Social phobia is a chronic disorder that results in substantial impairment. We conducted a qualitative review of randomized controlled trials (RCTs) of psychological interventions for social phobia.

Articles were identified through searches of electronic databases and manual searches of reference lists. They were classified by psychological interventions evaluated. Data regarding treatment, participants and results were then extracted and tabulated. We identified which psychological interventions are empirically supported, using the scheme proposed by Chambless & Hollon (Journal of Consulting and Clinical Psychology 1998, 66, 7–18).

Thirty studies evaluating the efficacy of social skills training (SST), exposure therapy and/or cognitive treatments were identified. Cognitive behavior therapy (CBT), involving cognitive restructuring and exposure to feared and avoided social situations or behavioral experiments, was found to be an efficacious and specific treatment for social phobia. Exposure therapy was found to be an efficacious treatment since most of the evidence of its efficacy was from comparisons with no treatment. There were mixed findings regarding the relative efficacy of CBT and in vivo exposure. Some studies reported that the interventions were equivalent, while others found that patients treated with CBT had a better outcome. There was little evidence to support the use of SST.

CBT is the psychological intervention of choice for social phobia. The findings of this review are compared to those of other major reviews and limitations are discussed.

Despite heightened awareness of the clinical significance of social phobia, information is still lacking about putative subtypes, functional impairment, and treatment-seeking. New epidemiologic data on these topics are presented from the National Comorbidity Survey Replication (NCS-R).

The NCS-R is a nationally representative household survey fielded in 2001–2003. The World Health Organization (WHO) Composite International Diagnostic Interview Version 3.0 (CIDI 3.0) was used to assess 14 performance and interactional fears and DSM-IV social phobia.

The estimated lifetime and 12-month prevalence of social phobia are 12.1% and 7.1% respectively. Performance and interactional fears load onto a single latent factor, and there is little evidence for distinct subtypes based either on the content or the number of fears. Social phobia is associated with significant psychiatric co-morbidity, role impairment, and treatment-seeking, all of which have a dose–response relationship with number of social fears. However, social phobia is the focus of clinical attention in only about half of cases where treatment is obtained. Among non-co-morbid cases, those with the most fears were least likely to receive social phobia treatment.

Social phobia is a common, under-treated disorder that leads to significant functional impairment. Increasing numbers of social fears are associated with increasingly severe manifestations of the disorder.

To investigate the extent to which three putative ‘environmental’ risk factors, maternal punitive discipline (MPD), paternal punitive discipline (PPD) and negative life events (NLEs), share genetic influences with, and moderate the heritability of, externalizing behavior.

The sample consisted of 2647 participants, aged 12–19 years, from the G1219 and G1219Twins longitudinal studies. Externalizing behavior was measured using the Youth Self-Report, MPD, PPD and exposure to NLEs were assessed using the Negative Sanctions Scale and the Life Event Scale for Adolescents respectively.

Genetic influences overlapped for externalizing behavior and each ‘environmental’ risk, indicating gene–environment correlation. When controlling for the gene–environment correlation, genetic variance decreased, and both shared and non-shared environmental influences increased, as a function of MPD. Genetic variance increased as a function of PPD, and for NLEs the only interaction effect was on the level of non-shared environment influence unique to externalizing behavior.

The magnitude of the influence of genetic risk on externalizing behavior is contextually dependent, even after controlling for gene–environment correlation.

Disinhibition and decision-making skills play an important role in theories on the cause and outcome of addictive behaviors such as substance use disorders and pathological gambling. In recent studies, both disinhibition and disadvantageous decision-making strategies, as measured by neurocognitive tests, have been found to influence the course of substance use disorders. Research on factors affecting relapse in pathological gambling is scarce.

This study investigated the effect of both self-reported impulsivity and reward sensitivity, and neurocognitively assessed disinhibition and decision-making under conflicting contingencies, on relapse in a group of 46 pathological gamblers.

