Studies of cognitive behavioural therapy delivered by computer (cCBT) show clinical efficacy for treating anxiety and depression, but have not focused on barriers to uptake. Potential barriers include adverse consequences, accessibility and acceptability.

An integrated systematic review was conducted of quantitative and qualitative studies and surveys from multiple electronic databases where computers delivered cCBT for anxiety or depression.

Substantial numbers of potential participants are lost prior to trials commencing with little explanation. Among trial participants, drop-outs may be higher in the cCBT groups (odds ratio 2.03, 95% confidence interval 0.81–5.09). Only a median of 56% completed a full course of cCBT and personal circumstance was a more common cause of drop-out than difficulties with the technology or social background. Risk was rarely assessed in the majority of programs. Significant staff time was needed to support clients. Therapists were more negative about cCBT than clients.

While cCBT is likely to be an effective and acceptable intervention for some people, there are barriers to its uptake that will substantially limit its impact if not addressed. These included investigating the outcome and attitudes of those who do not make it as far as cCBT trials and why so few finish a full course of cCBT.

Memory impairment is being recognized increasingly as an important feature of the neuropsychology of schizophrenia. Dysfunction of working memory, a system for the short-term storage and manipulation of information, may relate to a number of core symptoms of schizophrenia. Many studies have examined working memory function in schizophrenia but a clear understanding of the nature and extent of any deficit has been elusive.

A systematic review and meta-analysis of studies comparing working memory function in subjects with schizophrenia and healthy controls was performed. Following a comprehensive literature search, meta-analyses were conducted on 36 measures of phonological, visuospatial and central executive working memory functioning, encompassing 441 separate results from 187 different studies.

Statistically significant effect sizes were found for all working memory measures, indicating deficits in schizophrenia groups. Some of these were robust findings in the absence of evidence of significant heterogeneity or publication bias. Meta-regression analyses showed that the working memory deficit was not simply explained by discrepancies in current IQ between schizophrenia and control groups.

Large deficits in working memory were demonstrated in schizophrenia groups across all three working memory domains. There were, however, no clear differences across subdomains or between particular working memory tasks. There was substantial heterogeneity across results that could only be partly explained.

There is good evidence that psychotic symptoms segregate into symptom dimensions. However, it is still unclear how these dimensions are associated with risk indicators and other clinical variables, and whether they have advantages over categorical diagnosis in clinical practice. We investigated symptom dimensions in a first-onset psychosis sample and examined their associations with risk indicators and clinical variables. We then examined the relationship of categorical diagnoses to the same variables.

We recruited 536 patients as part of a population-based, incidence study of psychosis. Psychopathology was assessed using the Schedules for Clinical Assessment in Neuropsychiatry (SCAN). A principal axis factor analysis was performed on symptom scores. The relationship of dimension scores with risk indicators and with clinical variables was then examined employing regression analyses. Finally, regression models were compared to assess the contribution of dimensions versus diagnosis in explaining these variables.

Factor analysis gave rise to a five-factor solution of manic, reality distortion, negative, depressive and disorganization symptom dimensions. The scores of identified dimensions were differentially associated with specific variables. The manic dimension had the highest number of significant associations; strong correlations were observed with shorter duration of untreated psychosis, acute mode of onset and compulsory admission. Adding dimensional scores to diagnostic categories significantly increased the amount of variability explained in predicting these variables; the reverse was also true but to a lesser extent.

Categorical and dimensional representations of psychosis are complementary. Using both appears to be a promising strategy in conceptualising psychotic illnesses.

Spontaneous movement disorders (SMDs), such as spontaneous dyskinesia and parkinsonism, have been described in patients with schizophrenia who have never been treated with antipsychotic medication. Their presence has been documented extensively in chronic schizophrenia but not at the time of illness onset.

We performed a systematic review of studies investigating spontaneous abnormal movements elicited on clinical examination in antipsychotic-naive patients with first-episode psychosis.

