Background. To establish whether high-functioning children with autism spectrum disorder (ASD) have enlarged brains in later childhood, and if so, whether this enlargement is confined to the gray and/or to the white matter and whether it is global or more prominent in specific brain regions.

Method. Brain MRI scans were acquired from 21 medication-naive, high-functioning children with ASD between 7 and 15 years of age and 21 comparison subjects matched for gender, age, IQ, height, weight, handedness, and parental education, but not pubertal status.

Results. Patients showed a significant increase of 6% in intracranium, total brain, cerebral gray matter, cerebellum, and of more than 40% in lateral and third ventricles compared to controls. The cortical gray-matter volume was evenly affected in all lobes. After correction for brain volume, ventricular volumes remained significantly larger in patients.

Conclusions. High-functioning children with ASD showed a global increase in gray-matter, but not white-matter and cerebellar volume, proportional to the increase in brain volume, and a disproportional increase in ventricular volumes, still present after correction for brain volume. Advanced pubertal development in the patients compared to the age-matched controls may have contributed to the findings reported in the present study.

Four hundred ‘new’ long-stay patients were studied and assessments of their needs for treatment and accommodation were made. About one third appeared to need further care in hospital. A further third could possibly be discharged if suitable accommodation in the community were available: most of this group were more handicapped than present residents in hostels. The remaining third had diverse needs; many were multiply handicapped – for example, by physical disability or mental retardation in addition to psychiatric disorder. At the moment the psychiatric hospital is virtually the only agency to accept the care of such people.

Background. Schizophrenia is a debilitating chronic mental illness. However, the annual prevalence of schizophrenia is not well understood because of under-representation of schizophrenia patients in epidemiological surveys. This study used multiple administrative claims databases to estimate the annual prevalence of diagnosed schizophrenia in the USA.

Method. The annual prevalence of diagnosed schizophrenia in the USA was estimated for different health insurance coverage groups. The prevalence for privately insured individuals was calculated from an administrative claims database of approximately 3 million privately insured beneficiaries covering the period 1999–2003. The prevalence for Medicaid enrollees was calculated from California Medicaid claims covering the period 2000–2002. The prevalence for Medicare and Medicaid/Medicare dual eligibles was estimated using a combination of both databases. Published statistics were used to estimate the prevalence of schizophrenia in the uninsured and veteran populations and to weight the prevalence rates obtained to the population of the USA.

Results. The 12-month prevalence of diagnosed schizophrenia in the USA in 2002 was estimated at 5·1 per 1000 lives. The Medicaid population was identified with the highest prevalence rate among the populations studied. Sensitivity analyses taking into consideration the Veterans Affairs population only changed the estimate slightly to 5·3 per 1000 lives.

Conclusion. Analyses of administrative claims data contribute to the understanding of the prevalence of diagnosed schizophrenia.

Background. Past research has demonstrated that depression is associated with dysfunctional processing of emotional information. Recent studies demonstrate that a bias in the attentional processing of negative information may be an important cognitive vulnerability factor underlying the onset and maintenance of depression. However, to date, the nature of this attentional bias is still poorly understood and further exploration of this topic to advance current knowledge of attentional biases in depression seems imperative.

Method. This study examined attentional biases for angry facial expressions presented for 1000 ms in 20 patients with major depressive disorder (MDD) and 20 non-depressed control participants (NC) matched for age and gender using an emotional modification of the Exogenous Cueing task.

Results. Patients with MDD showed maintained attention for angry faces compared with neutral faces. In comparison with non-depressed participants they showed a stronger attentional engagement for angry faces. In contrast, the NC group directed attention away from angry faces, more rapidly disengaging their attention compared with neutral faces.

Conclusions. This pattern of results supports the assumption that MDD is characterized by deficits in the attentional processing of negative, interpersonal information and suggests a ‘protective’ bias in non-depressed individuals. Implications in relation to previous research exploring cognitive and interpersonal functioning in depression are discussed.

