the presence or absence of hostility in and between partners.
We present a case of folie à deux in immigrants, for whom the process of immigration changed the intrafamilial dependencies. Folie à deux only appeared in the previously dominant member once she became the dependent member. Follow-up showed resolution of the folie à deux with no change in the recent reversal of roles.
We examined a case of a family of induced insanity (folie à trois) which is characterized by its delusion of jealousy, and reported about the establishment and disappearance process of the delusion. We examined the background of the fact that the family members shared the same delusion and the family dynamics. We concluded that induced insanity is an extended expression of family illness which appears in the process in which the family expresses its problematic theme and tries to cope with it.
Two incidents of shared delusions are presented, one between two brothers and the other between an elderly couple. Their presentation and management are discussed. The possible role of projection and overvalued ideas as aetiological factors in Nigerians with shared delusions are highlighted.
The study of a 66 year old woman's medical chart revealed many discordant elements, leading to the diagnosis of Munchausen's syndrome. The patient had been treated over a period of 20 years at the Medical polyclinic for a variety of symptoms concerning virtually all organs. Her son's chart similarly contains discordant elements, rising the suspicion of a Munchausen Syndrome "by proxy". With this case report, historical aspects and the therapeutic challenge of this syndrome are outlined.
When dealing with Munchausen syndrome by proxy as well as with false allegations of sexual abuse, we normally were confronted with complex family dynamics especially between mother and child. To date there are no scientific discussions on the importance of these dynamics for the development of manifest symptoms in the child and regarding the child's contribution. The descriptions of the Munchausen syndrome by proxy stressed the maternal pathology from which the child's symptoms seemed to be derivable by the concept of simple induction. Regarding false allegations of sexual abuse, especially in divorce proceedings, even publications on the motives of the inducing parents were rare. This paper presents considerations on the object relation dynamics as well as on the intrapsychic dynamics of the children and adolescents in question. Related forensic psychiatric problems are discussed.
OBJECTIVES: Genetic associations between delusional disorder and paranoid schizophrenia are not well understood, although involvement of biological factors has been suspected. We investigated the incidence of human leukocyte antigen (HLA) class I alleles in patients with delusional disorder and paranoid schizophrenia, first, to explore a possible immunogenetic etiology of these paranoid disorders and, second, to determine whether they share similar etiologic mechanisms. METHOD: We employed a nested case-control study design. Psychiatric reference data were available for 38,500 patients attending a hospital-based psychiatric outpatient department between 1998 and 2005. We enrolled 100 patients with delusional disorder and 50 patients with paranoid schizophrenia as the subject cases, using DSM-IV criteria. We considered equivalent numbers of healthy volunteers matched for age and ethnic background as control subjects. All subjects came from an India-born Bengali population. We applied the polymerase chain reaction-based molecular typing method to all patients and healthy subjects. RESULTS: The HLA-A*03 gene is significantly associated with delusional disorder as well as with paranoid schizophrenia. This HLA gene alone or in linkage disequilibrium with other HLA genes or other closely linked non-HLA genes may influence susceptibility to delusional disorder and paranoid schizophrenia. CONCLUSIONS: The study reveals important associations between HLA genes and paranoid disorders. Delusional disorder and paranoid schizophrenia may share similar etiologic mechanisms. This preliminary observation may help our understanding of the genetic basis of these paranoid disorders.
BACKGROUND: The 'odd' or 'Cluster A' personality disorders (PDs) - paranoid, schizoid and schizotypal PDs - were created in DSM-III with little empirical foundation. We have examined the relationship between the genetic and environmental risk factors for dimensional representations of these three personality disorders. METHOD: These personality disorders were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV) in 1386 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel. Using Mx, a single-factor independent pathway twin model was fitted to the number of endorsed criteria for the three disorders. RESULTS: The best-fit model included genetic and unique environmental common factors and genetic and unique environmental effects specific to each personality disorder. Total heritability was modest for these personality disorders and ranged from 21% to 28%. Loadings on the common genetic and unique environmental factors were substantially higher for schizotypal than for paranoid or schizoid PD. The proportion of genetic liability shared with all Cluster A disorders was estimated at 100, 43 and 26% respectively for schizotypal, paranoid and schizoid PDs. CONCLUSION: In support of the validity of the Cluster A construct, dimensional representations of schizotypal, paranoid and schizoid PD are all modestly heritable and share a portion of their genetic and environmental risk factors. No evidence was found for shared environmental or sex effects for these PDs. Schizotypal PD most closely reflects the genetic and environmental liability common to all three Cluster A disorders. These results should be interpreted in the context of the limited power of this sample.