We identified a total of 13 studies. Findings suggest a spontaneous dyskinesia median rate of 9% and a spontaneous parkinsonism median rate of 17%. Information on akathisia and dystonia was limited. The presence of SMDs may be associated with negative symptoms and cognitive dysfunction.

These findings support the notion that spontaneous abnormal movements are part of a neurodysfunction intrinsic to the pathogenesis of schizophrenia. Future studies should further investigate the role of basal ganglia and extrapyramidal pathways in the pathophysiology of psychosis, with particular attention to treatment implications.

Strong evidence supports the association between childhood trauma and psychotic disorders. In two different high-risk populations, we looked for a correlation between the magnitude of schizotypal dimensions and the importance of self-reported childhood trauma.

A sample of 138 unaffected first-degree relatives was recruited (67 relatives of schizophrenic probands and 71 relatives of bipolar probands). The relationship between schizotypal dimensions and childhood trauma scores was analyzed by partial correlations.

A positive correlation was found between childhood trauma scores and total schizotypal scores in first-degree relatives of schizophrenic subjects but not in first-degree relatives of bipolar probands. This correlation was primarily due to a strong association with the positive dimension of schizotypy.

The significant correlation between childhood trauma and schizotypal dimensions in subjects at high genetic risk for schizophrenia suggests that susceptibility genes for schizophrenia may interact with childhood trauma to induce the emergence of schizotypal dimensions, mainly positive psychotic features.

Previous research has shown that adults with intellectual disability (ID) may be more at risk of developing dementia in old age than expected. However, the effect of age and ID severity on dementia prevalence rates has never been reported. We investigated the predictions that older adults with ID should have high prevalence rates of dementia that differ between ID severity groups and that the age-associated risk should be shifted to a younger age relative to the general population.

A two-staged epidemiological survey of 281 adults with ID without Down syndrome (DS) aged ⩾60 years; participants who screened positive with a memory task, informant-reported change in function or with the Dementia Questionnaire for Persons with Mental Retardation (DMR) underwent a detailed assessment. Diagnoses were made by psychiatrists according to international criteria. Prevalence rates were compared with UK prevalence and European consensus rates using standardized morbidity ratios (SMRs).

Dementia was more common in this population (prevalence of 18.3%, SMR 2.77 in those aged ⩾65 years). Prevalence rates did not differ between mild, moderate and severe ID groups. Age was a strong risk factor and was not influenced by sex or ID severity. As predicted, SMRs were higher for younger age groups compared to older age groups, indicating a relative shift in age-associated risk.

Criteria-defined dementia is 2–3 times more common in the ID population, with a shift in risk to younger age groups compared to the general population.

Cognitive behaviour therapy (CBT) has been shown to reduce psychological morbidity in people with cancer, but no randomized controlled trial (RCT) exists in palliative care. We aimed to determine whether home care nurses could be taught to deliver basic cognitive behavioural techniques and so reduce symptoms of anxiety and depression.

Clinical nurse specialists (CNSs) at St Christopher's Hospice were randomly allocated to receive training in CBT or continue their usual practice. At the end of the trial, nurses were rated on the Cognitive Therapy First Aid Rating Scale (CTFARS) for CBT competence. Home care patients who scored as possible cases on the Hospital Anxiety and Depression Scale (HADS) entered the trial. Participants received home care nursing visits. Assessments were carried out at baseline, 6, 10 and 16 weeks.

Eight nurses received CBT training and seven continued practice as usual. The mean CTFARS scores were 35.9 for the CBT nurses and 19.0 for the controls (p=0.02). A total of 328 patients (54%) were possible cases and 80 entered the trial; most of those excluded were too ill to participate. There was an interaction between group and time: individuals receiving CBT had lower anxiety scores over time [coefficient −0.20, 95% confidence interval (CI) −0.35 to −0.05, p=0.01]. No effect of the training was found for depression.

It is possible to conduct a randomized trial of psychological interventions in palliative care but there is considerable attrition from physical morbidity and mortality. Nurses can learn to integrate basic CBT methods into their clinical practice. This training may be associated with better outcomes for symptoms of anxiety.

