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ABSTRACTAssertive Community Treatment (ACT) is the most common ambulatory service delivery model for people with severe mental illness worldwide. Flexible ACT, a Dutch modification of ACT, provides comprehensive care for the entire population of people with severe mental illness (SMI). FACT combines the principles of individual case management with ACT services. Researchers found an association between model fidelity and treatment outcome. Consequently, scholars formulated fidelity scales based on previous research and expert opinion (operationalizations of multiple criteria of team structure, organization and treatment processes). The first FACT model fidelity scale from 2008 facilitated the dissemination of FACT and prevented programme drift. Ten years later, an update was necessary to address relevant local variations in implementation, due to specific population profiles and available regional network services, and to improve recovery-oriented and evidence-based practices. Authors and stakeholders tested and updated a new FACT-model fidelity scale in the Netherlands, Denmark and Sweden. The resulting scale assesses 16 quantitative items and 8 qualitative, descriptive topics on 5-point Likert scales. The scale includes FACT-criteria that evidently work and still allow a team to diversify. The FACTs 2017 is a new standard to assess FACT-team model fidelity for the care of people with severe mental illness in The Netherlands and Scandinavia.

Despite extensive research, interdependent problems such as severe mental illness and homelessness cause extreme disparities and health inequity. Handling complexity in careseeker–caregiver networks remains challenging. The local public health services in a Dutch city were enriched with a specialized team. An ethnographic policy evaluation was conducted to identify the essentials of an effective approach. We use the narrative of a homeless man who experiences psychoses for an in-depth analysis of the team’s functionality. The narrative data shows the challenges of caregiver networks and underlines the need to integrate care. It demonstrates how normal behavior, personal skills, and a socio-ecological system strategy merge into collaborative networks with the ability to diversify care and keep focus on recovery. This paper demonstrates the failure of the linear handicap model and the costs of overspecialized care systems. Building on socio-ecological recovery literature, it provides insight how care networks successfully can foster recovery.

Schizophrenia is a heritable complex phenotype associated with a background risk involving multiple common genetic variants of small effect and a multitude of environmental exposures. Early twin and family studies using proxy‐genetic liability measures suggest gene‐environment interaction in the etiology of schizophrenia spectrum disorders, but the molecular evidence is scarce. Here, by analyzing the main and joint associations of polygenic risk score for schizophrenia (PRS‐SCZ) and environmental exposures in 1,699 patients with a diagnosis of schizophrenia spectrum disorders and 1,542 unrelated controls with no lifetime history of a diagnosis of those disorders, we provide further evidence for gene‐environment interaction in schizophrenia. Evidence was found for additive interaction of molecular genetic risk state for schizophrenia (binary mode of PRS‐SCZ above 75% of the control distribution) with the presence of lifetime regular cannabis use and exposure to early‐life adversities (sexual abuse, emotional abuse, emotional neglect, and bullying), but not with the presence of hearing impairment, season of birth (winter birth), and exposure to physical abuse or physical neglect in childhood. The sensitivity analyses replacing the a prioriPRS‐SCZ at 75% with alternative cut‐points (50% and 25%) confirmed the additive interaction. Our results suggest that the etiopathogenesis of schizophrenia involves genetic underpinnings that act by making individuals more sensitive to the effects of some environmental exposures.

Important questions remain about the profile of cognitive impairment in psychotic disorders across adulthood and illness stages. The age-associated profile of familial impairments also remains unclear, as well as the effect of factors, such as symptoms, functioning, and medication. Using cross-sectional data from the EU-GEI and GROUP studies, comprising 8455 participants aged 18 to 65, we examined cognitive functioning across adulthood in patients with psychotic disorders (n= 2883), and their unaffected siblings (n= 2271), compared to controls (n= 3301). An abbreviated WAIS-III measured verbal knowledge, working memory, visuospatial processing, processing speed, and IQ. Patients showed medium to large deficits across all functions (ES range = –0.45 to –0.73, p< 0.001), while siblings showed small deficits on IQ, verbal knowledge, and working memory (ES = –0.14 to –0.33, p< 0.001). Magnitude of impairment was not associated with participant age, such that the size of impairment in older and younger patients did not significantly differ. However, first-episode patients performed worse than prodromal patients (ES range = –0.88 to –0.60, p< 0.001). Adjusting for cannabis use, symptom severity, and global functioning attenuated impairments in siblings, while deficits in patients remained statistically significant, albeit reduced by half (ES range = –0.13 to –0.38, p< 0.01). Antipsychotic medication also accounted for around half of the impairment in patients (ES range = –0.21 to –0.43, p< 0.01). Deficits in verbal knowledge, and working memory may specifically index familial, i.e., shared genetic and/or shared environmental, liability for psychotic disorders. Nevertheless, potentially modifiable illness-related factors account for a significant portion of the cognitive impairment in psychotic disorders.

