Structured psychiatric interviews are now the diagnostic gold standard in psychiatric research and are making a rapid inroad into daily clinical work. In research, non-clinicians equipped with structured interviews often perform diagnostic assessments. Structured interviews have been shown to yield high diagnostic reliability among novice interviewers (1).A structured interview is defined as "an interview consisting of… predetermined questions presented in a definite order". These questions "yield diagnostic information based on the patient's responses and the interviewer's observations. The interviews… identify symptoms and syndromes which meet specific diagnostic criteria" (2).Structured interviews made their appearance as part of the operational revolution in psychiatry, in the quest of improving diagnostic reliability. They were strongly advocated for by a major figure of the DSM-III project, Robert Spitzer, in a seminal article entitled "Are clinicians still necessary?" (3). The potential unreliability in the quality and quantity of the diagnostic information elicited across the patients ("information variance") is here countered by the application of identical questions, presented to the patients in a fixed sequence. Another source of unreliability, potentially involved in the process of converting clinical information into diagnostic criteria ("criterion variance"), is minimized by formulating the interview questions in a wording as close as possible to the phrasings of the diagnostic criteria. In sum, the structured interview reduces the initiative, inference and reflection by the interviewer almost to zero, obviating clinical psychiatric experience and education in psychopathology, thus allowing a suitably trained non-clinician to perform the diagnostic assessment.The validity of structured interviews has rarely been explored (4,5). Moreover, it is sometimes claimed to be untestable in principle, due to the unavailability of a "gold stanAssessing the diagnostic validity of a structured psychiatric interview in a first-admission hospital sample

Background/Aims: Although the very idea that the generative disorder in schizophrenia is a disturbance of the self is as old as the schizophrenia concept itself, empirical studies have only recently emerged, documenting that anomalous self-experiences (i.e. self-disorders, SDs) aggregate in schizophrenia spectrum disorders but not in other mental disorders. The aim of this study is to explore potential associations between SDs, neurocognitive performance, rationality and IQ in patients with schizophrenia. Methods: The sample comprises 31 patients diagnosed with schizophrenia (DSM-IV). All patients underwent comprehensive evaluation. SDs were assessed with the Examination of Anomalous Self-Experience scale. Neurocognitive performance was measured with 4 PC-implemented subtests from the Cambridge Neuropsychological Test Automated Battery. Rationality was measured using syllogism tests. The IQ was indexed by a summary score of 4 IST-2000-R computerized subtests. Results: No correlation was found between SDs and neurocognitive performance or between SDs and IQ. SDs were found to correlate with rationality. Neurocognitive performance correlated with rationality, and both correlated with IQ, respectively. Conclusions: The lack of correlation between SDs and neurocognitive performance is consistent with the results from the only previous study exploring this issue, suggesting that SDs depict something essential to schizophrenia, whereas neurocognitive impairment does not. The correlation between SDs and rationality indicates that the syllogism tests reflect something central for schizophrenia, but the result needs further corroboration from larger, empirical studies.

BackgroundEmpirical studies of rationality (syllogisms) in patients with schizophrenia have obtained different results. One study found that patients reason more logically if the syllogism is presented through an unusual content.AimsTo explore syllogism-based rationality in schizophrenia.MethodThirty-eight first-admitted patients with schizophrenia and 38 healthy controls solved 29 syllogisms that varied in presentation content (ordinary v. unusual) and validity (valid v. invalid). Statistical tests were made of unadjusted and adjusted group differences in models adjusting for intelligence and neuropsychological test performance.ResultsControls outperformed patients on all syllogism types, but the difference between the two groups was only significant for valid syllogisms presented with unusual content. However, when adjusting for intelligence and neuropsychological test performance, all group differences became non-significant.ConclusionsWhen taking intelligence and neuropsychological performance into account, patients with schizophrenia and controls perform similarly on syllogism tests of rationality.Declaration of interestNone.Copyright and usage© The Royal College of Psychiatrists 2015. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) licence.

The findings are the first of their kind and suggest that delays in early motor development may not only characterize psychopathological disorders such as schizophrenia, but may also be associated with the personality dimension of neuroticism in adulthood.

Negative neurocognitive bias is a core feature of major depressive disorder that is reversed by pharmacological and psychological treatments. This double-blind functional magnetic resonance imaging study investigated for the first time whether electroconvulsive therapy modulates negative neurocognitive bias in major depressive disorder. Patients with major depressive disorder were randomised to one active ( n=15) or sham electroconvulsive therapy ( n=12). The following day they underwent whole-brain functional magnetic resonance imaging at 3T while viewing emotional faces and performed facial expression recognition and dot-probe tasks. A single electroconvulsive therapy session had no effect on amygdala response to emotional faces. Whole-brain analysis revealed no effects of electroconvulsive therapy versus sham therapy after family-wise error correction at the cluster level, using a cluster-forming threshold of Z>3.1 ( p<0.001) to secure family-wise error <5%. Groups showed no differences in behavioural measures, mood and medication. Exploratory cluster-corrected whole-brain analysis ( Z>2.3; p<0.01) revealed electroconvulsive therapy-induced changes in parahippocampal and superior frontal responses to fearful versus happy faces as well as in fear-specific functional connectivity between amygdala and occipito-temporal regions. Across all patients, greater fear-specific amygdala - occipital coupling correlated with lower fear vigilance. Despite no statistically significant shift in neural response to faces after a single electroconvulsive therapy session, the observed trend changes after a single electroconvulsive therapy session point to an early shift in emotional processing that may contribute to antidepressant effects of electroconvulsive therapy.