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SummaryPoor research integrity is increasingly recognised as a serious problem in science. We outline some evidence for this claim and introduce the Royal College of Psychiatrists (RCPsych) journals’ Research Integrity Group, which has been created to address this problem.

SummaryWe present an account of why we decided to retract a paper. We discovered a lack of adherence to conventional trials registration, execution, interpretation and reporting, and consequently, with the authors, needed to correct the scientific record. We set out our responses in general to strengthen research integrity.Declaration of interestK.S.B. is Editor-in-Chief of the British Journal of Psychiatry. W.L., K.R.K. and S.M.L. are members of the senior editorial committee and the research integrity committee for the journal. In the past three years, S.M.L. has received research support from Janssen and Lundbeck, and personal support from Janssen, Otsuka and Sunovion.

BackgroundPsychotic symptoms and psychotic disorders occur at increased rates in adults with intellectual disability, including borderline intellectual functioning, compared with the general population. Little is known about the development of such symptoms in this population.AimsTo examine whether clinical factors predictive of psychotic disorder in a familial study of schizophrenia also apply to those with intellectual disability.MethodAdolescents with special educational needs (SEN) were assessed with the Structured Interview for Schizotypy (SIS) and Childhood Behavioural Checklist (CBCL). These scores were used to prospectively divide participants based on their anticipated risk for psychotic disorder. A subsample were reassessed three times over 6 years, using the Positive and Negative Syndrome Scale (PANSS).ResultsThe SEN group were more symptomatic than controls throughout (Cohen's d range for PANSS subscale scores: 0.54–1.4, all P < 0.007). Over 6 years of follow-up, those above the SIS and CBCL cut-off values at baseline were more likely than those below to display morbid positive psychotic symptoms (odds ratio, 3.5; 95% CI 1.3–9.0) and develop psychotic disorder (odds ratio, 11.4; 95% CI 2.6–50.1). Baseline SIS and CBCL cut-off values predicted psychotic disorder with sensitivity of 0.67, specificity of 0.85, positive predictive value of 0.26 and negative predictive value of 0.97.ConclusionsAdolescents with SEN have increased psychotic and non-psychotic symptoms. The personality and behavioural features associated with later psychotic disorder in this group are similar to those in people with familial loading. Relatively simple screening measures may help identify those in this vulnerable group who do and do not require monitoring for psychotic symptoms.Declaration of interestNone.

In schizophrenia, life expectancy is reduced by 20 years, primarily due to cardiovascular disease (CVD). Physical activity modifies CVD risk factors, but physical activity levels are low in this patient group. We urgently need evidence-based interventions that increase physical activity to improve health and reduce premature mortality in people with schizophrenia.

BackgroundSeveral magnetic resonance imaging (MRI) studies have identified structural abnormalities in association with bipolar disorder. The literature is, however, heterogeneous and there is remaining uncertainty about which brain areas are pivotal to the pathogenesis of the condition.AimsTo identify, appraise and summarise volumetric MRI studies of brain regions comparing bipolar disorder with an unrelated control group and individuals with schizophrenia.MethodA systematic review and random-effects meta-analysis was carried out to identify key areas of structural abnormality in bipolar disorder and whether the pattern of affected areas separated bipolar disorder from schizophrenia. Significant heterogeneity was explored using meta-regression.ResultsParticipants with bipolar disorder are characterised by whole brain and prefrontal lobe volume reductions, and also by increases in the volume of the globus pallidus and lateral ventricles. In comparison with schizophrenia, bipolar disorder is associated with smaller lateral ventricular volume and enlarged amygdala volume. Heterogeneity was widespread and could be partly explained by clinical variables and year of publication, but generally not by differences in image acquisition.ConclusionsThere appear to be robust changes in brain volume in bipolar disorder compared with healthy volunteers, although most changes do not seem to be diagnostically specific. Age and duration of illness appear to be key issues in determining the magnitude of observed effect sizes.

BackgroundMild to moderate intellectual disability affects 2.5% of the general population and is associated with an increased risk of several psychiatric disorders. Most cases are of unknown aetiology although genetic factors have an important role.AimsTo investigate the role of obstetric and neonatal complications in the aetiology of mild to moderate intellectual disability.MethodObstetric and neonatal complications recorded at the time of pregnancy and delivery were compared between participants with mild to moderate intellectual disability, age-matched siblings and unrelated controls using logistic regression.ResultsAdmission to a special care baby unit and not being breastfed on discharge were more common in people with mild to moderate intellectual disability. Not being breastfed on discharge was also more common in those with intellectual disability than unaffected siblings. Foetal distress was more common among controls than among those with mild to moderate intellectual disability.ConclusionsAdmission to a special care baby unit and not being breastfed on discharge may be related to the aetiology of intellectual disability, although the direction of this association is unclear.

BackgroundThere is evidence to suggest that among young people with mild intellectual disability there are those whose cognitive difficulties may predict the subsequent manifestation of a schizophrenic phenotype. It is suggested that they may be detectable by simple means.AimsTo gain adequate cooperation from educational services, parents and students so as to recruit a sufficiently large sample to test the above hypothesis, and to examine the hypothesis in the light of the findings.MethodThe sample was screened with appropriate instruments, and groups hypothesised as being likely or not likely to have the phenotype were compared in terms of psychopathology and neuropsychology.ResultsSimple screening methods detect a sample whose psychopathological and neuropsychological profile is consistent with an extended phenotype of schizophrenia.ConclusionsDifficulties experienced by some young people with mild and borderline intellectual disability are associated with enhanced liability to schizophrenia. Clinical methods can both identify those with this extended phenotype and predict those in whom psychosis will occur.

