Psychiatric disorders are common following traumatic brain injury (TBI). However, few studies have examined the course of disorder development and the influence of pre-injury psychiatric history. The present study aimed to examine the frequency of, and association between, psychiatric disorders occurring pre- and post-injury, and to examine the post-injury course of disorders.

Participants were 102 adults (75.5% male) with predominantly moderate-severe TBI. Participants were initially assessed for pre-injury and current disorders, and reassessed at 3, 6 and 12 months post-injury using the Structured Clinical Interview for DSM-IV Disorders (SCID).

Over half of the participants had a pre-injury psychiatric disorder; predominantly substance use, mood, and anxiety disorders. In the first year post-injury, 60.8% of participants had a psychiatric disorder, commonly anxiety and mood disorders. Post-injury disorders were associated with the presence of a pre-injury history (p<0.01), with 74.5% of participants with a pre-injury psychiatric history experiencing a post-injury disorder, which commonly presented at initial assessment or in the first 6 months. However, 45.8% of participants without a pre-injury history developed a novel post-injury disorder, which was less likely to emerge at the initial assessment and generally developed later in the year.

Despite evidence that most post-injury psychiatric disorders represent the continuation of pre-existing disorders, a significant number of participants developed novel psychiatric disorders. This study demonstrates that the timing of onset may differ according to pre-injury history. There seem to be different trajectories for anxiety and depressive disorders. This research has important implications for identifying the time individuals are most at risk of psychiatric disorders post-injury.

Anorexia nervosa (AN) is a serious disorder incurring high costs due to hospitalization. International treatments vary, with prolonged hospitalizations in Europe and shorter hospitalizations in the USA. Uncontrolled studies suggest that longer initial hospitalizations that normalize weight produce better outcomes and fewer admissions than shorter hospitalizations with lower discharge weights. This study aimed to compare the effectiveness of hospitalization for weight restoration (WR) to medical stabilization (MS) in adolescent AN.

We performed a randomized controlled trial (RCT) with 82 adolescents, aged 12–18 years, with a DSM-IV diagnosis of AN and medical instability, admitted to two pediatric units in Australia. Participants were randomized to shorter hospitalization for MS or longer hospitalization for WR to 90% expected body weight (EBW) for gender, age and height, both followed by 20 sessions of out-patient, manualized family-based treatment (FBT).

The primary outcome was the number of hospital days, following initial admission, at the 12-month follow-up. Secondary outcomes were the total number of hospital days used up to 12 months and full remission, defined as healthy weight (>95% EBW) and a global Eating Disorder Examination (EDE) score within 1 standard deviation (s.d.) of published means. There was no significant difference between groups in hospital days following initial admission. There were significantly more total hospital days used and post-protocol FBT sessions in the WR group. There were no moderators of primary outcome but participants with higher eating psychopathology and compulsive features reported better clinical outcomes in the MS group.

Outcomes are similar with hospitalizations for MS or WR when combined with FBT. Cost savings would result from combining shorter hospitalization with FBT.

Although specific phobia is highly prevalent, associated with impairment, and an important risk factor for the development of other mental disorders, cross-national epidemiological data are scarce, especially from low- and middle-income countries. This paper presents epidemiological data from 22 low-, lower-middle-, upper-middle- and high-income countries.

Data came from 25 representative population-based surveys conducted in 22 countries (2001–2011) as part of the World Health Organization World Mental Health Surveys initiative (n = 124 902). The presence of specific phobia as defined by the Diagnostic and Statistical Manual of Mental Disorders, fourth edition was evaluated using the World Health Organization Composite International Diagnostic Interview.

The cross-national lifetime and 12-month prevalence rates of specific phobia were, respectively, 7.4% and 5.5%, being higher in females (9.8 and 7.7%) than in males (4.9% and 3.3%) and higher in high- and higher-middle-income countries than in low-/lower-middle-income countries. The median age of onset was young (8 years). Of the 12-month patients, 18.7% reported severe role impairment (13.3–21.9% across income groups) and 23.1% reported any treatment (9.6–30.1% across income groups). Lifetime co-morbidity was observed in 60.5% of those with lifetime specific phobia, with the onset of specific phobia preceding the other disorder in most cases (72.6%). Interestingly, rates of impairment, treatment use and co-morbidity increased with the number of fear subtypes.

Specific phobia is common and associated with impairment in a considerable percentage of cases. Importantly, specific phobia often precedes the onset of other mental disorders, making it a possible early-life indicator of psychopathology vulnerability.

Little is known about the pattern of genetic and environmental influences on symptoms of anxiety and depression (SxAnxDep) from childhood to early adulthood.

Parental- and self-reported levels of SxAnxDep were assessed at ages 8–9, 13–14, 16–17 and 19–20 years in 2508 twins from the Swedish Twin Study of Child and Adolescent Development (TCHAD). Analysis conducted using the Mx program included SxAnxDep by parental and self-report.

