The nosological status of olfactory reference syndrome (ORS) is a matter of debate and there is uncertainty as to what treatments are effective.

The world literature was searched for reports of cases of ORS. Clinical, nosological and therapeutic information from cases meeting proposed diagnostic criteria for the disorder was summarized and tabulated.

A total of 84 case reports (52 male/32 female) were found. Age of onset was <20 years in almost 60% of cases. Smell-related precipitating events were recorded in 42%. Most patients could not smell the smell or only did so intermittently. Authors of the reports expressed reservations about the delusional nature of the belief in slightly under half of the cases. Over two-thirds were improved or recovered at follow-up, with the disorder responding to antidepressants and psychotherapy more frequently than to neuroleptics.

ORS is a primary psychiatric syndrome that does not fit well into its current classification as a subtype of delusional disorder, both in terms of its nosology and its response to treatment.

Cognitive impairment, particularly in memory and executive function, is a core feature of psychosis. Moreover, psychosis is characterized by a more prominent history of stress exposure, and by dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis. In turn, stress exposure and abnormal levels of the main HPA axis hormone cortisol are associated with cognitive impairments in a variety of clinical and experimental samples; however, this association has never been examined in first-episode psychosis (FEP).

In this study, 30 FEP patients and 26 controls completed assessment of the HPA axis (cortisol awakening response and cortisol levels during the day), perceived stress, recent life events, history of childhood trauma, and cognitive function. The neuropsychological battery comprised general cognitive function, verbal and non-verbal memory, executive function, perception, visuospatial abilities, processing speed, and general knowledge.

Patients performed significantly worse on all cognitive domains compared to controls. In patients only, a more blunted cortisol awakening response (that is, more abnormal) was associated with a more severe deficit in verbal memory and processing speed. In controls only, higher levels of perceived stress and more recent life events were associated with a worse performance in executive function and perception and visuospatial abilities.

These data support a role for the HPA axis, as measured by cortisol awakening response, in modulating cognitive function in patients with psychosis; however, this association does not seem to be related to the increased exposure to psychosocial stressors described in these patients.

It has long been acknowledged that hearing impairment may increase the risk for psychotic experiences. Recent work suggests that young people in particular may be at risk, indicating a possible developmental mechanism.

The hypothesis that individuals exposed to hearing impairment in early adolescence would display the highest risk for psychotic symptoms was examined in a prospective cohort study of a population sample of originally 3021 adolescents and young adults aged 14–24 years at baseline, in Munich, Germany (Early Developmental Stages of Psychopathology Study). The expression of psychosis was assessed at multiple time points over a period of up to 10 years, using a diagnostic interview (Munich Composite International Diagnostic Interview; CIDI) administered by clinical psychologists.

Hearing impairment was associated with CIDI psychotic symptoms [odds ratio (OR) 2.04, 95% confidence interval (CI) 1.10–3.81], particularly more severe psychotic symptoms (OR 5.66, 95% CI 1.64–19.49). The association between hearing impairment and CIDI psychotic symptoms was much stronger in the youngest group aged 14–17 years at baseline (OR 3.28, 95% CI 1.54–7.01) than in the older group aged 18–24 years at baseline (OR 0.82, 95% CI 0.24–2.84).

The finding of an age-specific association between hearing impairment and psychotic experiences suggests that disruption of development at a critical adolescent phase, in interaction with other personal and social vulnerabilities, may increase the risk for psychotic symptoms.

Early visual processing deficits are reliably detected in schizophrenia and show relationships to poor real-world functioning. However, the nature of this relationship is complex. Theoretical models and recent studies using statistical modeling approaches suggest that multiple intervening factors are involved. We previously reported that a direct and significant association between visual processing and functional status was mediated by a measure of social perception. The present study examined the contribution of negative symptoms to this model.