The validity and clinical utility of the concept of “clinical high risk” (CHR) for psychosis have so far been investigated only in risk‐enriched samples in clinical settings. In this population‐based prospective study, we aimed – for the first time – to assess the incidence rate of clinical psychosis and es­timate the population attributable fraction (PAF) of that incidence for preceding psychosis risk states and DSM‐IV diagnoses of non‐psychotic mental disorders (mood disorders, anxiety disorders, alcohol use disorders, and drug use disorders). All analyses were adjusted for age, gender and education. The incidence rate of clinical psychosis was 63.0 per 100,000 person‐years. The mutually‐adjusted Cox proportional hazards model indicated that preceding diagnoses of mood disorders (hazard ratio, HR=10.67, 95% CI: 3.12‐36.49), psychosis high‐risk state (HR=7.86, 95% CI: 2.76‐22.42) and drug use disorders (HR=5.33, 95% CI: 1.61‐17.64) were associated with an increased risk for clinical psychosis incidence. Of the clinical psychosis incidence in the population, 85.5% (95% CI: 64.6‐94.1) was attributable to prior psychopathology, with mood disorders (PAF=66.2, 95% CI: 33.4‐82.9), psychosis high‐risk state (PAF=36.9, 95% CI: 11.3‐55.1), and drug use disorders (PAF=18.7, 95% CI: –0.9 to 34.6) as the most important factors. Although the psychosis high‐risk state displayed a high relative risk for clinical psychosis outcome even after adjusting for other psychopathology, the PAF was comparatively low, given the low prevalence of psychosis high‐risk states in the population. These findings provide empirical evidence for the “prevention paradox” of targeted CHR early intervention. A comprehensive prevention strategy with a focus on broader psychopathology may be more effective than the current psychosis‐focused approach for achieving population‐based improvements in prevention of psychotic disorders.

Cell fusion in tumor progression mostly refers to the merging of a cancer cell with a cell that has migration and immune escape capabilities such as macrophages. Here we show that spontaneous hybrids made from the fusion of transformed mesenchymal cells with partners from the same lineage undergo nonrecurrent large-scale genomic rearrangements, leading to the creation of highly aneuploid cells with novel phenotypic traits, including metastatic spreading capabilities. Moreover, in contrast to their parents, hybrids were the only cells able to recapitulate in vivo all features of human pleomorphic sarcomas, a rare and genetically complex mesenchymal tumor. Hybrid tumors not only displayed specific mesenchymal markers, but also combined a complex genetic profile with a highly metastatic behavior, like their human counterparts. Finally, we provide evidence that patient-derived pleomorphic sarcoma cells are inclined to spontaneous cell fusion. The resulting hybrids also gain in aggressiveness, exhibiting superior growth capacity in mouse models. Altogether, these results indicate that cell fusion has the potential to promote cancer progression by increasing growth and/or metastatic capacities, regardless of the nature of the companion cell. Moreover, such events likely occur upon sarcoma development, paving the way for better understanding of the biology, and aggressiveness of these tumors.

Oncogenesis is considered to result from chromosomal instability, in addition to oncogene and tumor-suppressor alterations. Intermediate to aneuploidy and chromosomal instability, genome doubling is a frequent event in tumor development but the mechanisms driving tetraploidization and its impact remain unexplored. Cell fusion, one of the pathways to tetraploidy, is a physiological process involved in mesenchymal cell differentiation. Besides simple genome doubling, cell fusion results in the merging of two different genomes that can be destabilized upon proliferation. By testing whether cell fusion is involved in mesenchymal oncogenesis, we provide evidence that it induces genomic instability and mediates tumor initiation. After a latency period, the tumor emerges with the cells most suited for its development. Furthermore, hybrid tumor genomes were stabilized after this selection process and were very close to those of human pleomorphic mesenchymal tumors. Thus genome restructuring triggered by cell fusion may account for the chromosomal instability involved in oncogenesis.

