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Abnormal functional connectivity (FC, the temporal synchronization of activation across distinct brain regions) of the default mode (DMN), salience (SN), central executive (CEN), and motor (MN) networks is well established in psychosis. However, little is known about FC in individuals, particularly adolescents, reporting subthreshold psychotic experiences (PE) and their trajectory over time. Thus, the aim of this study was to investigate the FC of these networks in adolescents with PE. In this population-based case-control study, 24 adolescents (mean age = 13.58) meeting the criteria for PE were drawn from a sample of 211 young people recruited and scanned for a neuroimaging study, with a follow-up scan 2 years later (n = 18, mean age = 15.78) and compared to matched controls drawn from the same sample. We compared FC of DMN, SN, CEN, and MN regions between PE and controls using whole-brain FC analyses. At both timepoints, the PE group displayed significant hypoconnectivity compared to controls. At baseline, FC in the PE group was decreased between MN and DMN regions. At follow-up, dysconnectivity in the PE group was more widespread. Over time, controls displayed greater FC changes than the PE group, with FC generally increasing between MN, DMN, and SN regions. Adolescents with PE exhibit hypoconnectivity across several functional networks also found to be hypoconnected in established psychosis. Our findings highlight the potential for studies of adolescents reporting PE to reveal early neural correlates of psychosis and support further investigation of the role of the MN in PE and psychotic disorders.

SummaryThere has been a resurgence of interest in the role of childhood trauma in the aetiology of psychosis. In this review, recent findings on the association between childhood trauma and a continuum of psychotic symptoms are presented. Evidence of the association between specific childhood trauma subtypes and psychotic symptoms is examined, with a brief discussion of some current hypotheses about the potential mechanisms underlying the associations that have been found. Some practice implications of these findings are also highlighted.Learning Objectives• Identify findings from recent meta-analyses on the association between childhood trauma and a range of psychotic outcomes, from non-clinical psychotic experiences to psychotic disorders• Consider which childhood traumas are the most potent in the context of psychotic outcomes• Recognise that the relationships between childhood trauma, psychotic symptoms and other psychopathology are complex, dynamic and multidimensional

AIM:Psychotic-like experiences (PEs) have been associated with childhood adversity and psychopathology. However, few studies have examined the dynamic interplay between risk and protective factors and later life outcomes in people with PEs. This study aimed to explore and compare patterns of early adverse and protective experiences and young adult outcomes in a sample of young people with a history of PEs.METHOD:Longitudinal qualitative data spanning nine years were collected from a general population sample of seventeen young adults who had reported PEs in early adolescence. A qualitative comparative case study design was used to explore patterns of early life experiences and young adult outcomes.RESULTS:Four archetypal profiles of early life experiences and later outcomes were identified. Qualitative differences between types of early adverse experiences and the quality of attachment relationships were dominant discriminating factors between low-risk and at-risk archetypes for poor young adult outcomes. Experiences of multiple adversities, which included childhood trauma and occurred in the absence of secure attachment relationships was associated with the poorest young adult outcomes. The presence of secure attachment relationships was protective, even among individuals who had experienced adversity.CONCLUSIONS:Not all young people who report PEs have high levels of adversity. Those who experience multiple early adversities, childhood trauma and insecure attachment relationships are at highest risk for reoccurring PEs and poor young adult outcomes. Developing trusted attachment relationships and engaging in corrective experiences may be protective and could promote positive outcomes in youth with PEs.

