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IntroductionPathophysiological etiology of schizophrenia remains unclear due to the heterogeneous nature of its biological and clinical manifestations. Dysfunctional communication among large-scale brain networks and hub nodes have been reported. In this study, an exploratory approach was adopted to evaluate the dysfunctional connectome of brain in schizophrenia.MethodsTwo hundred adult individuals with schizophrenia and 200 healthy controls were recruited from Taipei Veterans General Hospital. All subjects received functional magnetic resonance imaging (fMRI) scanning. Functional connectivity (FC) between parcellated brain regions were obtained. Pair-wise brain regions with significantly different functional connectivity among the two groups were identified and further analyzed for their concurrent ratio of connectomic differences with another solitary brain region (single-FC dysfunction) or dynamically interconnected brain network (network-FC dysfunction).ResultsThe right thalamus had the highest number of significantly different pair-wise functional connectivity between schizophrenia and control groups, followed by the left thalamus and the right middle frontal gyrus. For individual brain regions, dysfunctional single-FCs and network-FCs could be found concurrently. Dysfunctional single-FCs distributed extensively in the whole brain of schizophrenia patients, but overlapped in similar groups of brain nodes. A dysfunctional module could be formed, with thalamus being the key dysfunctional hub.DiscussionThe thalamus can be a critical hub in the brain that its dysfunctional connectome with other brain regions is significant in schizophrenia patients. Interconnections between dysfunctional FCs for individual brain regions may provide future guide to identify critical brain pathology associated with schizophrenia.

Aim: Bipolar disorder (BD) and major depression have been associated with an increased risk of developing Parkinson's disease (PD); however, few studies have directly compared the risk of PD development between patients with BD and major depression while considering relevant risk factors and psychotropic medications. Methods: Using the Taiwan National Health Insurance Research Database, 21,186 patients with BD, 21,188 patients with major depression, and 42,374 controls were enrolled between 2001 and 2009, and followed until the end of 2011. Individuals who developed PD during the follow‐up period were identified. Cox regression models were used to analyze the hazard ratio (HR) of developing PD, adjusting for demographic factors, comorbidities, and psychotropic medication usage. Results: Both patients with BD [HR 8.63, 95% confidence interval (CI) 6.35–11.72] and those with major depression (HR 5.68, 95% CI 4.15–7.78) had an elevated risk of subsequent PD compared to the controls. Patients with BD were associated with a 51% increased risk of subsequent PD compared with patients with major depression. Long‐term treatment with antiepileptic mood stabilizers was associated with increased PD risk among patients with late‐onset BD and high Charlson comorbidity index scores. Lithium was not associated with an increased PD risk. Conclusions: The study highlights an elevated PD risk in patients with BD and major depression compared to the controls, with BD patients at highest risk. Further research is needed to elucidate the complex interplay between psychotropic medications and neurodegenerative processes in BD, aiming to optimize therapeutic strategies and improve patient outcomes. [ABSTRACT FROM AUTHOR]

© 2015 Lam et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Bac

Background: Sleep disturbance and impulsivity are key components of mood vulnerability in bipolar disorder (BD), but few studies have assessed the association between these two symptoms among patients with BD. Methods: Forty-seven euthymic patients with bipolar I disorder (BDI) or bipolar II disorder (BDII) and 58 age- and sex-matched healthy controls were enrolled in this cross-sectional study. Trait impulsivity was measured using the Barratt Impulsiveness Scale Version 11 (BIS-11), which yielded 3 second-order factors: attention, motor, and non-planning. Subjective sleep quality was assessed using the self-reported Pittsburgh Sleep Quality Index (PSQI). General linear models (GLMs) were used to assess the associations between subjective poor sleep and trait impulsivity with multiple testing corrections. Results: Patients with BD scored higher in BIS-11 and PSQI than healthy controls. PSQI total scores positively correlated with BIS-11 total scores, while sleep disturbance and daytime dysfunction were associated with attentional impulsiveness after controlling for covariates. Participants with higher PSQI total scores (>10) had higher scores in BIS-11 total, attention, and non-planning than those with low PSQI scores (≤5). Conclusion: These findings support the hypothesis that poor sleep quality might lead to impulsivity and add to the growing evidence that improving sleep quality may be a therapeutic target for patients with BD. [ABSTRACT FROM AUTHOR]

