400 research outputs found

    In an open publishing house not so far, far away
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    EditorialSUMMARY: As BJPsych Open completes its first circle around the sun and marks its first anniversary, we share with you its strengths and advantages that underpin its success as a new journal. First and foremost, the editorial team has maintained rigorous scientific standards while pursuing an open access publishing model that, by design, accommodates a broad range of clinical and scientific topics. Fundamental to BJPsych Open's mission has been our policy of accepting papers that are both methodologically sound and intellectually stimulating. The calibre of the journal has already been recognised, with recent notification of indexing all its content in PubMed Central. This reflects the quality of submissions and is the result of concerted efforts by the authors, the editorial board, the many selfless reviewers and our dedicated staff in the journal office. We urge you to join us on this exciting journey and look to your input as authors, readers and reviewers to help shape this fledgling enterprise, destined to become a force to be reckoned with. DECLARATION OF INTERESTS: None. COPYRIGHT AND USAGE: © The Royal College of Psychiatrists 2016. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) license

    A comparative study of engagement in mobile and wearable health monitoring for bipolar disorder

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    ObjectivesSelf‐monitoring is recommended for individuals with bipolar disorder, with numerous technological solutions available. This study aimed to identify basic components of these solutions that increase engagement with self‐monitoring.MethodsParticipants with bipolar disorder (n = 47) monitored their symptoms with a Fitbit and a smartphone app and were randomly assigned to either review or not review recorded symptoms weekly. We tested whether individuals would better adhere to and prefer monitoring with passive monitoring with an activity tracker compared to active monitoring with a smartphone app and whether individuals would better adhere to self‐monitoring if their recorded symptoms were reviewed with an interviewer.ResultsMonitoring with a smartphone app achieved similar adherence and preference to Fitbit (P > .85). Linear mixed effects modeling found adherence decreased significantly more over the study for the Fitbit (12% more, P < .001) even though more participants reported they would use the Fitbit over a year compared to the app (72.3% vs 46.8%). Reviewing symptoms weekly did not improve adherence, but most participants reported they would prefer to review symptoms with a clinician (74.5%) and on monthly basis (57.5%) compared to alternatives. Participants endorsed sleep as the most important symptom to monitor, forgetfulness as the largest barrier to self‐monitoring, and raising self‐awareness as the best reason for self‐monitoring.ConclusionsWe recommend a combined strategy of wearable and mobile monitoring that includes reminders, targets raising self‐awareness, and tracks sleep. A clinician may want to review symptoms on a monthly basis.Trial registration: ClinicalTrials.gov NCT03358238.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154615/1/bdi12849_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154615/2/bdi12849.pd

    Greater sleep disturbance and longer sleep onset latency facilitate SCR-specific fear reinstatement in PTSD

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    Fear reinstatement is one of several paradigms designed to measure fear return following extinction, as a laboratory model for the relapse of Posttraumatic Stress Disorder (PTSD) symptoms. Sleep is a key factor in emotional memory consolidation, and here we examined the relationship between sleep quality and fear reinstatement in PTSD, relative to trauma-exposed and non-exposed controls. The Pittsburgh Sleep Quality Index (PSQI) was used as a subjective measure of sleep quality, and skin conductance responses (SCR) and unconditioned stimulus (US)-expectancy ratings were used to index threat responses during a differential fear conditioning, extinction, and reinstatement paradigm. There were no significant between-group differences in the reinstatement of conditioned responding. Sleep disturbance and sleep onset latency were significant moderators between reinstatement of fear and PTSD symptom severity, such that there was a positive relationship between PTSD symptoms and fear reinstatement for higher levels - but not lower levels - of sleep disturbance and sleep onset latency. To our knowledge, this is the first study to investigate PTSD-specific reinstatement patterns and sleep as a boundary condition of reinstatement. Future research using polysomnographic measures of sleep-wave architecture may further clarify the relationship between fear reinstatement and sleep quality in clinical samples with PTSD relative to controls

    Open Sesame: a new generation journal.