BackgroundCognitive and motor dysfunction are hallmark features of the psychosis continuum, and have been detected during late childhood and adolescence in youth who report psychotic experiences (PE). However, previous investigations have not explored infancy and early childhood development. It remains unclear whether such deficits emerge much earlier in life, and whether they are associated with psychotic, specifically hallucinatory, experiences (HE).MethodsThis study included data from Gen2 participants of The Raine Study (n = 1101), a population-based longitudinal cohort study in Western Australia. Five areas of childhood development comprising: communication; fine motor; gross motor; adaptive (problem-solving); and personal-social skills, were assessed serially at ages 1, 2 and 3 years. Information on HE, depression and anxiety at ages 10, 14 and 17 years was obtained. HE were further subdivided into those with transient or recurrent experiences. Mixed effects logistic regression models and cumulative risk analyses based on multiple domain delays were performed.ResultsEarly poorer development in multiple areas was noted from ages 1, 2 and 3 years among youth who reported HE. Early developmental delays significantly increased the risk for later HE. This association was particularly marked in the recurrent HE group, with over 40% having early developmental delays in multiple domains. There was no significant association between early childhood development and later anxiety/depression apart from lower gross motor scores at age 3.ConclusionsThe findings suggest that early pan-developmental deficits are associated with later HE, with the effect strongest for young people who report recurrent HE throughout childhood and adolescence.

BackgroundPsychotic experiences (PE) are highly prevalent in childhood and are known to be associated with co-morbid mental health disorders and functional difficulties in adolescence. However, little is known about the long-term outcomes of young people who report PE.MethodsAs part of the Adolescent Brain Development Study, 211 young people were recruited in childhood (mean age 11.7 years) and underwent detailed clinical interviews, with 25% reporting PE. A 10 year follow-up study was completed and 103 participants returned (mean age 20.9 years). Structured clinical interviews for DSM-5 (SCID-5) and interviewer-rated assessments of functioning were conducted. A detailed neuropsychological battery was also administered. Analyses investigated group differences between those who had ever reported PE and controls in early adulthood.ResultsThe PE group was at a significantly higher risk of meeting DSM-5 criteria for a current (OR 4.08, CI 1.16–14.29, p = 0.03) and lifetime psychiatric disorder (OR 3.27, CI 1.43–7.47, p = 0.005). They were also at a significantly higher risk of multi-morbid lifetime psychiatric disorders. Significantly lower scores on current social and global functioning measures were observed for the PE group. Overall, there were no differences in neuropsychological performance between groups apart from significantly lower scores on the Stroop Word task and the Purdue Pegboard task for the PE group.ConclusionsOur findings suggest that reports of PE are associated with poorer mental health and functional outcomes in early adulthood, with some persisting cognitive and motor deficits. Young people who report such symptoms could be considered a target group for interventions to aid functional outcomes.

AIMS (a) To investigate the utility of childhood PE as a predictor of adolescent psychopathology while accounting for three known risk factors: childhood mental disorder; traumatic experiences and poor childhood functioning, and (b) to investigate the additive effects of including childhood PE in predictive clinical model of adolescent psychopathology. METHOD The study sample comprised of 86 Irish youths who completed two waves of the "Adolescent Brain Development" study (baseline age: 11.7 and follow-up age: 15.7). At baseline, participants completed a clinical interview assessing for PE, mental disorders, traumatic experiences and global functioning in childhood. The internalizing and externalizing problems sub-scales from the Youth Self Report questionnaire were used as follow-up outcomes variables in adolescence. RESULTS Logistic regression analyses revealed that childhood PE was the only predictor significantly associated with both internalizing (univariate OR: 7.58, CI: 2.59-22.15; multivariate OR: 5.43, CI: 1.53-19.29) and externalizing (univariate OR: 11.76, CI: 3.70-37.41; multivariate OR: 30.39, CI: 5.28-174.80) problems in adolescence. All predictive models with PE significantly predicted adolescent outcomes (area under the curve range: 0.70-0.81; all P

