Showing papers by "Robin M. Murray published in 2010"
TL;DR: Functional magnetic resonance imaging in healthy volunteers found that Δ-9-THC and CBD can have opposite effects on regional brain function, which may underlie their different symptomatic and behavioral effects, and CBD's ability to block the psychotogenic effects of Δ- 9- THC.
613 citations
TL;DR: The findings suggest that the origins of schizophrenia include two interrelated developmental processes evident from childhood to early adolescence (ages 7-13 years).
Abstract: ObjectivePremorbid cognitive deficits in schizophrenia are well documented and have been interpreted as supporting a neurodevelopmental etiological model. The authors investigated the following three unresolved questions about premorbid cognitive deficits: What is their developmental course? Do all premorbid cognitive deficits follow the same course? Are premorbid cognitive deficits specific to schizophrenia or shared by other psychiatric disorders? MethodParticipants were members of a representative cohort of 1,037 males and females born between 1972 and 1973 in Dunedin, New Zealand. Cohort members underwent follow-up evaluations at specific intervals from age 3 to 32 years, with a 96% retention rate. Cognitive development was analyzed and compared in children who later developed schizophrenia or recurrent depression as well as in healthy comparison subjects. ResultsChildren who developed adult schizophrenia exhibited developmental deficits (i.e., static cognitive impairments that emerge early and remain...
502 citations
TL;DR: Findings provide support for the hypothesis that exceptional intellectual ability is associated with bipolar disorder.
Abstract: Background
Anecdotal and biographical reports suggest that bipolar disorder may be associated with high IQ or creativity, but evidence for any such connection is weak.
Aims
To investigate possible associations between scholastic achievement and later bipolar disorder, using prospective data, in a whole-population cohort study.
Method
Using individual school grades from all individuals finishing compulsory schooling in Sweden between 1988 and 1997, we tested associations between scholastic achievement at age 15–16 and hospital admission for psychosis between ages 17 and 31, adjusting for potential confounders.
Results
Individuals with excellent school performance had a nearly fourfold increased risk of later bipolar disorder compared with those with average grades (hazard ratio HR = 3.79, 95% CI 2.11–6.82). This association appeared to be confined to males. Students with the poorest grades were also at moderately increased risk of bipolar disorder (HR = 1.86, 95% CI 1.06–3.28).
Conclusions
These findings provide support for the hypothesis that exceptional intellectual ability is associated with bipolar disorder.
294 citations
TL;DR: This article proposes an integrated model--of a sociodevelopmental pathway to psychosis--to account for the reported high rates in migrant and minority ethnic populations.
Abstract: There is consistent and strong evidence that the incidence of all psychoses is higher in many migrant and minority ethnic populations in a number of countries. The reasons for this are, however, unclear and a wide range of explanations have been proposed, from genetic to neurodevelopmental to psychosocial. In this article, we describe and evaluate the available evidence for and against each of these. What this shows is that: (1) there are few studies that have directly investigated specific risk factors in migrant and minority ethnic populations, with often only 1 or 2 studies of any relevance to specific explanations and (2) what limited research there has been tends to implicate a diverse range of social factors (including childhood separation from parents, discrimination and, at an area level, ethnic density) as being of potential importance. In an attempt to synthesize these disparate findings and provide a basis for future research, we go on to propose an integrated model—of a sociodevelopmental pathway to psychosis—to account for the reported high rates in migrant and minority ethnic populations. Aspects of this model will be directly tested in a new Europe-wide incidence and case–control study that we will conduct over the next 3 years, as part of the European Network of National Schizophrenia Networks studying Gene–Environment Interactions programme.
289 citations
TL;DR: It is shown that antipsychotics normalize diurnal cortisol hyper-secretion but not the blunted cortisol awakening response in FEP; factors other than the excess of psychosocial stress explain HPA axis abnormalities in F EP.
258 citations
TL;DR: The impact of parental history of mental disorder was not confined to elevated offspring risk of concordant disorders but rather offspring are at increased risk of a wide range of mental disorders, particularly those with 2 affected parents.