We employed structural equation modeling (sem) to test several models of outcome, using data from 174 schizophrenia out-patients. Specifically, we examined the direct and indirect relative contributions of early visual processing, social perception and negative symptoms to functional outcome.

First, we found that, similar to social perception, a measure of negative symptoms mediated the association between visual information processing and functional status. Second, we found that the inclusion of negative symptoms substantially enhanced the explanatory power of the model. Notably, it was the experiential aspect of negative symptoms (avolition and anhedonia) more than the expressive aspect (affective flattening and alogia) that accounted for significant variance in functional outcome, especially in the social component of the construct of functional outcome.

Social perception and negative symptoms play relevant roles in functional impairment in schizophrenia. Both social perception and negative symptoms statistically mediate the connection between visual processing and functional outcome. However, given the lack of association between social perception and negative symptoms, these constructs appear to have an impact on functioning through separate pathways.

By studying behavior, cognitive abilities and brain functioning in adolescents at high risk for psychosis, we can gain an insight into the vulnerability markers or protective factors in the development of psychotic symptoms. Although many high-risk studies have focused on impairments in neurocognitive functions, such as memory and attention, very few studies have investigated problems in processing social cues such as facial expressions as a possible vulnerability marker for psychosis.

Thirty-six adolescents at ultra-high risk (UHR) for psychosis and 21 non-clinical controls completed a face recognition test, a facial affect labeling test and an inhibitory control test. Schizotypal traits and schizophrenia symptoms were assessed using a schizotypy questionnaire and the Positive and Negative Syndrome Scale (PANSS).

The UHR group showed impairments in labeling facial expressions of others, in addition to a spared ability to recognize facial identity. More specifically, the UHR group made more errors in labeling neutral expressions compared to the controls, and an analysis of error types indicated that neutral faces were misattributed as being angry. The degree of misattribution of neutral-as-angry faces correlated significantly with reduced inhibitory control.

Our findings suggest that misattributing social cues might contribute to vulnerability for psychosis. This social cognitive deficit may be related to problems in inhibitory control, which potentially plays an important role in the selection of appropriate social meaning. These findings may have relevance for understanding the mechanisms underlying prodromal social dysfunction, which should be targeted in future remediation interventions.

Despite behavioural signs of flattened affect, patients affected by schizophrenia show enhanced sensitivity to negative stimuli. The current literature concerning neural circuitry for emotions supports dysregulations of cortico-limbic networks, but gives contrasting results. Adverse childhood experiences (ACEs) could persistently influence emotional regulation and neural correlates of response to emotional stimuli in healthy humans. This study evaluated the effect of ACEs and chronic undifferentiated schizophrenia on neural responses to emotional stimuli (negative facial expression).

Brain blood-oxygen-level-dependent functional magnetic resonance imaging neural responses to a face-matching paradigm, and regional grey matter (GM) volumes were studied at 3.0 T in the amygdala, hippocampus, anterior cingulated cortex (ACC) and prefrontal cortex (PFC). The severity of ACEs was assessed. Participants included 20 consecutively admitted in-patients affected by chronic undifferentiated schizophrenia, and 20 unrelated healthy volunteers from the general population.

Patients reported higher ACEs than controls. Worse ACEs proportionally led to decreasing responses in the amygdala and hippocampus, and to increasing responses in the PFC and ACC in all participants. Patients showed higher activations in the amygdala and hippocampus, and lower activations in the PFC and ACC. Higher ACEs were associated with higher GM volumes in the PFC and ACC, and schizophrenia was associated with GM reduction in all studied regions.

Structural and functional brain correlates of emotional reactivity are influenced by both current chronic undifferentiated schizophrenia and the severity of past ACEs.

Visual and verbal episodic memory deficits are putative endophenotypes for schizophrenia; however, the extent of any genetic overlap of these with schizophrenia is unclear. In this study, we set out to quantify the genetic and environmental contributions to variance in visual and verbal memory performance, and to quantify their genetic relationship with schizophrenia.

