Mechanisms of change during group metacognitive therapy for repetitive negative thinking in primary and non-primary generalized anxiety disorder

© 2015 Elsevier Ltd. Repetitive negative thinking (RNT) is a transdiagnostic process that serves to maintain emotional disorders. Metacognitive theory suggests that positive and negative metacognitive beliefs guide the selection of RNT as a coping strategy which, in turn, increases psychological distress. The aim of this study was to test the indirect effect of metacognitive beliefs on psychological distress via RNT. Patients (N=52) with primary and non-primary generalized anxiety disorder attended a brief, six-week group metacognitive therapy program and completed measures of metacognitive beliefs, RNT, and symptoms at the first and final treatment sessions, and at a one-month follow-up. Prospective indirect effects models found that negative metacognitive beliefs (but not positive metacognitive beliefs) had a significant indirect effect on psychological distress via RNT. As predicted by metacognitive theory, targeting negative metacognitions in treatment appears to reduce RNT and, in turn, emotional distress. Further research using alternative measures at multiple time points during therapy is required to determine whether the absence of a relationship with positive metacognitive beliefs in this study was a consequence of (a) psychometric issues, (b) these beliefs only being relevant to a subgroup of patients, or (c) a lack of awareness early in treatment

Group metacognitive therapy for repetitive negative thinking in primary and non-primary generalized anxiety disorder: An effectiveness trial

Background Generalized anxiety disorder (GAD) is a common and highly comorbid anxiety disorder characterized by repetitive negative thinking (RNT). Treatment trials tend to exclude individuals with non-primary GAD, despite this being a common presentation in real world clinics. RNT is also associated with multiple emotional disorders, suggesting that it should be targeted regardless of the primary disorder. This study evaluated the acceptability and effectiveness of brief group metacognitive therapy (MCT) for primary or non-primary GAD within a community clinic. Methods Patients referred to a specialist community clinic attended six, two-hour weekly sessions plus a one-month follow-up (N=52). Measures of metacognitive beliefs, RNT, symptoms, positive and negative affect, and quality of life were completed at the first, last, and follow-up sessions. Results Attrition was low and large intent-to-treat effects were observed on most outcomes, particularly for negative metacognitive beliefs and RNT. Treatment gains increased further to follow-up. Benchmarking comparisons demonstrated that outcomes compared favorably to longer disorder-specific protocols for primary GAD. Limitations No control group or independent assessment of protocol adherence. Conclusions Brief metacognitive therapy is an acceptable and powerful treatment for patients with primary or non-primary GAD

Considering sex as a biological variable in preclinical research

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154390/1/fsb2fj201600781r.pd

“PMA Sounds Fun”: Negotiating Drug Discourses Online

In 2007, a young woman, Annabel Catt, died after consuming a capsule sold as “ecstasy” that contained para-methoxyamphetamine. In this paper, we describe how this death was depicted in online drug-user communities and illustrate how the meanings of drug use are negotiated in online settings. News articles, public online discussions, and online fieldwork formed the data. This paper demonstrates how dominant drug discourses may be resisted by drug users, drawing on theories of health resistance and Kane Race’s concept of counter public health. Online environments may offer ways of engaging people who use drugs that acknowledge both pleasure and safety. The study’s limitations are noted

Pathways to ischemic neuronal cell death: are sex differences relevant?

We have known for some time that the epidemiology of human stroke is sexually dimorphic until late in life, well beyond the years of reproductive senescence and menopause. Now, a new concept is emerging: the mechanisms and outcome of cerebral ischemic injury are influenced strongly by biological sex as well as the availability of sex steroids to the brain. The principal mammalian estrogen (17 β estradiol or E2) is neuroprotective in many types of brain injury and has been the major focus of investigation over the past several decades. However, it is becoming increasingly clear that although hormones are a major contributor to sex-specific outcomes, they do not fully account for sex-specific responses to cerebral ischemia. The purpose of this review is to highlight recent studies in cell culture and animal models that suggest that genetic sex determines experimental stroke outcome and that divergent cell death pathways are activated after an ischemic insult. These sex differences need to be identified if we are to develop efficacious neuroprotective agents for use in stroke patients

Rodent models of focal cerebral ischemia: procedural pitfalls and translational problems

Rodent models of focal cerebral ischemia are essential tools in experimental stroke research. They have added tremendously to our understanding of injury mechanisms in stroke and have helped to identify potential therapeutic targets. A plethora of substances, however, in particular an overwhelming number of putative neuroprotective agents, have been shown to be effective in preclinical stroke research, but have failed in clinical trials. A lot of factors may have contributed to this failure of translation from bench to bedside. Often, deficits in the quality of experimental stroke research seem to be involved. In this article, we review the commonest rodent models of focal cerebral ischemia - middle cerebral artery occlusion, photothrombosis, and embolic stroke models - with their respective advantages and problems, and we address the issue of quality in preclinical stroke modeling as well as potential reasons for translational failure