Psychotic experiences (PEs) are common in early adolescence and are associated with nonpsychotic psychopathology. However, not all adolescents with PEs have subsequent psychopathology, and vice versa. To date, factors mediating the relationship between PEs and psychopathology have been understudied. The aims of this study were to investigate the bidirectional relationship between PEs and psychopathology in adolescence and to investigate potentially malleable mediators of these relationships. Data from 2 waves (age 13 and 17 years) of Cohort '98 of the Growing Up in Ireland study were examined (n = 6,206). Using KHB pathway decomposition, we investigated the following as potential mediators of the relationship between psychopathology and PEs: parent-child relationship (conflict and positive), self-concept, and child-peer relationship (alienation and trust). Supplementary counterfactual mediation and sensitivity analyses were conducted. Early adolescents with psychopathology had twofold increased odds of late adolescent PEs (internalizing problems: odds ratio [OR] = 2.03, 95% confidence interval [CI; 1.56, 2.62]; externalizing problems: OR = 1.99, CI [1.51, 2.60]). Parent-child conflict explained between 23% and 34% of the associations between internalizing and externalizing problems and subsequent PEs. Early adolescents with PEs had increased odds of late adolescent psychopathology (internalizing problems: OR = 2.01, CI [1.61, 2.50]; externalizing problems: OR = 1.70, CI [1.25, 2.31]). Self-concept alone accounted for 52% of the relationship between PEs and subsequent internalizing problems. There is a bidirectional heterotypic relationship between psychopathology and PEs. Parent-child conflict and self-concept are important characteristics that mediate a proportion of the relationship between PEs and psychopathology. Interventions targeting parent-child conflict in the context of psychopathology and self-concept in the context of PEs may assist in reducing the incidence of poorer outcomes. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Background Childhood risk factors for the development of adult schizophrenia have proved to have only modest and nonspecific effects, and most seem unrelated to the adult phenotype. We report the first direct examination of the longitudinal relationship between psychotic symptoms in childhood and adulthood. Methods We analyzed prospective data from a birth cohort (N = 761), in which children were asked about delusional beliefs and hallucinatory experiences at age 11 years, and then followed up to age 26 years. Structured diagnostic interviews were employed at both ages and self-report of schizophreniform symptoms was augmented by other data sources at age 26 years. Results Self-reported psychotic symptoms at age 11 years predicted a very high risk of a schizophreniform diagnosis at age 26 years (odds ratio, 16.4; 95% confidence interval, 3.9-67.8). In terms of attributable risk, 42% of the age-26 schizophreniform cases in the cohort had reported 1 or more psychotic symptoms at age 11 years. Age-11 psychotic symptoms did not predict mania or depression at age 26 years, suggesting specificity of prediction to schizophreniform disorder. The link between child and adult psychotic symptoms was not simply the result of general childhood psychopathology. Conclusion These findings provide the first evidence for continuity of psychotic symptoms from childhood to adulthood.

Background Little is known about the prevalence of inconsistent trauma reporting in community samples and about its associations with psychopathology. This study aimed to assess for the first time the prevalence of inconsistent trauma reporting in a community sample of children/adolescents and to explore associations with both psychotic experiences and with psychopathology more generally. Method A community-based sample of 86 children/adolescents (baseline mean age 11.5) were interviewed at two time points with data collected in relation to potentially traumatic events through the K-SADS. Emotional and behavioural problems were assessed at follow-up (mean age 15.7) through the Youth Self Report questionnaire while the presence of psychotic experiences was based on expert consensus post interview. Logistic regression models were used to test associations between inconsistent reporting and psychotic experiences at baseline and follow-up, with associations with emotional and behavioral problems at follow-up also assessed. Results Overall, 16.3% of adolescents failed to report previously reported potentially traumatic events at follow-up and were therefore defined as inconsistent trauma reporters. Inconsistent reporting was associated with emotional and behavioural problems as assessed by the Youth Self Report with the exception of rule breaking behaviour and with psychotic experiences as assessed on interview. Conclusions Inconsistent trauma reporting is associated with psychotic experiences and emotional and behavioural problems in young people and may represent an important marker for psychopathology in youth.

(2001). A Critique of the Idea and Science of Risk-Factor Research in Schizophrenia. International Journal of Mental Health: Vol. 30, Risk Factors for Schizophrenia and Implications for Prevention—3, pp. 82-90.

