Although there is agreement on the association between delay in treatment of psychosis and outcome, less is known regarding the pathways to care of patients suffering from a first psychotic episode. Pathways are complex, involve a diverse range of contacts, and are likely to influence delay in treatment. We conducted a systematic review on the nature and determinants of the pathway to care of patients experiencing a first psychotic episode.

We searched four databases (Medline, HealthStar, EMBASE, PsycINFO) to identify articles published between 1985 and 2009. We manually searched reference lists and relevant journals and used forward citation searching to identify additional articles. Studies were included if they used an observational design to assess the pathways to care of patients with first-episode psychosis (FEP).

Included studies (n=30) explored the first contact in the pathway and/or the referral source that led to treatment. In 13 of 21 studies, the first contact for the largest proportion of patients was a physician. However, in nine of 22 studies, the referral source for the greatest proportion of patients was emergency services. We did not find consistent results across the studies that explored the sex, socio-economic, and/or ethnic determinants of the pathway, or the impact of the pathway to care on treatment delay.

Additional research is needed to understand the help-seeking behavior of patients experiencing a first-episode of psychosis, service response to such contacts, and the determinants of the pathways to mental health care, to inform the provision of mental health services.

Cognitive impairment is considered to be a core characteristic of schizophrenia. The relationship between psychosis and cognitive deterioration, however, remains unclear. This longitudinal study investigated the neuropsychological functioning of patients before and after their first psychotic episode. Cognitive functioning of participants who later developed a psychosis was compared to that of people at ultra-high risk (UHR) for psychosis who did not develop psychosis at follow-up and healthy controls.

Participants were 41 persons at UHR for psychosis (the UHR group), of whom 17 developed psychosis between the first and second assessment. Seventeen healthy controls were included in the study. Cognitive performance was assessed at intake (T0) and again after 18 months (T1). The areas of cognitive functioning assessed include verbal memory and learning, visuospatial working memory, executive function, sustained attention and motor speed.

The transition group did not perform significantly worse at the second assessment than at the first on any of the outcome measures. The UHR group performed better on a verbal learning and memory test at T1 compared to T0. At T0, the control group scored significantly better than the UHR group and the transition group on the verbal learning and memory test and the verbal fluency test.

The results indicate that no cognitive deterioration occurs during the first psychotic episode. Problems in verbal memory may be present before the first episode of psychosis.

Schizophrenia out-patients have deficits in affective theory of mind (ToM) but also on more basal levels of social cognition, such as the processing of neutral and emotional expressions. These deficits are associated with changes in brain activation in the amygdala and the superior temporal sulcus (STS). However, until now there have been no studies that examined these different levels of social cognition and their neurobiological underpinnings in patients within one design.

Sixteen medicated schizophrenia out-patients and 16 matched healthy controls were studied with functional magnetic resonance imaging (fMRI) during a social cognition task that allows the investigation of affective ToM (aToM), emotion recognition and the processing of neutral facial expressions.

Patients showed a deficit in emotion recognition and a more prominent deficit in aToM. The performance in aToM and in emotion recognition was correlated in the control group but not in the schizophrenia group. Region-of-interest analysis of functional brain imaging data revealed no difference between groups during aToM, but a hyperactivation in the schizophrenia group in the left amygdala and right STS during emotion recognition and the processing of neutral facial expressions.

The results indicate that schizophrenia out-patients have deficits at several levels of social cognition and provide the first evidence that deficits on higher-order social cognitive processes in schizophrenia may be traced back to an aberrant processing of faces per se.

The effects of hospital-based rehabilitation including weekly supportive psychodynamic therapy compared with specialized assertive intervention and standard treatment has not previously been investigated in first-episode psychosis. The aim of the study was to examine long-term effect on use of institutional care of different intensive interventions for patients with first-episode schizophrenia spectrum disorder on use of psychiatric bed days and days in supported housing.

A total of 94 severely ill patients with first-episode schizophrenia spectrum disorders were included in a special part of the Copenhagen OPUS trial and randomized to either the specialized assertive intervention program (OPUS), standard treatment or hospital-based rehabilitation.