Logistic regression analysis indicated that longer duration of the disorder and neurocognitive indicators of disinhibition (Stop Signal Reaction Time) and decision-making (Card Playing Task) were significant predictors of relapse (explaining 53% of the variance in relapse), whereas self-reported impulsivity and reward sensitivity did not significantly predict relapse. Overall classification accuracy was 76%, with a positive classification accuracy of 76% and a negative classification accuracy of 75%.

Duration of the disorder and neurocognitive measures of disinhibition and decision-making are powerful predictors of relapse in pathological gambling. The results suggest that endophenotypical neurocognitive characteristics are more promising in the prediction of relapse in pathological gambling than phenotypical personality characteristics. Neurocognitive predictors may be useful to guide treatment planning of follow-up contacts and booster sessions.

We hypothesized that gender differences in average levels on the internalizing and externalizing factors that account for co-morbidity among common psychopathological syndromes in both men and women account for gender differences in the prevalence of specific syndromes.

The latent structure of 11 syndromes was examined in a middle-aged (mean age=52.66 years, s.d.=5.82) sample of 2992 (37% men) members of the community-based Minnesota Twin Registry (MTR) assessed using 10 scales of the Psychiatric Diagnostic Screening Questionnaire (PDSQ) and an adult antisocial behavior scale. Confirmatory factorial invariance models were applied to a best-fitting, internalizing–externalizing model.

A ‘strong gender invariance model’ fit best, indicating that gender differences in the means of individual syndromes were well accounted for by gender differences in mean levels of internalizing and externalizing. Women exhibited higher mean levels of internalizing (d=0.23) and lower mean levels of externalizing (d=−0.52) than men.

These findings suggest that risk factors for common mental disorders exhibiting gender differences may influence prevalence at the latent factor level. Future research may benefit from focusing on both the latent factor and individual syndrome levels in explaining gender differences in psychopathology.

Foetal nutrition and growth seem to affect the risk of developing schizophrenia. Exposure to famine during foetal development and low birthweight increase the risk. However, few studies have investigated the association between schizophrenia and adult height and weight or patterns of growth.

The study population consisted of two subpopulations: families with at least one member with schizophrenia, and families of offspring of mothers with psychotic disorder, and controls. Using a seven-parameter model of height growth curves, we compared the parameters of persons who later developed schizophrenia and their unaffected siblings from the same families. We also studied how growth curve parameters differed in children with genetic risk for schizophrenia and controls, and whether weight, height and body mass index (BMI) at different ages predicted later development of schizophrenia.

The predicted growth curves based on a parametric model were nearly identical for persons with schizophrenia and their unaffected siblings. Adult height of daughters of mothers with psychoses was borderline significantly (p=0.0536) lower compared to controls, while no difference was detected among sons (p=0.3283).

No association between growth characteristics and schizophrenia in families with at least one member with schizophrenia was found. Family-related factors should be taken into account as possible confounders in future studies on growth and schizophrenia.

An increased prevalence of minor physical anomalies (MPAs) has been extensively documented in schizophrenia but their specificity for the disorder remains unclear. We investigated the prevalence and the predictive power of MPAs in a large sample of first-episode psychotic patients across a range of diagnoses.

MPAs were examined in 242 subjects with first-episode psychosis (50% schizophrenia, 45% affective psychosis and 5% substance-induced psychosis) and 158 healthy controls. Categorical principal components analysis and analysis of variance were undertaken, and individual items with the highest loading were tested using the χ2 test.

Overall facial asymmetry, assymetry of the orbital landmarks, and frankfurt horizontal significantly differentiated patients with schizophrenia and affective psychosis from controls, as did a ‘V-shaped’ palate, reduced palatal ridges, abnormality of the left ear surface and the shape of the left and right ears. Patients with affective psychosis had significantly lowered eye fissures compared with control subjects.

MPAs are not specific to schizophrenia, suggesting a common developmental pathway for non-affective and affective psychoses. The topographical distribution of MPAs in this study is suggestive of an insult occurring during organogenesis in the first trimester of pregnancy.

