Although mental disorders have been shown to predict subsequent substance disorders, it is not known whether substance disorders could be cost-effectively prevented by large-scale interventions aimed at prior mental disorders. Although experimental intervention is the only way to resolve this uncertainty, a logically prior question is whether the associations of mental disorders with subsequent substance disorders are strong enough to justify mounting such an intervention. We investigated this question in this study using simulations to estimate the number of substance disorders that might be prevented under several hypothetical intervention scenarios focused on mental disorders.

Data came from the National Comorbidity Survey Replication (NCS-R), a nationally representative US household survey that retrospectively assessed lifetime history and age of onset of DSM-IV mental and substance disorders. Survival analysis using retrospective age-of-onset reports was used to estimate associations of mental disorders with subsequent substance dependence. Simulations based on the models estimated effect sizes in several hypothetical intervention scenarios.

Although successful intervention aimed at mental disorders might prevent some proportion of substance dependence, the number of cases of mental disorder that would have to be treated to prevent a single case of substance dependence is estimated to be so high that this would not be a cost-effective way to prevent substance dependence (in the range 76–177 for anxiety-mood disorders and 40–47 for externalizing disorders).

Treatment of prior mental disorders would not be a cost-effective way to prevent substance dependence. However, prevention of substance dependence might be considered an important secondary outcome of interventions for early-onset mental disorders.

Previous research indicates that alcohol and drug dependence constitute aspects of a general vulnerability to externalizing disorders that accounts for much of the parent-offspring resemblance for these and related disorders. This study examined how adolescent offspring risk for externalizing psychopathology varies with respect to parental alcoholism and illicit drug dependence.

Data from the Minnesota Twin Family Study, a community-based investigation of adolescents (age 17 years, n=1252) and their parents, were used. Lifetime diagnoses of alcohol and drug dependence (among both parents and offspring) and offspring attention deficit hyperactivity disorder, oppositional defiant disorder, conduct disorder, adult antisocial behavior, and nicotine dependence were assessed via structured interviews.

Parental alcohol dependence and parental drug dependence were similarly associated with increased risk for nearly all offspring disorders, with offspring of alcohol and drug-dependent parents having approximately 2–3 times the odds for developing a disorder by late adolescence compared to low-risk offspring. Compared to parental dependence on other illicit drugs, parental cannabis dependence was associated with weaker increased risk for offspring externalizing disorders.

Both parental alcohol and drug dependence are independently associated with an increased risk for a broad range of externalizing psychopathology among late-adolescent offspring.

Impairments in executive cognitive control, including a reduced ability to inhibit prepotent responses, have been reported in autism spectrum disorders (ASD). These deficits may underlie patterns of repetitive behaviors associated with the disorder.

Eighteen individuals with ASD and 15 age- and IQ-matched healthy individuals performed an antisaccade task and a visually guided saccade control task, each with gap and overlap conditions. Measures of repetitive behaviors were obtained using the Autism Diagnostic Inventory – Revised (ADI-R) and examined in relation to neurocognitive task performance.

Individuals with an ASD showed increased rates of prosaccade errors (failures to inhibit prepotent responses) on the antisaccade task regardless of task condition (gap/overlap). Prosaccade error rates were associated with the level of higher-order (e.g. compulsions, preoccupations) but not sensorimotor repetitive behaviors in ASD.

Neurocognitive disturbances in voluntary behavioral control suggest that alterations in frontostriatal systems contribute to higher-order repetitive behaviors in ASD.

It has been demonstrated that the mechanism of cognitive memory control in humans is sustained by the hippocampus and prefrontal cortices, which have been found to be structurally and functionally abnormal in borderline personality disorder (BPD). We investigated whether the memory control mechanism is affected in BPD.

Nineteen Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV BPD patients and 19 matched healthy controls (HC) performed a specific think/no-think paradigm exploring the capacity of remembering and suppressing pair of words previously learned. After the think–no think phase, the second member of each word pair has to be remembered either when subjects are presented with the cue word showed at the beginning of the test (Same Probe Test; SPT) or when they are presented with an extra-list categorical word (Independent Probe Test; IPT). We evaluated the effect of suppression and of retrieval activity on later retention of words.

