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Cognitive behaviour therapy (CBT) is widely used to treat depression. However, CBT is not always available to patients because of a shortage of therapists and long waiting times. Computerized CBT (CCBT) is one of several alternatives currently available to treat patients with depression. Evidence of its clinical effectiveness has led to programs being used increasingly within the UK and elsewhere. However, little information is available regarding the acceptability of CCBT to patients.
A systematic review of sources of information on acceptability to patients of CCBT for depression.
Sources of information on acceptability included: recruitment rates, patient drop-outs and patient-completed questionnaires. We identified 16 studies of CCBT for the treatment of depression that provided at least some information on these sources. Limited information was provided on patient take-up rates and recruitment methods. Drop-out rates were comparable to other forms of treatment. Take-up rates, when reported, were much lower. Six of the 16 studies included specific questions on patient acceptability or satisfaction although information was only provided for those who had completed treatment. Several studies have reported positive expectancies and high satisfaction in routine care CCBT services for those completing treatment.
Trials of CCBT should include more detailed information on patient recruitment methods, drop-out rates and reasons for dropping out. It is important that well-designed surveys and qualitative studies are included alongside trials to determine levels and determinants of patient acceptability.
Although empirical support for the efficacy of cognitive behavioural therapy (CBT) as a treatment for major depressive disorder (MDD) is well established, its mechanism of action is uncertain. In this investigation, we examined evidence for the cognitive mediational model in a randomized control trial involving CBT, interpersonal therapy (IPT) and pharmacotherapy (PHT) in patients with MDD.
One hundred and thirty participants diagnosed with MDD were treated with CBT, IPT or PHT. Participants completed the Hamilton Depression Rating Scale, Beck Depression Inventory – II and Dysfunctional Attitudes Scale prior to and following treatment.
The cognitive mediational model, in which dysfunctional attitudes are proposed to mediate depressive symptom reduction in response to treatment, provided a good fit to the data when contrasting CBT v. IPT, with results supporting a mediational role for dysfunctional attitude change in depressive symptom reduction. The complication model, in which dysfunctional attitudes are proposed to be a consequence of depressive symptom reduction, provided a good fit to the data when contrasting CBT v. PHT, with results supporting a mediational role for depressive symptom reduction in dysfunctional attitude change.
There was no evidence for a mediational role for dysfunctional attitude change in IPT. Changes in dysfunctional attitudes accompanied both CBT and PHT; however, empirical evidence suggests that the role of attitudes in treatment outcome may differ between these two treatments.
The overlap between anxiety and major depressive disorder (MDD), the increased risk for depression and anxiety in offspring of depressed parents, the sequence of onset with anxiety preceding MDD, and anxiety as a predictor of depression are well established. The specificity of anxiety disorders in these relationships is unclear. This study, using a longitudinal high-risk design, examined whether anxiety disorders associated with the emotions fear and anxiety mediate the association between parental and offspring depression.
Two hundred and twenty-four second-generation and 155 third-generation descendants at high and low risk for depression because of MDD in the first generation were interviewed over 20 years. Probit and Cox proportional hazard models were fitted with generation 2 (G2) or G3 depression as the outcome and parental MDD as the predictor. In G2 and G3, fear- (phobia or panic) and anxiety-related [overanxious or generalized anxiety disorder (GAD)] disorders were examined as potential mediators of increased risk for offspring depression, due to parental MDD.
In G2, fear-related disorders met criteria for mediating the association between parental MDD and offspring MDD whereas anxiety-related disorders did not. These results were consistent, regardless of the analytic methods used. Further investigation of the mediating effect of fear-related disorders by age of onset of offspring MDD suggests that the mediating effect occurs primarily in adolescent onset MDD. The results for G3 appear to follow similar patterns.
These findings support the separation of anxiety disorders into at least two distinct forms, particularly when examining their role in the etiology of depression.
The association between life events and anxious depression might be due to causality or to gene–environment correlation. We examined unidirectional and reciprocal causality and a gene–environment correlation model, in which genes that influence the vulnerability for anxious depression also increase the risk of exposure to life events. The effect of genes that influence environmental exposure might be mediated through personality and we therefore also examined the association between life events and personality (neuroticism and extraversion).
Information on life events, anxious depression, neuroticism and extraversion was collected in 5782 monozygotic (MZ) and dizygotic (DZ) twins who participated in a longitudinal survey study of the Netherlands Twin Register. To examine causality, data were analysed longitudinally. To examine gene–environment correlation, the co-twin control method was used.
Anxious depression and, to a lesser extent, neuroticism scores increased after exposure to life events. Anxious depression and neuroticism also predicted the experience of life events. Prospectively, extraversion was not associated with life events. Anxious depression, neuroticism and extraversion scores did not differ between the non-exposed subjects of MZ and DZ twin pairs and unrelated subjects discordant for life events.