BackgroundAn excess of non-right-handedness has been shown among patients with schizophrenia. However it is not clear whether this finding can be accounted for by an increase in left-handedness, mixed-handedness or both. It is not known whether atypical patterns of hand preferences occur in other functional psychotic illnesses.MethodThe Annett hand preference questionnaire was administered to patients with schizophrenia (n=120); affective psychosis (n=55); schizoaffective psychosis (n=41), and control subjects (n=86). Handedness was classified into three categories: right, mixed and left-handedness.ResultsThe hand preference patterns of patients with functional psychotic illnesses were not significantly different from controls. Patients with schizophrenia showed a non-significant excess of mixed-handedness compared with controls. Patients with schizophrenia and affective psychosis showed a non-significant decrease in left-handedness compared with controls.ConclusionsAlthough our results showed a trend in the hypothesised direction, we failed to demonstrate that patients with psychotic illness differed from controls on self-reported hand preference patterns.

Adults suffering from psychosis have high rates of cannabis use. However, there remains controversy as to whether this is a cause or consequence of the psychosis. This review tests the hypothesis that cannabis can cause psychosis by reviewing studies verifying three important criteria for causality in psychiatry: association, temporal priority, and direction, with the emphasis put on prospective longitudinal population-based studies that tested temporal priority. Evidence supports a causal role for cannabis in the development of psychosis but it appears that cannabis use is neither a sufficient nor a necessary cause for psychosis. Rather, it is a component cause - part of a complex constellation of factors leading to psychosis. On an individual level, cannabis use appears to confer only a two-to three-fold increase in the relative risk for later schizophrenia. On a population level, elimination of cannabis use could lead to a 7-13% reduction in incidence of schizophrenia. Thus, some cases of psychotic disorder could be prevented by discouraging cannabis use, particularly among vulnerable youths. More research is needed to better understand the mechanisms by which cannabis causes psychosis.

Background Deficits in working memory are widely reported in schizophrenia and are considered a trait marker for the disorder. Event-related potentials (ERPs) and imaging data suggest that these differences in working memory performance may be due to aberrant functioning in the prefrontal and parietal cortices. Research suggests that many of the same risk factors for schizophrenia are shared with individuals from the general population who report psychotic symptoms. Methods Forty-two participants (age range 11–13 years) were divided into those who reported psychotic symptoms (N = 17) and those who reported no psychotic symptoms, i.e. the control group (N = 25). Behavioural differences in accuracy and reaction time were explored between the groups as well as electrophysiological correlates of working memory using a Spatial Working Memory Task, which was a variant of the Sternberg paradigm. Specifically, differences in the P300 component were explored across load level (low load and high load), location (positive probe i.e. in the same location as shown in the study stimulus and negative probe i.e. in a different location to the study stimulus) and between groups for the overall P300 timeframe. The effect of load was also explored at early and late timeframes of the P300 component (250-430 ms and 430-750 ms respectively). Results No between-group differences in the behavioural data were observed. Reduced amplitude of the P300 component was observed in the psychotic symptoms group relative to the control group at posterior electrode sites. Amplitude of the P300 component was reduced at high load for the late P300 timeframe at electrode sites Pz and POz. Conclusions These results identify neural correlates of neurocognitive dysfunction associated with population level psychotic symptoms and provide insights into ERP abnormalities associated with the extended psychosis phenotype.

This paper reviews the literature on obstetric complications as a risk factor for schizophrenia. The authors trace the evolution of this literature through different methods and carry out a quantitative review of the results from prospective, population-based studies.Relevant papers were identified by a MEDLINE search, by examination of reference lists of published papers, and through personal contact with researchers in the field. Studies were grouped in chronological order according to common themes or methods. Meta-analytic techniques were used to summarize the findings of prospective population-based studies.The meta-analytic synthesis of the prospective population-based studies revealed that three groups of complications were significantly associated with schizophrenia: 1) complications of pregnancy (bleeding, diabetes, rhesus incompatibility, preeclampsia); 2) abnormal fetal growth and development: (low birthweight, congenital malformations, reduced head circumference), and 3) complications of delivery (uterine atony, asphyxia, emergency Cesarean section). Pooled estimates of effect sizes were generally less than 2.Current methods of investigating the relationship between obstetric complications and schizophrenia are reaching the limit of their usefulness. Lack of statistical power to measure small and interactive effects and lack of detailed information about the prenatal period are major problems with current approaches. A combination of disciplines and approaches will be needed to elucidate the mechanisms underlying these small but important associations.