The best-fit model revealed one genetic risk factor for SxAnxDep acting at ages 8–9, 13–14, 16–17 and 19–20, and new sets of genetic risk factors ‘coming on line’ in early adolescence, late adolescence and early adulthood. Together, these genetic factors were very strong influences on the levels of SxAnxDep reported in common by parents and twins with heritability estimates, correcting for rater- and time-specific effects, ranging from 72% to 89%. The first genetic factor, which accounted for 72% of the variance in SxAnxDep at ages 8–9, attenuated sharply in influence, accounting for only 12% of the variance by ages 19–20. No evidence was found for shared environmental influences. Although not statistically significant, the correlation between genetic risk factors for SxAnxDep in males and females declined with advancing age.

Genetic effects on SxAnxDep are developmentally dynamic from middle childhood to young adulthood, demonstrating both genetic innovation and genetic attenuation. The attenuation might explain the low levels of continuity observed for anxiety and depressive disorders from childhood to adulthood. Differences in genetic risk factors for SxAnxDep in males and females may increase during development.

The time of widespread outbreaks of infectious diseases can lead to elevated stress and mental health problems among all persons affected, and in particular those sub-groups of the population that are at an increased risk of mental health problems. One such vulnerable group constitutes university students. The aim of this study is to assess stress, depression, anxiety, and suicidality among different groups of university students (medical, psychology, and other).

Using a repeated cross-sectional study design, we collected survey data among a large sample of 7228 university students from Poland (mean age = 22.78, s.d. = 4.40; 81% female). Data were collected in five waves, during the first 2 months of the COVID-19 pandemic in Europe (March and April 2020).

The results demonstrate a significant increase in depression levels as the pandemic was progressing. We also found that female students scored significantly higher than male students on depression, anxiety, and stress. Psychology students recorded the lowest scores on depression and anxiety. Young adult students (aged 18–24 years) had more symptoms of depression, anxiety, and suicidality than adult students (⩾25 years).

These results provide insights into stress and mental health among university students during the early stages of the COVID-19 pandemic. Findings can be used for a more effective identification of students who may struggle during next stages of the pandemic and future crises.

Preconception, prenatal and postnatal maternal stress is associated with increased offspring psychopathology, but findings are inconsistent and need replication. We estimated associations between maternal bereavement stress and offspring autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, suicide attempt and completed suicide.

Using Swedish registers, we conducted the largest population-based study to date examining associations between stress exposure in 738 144 offspring born 1992–2000 for childhood outcomes and 2 155 221 offspring born 1973–1997 for adult outcomes with follow-up to 2009. Maternal stress was defined as death of a first-degree relative during (a) the 6 months before conception, (b) pregnancy or (c) the first two postnatal years. Cox proportional survival analyses were used to obtain hazard ratios (HRs) in unadjusted and adjusted analyses.

Marginal increased risk of bipolar disorder and schizophrenia following preconception bereavement stress was not significant. Third-trimester prenatal stress increased the risk of ASD [adjusted HR (aHR) 1.58, 95% confidence interval (CI) 1.15–2.17] and ADHD (aHR 1.31, 95% CI 1.04–1.66). First postnatal year stress increased the risk of offspring suicide attempt (aHR 1.13, 95% CI 1.02–1.25) and completed suicide (aHR 1.51, 95% CI 1.08–2.11). Bereavement stress during the second postnatal year increased the risk of ASD (aHR 1.30, 95% CI 1.09–1.55).

Further research is needed regarding associations between preconception stress and psychopathological outcomes. Prenatal bereavement stress increases the risk of offspring ASD and ADHD. Postnatal bereavement stress moderately increases the risk of offspring suicide attempt, completed suicide and ASD. Smaller previous studies may have overestimated associations between early stress and psychopathological outcomes.

Individuals with schizophrenia are at greater risk for metabolic syndrome (MetS) which is associated with cognitive deficits in the general population. MetS might be potentially an important contributing factor to cognitive impairment in schizophrenia.

In the current systematic review and meta-analysis, the findings of 18 studies investigating the association between MetS (and its components) with cognitive impairment in schizophrenia are reviewed.

Co-morbidity of MetS (d = 0.28) and diabetes mellitus (d = 0.28) were both associated with more severe cognitive deficits in schizophrenia. There was also evidence for a significant relationship between cognitive impairment in schizophrenia and each of the components of MetS including hypertension, dyslipidemia, abdominal obesity and diabetes.

MetS is significantly associated with cognitive impairment in schizophrenia and can potentially contribute to functional decline observed in some patients with schizophrenia throughout the course of illness.

The cortisol awakening response (CAR) has been shown to predict major depressive episodes (MDEs) over a 1-year period. It is unknown whether this effect: (a) is stable over longer periods of time; (b) is independent of prospective stressful life events; and (c) differentially predicts first onsets or recurrences of MDEs.