Mood lability is a concept widely used. However, data on its prevalence and morbid associations are scarce. We sought to establish the occurrence and importance of mood lability in a large community sample of children and adolescents by testing a priori hypotheses.

Cross-sectional data were taken from a national mental health survey including 5326 subjects aged 8–19 years in the UK. The outcomes were prevalence and characteristics of mood lability and its associations with psychopathology and overall impairment.

Mood lability occurred in more than 5% of the population of children and adolescents, both by parent and self-report. Mood lability was strongly associated with a wide range of psychopathology and was linked to significant impairment even in the absence of psychiatric disorders. Mood lability was particularly strongly associated with co-morbidity between internalizing and externalizing disorders, even when adjusting for the association with individual disorders. The pattern of results did not change after excluding youth with bipolar disorder or with episodes of elated mood.

Clinically significant mood lability is relatively common in the community. Our findings indicate that mood lability is not a mere consequence of other psychopathology in that it is associated with significant impairment even in the absence of psychiatric diagnoses. Moreover, the pattern of association of mood lability with co-morbidity suggests that it could be a risk factor shared by both internalizing and externalizing disorders. Our data point to the need for greater awareness of mood lability and its implications for treatment.

The potential effects of antipsychotic drugs on brain structure represent a key factor in understanding neuroanatomical changes in psychosis. This review addresses two issues: (1) do antipsychotic medications induce changes in total or regional human brain volumes and (2) do such effects depend on antipsychotic type?

A systematic review of studies reporting structural brain magnetic resonance imaging (MRI) measures: (1) directly in association with antipsychotic use; and (2) in patients receiving lifetime treatment with antipsychotics in comparison with drug-naive patients or healthy controls. We searched Medline and EMBASE databases using the medical subject heading terms: ‘antipsychotics’ AND ‘brain’ AND (MRI NOT functional). The search included studies published up to 31 January 2007. Wherever possible, we reported the effect size of the difference observed.

Thirty-three studies met our inclusion criteria. The results suggest that antipsychotics act regionally rather than globally on the brain. These volumetric changes are of a greater magnitude in association with typical than with atypical antipsychotic use. Indeed, there is evidence of a specific effect of antipsychotic type on the basal ganglia, with typicals specifically increasing the volume of these structures. Differential effects of antipsychotic type may also be present on the thalamus and the cortex, but data on these and other brain areas are more equivocal.

Antipsychotic treatment potentially contributes to the brain structural changes observed in psychosis. Future research should take into account these potential effects, and use adequate sample sizes, to allow improved interpretation of neuroimaging findings in these disorders.

Two alternative models of post-traumatic stress disorder (PTSD) appear to represent the disorder's latent structure better than the traditional Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) three-factor PTSD model. The present study examines the impact of using these structural models for the diagnosis of lifetime PTSD while retaining the DSM-IV PTSD's six-symptom diagnostic requirement.

Data were gathered from large-scale, epidemiological datasets collected with adults (National Comorbidity Survey Replication) and adolescents (National Survey of Adolescents). Two alternative, empirically supported four-factor models of PTSD were compared with the DSM-IV three-factor PTSD diagnostic model.

Results indicated that the diagnostic alterations resulted in substantially improved structural validity, downward adjustments of PTSD's lifetime prevalence (roughly 1 percentage point decreases in adults, 1–2.5 percentage point decreases in adolescents), and equivalent psychiatric co-morbidity and sociodemographic associations.

Implications for modifying PTSD diagnostic criteria in future editions of DSM are discussed.

Although minor motor and sensory deficits, or neurological soft signs (NSS), are a well-established finding in schizophrenia, the cerebral changes underlying these signs are only partly understood. We therefore investigated the cerebral correlates of NSS by using magnetic resonance imaging (MRI) in patients with schizophrenia and healthy controls.