It was a stable pattern that patients randomized to hospital-based rehabilitation spent more days in psychiatric wards and in supported housing throughout the 5-year follow-up period compared with the two other groups. Patients in OPUS treatment spent significantly fewer days in psychiatric wards and supported housing in the first 3 years compared with patients in hospital-based rehabilitation. Due to attrition and small sample size, differences in level of psychotic and negative symptoms at 5-year follow-up could not be evaluated.

The study indicates that hospital-based rehabilitation together with weekly supportive psychodynamic therapy was associated with a continued increased use of psychiatric bed days and days in supported housing. The data cannot justify using hospital-based rehabilitation in first-episode psychosis.

Adolescent cannabis use has been shown in many studies to increase the risk of later psychosis. Childhood trauma is associated with both substance misuse and risk for psychosis. In this study our aim was to investigate whether there is a significant interaction between cannabis use and childhood trauma in increasing the risk for experiencing psychotic symptoms during adolescence.

Psychiatric interviews using the Schedule for Affective Disorders and Schizophrenia for School-Age Children (K-SADS) semi-structured instrument were carried out with 211 adolescents aged between 12 and 15 years and their parents as part of a population-based study. The interview enquired about early traumatic events, cannabis use and psychiatric symptoms in adolescence.

In separate analyses both cannabis use and childhood trauma were significantly associated with risk of experiencing psychotic symptoms. However, the presence of both childhood trauma and early cannabis use significantly increased the risk for psychotic symptoms beyond the risk posed by either risk factor alone, indicating that there was a greater than additive interaction between childhood trauma and cannabis use.

Our finding of a greater than additive interaction between childhood trauma and cannabis use may have implications for the identification of individuals at high risk of experiencing psychotic symptoms. For example, measures to actively discourage or intensively treat cannabis use in children and adolescents who have experienced abuse may help to prevent the development of psychosis in this vulnerable group. Our findings require replication in larger samples to confirm this interaction effect.

The effects of cannabis use on neuropsychological indices that show characteristic disturbances in schizophrenia are unclear. The effect of cannabis use on these cognitive functions is of particular interest given the hypothesized association between cannabis use and schizophrenia. Therefore, this study aimed to examine the effects of cannabis use on attentional control, working memory and executive functioning, in both healthy individuals and patients with schizophrenia.

Neuropsychological performance was assessed in 36 cannabis users who were otherwise healthy, 35 healthy non-users, 22 cannabis-using patients with schizophrenia, and 49 non-using patients with schizophrenia. Participants were administered the Stroop task, the letter–number sequencing and spatial span subtests of the Wechsler Memory Scale, and the Wisconsin Card Sorting Test (WCST).

Patients with schizophrenia (both cannabis users and non-users) showed significantly poorer performance across all neuropsychological tasks, relative to controls; however, there were no significant differences between schizophrenic cannabis users and schizophrenic non-users on any measures, with the exception of increased non-perseverative errors on the WCST in cannabis-using patients. Similarly, healthy cannabis users showed no significant differences from healthy non-users in any of the cognitive domains, with the exception of a schizophrenic-like increase in perseveration on the WCST.

Amongst both healthy individuals and patients with schizophrenia there appears to be little difference in cognitive performance between cannabis users and non-users, suggesting that cannabis use has only subtle effects on the neurocognitive performance indices assessed here, which have been well established to be disturbed in schizophrenia.

Childhood adversity (CA) is associated with adult mental disorders, but the mechanisms underlying this association remain inadequately understood. Stress sensitization, whereby CA increases vulnerability to mental disorders following adult stressful life events, has been proposed as a potential mechanism. We provide a test of the stress sensitization hypothesis in a national sample.

We investigated whether the association between past-year stressful life events and the 12-month prevalence of major depression, post-traumatic stress disorder (PTSD), other anxiety disorders, and perceived stress varies according to exposure to CA. We used data from the National Epidemiological Survey of Alcohol and Related Conditions (NESARC) (n=34 653).

