Due to neuropsychological conceptualizations of orbitoprefrontal cortex (OFC) dysfunction underpinning impulsive aggression and the incidence of such behaviour in post-traumatic stress disorder (PTSD), this study aimed to explore olfactory identification (OI) ability in war veterans with PTSD as a probe of putative OFC dysfunction; and to explore the utility of OI ability in predicting aggressive and impulsive behavior in this clinical population.

Participants comprised 31 out-patient male war veterans with PTSD (mean=58.23 years, s.d.=2.56) recruited from a Melbourne Veterans Psychiatry Unit, and 31 healthy age- and gender-matched controls (mean=56.84 years, s.d.=7.24). All participants were assessed on clinical measures of PTSD, depression, anxiety, and alcohol misuse; olfactory identification; neurocognitive measures of dorsolateral prefrontal, lateral prefrontal and mesial temporal functioning; and self-report measures of aggression and impulsivity.

War veterans with PTSD exhibited significant OI deficits (OIDs) compared to controls, despite uncompromised performance on cognitive measures. OIDs remained after covaring for IQ, anxiety, depression and alcohol misuse, and were significant predictors of aggression and impulsivity.

This research contributes to emerging evidence of orbitoprefrontal dysfunction in the pathophysiology underlying PTSD. This is the first study to report OIDs as a predictor of aggression and impulsivity in this clinical population. It prompts further exploration of the potential diagnostic utility of OIDs in the assessment of PTSD. Such measures may help delineate the clinical complexity of PTSD, and support more targeted interventions for individuals with a greater susceptibility to aggressive and impulsive behaviors.

The aim was to determine the prevalence of chronic fatigue syndrome (CFS), chronic fatigue and fibromyalgia in UK military personnel after the Gulf War 1990–1991.

A two-phase cohort study was used. Three randomly selected subsamples identified from a population-based cross-sectional postal survey of over 10 000 current and ex-service UK military personnel (Gulf veterans were those deployed to the Gulf War 1990–1991; non-Gulf veterans were Bosnia peacekeepers 1992–1997 and those on active duty during the Gulf War 1990–1991 but not deployed) were recruited. Their disability status was assessed using the Short Form 36 physical functioning scale; Gulf veterans who reported physical disability (n=111) were compared with non-Gulf (n=133) veterans who reported similar levels of physical disability. Screening for known medical and psychiatric conditions was conducted to exclude medical explanations for disability and symptomatic distress. Standardised criteria for CFS, chronic fatigue and fibromyalgia were used.

Disabled Gulf veterans were more likely to be overweight, have elevated γ-glutamyl transferase levels and screen positive for hypertension. There were no other clinically significant differences in clinical markers for medically explainable conditions. Disabled Gulf veterans were more likely than similarly disabled Bosnia and Era veterans (adjusted odds ratio 7.8, 95% confidence interval 2.5–24.5) to meet the criteria for CFS. Rates for other medically unexplained conditions were not significantly increased.

Symptoms in keeping with CFS account for a significant part of the symptomatic distress in Gulf veterans.

In recent years a close association between anxiety and persecutory ideation has been established, contrary to the traditional division of neurosis and psychosis. Nonetheless, the two experiences are distinct. The aim of this study was to identify factors that distinguish the occurrence of social anxiety and paranoid thoughts in an experimental situation.

Two hundred non-clinical individuals broadly representative of the UK general population were assessed on a range of psychological factors, experienced a neutral virtual reality social environment, and then completed state measures of paranoia and social anxiety. Clustered bivariate logistic regressions were carried out, testing interactions between potential predictors and the type of reaction in virtual reality.

The strongest finding was that the presence of perceptual anomalies increased the risk of paranoid reactions but decreased the risk of social anxiety. Anxiety, depression, worry and interpersonal sensitivity all had similar associations with paranoia and social anxiety.

The study shows that social anxiety and persecutory ideation share many of the same predictive factors. Non-clinical paranoia may be a type of anxious fear. However, perceptual anomalies are a distinct predictor of paranoia. In the context of an individual feeling anxious, the occurrence of odd internal feelings in social situations may lead to delusional ideas through a sense of ‘things not seeming right’. The study illustrates the approach of focusing on experiences such as paranoid thinking rather than diagnoses such as schizophrenia.

Victims of war captivity sometimes suffer from complex post-traumatic stress disorder (PTSD), a unique form of PTSD that entails various alterations in personality. These alterations may involve changes in attachment orientation.

The sample comprised two groups of veterans from the 1973 Yom Kippur War: 103 ex-prisoners of war (ex-POWs) and 106 comparable control veterans. They were assessed at two points in time, 18 years and 30 years after the war.