Forty-two patients, all receiving atypical neuroleptics, with first-episode schizophrenia or schizophreniform disorder and 22 healthy controls matched for age and gender were included. NSS were examined on the Heidelberg Scale after remission of the acute symptoms before discharge and correlated to density values by using optimized voxel-based morphometry (VBM).

NSS scores were significantly higher in patients than healthy controls. Within the patient group NSS were significantly associated with reduced grey or white-matter densities in the pre- and post-central gyrus, pre-motor area, middle and inferior frontal gyri, cerebellum, caudate nucleus and thalamus. These associations did not apply for the control group, in whom only the associations between NSS and reduced frontal gyri densities could be confirmed.

The pattern of cerebral changes associated with NSS clearly supports the model of ‘cognitive dysmetria’ with a disrupted cortico-cerebellar-thalamic-cortical circuit in schizophrenia. The variety of sites may correspond with the clinical diversity of NSS, which comprises both motor and sensory signs, and with the putative heterogeneity of the pathogenetic changes involved. That the respective associations did not apply for the healthy control group indicates that NSS in patients and controls refer to different pathogenetic factors.

This analysis aimed to show whether symptoms of either pole change in their persistence as individuals move through two decades, whether such changes differ by age grouping, and whether age of onset plays an independent role in symptom persistence.

Participants in the National Institute of Mental Health (NIMH) Collaborative Depression Study (CDS) who completed at least 20 years of follow-up and who met study criteria for bipolar I or schizo-affective manic disorder, before intake or during follow-up, were divided by age at intake into youngest (18–29 years, n=56), middle (30–44 years, n=68) and oldest (>44 years, n=24) groups.

The persistence of depressive symptoms increased significantly in the two younger groups. Earlier ages of onset were associated with higher depressive morbidity throughout the 20 years of follow-up but did not predict changes in symptom persistence. The proportions of weeks spent in episodes of either pole correlated across follow-up periods in all age groupings, although correlations were stronger for depressive symptoms and for shorter intervals.

Regardless of age at onset, the passage of decades in bipolar illness seems to bring an increase in the predominance of depressive symptoms in individuals in their third, fourth and fifth decades and an earlier age of onset portends a persistently greater depressive symptom burden. The degree to which either depression or manic/hypomanic symptoms persist has significant stability over lengthy periods and seems to reflect traits that manifest early in an individual's illness.

Adverse childhood experiences have been described as one of the major environmental risk factors for depressive disorder. Similarly, the deleterious impact of early traumatic experiences on depression seems to be moderated by individual genetic variability. Serotonin transporter (5-HTT) and brain-derived neurotrophic factor (BDNF) modulate the effect of childhood adversity on adult depression, although inconsistencies across studies have been found. Moreover, the gene×environment (G×E) interaction concerning the different types of childhood adversity remains poorly understood. The aim of this study was to analyse the putative interaction between the 5-HTT gene (5-HTTLPR polymorphism), the BDNF gene (Val66Met polymorphism) and childhood adversity in accounting for adult depressive symptoms.

A sample of 534 healthy individuals filled in self-report questionnaires of depressive symptomatology [the Symptom Check List 90 Revised (SCL-90-R)] and different types of childhood adversities [the Childhood Trauma Questionnaire (CTQ)]. The 5-HTTLPR polymorphism (5-HTT gene) and the Val66Met polymorphism (BDNF gene) were genotyped in the whole sample.

Total childhood adversity (β=0.27, p<0.001), childhood sexual abuse (CSA; β=0.17, p<0.001), childhood emotional abuse (β=0.27, p<0.001) and childhood emotional neglect (β=0.22, p<0.001) had an impact on adult depressive symptoms. CSA had a greater impact on depressive symptoms in Met allele carriers of the BDNF gene than in the Val/Val group (F=5.87, p<0.0001), and in S carriers of the 5-HTTLPR polymorphism (5-HTT gene) (F=5.80, p<0.0001).

Childhood adversity per se predicted higher levels of adult depressive symptoms. In addition, BDNF Val66Met and 5-HTTLPR polymorphisms seemed to moderate the effect of CSA on adult depressive symptoms.