Our findings suggest that reciprocal causation explains the relationship between life events and anxious depression and between life events and neuroticism. Extraversion is not related to life events. No evidence was found for gene–environment correlation, i.e. the genes that influence anxious depression, neuroticism or extraversion do not overlap with the genes that increase the risk of exposure to life events.
Little is known about the pattern of genetic and environmental influences on symptoms of anxiety and depression (SxAnxDep) from childhood to early adulthood.
Parental- and self-reported levels of SxAnxDep were assessed at ages 8–9, 13–14, 16–17 and 19–20 years in 2508 twins from the Swedish Twin Study of Child and Adolescent Development (TCHAD). Analysis conducted using the Mx program included SxAnxDep by parental and self-report.
The best-fit model revealed one genetic risk factor for SxAnxDep acting at ages 8–9, 13–14, 16–17 and 19–20, and new sets of genetic risk factors ‘coming on line’ in early adolescence, late adolescence and early adulthood. Together, these genetic factors were very strong influences on the levels of SxAnxDep reported in common by parents and twins with heritability estimates, correcting for rater- and time-specific effects, ranging from 72% to 89%. The first genetic factor, which accounted for 72% of the variance in SxAnxDep at ages 8–9, attenuated sharply in influence, accounting for only 12% of the variance by ages 19–20. No evidence was found for shared environmental influences. Although not statistically significant, the correlation between genetic risk factors for SxAnxDep in males and females declined with advancing age.
Genetic effects on SxAnxDep are developmentally dynamic from middle childhood to young adulthood, demonstrating both genetic innovation and genetic attenuation. The attenuation might explain the low levels of continuity observed for anxiety and depressive disorders from childhood to adulthood. Differences in genetic risk factors for SxAnxDep in males and females may increase during development.
A tendency to make hasty decisions on probabilistic reasoning tasks and a difficulty attributing mental states to others are key cognitive features of persecutory delusions (PDs) in the context of schizophrenia. This study examines whether these same psychological anomalies characterize PDs when they present in the context of psychotic depression.
Performance on measures of probabilistic reasoning and theory of mind (ToM) was examined in five subgroups differing in diagnostic category and current illness status.
The tendency to draw hasty decisions in probabilistic settings and poor ToM tested using story format feature in PDs irrespective of diagnosis. Furthermore, performance on the ToM story task correlated with the degree of distress caused by and preoccupation with the current PDs in the currently deluded groups. By contrast, performance on the non-verbal ToM task appears to be more sensitive to diagnosis, as patients with schizophrenia spectrum disorders perform worse on this task than those with depression irrespective of the presence of PDs.
The psychological anomalies associated with PDs examined here are transdiagnostic but different measures of ToM may be more or less sensitive to indices of severity of the PDs, diagnosis and trait- or state-related cognitive effects.
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.
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.
In this meta-analysis, we investigated whether response inhibition is sensitive to attention deficit hyperactivity disorder (ADHD) status and, if so, what influence maturation has on this attentional symptom of ADHD.
We examined 25 studies that reported data on the Stroop color word test in children and adults with ADHD and in age-matched controls; average ages ranged from 9 to 41 years. We utilized a hierarchical approach to analyze the strength of the Stroop effect and whether the effect varies as a function of age. Additionally, we assessed potential differences in maturation rates based on reaction time (RT) of color and color-word conditions.
First, we found that the relationship between color-word and color RT was multiplicative, and the slope of this function (the ratio of color-word RT over color RT) was identical across age groups and ADHD status. Second, we found that although ADHD individuals were on average 1.14 times slower than age-matched controls in both the color and the color-word condition, the maturation rate was identical for both groups.
The results from this analysis indicate that the Stroop interference effect is not larger in ADHD individuals than in age-matched controls. Further, we did not find evidence for differential maturation rates for persons with ADHD and the control groups. The Stroop interference effect appears to be immune to age, regardless of ADHD status.
The personality disorders (PDs) in the ‘dramatic’ cluster B [antisocial (ASPD), histrionic (HPD), narcissistic (NPD) and borderline (BPD)] demonstrate co-morbidity. However, the degree to which genetic and/or environmental factors influence their co-occurrence is not known and, with the exception of ASPD, the relative impact of genetic and environmental risk factors on liability to the cluster B PDs has not been conclusively established.
PD traits were assessed in 1386 Norwegian twin pairs between the age of 19 and 35 years using the Structured Interview for DSM-IV Personality Disorders (SIDP-IV). Using the statistical package Mx, multivariate twin models were fitted to dimensional representations of the PDs.
The best-fitting model, which did not include sex or shared family environment effects, included common genetic and environmental factors influencing all four dramatic PD traits, and factors influencing only ASPD and BPD. Heritability was estimated at 38% for ASPD traits, 31% for HPD traits, 24% for NPD traits and 35% for BPD traits. BPD traits had the lowest and ASPD traits the highest disorder-specific genetic variance.