We applied bivariate genetic modelling to 280 twins in a classic twin study design, including monozygotic (MZ) and dizygotic (DZ) pairs concordant and discordant for schizophrenia, and healthy control twins. We assessed episodic memory using subtests of the Wechsler Memory Scale – Revised (WMS-R).

Genetic influences (i.e. heritability) contributed significantly to variance in immediate recall of both verbal memory and visual learning, and the delayed recall of verbal and visual memory. Liability to schizophrenia was associated with memory impairment, with evidence of significant phenotypic correlations between all episodic memory measures and schizophrenia. Genetic factors were the main source of the phenotypic correlations for immediate recall of visual learning material; both immediate and delayed recall of verbal memory; and delayed recall of visual memory that, for example, shared genetic variance with schizophrenia, which accounted for 88% of the phenotypic correlation (rph=0.41) between the two.

Verbal memory and visual learning and memory are moderately heritable, share a genetic overlap with schizophrenia and are valid endophenotypes for the condition. The inclusion of these endophenotypes in genetic association studies may improve the power to detect susceptibility genes for schizophrenia.

Many patients with schizophrenia exhibit neurocognitive impairments, namely, in attentional, mnestic and executive functions. While these deficits limit psychosocial rehabilitation, their effect on psychoeducation is unknown. Within the framework of the longitudinal Munich Cognitive Determinants of Psychoeducation and Information in Schizophrenic Psychoses (COGPIP) study, we examined: (a) whether illness knowledge after psychoeducation could be predicted more precisely from the neurocognitive than from the psychopathological status of the patients; (b) which neurocognitive domains are best predictors.

A total of 116 in-patients with schizophrenic or schizoaffective disorders were randomized to a neurocognitive training or control condition (2 weeks) followed by a manualized psychoeducational group programme (4 weeks) and then observed over a 9-month follow-up. Repeated measurements included – among others – the Positive and Negative Syndrome Scale and a comprehensive neuropsychological test battery from which normative T scores were used to calculate one global and five domain-specific neurocognitive composite scores. Illness knowledge was measured by a questionnaire (WFB-52) tailored to the psychoeducational programme.

Multiple linear regression analyses showed that, apart from baseline illness knowledge, neurocognition significantly predicted knowledge outcome as well as knowledge gain (measured by reliable change indices) after psychoeducation. This was not true for psychopathology. Among the domain-specific neurocognitive composite scores, only memory acquisition was a significant predictor of knowledge outcome and gain.

Neurocognition, not psychopathology, is a significant predictor of illness knowledge after psychoeducation in schizophrenia. This finding should guide efforts to tailor psychoeducational interventions more closely to the patient's needs and resources.

Interpersonal functioning is central to social anxiety disorder (SAD). Empirical examinations of interpersonal behaviors in individuals with SAD have frequently relied on analogue samples, global retrospective reports and laboratory observation. Moreover, research has focused on avoidance and safety behaviors, neglecting potential links between SAD and affiliative behaviors.

The influence of situational anxiety and emotional security on interpersonal behaviors was examined for individuals with SAD (n=40) and matched normal controls (n=40). Participants monitored their behavior and affect in naturally occurring social interactions using an event-contingent recording procedure.

Individuals with SAD reported higher levels of submissive behavior and lower levels of dominant behavior relative to controls. Consistent with cognitive–behavioral and evolutionary theories, elevated anxiety in specific events predicted increased submissiveness among individuals with SAD. Consistent with attachment theory, elevations in event-level emotional security were associated with increased affiliative behaviors (increased agreeable behavior and decreased quarrelsome behavior) among members of the SAD group. Results were not accounted for by concurrent elevations in sadness or between-group differences in the distribution of social partners.

These findings are consistent with predictions based on several theoretical perspectives. Further, the present research documents naturally occurring interpersonal patterns of individuals with SAD and identifies conditions under which these individuals may view social interactions as opportunities for interpersonal connectedness.

