Childhood abuse in the etiological continuum underlying psychosis from first-episode psychosis to psychotic experiences

Goal The present study aimed to examine the prevalence of child abuse across the continuum of psychosis. Patients and methods The sample consisted of 198 individuals divided in three groups: (1) 48 FEP patients, (2) 77 individuals scoring high in Community Assessment of Psychic Experiences (CAPE), classified as “High CAPE” group and (3) 73 individuals scoring low, classified as “Low CAPE” group. Childhood abuse was assessed using self-report instruments. Chi2 tests and logistic regression models controlling by sex, age and cannabis were used to perform three comparisons: (i) FEP vs. Low CAPE; (ii) FEP vs. High CAPE and (iii) High CAPE vs. Low CAPE. Results The frequency of individuals exposed to childhood abuse for FEP, High CAPE and Low CAPE groups were 52.1%, 41.6% and 11%, respectively. FEP and High CAPE group presented significantly higher rates of childhood abuse compared to Low CAPE group, however, no significant differences were found between FEP and High CAPE groups regarding the frequency of childhood abuse. Conclusion There is an increasing frequency of childhood abuse from low subclinical psychosis to FEP patients. However, childhood abuse is equally common in FEP and at risk individuals

Efecto del pastoreo caprino y vacuno en pastos oligotrofos del Espacio Natural de Doñana

Se estudia el efecto del pastoreo sobre la composición del pasto, la frecuencia de plantas y suelo (descubierto y/o cubierto de acículas de pino), la producción, la biomasa acumulada y el tamaño del banco de semillas, en tres tipos de vegetación (alcornocal adehesado, pinar adehesado y pinar con sotobosque de matorral y claros herbáceos) en una formación forestal representativa de la provincia de Huelva. Los resultados indican un aumento significativo de suelo descubierto, por efecto del pastoreo, tanto en el pinar adehesado como en los claros de pinar pero no en el alcornocal adehesado. El pastoreo también redujo significativamente la frecuencia de herbáceas en todas las unidades de vegetación y produjo una tendencia a la reducción de acículas de pino. La composición del pasto varió considerablemente entre el alcornocal adehesado, mucho más productivo (327±20 gMS .m-2 .año-1) y las otras unidades, mucho menos productivas (43 a 97 gMS .m-2 .año-1) pero no hubo diferencias en composición entre el pinar adehesado y los claros de pinar. El banco de semillas se redujo significativamente por pastoreo en el alcornocal y en el pinar adehesado, pero no en los claros del pinar

Risk assessment and suicide by patients with schizophrenia in secondary mental healthcare: a case-control study

Objectives: To investigate the role of risk assessment in predicting suicide in patients with schizophrenia spectrum disorders (SSDs) receiving secondary mental healthcare. We postulated that risk assessment plays a limited role in predicting suicide in these patients. Design: Retrospective case–control study. Setting: Anonymised electronic mental health record data from the South London and Maudsley National Health Service (NHS) Foundation Trust (SLaM) (London, UK) linked with national mortality data. Participants: In 242 227 SLaM service users up to 31 December 2013, 635 suicides were identified. 96 (15.1%) had a SSD diagnosis. Those who died before 1 January 2007 (n=25) were removed from the analyses. Thus, 71 participants with SSD who died from suicide over the study period (cases) were compared with 355 controls. Main outcome measure: Risk of suicide in relation to risk assessment ratings. Results: Cases were younger at first contact with services (mean±SD 34.5±12.6 vs 39.2±15.2) and with a higher preponderance of males (OR=2.07, 95% CI 1.18 to 3.65, p=0.01) than controls. Also, suicide occurred within 10 days after last contact with services in half of cases, with the most common suicide methods being hanging (14) and jumping (13). Cases were more likely to have the following ‘risk assessment’ items previously recorded: suicidal history (OR=4.42, 95% CI 2.01 to 9.65, p<0.001), use of violent method (OR=3.37, 95% CI 1.47 to 7.74, p=0.01), suicidal ideation (OR=3.57, 95% CI 1.40 to 9.07, p=0.01) and recent hospital discharge (OR=2.71, 95% CI 1.17 to 6.28, p=0.04). Multiple regression models predicted only 21.5% of the suicide outcome variance. Conclusions: Predicting suicide in schizophrenia is highly challenging due to the high prevalence of risk factors within this diagnostic group irrespective of outcome, including suicide. Nevertheless, older age at first contact with mental health services and lack of suicidal history and suicidal ideation are useful protective markers indicative of those less likely to end their own lives

