The prevalence of human immunodeficiency virus (HIV) is elevated among individuals with a severe mental illness (SMI). Because of the benefits of HIV testing, it is important for individuals with SMI to have routine access to testing. The goals of this review are: to summarize knowledge about HIV testing prevalence, correlates, and interventions among individuals with an SMI; to identify research needs; and to discuss clinical implications of the studies reviewed.

Literature searches were conducted using PsycINFO, PubMed, and Medline. Additional articles were obtained from reference lists of relevant articles.

Fewer than one-half of individuals with an SMI have been tested for HIV in the past year. Engaging in sex or drug risk behavior was the only consistent correlate of HIV testing. Interventions for promoting HIV testing among individuals with an SMI have not been well developed or evaluated.

Research on HIV testing among individuals with an SMI is needed. Mental health settings may be opportune venues for HIV testing, even though providers face ethical challenges when implementing testing programs in these settings.

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.

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.

A key neuropsychological proposal in schizophrenia is that negative and disorganization symptoms are associated with different patterns of impairment on executive tasks.

Studies reporting correlations between positive, negative or disorganization symptoms and any type of executive test were meta-analysed. The influence of moderating factors was also examined, including age, treatment and stage of illness and whether symptoms were relapsing or persistent. The magnitudes of the correlations were compared with those for general intellectual impairment.

Pooled correlations between executive impairment and both negative symptoms and disorganization were significant in the small-to-moderate range. That for positive symptoms (‘reality distortion’), however, was close to zero. The pattern of correlations among different executive tests differed significantly for negative symptoms and disorganization. Patients with stable clinical pictures showed significantly higher correlations with executive impairment than those with relapsing and remitting illnesses. Both negative symptoms and disorganization also correlated significantly with general intellectual function as indexed by current IQ.

Meta-analysis supports the view that negative symptoms and disorganization are associated with partially dissociable patterns of executive impairment. However, co-existent general intellectual impairment has been an important confounding factor in the studies to date.

Although cognitive variables have been shown to be useful in predicting outcomes in late-life depression, there has not yet been a comprehensive study in younger persons with depression.

The clinical symptoms and cognitive performance of participants were evaluated at admission to one of two university teaching hospitals and again at 3 months after remission and discharge. A total of 52 participants with a DSM-IV diagnosis of major depressive disorder, aged between 20 and 60 years and with a Hamilton Depression Rating Scale score ⩾17 entered the study. The sample for this paper comprises the 48 subjects (mean age 37.9 years, s.d.=10.7) who received admission and follow-up assessments; an attrition rate of 7.7%.

More perseverative errors on the shortened Wisconsin Card Sorting Test at admission predicted a worse clinical outcome at follow-up. Poor event-based prospective memory and more perseverative errors on the shortened Wisconsin Card Sorting Test at admission predicted worse social and occupational outcome at follow-up.

These results suggest that a brief cognitive screen at hospital admission, focusing on executive function, would have a useful prognostic value in depression. Determining early predictors of individuals at risk of poorer outcomes is important for identifying those who may need altered or additional treatment approaches.

Research on the long-term course of major depressive disorder (MDD) is hindered by the absence of established course criteria and by idiosyncratic definitions of chronicity. The aims of this study were to derive an empirical index of MDD course, to examine its predictive validity, and to identify the adulthood outcomes associated with a chronic course.

Indicators for a MDD course factor were rationally selected and subjected to principal components (PCA) and confirmatory factor analyses (CFA) among 426 subjects with a lifetime history of MDD by age 30. Scores on the index prior to age 19 were examined as predictors of course from age 19 to 30. Associations between the index and outcomes of interest at age 30 were examined.

Three indicators loaded highly on a chronic course index and displayed adequate internal consistency: early onset age, number of episodes, and duration of ill time. Predictive validity of the index was supported. A more chronic course was associated with greater symptom severity, greater likelihood of treatment utilization, and greater psychosocial impairment in multiple domains. Treatment utilization interacted with chronicity to predict relatively few outcomes and did not reduce the negative impact of a chronic course.

The course of MDD through early adulthood is best represented by a composite of early onset age, number of episodes, and duration of ill time. A chronic course through early adulthood is associated with numerous indicators of psychosocial impairment. Mental health treatment utilization in a naturalistic setting does not appear to reduce the negative impact of chronic MDD.