A total of 270 older adolescents (mean age 17.06 years at cortisol measurement) from the larger prospective Northwestern-UCLA Youth Emotion Project completed baseline diagnostic and life stress interviews, questionnaires, and a 3-day cortisol sampling protocol measuring the CAR and diurnal rhythm, as well as up to four annual follow-up interviews of diagnoses and life stress.

Non-proportional person-month survival analyses revealed that higher levels of the baseline CAR significantly predict MDEs for 2.5 years following cortisol measurement. However, the strength of prediction of depressive episodes significantly decays over time, with the CAR no longer significantly predicting MDEs after 2.5 years. Elevations in the CAR did not significantly increase vulnerability to prospective major stressful life events. They did, however, predict MDE recurrences more strongly than first onsets.

These results suggest that a high CAR represents a time-limited risk factor for onsets of MDEs, which increases risk for depression independently of future major stressful life events. Possible explanations for the stronger effect of the CAR for predicting MDE recurrences than first onsets are discussed.

Identifying risk factors for the development of post-traumatic stress disorder (PTSD) is important for understanding and ultimately preventing the disorder. This study assessed pain shortly after traumatic injury (i.e. peritraumatic pain) as a risk factor for PTSD.

Participants (n=115) were patients admitted to a Level 1 Surgical Trauma Center. Admission to this service reflected a severe physical injury requiring specialized, emergent trauma care. Participants completed a pain questionnaire within 48 h of traumatic injury and a PTSD diagnostic module 4 and 8 months later.

Peritraumatic pain was associated with an increased risk of PTSD, even after controlling for a number of other significant risk factors other than acute stress disorder symptoms. An increase of 0.5 s.d. from the mean in a 0–10 pain rating scale 24–48 h after injury was associated with an increased odds of PTSD at 4 months by more than fivefold, and at 8 months by almost sevenfold. A single item regarding amount of pain at the time of hospital admission correctly classified 65% of participants.

If these findings are replicated in other samples, high levels of peritraumatic pain could be used to identify individuals at elevated risk for PTSD following traumatic injury.

Diffusion tensor imaging (DTI) can be used to investigate cerebral structural connectivity in never-medicated individuals with first-episode schizophrenia.

Subjects with first-episode schizophrenia according to DSM-IV-R who had never been exposed to antipsychotic medication (n=25) and healthy controls (n=26) were recruited. Groups were matched for age, gender, best parental socio-economic status and ethnicity. All subjects underwent DTI and structural magnetic resonance imaging (MRI) scans. Voxel-based analysis was performed to investigate brain regions where fractional anisotropy (FA) values differed significantly between groups. A confirmatory region-of-interest (ROI) analysis of FA scores was performed in which regions were placed blind to group membership.

In patients, FA values significantly lower than those in healthy controls were located in the left fronto-occipital fasciculus, left inferior longitudinal fasciculus, white matter adjacent to right precuneus, splenium of corpus callosum, right posterior limb of internal capsule, white matter adjacent to right substantia nigra, and left cerebral peduncle. ROI analysis of the corpus callosum confirmed that the patient group had significantly lower mean FA values than the controls in the splenium but not in the genu. The intra-class correlation coefficient (ICC) for independent ROI measurements was 0.90 (genu) and 0.90 (splenium). There were no regions where FA values were significantly higher in the patients than in the healthy controls.

Widespread structural dysconnectivity, including the subcortical region, is already present in neuroleptic-naive patients in their first episode of illness.

To assess the prevalence and clinical impact of co-morbid social anxiety disorder (SAD) and alcohol use disorders (AUD, i.e. alcohol abuse and alcohol dependence) in a nationally representative sample of adults in the United States.

Data came from a large representative sample of the US population. Face-to-face interviews of 43093 adults residing in households were conducted during 2001–2002. Diagnoses of mood, anxiety, alcohol and drug use disorders and personality disorders were based on the Alcohol Use Disorder and Associated Disabilities Interview Schedule – DSM-IV version.

Lifetime prevalence of co-morbid AUD and SAD in the general population was 2.4%. SAD was associated with significantly increased rates of alcohol dependence [odds ratio (OR) 2.8] and alcohol abuse (OR 1.2). Among respondents with alcohol dependence, SAD was associated with significantly more mood, anxiety, psychotic and personality disorders. Among respondents with SAD, alcohol dependence and abuse were most strongly associated with more substance use disorders, pathological gambling and antisocial personality disorders. SAD occurred before alcohol dependence in 79.7% of co-morbid cases, but co-morbidity status did not influence age of onset for either disorder. Co-morbid SAD was associated with increased severity of alcohol dependence and abuse. Respondents with co-morbid SAD and alcohol dependence or abuse reported low rates of treatment-seeking.

Co-morbid lifetime AUD and SAD is a prevalent dual diagnosis, associated with substantial rates of additional co-morbidity, but remaining largely untreated. Future research should clarify the etiology of this co-morbid presentation to better identify effective means of intervention.