We investigated whether women who participated in a household survey in England were more likely to screen positive for possible generalised anxiety disorder and depression during and after menopause. We used logistic regression in secondary cross-sectional analyses of 1413 participants from the 2014 Adult Psychiatric Morbidity Survey data, adjusting for potential confounders (including age, deprivation score and chronic disease).

We found that participants who were post-menopausal were more likely to screen positive for possible depression compared with participants who were pre-menopausal (3.9% v. 1.7%; adjusted odds ratio 3.91, 95% CI 1.23–12.46), but there was no association with perimenopause. We found no evidence of an association between menopausal stage and possible generalised anxiety disorder or symptom score. Clinicians should be aware of the association between menopause and depression, to best support women. Future research could focus on to what extent associations are driven by somatic features, and how this might be modified.

Since its inclusion in the DSM-III, various theories and treatment approaches have been developed for generalised anxiety disorder (GAD). Aaron T. Beck was the first to offer a cognitive conceptualisation of GAD in Anxiety Disorders and Phobias: A Cognitive Perspective. This original cognitive model of GAD was initially found to be promising in treating GAD but has not been developed further. Other theoretical models and treatments of GAD have gained more research attention, such as the Intolerance of Uncertainty model and Meta-Cognitive model. This article offers a brief overview of multiple theories and treatment approaches of GAD followed by an extensive discussion about the original cognitive model and a revised cognitive model of GAD in the Beckian tradition. Specifically, this paper describes how known key psychological maintenance factors of anxiety disorders, i.e. threat beliefs, safety-seeking behaviours and selective attention, can be used to conceptualise the experience of people with GAD and guide treatment. This is done with theoretical discussion as well as clinical examples. Finally, the paper offers suggestions for key ingredients to be included in cognitive therapy for GAD and future directions for research.

Clinical assessments of sleep and subjective state upon waking were performed in normal controls and patients with generalised anxiety disorder, panic disorder, obsessive-compulsive disorder, primary dysthymia and major depression. Subjects were selected according to DSM-III-R criteria. As compared to normal controls, patients with generalised anxiety, dysthymia and major depression exhibit pervasive and intense complaints of insomnia, and no clear distinctions can be drawn among these groups. Patients with panic disorder do not differ from normal controls, whereas obsessive compulsive patients present limited sleep symptoms. These findings suggest that subjective sleep variables are relevant for the diagnostic discrimination of panic and obsessive-compulsive disorders.

This randomised, double-blind, placebo-controlled study compared the efficacy of venlafaxine XR (75 or 150 mg/d) with diazepam (15 mg/d) over an 8-week treatment period in 540 non-depressed outpatients with generalised anxiety disorder (GAD). At week 8, significant improvements from baseline were observed in the venlafaxine XR, diazepam and placebo groups. Although these improvements were higher in the first two groups than in the placebo group for each of the primary efficacy variables (Hamilton Rating Scale for Anxiety (HAM-A) total, HAM-A psychic anxiety factor, Hospital Anxiety and Depression Scale (HAD) anxiety sub-scale and Clinical Global Impression (CGI) improvement), there were no statistically significant differences between groups. These non-positive results were thought to be due to the very high placebo response observed in some centres. To understand the variability of the study, a secondary preplanned analysis was performed. This involved sub-dividing the study centres according to their ability to detect a two-point mean difference between diazepam and placebo at week 8 on the HAM-A total score. Centres able to show such a difference were termed verum-sensitive. Improvements from baseline to week 8 in venlafaxine XR-treated patients from verum-sensitive centres were significantly greater than in placebo on each of the primary efficacy measures (P ≤ 0.05). This suggests that those centres able to detect an anxiolytic effect of diazepam were also able to detect an anxiolytic effect of venlafaxine XR. Significant differences in baseline demographics, rates of adverse event reporting and rates of patient discontinuations were noted between patients enrolled at verum-sensitive and verum-insensitive sites. These results reflect the importance of study centre selection in accurately determining efficacy in placebo-controlled trials.

The objective of this analysis was to evaluate the short- (8 weeks) and long-term (24 weeks) efficacy of three fixed doses of venlafaxine extended release (ER) and placebo on the social adjustment of patients with generalised anxiety disorder (GAD). We analysed data from 544 outpatients who participated in a 24-week, double-blind, multicentre, parallel-group, placebo-controlled study conducted at 55 centres in five countries. All patients meet the DSM-IV criteria for GAD and were randomly assigned to receive venlafaxine ER 37.5, 75, and 150 mg or matched placebo administered orally once daily. Social adjustment was measured using the Social Adjustment Scale-Self Report, which explores social adaptation in the areas of work, social and leisure, extended family, primary relationship (marital), parental, and family unit. At baseline, the GAD patients had a high level of social dysfunction. Venlafaxine ER showed a dose-related improvement in social impairment during short-term treatment and in sustaining this improvement over the long-term. In the most severely socially impaired subgroup, placebo remission rates on the HAM-A were low, and the magnitude of the venlafaxine-placebo difference on the mean HAM-A total score was high, reaching more than 7 points. The benefits of venlafaxine ER treatment of GAD extend beyond that of improvement of anxiety symptoms to a significant improvement in the impairment of functioning that is associated with the illness.