Mummification is the preservation of the effects and/or corpse of a loved one. Psychiatric literature regarding this condition is reviewed and a case is presented in which a mother's paranoid psychosis is discovered following her apparent mummification of her son's corpse. In retrospect, it appears that a diagnosis of folie à deux pertained to this pair. The authors contend that mummification may represent the outcome of a shared delusional system and that failure to establish psychiatric diagnoses in those who practice mummification has been the result of inherent difficulties in diagnosing paranoid disorders.
Evidence implicating genetic or prenatal-perinatal environmental causes in the familial aggregation of schizophrenia led us to study 53 sets of siblings, two or more of whom had chronic psychosis, either schizophrenia or schizoaffective disorder. We looked for similarities in clinical features and concordance of diagnosis within sibships to test for shared familial causes. Clinical variables, including diagnosis, specific symptoms, age at onset, and nongenetic perinatal factors, were studied. Auditory hallucinations, paranoid delusions, thought disorder, negative symptoms, and poor premorbid social adjustment did not significantly correlate in siblings. Concordance was found for schizoaffective disorder and history of major depressive episodes, suggesting that schizophrenia with a depressive component and Research Diagnostic Criteria schizoaffective illness may represent a specific etiologic subtype(s) of the illness, whereas the other noted symptoms may represent the variable expression of the disorder. Age at onset and at first hospitalization were significantly correlated, consistent with genetic or other familial factors on time of onset. Birth complications were significantly more frequent among the schizophrenic compared with non-psychotic siblings, had a familial component, and tended to be associated with an earlier age at onset. Thus, nongenetic perinatal factors may increase the risk for schizophrenia in a familial form of the illness and contribute to the correlation of ages at onset in siblings.
The plasma cortisol suppression following 1 mg dexamethasone was studied in 45 recently hospitalized female patients who met DSM-III criteria for a schizophrenic (or 'schizophreniform') disorder. 19 patients showed nonsuppression (42%): 4 out of 6 within the disorganized (hebephrenic) subtype, 9 out of 10 within the catatonic subtype, 6 out of 11 within the acute ('schizophreniform') subtype and non of the 18 within the paranoid subtype. The distribution is heterogeneous, suggesting that schizophrenic disorders may contain different conditions in terms of limbic pathology. Catatonic patients revealed a very high frequency of nonsuppression, which may indicate that this subtype shares some features of the affective disorders.
BACKGROUND: Personality disorders (PDs) as assessed by questionnaires and personal interviews are heritable. However, we know neither how much unreliability of measurement impacts on heritability estimates nor whether the genetic and environmental risk factors assessed by these two methods are the same. We wish to know whether the same set of PD vulnerability factors are assessed by these two methods. METHOD: A total of 3334 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel (NIPHTP) completed a questionnaire containing 91 PD items. One to 6 years later, 1386 of these pairs were interviewed with the Structured Interview for DSM-IV Personality (SIDP-IV). Self-report items predicting interview results were selected by regression. Measurement models were fitted using Mx. RESULTS: In the best-fit models, the latent liabilities to paranoid personality disorder (PPD), schizoid personality disorder (SPD) and schizotypal personality disorder (STPD) were all highly heritable with no evidence of shared environmental effects. For PPD and STPD, only unique environmental effects were specific to the interview measure whereas both environmental and genetic effects were found to be specific to the questionnaire assessment. For SPD, the best-fit model contained genetic and environmental effects specific to both forms of assessment. CONCLUSIONS: The latent liabilities to the cluster A PDs are highly heritable but are assessed by current methods with only moderate reliability. The personal interviews assessed the genetic risk for the latent trait with excellent specificity for PPD and STPD and good specificity for SPD. However, for all three PDs, the questionnaires were less specific, also indexing an independent set of genetic risk factors.
