Although guided self-help for depression and anxiety disorders has been examined in many studies, it is not clear whether it is equally effective as face-to-face treatments.

We conducted a meta-analysis of randomized controlled trials in which the effects of guided self-help on depression and anxiety were compared directly with face-to-face psychotherapies for depression and anxiety disorders. A systematic search in bibliographical databases (PubMed, PsycINFO, EMBASE, Cochrane) resulted in 21 studies with 810 participants.

The overall effect size indicating the difference between guided self-help and face-to-face psychotherapy at post-test was d=−0.02, in favour of guided self-help. At follow-up (up to 1 year) no significant difference was found either. No significant difference was found between the drop-out rates in the two treatments formats.

It seems safe to conclude that guided self-help and face-to-face treatments can have comparable effects. It is time to start thinking about implementation in routine care.

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).

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.

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.

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.

Encoding and maintenance of information in working memory, followed by internal manipulation of that information for planning adaptive behavior, are two key components of working-memory systems. Both processes have been reported to be impaired in schizophrenia, but few studies have directly compared the relative severity of these abnormalities, or the degree to which manipulation deficits might be secondary to alterations in maintenance processes.

Clinically stable schizophrenia patients (n=25) and a demographically similar healthy comparison group (n=24) were administered a verbal span task with three levels of working-memory load. Maintenance was assessed using sequential position questions. Manipulation processes were assessed by requiring comparison of the relative sequential position of test items, which entailed simultaneous serial search strategies regarding item order.

Both groups showed reduced accuracy and increased reaction time for manipulation compared with maintenance processing. There were significant patient impairments across working-memory loads. There was no differential deficit in manipulation processing, and effect sizes of relative deficit in the patient group were higher for maintenance than manipulation processing.

The strong correlation for maintenance and manipulation deficits suggest that impairments in the ability to internally manipulate information stored in working-memory systems are not greater than alterations in the encoding and maintaining of information in working memory and that disturbances in maintenance processing may contribute to deficits in higher-order working-memory operations.

Impaired spatial working memory (SWM) is a robust feature of schizophrenia and has been linked to the risk of developing psychosis in people with an at-risk mental state (ARMS). We used functional magnetic resonance imaging (fMRI) to examine the neural substrate of SWM in the ARMS and in patients who had just developed schizophrenia.

fMRI was used to study 17 patients with an ARMS, 10 patients with a first episode of psychosis and 15 age-matched healthy comparison subjects. The blood oxygen level-dependent (BOLD) response was measured while subjects performed an object–location paired-associate memory task, with experimental manipulation of mnemonic load.

In all groups, increasing mnemonic load was associated with activation in the medial frontal and medial posterior parietal cortex. Significant between-group differences in activation were evident in a cluster spanning the medial frontal cortex and right precuneus, with the ARMS groups showing less activation than controls but greater activation than first-episode psychosis (FEP) patients. These group differences were more evident at the most demanding levels of the task than at the easy level. In all groups, task performance improved with repetition of the conditions. However, there was a significant group difference in the response of the right precuneus across repeated trials, with an attenuation of activation in controls but increased activation in FEP and little change in the ARMS.

Abnormal neural activity in the medial frontal cortex and posterior parietal cortex during an SWM task may be a neural correlate of increased vulnerability to psychosis.

The same executive dysfunctions and alterations in neuroimaging tests (both functional and structural) have been found in obsessive-compulsive patients and their first-degree relatives. These neurobiological findings are considered to be intermediate markers of the disease. The aim of our study was to assess verbal and non-verbal memory in unaffected first-degree relatives, in order to determine whether these neuropsychological functions constitute a new cognitive marker for obsessive-compulsive disorder (OCD).

Recall and use of organizational strategies in verbal and non-verbal memory tasks were measured in 25 obsessive-compulsive patients, 25 unaffected first-degree relatives and 25 healthy volunteers.

First-degree relatives and healthy volunteers did not show differences on most measures of verbal memory. However, during the recall and processing of non-verbal information, deficits were found in first-degree relatives and patients compared with healthy volunteers.

The presence of the same deficits in the execution of non-verbal memory tasks in OCD patients and unaffected first-degree relatives suggests the influence of certain genetic and/or familial factors on this cognitive function in OCD and supports the hypothesis that deficits in non-verbal memory tasks could be considered as cognitive markers of the disorder.

Cognitive-behavioral therapy (CBT) consisting of exposure and response prevention (EX/RP) is efficacious as a treatment for obsessive–compulsive disorder (OCD). However, about half of patients have a partial or poor response to EX/RP treatment. This study examined potential predictors and moderators of CBT augmentation of pharmacotherapy, to identify variables associated with a poorer response to OCD treatment.