Abstract: Context While concordant parent/offspring risks for specific mental disorders are well established, knowledge of the broader range of psychiatric outcomes among offspring with parental history of mental disorder is lacking. Objective To examine the full range of mental health outcomes among offspring of parents with serious and other mental disorders compared with those whose parents had no such history. Design Population-based cohort study. Offspring were followed up from their 14th birthday for the development of mental disorders based on both outpatient and inpatient hospital data. Setting Danish population. Participants All offspring born in Denmark between 1980 and 1994 (N = 865 078) with follow-up to December 2008. Main Outcome Measures Incidence rates, incidence rate ratios, and cumulative incidences for offspring psychiatric outcomes. Results Parental serious mental disorder (SMD) (nonaffective or affective psychosis) was found to be positively associated with virtually all offspring psychiatric outcomes, including those not hitherto regarded as clinically related. Offspring of parents without SMD but with a history of “other mental disorder” were also found to be at increased risk of developing a range of mental disorders. The strongest associations were found where both parents had a history of mental disorder (eg, offspring of 2 parents with SMD were 13 times more likely to develop schizophrenia). Elevated risks were not confined to concordant parent/offspring disorders (eg, offspring of 2 parents with SMD were 8 times more likely to develop substance misuse disorders). Conclusions The impact of parental history of mental disorder was not confined to elevated offspring risk of concordant disorders but rather offspring are at increased risk of a wide range of mental disorders, particularly those with 2 affected parents. Our results imply an important role for etiological factors giving rise to broad, as well as specific, familial vulnerabilities. These findings also have potential implications for diagnostic classification.
242 citations
TL;DR: Only specific adverse childhood experiences are associated with psychotic disorders and only in a minority of cases, suggesting that research into the mechanisms underlying the pathway from childhood adversity to psychosis is more fruitful.
Abstract: Background Childhood adversity has been associated with onset of psychosis in adulthood but these studies have used only general definitions of this environmental risk indicator. Therefore, we sought to explore the prevalence of more specific adverse childhood experiences amongst those with and without psychotic disorders using detailed assessments in a large epidemiological case-control sample (AESOP).
Method Data were collected on 182 first-presentation psychosis cases and 246 geographically matched controls in two UK centres. Information relating to the timing and frequency of exposure to different types of childhood adversity (neglect, antipathy, physical and sexual abuse, local authority care, disrupted living arrangements and lack of supportive figure) was obtained using the Childhood Experience of Care and Abuse Questionnaire.
Results Psychosis cases were three times more likely to report severe physical abuse from the mother that commenced prior to 12 years of age, even after adjustment for other significant forms of adversity and demographic confounders. A non-significant trend was also evident for greater prevalence of reported severe maternal antipathy amongst those with psychosis. Associations with maternal neglect and childhood sexual abuse disappeared after adjusting for maternal physical abuse and antipathy. Paternal maltreatment and other forms of adversity were not associated with psychosis nor was there evidence of a dose–response effect.
Conclusions These findings suggest that only specific adverse childhood experiences are associated with psychotic disorders and only in a minority of cases. If replicated, this greater precision will ensure that research into the mechanisms underlying the pathway from childhood adversity to psychosis is more fruitful.
189 citations
TL;DR: Early in their course, cognitive deficits are present in all psychotic disorders but are most severe and pervasive in schizophrenia and least pervasive in bipolar disorder and mania.
Abstract: ObjectiveOverwhelming evidence suggests that compromised neuropsychological function is frequently observed in schizophrenia. Neurocognitive dysfunction has often been reported in other psychotic disorders, although there are inconsistencies in the literature. In the context of four distinct diagnostic groups, the authors compared neuropsychological performance among patients experiencing their first psychotic episode. MethodData were derived from a population-based, case-control study of patients with first-episode psychosis. A neuropsychological test battery was administered to patients with a diagnosis of schizophrenia (N=65), bipolar disorder or mania (N=37), depressive psychosis (N=39), or other psychotic disorders (N=46) following index presentation, as well as to healthy comparison subjects (N=177). The presence of specific and generalized cognitive deficits was examined. ResultsThe schizophrenia group presented widespread neuropsychological impairments and performed significantly worse than health...
