The Beck Depression Inventory, 2nd edition (BDI-II) is widely used in research on depression. However, the minimal clinically important difference (MCID) is unknown. MCID can be estimated in several ways. Here we take a patient-centred approach, anchoring the change on the BDI-II to the patient's global report of improvement.

We used data collected (n = 1039) from three randomized controlled trials for the management of depression. Improvement on a ‘global rating of change’ question was compared with changes in BDI-II scores using general linear modelling to explore baseline dependency, assessing whether MCID is best measured in absolute terms (i.e. difference) or as percent reduction in scores from baseline (i.e. ratio), and receiver operator characteristics (ROC) to estimate MCID according to the optimal threshold above which individuals report feeling ‘better’.

Improvement in BDI-II scores associated with reporting feeling ‘better’ depended on initial depression severity, and statistical modelling indicated that MCID is best measured on a ratio scale as a percentage reduction of score. We estimated a MCID of a 17.5% reduction in scores from baseline from ROC analyses. The corresponding estimate for individuals with longer duration depression who had not responded to antidepressants was higher at 32%.

MCID on the BDI-II is dependent on baseline severity, is best measured on a ratio scale, and the MCID for treatment-resistant depression is larger than that for more typical depression. This has important implications for clinical trials and practice.

A number of scales are used to estimate the severity of depression. However, differences between self-report and clinician rating, multi-dimensionality and different weighting of individual symptoms in summed scores may affect the validity of measurement. In this study we examined and integrated the psychometric properties of three commonly used rating scales.

The 17-item Hamilton Depression Rating Scale (HAMD-17), the Montgomery–Asberg Depression Rating Scale (MADRS) and the Beck Depression Inventory (BDI) were administered to 660 adult patients with unipolar depression in a multi-centre pharmacogenetic study. Item response theory (IRT) and factor analysis were used to evaluate their psychometric properties and estimate true depression severity, as well as to group items and derive factor scores.

The MADRS and the BDI provide internally consistent but mutually distinct estimates of depression severity. The HAMD-17 is not internally consistent and contains several items less suitable for out-patients. Factor analyses indicated a dominant depression factor. A model comprising three dimensions, namely ‘observed mood and anxiety’, ‘cognitive’ and ‘neurovegetative’, provided a more detailed description of depression severity.

The MADRS and the BDI can be recommended as complementary measures of depression severity. The three factor scores are proposed for external validation.

People with schizophrenia are often found to have smaller brains and larger brain ventricles than normal, but the role of antipsychotic medication remains unclear.

We conducted a systematic review of magnetic resonance imaging (MRI) studies. We included longitudinal studies of brain changes in patients taking antipsychotic drugs and we examined studies of antipsychotic-naive patients for comparison purposes.

Fourteen out of 26 longitudinal studies showed a decline in global brain or grey-matter volume or an increase in ventricular or cerebrospinal fluid (CSF) volume during the course of drug treatment, including the largest studies conducted. The frontal lobe was most consistently affected, but overall changes were diffuse. One large study found different degrees of volume loss with different antipsychotics, and another found that volume changes were associated with taking medication compared with taking none. Analyses of linear associations between drug exposure and brain volume changes produced mixed results. Five out of 21 studies of patients who were drug naive, or had only minimal prior treatment, showed some differences from controls in volumes of interest. No global differences were reported in three studies of drug-naive patients with long-term illness. Studies of high-risk groups have not demonstrated differences from controls in global or lobar brain volumes.

Some evidence points towards the possibility that antipsychotic drugs reduce the volume of brain matter and increase ventricular or fluid volume. Antipsychotics may contribute to the genesis of some of the abnormalities usually attributed to schizophrenia.

We examined longitudinally the course and predictors of treatment resistance in a large cohort of first-episode psychosis (FEP) patients from initiation of antipsychotic treatment. We hypothesized that antipsychotic treatment resistance is: (a) present at illness onset; and (b) differentially associated with clinical and demographic factors.

The study sample comprised 323 FEP patients who were studied at first contact and at 10-year follow-up. We collated clinical information on severity of symptoms, antipsychotic medication and treatment adherence during the follow-up period to determine the presence, course and predictors of treatment resistance.