Both on the SPT and on the IPT, HC showed the expected improvement of memory retrieval on to-be-remembered words, unlike BPD patients. On the SPT, HC, but not BPD patients, correctly recalled significantly more words among remembered words (RW) than among suppressed words (SW). Similarly to HC, subjects with BPD without a history of childhood abuse showed a significantly higher percentage of correctly recalled words among RW than among SW.

The mechanism of active retrieval of memories and of improvement through repetition is impaired in BPD, particularly in those who experienced traumatic experiences. This impairment might play an important role, possibly resulting in the emergence of unwanted memories and dissociative symptoms.

Communication disturbance (thought disorder) is a central feature of schizophrenia that predicts poor functioning. We investigated the hypothesis that memory and attention deficits interact with beliefs about the gravity of being rejected (i.e. evaluation sensitivity) to produce the symptoms of communication disorder.

Seventy-four individuals diagnosed with schizophrenia or schizo-affective disorder completed a battery of tests assessing neurocognition (attention, working and verbal memory, abstraction), symptomatology (positive, negative and affective), functioning, and dysfunctional beliefs.

Patients with communication deviance (n=33) performed more poorly on the neurocognitive tests and reported a greater degree of sensitivity to rejection than patients with no thought disorder (n=41). In a logistic regression analysis, evaluation sensitivity moderated the relationship between cognitive impairment and the presence of communication disorder. This finding was independent of hallucinations, delusions, negative symptoms, depression and anxiety.

We propose that negative appraisals about acceptance instigate communication anomalies in individuals with a pre-existing diathesis for imperfect speech production.

Millions of people seek emergency department (ED) care for injuries each year, the majority for minor injuries. Little is known about the effect of psychiatric co-morbid disorders that emerge after minor injury on functional recovery. This study examined the effect of post-injury depression on return to pre-injury levels of function.

This was a longitudinal cohort study with follow-up at 3, 6 and 12 months post-injury: 275 adults were randomly selected from those presenting to the ED with minor injury; 248 were retained over the post-injury year. Function was measured with the Functional Status Questionnaire (FSQ). Psychiatric disorders were diagnosed using the Structured Clinical Interview for DSM-IV-TR disorders (SCID).

During the post-injury year, 18.1% [95% confidence interval (CI) 13.3–22.9] were diagnosed with depression. Adjusting for clinical and demographic covariates, the depressed group was less likely to return to pre-injury levels of activities of daily living [odds ratio (OR) 8.37, 95% CI 3.78–18.53] and instrumental activities of daily living (OR 3.25, 95% CI 1.44–7.31), less likely to return to pre-injury work status (OR 2.37, 95% CI 1.04–5.38), and more likely to spend days in bed because of health (OR 2.41, 95% CI 1.15–5.07).

Depression was the most frequent psychiatric diagnosis in the year after minor injury requiring emergency care. Individuals with depression did not return to pre-injury levels of function during the post-injury year.

Children with attention deficit/hyperactivity disorder (ADHD) are at risk of negative academic outcomes. However, relatively few studies in this area have been based on long-term longitudinal designs and community-based settings. This study examined the link between childhood hyperactivity-inattention symptoms (HI-s) and subsequent academic achievement in a community setting, controlling for other behavioural symptoms, socio-economic status (SES) and environmental factors at baseline.

The sample consisted of 1264 subjects (aged 12 to 26 years at follow-up) recruited from the longitudinal GAZEL Youth study. Psychopathology, environmental variables and academic outcomes were measured through self-reports. Multivariate modelling was performed to evaluate the effects of childhood HI-s and other risk factors on academic achievement 8 years later.