Cognitive theories of generalised anxiety disorder (GAD) posit that cognitive and behavioural factors maintain the disorder. This study examined whether avoidance and safety behaviours mediated the relationship between cognitive factors and GAD symptoms. We also examined the reverse mediation model; that is, whether cognitive factors mediated the relationship between maladaptive behaviours and GAD symptoms. Undergraduate psychology students (N = 125 and N = 292) completed the Worry Behaviours Inventory (a recently developed measure of maladaptive behaviours associated with GAD), in addition to measures of intolerance of uncertainty, cognitive avoidance, metacognitive beliefs, and symptoms of GAD and depression. Analyses supported the reliability and validity of the WBI. We consistently found that engagement in maladaptive behaviours significantly mediated the relationship between cognitive factors and symptoms of GAD. The reverse mediation model was also supported. Our results are consistent with the contention that cognitive and behavioural factors contribute to GAD symptom severity.

Generalised anxiety disorder (GAD) is a common psychiatric illness characterised by selective morpho-functional brain alterations. The breath of neuroimaging studies investigating the neural basis of GAD is extensive; however, its pathophysiology is still largely unknown. Specifically for proton Magnetic Resonance Spectroscopy (¹H MRS) investigations, which have the aim of identifying differences in metabolite levels between conditions in key brain areas, often showed contrasting results. Indeed, there are selected ¹H MRS studies reporting deficits of key metabolites in GAD patients; however, collectively the literature remains mixed with respect to consistency of major findings. In this review, we evaluate published ¹H MRS studies on GAD with the final aim of providing a comprehensive overview of the extent of neurometabolic dysfunctions associated with GAD. Interestingly, the majority of the studies reviewed showed altered metabolite levels in the dorsolateral prefrontal cortex and hippocampus suggesting regional specificity. These results also provide evidence of the utility of ¹H MRS not only for elucidating the pathophysiology of neuropsychiatric diseases, but also for the identification of more beneficial and targeted pharmacological interventions. Additionally, future studies are warranted to overcome methodological differences observed across the studies.

This article appraises the ability of several measures, assessing symptomatology theoretically relevant to generalised anxiety disorder (GAD), to accomplish successful classification of individuals with DSM-IV GAD and individuals with mood or other anxiety disorders. Participants were 197 individuals (average age = 36.43; 67.5% female) receiving treatment at a clinic, who completed pretreatment self-report measures. Receiver operator characteristic analyses and logistic regression analyses were employed to determine the classificatory abilities, including sensitivity and specificity, of several GAD relevant measures. The Penn State Worry Questionnaire (PSWQ) accomplished significant classification in both comparison group dyads: GAD-Anxiety and GAD-Mood. Whereas the general distress of depression subscale of the Mood and Anxiety Symptoms Questionnaire (MASQ) accomplished significant classification in the GAD-Anxiety group dyad, both the general distress of anxiety and anxious arousal subscales of the MASQ did so in the GAD-Mood group dyad. Only the PSWQ significantly predicted the presence of GAD, while controlling for other symptom variables. Though evidence supports the uniqueness of some symptoms of GAD, including worry, often considered pathognomonic to GAD, the modest areas under the curve, sensitivity, and specificity of the measures afford tenuous support for the utility of these measures. The lack of highly sensitive and specific symptomatology comport with critiques of GAD as a diagnostically delimited category.

This study explored how meta-worry and intolerance of uncertainty relate to pathological worry, generalised anxiety, obsessive–compulsive disorder, social phobia, and depression. University students (n = 253) completed a questionnaire battery. A series of regression analyses were conducted. The results indicated that meta-worry was associated with GAD, social phobia, obsessive–compulsive, and depressive symptoms. Intolerance of uncertainty was related to GAD, social phobia, and obsessive–compulsive symptoms, but not depressive symptoms. The importance of meta-worry and intolerance of uncertainty as predictors of pathological worry, GAD, social phobia, obsessive–compulsive and depressive symptoms was also examined. Even though both factors significantly predicted the aforementioned symptoms, meta-worry emerged as a stronger predictor of GAD and obsessive compulsive symptoms than did intolerance of uncertainty. Intolerance of uncertainty, compared with meta-worry, appeared as a stronger predictor of social phobia symptoms. Findings emphasise the importance of addressing meta-worry and/or intolerance of uncertainty not only for the assessment and treatment of generalised anxiety disorder (GAD), but also obsessive–compulsive disorder, social phobia, and depression.