BackgroundWe investigated the hypothesis that prenatal exposure to the 1957 A2 influenza increases the risk of schizophrenia in adulthood.MethodWe traced a cohort of individuals known to have been exposed to the 1957 influenza epidemic during gestation and an unexposed cohort matched for period of gestation and hospital of birth. Follow-up information on psychiatric illness in subjects was sought from two sources: maternal interview and psychiatric hospital admission data.ResultsFollow-up information was obtained on 54% of the sample: 238 subjects from the influenza-exposed group and 287 subjects from the unexposed group. There was no increased risk of schizophrenia among the exposed cohort compared to the unexposed cohort (relative risk 1.1; 95% CI 0.41–2.95), although there was an increase in depressive illness (relative risk 1.59; 95% CI 1.15–2.19).ConclusionsThe association between prenatal influenza and an increased risk of schizophrenia in adulthood has thus far been found only in population-based data and is not supported by the present observational study which has information about exposure and outcome in individuals.

Background Childhood developmental abnormalities have been previously described in schizophrenia. It is not known, however, whether childhood developmental impairment is specific to schizophrenia or is merely a marker for a range of psychiatric outcomes. Methods A 1-year birth cohort (1972-1973) of 1037 children enrolled in the Dunedin Multidisciplinary Health and Development Study was assessed at biennial intervals between ages 3 and 11 years on emotional, behavioral, and interpersonal problems, motor and language development, and intelligence. At age 11 years, children were asked about psychotic symptoms. At age 26 years, DSM-IV diagnoses were made using the Diagnostic Interview Schedule. Study members having schizophreniform disorder (n = 36 [3.7%]) were compared with healthy controls and also with groups diagnosed as having mania (n = 20 [2%]) and nonpsychotic anxiety or depression disorders (n = 278 [28.5%]) on childhood variables. Results Emotional problems and interpersonal difficulties were noted in children who later fulfilled diagnostic criteria for any of the adult psychiatric outcomes assessed. However, significant impairments in neuromotor, receptive language, and cognitive development were additionally present only among children later diagnosed as having schizophreniform disorder. Developmental impairments also predicted self-reported psychotic symptoms at age 11 years. These impairments were independent of the effects of socioeconomic, obstetric, and maternal factors. Conclusions The results provide evidence for an early-childhood, persistent, pan-developmental impairment that is specifically associated with schizophreniform disorder and that predicts psychotic symptoms in childhood and adulthood.

Foreword William Carpenter Preface Part I. The Social Epidemiology of Schizophrenia: Introduction 1. Investigating socio-environmental influences in schizophrenia: conceptual and design issues Michaeline Bresnahan and Ezra Susser 2. Geographical variation in incidence, course and outcome in schizophrenia: a comparison of developing and developed countries Michealine Bresnahan, Paulo Menezes, Vijoy Varma and Ezra Susser 3. Temporal variation in the incidence, course and outcome of schizophrenia Michaeline Bresnahan, Jane Boydell, Robin Murray and Ezra Susser 4. Urbanisation, migration and risk of schizophrenia Jane Boydell and Robin Murray Part II. The Developmental Epidemiology of Schizophrenia: Introduction 5. Prenatal and perinatal risk factors for schizophrenia Mary Cannon, Robert Kendell, Ezra Susser and Peter Jones 6. Childhood development and later schizophrenia: evidence from genetic high risk and birth cohort studies Mary Cannon, C. Jane Tarrant, Matti O. Huttunen and Peter Jones 7. Prodrome, onset and early course of schizophrenia Heinz Hafner 8. The value of first-episode studies of schizophrenia Mary Clarke and Eadbhard O'Callaghan 9. Schizophrenia at the extremes of life Kenneth G. D. Orr and David J. Castle Part III. The Genetic Epidemiology of Schizophrenia: Introduction 10. The 'classical' genetic epidemiology of schizophrenia Alastair Cardno and Robin Murray 11. Molecular genetics and epidemiology in schizophrenia: a necessary partnership Stanley Zammit, Glyn Lewis and Michael J. Owen 12. Gene-environment correlation and interaction in schizophrenia Jim van Os and Pak Sham 13. Investigating gene-environment interaction in schizophrenia using neuroimaging Theo G. M. van Erp, Timothy L. Gasperoni, Isabelle M. Rosso and Tyrone D. Cannon Part IV. Special Issues in the Epidemiology of Schizophrenia: Introduction 14. Mortality and physical illness in schizophrenia Preben Bo Mortensen 15. The clinical epidemiology of suicide in schizophrenia Hannele Heila and Jouko Loennqvist 16. What is the relationship between substance abuse and schizophrenia? Robin Murray, Anton Grech, Peter Phillips and Sonia Johnson 17. Criminal and violent behaviour in schizophrenia Elizabeth Walsh and Alec Buchanan Part V. Future Directions and Emerging Issues: Introduction 18. Diagnosis and classification of schizophrenia: categories vs dimensions, distributions vs disease Jim van Os and Helene Verdoux 19. The implications of epidemiology for service planning in schizophrenia Graham Thornicroft and Michele Tansella 20. Prevention of schizophrenia - not an impossible dream John McGrath Glossary Index.