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    SUMMARY: The Royal College of Psychiatrists welcomes you to its newest peer-reviewed research journal, British Journal of Psychiatry Open (BJPsych Open), which has been created to maximise the College's efforts to publish and disseminate the most exciting and progressive research in psychiatry and allied disciplines. BJPsych Open will maintain the same high quality standards established by the British Journal of Psychiatry (BJPsych). As an online journal without print restrictions, BJPsych Open will be able to publish many more excellent articles and article types not currently accommodated within BJPsych. The breadth of BJPsych Open is outlined in 'What we publish' and its strength is realised in our first issue, 'Powerful papers'. As editors, we welcome both your submissions and comments as our new generation journal grows. DECLARATION OF INTEREST: None. COPYRIGHT AND USAGE: © The Royal College of Psychiatrists 2015. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) licence

    Protocol and rationale-the efficacy of minocycline as an adjunctive treatment for major depressive disorder: a double blind, randomised, placebo controlled trial

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    While current pharmacotherapies are efficacious, there remain a clear shortfall between symptom remission and functional recovery. With the explosion in our understanding of the biology of these disorders, the time is ripe for the investigation of novel therapies. Recently depression is conceptualized as an immune-inflammatory and nitro-oxidative stress related disorder. Minocycline is a tetracycline antibiotic that has anti-inflammatory, pro-oxidant, glutamatergic, neurotrophic and neuroprotective properties that make it a viable target to explore as a new therapy. This double blind, randomised, placebo controlled adjunctive trial will investigate the benefits of 200 mg/day of minocycline treatment, in addition to any usual treatment, as an adjunctive treatment for moderate-severe major depressive disorder. Sixty adults are being randomised to 12 weeks of treatment (with a 4 week follow-up post-discontinuation). The primary outcome measure for the study is mean change on the Montgomery-Asberg Depression Rating Scale (MADRS), with secondary outcomes including the Social and Occupational Functioning Assessment Scale (SOFAS), Clinical Global Impressions (CGI), Hamilton Rating Scale for Anxiety (HAM-A), Patient Global Impression (PGI), Quality of Life Enjoyment and Satisfaction Questionnaire (Q-LES-Q) and Range of Impaired Functioning Tool (LIFE-RIFT). Biomarker analyses will also be conducted at baseline and week 12. The study has the potential to provide new treatment targets, both by showing efficacy with a new class of \u27antidepressant\u27 but also through the analysis of biomarkers that may further inform our understanding of the pathophysiology of unipolar depression

    Lack of cortico-limbic coupling in bipolar disorder and schizophrenia during emotion regulation

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    Bipolar disorder (BD) and schizophrenia (Sz) share dysfunction in prefrontal inhibitory brain systems, yet exhibit distinct forms of affective disturbance. We aimed to distinguish these disorders on the basis of differential activation in cortico-limbic pathways during voluntary emotion regulation. Patients with DSM-IV diagnosed Sz (12) or BD-I (13) and 15 healthy control (HC) participants performed a well-established emotion regulation task while undergoing functional magnetic resonance imaging. The task required participants to voluntarily upregulate or downregulate their subjective affect while viewing emotionally negative images or maintain their affective response as a comparison condition. In BD, abnormal overactivity (hyperactivation) occurred in the right ventrolateral prefrontal cortex (VLPFC) during up- and downregulation of negative affect, relative to HC. Among Sz, prefrontal hypoactivation of the right VLPFC occurred during downregulation (opposite to BD), whereas upregulation elicited hyperactivity in the right VLPFC similar to BD. Amygdala activity was significantly related to subjective negative affect in HC and BD, but not Sz. Furthermore, amygdala activity was inversely coupled with the activity in the left PFC during downregulation in HC (r=−0.76), while such coupling did not occur in BD or Sz. These preliminary results indicate that differential cortico-limbic activation can distinguish the clinical groups in line with affective disturbance: BD is characterized by ineffective cortical control over limbic regions during emotion regulation, while Sz is characterized by an apparent failure to engage cortical (hypofrontality) and limbic regions during downregulation