The initial enthusiasm about the second-generation or atypical antipsychotic drugs soon changed into criticism and debate, culminating in the controversial CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness), CUtLASS (Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study) and EUFEST (European First-Episode Schizophrenia Trial) effectiveness trials. This review summarizes the results of three recent meta-analyses that compared second-generation antipsychotics (SGAs) with placebo, with conventional antipsychotics, and with SGAs head-to-head. We compare the meta-analyses with previous reviews and put them in the perspective of CATIE, CUtLASS and EUFEST. The data show that the SGAs are not a homogeneous group and that this confusing classification should be abandoned. We find that, overall, the data are consistent but experts interpret the same results differently. The debate seems to be driven more by values than by data; some place an emphasis on cost, others focus on extrapyramidal side-effects (EPS), weight gain, or efficacy. In our opinion, the SGAs are not the breakthrough that industry would like to maintain. They have different properties, so a clinician may individualize a treatment plan to a given patient's problems, a decision that should be shared with the patient. However, these drugs are important contributions to treatment, and most psychiatrists, let alone patients, would probably not want to do without them.

In view of the very extensive and often prolonged use of benzodiazepines in therapeutic practice, this study was designed to investigate whether or not cognitive ability is impaired in longterm benzodiazepine users, and to determine the nature and extent of any deficit. Fifty patients currently taking benzodiazepines for at least one year, thirty-four who had stopped taking benzodiazepines, and a matched control group of subjects who had never taken benzodiazepines or who had taken benzodiazepines in the past for less than one year were administered a battery of neuropsychological tests designed to measure a wide range of cognitive functions. It was found that patients taking high doses of benzodiazepines for long periods of time perform poorly on tasks involving visual-spatial ability and sustained attention. This is consistent with deficits in posterior cortical cognitive function.

Background. Recent developments in research suggest that particular attempts to control thoughts may contribute to the problem of intrusion. An instrument capable of identifying strategies for dealing with unwanted intrusions in clinical populations may be used for differentiating between thought control strategies that may or may not be helpful.

Methods. The Thought Control Questionnaire (TCQ) (Wells & Davies, 1994) developed and validated on a normal sample, was administered to a clinical sample in order to investigate the consistency of the original factor structure and its psychometric properties. The sensitivity of the scale to change associated with recovery was also examined. Relationships between individual differences in thought control strategies and psychiatric symptoms in patients with DSM-IV major depression, and PTSD with or without major depression were investigated.

Results. The Scree Test suggested a six-factor solution which was rotated. This solution split the original distraction subscale into separate behavioural and cognitive distraction, otherwise the subscales were almost identical to those obtained in non-clinical subjects. As this split has been shown to be unreliable, further analyses in this study were based on the five-factor version of the TCQ obtained by Wells & Davies (1994). Predictors of recovery and of symptoms in PTSD and depression were explored.

Conclusions. Correlations between the TCQ subscales and other measures suggest that particular thought control strategies may be associated with the symptoms of PTSD and depression. The TCQ scales appear to be sensitive to changes associated with recovery. Significant differences emerged in thought control strategies between depressed and PTSD patients. Hierarchical regression analysis showed distraction, punishment and reappraisal control strategies predicted depression scores in depressed patients while use of distraction predicted intrusions in PTSD.

Background. We investigated the links between familial loading, preadolescent temperament, and internalizing and externalizing problems in adolescence, hereby distinguishing effects on maladjustment in general versus dimension-specific effects on either internalizing or externalizing problems.

Method. In a population-based sample of 2230 preadolescents (10–11 years) familial loading (parental lifetime psychopathology) and offspring temperament were assessed at baseline by parent report, and offspring psychopathology at 2·5-years follow-up by self-report, teacher report and parent report. We used purified measures of temperament and psychopathology and partialled out shared variance between internalizing and externalizing problems.

Results. Familial loading of internalizing psychopathology predicted offspring internalizing but not externalizing problems, whereas familial loading of externalizing psychopathology predicted offspring externalizing but not internalizing problems. Both familial loadings were associated with Frustration, low Effortful Control, and Fear. Frustration acted as a general risk factor predicting severity of maladjustment; low Effortful Control and Fear acted as dimension-specific risk factors that predicted a particular type of psychopathology; whereas Shyness, High-Intensity Pleasure, and Affiliation acted as direction markers that steered the conditional probability of internalizing versus externalizing problems, in the event of maladjustment. Temperament traits mediated one-third of the association between familial loading and psychopathology. Findings were robust across different composite measures of psychopathology, and applied to girls as well as boys.