Background There has been a surge of interest into the relationship between psychotic experiences (PEs) and bullying. However, the methods of bullying and impact of bullying varies across individuals and the prevalence may also vary by respondent (parent or children). For this reason, a thorough investigation into this relationship is warranted. Methods A longitudinal analysis was conducted on waves 1 and 2 (ages 9 and 13) of the nationally representative Growing Up in Ireland study. Data from n=7163 families were included in this study. Information regarding bullying, being a bully, bullying type, reasons for the bullying, the impact of the bullying was collected from the participating child and their primary care giver (PCG) at both waves. Psychotic experiences were reported by the child at the second wave using the Adolescent Psychotic Symptoms Screener. Results 13.12% of children met validated criteria for psychotic experiences. Based on the PCG’s account, 32.89% of those with PEs at age 13 were bullied at age 9 and this was independently associated with PEs even after accounting for bullying at 13 (OR: 1.40, CI: 1.19–1.65). Physical, verbal, electronic bullying and bullying by exclusion were associated with an increased risk of PE. However, in a multivariate analysis only verbal bullying was independently associated with an increased risk of psychotic experiences (OR: 1.56, CI: 1.27–1.93; adjusted for bullying at 13: OR: 1.47, CI: 1.19–1.82). There was a linear relationship between the number of different methods of bullying experienced at 9 and the risk of PEs at 13 (continuous OR: 1.24, CI: 1.14–1.34). Of the reasons for bullying given by the PCG, only ethnicity (OR: 2.36, CI: 1.46–3.80), being a teacher’s pet (OR: 2.09, CI: 1.17–3.73) and jealously (OR: 2.28, CI: 1.5–3.39) were significantly associated with PEs. Persistent bullying was associated with a higher risk of PEs relative to their peers (never bullied OR: 2.31, CI: 1.73–3.08; and bullied at one-time point: OR: 1.49, CI: 1.10–2.03). Based on the child’s account, the vast majority of those who report being a bully (13.87%) at age 9 were also bullied (76.48%, OR: 7.04, 5.97–8.31). Both being a bully and being bullied at age 9 were associated with an increased risk of PEs (16.91%, OR: 1.34, CI: 1.09–1.64; and 50.48% OR: 1.71, CI: 1.48–1.98, respectively). In a multivariate analysis only being bullied was independently associated with PEs (OR: 1.68, CI: 1.44–1.96; adjusted for bullying at 13: OR: 1.57, CI: 1.34–1.83). Verbally bullying another was the only method of bullying associated with an increased risk of PEs at 13 (OR: 1.59, CI: 1.06–2.39). Of those reporting being bullied, verbal and written bullying at age 9 were associated with an increased risk of PEs at age 13 (OR: 1.25, CI: 0.97–1.6; and OR: 1.44, CI: 1.05–1.97, respectively). In a multivariate analysis only written bullying was associated with an increased risk of PEs (OR: 1.47, CI: 1.05–2.06; adjusted for bullying at 13: OR: 1.41, CI: 1.01–1.99). The impact of the bullying on well-being was also associated with an increased risk of PEs at 13 (OR: 1.36, CI: 1.09–1.72; adjusted for bullying at 13: OR: 1.30, CI: 1.04–1.63). Persistent bullying was associated with a vastly higher risk of PEs relative to their peers (never bullied: OR: 4.42, CI: 3.44–5.69; and bullied at one time point OR: 2.71, CI: 2.10–3.50). Discussion Bullying is pervasive in the childhood of those who subsequent report PE. Bullying at age 9, particularly verbal and written bullying methods are risk factors for PEs in adolescence even when controlling for adolescent bullying. Persistent bullying was associated with a vastly higher risk of PEs. Reducing the rates of bullying in childhood may moderate the likelihood of PEs in adolescents.