A lack of longitudinal studies has made it difficult to establish the direction of associations between circulating concentrations of low-grade chronic inflammatory markers, such as C-reactive protein and interleukin-6, and cognitive symptoms of depression. The present study sought to assess whether C-reactive protein and interleukin-6 predict cognitive symptoms of depression or whether these symptoms predict inflammatory markers.

In a prospective occupational cohort study of British white-collar civil servants (the Whitehall II study), serum C-reactive protein, interleukin-6 and cognitive symptoms of depression were measured at baseline in 1991–1993 and at follow-up in 2002–2004, an average follow-up of 11.8 years. Symptoms of depression were measured with four items describing cognitive symptoms of depression from the General Health Questionnaire. The number of participants varied between 3339 and 3070 (mean age 50 years, 30% women) depending on the analysis.

Baseline C-reactive protein (β=0.046, p=0.004) and interleukin-6 (β=0.046, p=0.005) predicted cognitive symptoms of depression at follow-up, while baseline symptoms of depression did not predict inflammatory markers at follow-up. After full adjustment for sociodemographic, behavioural and biological risk factors, health conditions, medication use and baseline cognitive systems of depression, baseline C-reactive protein (β=0.038, p=0.036) and interleukin-6 (β=0.041, p=0.018) remained predictive of cognitive symptoms of depression at follow-up.

These findings suggest that inflammation precedes depression at least with regard to the cognitive symptoms of depression.

Recent studies have shown a temporal association between depressive symptoms and cognitive decline. However, the relationship between syndromes of depression and dementia is unknown.

A total of 1736 people aged ⩾65 years in China and 5222 older people in the UK were interviewed using the Geriatric Mental State Examination (GMS) and reinterviewed at follow-up. Five levels of syndromes of depression and dementia were diagnosed using the Automated Geriatric Examination for Computer Assisted Taxonomy (AGECAT).

Although there were fewer depressive syndromes in Chinese than British participants, both populations showed a similarly high level of syndromes of dementia (organic disorder) (20% for women, 14% for men). There was a significant cross-sectional correlation between syndrome levels of depression and dementia (correlation coefficients: 0.141–0.248 for Chinese, 0.168–0.248 for British). This was maintained for different age, gender and people with and without cardiovascular disease (CVD). The relationship between syndromes of baseline depression and follow-up dementia was less substantial: the correlation coefficient was 0.075 [95% confidence interval (CI) 0.021–0.128] for the Chinese sample at the 1-year follow-up, and 0.093 (95% CI 0.061–0.125) for the British at the 2-year follow-up and 0.093 (95% CI 0.049–0.130) at the 4-year follow-up. This relationship disappeared in participants without baseline organic syndromes. In a multiple adjusted logistic regression analysis, an increased risk of organic syndromes seemed to be associated with baseline, mainly in the highest level of, depressive syndromes.

The relationship between syndromes of depression and dementia might be temporal. The lack of an obvious dose–response relationship between baseline depressive syndromes and follow-up dementia syndromes suggests that the causal relationship between depression and dementia needs further investigation.

Few genetically informative studies have examined the effects of different types of trauma on risk for depression over time. The aim of the present study was to examine the relative contributions over time of assaultive trauma, non-assaultive trauma, and familial effects to risk for depression.

Histories of depression and trauma were obtained during structured diagnostic interviews with 5266 (mean age 29.9 years, s.d.=2.4) members of a volunteer Australian twin panel from the general population. Age at first onset of a DSM-IV major depressive episode was the dependent variable. Associations of depression with traumatic events were examined while accounting for the temporal sequence of trauma and depression and familial effects.

Assaultive traumatic events that occurred during childhood had the strongest association with immediate and long-term risk for depression, and outweighed familial effects on childhood-onset depression for most twins. Although men and women endorsed equal rates of assaultive trauma, women reported a greater accumulation of assaultive events at earlier ages than men, whereas men reported a greater accumulation of non-assaultive events at all ages.

Early exposure to assaultive trauma can influence risk for depression into adulthood. Concordance for early trauma is a significant contributor to the familiality of early-onset depression.

Few controlled studies have specifically investigated aspects of mental health care in relation to suicide risk among recently discharged psychiatric patients. We aimed to identify risk factors, including variation in healthcare received, for suicide within 3 months of discharge.

We conducted a national population-based case-control study of 238 psychiatric patients dying by suicide within 3 months of hospital discharge, matched on date of discharge to 238 living controls.