The frequently observed co-morbidity between cluster B PDs results from both common genetic and environmental influences. Etiologically, cluster B has a ‘substructure’ in which ASPD and BPD are more closely related to each other than to the other cluster B disorders.
Both mental disorders and personality characteristics are associated with impaired work functioning, but these determinants have not yet been studied together. The aim of this paper is to examine the impairing effects that mental disorders and personality characteristics (i.e. neuroticism, locus of control and self-esteem) have on work functioning.
Data for a representative sample of 3570 working people were derived from the first two waves of the Netherlands Mental Health Survey and Incidence Study (NEMESIS), a prospective cohort study in the Dutch adult population.
Higher neuroticism, more external locus of control and lower self-esteem were each significantly associated with subsequent impairment in work functioning, independently of any effects from mental disorders. Associations between mental disorders and subsequent work impairment disappeared once personality traits were taken into account. Personality traits did not moderate the relationships between mental disorders and work functioning.
Working people with vulnerable personalities have a greater risk of impaired work functioning, independent of the risk from any mental disorder they may have.
Prior studies in the USA have reported higher rates of mental disorders among
persons with arthritis but no cross-national studies have been conducted. In
this study the prevalence of specific mental disorders among persons with
arthritis was estimated and their association with arthritis across diverse
The study was a series of cross-sectional population sample surveys. Eighteen
population surveys of household-residing adults were carried out in 17
countries in different regions of the world. Most were carried out between
2001 and 2002, but others were completed as late as 2007. Mental disorders
were assessed with the World Health Organization (WHO)
World Mental Health–Composite International Diagnostic Interview
(WMH-CIDI). Arthritis was ascertained by self-report.
The association of anxiety disorders, mood disorders and alcohol use
disorders with arthritis was assessed, controlling for age and sex.
Prevalence rates for specific mental disorders among persons with and
without arthritis were calculated and odds ratios
(ORs) with 95% confidence intervals were
used to estimate the association.
After adjusting for age and sex, specific mood and anxiety disorders occurred
among persons with arthritis at higher rates than among persons without
arthritis. Alcohol abuse/dependence showed a weaker and less
consistent association with arthritis. The pooled estimates of the age- and
sex-adjusted ORs were about 1.9 for mood disorders and for anxiety disorders
and about 1.5 for alcohol abuse/dependence among persons with
versus without arthritis. The pattern
of association between specific mood and anxiety disorders and arthritis was
similar across countries.
Mood and anxiety disorders occur with greater frequency among persons with
arthritis than those without arthritis across diverse countries. The
strength of association of specific mood and anxiety disorders with
arthritis was generally consistent across disorders and across
Recent evidence suggests that dopamine (DA) agonist-induced disruption of prepulse inhibition (PPI) depends on basal PPI values, in a manner that suggests an inverted U-shaped relationship between PPI and prefrontal DA levels. This is the first study to examine possible genetic determinants of PPI and the catechol O-methyltransferase (COMT) Val158Met polymorphism, the main catabolic pathway of released DA in the prefrontal cortex (PFC).
PPI was measured in 93 healthy males presented with 75-dB and 85-dB prepulses at 60-ms and 120-ms prepulse–pulse intervals. Subjects were grouped according to their COMT status into a Val/Val, a Val/Met and a Met/Met group.
ANOVAs showed that at all prepulse and interval conditions, Val/Val individuals had the lowest PPI, Met/Met the highest, and Val/Met were intermediate.
These results suggest that PPI is regulated by DA neurotransmission in the PFC and its levels depend on the COMT Val158Met gene polymorphism. These findings enhance the value of the PPI paradigm in examining individual variability of early information processing in healthy subjects and psychiatric disorders associated with changes in PFC DA activity and attentional deficits such as schizophrenia.
Physical morbidity is a potent risk factor for depression onset and clearly increases with age, yet prior research has often found depressive disorders to decrease with age. This study tests the possibility that the relationship between age and mental disorders differs as a function of physical co-morbidity.
Eighteen general population surveys were carried out among household-residing adults as part of the World Mental Health (WMH) surveys initiative (n=42 697). DSM-IV disorders were assessed using face-to-face interviews with the Composite International Diagnostic Interview (CIDI 3.0). The effect of age was estimated for 12-month depressive and/or anxiety disorders with and without physical or pain co-morbidity, and for physical and/or pain conditions without mental co-morbidity.
Depressive and anxiety disorders decreased with age, a result that cannot be explained by organic exclusion criteria. No significant difference was found in the relationship between mental disorders and age as a function of physical/pain co-morbidity. The majority of older persons have chronic physical or pain conditions without co-morbid mental disorders; by contrast, the majority of those with mental disorders have physical/pain co-morbidity, particularly among the older age groups.
CIDI-diagnosed depressive and anxiety disorders in the general population decrease with age, despite greatly increasing physical morbidity with age. Physical morbidity among persons with mental disorder is the norm, particularly in older populations. Health professionals, including mental health professionals, need to address barriers to the management of physical co-morbidity among those with mental disorders.