Biphenotypic sinonasal sarcoma (BSNS) is a locally aggressive tumor occurring in the sinonasal region. It harbors both myogenic and neural differentiation and is characterized by PAX3rearrangement with MAML3as the most frequent fusion partner, but the partner of PAX3remains unidentified in a subset of cases. About 70 cases have been reported so far. In this study, we report a series of 41 cases with clinical, pathologic, and molecular description. Twenty-five (61%) patients were female individuals, and the median age was 49 years. Tumors arose predominantly in the nasal cavity and ethmoidal sinuses. Local recurrences occurred in 8 cases of the 25 (32%). Histologic features were characteristic of BSNS, with 5 cases showing focal rhabdomyoblastic differentiation. Immunohistochemistry showed a constant positivity of S100 protein and PAX3 and negativity of SOX10. MyoD1 was focally positive in 91% of cases, whereas only 20% were positive for myogenin. Molecular analysis showed a PAX3-MAML3transcript in 37 cases (90%). RNA sequencing was performed in the 4 negative cases for PAX3-MAML3fusion, and it showed that 1 case harbored a PAX3-FOXO1fusion, as previously described in the literature, and 2 novel fusions: PAX3-WWTR1fusion in 2 cases and PAX3-NCOA2fusion in 1 case. RNA sequencing results were confirmed by fluorescence in situ hybridization, reverse transcription-polymerase chain reaction, and Sanger sequencing. The PAX3-NCOA2-positive case showed focal rhabdomyoblastic differentiation. In conclusion, we report 2 novel fusions (PAX3-WWTR1and PAX3-NCOA2) in BSNS and show that MyoD1 is more sensitive than myogenin for demonstrating myogenic differentiation in this tumor.

The content and organization of mental health care have been heavily influenced by the view that mental difficulties come as diagnosable disorders that can be treated by specialist practitioners who apply evidence‐based practice (EBP) guidelines of symptom reduction at the group level. However, the EBP symptom‐reduction model is under pressure, as it may be disconnected from what patients need, ignores evidence of the trans‐syndromal nature of mental difficulties, overestimates the contribution of the technical aspects of treatment compared to the relational and ritual components of care, and underestimates the lack of EBP group‐to‐individual generalizability. A growing body of knowledge indicates that mental illnesses are seldom “cured” and are better framed as vulnerabilities. Important gains in well‐being can be achieved when individuals learn to live with mental vulnerabilities through a slow process of strengthening resilience in the social and existential domains. In this paper, we examine what a mental health service would look like if the above factors were taken into account. The mental health service of the 21st century may be best conceived of as a small‐scale healing community fostering connectedness and strengthening resilience in learning to live with mental vulnerability, complemented by a limited number of regional facilities. Peer support, organized at the level of a recovery college, may form the backbone of the community. Treatments should be aimed at trans‐syndromal symptom reduction, tailored to serve the higher‐order process of existential recovery and social participation, and applied by professionals who have been trained to collaborate, embrace idiography and maximize effects mediated by therapeutic relationship and the healing effects of ritualized care interactions. Finally, integration with a public mental health system of e‐communities providing information, peer and citizen support and a range of user‐rated self‐management tools may help bridge the gap between the high prevalence of common mental disorder and the relatively low capacity of any mental health service.

The self-medication hypothesis postulates that the high prevalence of smoking in patients with psychosis can be explained by the ameliorating effect of smoking on symptoms. However, there are few large prospective studies testing this hypothesis. We aimed to examine the multi-cross-sectional and prospective associations of changes in smoking behaviour with symptoms and quality of life.

Dermatofibrosarcoma protuberans is underlined by recurrent collagen type I alpha 1 chain-platelet-derived growth factor B chain(COL1A1-PDGFB) fusions but ~ 4% of typical dermatofibrosarcoma protuberans remain negative for this translocation in routine molecular screening. We investigated a series of 21 cases not associated with the pathognomonic COL1A1-PDGFBfusion on routine fluorescence in situ hybridization (FISH) testing. All cases displayed morphological and clinical features consistent with the diagnosis of dermatofibrosarcoma protuberans. RNA-sequencing analysis was successful in 20 cases. The classical COL1A1-PDGFBfusion was present in 40% of cases (n= 8/20), and subsequently confirmed with a COL1A1break-apart FISH probe in all but one case (n= 7/8). 55% of cases (n= 11/20) displayed novel PDGFDrearrangements; PDGFDbeing fused either to the 5′ part of COL6A3(2q37.3) (n= 9/11) or EMILIN2(18p11) (n= 2/11). All rearrangements led to in-frame fusion transcripts and were confirmed at genomic level by FISH and/or array-comparative genomic hybridization. PDGFD-rearranged dermatofibrosarcoma protuberans presented clinical outcomes similar to typical dermatofibrosarcoma protuberans. Notably, the two EMILIN2-PDGFDcases displayed fibrosarcomatous transformation and homozygous deletions of CDKN2Aat genomic level. We report the first recurrent molecular variant of dermatofibrosarcoma protuberans involving PDGFD, which functionally mimic bona fide COL1A1-PDGFB fusions, leading presumably to a similar autocrine loop-stimulating PDGFRB. This study also emphasizes that COL1A1-PDGFBfusions can be cytogenetically cryptic on FISH testing in a subset of cases, thereby representing a diagnostic pitfall that pathologists should be aware of.