Conclusions. With regard to familial loading and temperament, it is important to distinguish general risk factors (Frustration) from dimension-specific risk factors (familial loadings, Effortful Control, Fear), and direction markers that act as pathoplastic factors (Shyness, High-Intensity Pleasure, Affiliation) from both types of risk factors. About one-third of familial loading effects on psychopathology in early adolescence are mediated by temperament.

This essay, which seeks to provide an historical framework for our efforts to develop a scientific psychiatric nosology, begins by reviewing the classificatory approaches that arose in the early history of biological taxonomy. Initial attempts at species definition used top-down approaches advocated by experts and based on a few essential features of the organism chosen a priori. This approach was subsequently rejected on both conceptual and practical grounds and replaced by bottom-up approaches making use of a much wider array of features. Multiple parallels exist between the beginnings of biological taxonomy and psychiatric nosology. Like biological taxonomy, psychiatric nosology largely began with ‘expert’ classifications, typically influenced by a few essential features, articulated by one or more great 19th-century diagnosticians. Like biology, psychiatry is struggling toward more soundly based bottom-up approaches using diverse illness characteristics. The underemphasized historically contingent nature of our current psychiatric classification is illustrated by recounting the history of how ‘Schneiderian’ symptoms of schizophrenia entered into DSM-III. Given these historical contingencies, it is vital that our psychiatric nosologic enterprise be cumulative. This can be best achieved through a process of epistemic iteration. If we can develop a stable consensus in our theoretical orientation toward psychiatric illness, we can apply this approach, which has one crucial virtue. Regardless of the starting point, if each iteration (or revision) improves the performance of the nosology, the eventual success of the nosologic process, to optimally reflect the complex reality of psychiatric illness, is assured.

Background. The frequency and clinical, neuropsychological and neuroimaging correlates of apathy in patients who have had a stroke are inadequately defined.

Method. A total of 167 consecutive patients admitted to the stroke units of two university hospitals after an ischaemic stroke and 109 controls received extensive medical, psychiatric and neuropsychological assessments; a subset received a magnetic resonance imaging (MRI) scan. The groups were matched for sex and age. Patients were assessed 3–6 months after their stroke. The sample for this study comprised 135 patients and 92 controls who completed the Apathy Evaluation Scale (AES).

Results. Apathy was present in 26·7% of stroke patients compared to 5·4% of controls. Apathetic stroke patients were older, more functionally dependent and had lower Mini-Mental State Examination (MMSE) scores than those without apathy. Apathy was not associated with risk factors for cerebrovascular disease or stroke severity. There was a weak but significant correlation between apathy and self-reported depression but not with clinician-rated depression. Neuropsychologically, after correction for age, premorbid intelligence (IQ) and depression, apathy was associated with reduced attention and speed of information processing. On neuroimaging there were trends for associations of apathy with the extent of hyperintensities in the right hemisphere and right fronto-subcortical circuit, but not with total stroke volume or number of strokes.

Conclusions. Apathy is common following a cerebrovascular event. Presence of apathy may be related to older age and right fronto-subcortical pathway pathology, rather than stroke severity. It is associated with functional impairment and cognitive deficits.

Background. Depressed patients show deficits on neuropsychological tests. However, the basis of these impairments and their relationship with mood disturbance remains unclear.

Methods. This paper reviews the literature regarding the relationship between mood disturbance and neuropsychological impairment in depression and the evidence for serotonergic and hypothalamic–pituitary–adrenal (HPA) axis involvement in these two domains.

Results. Mood disturbance and neuropsychological impairment both occur in depression, but have no clear relationship in time or degree. Impairment of post-synaptic 5-HT1A receptor function may result in the symptom of low mood in depression. Depressed patients demonstrate abnormalities in the functional control of the HPA axis with a resultant hypercortisolaemia, which may impair neuropsychological function. These processes may be related given the extensive interactions between the serotonergic system and the HPA axis.

Conclusions. We argue that there is a neurobiological cause of impaired neuropsychological function in depression. The complex relationship between neuropsychological function and mood may be a result of interactions between the serotonergic system and the HPA axis, particularly in the hippocampus with involvement of serotonergic 5-HT1A and glucocorticoid receptors. A primary dysfunction in these receptors will produce a lowering of mood and neuropsychological impairment respectively. Either dysfunction will result in a secondary impairment of the alternate system. Thus, the affective and psychological changes of depressive illness are likely to have complex relationships in time and severity to one another and the illness as a whole may result from a range of primary aetio-pathologies.