185 citations
TL;DR: The highest risk of suicide after a psychotic episode occurs soon after presentation, yet physicians should still be vigilant in assessing risk a decade or longer after first contact, according to the widely held view that 10% to 15% die of suicide.
Abstract: Context: The long-term risk of suicide after a first episode of psychosis is unknown because previous studies often have been based on prevalence cohorts, been biased to more severely ill hospitalized patients, extrapolated from a short follow-up time, and have made a distinction between schizophrenia and other psychoses. Objective: To determine the epidemiology of suicide in a clinically representative cohort of patients experiencing their first episode of psychosis.
156 citations
TL;DR: It is suggested that smaller hippocampal volume in first-episode psychosis can partly be explained by stress-related processes in the brain, as measured by cortisol hyper-secretion.
126 citations
TL;DR: Exaggerated medial prefrontal cortical and subcortical responses to emotional signals may represent heritable neurobiological abnormalities underlying bipolar disorder.
TL;DR: It is concluded that further study of the mechanisms underlying the link between cannabis and psychosis may be conducted productively from the perspective of progressive developmental sensitization, resulting from gene-environment interactions.
TL;DR: Using the largest international familial schizophrenia cohort to date, it is shown that a substantial portion of the phenotypic correlation between schizophrenia and cognition is caused by shared genetic effects.
Abstract: Content The DSM-IV concept of schizophrenia offers diagnostic reliability but etiologic and pathologic heterogeneity, which probably contributes to the inconsistencies in genetic studies. One solution is to identify intermediate phenotypes, “narrower” constructs of liability, that hypothetically share genetic risk with the disorder. Although a variety of candidate intermediate phenotypes have emerged, few have explicitly quantified the extent of their genetic overlap with schizophrenia. Objective To quantify the net-shared genetic effects between schizophrenia and specific cognitive candidate intermediate phenotypes. Design Twin and family design. Setting Adult psychiatric research centers in the United States and the United Kingdom. Participants A total of 2056 participants: 657 patients with schizophrenia, 674 first-degree relatives (including co-twins), and 725 controls. Main Outcome Measures (1) Latent factors capturing the common variance between cognitive tasks, (2) separation of the latent factors into their genetic and environmental components, and (3) estimation of the net-shared genetic variance between the latent cognitive factors or intelligence and schizophrenia. Results Genetic factors contributed substantially to the total variance in cognition (immediate recall latent factor: 0.66; 95% confidence interval [CI], 0.62 to 0.85; delayed recall latent factor: 0.48; 0.42 to 0.55; and intelligence: 0.66; 0.62 to 0.71). The latent common factors for modality-specific immediate and delayed recall and intelligence showed similar levels of phenotypic covariance with schizophrenia (immediate recall: −0.35; delayed recall: −0.37; and intelligence: −0.38), with 72%, 86%, and 89%, respectively, due to shared genetic effects with schizophrenia. Environmental effects accounted for little phenotypic correlation between cognition and schizophrenia. Conclusions Using the largest international familial schizophrenia cohort to date, we showed that a substantial portion of the phenotypic correlation between schizophrenia and cognition is caused by shared genetic effects. However, because the phenotypic and genetic correlations are far from unity, the genetics of schizophrenia are clearly not merely the genetics of cognition.
TL;DR: Reduced general neuropsychological function was linked to poor symptom relabelling ability and the cingulate gyrus (as part of a midline cortical system) along with right hemisphere regions may be involved in illness and symptom self-appraisal in first-onset psychosis.
Abstract: BACKGROUND: Several studies have suggested that neuropsychological and structural brain deficits are implicated in poor insight. Few insight studies however have combined neurocognitive and structural neuroanatomical measures.
AIMS: Focusing on the ability to relabel psychotic symptoms as pathological, we examined insight, brain structure and neurocognition in first-onset psychosis.