Past-year stressful life events were associated with an increased risk of major depression, PTSD, anxiety disorders, and perceived stress. However, the magnitude of the increased risk varied according to respondents' history of CA. For example, past-year major stressors were associated with a 27.3% increase in the 12-month risk of depression among individuals with ⩾3 CAs and a 14.8% increased risk among individuals without CAs. Stress sensitization effects were present for depression, PTSD, and other anxiety disorders in women and men, although gender differences were found in the threshold of past-year stress needed to trigger such effects. Stress sensitization was most evident among individuals with ⩾3 CAs.

CA is associated with increased vulnerability to the deleterious mental health effects of adult stressors in both men and women. High levels of CA may represent a general diathesis for multiple types of psychopathology that persists throughout the life course.

There is growing evidence on the importance of experiences of stressful events in the development of psychopathology. This study aimed to investigate the role of stressful events in the continuity of internalizing and externalizing problems, as well as the cross-influence of these problems from early childhood to late adolescence.

Data came from a general population sample of 396 children followed from the ages of 3 to 18 years. Parent-ratings of internalizing and externalizing problems at ages 3, 5, 10 and 18 years were used. Parents also reported on the presence of stressful events between the ages of 3 and 5 years, and 5 and 10 years. Adolescent reports on stressful events over the ages of 10–18 years were used. Structural equation models were used to disentangle/analyse the role of stressful events in the development of internalizing and externalizing problems.

From the age of 3 years onwards externalizing symptoms predicted experiences of stressful events. In turn, these experiences predicted later externalizing problems. Stressful events also explained part of the continuity of internalizing problems from the age of 10 years onwards, but not during childhood. From childhood onwards, cross-influences from externalizing problems to subsequent internalizing problems were found to run through stressful events. Only in adolescence cross-influences from internalizing problems to externalizing problems were found, again via stressful events.

From childhood onwards to late adolescence, stressful events play a significant role in both the continuity and the co-occurrence of externalizing and internalizing problems. Theoretical and methodological implications of these findings are discussed.

Symptoms of post-traumatic stress disorder (PTSD) and depression are highly co-morbid following a traumatic event. Nevertheless, decisive evidence regarding the direction of the relationship between these clinical entities is missing.

The aim of the present study was to examine the nature of this relationship by comparing a synchronous change model (PTSD and depression are time synchronous, possibly stemming from a third common factor) with a demoralization model (i.e. PTSD symptoms causing depression) and a depressogenic model (i.e. depressive symptoms causing PTSD symptoms). Israeli adult victims of single-event traumas (n=156) were assessed on measures of PTSD and depression at 2, 4 and 12 weeks post-event.

A cross-lagged structural equation modeling (SEM) analysis provided results consistent with the synchronous change model and the depressogenic model.

Depressive symptoms may play an important role in the development of post-traumatic symptoms.

The DSM-IV symptomatic criteria for major depression (MD) derive primarily from clinical experience with modest empirical support.

The sample studied included 1015 (518 males, 497 females) Caucasian twins from a population-based registry who met criteria for MD in the year prior to the interview. Logistic regression analyses were conducted to compare the associations of: (1) single symptomatic criterion, (2) two groups of criteria reflecting cognitive and neurovegetative symptoms, with a wide range of potential validators including demographic factors, risk for future episodes, risk of MD in the co-twin, characteristics of the depressive episode, the pattern of co-morbidity and personality traits.

The individual symptomatic criteria showed widely varying associations with the pattern of co-morbidity, personality traits, features of the depressive episode and demographic characteristics. When examined separately, these two criteria groups showed robust differences in their patterns of association, with the validators with the cognitive criteria generally producing stronger associations than the neurovegetative.

Among depressed individuals, individual DSM-IV symptomatic criteria differ substantially in their predictive relationship with a range of clinical validators. These results challenge the equivalence assumption for the symptomatic criteria for MD and suggest a more than expected degree of ‘covert’ heterogeneity among these criteria. Part of this heterogeneity is captured by the distinction between cognitive versus neurovegetative symptoms, with cognitive symptoms being more strongly associated with most clinically relevant characteristics. Detailed psychometric evaluation of DSM-IV criteria is overdue.