Ex-POWs suffered from more post-traumatic symptoms than controls at both measurements points and these symptoms increased only among ex-POWs from Time 1 to Time 2. In addition, both attachment anxiety and attachment avoidance increased with time among ex-POWs, whereas they decreased slightly or remained stable among controls. Finally, the increases in attachment anxiety and avoidance were positively associated with the increase in post-traumatic symptoms among both study groups. Further analyses indicated that early PTSD symptoms predicted later attachment better than early attachment predicted later PTSD symptoms.

The results suggest that: (1) complex traumas are implicated in attachment orientations and PTSD symptoms even many years after captivity; (2) there is an increase in attachment insecurities (anxiety, avoidance) and an increase in PTSD symptoms decades after the captivity; (3) and post-traumatic stress symptoms predict attachment orientations better than attachment orientations predict an increase in PTSD symptoms.

Studies of hypothalamic–pituitary–adrenal (HPA) axis function in chronic fatigue syndrome (CFS) point to hypofunction, although there are negative reports. Suggested mechanisms include a reduced hypothalamic or supra-hypothalamic stimulus to the HPA axis and enhanced sensitivity to the negative feedback of glucocorticoids. The aim of the current study was to investigate HPA axis function in CFS with the dexamethasone/corticotropin-releasing factor (Dex/CRF) test, in analogy with research in affective disorders.

Thirty-four well-characterized female CFS patients and 25 healthy control subjects participated in the low-dose Dex/CRF test. Current major depressive episode was an exclusion criterion. History of early-life stress (ELS) was assessed with the Structured Trauma Interview.

Salivary cortisol responses after 0.5 mg Dex were lower in CFS patients than in controls (before 100 μg CRF, p=0.038; after 100 μg CRF, p=0.015). A secondary analysis revealed an influence of early-life stress and of oestrogen intake. After removal of the 10 participants who were taking an oral oestrogen, patients without a history of ELS showed lower cortisol responses than patients with ELS and controls (before CRF, p=0.005; after CRF, p=0.008).

CFS is globally associated with reduced cortisol responses in the combined low-dose Dex/CRF test, but this effect is only clearly present in CFS patients without a history of ELS. This study provides further support for an enhanced glucocorticoid negative feedback and/or a reduced central HPA axis drive in CFS. Furthermore, it demonstrates that ELS is an important variable to consider in CFS research.

There is abundant evidence that schizophrenia is associated with cognitive deficits in childhood. However, previous studies investigating school performance have been inconclusive. Furthermore, there are several biological and social factors that could confound the association. We investigated whether school performance at age 16 is associated with risk of adult schizophrenia and other psychoses in a large national cohort, while controlling for multiple confounders.

Using a national sample of 907 011 individuals born in Sweden between 1973 and 1983, we used Cox regression to assess whether scholastic achievement at age 15–16 predicted hospital admission for psychosis between ages 17 and 31, adjusting for potential confounders.

Poor school performance was associated with increased rates of schizophrenia [hazard ratio (HR) 3.9, 95% confidence interval (CI) 2.8–5.3], schizo-affective disorder (HR 4.2, 95% CI 1.9–9.1) and other psychoses (HR 3.0, 95% CI 2.3–4.0). Receiving the lowest (E) grade was significantly associated with risk for schizophrenia and other psychoses in every school subject. There was no evidence of confounding by migrant status, low birthweight, hypoxia, parental education level or socio-economic group.

Poor school performance across all domains is strongly associated with risk for schizophrenia and other psychoses.

Differential association of risk factors associated with relapse following treatment of first-episode psychosis (FEP) have not been studied adequately, especially for patients treated in specialized early intervention (SEI) services, where some of the usual risk factors may be ameliorated.

Consecutive FEP patients treated in an SEI service over a 4-year period were evaluated for relapse during a 2-year follow-up. Relapse was based on ratings on the Scale for Assessment of Positive Symptoms (SAPS) and weekly ratings based on the Life Chart Schedule (LCS). Predictor variables included gender, duration of untreated psychosis (DUP), total duration of untreated illness (DUI), age of onset, pre-morbid adjustment, co-morbid diagnosis of substance abuse during follow-up and adherence to medication. Univariate analyses were followed by logistic regression for rate of relapse and survival analysis with the Cox proportional-hazards regression model for time to relapse as the dependent variables.