METHOD: Voxel-based magnetic resonance imaging data were acquired from 82 individuals with psychosis and 91 controls assessed with a brief neuropsychological test battery. Insight was measured using the Schedule for the Assessment of Insight.
RESULTS: The principal analysis showed reduced general neuropsychological function was linked to poor symptom relabelling ability. A subsequent between-psychosis group analysis found those with no symptom relabelling ability had significant global and regional grey matter deficits primarily located at the posterior cingulate gyrus and right precuneus/cuneus.
CONCLUSIONS: The cingulate gyrus (as part of a midline cortical system) along with right hemisphere regions may be involved in illness and symptom self-appraisal in first-onset psychosis.
01 Jan 2010
TL;DR: Whether more progress would be achieved in DSM-V by abandoning the familiar categorical system and instead moving to a dimensional system which rates both developmental impairment and symptom factor scores is discussed.
Abstract: The diagnostic criteria for schizophrenia in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV1) are based on the premise that it is a discrete illness entity, in particular, distinct from the affective psychoses. This assumption has persisted for more than a century, even though patients with a diagnosis of schizophrenia show a wide diversity of symptoms and outcomes, and no biological or psychological feature has been found to be pathognomonic of the disorder. However, there has been sustained, and indeed growing, criticism of the concept. For example, writing about the diagnosis of schizophrenia more than a decade ago,2 one of Britain's most sophisticated nosological experts, Ian Brockington, enjoined “It is important to loosen the grip which the concept of ‘schizophrenia’ has on the minds of psychiatrists. Schizophrenia is an idea whose very essence is equivocal, a nosological category without natural boundaries, a barren hypothesis. Such a blurred concept is ‘not a valid object of scientific enquiry’.”3 Should Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition(DSM-V), persist with the neo-Kraepelinian concept of schizophrenia with all its defects, or should it deconstruct psychosis into its component dimensions? In this article, we will address the question by considering 2 main themes, firstly, the role of culture and ethnicity in the diagnosis of psychosis, and secondly, a life course approach to understanding psychosis. We will then discuss whether more progress would be achieved in DSM-V by abandoning the familiar categorical system and instead moving to a dimensional system which rates both developmental impairment and symptom factor scores. However, we will begin by briefly reviewing the recent history of the classification of the psychoses.
TL;DR: In this article, the reproducibility of VBM and cortical thickness measurement was investigated to detect group differences and estimate heritability when MRI scans from different scanners running different acquisition protocols in a multicenter setup are included.
Abstract: Multicenter structural MRI studies can have greater statistical power than single-center studies. However, across-center differences in contrast sensitivity, spatial uniformity, etc., may lead to tissue classification or image registration differences that could reduce or wholly offset the enhanced statistical power of multicenter data. Prior work has validated volumetric multicenter MRI, but robust methods for assessing reliability and power of multisite analyses with voxel-based morphometry (VBM) and cortical thickness measurement (CORT) are not yet available. We developed quantitative methods to investigate the reproducibility of VBM and CORT to detect group differences and estimate heritability when MRI scans from different scanners running different acquisition protocols in a multicenter setup are included. The method produces brain maps displaying information such as lowest detectable effect size (or heritability) and effective number of subjects in the multicenter study. We applied the method to a five-site multicenter calibration study using scanners from four different manufacturers, running different acquisition protocols. The reliability maps showed an overall good comparability between the sites, providing a reasonable gain in sensitivity in most parts of the brain. In large parts of the cerebrum and cortex scan pooling improved heritability estimates, with "effective-N" values upto the theoretical maximum. For some areas, "optimal-pool" maps indicated that leaving out a site would give better results. The reliability maps also reveal which brain regions are in any case difficult to measure reliably (e.g., around the thalamus). These tools will facilitate the design and analysis of multisite VBM and CORT studies for detecting group differences and estimating heritability.
TL;DR: The presence of schizophrenia was specifically related to reduced GMV in frontal, insular, cingulate, medial parietal, and temporal cortex, over and above effects of genetic risk for the disorder.