Background Individuals with schizophrenia show significant brain morphological abnormalities. The ENIGMA consortium identified that patients with schizophrenia had smaller hippocampus, amygdala, thalamus, accumbens and intracranial volumes.1 Reduced hippocampal volume is one of the most consistent findings in schizophrenia research.2–4 Also, Previous research has reported differences in hippocampal volume and white matter integrity in young adolescents who report psychotic experiences.5,6 However there has been little longitudinal research to investigate the developmental trajectory of these regions in adolescence with an increased susceptibility to psychotic disorders. Aims to investigate two-year longitudinal changes in hippocampal volume in a sample of adolescents who reported psychotic experiences relative to their peers. To investigate the role of presence of co-morbid DSM IV mental disorders and stressful life events in influencing hippocampal volume and study the differences in hippocampus volume between adolescents who were having persistent symptoms versus adolescents with remitting symptoms. Methods A longitudinal case-control study of 50 community-based adolescents aged 13–16 years (25 with psychotic experiences and a matched sample of 25 without psychotic experiences), compared hippocampal volume. All participants were assessed at baseline and two years follow up. T1 weighted anatomical high-resolution imaging and high angular resolution diffusion imaging data were used to conduct quantitative anatomical volumetric evaluations of global hippocampal volume. Clinical interviews also provided information on psychotic experiences, co-morbid disorders and adverse life events. Results There were significant differences in the Right and Left Whole hippocampus between PE and Control group at baseline and 2-year follow up (p≤ 0.05). There were significant differences between PE persist and Control group in the left and right whole hippocampus (p≤ 0.05). Discussion The differences identified in our study suggest that early hippocampal reductions, may play a role in increasing vulnerability to psychosis. References 1. van Erp TG, Hibar DP, Rasmussen JM, et al. Subcortical brain volume abnormalities in 2028 individuals with schizophrenia and 2540 healthy controls via the ENIGMA consortium. Mol Psychiatry. 2016;21(4):585. 2. Wright IC, Rabe-Hesketh S, Woodruff PW, David AS, Murray RM, Bullmore ET. Meta-analysis of regional brain volumes in schizophrenia. Am J Psychiatry. 2000;157(1):16–25. 3. Nelson MD, Saykin AJ, Flashman LA, Riordan HJ. Hippocampal volume reduction in schizophrenia as assessed by magnetic resonance imaging: a meta-analytic study. Arch Gen Psychiatry. 1998;55(5):433–440. 4. Stein JL, Medland SE, Vasquez AA, et al. Identification of common variants associated with human hippocampal and intracranial volumes. Nat Genet. 2012;44(5):552–561. 5. Drakesmith M, Caeyenberghs K, Dutt A, et al. Schizophrenia-like topological changes in the structural connectome of individuals with subclinical psychotic experiences. Hum Brain Mapp. 2015;36(7):2629–2643. 6. Satterthwaite TD, Wolf DH, Calkins ME, et al. Structural Brain Abnormalities in Youth With Psychosis Spectrum Symptoms. JAMA psychiatry. 2016;73(5):515–524.