Severity is an important characteristic of major depression (MD) and an ‘episode specifier’ in DSM-IV classifying depressive episodes as ‘mild’, ‘moderate’ or ‘severe’. These severity subtypes rely on three different measures of severity: number of criteria symptoms, severity of the symptoms and degree of functional disability. No prior empirical study has evaluated the coherence and validity of the DSM-IV definition of severity of MD.

In a sample of 1015 (518 males, 497 females) Caucasian twins from a population-based registry who met criteria for MD in the year prior to interview, factor analysis and logistic regression were conducted to examine the inter-relationships of the three severity measures and their associations with a wide range of potential validators including demographic factors, risk for future episodes, risk of MD in the co-twin, characteristics of the depressive episode, the pattern of co-morbidity, and personality traits.

Correlations between the three severity measures were significant but moderate. Factor analysis indicated the existence of a general severity factor, but the factor was not highly coherent. The three severity measures showed differential predictive ability for most of the validators.

Severity of MD as defined by the DSM-IV is a multifaceted and heterogeneous construct. The three proposed severity measures reflect partly overlapping but partly independent domains with differential validity as assessed by a wide range of clinical characteristics. Clinicians should probably use a combination of severity measures as proposed in DSM-IV rather than privileging one.

Depressed patients show impaired performance following negative feedback; the probability of committing an error is increased immediately after an error. This deficit is assumed to be highly specific and to represent a trait marker of major depressive disorder (MDD). Inconsistencies in currently available data could reflect inter-individually different strategies to regulate negative affect. The present study examined modulation of performance following negative feedback by cognitive reappraisal to regulate aversive affect in depressed patients.

Thirty-three depressed patients and 33 control subjects performed tasks of varying difficulty over a prolonged time. Emotional feedback was given immediately after each trial. Performance was further analysed within subgroups using cognitive reappraisal of aversive events with high and low frequency.

A significant group by task difficulty interaction for absolute number of subsequent errors revealed that depressed patients were especially impaired when receiving negative feedback more frequently. An increased probability of subsequent errors was shown in patients irrespective of task difficulty. Analysis of subgroups revealed higher absolute number and probability of subsequent errors only in depressed patients habitually not using cognitive reappraisal to regulate aversive emotions. Depressed patients using this strategy did not differ from controls.

The present results replicate the observation of impaired performance in depressed patients following failure feedback. Most importantly, a subgroup of patients who habitually rely on cognitive reappraisal of aversion-eliciting events, such as negative performance feedback, was not impaired. This modulatory influence of emotion regulation strategies on performance subsequent to negative feedback suggests that training emotion regulation in achievement situations should be incorporated in current concepts to prevent relapse.

It is not known whether social support modifies the association between depression and impairment or disability in older people from developing countries in Asia.

We used a Thai version of the EURO-D scale to measure depression in 1104 Thai rural community-dwelling parents aged ⩾60 years. These were all those providing data on depression who were recruited as part of a study of older adults with at least one living child (biological, stepchild or adopted child). Logistic regression modelling was used to determine: (a) whether impairment, disability and social support deficits were associated with depression; (b) whether social support modified this association.

There were strong graded relationships between impairment, disability, social support deficits and EURO-D caseness. Level of impairment, but not disability, interacted with poor social support in that depression was especially likely in those who had more physical impairments as well as one or more social support deficits (p value for interaction=0.018), even after full adjustment.

Social support is important in reducing the association between physical impairment and depression in Thai older adults, especially for those with a large number of impairments. Enhancing social support as well as improving healthcare and disability facilities should be emphasized in interventions to prevent depression in older adults.

Concerns have been expressed about possible adverse effects of the use of antidepressant medication during pregnancy, including risk for neonatal pathology and the presence of congenital malformations.