Wnt signaling, which encompasses multiple biochemical pathways that regulate neural development downstream of extracellular Wnt glycoprotein ligands, has been suggested to contribute to major psychiatric disorders including autism spectrum disorders (ASD). We used next-generation sequencing and Sequenom genotyping technologies to resequence 10 Wnt signaling pathway genes in 198 ASD patients and 240 matched controls. Results for single-nucleotide polymorphisms (SNPs) of interest were confirmed in a second set of 91 ASD and 144 control samples. We found a significantly increased burden of extremely rare missense variants predicted to be deleterious by PolyPhen-2, distributed across seven genes in the ASD sample (3.5% in ASD vs 0.8% in controls; Fisher's exact test, odds ratio (OR)=4.37, P=0.04). We also found a missense variant in WNT1 (S88R) that was overrepresented in the ASD sample (8 A/T in 267 ASD (minor allele frequency (MAF)=1.69%) vs 1 A/T in 377 controls (MAF=0.13%), OR=13.0, Fisher's exact test, P=0.0048; OR=8.2 and P=0.053 after correction for population stratification). Functional analysis revealed that WNT1-S88R is more active than wild-type WNT1 in assays for the Wnt/β-catenin signaling pathway. Our findings of a higher burden in ASD of rare missense variants distributed across 7 of 10 Wnt signaling pathway genes tested, and of a functional variant at the WNT1 locus associated with ASD, support that dysfunction of this pathway contributes to ASD susceptibility. Given recent findings of common molecular mechanisms in ASD, schizophrenia and affective disorders, these loci merit scrutiny in other psychiatric conditions as well.

Objective: We intended to investigate the risk of developing migraine among patients with posttraumatic stress disorder (PTSD). Methods: With the Taiwan's National Health Insurance Research Database, we examined 5,644 patients with PTSD and 22,576 age- and sex-matched controls between 2002 and 2009 and followed them to the end of 2011. Individuals who developed migraine during the follow-up period were identified. Results: Patients with PTSD had a significantly higher incidence of developing migraine (5.74 vs. 1.22 per 1,000 person-years, p < 0.001) during the follow-up period than the controls. We did Cox regression analysis with adjustments of demographic data and medical comorbidities and found that patients with PTSD were more likely to develop migraine (hazard ratio [HR] = 3.83, 95% confidence interval [CI] = 2.82–5.20) than the control group. Sensitivity analyses after excluding the 1st year (HR = 2.89; 95% CI = 2.04–4.08) or the first 3 years (HR = 2.07; 95% CI = 1.32–3.24) of observation showed consistent findings. Moreover, a high frequency of psychiatric clinics visiting for PTSD was associated with an increased risk of developing migraine. Conclusion: Patients with PTSD had a higher risk of migraine than the controls. The symptom severity of PTSD may be associated with an increased risk of migraine. Further studies are required to investigate the underlying pathophysiology between PTSD and migraine.

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Copyright of Tijdschrift voor Jeugdrecht is the property of Boom uitgevers Den Haag and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Anabolic-androgenic steroids (AASs) are highly sought-after in order to achieve muscle growth and better physical attributes. The study was conducted to measure the prevalence and attitudes towards the use of AASs among university students. 1008 male students from Isfahan University, Iran, between the ages of 18 and 25 years (23.3 ± 1.2 years) completed a questionnaire that investigated participation in bodybuilding, level of sport competition, participation in sports and recreational activities, AASs use, prevalence, knowledge among users, attitudes, as well as intent to continue using AASs in the future. 8% of respondents had used AASs and 6% currently use AASs. 71% of users believed using only a small amount of AASs or using AASs with anti-toxic drugs would not result in any harm, 10% indicated that AASs were harmless and 19% admitted to taking AASs despite knowing the adverse effects. 33% of respondents believed that they needed to use AASs to ensure athletic success and 26% believed that athletes should be allowed to use AASs without consequence. The prevalent use of AASs is a public health concern which implies that educational programmes at university level are needed to educate students about the adverse effects of AASs use