Many patients with psychotic disorders have persistent paranoid ideation and avoid social situations because of suspiciousness and anxiety. We investigated the effects of virtual-reality-based cognitive behavioural therapy (VR-CBT) on paranoid thoughts and social participation.

In verschillende richtlijnen en zorgstandaarden wordt benadrukt dat het voor het effect van de behandeling van patiënten met een ernstige psychische aandoening (EPA) belangrijk is om te investeren in een goede therapeutische relatie. Toch is er nog maar weinig onderzoek gedaan naar hoe je een goede therapeutische relatie met EPA-patiënten opbouwt en in standhoudt.

Dermatofibrosarcoma protuberans is underlined by recurrent collagen type I alpha 1 chain-platelet-derived growth factor B chain(COL1A1-PDGFB) fusions but ~ 4% of typical dermatofibrosarcoma protuberans remain negative for this translocation in routine molecular screening. We investigated a series of 21 cases not associated with the pathognomonic COL1A1-PDGFBfusion on routine fluorescence in situ hybridization (FISH) testing. All cases displayed morphological and clinical features consistent with the diagnosis of dermatofibrosarcoma protuberans. RNA-sequencing analysis was successful in 20 cases. The classical COL1A1-PDGFBfusion was present in 40% of cases (n= 8/20), and subsequently confirmed with a COL1A1break-apart FISH probe in all but one case (n= 7/8). 55% of cases (n= 11/20) displayed novel PDGFDrearrangements; PDGFDbeing fused either to the 5′ part of COL6A3(2q37.3) (n= 9/11) or EMILIN2(18p11) (n= 2/11). All rearrangements led to in-frame fusion transcripts and were confirmed at genomic level by FISH and/or array-comparative genomic hybridization. PDGFD-rearranged dermatofibrosarcoma protuberans presented clinical outcomes similar to typical dermatofibrosarcoma protuberans. Notably, the two EMILIN2-PDGFDcases displayed fibrosarcomatous transformation and homozygous deletions of CDKN2Aat genomic level. We report the first recurrent molecular variant of dermatofibrosarcoma protuberans involving PDGFD, which functionally mimic bona fide COL1A1-PDGFB fusions, leading presumably to a similar autocrine loop-stimulating PDGFRB. This study also emphasizes that COL1A1-PDGFBfusions can be cytogenetically cryptic on FISH testing in a subset of cases, thereby representing a diagnostic pitfall that pathologists should be aware of.

Met de deze brief reageert de auteur op een eerder verschenen opinie van Bob Cools, directeur van het CGG De pont in Mechelen: ‘De Nieuwe GGZ: een apologie en utopie’.

People with psychotic disorders can experience a lack of active involvement in their decisional process. Clinical decision aids are shared decision-making tools which are currently rarely used in mental healthcare. We examined the effects of Treatment E-Assist (TREAT), a computerized clinical decision aid in psychosis care, on shared decision-making and satisfaction with consultations as assessed by patients.

Aims.To study the systematic assessment of need for care and clinical parameters for use in treatment plans in patients diagnosed with severe mental illness.Methods.The Cumulative Needs for Care Monitor (CNCM) includes various validated instruments, such as the Camberwell Assessment of Need. A Markov-type cost-effectiveness model (health care perspective, 5-year time horizon) was used to compare CNCM with care as usual (CAU). Two studies were used to determine model parameters: a before–after study (n= 2155) and a matched-control study (n= 937).Results.The CNCM may lead to a gain in psychiatric functioning according to the models. CNCM patients remain in (outpatient) care, while CAU patients drop out more frequently. There is only a small difference in inpatient care. As a result, average costs per patient in the CNCM group are between €2809 (before–after model) and €5251 (matched-control model) higher. The iCER was between €45 127 and €57 839 per life year without psychiatric dysfunction gained.Conclusions.CNCM may be only cost-effective when willingness to pay for a life year without psychiatric dysfunction is higher than €45 000. However, this result is highly sensitive to the level of psychiatric dysfunctioning in patients who do not receive care.