Homocysteine and cognition: A systematic review of 111 studies

Background Elevated plasma homocysteine ​​(Hcy) levels have been associated with cognitive dysfunction in a wide range of conditions. The aim of this review is to establish which cognitive domains and populations are the most affected. Methods We systematically review the literature and consider all articles that showed any relationship between plasma Hcy levels and scores achieved on cognitive performance tests in both, the general population and patients suffering from central nervous system disorders and other diseases. When effect sizes were available and combinable, several meta-analyses were performed. Results We found 111 pertinent articles. There were 24 cohort studies, 18 randomized trials, 21 case-control studies, and 48 cross-sectional studies. This review reveals a positive trend between cognitive decline and increased plasma Hcy concentrations in general population and in patients with cognitive impairments. Results from the meta-analyses also confirm this trend. Treatment with vitamin supplementation fails to show a reduction in cognitive decline. Discussion Further investigations are warranted to clarify this relationship. Earlier detection of the elevated Hcy levels may be an effective intervention to prevent cognitive impairment and dementia

Stability of schizophrenia diagnosis in a ten-year longitudinal study on first episode of non-affective psychosis: conclusions from the PAFIP cohort

OBJECTIVE: To evaluate the ten-year stability of schizophrenia diagnosis in a cohort of first-episode psychosis (FEP) patients and the factors associated with it. METHODS: Changes in diagnosis of 209 FEP patients were described during ten years of follow-up. Related factors with maintenance or change of schizophrenia diagnosis were evaluated in prospective and retrospective approaches through Binary Logistic Regressions, ROC and survival curves. RESULTS: Out of the 209 patients, 126 were diagnosed of schizophrenia six months after their inclusion in the clinical program. Prospective analyses showed that eight of those 126 schizophrenia patients had changed to a different diagnosis after ten years, and predictors of change were better childhood premorbid adjustment, less severity of clinical global impression at baseline, and diagnosis of comorbid personality disorder during follow-up. Retrospectively, out of the 154 patients with schizophrenia in the ten-year assessment, 36 had a different diagnosis at baseline, and those factors related with a different prior diagnosis than schizophrenia were better socioeconomic status and shorter duration of untreated psychosis (DUP). A survival analysis on the timing of schizophrenia diagnosis showed that male gender and longer DUP were predictors of earlier definite diagnosis. CONCLUSIONS: Diagnostic stability of schizophrenia in our FEP sample is high, especially prospective stability, and the group of patients with diagnostic change corresponded to a milder psychopathological profile before and at the onset of disease. Moreover, we observed a cautious attitude in the diagnosis of schizophrenia in patients with shorter DUP who had schizophrenia diagnosis after ten years

Implementation of a multidisciplinary psychoeducational intervention for Parkinson's disease patients and carers in the community: study protocol

Background: Parkinson’s disease progressively limits patients at different levels and as a result family members play a key role in their care. However, studies show lack of an integrative approach in Primary Care to respond to the difficulties and psychosocial changes experienced by them. The aim of this study is to evaluate the effects of a multidisciplinary psychoeducational intervention focusing on improving coping skills, the psychosocial adjustment to Parkinson’s disease and the quality of life in patients and family carers in a Primary Care setting. Methods: This quasi-experimental study with control group and mixed methods was designed to evaluate a multidisciplinary psychoeducational intervention. Based on the study power calculations, 100 people with Parkinson’s disease and 100 family carers will be recruited and assigned to two groups. The intervention group will receive the ReNACE psychoeducational intervention. The control group will be given a general educational programme. The study will be carried out in six community-based health centres. The results obtained from the two groups will be collected for evaluation at three time points: at baseline, immediately after the intervention and at 6 months post-intervention. The results will be measured with these instruments: the Quality of Life Scale PDQ39 for patients and the Scale of Quality of Life of Care-givers SQLC for family carers, and for all participants the Psychosocial Adjustment to Illness scale and the Brief COPE Inventory. Focus groups will be organised with some patients and family carers who will have received the ReNACE psychoeducational intervention and also with the healthcare professionals involved in its development. Discussion: An important gap exists in the knowledge and application of interventions with a psychosocial approach for people with PD and family carers as a whole. This study will promote this comprehensive approach in Primary Care, which will clearly contribute in the existing knowledge and could reduce the burden of PD for patients and family carers, and also in other long-term conditions