The impact of co-morbid substance use in first-episode schizophrenia has not been fully explored.

This naturalistic follow-up of a cohort of 152 people with first-episode schizophrenia examined substance use and clinical outcome in terms of symptoms and social and neuropsychological function.

Data were collected on 85 (56%) of the patient cohort after a median period of 14 months. Over the follow-up period, the proportion of smokers rose from 60% at baseline to 64%. While 30% reported lifetime problem drinking of alcohol at baseline, only 15% had problem drinking at follow-up. Furthermore, while at baseline 63% reported lifetime cannabis use and 32% were currently using the drug, by the follow-up assessment the latter figure had fallen to 18.5%. At follow-up, persistent substance users had significantly more severe positive and depressive symptoms and greater overall severity of illness. A report of no lifetime substance use at baseline was associated with greater improvement in spatial working memory (SWM) at follow-up.

Past substance use may impede recovery of SWM performance in people with schizophrenia in the year or so following first presentation to psychiatric services. The prevalence of substance use other than tobacco tends to diminish over this period, in the absence of specific interventions. Persistent substance use in first-episode schizophrenia is associated with more severe positive and depressive symptoms but not negative symptoms, and should be a target for specific treatment intervention.

Velo-cardio-facial syndrome (VCFS) is associated with deletions at chromosome 22q11, abnormalities in brain anatomy and function, and schizophrenia-like psychosis. Thus it is assumed that one or more genes within the deleted region are crucial to brain development. However, relatively little is known about how genetic variation at 22q11 affects brain structure and function. One gene on 22q11 is catechol-O-methyltransferase (COMT): an enzyme that degrades dopamine and contains a functional polymorphism (Val158Met) affecting enzyme activity. Here, we investigated the effect of COMT Val158Met polymorphism on brain anatomy and cognition in adults with VCFS.

The COMT Val158Met polymorphism was genotyped for 26 adults with VCFS on whom DNA was available. We explored its effects on regional brain volumes using hand tracing approaches; on regional grey- and white-matter density using computerized voxel-based analyses; and measures of attention, IQ, memory, executive and visuospatial function using a comprehensive neuropsychological test battery.

After corrections for multiple comparisons Val-hemizygous subjects, compared with Met-hemizygotes, had a significantly larger volume of frontal lobes. Also, Val-hemizygotes had significantly increased grey matter density in cerebellum, brainstem, and parahippocampal gyrus, and decreased white matter density in the cerebellum. No significant effects of COMT genotype on neurocognitive performance were found.

COMT genotype effects on brain anatomy in VCFS are not limited to frontal regions but also involve other structures previously implicated in VCFS. This suggests variation in COMT activity is implicated in brain development in VCFS.

Paranoia is increasingly being studied in clinical and non-clinical populations. However there is no multi-dimensional measure of persecutory ideas developed for use across the general population-psychopathology continuum. This paper reports the development of such a questionnaire: the ‘Green et al. Paranoid Thought Scales’. The aim was to devise a tool to assess ideas of persecution and social reference in a simple self-report format, guided by a current definition of persecutory ideation, and incorporating assessment of conviction, preoccupation and distress.

A total of 353 individuals without a history of mental illness, and 50 individuals with current persecutory delusions completed a pool of paranoid items and additional measures to assess validity. Items were devised from a recent definition of persecutory delusions, current assessments of paranoia, the authors' clinical experience, and incorporated dimensions of conviction, preoccupation and distress. Test–retest reliability in the non-clinical group was assessed at 2 weeks follow-up, and clinical change in the deluded group at 6 months follow-up.

Two 16-item scales were extracted, assessing ideas of social reference and persecution. Good internal consistency and validity was established for both scales and their dimensions. The scales were sensitive to clinical change. A hierarchical relationship between social reference and persecution was found. The data provide further evidence for a continuum of paranoid ideas between deluded and healthy individuals.