Data were drawn from a large randomized controlled trial that compared the augmenting effects of EX/RP to stress management training (SMT; an active CBT control) among 108 participants receiving a therapeutic dose of a serotonin reuptake inhibitor (SRI). Stepwise regression was used to determine the model specification.

Pretreatment OCD severity and gender were significant moderators of outcome: severity affected SMT (but not EX/RP) outcome; and gender affected EX/RP (but not SMT) outcome. Adjusting for treatment type and pretreatment severity, significant predictors included greater co-morbidity, number of past SRI trials, and lower quality of life (QoL). Significant moderators, including their main-effects, and predictors accounted for 37.2% of the total variance in outcome, comparable to the impact of treatment type alone (R2=30.5%). These findings were replicated in the subgroup analysis of EX/RP alone (R2=55.2%).

This is the first randomized controlled study to examine moderators and predictors of CBT augmentation of SRI pharmacotherapy. Although effect sizes for individual predictors tended to be small, their combined effect was comparable to that of treatment. Thus, future research should examine whether monitoring for a combination of these risk factors and targeting them with multi-modular strategies can improve EX/RP outcome.

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.

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.

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.

Bipolar disorder may be associated with an inherited abnormality of a neural network incorporating left prefrontal cortex and bilateral retrosplenial cortex.

Childhood traumatic events and functional abnormalities of the hypothalamus–pituitary–adrenal (HPA) axis have been widely reported in psychiatric patients, although neither is specific for any diagnosis. Among the limited number of studies that have evaluated these topics, none has adopted a trans-diagnostic approach. The aim of the present research is to explore the relationship between childhood stressors, HPA axis function and psychiatric symptoms, independent of the diagnosis.

A total of 93 moderate to severely ill psychiatric out-patients of Florence and Pisa University Psychiatric Units and 33 healthy control subjects were recruited. The assessment consisted of salivary cortisol pre- and post-low dose (0.5 mg) Dexamethasone, early and recent life events, 121 psychiatric symptoms independent of diagnosis, SCID, BPRS.

In total, 33.5% of patients were Dexamethasone Suppression Test (DST) non-suppressors, compared with 6.1% of controls (p=0.001). Among patients, non-suppression was associated with particular symptoms (i.e. depressive and psychotic), but not to any specific diagnosis. Early stressful life events were significantly associated with higher salivary cortisol levels, with DST non-suppression and with approximately the same subset of symptoms. A recent stressful event seemed to be associated to the HPA response only in those subjects who were exposed to early traumata.

Our report suggests a relationship between life stress, HPA axis and psychopathology. A cluster of specific psychiatric symptoms seems to be stress related. Moreover, it seems that an abnormal HPA response is possibly triggered by an excessive pressure in vulnerable individuals.

Little is known about how to remedy the unmet mental health needs associated with major terrorist attacks, or what outcomes are achievable with evidence-based treatment. This article reports the usage, diagnoses and outcomes associated with the 2-year Trauma Response Programme (TRP) for those affected by the 2005 London bombings.

Following a systematic and coordinated programme of outreach, the contact details of 910 people were obtained by the TRP. Of these, 596 completed a screening instrument that included the Trauma Screening Questionnaire (TSQ) and items assessing other negative responses. Those scoring ⩾6 on the TSQ, or endorsing other negative responses, received a detailed clinical assessment. Individuals judged to need treatment (n=217) received trauma-focused cognitive-behaviour therapy (TF-CBT) or eye movement desensitization and reprocessing (EMDR). Symptom levels were assessed pre- and post-treatment with validated self-report measures of post-traumatic stress disorder (PTSD) and depression, and 66 were followed up at 1 year.

Case finding relied primarily on outreach rather than standard referral pathways such as primary care. The effect sizes achieved for treatment of DSM-IV PTSD exceeded those usually found in randomized controlled trials (RCTs) and gains were well maintained an average of 1 year later.

Outreach with screening, linked to the provision of evidence-based treatment, seems to be a viable method of identifying and meeting mental health needs following a terrorist attack. Given the failure of normal care pathways, it is a potentially important approach that merits further evaluation.

Anxiety disorders are the most prevalent mental health disorders and are associated with substantial disability and reduced well-being. It is unknown whether the relative impact of different anxiety disorders is due to the anxiety disorder itself or to the co-occurrence with other anxiety disorders. This study compared the functional impact of combinations of anxiety disorders in primary care out-patients.