Data from the Swedish Medical Birth Register (MBR) from 1 July 1995 up to 2007 were used to identify women who reported the use of antidepressants in early pregnancy or were prescribed antidepressants during pregnancy by antenatal care: a total of 14 821 women with 15 017 infants. Maternal characteristics, maternal delivery diagnoses, infant neonatal diagnoses and the presence of congenital malformations were compared with all other women who gave birth, using the Mantel–Haenszel technique and with adjustments for certain characteristics.

There was an association between antidepressant treatment and pre-existing diabetes and chronic hypertension but also with many pregnancy complications. Rates of induced delivery and caesarean section were increased. The preterm birth rate was increased but not that of intrauterine growth retardation. Neonatal complications were common, notably after tricyclic antidepressant (TCA) use. An increased risk of persistent pulmonary hypertension of the newborn (PPHN) was verified. The congenital malformation rate was increased after TCAs. An association between use of paroxetine and congenital heart defects was verified and a similar effect on hypospadias was seen.

Women using antidepressants during pregnancy and their newborns have increased pathology. It is not clear how much of this is due to drug use or underlying pathology. Use of TCAs was found to carry a higher risk than other antidepressants and paroxetine seems to be associated with a specific teratogenic property.

Anorexia nervosa (AN) and bulimia nervosa (BN) are marked by longitudinal symptom fluctuations. DSM-IV-TR does not address how to classify eating disorder (ED) presentations in individuals who no longer meet full criteria for these disorders. To consider this issue, we examined subthreshold presentations in women with initial diagnoses of AN and BN.

A total of 246 women with AN or BN were followed for a median of 9 years; weekly symptom data were collected at frequent intervals using the Longitudinal Interval Follow-up Evaluation of Eating Disorders (LIFE-EAT-II). Outcomes were ED presentations that were subthreshold for ⩾3 months, including those narrowly missing full criteria for AN or BN, along with binge eating disorder (BED) and purging disorder.

During follow-up, most women (77.6%) experienced a subthreshold presentation. Subthreshold presentation was related to intake diagnosis (Wald χ2=8.065, df=2, p=0.018). Individuals with AN most often developed subthreshold presentations resembling AN; those with BN were more likely to develop subthreshold BN. Purging disorder was experienced by half of those with BN and one-quarter of those with AN binge/purge type (ANBP); BED occurred in 20% with BN. Transition from AN or BN to most subthreshold types was associated with improved psychosocial functioning (p<0.001).

Subthreshold presentations in women with lifetime AN and BN were common, resembled the initial diagnosis, and were associated with modest improvements in psychosocial functioning. For most with lifetime AN and BN, subthreshold presentations seem to represent part of the course of illness and to fit within the original AN or BN diagnosis.

Puberty moderates genetic influences on disordered eating attitudes and behaviors, with little genetic influence before puberty but large (⩾50%) genetic effects during and after puberty. To date, however, nothing is known about the mechanisms that underlie these effects. Estradiol is a particularly promising candidate, as estrogens become elevated at puberty and regulate gene transcription within neurotransmitter systems important for eating-related phenotypes. The aim of this pilot study was to examine whether estradiol levels moderate genetic influences on disordered eating during puberty.

Participants included 198 female twins (ages 10–15 years) from the Michigan State University Twin Registry. Disordered eating attitudes and behaviors were assessed with the total score, weight preoccupation, body dissatisfaction and binge eating/compensatory behavior subscales of the Minnesota Eating Behavior Survey (MEBS). Afternoon saliva samples were assayed for estradiol levels. Moderation of genetic effects was examined by comparing twin correlations in low versus high estradiol groups.

In the low estradiol group, monozygotic (MZ) and dizygotic (DZ) twin correlations for all MEBS scales were similar, suggesting little genetic influence. In the high estradiol group, the MZ twin correlation was more than double the DZ twin correlation, indicating the presence of genetic effects. Findings could not be accounted for by age, body mass index or the physical changes of puberty.

Estradiol may be one important moderator of genetic effects on disordered eating during puberty. Larger twin studies are needed to replicate this pilot work and quantify the extent of genetic moderation.