HI-s independently predicted grade retention [adjusted odds ratio (OR) 3.58, 95% confidence interval (CI) 2.38–5.39], failure to graduate from secondary school (adjusted OR 2.41, 95% CI 1.43–4.05), obtaining a lower-level diploma (adjusted OR 3.00, 95% CI 1.84–4.89), and lower academic performance. These results remained significant even after accounting for school difficulties at baseline. Negative academic outcomes were also significantly associated with childhood symptoms of conduct disorder (CD), even after accounting for adjustment variables.

This longitudinal survey replicates, in a general population-based setting, the finding of a link between HI-s and negative academic outcomes.

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.

Several prior reports have found that some young children with autism spectrum disorder [ASD; including autism and Asperger's syndrome and pervasive developmental disorder – not otherwise specified (PDD-NOS)] have a significant increase in head size and brain weight. However, the findings from older children and adults with ASD are inconsistent. This may reflect the relatively small sample sizes that were studied, clinical heterogeneity, or age-related brain differences.

Hence, we measured head size (intracranial volume), and the bulk volume of ventricular and peripheral cerebrospinal fluid (CSF), lobar brain, and cerebellum in 114 people with ASD and 60 controls aged between 18 and 58 years. The ASD sample included 80 people with Asperger's syndrome, 28 with autism and six with PDD-NOS.

There was no significant between-group difference in head and/or lobar brain matter volume. However, compared with controls, each ASD subgroup had a significantly smaller cerebellar volume, and a significantly larger volume of peripheral CSF.

Within ASD adults, the bulk volume of cerebellum is reduced irrespective of diagnostic subcategory. Also the significant increase in peripheral CSF may reflect differences in cortical maturation and/or ageing.

Diagnosing attention deficit hyperactivity disorder (ADHD) in adults is difficult when diagnosticians cannot establish onset prior to the DSM-IV criterion of age 7 or if the number of symptoms does not achieve the DSM threshold for diagnosis. Previous work has assessed the validity of such diagnoses based on psychiatric co-morbidity, family history and neuropsychological functions but none of these studies have used personality as a validation criterion.

We compared four groups of adults: (1) full ADHD subjects who met all DSM-IV criteria for childhood-onset ADHD; (2) late-onset subjects who met all criteria except the age at onset criterion, (3) subthreshold subjects who did not meet full symptom criteria and (4) non-ADHD subjects who did not meet any of the above criteria. Diagnoses were made by using the Structured Clinical Interview for DSM-IV (SCID) and the Temperament and Character Inventory (TCI) was used to assess personality traits.

We found that full ADHD and late-onset ADHD showed similar personality profiles with significant deviations on all TCI scales except reward dependence and self-transcendence. By contrast, subthreshold cases only showed deviations on novelty seeking and self-directiveness.

These data call into question the stringent age of onset of ADHD symptom criteria for adults when making retrospective diagnoses of ADHD. Subthreshold ADHD seems to be a milder form of the disorder that is consistent with dimensional views of the disorder.

Studies of patients with anorexia nervosa (AN) have shown that they do not perform well in set-shifting tasks but little is known about the neurobiological correlates of this aspect of executive function. The aim of this study was to measure serum brain-derived neurotrophic factor (BDNF) and to establish whether set-shifting difficulties are present in people with current AN and in those recovered from AN, and whether serum BDNF concentrations are correlated with set-shifting ability.

Serum BDNF concentrations were measured in 29 women with current AN (AN group), 18 women who had recovered from AN (ANRec group) and 28 age-matched healthy controls (HC group). Set-shifting was measured using the Wisconsin Card Sorting Test (WCST). Eating-related psychopathology and depressive, anxiety and obsessive–compulsive symptomatology were evaluated using the Eating Disorder Examination Questionnaire (EDEQ), the Hospital Anxiety and Depression Scale (HADS), and the Maudsley Obsessive–Compulsive Inventory (MOCI) respectively.

Serum BDNF concentrations (mean±s.d.) were significantly lower in the AN group (11.7±4.9 ng/ml) compared to the HC group (15.1±5.5 ng/ml, p=0.04) and also compared to the ANRec group (17.6±4.8 ng/ml, p=0.001). The AN group made significantly more errors (total and perseverative) in the WCST relative to the HC group. There was no significant correlation between serum BDNF concentrations and performance on the WCST.