TL;DR: It is concluded that the use of cannabis and the amphetamines significantly contributes to the risk of psychosis.
Abstract: Adolescence is a time of exploration of the self, and this exploration may involve the use of alcohol and drugs. Sadly, for some, adolescence also marks the first signs of a psychosis. The temporal proximity between the onset of substance use and of psychosis has been the cause of much debate. Here we review the association of alcohol, cannabis, stimulants, and other drugs with psychosis, and we conclude that the use of cannabis and the amphetamines significantly contributes to the risk of psychosis.
TL;DR: The use of illicit substance use and its correlates in first episode psychosis are studied to find out if it is a positive or negative sign for psychosis.
Abstract: Objective: To determine if substance use (particularly cannabis) is more frequent among first episode psychosis patients and associated with a more problematic clinical presentation. Method: All first episode psychosis (FEP) patients presenting to secondary services were recruited from London and Nottingham, over 2 years, in the Aetiology and Ethnicity of Schizophrenia and Other Psychoses study broad framework. Clinical and sociodemographic variables were assessed using a set of standardized instruments. A schedule was created to retrospectively collate substance use data from patients, relatives and clinicians. Results: Five hundred and eleven FEP were identified. They used three to five times more substances than general population. Substance use was associated with poorer social adjustment and a more acute mode of onset. Cannabis use did not affect social adjustment, but was associated with a more acute mode of onset. Conclusion: Cannabis has a different impact on FEP than other substances. Large epidemiological studies are needed to disentangle cannabis effect.
TL;DR: Bipolar disorder may be associated with an inherited abnormality of a neural network incorporating left prefrontal cortex and bilateral retrosplenial cortex, which is related to genetic susceptibility for illness.
Abstract: Background Individuals with a history of bipolar disorder demonstrate abnormalities of executive function, even during euthymia. The neural architecture underlying this and its relationship with genetic susceptibility for illness remain unclear. Method We assessed 18 remitted individuals with bipolar disorder, 19 of their unaffected first degree relatives and 19 healthy controls using functional magnetic resonance imaging (fMRI) and a paced verbal fluency task with two levels of difficulty. Results Bipolar patients made significantly more errors in the easy level of the verbal fluency task than their relatives or controls. Analysis of variance of fMRI data demonstrated a significant main effect of group in a large cluster including retrosplenial cortex and adjacent precuneate cortex (x=7, y=-56, x=15). All three groups showed deactivation in these areas during task performance relative to a neutral or rest condition. Group differences comprised a lesser amount of deactivation in unaffected relatives compared with controls in the easy condition [F(2, 55)=3.42, p=0.04] and in unaffected relatives compared with bipolar patients in the hard condition [F(2, 55)=4.34, p=0.018]. Comparison with the control group indicated that both bipolar patients and their relatives showed similar deficits of deactivation in retrosplenial cortex and reduced activation of left prefrontal cortex. Conclusions Bipolar disorder may be associated with an inherited abnormality of a neural network incorporating left prefrontal cortex and bilateral retrosplenial cortex.
Copenhagen University Hospital1, University of Bonn2, University of Copenhagen3, Aalborg University4, GlaxoSmithKline5, Utrecht University6, Ludwig Maximilian University of Munich7, University of Oslo8, Oslo University Hospital9, Hebrew University of Jerusalem10, University of Helsinki11, National Institutes of Health12, King's College London13, University of Verona14, University of California, Los Angeles15, Heidelberg University16, Cardiff University17, Wellcome Trust Sanger Institute18, Broad Institute19, University of Aberdeen20
TL;DR: Results of a replication study of AHI1 locus markers, previously implicated in schizophrenia, in a large European sample and a meta-analysis of the implicated markers show evidence for significant overrepresentation of all tested alleles in patients compared with controls.