Of the 189 eligible patients, 145 achieved remission of positive symptoms. A high rate of medication adherence (85%) and relatively low relapse rates (29.7%) were observed over the 2-year follow-up. A higher relapse rate was associated with a co-morbid diagnosis of substance abuse assessed during the follow-up period [odds ratio (OR) 2.84, 95% confidence interval (CI) 1.24–6.51]. The length of time to relapse was not associated with any single predictor.

Specialized treatment of substance abuse may be necessary to further reduce risk of relapse even after improving adherence to medication.

Recent studies suggest that purging disorder (PD) may be a common eating disorder that is associated with clinically significant levels of distress and high levels of psychiatric co-morbidity. However, no study has established evidence of disorder-related impairment or whether distress is specifically related to PD rather than to co-morbid disorders.

Three groups of normal-weight women [non-eating disorder controls (n=38), with PD (n=24), and with bulimia nervosa (BN)-purging subtype (n=57)] completed structured clinical interviews and self-report assessments.

Both PD and BN were associated with significant co-morbidity and elevations on indicators of distress and impairment compared to controls. Compared to BN, PD was associated with lower rates of current and lifetime mood disorders but higher rates of current anxiety disorders. Elevated distress and impairment were maintained in PD and BN after controlling for Axis I and Axis II disorders.

PD is associated with elevated distress and impairment and should be considered for inclusion as a provisional disorder in nosological schemes such as the Diagnostic and Statistical Manual to facilitate much-needed research on this clinically significant syndrome.

Identifying risk factors for the development of post-traumatic stress disorder (PTSD) is important for understanding and ultimately preventing the disorder. This study assessed pain shortly after traumatic injury (i.e. peritraumatic pain) as a risk factor for PTSD.

Participants (n=115) were patients admitted to a Level 1 Surgical Trauma Center. Admission to this service reflected a severe physical injury requiring specialized, emergent trauma care. Participants completed a pain questionnaire within 48 h of traumatic injury and a PTSD diagnostic module 4 and 8 months later.

Peritraumatic pain was associated with an increased risk of PTSD, even after controlling for a number of other significant risk factors other than acute stress disorder symptoms. An increase of 0.5 s.d. from the mean in a 0–10 pain rating scale 24–48 h after injury was associated with an increased odds of PTSD at 4 months by more than fivefold, and at 8 months by almost sevenfold. A single item regarding amount of pain at the time of hospital admission correctly classified 65% of participants.

If these findings are replicated in other samples, high levels of peritraumatic pain could be used to identify individuals at elevated risk for PTSD following traumatic injury.

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.

To test whether scores on depression inventories on entry to a longitudinal study predict mental ability over the next 4–16 years.

Associations between scores on the Beck Depression Inventory and on tests of intelligence, vocabulary and memory were analysed in 5070 volunteers aged 49–93 years after differences in prescribed drug consumption, death and drop-out, sex, socio-economic advantage and recruitment cohort effects had also been considered.

On all cognitive tasks Beck scores on entry, even in the range 0–7 indicating differences in above average contentment, affected overall levels of cognitive performance but not rates of age-related cognitive decline suggesting effects of differences in life satisfaction rather than in depression.

A new finding is that, in old age, increments in life satisfaction are associated with better cognitive performance. Implications for interpreting associations between depression inventory scores and cognitive performance in elderly samples are discussed.

In previous studies we suggested that liberal acceptance (LA) represents a fundamental cognitive bias in schizophrenia and may explain why patients are more willing to accept weak response alternatives and display overconfidence in incorrect responses. The aim of the present study was to test a central assumption of the LA account: false alarms in schizophrenia should be particularly increased when the distractor–target resemblance is weak relative to a control group.

Sixty-eight schizophrenia patients were compared to 25 healthy controls on a visual memory task. At encoding, participants studied eight complex displays, each consisting of a unique pairing of four stimulus attributes: symbol, shape, position and colour. At recognition, studied items were presented along with distractors that resembled the targets to varying degrees (i.e. the match between distractors and targets ranged from one to three attributes). Participants were required to make old/new judgements graded for confidence.

The hypotheses were confirmed: false recognition was increased for patients compared to controls for weakly and moderately related distractors only, whereas strong lure items induced similar levels of false recognition for both groups. In accordance with prior research, patients displayed a significantly reduced confidence gap and enhanced knowledge corruption compared to controls. Finally, higher neuroleptic dosage was related to a decreased number of high-confident ratings.

These data assert that LA is a core mechanism contributing to both enhanced acceptance of weakly supported response alternatives and metamemory deficits, and this may be linked to the emergence of positive symptomatology.

To date, there has been no large-scale survey of geriatric depression (GD) involving both rural and urban areas in China using standardized assessment tools and diagnostic criteria. This study aimed to determine the 12-month and lifetime prevalence rates of GD and sociodemographic correlates in urban and rural regions of Beijing, China.