Serum BDNF may be a biological marker for eating-related psychopathology and of recovery in AN. Longitudinal studies are needed to explore possible associations between serum BDNF concentrations, illness and recovery and neuropsychological traits.

This study attempted to longitudinally investigate neuropsychological function, illness representations, self-esteem, mood and quality of life (QoL) in individuals with chronic fatigue syndrome (CFS) and compared them with both healthy participants and a clinical comparison group of individuals with autoimmune thyroid disease (AITD).

Neuropsychological evaluation was administered at two time points, five weeks apart. Twenty-one individuals with CFS, 20 individuals with AITD and 21 healthy participants were matched for age, pre-morbid intelligence, education level and socio-economic status (SES). All groups also completed measures of illness perceptions, mood, self-esteem and QoL at both time points.

The CFS group showed significantly greater impairment on measures of immediate and delayed memory, attention and visuo-constructional ability, and reported significantly higher levels of anxiety and depression. After controlling for the effects of mood, the CFS group still demonstrated significant impairment in attention. The CFS group also reported significantly lower self-reported QoL than the AITD and healthy participants. In terms of illness perceptions, the AITD group believed that their condition would last longer, that they had more treatment control over their condition, and reported less concern than the CFS group.

These results suggest that the primary cognitive impairment in CFS is attention and that this is not secondary to affective status. The lower treatment control perceptions and greater illness concerns that CFS patients report may be causally related to their affective status.

The ability to decode emotional information from facial expressions is crucial for successful social interaction. Borderline personality disorder (BPD) is characterized by serious problems in interpersonal relationships and emotional functioning. Empirical research on facial emotion recognition in BPD has been sparsely published and results are inconsistent. To specify emotion recognition deficits in BPD more closely, the present study implemented two emotion recognition tasks differing in response format.

Nineteen patients with BPD and 19 healthy subjects were asked to evaluate the emotional content of visually presented stimuli (emotional and neutral faces). The first task, the Fear Anger Neutral (FAN) Test, required a rapid discrimination between negative or neutral facial expressions whereas in the second task, the Emotion Recognition (ER) Test, a precise decision regarding default emotions (sadness, happiness, anger, fear and neutral) had to be achieved without a time limit.

In comparison to healthy subjects, BPD patients showed a deficit in emotion recognition only in the fast discrimination of negative and neutral facial expressions (FAN Test). Consistent with earlier findings, patients demonstrated a negative bias in the evaluation of neutral facial expressions. When processing time was unlimited (ER Test), BPD patients performed as well as healthy subjects in the recognition of specific emotions. In addition, an association between performance in the fast discrimination task (FAN Test) and post-traumatic stress disorder (PTSD) co-morbidity was indicated.

Our data suggest a selective deficit of BPD patients in rapid and direct discrimination of negative and neutral emotional expressions that may underlie difficulties in social interactions.

It is unclear whether Axis II psychopathology or co-morbid clinical syndromes result in the treatment-seeking behaviour and social impairment of patients with borderline personality disorder (BPD). This study examined the independent associations between social functioning and service use and Axis I and Axis II disorders in persons with BPD in the national household population of Britain.

The study was a cross-sectional survey of adults aged 16–74 years in households (n=8397). Data included self-reported consultations with health-care professionals and behavioural problems. Diagnosis was determined by computer-assisted interviews. Analyses included logistic regression adjusting for demography, co-morbid Axis I clinical syndromes and other Axis II disorders.

Consultation in the past year was reported by 57.5% of persons with BPD but only 13.4% reported lifetime psychiatric admission. BPD was not independently associated with impaired functioning but was associated with co-morbid psychotic, depressive and anxiety disorders. Only general practitioners (GPs) were consulted for problems independently due to BPD.

Functional effects of BPD are mediated through co-morbid clinical syndromes, not Axis II psychopathology. A subgroup do not have co-morbid disorders or seek treatment, and are high functioning.