Background:Blockade of the dopamine D2receptor is a key mechanism in the antipsychotic treatment of patients with a psychotic disorder, but may also induce emotional deficits. The partial D2agonistic profile of aripiprazole has, therefore, been suggested to favor emotional wellbeing compared with the pure dopamine antagonistic properties of traditional antipsychotics. Method:The current study used the experience sampling method (a structured diary technique) to assess the effects of switching from treatment with traditional dopamine antagonist antipsychotics to treatment with the partial dopamine agonist aripiprazole on emotional wellbeing in the daily life of 13 patients with a diagnosis of schizophrenia. Results:More than half of all patients experienced exacerbation of psychotic symptoms after they had switched to the aripiprazole medication regime, consequently resulting in dropout of the study. Furthermore, switching to aripiprazole treatment, when effective in terms of symptom reduction, was accompanied by decreased feelings of both positive and negative affect in daily life, suggestive of a general state of emotional dampening. Conclusions:Although the scale of the current study and the 54% dropout rate call for careful interpretation of the data, implementation of ecological monitoring in psychopharmacological research may open up new avenues for untangling the working mechanisms of compounds with regard to their impact on mental states.

Objective: The implementation of assertive community treatment (ACT) varies widely. To date, the association between model fidelity and effect has not been investigated in Europe. We investigated the association between model fidelity and outcome in the Dutch mental health system.Method: In a prospective longitudinal study, ACT model fidelity and patient outcomes were assessed in 20 outpatient treatment teams. Patients with severe mental illness (n= 530) participated in the study. Outcomes were assessed 3 times using the Health of the Nation Outcome Scales (HoNOS), the Camberwell Assessment of Need Short Assessment Schedule (CANSAS), and the number of hospital days and homeless days during a 2-year follow-up period. Data were analyzed using multilevel statistics.Results: High ACT model fidelity was associated with better outcomes on the HoNOS and less homeless days. Among all of the ACT ingredients, team structure was associated with better outcomes. No associations were found between ACT model fidelity, number of hospital days, and CANSAS scores.Conclusions: Our evidence supports the importance of model fidelity for improving patient outcomes.

Social phobia (SPh) and paranoid symptoms (PS) are associated. They may overlap because they share psychological and behavioural mechanisms such as selective attention for social threats and avoidance behaviour. Possibly, one leads to the other. The aim of this study is to explore the association between SPh and PS in a prospective general population sample.Adults (7076) from the NEMESIS general population were assessed for SPh and PS using the Composite International Diagnostic Interview (CIDI) at baseline, and one and three years later. Odds ratios, dose–response relationships and confidence intervals were calculated.Lifetime SPh and PS were associated (OR=3.08; 95% CI=2.49–3.82; p<.001), with a dose response. SPh emerging after PS was significant (OR=4.07; 95% CI=2.50–6.63; p<.001), also with a dose response, i.e. more PS symptoms yield more SPh symptoms. PS emerging after SPh was not significant.This study confirmed the association of SPh and PS in a general population. Possibly this is caused by shared underlying psychological and behavioural processes. There was some indication that paranoid ideation precedes the development of SPh, but this must be considered with caution. Clinical implications are discussed.

To examine, using a cross-twin cross-trait design, the hypotheses 1) that the genetic and environmental susceptibility to depression is expressed, in part, as alterations in cortisol day curves and 2) that cortisol abnormalities are not merely the consequence of depressive states or the stressors associated with its onset. Alteration of diurnal secretion of cortisol is a possible endophenotype of depression, as depressed patients show alterations in cortisol dynamics over the day.

Individual differences in stress reactivity constitute a crucially important mechanism of risk for depression. Because stress can be conceptualized as the continuous occurrence of minor daily hassles, this study focused on emotional reactivity to stress in the flow of daily life and examined to what degree individual differences in emotional reactivity could be explained by genetic and/or environmental factors.

Screening for preschizophrenia in the general population with the aim of preventing transition to full-blown illness is an epidemiological impossibility because a rare disease cannot be predicted. The lack of specificity resulting in abundance of false-positives can be remedied in part by using much more restrictive screening criteria that combine several indicators of risk for transition to schizophrenia. Raising the specificity (reducing the false-positives), however, can only be done at the expense of sensitivity (increasing the false-negatives). The most commonly used strategy to raise specificity is the sample enrichment strategy. This involves the creation of samples enriched with schizophrenia risk by selectively filtering at-risk people out over a range of consecutive referral processes starting in the general population, through to general practioners, mental health services, and the early detection clinic. However, improvements in specificity obtained by the sample enrichment strategy should not be attributed to the use of some predictive instrument that supposedly identifies high-risk individuals. The epidemiologically and ethically most viable way for screening and early detection is to selectively increase the permeability of the filters on the pathway to mental health care. This will occasion samples of help-seekers enriched with schizophrenia risk at the level of mental health services (thus reducing false-positives), while at the same time making an attempt to "attract" as many detectable schizophrenia prodromes as possible through the filters along the pathway to mental health care (thus reducing false-negatives). Early psychosis research has yielded some useful suggestions in that it is becoming increasingly clear that it is not just psychosis itself, but rather the clinical context of the psychotic experience that determines risk for transition to schizophrenia. Thus, risk for transition to full-blown psychotic disorder is to a large degree determined by size of psychosis "load," comorbid distress and depression, cannabis use, cognitive ability, and subjective reports of impairment and coping. Making a diagnosis of psychotic disorder is not an exact science: it involves an arbitrary cutoff imposed on dimensional variation of psychopathology and need for care over time. Gaining insight into the cognitive and biological factors that drive the dimensional variation, including therapeutic interventions, is arguably more useful than sterile dichotomous prediction models.