A reliable and valid tool for assessing paranoid thoughts is presented. It will provide an effective way for researchers to ensure consistency in research and for clinicians to assess change with treatment.

We investigated whether the predictive accuracy of mild cognitive impairment (MCI) for Alzheimer-type dementia (AD) in a clinical setting is dependent on age and the definition of MCI used.

Non-demented subjects older than 40 (n=320) who attended a memory clinic of a university hospital were reassessed 5 years later for the presence of AD. MCI was diagnosed according to the criteria of amnestic MCI, mild functional impairment (MFI), ageing-associated cognitive decline (AACD), and age-associated memory impairment (AAMI). The main outcome measure was the area under the curve (AUC) of a receiver operating characteristic (ROC) curve. Analyses were conducted on the entire sample and on subgroups of subjects aged 40–54, 55–69 and 70–85 years.

A diagnosis of AD at follow-up was made in 58 subjects. Four of them were in the 40–54 age group, 29 in the 55–69 age group and 25 in the 70–85 age group. The diagnostic accuracy in the entire sample was low to moderately high with AUCs ranging from 0.56 (AACD) to 0.75 (amnestic MCI). A good predictive accuracy with an AUC >0.80 was only observed in subjects aged 70–85 using the criteria of amnestic MCI (AUC=0.84).

The predictive accuracy of MCI for AD is dependent on age and the definition of MCI used. The predictive accuracy is good only for amnestic MCI in subjects 70–85 years. As subjects with prodromal AD are often younger than 70, the usefulness of MCI as predictor of AD in clinical practice is limited.

Patients treated in primary care settings report better mental outcomes when they agree with practitioners about the nature of their core presenting problems. However, no study has examined the impact of staff–patient agreement on treatment outcomes in specialist mental health services. We investigated whether a better staff–patient agreement on needs for care predicts more favourable outcome in patients receiving community-based psychiatric care.

A 3-month prevalence cohort of 188 patients with the full spectrum of psychiatric conditions was assessed at baseline and at 4 years using the Camberwell Assessment of Need (CAN), both staff (CAN-S) and patient versions (CAN-P), and a set of standardized outcome measures. Baseline staff–patient agreement on needs was included among predictors of outcome. Both clinician-rated (psychopathology, social disability, global functioning) and patient-rated (subjective quality of life and satisfaction with services) outcomes were considered.

Controlling for the effect of sociodemographics, service utilization and changes in clinical status, better staff–patient agreement makes a significant additional contribution in predicting treatment outcomes not only on patient-rated but also on clinician-rated measures.

Mental health care should be provided on the basis of a negotiation process involving both professionals and service users to ensure effective interventions; every effort should be made by services to implement strategies aiming to increase consensus between staff and patients.

Social dysfunction in personality disorder is commonly ascribed to abnormal temperamental traits but may also reflect deficits in social processing. In this study, we examined whether borderline and avoidant personality disorders (BPD, APD) may be differentiated by deficits in different social domains and whether disorganization of social domain functioning uniquely characterizes BPD.

Patients were recruited from psychiatric clinics in Pittsburgh, USA, to provide a sample with BPD, APD and a no-personality disorder (no-PD) comparison group. Standardized assessments of Axis I and Axis II disorders and social domain dysfunction were conducted, including a new scale of ‘domain disorganization’ (DD).

Pervasive social dysfunction was associated with a 16-fold increase in the odds of an Axis II disorder. Both APD and BPD were associated with elevated social dysfunction. Romantic relationship dysfunction was associated specifically with BPD symptoms and diagnosis. DD was associated specifically with a categorical BPD diagnosis and with a dimensional BPD symptom count.

A focus on the inherently interpersonal properties of personality disorders suggests specific mechanisms (within and across interpersonal domains) that may help to account for the origins and maintenance of some disorders. In particular, BPD reflects disturbances in romantic relationships, consistent with a role for attachment processes, and in the organization of functioning across social domains.