Abstract: The Abelson helper integration site 1 (AHI1) gene locus on chromosome 6q23 is among a group of candidate loci for schizophrenia susceptibility that were initially identified by linkage followed by linkage disequilibrium mapping, and subsequent replication of the association in an independent sample. Here, we present results of a replication study of AHI1 locus markers, previously implicated in schizophrenia, in a large European sample (in total 3907 affected and 7429 controls). Furthermore, we perform a meta-analysis of the implicated markers in 4496 affected and 18 920 controls. Both the replication study of new samples and the meta-analysis show evidence for significant overrepresentation of all tested alleles in patients compared with controls (meta-analysis; P = 8.2 × 10−5–1.7 × 10−3, common OR = 1.09–1.11). The region contains two genes, AHI1and C6orf217, and both genes—as well as the neighbouring phosphodiesterase 7B (PDE7B)—may be considered candidates for involvement in the genetic aetiology of schizophrenia.
TL;DR: This article examined whether ASz children display brain function abnormalities during error processing that are similar to those exhibited by adults with schizophrenia using the same Go/NoGo paradigm and found that children with a triad of putative antecedents of schizophrenia exhibited specific early error-processing deficits rather than a generalized deficit in self-monitoring.
01 Jan 2010
TL;DR: The Abelson helper integration site 1 (AHI1) gene locus on chromosome 6q23 is among a group of candidate loci for schizophrenia susceptibility that were initially identified by linkage followed by linkage disequilibrium mapping and subsequent replication of the association in an independent sample.
Abstract: The Abelson helper integration site 1 (AHI1) gene locus on chromosome 6q23 is among a group of candidate loci for schizophrenia susceptibility that were initially identified by linkage followed by linkage disequilibrium mapping, and subsequent replication of the association in an independent sample. Here, we present results of a replication study of AHI1 locus markers, previously implicated in schizophrenia, in a large European sample (in total 3907 affected and 7429 controls). Furthermore, we perform a meta-analysis of the implicated markers in 4496 affected and 18,920 controls. Both the replication study of new samples and the meta-analysis show evidence for significant overrepresentation of all tested alleles in patients compared with controls (meta-analysis; P = 8.2 x 10(-5)-1.7 x 10(-3), common OR = 1.09-1.11). The region contains two genes, AHI1 and C6orf217, and both genes-as well as the neighbouring phosphodiesterase 7B (PDE7B)-may be considered candidates for involvement in the genetic aetiology of schizophrenia.
01 Jan 2010
TL;DR: Nosarti et al. as discussed by the authors studied the effect of preterm birth on the development of the preterm brain and found that preterm infants are more likely to experience neurological sequelae.
Abstract: Part I. Introduction: 1. Epidemiology of preterm birth Sven Cnattigius and Stefan Johansson 2. The changing face of intensive care for preterm newborns John Wyatt 3. Clinical outcome: neurological sequelae following preterm birth Ingeborg Krageloh-Mann Part II. Neuroimaging: 4. Imaging the preterm brain Terrie E. Inder, Russell Lawrence and Jeffrey J. Neil 5. Structural Magnetic Resonance Imaging Richard W. I. Cooke 6. Magnetic Resonance Imaging findings from adolescence to adulthood Matthew Allin and Muriel Walshe 7. Functional neuroimaging following very preterm birth Chiara Nosarti and Larry Rifkin 8. Diffusion tensor imaging findings in preterm and low birth weight populations Matthew Allin Part III. Behavioural Outcome: 9. Behavioural outcome of preterm birth in childhood and adolescence Elaine Healy 10. Preterm birth and fetal growth in relation to adult psychopathology Christina M. Hultman and Chiara Nosarti Part IV. Neuropsychological Outcome: 11. Cognitive and functional outcomes of children born preterm Betty Vohr 12. Methodological considerations in neurodevelopmental outcome studies of infants born prematurely Glen P. Aylward 13. Language function after preterm birth Teresa M. Rushe 14. A cognitive neuroscience perspective on the development of memory in children born preterm Michelle De Haan 15. Executive function development in preterm children Peter John Anderson, Kelly Howard and Lex W. Doyle Part V. Applied Research: 16. Academic performance and learning disabilities H. Gerry Taylor 17. Pathways of risk and resiliency after prematurity: role of socioeconomical status Michael M. Msall, Mary C. Sullivan and Jennifer Park 18. Cognitive and behavioural interventions Marie C. McCormick and Beth Marie McManus Part VI. Conclusions: 19. Integrative summary and future directions Chiara Nosarti, Robin M. Murray and Maureen Hack.