    Acute coronary syndrome-associated depression: Getting to the heart of the data

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    Objectives: We sought to identify and consider methodological issues that may have limited or confounded investigations into links between depression and acute coronary syndrome (ACS) events. Methods: We reviewed salient research studies to identify such issues. Results: Against previous conclusions, we found that lifetime depression is unlikely to have any primary ACS impact, while we clarify that ‘incident depression’ (depression commencing at variable periods around the time of the ACS event) appears to confer a greater risk than non-incident depression. As the time periods of incident depressions are likely to have quite differing causes, evaluating any consolidated risk period appears unwise. It remains unclear whether it is ‘depression’ that provides the risk for ACS events or a higher order factor. Variable use of depression measures and failure to evaluate depressive sub-types have further limited clarification. The response by ACS patients to antidepressant medication appears limited, and it remains to be determined whether exposure to an antidepressant might be a contributing factor. Finally, studies may have focused on an excessively refined association, and neglected to recognise that depression is associated with a wide range of vascular events, suggesting that a broader conceptual model may be required. Limitations: The authors have considered only a limited set of studies in preparing this review, with the critique relying at times on subjective interpretation. Conclusions: After decades of research pursuing links between depression and ACS events explanatory links remain obscure, presumably reflecting a range of methodological issues that we have discussed in this paper

    Treatment and outcomes of an Australian cohort of outpatients with bipolar 1 or schizoaffective disorder over twenty-four months : implications for clinical practice

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    Background The Bipolar Comprehensive Outcomes Study (BCOS) is a 2-year, prospective, non-interventional, observational study designed to explore the clinical and functional outcomes associated with &lsquo;real-world&rsquo; treatment of participants with bipolar I or schizoaffective disorder. All participants received treatment as usual. There was no study medication.Methods Participants prescribed either conventional mood stabilizers (CMS; n&thinsp;=&thinsp;155) alone, or olanzapine with, or without, CMS (olanzapine&thinsp;&plusmn;&thinsp;CMS; n&thinsp;=&thinsp;84) were assessed every 3&thinsp;months using several measures, including the Young Mania Rating Scale, 21-item Hamilton Depression Rating Scale, Clinical Global Impressions Scale &ndash; Bipolar Version, and the EuroQol Instrument. This paper reports 24-month longitudinal clinical, pharmacological, functional, and socioeconomic data.Results On average, participants were 42 (range 18 to 79) years of age, 58%; were female, and 73%; had a diagnosis of bipolar I. Polypharmacy was the usual approach to pharmacological treatment; participants took a median of 5 different psychotropic medications over the course of the study, and spent a median proportion of time of 100%; of the study on mood stabilizers, 90%; on antipsychotics, 9%; on antidepressants, and 5%; on benzodiazepines/hypnotics. By 24&thinsp;months, the majority of participants had achieved both symptomatic and syndromal remission of both mania and depression. Symptomatic relapse rates were similar for both the CMS alone (65%;) and the olanzapine&thinsp;&plusmn;&thinsp;CMS (61%;) cohorts.Conclusions Participants with bipolar I or schizoaffective disorder in this study were receiving complex medication treatments that were often discordant with recommendations made in contemporary major treatment guidelines. The majority of study participants demonstrated some clinical and functional improvements, but not all achieved remission of symptoms or syndrome.<br /

    The BDNF Val66Met polymorphism moderates the relationship between Posttraumatic Stress Disorder and fear extinction learning

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    The low expression Met allele of the BDNF Val66Met polymorphism is associated with impaired fear extinction in healthy controls, and poorer response to exposure therapy in patients with Posttraumatic Stress Disorder (PTSD). Given that fear extinction underlies exposure therapy, this raises the question of the impact of BDNFVal66Met polymorphism on fear extinction in PTSD, yet this question has not yet been examined. One hundred and six participants (22 PTSD, 46 trauma-exposed controls (TC) and 38 non-trauma exposed controls (NTC)) completed a fear conditioning and extinction task and saliva samples were taken for DNA extraction and genotyped for the BDNF Val66Met polymorphism. Moderation analyses using PROCESS examined whether BDNF genotype (Val–Val vs Met carriers) moderated the relationship between PTSD symptom severity (and diagnostic status) and skin conductance response (SCR) amplitude during fear extinction. The PTSD group displayed significantly slower fear extinction learning compared to TC and NTC in the early extinction phase. The BDNF Val66Met polymorphism moderated the relationship between PTSD and fear extinction learning, such that poorer fear extinction learning was associated with greater PTSD symptom severity (and PTSD diagnostic status) in individuals with the low-expression Met allele, but no relationship was demonstrated in individuals with the Val–Val allele. This study reveals that impaired fear extinction learning is particularly evident in individuals with PTSD who carry the low-expression BDNF Met Val–Val allele and importantly not in those with the allele. This provides novel evidence of a link between BDNF and impaired fear extinction learning in PTSD, which may contribute to poorer response to exposure therapy
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