From the 23% of the patients, who were treatment resistant, 84% were treatment resistant from illness onset. Multivariable regression analysis revealed that diagnosis of schizophrenia, negative symptoms, younger age at onset, and longer duration of untreated psychosis predicted treatment resistance from illness onset.

The striking majority of treatment-resistant patients do not respond to first-line antipsychotic treatment even at time of FEP. Clinicians must be alert to this subgroup of patients and consider clozapine treatment as early as possible during the first presentation of psychosis.

Non-medical use of prescription opioids represents a national public health concern of growing importance. Mood and anxiety disorders are highly associated with non-medical prescription opioid use. The authors examined longitudinal associations between non-medical prescription opioid use and opioid disorder due to non-medical opioid use and mood/anxiety disorders in a national sample, examining evidence for precipitation, self-medication and general shared vulnerability as pathways between disorders.

Data were drawn from face-to-face surveys of 34 653 adult participants in waves 1 and 2 of the National Epidemiologic Survey on Alcohol and Related Conditions. Logistic regression models explored the temporal sequence and evidence for the hypothesized pathways.

Baseline lifetime non-medical prescription opioid use was associated with incidence of any mood disorder, major depressive disorder (MDD), bipolar disorder, any anxiety disorder and generalized anxiety disorder (GAD in wave 2, adjusted for baseline demographics, other substance use, and co-morbid mood/anxiety disorders). Lifetime opioid disorder was not associated with any incident mood/anxiety disorders. All baseline lifetime mood disorders and GAD were associated with incident non-medical prescription opioid use at follow-up, adjusted for demographics, co-morbid mood/anxiety disorders, and other substance use. Baseline lifetime mood disorders, MDD, dysthymia and panic disorder were associated with incident opioid disorder due to non-medical prescription opioid use at follow-up, adjusted for the same covariates.

These results suggest that precipitation, self-medication as well as shared vulnerability are all viable pathways between non-medical prescription opioid use and opioid disorder due to non-medical opioid use and mood/anxiety disorders.

Clozapine remains the only evidence-based antipsychotic for treatment-resistant schizophrenia (TRS). The ability to predict which patients with their first onset of schizophrenia would subsequently meet criteria for treatment resistance (TR) could help to diminish the severe functional disability which may ensue if TR is not recognized and correctly treated.

This is a 5-year longitudinal assessment of clinical outcomes in a cohort of 246 first-episode schizophrenia spectrum patients recruited as part of the NIHR Genetics and Psychosis (GAP) study conducted in South London from 2005 to 2010. We examined the relationship between baseline demographic and clinical measures and the emergence of TR. TR status was determined from a review of electronic case records. We assessed for associations with early-, and late-onset TR, and non-TR, and differences between those TR patients treated with clozapine and those who were not.

Seventy per cent (n = 56) of TR patients, and 23% of the total study population (n = 246) were treatment resistant from illness onset. Those who met criteria for TR during the first 5 years of illness were more likely to have an early age of first contact for psychosis (<20 years) [odds ratio (OR) 2.49, 95% confidence interval (CI) 1.25–4.94] compared to those with non-TR. The relationship between an early age of first contact (<20 years) and TR was significant in patients of Black ethnicity (OR 3.71, 95% CI 1.44–9.56); and patients of male gender (OR 3.13 95% CI 1.35–7.23).

For the majority of the TR group, antipsychotic TR is present from illness onset, necessitating increased consideration for the earlier use of clozapine.

Childhood early life stress (ELS) increases risk of adulthood major depressive disorder (MDD) and is associated with altered brain structure and function. It is unclear whether specific ELSs affect depression risk, cognitive function and brain structure.

This cross-sectional study included 64 antidepressant-free depressed and 65 never-depressed individuals. Both groups reported a range of ELSs on the Early Life Stress Questionnaire, completed neuropsychological testing and 3T magnetic resonance imaging (MRI). Neuropsychological testing assessed domains of episodic memory, working memory, processing speed and executive function. MRI measures included cortical thickness and regional gray matter volumes, with a priori focus on the cingulate cortex, orbitofrontal cortex (OFC), amygdala, caudate and hippocampus.