TL;DR: Children aged 9-12 years who present multiple antecedents of schizophrenia display poorer neurocognition than healthy peers on several domains showing pronounced deficits in schizophrenia, first-episode psychosis, and youth with prodromal symptoms.
TL;DR: There was evidence that, as levels of ethnic identification increased, the odds of psychosis increased in the BME but not in the White British group, independent of potential confounders, but the association between strong ethnic identity and psychosis in BME individuals was attenuated and non-significant when controlled for perceived disadvantage.
TL;DR: This analysis demonstrates potential importance in another light to move beyond current epidemiological approaches to elucidate exact socio-environmental factors that underpin urbanicity and ethnic minority status as markers of increased risk by incorporating gene-environment interactions that adopt a multi disciplinary perspective.
Abstract: Genetic and environmental factors are associated with psychosis risk, but the latter present more tangible markers for prevention. We conducted a theoretical exercise to estimate the proportion of psychotic illnesses that could be prevented if we could identify and remove all factors that lead to increased incidence associated with ethnic minority status and urbanicity. Measures of impact by population density and ethnicity were estimated from incidence rate ratios [IRR] obtained from two methodologically-similar first episode psychosis studies in four UK centres. Multilevel Poisson regression was used to estimate IRR, controlling for confounders. Population attributable risk fractions [PAR] were estimated for our study population and the population of England. We considered three outcomes; all clinically relevant ICD-10 psychotic illnesses [F10-39], non-affective psychoses [F20-29] and affective psychoses [F30-39]. One thousand and twenty-nine subjects, aged 18-64, were identified over 2.4 million person-years. Up to 22% of all psychoses in England (46.9% within our study areas) could be prevented if exposures associated with increased incidence in ethnic minority populations could be removed; this is equivalent to 66.9% within ethnic minority groups themselves. For non-affective psychoses only, PAR for population density was large and significant (27.5%); joint PAR with ethnicity was 61.7%. Effect sizes for common socio-environmental risk indicators for psychosis are large; inequalities were marked. This analysis demonstrates potential importance in another light: we need to move beyond current epidemiological approaches to elucidate exact socio-environmental factors that underpin urbanicity and ethnic minority status as markers of increased risk by incorporating gene-environment interactions that adopt a multi disciplinary perspective.
TL;DR: Preterm birth leads to functional neuronal differences in adulthood, which are meditated by both structural variations in task-specific regions, and gestational age.
TL;DR: It is found that never-smokers had a younger age at examination and earlier onset and longer duration of illness than smokers and ex-smoking, and longerduration of illness was significantly associated with higher RTQ scores.
Abstract: Rates of cigarette smoking in individuals with schizophrenia well exceed those in the general population and in other mental illnesses. In the present study, we examined the relationship between smoking status, clinical characteristics and cognitive functions in 230 male Chinese schizophrenia patients. They were interviewed by experienced psychiatrists using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) (SCID-P). Clinical symptoms were rated using the Positive and Negative Syndrome Scale (PANSS), and the Revised Tolerance Questionnaire (RTQ) used to evaluate the severity of nicotine dependence. Nine neuropsychological tests were used to assess cognitive function. We found that never-smokers had a younger age at examination and earlier onset and longer duration of illness than smokers and ex-smokers. The age of initiation of regular smoking in patients was significantly earlier than their age of illness onset. We found that longer duration of illness was significantly associated with higher RTQ scores. Ex-smokers with schizophrenia performed significantly more poorly on the Stroop C test than smokers. The results imply that smoking may affect cognitive function and illness onset time in patients with schizophrenia.
TL;DR: This study replicates the association between the KIBRA gene and episodic memory and suggests a possibly differential effect of the polymorphism in psychotic and non-psychotic individuals.