To show which aspects of the environment increase the risk for schizophrenia and how they interact with pre-existing liability for psychosis.

Associations between disability and depression have been shown to be consistent across cultures among middle-aged adults. In later life the association between disability and depression is much more substantial and may be amenable to influences by health care facilities as well as economic and sociocultural factors. Fourteen community-based studies on depression in later life in 11 western European countries contribute to a total study sample of 22,570 respondents aged 65 years or older. Measures are harmonised for depressive symptoms (EURO-D scale) and disability. Using multilevel modelling to control for the stratified data structure we examined whether the association between disability and depressive symptoms is modified by national health care and mental health care availability, national economic circumstances, demographic characteristics and religious tradition. The association between depressive symptoms and disability is attenuated by health care expenditure and availability of mental health care and also by gross domestic product; it was more pronounced in countries with high levels of orthodox religious beliefs. Higher levels of depressive symptoms are found in countries with a larger gross domestic product (per capita) and higher health care expenses but are interpreted with care because of measurement differences between the centres. The findings from this contextual perspective indicate that general and mental health care should be geared to one another wherever possible.

Previous work suggests that auditory hallucinations in children and adolescents occur frequently in the absence of psychotic illness, although a number of such children go on to develop more severe psychotic symptomatology and need for care. We examined prospectively what factors are associated with formation of delusions in adolescents who are hearing voices. Eighty adolescents (mean age 12.9 years, SD = 3.1) who reported hearing voices were examined at baseline and followed-up three times over a period of 3 years. Fifty percent were receiving professional care, but 50% were not in need of care. Baseline measurement of voice appraisals, attributions, psychopathology, global functioning, dissociation, stressful life events, coping mechanisms, and receipt of professional care were used as predictors of delusion formation, measured as a score of 6 or greater on the extended BPRS items: “suspiciousness,” “unusual thought content” and “grandiosity.” Thirteen children (16%) displayed evidence of delusional ideation over at least one of the three follow-up periods, of which seven (9%) de novo. Adjusting for presence of baseline delusional ideation, delusion formation over the follow-up period was associated with baseline voice appraisals and attributions such as tone of the voice (hazard ratio voice “variably friendly and hostile” compared to “always friendly”: HR = 6.8, 95% CI: 1.1, 41.0), perceived location of the voice (outside vs. inside head: HR = 2.9, 95% CI: 1.0, 8.7), and whether the voice resembled that of a parent (HR = 3.5, 95% CI: 1.0, 12.0); baseline BPRS anxiety/depression (HR = 6.4, 95% CI: 1.9, 21.4), baseline BPRS disorganization (HR = 5.0, 95% CI: 0.98, 26.1) and the baseline amount of reported recent stressful life events (HR continuous life events score: 1.8, 95% CI: 1.0, 3.3). In addition, in older children, the perceived influence of the voices on emotions and behavior was strongly associated with delusion formation (HR = 5.1, 95% CI: 1.0, 25.9). Delusion formation in children hearing voices may be responsive to triggering events and facilitated by feelings of anxiety/depression. The results also highlight the role of attributions associated with external sources, authority figures, perceived influence or “power” over the person, as well as emotional appraisal processes and cognitive disorganization. © 2001 Wiley-Liss, Inc.