BackgroundDespite interest in early treatment of schizophrenia, premorbid and prodromal symptomatology remain poorly delineated.AimsTo compare pre-illness symptomatology in patients at high risk of schizophrenia who progress to illness with that of high-risk subjects who remain well and with normal controls.MethodUsing Present State Examination (PSE) data, symptomatic scales were devised from participants of the Northwick Park Study of first-episode schizophrenia and scores were compared on the first and last PSEs of participants of the Edinburgh High Risk Study.ResultsAt entry, when still well, high-risk individuals who subsequently became ill (mean time to diagnosis 929 days; s.e.=138 days) scored significantly higher on ‘situational anxiety’, ‘nervous tension’, ‘depression’, ‘changed perception’ and ‘hallucinations' than those remaining well and normal controls, who did not differ. With illness onset, affective symptomatology remained high but essentially stable.ConclusionsIn genetically predisposed individuals, affective and perceptual disorders are prominent before any behavioural or subjective change that usually characterises the shift to schizophrenic prodrome or active illness.

BackgroundThe hypothesis that schizophrenia is neurodevelopmental was investigated in a prospective study of young people with a postulated 10–15% risk for the development of schizophrenia.AimsTo determine premorbid variables distinguishing high-risk people who will go on to develop schizophrenia from those who will not.MethodA high-risk sample of 163 young adults with two relatives with schizophrenia was recruited. They and 36 controls were serially examined. Baseline measures were compared between those who did develop schizophrenia, a well control group, a well high-risk group and high-risk participants with partial or isolated psychotic symptoms.ResultsOf those at high risk, 20 developed schizophrenia within 2½ years. More experienced isolated or partial psychotic symptoms. Those who developed schizophrenia differed from those who did not on social anxiety, withdrawal and other schizotypal features. The whole high-risk sample differed from the control group on developmental and neuropsychological variables.ConclusionsThe genetic component of schizophrenia affects many more individuals than will develop the illness, and partial impairment can be found in them. Highly significant predictors of the development of schizophrenia are detectable years before onset.

BackgroundMagnetic resonance imaging (MRI) has demonstrated abnormalities of brain structure, particularly of the temporal lobes, in schizophrenia. These are thought to be neurodevelopmental in origin, but when they become evident is unknown.AimsTo determine iftemporal lobe volumes reduce during the development of symptoms of schizophrenia in initially well people at high riskofthis disorder.MethodA group of 66 people who had at least two first— or second-degree relatives with schizophrenia and a control group of 20 healthy people had a structural MRI scan ofthe whole brain which was repeated after approximately 2 years. Regions of interest, specifically the amygdala-hippocampus complex and the temporal lobes, were traced semi-automatically by three masked raters with good inter— and intrarater reliabilityResultsRegional brain volume changes over 2 years did notdiffer between high-risk and healthy participants. Within the high-risk group, the 19 people with psychotic symptoms (12 at first assessment) had a mean reduction of 2163 mm3 intherighttemporal lobe compared with 97 mm3 in the 47 without symptoms (P⩵0.02).ConclusionsOur findings suggest that people at high risk of schizophrenia with psychotic symptoms show reductions in temporal lobe volumes.

BackgroundNeurological ‘soft signs’ and minor physical anomalies (MPAs) are reported to be more frequent in patients with schizophrenia than in controls.AimsTo determine whether these disturbances are genetically mediated, and whether they are central to the genesis of symptoms or epiphenomena.MethodWe obtained ratings in 152 individuals who were antipsychotic drug-free and at high risk, some of whom had experienced psychotic symptoms, as well as 30 first-episode patients and 35 healthy subjects.ResultsMPAs and Neurological Evaluation Scale (NES) ‘sensory integration abnormalities’ were more frequent in high-risk subjects than in healthy controls, but there were no reliable differences between high-risk subjects with and without psychotic symptoms. MPAs were most frequent in high-risk subjects with least genetic liability and NES scores showed no genetic associations.ConclusionsThe lack of associations with psychotic symptoms and genetic liability to schizophrenia suggests that soft signs and physical anomalies are non-specific markers of developmental deviance that are not mediated by the gene(s) for schizophrenia.

BackgroundPatients with schizophrenia differ from controls in several measures of brain structure and function, but it is uncertain how these relate to clinical features of the illness. We dichotomised patient groups by treatment response to test the hypothesis that treatment-resistant patients exhibit more marked biological abnormalities than treatment-responsive parients.MethodTwenty treatment-responsive and 20 treatment-resistant patients with schizophrenia, matched for sex, age, and illness duration, were compared by magnetic resonance imaging, single photon emission tomography, and detailed neuropsychological assessment.ResultsBrain-imaging variables were not statistically related to treatment response, although poorly responsive patients had lower volumes of most brain structures. Several highly significant differences emerged between patient groups on neuropsychological testing. Episodic memory functioning distinguished patient groups even after we controlled for global cognitive impairment.ConclusionsCerebral structure and blood flow have a limited effect on treatment response in schizophrenia, but long-term episodic memory impairment is associated with, and may predict, poor prognosis.

A case of Munchausen's syndrome was probably caused by brain damage sustained during a necessary cholecystectomy. Doctors should not be discouraged from seeking treatable disorder because of such patients' behaviour.