Delusions of fatal contagion were encountered in about 10% of refugee psychiatric patients from Southeast Asia belonging to one ethnic group, the Hmong. Psychotic depression was the most common diagnosis among the Hmong patients with delusions of contagion, whereas paranoid and schizophrenic diagnoses predominate in patients with similar delusions from other refugee groups. Some cases also occurred as a shared delusional disorder. Associated findings included isolation from the community, intrafamilial conflict, failure to acculturate, and sexual frustration or conflict. Most patients responded to tricyclic medication, later supplemented in about half of the cases with a neuroleptic. This syndrome, which does not appear to have been described previously, should be considered in cases of somatizing refugees who present repeatedly to medical facilities.
OBJECTIVE: The authors examined the relationship of borderline personality disorder to posttraumatic stress disorder (PTSD) with respect to the role of trauma and its timing. METHOD: The Trauma History Questionnaire and the PTSD module of the Structured Clinical Interview for DSM-III-R were administered to 180 male and female outpatients with a diagnosis of one or more DSM-III-R personality disorders. Path analysis was used to evaluate the relationship between borderline personality disorder and PTSD. RESULTS: High rates of early and lifetime trauma were found for the subject group as a whole. Compared to subjects without borderline personality disorder, subjects with borderline personality disorder had significantly higher rates of childhood/adolescent physical abuse (52.8% versus 34.3%) and were twice as likely to develop PTSD. In the path analysis of the relationship between borderline personality disorder and PTSD, none of the different types of paths (direct path, indirect paths through adulthood traumas, paths sharing the antecedent of childhood abuse) was significant. The associations with both trauma and PTSD were not unique to borderline personality disorder; paranoid personality disorder subjects had an even higher rate of comorbid PTSD than subjects without paranoid personality disorder, as well as elevated rates of physical abuse and assault in childhood/adolescence and adulthood. CONCLUSIONS: The associations of personality disorder with early trauma and PTSD were evident, but modest, in borderline personality disorder and were not unique to this type of personality disorder. The results do not appear substantial or distinct enough to support singling out borderline personality disorder from the other personality disorders as a trauma-spectrum disorder or variant of PTSD.
We investigated whether schizophrenia spectrum disorders share common personality characteristics or traits. Participants with a diagnosis of schizophrenia or schizoaffective disorder (SZ) or with a schizophrenia spectrum personality disorder (schizophrenia spectrum PD: schizoid, paranoid, and schizotypal personality disorder) were compared with non-psychiatric control subjects on the five-factor model of personality and the psychosis-proneness scales. On the five-factor personality scales, SZ subjects showed higher levels of neuroticism, and lower levels of openness, agreeableness, extraversion, and conscientiousness than control subjects. Higher scores on openness and lower scores on neuroticism distinguished schizophrenia spectrum PD from SZ. On the psychosis-proneness scales, both PD and SZ participants scored high relative to non-psychiatric control participants on magical ideation and perceptual aberration, while PD participants scored intermediate between non-psychiatric control participants and SZ on social anhedonia. Discriminant analysis indicated that schizophrenia spectrum patients could be distinguished from PDs by more severe social withdrawal and maladjustment, while subjects with PDs could be best distinguished from control subjects on the basis of odd or novel ideation and decreased conscientiousness.
A substantial number of patients do not meet diagnostic criteria for schizophrenia yet exhibit psychotic phenomena characteristic of that disorder (e.g., schizophreniform disorder, schizoaffective disorder, paranoid disorder, atypical psychosis). The relationship between schizophrenia and these disorders is poorly understood. This paper describes how the two-threshold multifactorial model of familial transmission can be applied to test the hypothesis that these disorders share a multifactorial etiology with schizophrenia. The procedure is illustrated using data from a blind family study of the major psychoses. Results support the hypothesis that the disorders under examination share a common multifactorial familial etiology. Methodological issues are discussed along with suggestions for future research in this area.