Forty-three per cent of suicides occurred within a month of discharge, 47% of whom died before their first follow-up appointment. The first week and the first day after discharge were particular high-risk periods. Risk factors for suicide included a history of self-harm, a primary diagnosis of affective disorder, recent last contact with services and expressing clinical symptoms at last contact with staff. Suicide cases were more likely to have initiated their own discharge and to have missed their last appointment with services. Patients who were detained for compulsory treatment at last admission, or who were subject to enhanced levels of aftercare, were less likely to die by suicide.

The weeks after discharge from psychiatric care represent a critical period for suicide risk. Measures that could reduce risk include intensive and early community follow-up. Assessment of risk should include established risk factors as well as current mental state and there should be clear follow-up procedures for those who have self-discharged. Recent detention under the Mental Health Act and current use of enhanced levels of aftercare may be protective.

Anorexia nervosa (AN) is associated with behavioral traits that predate the onset of AN and persist after recovery. We identified patterns of behavioral traits in AN trios (proband plus two biological parents).

A total of 433 complete trios were collected in the Price Foundation Genetic Study of AN using standardized instruments for eating disorder (ED) symptoms, anxiety, perfectionism, and temperament. We used latent profile analysis and ANOVA to identify and validate patterns of behavioral traits.

We distinguished three classes with medium to large effect sizes by mothers' and probands' drive for thinness, body dissatisfaction, perfectionism, neuroticism, trait anxiety, and harm avoidance. Fathers did not differ significantly across classes. Classes were distinguished by degree of symptomatology rather than qualitative differences. Class 1 (~33%) comprised low symptom probands and mothers with scores in the healthy range. Class 2 (~43%) included probands with marked elevations in drive for thinness, body dissatisfaction, neuroticism, trait anxiety, and harm avoidance and mothers with mild anxious/perfectionistic traits. Class 3 (~24%) included probands and mothers with elevations on ED and anxious/perfectionistic traits. Mother–daughter symptom severity was related in classes 1 and 3 only. Trio profiles did not differ significantly by proband clinical status or subtype.

A key finding is the importance of mother and daughter traits in the identification of temperament and personality patterns in families affected by AN. Mother–daughter pairs with severe ED and anxious/perfectionistic traits may represent a more homogeneous and familial variant of AN that could be of value in genetic studies.

Assessment of eating disorders at the symptom level can facilitate the refinement of phenotypes. We examined genetic and environmental contributions to liability to anorexia nervosa (AN) symptoms in a population-based twin sample using a genetic common pathway model.

Participants were from the Norwegian Institute of Public Health Twin Panel (NIPHTP) and included all female monozygotic (MZ; 448 complete pairs and four singletons) and dizygotic (DZ; 263 complete pairs and four singletons) twins who completed the Composite International Diagnostic Interview (CIDI) assessing DSM-IV Axis I and ICD-10 criteria. Responses to items assessing AN symptoms were included in a model fitted using the marginal maximum likelihood (MML) approach.

Heritability of the overall AN diagnosis was moderate [a2=0.22, 95% confidence interval (CI) 0.0–0.50] whereas heritabilities of the specific items varied. Heritability estimates for weight loss items were moderate (a2=0.31–0.34) and items assessing weight concern when at a low weight were smaller (0.18–0.29). Additive genetic factors contributed little to the variance of amenorrhea, which was most strongly influenced by unshared environment (a2=0.16, e2=0.71).

AN symptoms are differentially heritable. Specific criteria such as those related to body weight and weight loss history represent more biologically driven potential endophenotypes or liability indices. The results regarding weight concern differ somewhat from those of previous studies, highlighting the importance of assessing genetic and environmental influences on variance of traits within specific subgroups of interest.

Understanding the pathways to psychiatric care and recognition of delay points are crucial for the development of interventions that aim to improve access to mental health-care services.

Over a 2-month period in 2003, a total of 1044 patients at the commencement of new episodes of care at Amanuel Specialized Mental Hospital in Addis Ababa, Ethiopia were interviewed using the encounter form that was developed by the World Health Organization (WHO) for the study of pathways to psychiatric care.

The mental hospital was contacted directly by 41% of patients. The remaining patients sought care from up to four different caregivers before arriving at the psychiatric hospital. Where the initial service was not received at the psychiatric hospital, 30.9% of patients sought care from priests/holy water/church. The median delay between onset of illness and arrival at the psychiatric hospital was 38 weeks. The longest delays before arriving at the mental hospital were associated with having no formal education, joblessness, and diagnoses of epilepsy and physical conditions.