A total of 1601 elderly patients (aged ⩾60 years) were randomly selected and interviewed in Beijing using the Composite International Diagnostic Interview (CIDI 1.0). Basic sociodemographic and clinical data were also collected during the interviews.

The overall 12-month prevalence of GD was 4.33%, and the 12-month prevalence rates for men and women were 2.65% and 5.83% respectively. The overall lifetime prevalence of GD was 7.83%, and lifetime prevalence rates for men and women were 4.65% and 10.66% respectively. Female sex, lower educational level, monthly income, rural abode, and the presence of one or more major medical conditions were associated with increased risk of GD. Of the GD subjects interviewed, 25.2% were receiving some type of treatment, with only 4.7% preferring to seek treatment from mental health professionals.

Although still relatively low by international standards, there is an increasing trend in the prevalence of GD in China. The low percentage of subjects treated for GD is a major public health concern that should be addressed urgently.

The association between personality traits and the first lifetime onset of clinically significant depression has not been studied in older adults.

Experienced psychiatrists conducted interviews and chart reviews at baseline and throughout the 15-year follow-up period. Survival analyses were conducted on the presence/absence of a DSM-III-R mood disorder at follow-up.

There were 59 cases of first lifetime episodes of depression. Analyses showed that Neuroticism [hazard ratio (HR) per one point increase in the Maudsley Personality Inventory (MPI)=1.05, 95% confidence interval (CI) 1.02–1.08] but not Extroversion (HR 1.02, 95% CI 0.97–1.06) amplified risk for mood disorder.

This prospective study on a randomly sampled birth cohort of older adults showed that Neuroticism confers risk for a first lifetime episode of clinically significant depression. Findings have implications for understanding the etiology of late-life depression (LLD) and could also aid in the identification and treatment of people at risk.

Depression and anxiety are highly co-morbid disorders. Two latent trait models have been proposed to explain the nature of the relationship between these disorders. The first posits that depressive and anxiety disorders are both manifestations of a single internalizing factor. The second model, based on a tripartite model proposed by Clark & Watson [Journal of Abnormal Psychology (1991) 100, 316–336], proposes that depressive and anxiety disorders reflect a combination of shared and disorder-specific factors.

We directly compared the two models in a sample of 891 individuals from the Oregon Adolescent Depression Project who participated in up to four diagnostic assessments over approximately 15 years. Structural equation models were used to examine the relationship between depressive and anxiety disorders across different developmental periods (<14, 14–18, 19–23, 24–30 years of age).

The one- and three-factor models were hierarchically related. Thus, a direct comparison between the one- and three-factor models was possible using a χ2 difference test. The result found that the three-factor model fit the data better than the one-factor model.

The three-factor model, positing that depressive and anxiety disorders were caused by a combination of shared and disorder-specific factors, provided a significantly better fit to the data than the one-factor model postulating that a single factor influences the development of both depressive and anxiety disorders.

To investigate the association between nicotine dependence (ND), by cigarette smoking and use of smokeless tobacco (UST), and mental disorders.

Face-to-face surveys (n=43 093) were conducted in the 2001–2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Nicotine use, ND, and mental disorders were assessed using DSM-IV criteria.

UST-ND was associated with a significantly increased likelihood of any anxiety disorder, specific phobia, alcohol abuse and dependence. Consistent with previous findings, cigarette smoking-ND was associated with an increased likelihood of all mental disorders examined. Among those without ND, cigarette smoking was specifically associated with panic attacks and panic disorder; non-dependent UST was not associated with mental disorders.

Our findings suggest that the association between ND and mental disorders is relatively specific to the mode of nicotine administration. Among those who are nicotine dependent, cigarette use is associated with most major psychiatric disorders, whereas UST is associated with dysthymia and specific phobia. Among those who use tobacco but are not nicotine dependent, cigarette use is associated with dysthymia and panic disorder; UST is not associated with any major mood or anxiety disorders. The link between mental disorders and nicotine is complex, and is associated primarily with dependence, and not with non-dependent use.

Although poor neuropsychological test performance is well documented in schizophrenia, how closely it resembles that seen in patients with brain damage in terms of cognitive failures in daily life and stability over time has been little studied.

Thirty patients with chronic schizophrenia, 24 patients with frontal or temporal brain damage and 30 healthy controls were given a battery of memory and executive tests. Carers of the two patient groups also completed questionnaires rating memory and executive failures in daily life. Testing was repeated 6 weeks later.

