A multi-centre, double-blind, 12-week, randomized, placebo-controlled trial of adjunctive N-Acetylcysteine for treatment-resistant PTSD.

BACKGROUND: PTSD may involve oxidative stress, and N-acetylcysteine (NAC) may reduce the impact of oxidative stress in the brain. This study aims to investigate the efficacy of adjuvant NAC in people with treatment-resistant PTSD. METHODS: A multicentre, randomised, double-blind, placebo-controlled trial for adults with PTSD unresponsive to first-line treatment. The intervention was either oral NAC 2.7 g/day or placebo for 12 weeks. The primary outcome was change in Clinician-Administered PTSD Scale for DSM-5 (CAPS-5) at 12 weeks compared with baseline. Secondary outcomes included depression and substance craving. Follow-up measures were obtained at 16 and 64-weeks. RESULTS: 133 patients were assessed, with 105 randomised; 81 participants completed the 12-week trial, 79 completed week-16 follow-up, and 21 completed week-64 follow-up. There were no significant differences between those taking NAC and those taking placebo in CAPS-5 scores at week 12, nor in secondary outcomes. Significant between-group differences were observed at week 64 in craving duration (Cohen's d = 1.61) and craving resistance (Cohen's d = 1.03), both in favour of NAC. CONCLUSION: This was the first multicentre, double-blind, randomised, placebo-controlled trial of adjunctive NAC for treatment-resistant PTSD. No benefit of NAC was observed in this group beyond that provided by placebo at end of the trial. TRIAL REGISTRATION: ACTRN12618001784202, retrospectively registered 31/10/2018, URL: http://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=376004.

Issues for eHealth in Psychiatry: Results of an Expert Survey.

BACKGROUND: Technology has changed the landscape in which psychiatry operates. Effective, evidence-based treatments for mental health care are now available at the fingertips of anyone with Internet access. However, technological solutions for mental health are not necessarily sought by consumers nor recommended by clinicians. OBJECTIVE: The objectives of this study are to identify and discuss the barriers to introducing eHealth technology-supported interventions within mental health. METHODS: An interactive polling tool was used to ask "In this brave new world, what are the key issues that need to be addressed to improve mental health (using technology)?" Respondents were the multidisciplinary attendees of the "Humans and Machines: A Quest for Better Mental Health" conference, held in Sydney, Australia, in 2016. Responses were categorized into 10 key issues using team-based qualitative analysis. RESULTS: A total of 155 responses to the question were received from 66 audience members. Responses were categorized into 10 issues and ordered by importance: access to care, integration and collaboration, education and awareness, mental health stigma, data privacy, trust, understanding and assessment of mental health, government and policy, optimal design, and engagement. In this paper, each of the 10 issues are outlined, and potential solutions are discussed. Many of the issues were interrelated, having implications for other key areas identified. CONCLUSIONS: As many of the issues identified directly related to barriers to care, priority should be given to addressing these issues that are common across mental health delivery. Despite new challenges raised by technology, technology-supported mental health interventions represent a tremendous opportunity to address in a timely way these major concerns and improve the receipt of effective, evidence-based therapy by those in need.

Modulatory effects of brain-derived neurotrophic factor Val66Met polymorphism on prefrontal regions in major depressive disorder.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism contributes to the development of depression (major depressive disorder, MDD), but it is unclear whether neural effects observed in healthy individuals are sustained in MDD. AIMS: To investigate BDNF Val66Met effects on key regions in MDD neurocircuitry: amygdala, anterior cingulate, middle frontal and orbitofrontal regions. METHOD: Magnetic resonance imaging scans were acquired in 79 persons with MDD (mean age 49 years) and 74 healthy volunteers (mean age 50 years). Effects on surface area and cortical thickness were examined with multiple comparison correction. RESULTS: People who were Met allele carriers showed reduced caudal middle frontal thickness in both study groups. Significant interaction effects were found in the anterior cingulate and rostral middle frontal regions, in which participants in the MDD group who were Met carriers showed the greatest reduction in surface area. CONCLUSIONS: Modulatory effects of the BDNF Val66Met polymorphism on distinct subregions in the prefrontal cortex in MDD support the neurotrophin model of depression.