Of 19 ELSs, only emotional abuse, sexual abuse and severe family conflict independently predicted adulthood MDD diagnosis. The effect of total ELS score differed between groups. Greater ELS exposure was associated with slower processing speed and smaller OFC volumes in depressed subjects, but faster speed and larger volumes in non-depressed subjects. In contrast, exposure to ELSs predictive of depression had similar effects in both diagnostic groups. Individuals reporting predictive ELSs exhibited poorer processing speed and working memory performance, smaller volumes of the lateral OFC and caudate, and decreased cortical thickness in multiple areas including the insula bilaterally. Predictive ELS exposure was also associated with smaller left hippocampal volume in depressed subjects.

Findings suggest an association between childhood trauma exposure and adulthood cognitive function and brain structure. These relationships appear to differ between individuals who do and do not develop depression.

Longitudinal symptoms of post-traumatic stress disorder (PTSD) are often characterized by heterogeneous trajectories, which may have unique pre-, peri- and post-trauma risk and protective factors. To date, however, no study has evaluated the nature and determinants of predominant trajectories of PTSD symptoms in World Trade Center (WTC) responders.

A total of 10835 WTC responders, including 4035 professional police responders and 6800 non-traditional responders (e.g. construction workers) who participated in the WTC Health Program (WTC-HP), were evaluated an average of 3, 6 and 8 years after the WTC attacks.

Among police responders, longitudinal PTSD symptoms were best characterized by four classes, with the majority (77.8%) in a resistant/resilient trajectory and the remainder exhibiting chronic (5.3%), recovering (8.4%) or delayed-onset (8.5%) symptom trajectories. Among non-traditional responders, a six-class solution was optimal, with fewer responders in a resistant/resilient trajectory (58.0%) and the remainder exhibiting recovering (12.3%), severe chronic (9.5%), subsyndromal increasing (7.3%), delayed-onset (6.7%) and moderate chronic (6.2%) trajectories. Prior psychiatric history, Hispanic ethnicity, severity of WTC exposure and WTC-related medical conditions were most strongly associated with symptomatic trajectories of PTSD symptoms in both groups of responders, whereas greater education and family and work support while working at the WTC site were protective against several of these trajectories.

Trajectories of PTSD symptoms in WTC responders are heterogeneous and associated uniquely with pre-, peri- and post-trauma risk and protective factors. Police responders were more likely than non-traditional responders to exhibit a resistant/resilient trajectory. These results underscore the importance of prevention, screening and treatment efforts that target high-risk disaster responders, particularly those with prior psychiatric history, high levels of trauma exposure and work-related medical morbidities.

Meta-analyses have established a high prevalence of childhood maltreatment (CM) in patients with eating disorders (EDs) relative to the general population. Whether the prevalence of CM in EDs is also high relative to that in other mental disorders has not yet been established through meta-analyses nor to what extent CM affects defining features of EDs, such as number of binge/purge episodes or age at onset. Our aim is to provide meta-analyses on the associations between exposure to CM (i.e. emotional, physical and sexual abuse) on the occurrence of all types of EDs and its defining features.

Systematic review and meta-analyses. Databases were searched until 4 June 2016.

CM prevalence was high in each type of ED (total N = 13 059, prevalence rates 21–59%) relative to healthy (N = 15 092, prevalence rates 1–35%) and psychiatric (N = 7736, prevalence rates 5–46%) control groups. ED patients reporting CM were more likely to be diagnosed with a co-morbid psychiatric disorder [odds ratios (ORs) range 1.41–2.46, p < 0.05] and to be suicidal (OR 2.07, p < 0.001) relative to ED subjects who were not exposed to CM. ED subjects exposed to CM also reported an earlier age at ED onset [effect size (Hedges’ g) = −0.32, p < 0.05], to suffer a more severe form of the illness (g = 0.29, p < 0.05), and to binge-purge (g = 0.31, p < 0.001) more often compared to ED patients who did not report any CM.

CM, regardless of type, is associated with the presence of all types of ED and with severity parameters that characterize these illnesses in a dose dependent manner.