We aimed to compare the rate of cognitive decline in patients with early and late onset Alzheimer's disease (AD) and to investigate the potentially modifying influence of the apolipoprotein E (APOE) genotype.

We included 99 patients with early onset AD (age ⩽65 years) and 192 patients with late onset AD (age >65 years) who had at least two scores on the Mini-Mental State Examination (MMSE) (range 2–14) obtained at least 1 year apart. Linear mixed models were performed to investigate the rate of cognitive decline dependent on age at onset (AAO) and APOE genotype.

The mean (s.d.) age for patients with early onset AD was 57.7 (4.5) years, and 74.5 (5.1) years for patients with late onset AD. AAO was not associated with baseline MMSE [β (s.e.)=0.8 (0.5), p=0.14]. However, patients with early onset showed a faster decline on the MMSE [β (s.e.)=2.4 (0.1) points/year] than those with late onset [β (s.e.)=1.7 (0.1) points/year, p=0.00]. After stratification according to APOE genotype, APOE ε4 non-carriers with early onset showed faster cognitive decline than non-carriers with late onset [2.4 (0.3) v. 1.3 (0.3) points/year, p=0.01]. In APOE ε4 carriers, no difference in rate of cognitive decline was found between patients with early and late onset [β (s.e.)=0.2 (0.2), p=0.47].

Patients with early onset AD show more rapid cognitive decline than patients with late onset, suggesting that early onset AD follows a more aggressive course. Furthermore, this effect seems to be most prominent in patients with early onset who do not carry the genetic APOE ε4 risk factor for AD.

Mild traumatic brain injury (mTBI) is being claimed as the ‘signature’ injury of the Iraq war, and is believed to be the cause of long-term symptomatic ill health (post-concussional syndrome; PCS) in an unknown proportion of military personnel.

We analysed cross-sectional data from a large, randomly selected cohort of UK military personnel deployed to Iraq (n=5869). Two markers of PCS were generated: ‘PCS symptoms’ (indicating the presence of mTBI-related symptoms: none, 1–2, 3+) and ‘PCS symptom severity’ (indicating the presence of mTBI-related symptoms at either a moderate or severe level of severity: none, 1–2, 3+).

PCS symptoms and PCS symptom severity were associated with self-reported exposure to blast whilst in a combat zone. However, the same symptoms were also associated with other in-theatre exposures such as potential exposure to depleted uranium and aiding the wounded. Strong associations were apparent between having PCS symptoms and other health outcomes, in particular being a post-traumatic stress disorder or General Health Questionnaire case.

PCS symptoms are common and some are related to exposures such as blast injury. However, this association is not specific, and the same symptom complex is also related to numerous other risk factors and exposures. Post-deployment screening for PCS and/or mTBI in the absence of contemporaneous recording of exposure is likely to be fraught with hazards.

Previous research has found that many patients with anorexia nervosa (AN) are unable to maintain normal weight after weight restoration. The objective of this study was to identify variables that predicted successful weight maintenance among weight-restored AN patients.

Ninety-three patients with AN treated at two sites (Toronto and New York) through in-patient or partial hospitalization achieved a minimally normal weight and were then randomly assigned to receive fluoxetine or placebo along with cognitive behavioral therapy (CBT) for 1 year. Clinical, demographic and psychometric variables were assessed after weight restoration prior to randomization and putative predictors of successful weight maintenance at 6 and 12 months were examined.

The most powerful predictors of weight maintenance at 6 and 12 months following weight restoration were pre-randomization body mass index (BMI) and the rate of weight loss in the first 28 days following randomization. Higher BMI and lower rate of weight loss were associated with greater likelihood of maintaining a normal BMI at 6 and 12 months. An additional predictor of weight maintenance was site; patients in Toronto fared better than those in New York.

This study found that the best predictors of weight maintenance in weight-restored AN patients over 6 and 12 months were the level of weight restoration at the conclusion of acute treatment and the avoidance of weight loss immediately following intensive treatment. These results suggest that outcome might be improved by achieving a higher BMI during structured treatment programs and on preventing weight loss immediately following discharge from such programs.