Effects of copy number variations on brain structure and risk for psychiatric illness: large-scale studies from the ENIGMA working groups on CNVs

The Enhancing NeuroImaging Genetics through Meta-Analysis copy number variant (ENIGMA-CNV) and 22q11.2 Deletion Syndrome Working Groups (22q-ENIGMA WGs) were created to gain insight into the involvement of genetic factors in human brain development and related cognitive, psychiatric and behavioral manifestations. To that end, the ENIGMA-CNV WG has collated CNV and magnetic resonance imaging (MRI) data from ~49,000 individuals across 38 global research sites, yielding one of the largest studies to date on the effects of CNVs on brain structures in the general population. The 22q-ENIGMA WG includes 12 international research centers that assessed over 533 individuals with a confirmed 22q11.2 deletion syndrome, 40 with 22q11.2 duplications, and 333 typically developing controls, creating the largest-ever 22q11.2 CNV neuroimaging data set. In this review, we outline the ENIGMA infrastructure and procedures for multi-site analysis of CNVs and MRI data. So far, ENIGMA has identified effects of the 22q11.2, 16p11.2 distal, 15q11.2, and 1q21.1 distal CNVs on subcortical and cortical brain structures. Each CNV is associated with differences in cognitive, neurodevelopmental and neuropsychiatric traits, with characteristic patterns of brain structural abnormalities. Evidence of gene-dosage effects on distinct brain regions also emerged, providing further insight into genotype-phenotype relationships. Taken together, these results offer a more comprehensive picture of molecular mechanisms involved in typical and atypical brain development. This "genotype-first" approach also contributes to our understanding of the etiopathogenesis of brain disorders. Finally, we outline future directions to better understand effects of CNVs on brain structure and behavior.Funding information: European Union's Horizon2020 Research and Innovation Programme, Grant/Award Number: CoMorMent project; Grant #847776; KG Jebsen Stiftelsen; National Institutes of Health, Grant/Award Number: U54 EB020403; Norges Forskningsråd, Grant/Award Number: #223273; South-Eastern Norway Regional Health Authority, Grant/Award Number: #2020060ACKNOWLEDGMENTS: The ENIGMA Consortium is supported by the NIH Big Data to Knowledge (BD2K) program under consortium grant number U54 EB020403 (PI: Thompson). OAA is supported by the Research Council of Norway, South East Norway Health Authority, KG Jebsen Stiftelsen, EU H2020. C. A. has been funded by the Spanish Ministry of Science and Innovation; Instituto de Salud Carlos III (SAM16PE07CP1, PI16/02012, PI19/ 024), co-financed by ERDF Funds from the European Commission, “A way of making Europe”, CIBERSAM; Madrid Regional Government (B2017/BMD-3740 AGES-CM-2), European Union Structural Funds; European Union Seventh Framework Program under grant agreements FP7-4-HEALTH-2009-2.2.1-2-241,909 (Project EU-GEI), FP7- HEALTH-2013-2.2.1-2-603,196 (Project PSYSCAN) and FP7- HEALTH-2013- 2.2.1-2-602,478 (Project METSY); and European Union H2020 Program under the Innovative Medicines Initiative two Joint Undertaking (grant agreement No 115916, Project PRISM, and grant agreement No 777394, Project AIMS-2-TRIALS), Fundación Familia Alonso and Fundación Alicia Koplowitz. R. A-A is funded by a Miguel Servet contract from the Carlos III Health Institute (CP18/00003). G. B. is supported by the Dutch Organization for Health Research and Development ZonMw (grants 91112002 & 91712394). A. S. B. is supported by the Dalglish Family Chair in 22q11.2 Deletion Syndrome, Canadian Institutes of Health Research (CIHR) grants MOP-79518, MOP89066, MOP-97800 and MOP-111238, and NIMH grant number U01 MH101723–01(3/5). C. E. B. is also supported by the National Institute of Mental Health: RO1 MH085953, R01 MH100900 and 1U01MH119736. N. E. B. is granted the KNAW Academy Professor Award (PAH/6635). V. D. C. is supported by NIH R01 MH094524. S. C. is supported by the European Union's Horizon 2020 Framework Programme for Research and Innovation under the Specific Grant Agreement No. 945539 (Human Brain Project SGA3); Helmholtz Initiative and Networking Fund. C. R. K. C. is supported by NIA T32AG058507. E. W. C. C. is supported by the Canadian Institutes of Health Research, Ontario Mental Health Foundation grant MOP-74631 and NIMH grant U01MH101723–01(3/5). S. Ci. has received funding from the European Union's Horizon 2020 Framework Programme for Research and Innovation under