Fixed hippocampal volume reductions and shape abnormalities are established findings in schizophrenia, but the relationship between hippocampal volume change and clinical outcome has been relatively unexplored in schizophrenia and other psychotic disorders. In light of recent findings correlating hippocampal volume change and clinical outcome in first-episode psychotic adults, we hypothesized that fewer decreases in hippocampal volume would be associated with better functional outcome and fewer psychotic symptoms in our rare and chronically ill population of childhood-onset schizophrenia (COS) patients.

We prospectively obtained 114 structural brain magnetic resonance images (MRIs) from 27 COS subjects, each with three or more scans between the ages of 10 and 30 years. Change in hippocampal volume, measured by fit slope and percentage change, was regressed against clinical ratings (Children's Global Assessment Scale, Scale for the Assessment of Positive Symptoms, Scale for the Assessment of Negative Symptoms) at last scan (controlling for sex, time between scans and total intracranial volume).

Fewer negative symptoms were associated with less hippocampal volume decrease (fit slope: p = 0.0003, and percentage change: p = 0.005) while positive symptoms were not related to hippocampal change. There was also a relationship between improved clinical global functioning and maintained hippocampal volumes (fit slope: p = 0.025, and percentage change: p = 0.043).

These results suggest that abnormal hippocampal development in schizophrenia can be linked to global functioning and negative symptoms. The hippocampus can be considered a potential treatment target for future therapies.

Individual variation in the clinical course of bipolar disorder may have prognostic and therapeutic implications but is poorly reflected in current classifications. We aimed to establish a typology of the individual clinical trajectories based on detailed prospective medium-term follow-up.

Latent class analysis (LCA) of nine characteristics of clinical course (time depressed, severity of depression, stability of depression, time manic, severity of mania, stability of mania, mixed symptoms, mania-to-depression and depression-to-mania phase switching) derived from life charts prospectively tracking the onsets and offsets of (hypo)manic, depressive, mixed and subsyndromal episodes in a representative sample of 176 patients with bipolar disorder.

The best-fitting model separated patients with bipolar disorder into large classes of episodic bipolar (47%) and depressive type (32%), moderately sized classes characterized by prolonged hypomanias (10%) and mixed episodes (5%) and five small classes with unusual course characteristics including mania-to-depression and depression-to-mania transitions and chronic mixed affective symptoms. This empirical typology is relatively independent of the distinction between bipolar disorder type I and type II. Lifetime co-morbidity of alcohol use disorders is characteristic of the episodic bipolar course type.

There is potential for a new typology of clinical course based on medium-term naturalistic follow-up of a representative clinical sample of patients with bipolar disorder. Predictive validity and stability over longer follow-up periods remain to be established.

Cognitive deficits in alcohol dependence (AD) have been observed, poorer verbal ability being among the most consistent findings. Genetic factors influence both cognitive ability and AD, but whether these influences overlap is not known.

A subset of 602 monozygotic (MZ) and dizygotic (DZ) twins from FinnTwin16, a population-based study of Finnish twins, was used to study the associations of verbal ability with DSM-III-R diagnosis and symptoms of AD, the maximum number of drinks consumed in a 24-h period, and the Rutgers Alcohol Problem Index (RAPI) scores. These twins, most of them selected for within-pair discordance or concordance for their RAPI scores at age 18.5 years, were studied with neuropsychological tests and interviewed with the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) in young adulthood (mean age 26.2 years, range 23–30 years).

All alcohol problem measures were associated with lower scores on the Vocabulary subtest of the Wechsler Adult Intelligence Scale – Revised (WAIS-R), a measure of verbal ability. In bivariate genetic models, Vocabulary and the alcohol problem measures had moderate heritabilities (0.54–0.72), and their covariation could be explained by correlated genetic influences (genetic correlations −0.20 to −0.31).

Poorer verbal ability and AD have partly overlapping biological etiology. The genetic and environmental influences on the development of cognitive abilities, alcohol problems and risk factors for AD should be studied further with prospective longitudinal designs.

Psychiatry and clinical psychology are the two dominant disciplines in mental health research, but the structure of scientific influence and information flow within and between them has never been mapped.

Citations among 96 of the highest impact psychiatry and clinical psychology journals were examined, based on 10 052 articles published in 2008. Network analysis explored patterns of influence between journal clusters.

Psychiatry journals tended to have greater influence than clinical psychology journals, and their influence was asymmetrical: clinical psychology journals cited psychiatry journals at a much higher rate than the reverse. Eight journal clusters were found, most dominated by a single discipline. Their citation network revealed an influential central cluster of ‘core psychiatry’ journals that had close affinities with a ‘psychopharmacology’ cluster. A group of ‘core clinical psychology’ journals was linked to a ‘behavior therapy’ cluster but both were subordinate to psychiatry journals. Clinical psychology journals were less integrated than psychiatry journals, and ‘health psychology/behavioral medicine’ and ‘neuropsychology’ clusters were relatively peripheral to the network.

Scientific publication in the mental health field is largely organized along disciplinary lines, and is to some degree hierarchical, with clinical psychology journals tending to be structurally subordinate to psychiatry journals.