One third of referrals from primary to secondary care are for medically unexplained symptoms (MUS). We aimed to determine the association of depression and anxiety disorders with high use of specialist services by patients with MUS. We did this by comparing their prevalence in patients who had been repeatedly referred with symptoms for which they had received repeated specialist diagnoses of MUS with that in two control groups. We also determined the adequacy of treatment received.

A case-control study in five general practices in Edinburgh, UK. Data collection was by case note review and questionnaire. Cases were 193 adults with three or more referrals over 5 years, at least two of which resulted in a diagnosis of MUS. Controls were: (a) patients referred only once over 5 years (n=152); (b) patients with three or more referrals for symptoms always diagnosed as medically explained (n=162).

In total, 93 (48%) of the cases met our criteria for current depression, anxiety or panic disorders. This compared with 38 (25%) and 52 (35.2%) of the control groups; odds ratios (95% confidence intervals) of 2.6 (1.6–4.1) and 1.6 (1.01–2.4), respectively. Almost half (44%) of the cases with current depression or anxiety had not received recent minimum effective therapy.

Depression, anxiety and panic disorders are common in patients repeatedly referred to hospital with MUS. Improving the recognition and treatment of these disorders in these patients has the potential to provide better, more appropriate and more cost-effective medical care.

Understanding how common mental disorders such as anxiety and depression vary with socio-economic circumstances as people age can help to identify key intervention points. However, much research treats these conditions as a single disorder when they differ significantly in terms of their disease burden. This paper examines the socio-economic pattern of anxiety and depression separately and longitudinally to develop a better understanding of their disease burden for key social groups at different ages.

The Twenty-07 Study has followed 4510 respondents from three cohorts in the West of Scotland for 20 years and 3846 respondents had valid data for these analyses. Hierarchical repeated-measures models were used to investigate the relationship between age, social class and the prevalence of anxiety and depression over time measured as scores of 8 or more out of 21 on the relevant subscale of the Hospital Anxiety and Depression Scale (HADS).

Social class differences in anxiety and depression widened with age. For anxiety there was a nonlinear decrease in prevalence with age, decreasing more slowly for those from manual classes compared to non-manual, whereas for depression there was a non-linear increase in prevalence with age, increasing more quickly for those from manual classes compared to non-manual. This relationship is robust to cohort, period and attrition effects.

The more burdensome disorder of depression occurs more frequently at ages where socio-economic inequalities in mental health are greatest, representing a ‘double jeopardy’ for older people from a manual class.

Although psychiatric diagnostic systems have conceptualized mania as a discrete phenomenon, appropriate latent structure investigations testing this conceptualization are lacking. In contrast to these diagnostic systems, several influential theories of mania have suggested a continuous conceptualization. The present study examined whether mania has a continuous or discrete latent structure using a comprehensive approach including taxometric, information-theoretic latent distribution modeling (ITLDM) and predictive validity methodologies in the Epidemiologic Catchment Area (ECA) study.

Eight dichotomous manic symptom items were submitted to a variety of latent structural analyses, including factor analyses, taxometric procedures and ITLDM, in 10105 ECA community participants. In addition, a variety of continuous and discrete models of mania were compared in terms of their relative abilities to predict outcomes (i.e. health service utilization, internalizing and externalizing disorders, and suicidal behavior).

Taxometric and ITLDM analyses consistently supported a continuous conceptualization of mania. In ITLDM analyses, a continuous model of mania demonstrated 6.52:1 odds over the best-fitting latent class model (LCM) of mania. Factor analyses suggested that the continuous structure of mania was best represented by a single latent factor. Predictive validity analyses demonstrated a consistent superior ability of continuous models of mania relative to discrete models.

The present study provided three independent lines of support for a continuous conceptualization of mania. The implications of a continuous model of mania are discussed.