the Specific Grant Agreement No. 945539 (Human Brain Project SGA3). M. C. C. is supported by the Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London. N. A. C. is supported by Agencia Nacional de Investigación y Desarrollo (ANID Chile) PIA ACT192064. GId. Z. is supported by the NHMRC. J. L. D. and D. E. J. L. are supported by the Wellcome Trust. T. B. C. is supported by NICHD grant PO1-HD070454, NIH grant UO1-MH191719, and NIMH grant R01 MH087636-01A1. AMD is supported by U24DA041147. B. D. is supported by the Swiss National Science Foundation (NCCR Synapsy, project grant numbers 32003B_135679, 32003B_159780, 324730_192755 and CRSK3_190185), the Leenaards Foundation and the Roger De Spoelberch Foundation. SE is supported by the NARSAD-Young Investigator Grant “Epigenetic Regulation of Intermediate Phenotypes in Schizophrenia”. B. E. S. is supported by the NIH (NIMH). D. C. G. is supported by NIH grant numbers MH078143, MH083824, AG058464. W. R. K. is supported by NIH/MH R0106824. R. E. G. is supported by NIH/NIMH grant numbers MH087626, MH119737. DMMcD-McG is supported by National Institutes of Mental Health (NIMH), grant numbers MH119737-02; MH191719; and MH087636-01A1. S. E. M. is supported by NHMRC grants APP1103623; APP1158127; APP1172917. TM is supported by Research Council of Norway - grant number 273345. D. G. M. is supported by the National Institute for Health Research Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London and S (European Autism Interventions)/EU AIMS-2-TRIALS, a European Innovative Medicines Initiative Joint Undertaking under grant agreements 115300 and 777394. T. N. was supported by Stiftelsen KG Jebsen under grant number SKGJ-MED-021. R. A. O. is supported by NIMH R01 MH090553. S. Y. S. has been funded by the Canadain Institutes of Health Research. M. J. O. is supported by MRC Centre grant MR/L010305/1 and Wellcome Trust grant 100,202/Z/12/Z; Dr. Owen has received research support from Takeda. Z. P. is supported by CIHR, CFI, HSFC. B. G. P. is supported by CIHR FDN 143290 and CAIP Chair. G. M. R. is supported by Fondecyt-Chile #1171014 and ANID-Chile ACT192064. A. Re. was supported by a grant from the Swiss National Science Foundation (31003A_182632). DRR is supported by R01 MH120174 (PI: Roalf). This report represents independent research funded by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London (to J. J. R). PSS is supported by NHMRC (Australia) program grant 1093083. J. E. S. is supported by NIH K01-ES026840. S. M. S. is supported by the Epilepsy Society. T. J. S. is supported by NIH grants R01MH107108, R01HD042794, and HDU54079125. I. E. S. is supported by South-Eastern Norway Regional Health Authority (#2020060), European Union's Horizon2020 Research and Innovation Programme (CoMorMent project; grant #847776) and the KG Jebsen Foundation (SKGJ-MED-021). V. M. S. is supported by Research Council of Norway (CoE funding scheme, grant number 223273). D. J. S. is supported by the SA MRC. C. K. T. is supported by Research Council of Norway (#230345, #288083, #223273) and South-Eastern Norway Regional Health Authority (#2019069, #2021070, #500189). D. T.-G. was supported by the Instituto de Salud Carlos III (PI14/00639 and PI14/00918) and Fundación Instituto de Investigación Marqués de Valdecilla (NCT0235832 and NCT02534363). Dvd. M. is supported by Research Council of Norway #276082. F. V. R. is supported by the Michael Smith Foundation for Health Research Scholar Award. deCODE genetics has received support from the Innovative Medicines Initiative Joint Undertaking under grant agreements' no. 115008 (NEWMEDS) and no. 115300 (EUAIMS), of which resources are composed of EFPIA in-kind contribution and financial contribution from the European Union's Seventh Framework Programme (EU-FP7/ 2007–2013). L. T. W. is supported by Research Council of Norway, European Research Council. The IDIVAL neuroimage unit is supported by Instituto de Salud Carlos III PI020499, research funding SCIII-INT13/0014, MICINN research funding SAF2010-20840-C02- 02, SAF2013-46292-R. The TOP/NORMENT study are supported by the Research Council of Norway (#223273). The GOBS study data collection was supported in part by the National Institutes of Health (NIH) grants: R01 MH078143, R01 MH078111, and R01 MH083824 with work conducted in part in facilities constructed under the support of NIH grant number C06 RR020547. The Sydney Memory and Ageing Study has been funded by three National Health & Medical Research Council (NHMRC) Program Grants (ID