Depression increases the risk of subsequent vascular events in both cardiac and non-cardiac patients. Atherosclerosis, the underlying process leading to vascular events, has been associated with depression. This association, however, may be confounded by the somatic-affective symptoms being a consequence of cardiovascular disease. While taking into account the differentiation between somatic-affective and cognitive-affective symptoms of depression, we examined the association between depression and atherosclerosis in a community-based sample.

In 1261 participants of the Nijmegen Biomedical Study (NBS), aged 50–70 years and free of stroke and dementia, we measured the intima–media thickness (IMT) of the carotid artery as a measure of atherosclerosis and we assessed depressive symptoms using the Beck Depression Inventory (BDI). Principal components analysis (PCA) of the BDI items yielded two factors, representing a cognitive-affective and a somatic-affective symptom cluster. While correcting for confounders, we used separate multiple regression analyses to test the BDI sum score and both depression symptom clusters.

We found a significant correlation between the BDI sum score and the IMT. Cognitive-affective, but not somatic-affective, symptoms were also associated with the IMT. When we stratified for coronary artery disease (CAD), the somatic-affective symptom cluster correlated significantly with depression in both patients with and patients without CAD.

The association between depressive symptoms and atherosclerosis is explained by the somatic-affective symptom cluster of depression. Subclinical vascular disease thus may inflate depressive symptom scores and may explain why treatment of depression in cardiac patients hardly affects vascular outcome.

Current theories of post-traumatic stress disorder (PTSD) place considerable emphasis on the role cognitive distortions such as self-blame, hopelessness or preoccupation with danger play in the etiology and maintenance of the disorder. Previous studies have shown that cognitive distortions in the early aftermath of traumatic events can predict future PTSD severity but, to date, no studies have investigated the neural correlates of this association.

We conducted a prospective study with 106 acutely traumatized subjects, assessing symptom severity at three time points within the first 3 months post-trauma. A subsample of 20 subjects additionally underwent a functional 4-T magnetic resonance imaging (MRI) scan at 2 to 4 months post-trauma.

Cognitive distortions proved to be a significant predictor of concurrent symptom severity in addition to diagnostic status, but did not predict future symptom severity or diagnostic status over and above the initial symptom severity. Cognitive distortions were correlated with blood oxygen level-dependent (BOLD) signal strength in brain regions previously implicated in visual processing, imagery and autobiographic memory recall. Intrusion characteristics accounted for most of these correlations.

This investigation revealed significant predictive value of cognitive distortions concerning concurrent PTSD severity and also established a significant relationship between cognitive distortions and neural activations during trauma recall in an acutely traumatized sample. These data indicate a direct link between the extent of cognitive distortions and the intrusive nature of trauma memories.

Refugees are at risk of experiencing a combined constellation of complicated bereavement and posttraumatic stress disorder (PTSD) symptoms following exposure to complex traumas associated with personal threat and loss. Features of identity confusion are central to both complicated bereavement and PTSD and these characteristics may be particularly prominent amongst refugees from traditional cultures displaced from their homelands, families, and kinship groups. We investigate whether a combined pattern of complicated bereavement and PTSD can be identified amongst West Papuan refugees participating in an epidemiological survey (n = 486, response rate: 85.8%) in a remote town in Papua New Guinea.

Latent class analysis was applied to derive subpopulations of refugees based on symptoms of complicated bereavement and PTSD. Associations were examined between classes and traumatic loss events, post-migration living difficulties (PMLDs), and psychosocial support systems.

The four classes identified comprised a complicated bereavement class (11%), a combined posttraumatic bereavement class (10%), a PTSD class (11%), and a low symptom class (67%). Symptoms of identity confusion were prominent in the posttraumatic bereavement class. Compared with the low symptom class, the combined posttraumatic bereavement class reported greater exposure to traumatic loss events (OR 2.43, 95% CI 1.11–5.34), PMLDs (OR 2.24, 95% CI 1.01–4.6), disruptions to interpersonal bonds and networks (OR 3.3, 95% CI 1.47–7.38), and erosion of roles and identities (OR 2.18, 95% CI 1.11–4.27).

Refugees appear to manifest a combined pattern of complicated bereavement and PTSD symptoms in which identity confusion is a prominent feature. This response appears to reflect the combined impact of high levels of exposure to traumatic losses, PMLDs, and disruption of relevant psychosocial systems.

Previous studies hypothesized that neurodevelopmental risk factors may play a role in the pathogenesis of obsessive-compulsive disorder (OCD). Cortical folding has been shown to be a reliable indicator for normal and altered neurodevelopment, but in OCD it has barely been investigated up to now. The present study investigates whether alterations in gyrification are detectable in OCD and, if so, how these are associated with clinical characteristics.

We compared the local Gyrification Index (lGI) between 75 OCD patients and 75 matched healthy subjects across the whole brain. In addition, for those regions exhibiting an altered lGI in patients we explored a potential relationship to symptom severity, age of onset, and influence of medication.

OCD patients had a significantly decreased lGI in right parietal, precentral but also insula, temporal, pars triangularis and rostral middle frontal regions compared to healthy subjects. A positive association with age of onset was found but no association with symptom severity. There was no effect of co-morbidity or medication.

The reduced gyrification found in OCD confirms previous findings in other psychiatric disorders and suggests that alterations may already occur during early stages of brain development. Our findings support the idea that altered cortical folding might represent a trait characteristic of the disorder although longitudinal studies are needed to clarify the trajectory of this morphological measure in OCD.