The fact that relatives of patients with schizophrenia display subtle cognitive abnormalities suggests genetic transmission of an underlying cognitive endophenotype. It was examined to what extent the cognitive abnormalities that discriminate patients and relatives from controls do so independently of each other, and independent of IQ. Neuropsychological measures were assessed in 50 patients with schizophrenia, 50 first-degree relatives of patients with schizophrenia, and 50 healthy controls. The assessment focused on episodic memory, attentional span, simple and complex speed of information, and semantic memory. Factor analysis of the cognitive test results yielded four factors reflecting speed, episodic memory, working memory, and semantic fluency. Performance of the relatives was intermediate to that of the patients and the controls after adjustment for age, sex, educational level, and IQ. For both patients and relatives, speed of information processing, working memory, and episodic memory independently discriminated from control performance, with a similar pattern in the order of the size of the effects. The results suggest the existence of more than one familial cognitive risk factor for schizophrenia. Independent familial cognitive risk factors may represent separate causal influences or separate indicators of risk related to the same genetic mechanism. © 2001 Wiley-Liss, Inc.

“Expressed emotion” (EE) is considered a marker of dysfunctional family interaction in patients with schizophrenia. An alternative hypothesis, however, is that at least some of the different elements of EE really represent attempts on the part of carers to cope with and care for a relative with a psychiatric disorder. EE (criticism and emotional overinvolvement) was measured in relatives (n = 31) of patients with psychotic illness using the Five-Minute Speech Sample (FMSS). Level of EE was examined in relation to (1) patient-reported family involvement in care over the previous 2 years as indicated by medication monitoring, involvement in treatment decisions, and providing a substitute for institutional care; and (2) symptom severity and number of psychotic episodes. Presence of EE in the relative was strongly associated with the degree of family involvement in care (odds ratio [OR] over three levels: 3.2; 95% confidence interval [CI], 1.1 to 9.0). In addition, presence of high EE was associated with number of psychotic episodes in the previous 5 years in the proband (OR over 0, 1, or 2 episodes: 6.2; 95% CI, 1.2 to 31.9). The association with family involvement was confined to emotional overinvolvement (OR = 9.1; 95% CI, 2.0 to 42.2), whereas the association with previous psychotic episodes was confined to criticism (OR = 20.6; 95% CI, 2.8 to 149.3). Emotional overinvolvement may be a state marker for attempts on the part of relatives to be partners in the care for patients with psychotic illness. High level of criticism may be a trait marker in relatives associated with poor prognosis, but could also develop in reaction to a frequently relapsing illness.

AbstractThe existing methods for studying the antimicrobial activity of essential oils (e.g. the dilution of the test substances in broth or agar medium) are not adequate to evaluate the effects of the volatile components. Growth inhibition of fungi by various essential oils was determined by direct contact in broth and agar media and compared with the fungistatic action of their vapors using the micro-atmosphere method. Tests were performed on eight cellulolytic mold strains that often contaminate archive and museum reserves. Thirty-seven essential oils were screened to find the most antifungal ones with potential to be employed as atmospheric preservatives. Chenopodium ambrosioidesL. var. anthelminticum, Cymbopogon martinii(Roxb.) W. Watson var. martinii, Cymbopogon nardus(L.) W. Watson var. nardus, Syzygium aromaticum(L.) Merr. et L. M. Perry and Pimenta racemosa(Mill.) J.W. Moore were the most active essential oils on the eight strains tested according to direct contact methods. C. martiniiwas inhibitory even after 12 days of incubation. Using the micro-atmosphere method, C. nardusand C. martiniivolatiles were the most fungistatic, but the vapors of Ch. ambrosioides, S. aromaticumand P. racemosagave moderate results with a specific short effect of P. racemosa.

AbstractAimsPeople with psychotic disorders receive mental healthcare services mainly for their psychiatric care needs. However, patients often experience multiple physical or social wellbeing-related care needs as well. This study aims to identify care needs, investigate their changes over time and examine their association with mental healthcare consumption and evidence-based pharmacotherapy.MethodsThis study combined annually obtained routine outcome monitoring (ROM) data with care consumption data of people with a long-term psychotic illness receiving treatment in four Dutch mental healthcare institutes between 2012 and 2016. Existing treatment algorithms were used to determine psychiatric, physical and social wellbeing-related care needs based on self-report questionnaires, semi-structured interviews and physical parameters. Care consumption was measured in hours of outpatient mental healthcare consumption per year. Generalised estimating equation models were used to calculate odds ratios of care needs and their associations with time, mental healthcare consumption and medication use.ResultsParticipants (n= 2054) had on average 7.4 care needs per measurement and received 25.4 h of care per year. Physical care needs are most prevalent and persistent and people with more care needs receive more mental healthcare. Care needs for psychotic symptoms and most social wellbeing-related care needs decreased, whereas the chance of being overweight significantly increased with subsequent years of care. Several positive associations were found between care needs and mental healthcare consumption as well as positive relations between care needs and evidence-based pharmacotherapy.ConclusionsThis longitudinal study present a novel approach in identifying care needs and their association with mental healthcare consumption and pharmacotherapy. Identification of care needs in this way based on ROM can assist daily clinical practice. A recovery-oriented view and a well-coordinated collaboration between clinicians and general practitioners together with shared decisions about which care needs to treat, can improve treatment delivery. Special attention is required for improving physical health in psychosis care which, despite appropriate pharmacotherapy and increasing care consumption, remains troublesome.