A total of 1004 patients with panic disorder (PD), generalized anxiety disorder (GAD), social anxiety disorder (SAD) or post-traumatic stress disorder (PTSD) provided data on their mental and physical functioning, and disability. Multivariate regressions compared functional levels for patients with different numbers and combinations of disorders.

Of the patients, 42% had one anxiety disorder only, 38% two, 16% three and 3% all four. There were few relative differences in functioning among patients with only one anxiety disorder, although those with SAD were most restricted in their work, social and home activities and those with GAD were the least impaired. Functioning levels tended to deteriorate as co-morbidity increased.

Of the four anxiety disorders examined, GAD appears to be the least disabling, although they all have more in common than in distinction when it comes to functional impairment. A focus on unique effects of specific anxiety disorders is inadequate, as it fails to address the more pervasive impairment associated with multiple anxiety disorders, which is the modal presentation in primary care.

The impact of different levels of depression severity on quality of life (QoL) is not well studied, particularly regarding ICD-10 criteria. The ICD classification of depressive episodes in three levels of severity is also controversial and the less severe category, mild, has been considered as unnecessary and not clearly distinguishable from non-clinical states. The present work aimed to test the relationship between depression severity according to ICD-10 criteria and several dimensions of functioning as assessed by Medical Outcome Study (MOS) 36-item Short Form general health survey (SF-36) at the population level.

A sample of 551 participants from the second phase of the Outcome of Depression International Network (ODIN) study (228 controls without depression and 313 persons fulfilling ICD criteria for depressive episode) was selected for a further assessment of several variables, including QoL related to physical and mental health as measured with the SF-36.

Statistically significant differences between controls and the depression group were found in both physical and mental markers of health, regardless of the level of depression severity; however, there were very few differences in QoL between levels of depression as defined by ICD-10. Regardless of the presence of depression, disability, widowed status, being a woman and older age were associated with worse QoL in a structural equation analysis with covariates. Likewise, there were no differences according to the type of depression (single-episode versus recurrent).

These results cast doubt on the adequacy of the current ICD classification of depression in three levels of severity.

Although a substantial body of research points to a link between psychological distress and inflammatory responses in middle-aged and older adults, particularly those with cardiovascular disease, the relationship between inflammation and distress in young, healthy individuals has not been established. This study was designed to investigate the cross-sectional association between psychological distress and inflammatory proteins in a young, healthy representative population of English adults.

Participants were 1338 individuals aged 16–34 years from the 2006 Health Survey for England (HSE). Blood samples to measure plasma fibrinogen and high sensitivity C-reactive protein (hsCRP), as well as measures of psychological distress (using the General Health Questionnaire 12-item scale, GHQ-12) and covariates, were collected during home visits. Linear regression was used to assess the relationship between psychological distress and fibrinogen and hsCRP.

Higher self-rated distress was positively associated with fibrinogen level in this young population, independently of age, sex, ethnicity, body mass index (BMI), high density lipoprotein (HDL) cholesterol, smoking, and alcohol and medication use (β=0.024, p<0.01). Psychological distress was not related to hsCRP.

Psychological distress may negatively impact inflammatory processes in young adulthood before the onset of chronic health problems such as hypertension and cardiovascular disease. Longitudinal research is needed to elucidate the relationship between distress and inflammation in young adults and its significance for later disease states.

Oppositional defiant disorder (ODD) is frequently co-occurring with attention deficit hyperactivity disorder (ADHD) in children and adolescents. Because ODD is a precursor of later conduct disorder (CD) and affective disorders, early diagnostic identification is warranted. Furthermore, the predictability of three recently confirmed ODD dimensions (ODD-irritable, ODD-headstrong and ODD-hurtful) may assist clinical decision making.

Receiver-operating characteristic (ROC) analysis was used in order to test the diagnostic accuracy of the Conners' Parent Rating Scale revised (CPRS-R) and the parent version of the Strength and Difficulties Questionnaire (PSDQ) in the prediction of ODD in a transnational sample of 1093 subjects aged 5–17 years from the International Multicentre ADHD Genetics study. In a second step, the prediction of three ODD dimensions by the same parent rating scales was assessed by backward linear regression analyses.

ROC analyses showed adequate diagnostic accuracy of the CPRS-R and the PSDQ in predicting ODD in this ADHD sample. Furthermore, the three-dimensional structure of ODD was confirmed by confirmatory factor analysis and the CPRS-R emotional lability scale significantly predicted the ODD irritable dimension.

The PSDQ and the CPRS-R are both suitable screening instruments in the identification of ODD. The emotional lability scale of the CPRS-R is an adequate predictor of irritability in youth referred for ADHD.