Analyses of co-morbidity patterns among common mental disorders have repeatedly indicated that relationships among disorders can be understood in terms of broad superordinate dimensions. However, these analyses have been based on syndromal-level indicators, which are often heterogeneous, rather than on symptoms, which are presumably more homogeneous.

Symptom-level exploratory and confirmatory analyses were used to explore the joint hierarchical organization of Axis I and II psychopathology, using data on 8405 individuals from the 2000 British Psychiatric Morbidity Survey.

Analyses indicated that 20 identified subordinate dimensions of psychopathology could be organized into four broad superordinate dimensions: Internalizing, Externalizing, Thought Disorder, and Pathological Introversion.

These results extend existing model frameworks ‘downward’ as well as ‘outward’, by analyzing symptoms rather than diagnoses, and by integrating symptoms from Axis I and II disorders in a common framework. This model demonstrates the importance of hierarchy in psychopathology structure, comprises replicable features of psychopathology structure, and has important implications for understanding the nature and organization of mental disorders.

A better understanding of the long-term scope and impact of the co-morbidity with oppositional defiant disorder (ODD) and conduct disorder (CD) in attention deficit hyperactivity disorder (ADHD) youth has important clinical and public health implications.

Subjects were assessed blindly at baseline (mean age=10.7 years), 1-year (mean age=11.9 years), 4-year (mean age=14.7 years) and 10-year follow-up (mean age=21.7 years). The subjects' lifetime diagnostic status of ADHD, ODD and CD by the 4-year follow-up were used to define four groups (Controls, ADHD, ADHD plus ODD, and ADHD plus ODD and CD). Diagnostic outcomes at the 10-year follow-up were considered positive if full criteria were met any time after the 4-year assessment (interval diagnosis). Outcomes were examined using a Kaplan–Meier survival function (persistence of ODD), logistic regression (for binary outcomes) and negative binomial regression (for count outcomes) controlling for age.

ODD persisted in a substantial minority of subjects at the 10-year follow-up. Independent of co-morbid CD, ODD was associated with major depression in the interval between the 4-year and the 10-year follow-up. Although ODD significantly increased the risk for CD and antisocial personality disorder, CD conferred a much larger risk for these outcomes. Furthermore, only CD was associated with significantly increased risk for psychoactive substance use disorders, smoking, and bipolar disorder.

These longitudinal findings support and extend previously reported findings from this sample at the 4-year follow-up indicating that ODD and CD follow a divergent course. They also support previous findings that ODD heralds a compromised outcome for ADHD youth grown up independently of the co-morbidity with CD.

Injured survivors of individual and mass trauma are at risk for developing post-traumatic stress disorder (PTSD). Few investigations have assessed PTSD after injury in large samples across diverse acute care hospital settings.

A total of 2931 injured trauma survivors aged 18–84 who were representative of 9983 in-patients were recruited from 69 hospitals across the USA. In-patient medical records were abstracted, and hospitalized patients were interviewed at 3 and 12 months after injury. Symptoms consistent with a DSM-IV diagnosis of PTSD were assessed with the PTSD Checklist (PCL) 12 months after injury.

Approximately 23% of injury survivors had symptoms consistent with a diagnosis of PTSD 12 months after their hospitalization. Greater levels of early post-injury emotional distress and physical pain were associated with an increased risk of symptoms consistent with a PTSD diagnosis. Pre-injury, intensive care unit (ICU) admission [relative risk (RR) 1·17, 95% confidence interval (CI) 1·02–1·34], pre-injury depression (RR 1·33, 95% CI 1·15–1·54), benzodiazepine prescription (RR 1·46, 95% CI 1·17–1·84) and intentional injury (RR 1·32, 95% CI 1·04–1·67) were independently associated with an increased risk of symptoms consistent with a PTSD diagnosis. White injury survivors without insurance demonstrated approximately twice the rate of symptoms consistent with a diagnosis of PTSD when compared to white individuals with private insurance. By contrast, for Hispanic injury survivors PTSD rates were approximately equal between uninsured and privately insured individuals.

Nationwide in the USA, more than 20% of injured trauma survivors have symptoms consistent with a diagnosis of PTSD 12 months after acute care in-patient hospitalization. Coordinated investigative and policy efforts could target mandates for high-quality PTSD screening and intervention in acute care medical settings.