The schizophrenia and the brain-damaged patients were significantly impaired on most, but not all tests. The degree of carer-rated memory or executive failure was similar in the two groups, but the schizophrenia patients were rated as having significantly more executive failures than memory failures, whereas the brain-damaged patients showed the reverse pattern. Both groups of patients showed similar consistency of performance across sessions.

Neuropsychological impairment in schizophrenia resembles that seen in patients with brain damage, not only in terms of overall severity, but also in terms of stability and the degree to which poor test performance translates into cognitive failures in daily life.

Although generalized anxiety disorder (GAD) and major depressive episode (MDE) are known to be highly co-morbid, little prospective research has examined whether these two disorders predict the subsequent first onset or persistence of the other or the extent to which other predictors explain the time-lagged associations between GAD and MDE.

Data were analyzed from the nationally representative two-wave panel sample of 5001 respondents who participated in the 1990–1992 National Comorbidity Survey (NCS) and the 2001–2003 NCS follow-up survey. Both surveys assessed GAD and MDE. The baseline NCS also assessed three sets of risk factors that are considered here: childhood adversities, parental history of mental-substance disorders, and respondent personality.

Baseline MDE significantly predicted subsequent GAD onset but not persistence. Baseline GAD significantly predicted subsequent MDE onset and persistence. The associations of each disorder with the subsequent onset of the other attenuated with time since onset of the temporally primary disorder, but remained significant for over a decade after this onset. The risk factors predicted onset more than persistence. Meaningful variation was found in the strength and consistency of associations between risk factors and the two disorders. Controls for risk factors did not substantially reduce the net cross-lagged associations of the disorders with each other.

The existence of differences in risk factors for GAD and MDE argues against the view that the two disorders are merely different manifestations of a single underlying internalizing syndrome or that GAD is merely a prodrome, residual, or severity marker of MDE.

Smoking initiation and persistence are clearly associated with factors commonly thought to be environmental in origin, including socio-economic status. However, twin models that incorporate gene–environment correlation and gene×environment interaction have not been applied to elucidate the genetic or environmental role that socio-economic status plays in smoking initiation and nicotine dependence.

Twin structural equation modelling was used to examine gene–environment correlation and gene×environment interaction of one index of socio-economic status, educational attainment, with smoking initiation and nicotine dependence among 5119 monozygotic and 4295 dizygotic male–male Vietnam-era twins from the Vietnam Era Twin Registry, a national registry of twin pairs who served in the military during the Vietnam era.

Educational attainment correlated significantly with smoking initiation (r=−0.27, p<0.001). Additive genetic (p=0.011), shared environment (p=0.002) and unique environment (p=0.027) components contributed to the correlation between educational attainment and smoking initiation. Educational attainment also significantly moderated the variance in smoking initiation (p<0.001), suggestive of gene×environment interaction, although the interaction with the additive genetic, shared environmental and unique environmental components could not be resolved due to multicollinearity. In contrast, educational attainment neither correlated with nor moderated nicotine dependence, once smokers had initiated.

Our study suggests that educational attainment is associated with smoking initiation, in part due to gene–environment correlation and gene×environment interaction. However, once smoking initiation is taken into account, there are no effects – be they gene–environment correlation or gene×environmental interaction – of educational attainment on nicotine dependence.

Impairments in executive functioning (EF) and intelligence quotient (IQ) are frequently observed in children with attention deficit hyperactivity disorder (ADHD). The aim of this paper was twofold: first, to examine whether both domains are viable endophenotypic candidates for ADHD and second to investigate whether deficits in both domains tend to co-segregate within families.

A large family-based design was used, including 238 ADHD families (545 children) and 147 control families (271 children). Inhibition, visuospatial and verbal working memory, and performance and verbal IQ were analysed.

Children with ADHD, and their affected and non-affected siblings were all impaired on the EF measures and verbal IQ (though unimpaired on performance IQ) and all measures correlated between siblings. Correlations and sibling cross-correlations were not significant between EF and IQ, though they were significant between the measures of one domain. Group differences on EF were not explained by group differences on IQ and vice versa. The discrepancy score between EF and IQ correlated between siblings, indicating that siblings resembled each other in their EF–IQ discrepancy instead of having generalized impairments across both domains. Siblings of probands who had an EF but not IQ impairment, showed a comparable disproportionate lower EF score in relation to IQ score. The opposite pattern was not significant.

The results supported the viability of EF and IQ as endophenotypic candidates for ADHD. Most findings support an independent familial segregation of both domains. Within EF, similar familial factors influenced inhibition and working memory. Within IQ, similar familial factors influenced verbal and performance IQ.