The purpose of this research is to describe in greater detail than is typically done the daily life experienes of 11 ambulatory chronic mental patients and 11 nonpsychiatric controls. The subjects, although diagnostically heterogeneous, were representative of Dutch chronic mental patients. The Experience-Sampling Method was used to signal subjects randomly 10 times a day for 6 consecutive days to fill out self-rating forms assessing mental state and contextual information at the moment of the signal. Compliance was good. In time-allocation comparisons with nonpsychiatric subjects the patients were found to live relatively “normal” lives. As expected, their psychopathology was influenced by social environments such as being alone, at home, or in soclety at large. Contrary to other studies that stress the social isolation of such individuals, the chronic subjects reported feeling better away from home and among people than normal subjects. When alone, chronic patients reported daydreaming more and noted a fendency to drift away from thouhts about current activities. Mental state fluctuations and daily interactions, characteristic of this group, are examined in relation to theories of vulnerability and coping style of chronic mental patients, with an eye to individualized treatment applications.

Met veel interesse hebben wij kennisgenomen van de reactie van prof. dr. Greet Vanaerschot op onze opiniebijdrage in GZ-psychologie, nr. 1 (Onderzoek naar de therapeutische relatie: Golden Oldie of toekomstmuziek?). Grote delen van haar betoog onderschrijven wij van harte.

Research in psychiatry could speeden its progress by taking the manifest heterogenity and variability of symptom expression within diagnostic groups more fully into account. Since Kraepelin symptom variation has been recognized to have both biological and environmental roots. If investigated systematically, such variations in illness experience will yield new subtypes that will provide greater insight into the onset, course and vulnerability of mental disorders. Studies ranging from population surveys to the laboratory have demonstrated that psychopathology is not randomly distributed in a population, nor is it constantly present in the lives of individuals. At both the population and the person levels, psychopathology varies with time and place. At the population level, illness processes localize in risk groups, who often reside in specific neighbourhoods or social settings. The individual experience of psychopathology also fluctuates with time, place and culture. This variability requires methods for case detection and treatment planning that take this into account.

AbstractAimsPsychosis spectrum disorder has a complex pathoetiology characterised by interacting environmental and genetic vulnerabilities. The present study aims to investigate the role of gene–environment interaction using aggregate scores of genetic (polygenic risk score for schizophrenia (PRS-SCZ)) and environment liability for schizophrenia (exposome score for schizophrenia (ES-SCZ)) across the psychosis continuum.MethodsThe sample consisted of 1699 patients, 1753 unaffected siblings, and 1542 healthy comparison participants. The Structured Interview for Schizotypy-Revised (SIS-R) was administered to analyse scores of total, positive, and negative schizotypy in siblings and healthy comparison participants. The PRS-SCZ was trained using the Psychiatric Genomics Consortiums results and the ES-SCZ was calculated guided by the approach validated in a previous report in the current data set. Regression models were applied to test the independent and joint effects of PRS-SCZ and ES-SCZ (adjusted for age, sex, and ancestry using 10 principal components).ResultsBoth genetic and environmental vulnerability were associated with case-control status. Furthermore, there was evidence for additive interaction between binary modes of PRS-SCZ and ES-SCZ (above 75% of the control distribution) increasing the odds for schizophrenia spectrum diagnosis (relative excess risk due to interaction = 6.79, [95% confidential interval (CI) 3.32, 10.26], p< 0.001). Sensitivity analyses using continuous PRS-SCZ and ES-SCZ confirmed gene–environment interaction (relative excess risk due to interaction = 1.80 [95% CI 1.01, 3.32], p= 0.004). In siblings and healthy comparison participants, PRS-SCZ and ES-SCZ were associated with all SIS-R dimensions and evidence was found for an interaction between PRS-SCZ and ES-SCZ on the total (B= 0.006 [95% CI 0.003, 0.009], p< 0.001), positive (B= 0.006 [95% CI, 0.002, 0.009], p= 0.002), and negative (B= 0.006, [95% CI 0.004, 0.009], p< 0.001) schizotypy dimensions.ConclusionsThe interplay between exposome load and schizophrenia genetic liability contributing to psychosis across the spectrum of expression provide further empirical support to the notion of aetiological continuity underlying an extended psychosis phenotype.