No. ID350833, ID568969, and APP1093083). We thank the participants and their informants for their time and generosity in contributing to this research. We also acknowledge the MAS research team: https://cheba.unsw.edu.au/researchprojects/sydney-memory-and-ageing-study. We acknowledge the contribution of the OATS research team (https://cheba.unsw.edu.au/ project/older-australian-twins-study) to this study. The OATS study has been funded by a National Health & Medical Research Council (NHMRC) and Australian Research Council (ARC) Strategic Award Grant of the Aging Well, Aging Productively Program (ID No. 401162); NHMRC Project (seed) Grants (ID No. 1024224 and 1025243); NHMRC Project Grants (ID No. 1045325 and 1085606); and NHMRC Program Grants (ID No. 568969 and 1093083). We thank the participants for their time and generosity in contributing to this research. This research was facilitated through access to Twins Research Australia, a national resource supported by a Centre of Research Excellence Grant (ID No. 1079102) from the National Health and Medical Research Council. The NCNG sample collection was supported by grants from the Bergen Research Foundation and the University of Bergen, the Dr Einar Martens Fund, the KG Jebsen Foundation, the Research Council of Norway, to S. L. H., V. M. S., A. J. L., and T. E. The authors thank Dr. Eike Wehling for recruiting participants in Bergen, and Professor Jonn-Terje Geitung and Haraldplass Deaconess Hospital for access to the MRI facility. Additional support by RCN grants 177458/V50 and 231286/F20. The Betula study was supported by a Wallenberg Scholar Grant (KAW). The HUNT Study is a collaboration between HUNT Research Centre (Faculty of Medicine and Health Sciences, NTNU—Norwegian University of Science and Technology), Nord-Trøndelag County Council, Central Norway Health Authority, and the Norwegian Institute of Public Health. HUNT-MRI was funded by the Liaison Committee between the Central Norway Regional Health Authority and the Norwegian University of Science and Technology, and the Norwegian National Advisory Unit for functional MRI. Research for the GAP cohort was supported by the Department of Health via the National Institute for Health Research (NIHR) Specialist Biomedical Research Center for Mental Health award to South London and Maudsley NHS Foundation Trust (SLaM) and the Institute of Psychiatry at King's College London, London. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. S.J. is supported by Calcul Quebec (http:// www.calculquebec.ca), Compute Canada (http://www.computecanada. ca), the Brain Canada Multi investigator research initiative (MIRI), the Institute of Data Valorization (Canada First Research Excellence Fund), CHIR, Canada Research Chairs and the Jeanne et Jean Louis Levesque Foundation. The NTR cohort was supported by the Netherlands Organization for Scientific Research (NWO), MW904-61-193 (de Geus & Boomsma), MaGWnr: 400-07-080 (van 't Ent), MagW 480-04-004 (Boomsma), NWO/SPI 56-464-14,192 (Boomsma), the European Research Council, ERC-230374 (Boomsma), and Amsterdam Neuroscience. Funding for genotyping was obtained from the National Institutes of Health (NIMH U24 MH068457-06; Grand Opportunity grants 1RC2 MH089951, and 1RC2 MH089995); the Avera Institute for Human Genetics, Sioux Falls, South Dakota (USA). Part of the genotyping and analyses were funded by the Genetic Association Information Network (GAIN) of the Foundation for the National Institutes of Health. The Brainscale study was supported by the Netherlands Organization for Scientific Research MagW 480-04-004 (Boomsma), 51.02.060 (Hilleke Hulshoff Pol), 668.772 (Boomsma & Hulshoff Pol); NWO/SPI 56-464-14192 (Boomsma), the European Research Council (ERC230374) (Boomsma), High Potential Grant Utrecht University (Hulshoff Pol), NWO Brain and Cognition 433-09-220 (Hulshoff Pol). SHIP is part of the Community Medicine Research net of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research (grants no. 01ZZ9603, 01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs and the Social Ministry of the Federal State of Mecklenburg-West Pomerania. Genome-wide SNP typing in SHIP and MRI scans in SHIP and SHIP-TREND have been supported by a joint grant from Siemens Healthcare, Erlangen, Germany and the Federal State of Mecklenburg-West Pomerania. The ENIGMA-22q11.2 Deletion Syndrome Working Group wishes to acknowledge our dear colleague Dr. Clodagh Murphy, who sadly passed away in April 2020. Open access funding enabled and organized by Projekt DEAL