Implementing a robust referral system and establishing a strong working relationship with both traditional and modern health-care providers, as well as designing a service delivery model that targets particular segments of the population, such as those who are uneducated, jobless and/or suffer from epilepsy and somatic conditions, should be the most important strategies towards improving mental health service delivery and shortening of undue delay for patients receiving psychiatric care in Ethiopia.

A proper understanding of patterns of care represents a crucial step in improving clinical decision making and enhancing service provision. Only a few studies, however, have explored global patterns of psychiatric admissions nationwide, and none have been undertaken in Italy.

Sociodemographic, clinical and treatment-related information was collected for 1577 patients admitted to 130 public and 36 private in-patient facilities in Italy during an index period in the year 2004. All patients were also rated using the 24-item Brief Psychiatric Rating Scale (BPRS) and the Personal and Social Performance (PSP) rating scales.

Non-affective psychoses (36%) were the most common diagnoses and accounted to a large extent for compulsory admissions. Private facilities were more likely to admit patients with organic mental disorders and substance abuse/dependence and less likely to admit patients with non-affective psychoses. Overall, 77.8% of patients had been receiving treatment by a mental health professional in the month prior to admission. In 54% of cases, the admission was solicited by patients' family members. The main factors preceding admission were impairment in work or social functioning, social withdrawal, and conflict with family members. Agitation, delusions and/or hallucinations, and the presence of multiple problems were associated with compulsory admissions, whereas depressive and anxiety symptoms were associated with voluntary admissions.

In a mixed, public–private psychiatric care system, like the Italian one, public and private facilities admit patients with widely different clinical characteristics and needs. Family support represents an important resource for most patients, and interventions specifically addressed to relieving family burden are warranted.

The mechanisms underlying the co-occurrence of the functional somatic syndromes are largely unknown. No empirical study has explicitly examined how genetic and environmental factors influence the co-morbidity of these syndromes. We aimed to examine how the co-morbidity of functional somatic syndromes is influenced by genetic and environmental factors that are in common to the syndromes.

A total of 31318 twins in the Swedish Twin Registry aged 41–64 years underwent screening interviews via a computer-assisted telephone system from 1998 to 2002. Four functional somatic syndromes (chronic widespread pain, chronic fatigue, irritable bowel syndrome, and recurrent headache) and two psychiatric disorders (major depression and generalized anxiety disorder) were assessed using structured questions based on standard criteria for each illness in a blinded manner.

Multivariate twin analyses revealed that a common pathway model with two latent traits that were shared by the six illnesses fit best to the women's data. One of the two latent traits loaded heavily on the psychiatric disorders, whereas the other trait loaded on all four of the functional somatic syndromes, particularly chronic widespread pain, but not on the psychiatric disorders. All illnesses except the psychiatric disorders were also affected by genetic influences that were specific to each.

The co-occurrence of functional somatic syndromes in women can be best explained by affective and sensory components in common to all these syndromes, as well as by unique influences specific to each of them. The findings clearly suggest a complex view of the multifactorial pathogenesis of these illnesses.

Recall of adverse life events under brain imaging conditions has been shown to coincide with activation of limbic and prefrontal brain areas in borderline personality disorder (BPD). We investigate changes of functional magnetic resonance imaging (fMRI) activation patterns during the recall of unresolved adverse life events (ULE) over 1 year.

Thirteen female BPD patients participated in the study. During fMRI measurement subjects recalled ULE and negative but resolved life events (RLE) after individual cue words to stimulate autobiographical memory retrieval. Subjective intensity of emotional and sensoric experiences during recall was assessed as well as standardized measures of psychopathology.

A 2×2 factorial analysis of fMRI data (Δt1/t2×ΔULE/RLE) revealed major right more than left differences of activation (i.e. t1>t2) of the posterior more than anterior cingulate, superior temporal lobes, insula, and right middle and superior frontal lobes (second-level analysis, t=3.0, puncorrected=0.003). The opposite contrast (Δt2/t1×ΔULE/RLE) did not reveal any differences. We did not find changes of emotional or sensoric qualities during recall (ULE versus RLE) or of psychopathology measures over the 1-year period.

Although subjective and clinical data did not change within 1 year, we observed a substantial decrease of temporo-frontal activation during the recall of ULE from t1 to t2. If future research confirms these findings, the question arises whether the decrease of neural activation precedes clinical improvement in BPD.