The current study investigates whether the underlying factor structure of psychopathic personality traits found in adults is similar to that in children and what the extent of the genetic and environmental influences are on these psychopathic traits.

Psychopathic personality traits were assessed in a community sample of 1219 twins and triplets (age 9–10 years) through caregiver reports of each child's behavior using the Child Psychopathy Scale (CPS).

Confirmatory factor analyses revealed an optimal two-factor solution (callous/disinhibited and manipulative/deceitful) to the CPS subscales. Bivariate genetic modeling of the two computed factor scores revealed significant genetic as well as unique environmental influences on psychopathic personality traits in both boys and girls, with heritability estimates of 0.64 and 0.46, respectively, in boys and 0.49 and 0.58, respectively, in girls. No shared environmental influences on psychopathic personality traits were found.

The relationship between the two factors was mediated by both genetic and unique environmental factors common to both traits.

The aim of this study was to investigate three main aspects of executive functions (EFs), i.e. shifting, updating and inhibition, in adolescents engaging in non-suicidal self-injury (NSSI) as compared with healthy controls.

EFs were assessed using the Intra/Extradimensional Set Shift, the Spatial Working Memory (SWM) Test and the Stop Signal Test (SST) from the Cambridge Neuropsychological Test Automated Battery (CANTAB), in a high-severity NSSI group (n=33), a low-severity NSSI group (n=29) and a healthy control group (n=35). Diagnostic characteristics were examined using the Kiddie-Sads-Present and Lifetime Version.

There were group differences on the SWM Test. A trend towards an interaction effect of sex revealed that males in the high-severity NSSI group made significantly more errors than males and females in the control group. Both males and females in the high-severity NSSI group made poor use of an efficient strategy in completing the test. The low-severity NSSI group performed poorly on the SST, making more errors than the control group and showing an impaired ability to inhibit initiated responses, as compared with the high-severity NSSI group. There were group differences in frequencies of current and previous major depressive disorder. However, no effects of these diagnoses were found on any of the EF tests.

This study demonstrates that NSSI subgroups have distinct deficits in EFs. The high-severity NSSI group has working memory deficits, while the low-severity NSSI group has impaired inhibitory control. This supports the emotion regulation hypothesis.

Impairments in working memory are present in many psychiatric illnesses such as attention-deficit hyperactivity disorder (ADHD) and schizophrenia. The dopamine transporter and catechol-O-methyltransferase (COMT) are proteins involved in dopamine clearance and the dopamine system is implicated in the modulation of working memory (WM) processes and neurochemical models of psychiatric diseases. The effects of functional polymorphisms of the dopamine transporter gene (DAT1) and the COMT gene were investigated using a visuospatial and numerical n-back working memory paradigm. Our n-back task was designed to reflect WM alone, and made no demands on higher executive functioning.

A total of 291 healthy volunteers (aged 18–45 years) were genotyped and matched for age, sex, and Barratt Impulsivity Scale (BIS) and National Adult Reading Test (NART) scores. To assess individual gene effects on WM, factorial mixed model analysis of variances (ANOVAs) were conducted with the between-subjects factor as genotype and difficulty level (0-, 1-, 2- and 3-back) entered as the within-subjects factor.

The analysis revealed that the DAT1 or COMT genotype alone or in combination did not predict performance on the n-back task in our sample of healthy volunteers.

Behavioral effects of DAT1 and COMT polymorphisms on WM in healthy volunteers may be non-existent, or too subtle to identify without exceedingly large sample sizes. It is proposed that neuroimaging may provide more powerful means of elucidating the modulatory influences of these polymorphisms.

Autism spectrum disorder (ASD) was once considered to be highly associated with intellectual disability and to show a characteristic IQ profile, with strengths in performance over verbal abilities and a distinctive pattern of ‘peaks’ and ‘troughs’ at the subtest level. However, there are few data from epidemiological studies.