Large-scale analysis of structural brain asymmetries in schizophrenia via the ENIGMA consortium

BACKGROUND Left-right asymmetry is an important organizing feature of the healthy brain that may be altered in schizophrenia, but most studies have used relatively small samples and heterogeneous approaches, resulting in equivocal findings. We carried out the largest case-control study of structural brain asymmetries in schizophrenia (N = 11,095), using a single image analysis protocol. METHODS We included T1-weighted data from 46 datasets (5,080 affected individuals and 6,015 controls) from the ENIGMA Consortium. Asymmetry indexes were calculated for global and regional cortical thickness, surface area, and subcortical volume measures. Differences of asymmetry were calculated between affected individuals and controls per dataset, and effect sizes were meta-analyzed across datasets. Analyses were also performed with respect to the use of antipsychotic medication and other clinical variables, as well as age and sex. Case-control differences in a multivariate context were assessed in a subset of the data (N = 2,029). RESULTS Small average differences between cases and controls were observed for asymmetries in cortical thickness, specifically of the rostral anterior cingulate (d = −0.08, pFDR = 0.047) and the middle temporal gyrus (d = −0.07, pFDR = 0.048), both driven primarily by thinner cortices in the left hemisphere in schizophrenia. These asymmetries were not significantly associated with the use of antipsychotic medication or other clinical variables. Older individuals with schizophrenia showed a stronger average leftward asymmetry of pallidum volume than older controls (d = 0.08, pFDR = 9.0 × 10−3). The multivariate analysis revealed that 7% of the variance across all structural asymmetries was explained by case-control status (F = 1.87, p = 1.25 × 10−5). CONCLUSIONS Altered trajectories of asymmetrical brain development and/or lifespan asymmetry may contribute to schizophrenia pathophysiology. Small case-control differences of brain macro-structural asymmetry may manifest due to more substantial differences at the molecular, cytoarchitectonic or circuit levels, with functional relevance for lateralized cognitive processes