Comprehensive clinical assessments were conducted with 156 children aged 10–14 years [mean (s.d.)=11.7 (0.9)], seen as part of an epidemiological study (81 childhood autism, 75 other ASD). A sample weighting procedure enabled us to estimate characteristics of the total ASD population.

Of the 75 children with ASD, 55% had an intellectual disability (IQ<70) but only 16% had moderate to severe intellectual disability (IQ<50); 28% had average intelligence (115>IQ>85) but only 3% were of above average intelligence (IQ>115). There was some evidence for a clinically significant Performance/Verbal IQ (PIQ/VIQ) discrepancy but discrepant verbal versus performance skills were not associated with a particular pattern of symptoms, as has been reported previously. There was mixed evidence of a characteristic subtest profile: whereas some previously reported patterns were supported (e.g. poor Comprehension), others were not (e.g. no ‘peak’ in Block Design). Adaptive skills were significantly lower than IQ and were associated with severity of early social impairment and also IQ.

In this epidemiological sample, ASD was less strongly associated with intellectual disability than traditionally held and there was only limited evidence of a distinctive IQ profile. Adaptive outcome was significantly impaired even for those children of average intelligence.

ICD-10 includes a craving criterion for alcohol dependence while DSM-IV does not. Little is known about whether craving fits with or improves the DSM-IV criteria set for alcohol-use disorders.

Data were derived from current drinkers (n=18 352) in the 1991–1992 National Longitudinal Alcohol Epidemiologic Survey (NLAES), a nationally representative survey of US adults >17 years of age. The Alcohol Use Disorder and Associated Disabilities Interview Schedule was used to assess the eleven DSM-IV dependence and abuse criteria, and alcohol craving. Exploratory factor, item response theory, and regression analyses were used to evaluate the psychometric properties and concurrent validity of DSM-based alcohol disorder criteria with the addition of alcohol craving.

The past 12-month prevalence of craving was 1.3%. Craving formed part of a unidimensional latent variable that included existing DSM-IV criteria. Craving demonstrated high severity on the alcohol-use disorder continuum, resulting in an improved dimensional model with greater discriminatory ability compared with current DSM-IV criteria. Correlates of the diagnosis did not change with the addition of craving, and past 12-month craving was associated with prior alcohol dependence, depression, and earlier age of alcohol disorder onset among those with current DSM-IV alcohol dependence.

The addition of craving to the existing DSM-IV criteria yields a continuous measure that better differentiates individuals with and without alcohol problems along the alcohol-use disorder continuum. Few individuals are newly diagnosed with alcohol dependence given the addition of craving, indicating construct validity but redundancy with existing criteria.

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.

For the emerging DSM-V, it has been recommended that dimensional and categorical methods be used simultaneously in diagnostic classification; however, little is known about this combined approach for abuse and dependence.

Using data (n=37 708) from the 2007 National Survey on Drug Use and Health (NSDUH), DSM-IV criteria for prescription opioid abuse and dependence among non-prescribed opioid users (n=3037) were examined using factor analysis (FA), latent class analysis (LCA, categorical), item response theory (IRT, dimensional), and factor mixture (hybrid) approaches.

A two-class factor mixture model (FMM) combining features of categorical latent classes and dimensional IRT estimates empirically fitted more parsimoniously to abuse and dependence criteria data than models from FA, LCA and IRT procedures respectively. This mixture model included a severely affected group (7%) with a comparatively moderate to high probability (0.32−0.88) of endorsing all abuse and dependence criteria items, and a less severely affected group (93%) with a low probability (0.003−0.16) of endorsing all criteria. The two empirically defined groups differed significantly in the pattern of non-prescribed opioid use, co-morbid major depression, and substance abuse treatment use.

A factor mixture model integrating categorical and dimensional features of classification fits better to DSM-IV criteria for prescription opioid abuse and dependence in adults than a categorical or dimensional approach. Research is needed to examine the utility of this mixture classification for substance use disorders and treatment response.