Explore the vast range of titles available.

The cerebral cortex of the human brain has a complex morphological structure consisting of folded or smooth cortical surfaces. These morphological features are referred to as cortical gyrification and are characterized by the gyrification index (GI). A number of cortical gyrification studies have been published using the manual tracing GI, automated GI, and local GI in patients with schizophrenia. In this review, we highlighted abnormal cortical gyrification in patients with schizophrenia, first-episode schizophrenia, siblings of patients, and high-risk and at-risk individuals. Previous researches also indicated that abnormalities in cortical gyrification may underlie the severity of clinical symptoms, neurological soft signs, and executive functions. A substantial body of research has been conducted; however, some researches showed an increased GI, which is called as \"hypergyria,\" and others showed a decreased GI, which is called as \"hypogyria.\" We discussed that different GI methods and a wide variety of characteristics, such as age, sex, stage, and severity of illness, might be important reasons for the conflicting findings. These issues still need to be considered, and future studies should address them.

There is growing evidence that glutamatergic signaling may be involved in major depressive disorder (MDD). In regard to peripheral blood glutamate changes in MDD, inconsistent findings have been reported. The purpose of the present study was to evaluate whether blood glutamate levels differed between MDD patients and control participants. We conducted a systematic review and meta-analysis of 12 association studies between blood glutamate levels and MDD in a total of 529 MDD patients and 590 controls. Subsequently, we conducted subgroup analyses and a meta-regression analysis to examine the sources of potential heterogeneity. A random effects model showed that blood glutamate levels were significantly higher in MDD patients than in controls (standardized mean difference=0.54, 95% CI=0.27-0.82, =8.5×10 ) with high heterogeneity ( =75.0%, <0.05). Subgroup analyses showed elevated glutamate levels in MDD patients compared with controls in plasma, but not serum studies, and in studies using high-performance liquid chromatography but not with mass spectrometry for glutamate assay. A meta-regression analysis showed no effects of age, gender, medication use, sample size, and published year on blood glutamate levels. Our findings suggest that altered glutamate levels may be implicated in MDD, which provides further evidence of glutamatergic dysfunction in MDD.

Several psychological studies have shown that depressive rumination is associated with the onset and severity of depression. However, it is unclear how rumination interacts with other predisposing factors to cause depression. In this study, we hypothesized that rumination mediates the association between depression and two predisposing factors of depression, ie, childhood maltreatment and trait anxiety. Between 2017 and 2018, 473 adult volunteers were surveyed using self-report questionnaires regarding the following: demographic information, rumination (Ruminative Responses Scale), trait anxiety (State-Trait Anxiety Inventory-Y), and the experience of childhood maltreatment (Child Abuse and Trauma Scale). The effects of these factors on depression (Patient Health Questionnaire-9) were analyzed by multiple regression and path analysis to analyze the mediating effects of rumination. This study was conducted with approval from the relevant ethics committee. Multiple regression analysis using depression as a dependent variable demonstrated that trait anxiety, rumination, childhood maltreatment, and living alone were significantly associated with depression. Path analysis showed that childhood maltreatment had a positive effect on trait anxiety, rumination, and depression; trait anxiety had a positive effect on rumination and depression; and rumination had a positive effect on depression. Regarding indirect effects, the experience of childhood maltreatment increased rumination and depression indirectly via trait anxiety. Furthermore, the experience of childhood maltreatment increased depression indirectly via rumination, and trait anxiety significantly increased depression via rumination. In other words, rumination mediated the indirect effects of abusive experiences and trait anxiety on depression. This model accounted for 50% of the variance in depression in adult volunteers. Our results suggest that rumination mediates the association between childhood maltreatment, trait anxiety, and depression in adulthood.

Anhedonia in major depressive disorder may be resistant to first-line antidepressants. We examined the effect of vortioxetine, a multimodal antidepressant, on anhedonia-like symptoms in Japanese patients with major depressive disorder. This was a post hoc analysis of an 8-week, randomized, double-blind, placebo-controlled, phase 3 study of vortioxetine (10 mg or 20 mg) in Japanese patients aged 20-75 years with recurrent major depressive disorder and a Montgomery-Åsberg Depression Rating Scale (MADRS) total score of at least 26. The primary outcome was the mean change from baseline to week 8 in anhedonia-like symptoms as measured by MADRS anhedonia factor score, composed of: Q1, apparent sadness; Q2, reported sadness; Q6, concentration; Q7, lassitude; and Q8, inability to feel. Mean change in MADRS total score and anhedonia factor score were compared among treatment groups, with data categorized by median baseline anhedonia factor score (0-17 or ≥18). Data were available for 489 patients. The least-squares mean difference in MADRS anhedonia factor score change from baseline to week 8 versus placebo was -1.34 for vortioxetine 10 mg ( = 0.0300) and -1.77 for vortioxetine 20 mg ( = 0.0044). The least-squares mean difference between vortioxetine and placebo in MADRS total score change from baseline to week 8 was -3.11 (10 mg dose) and -3.37 (20 mg dose) for patients with a higher baseline anhedonia factor score (≥18), and -2.08 (10 mg) and -2.61 (20 mg) for patients with a lower baseline score (0-17). This post hoc analysis suggests that vortioxetine may have therapeutic potential in patients with anhedonia-like symptoms of major depressive disorder. ClinicalTrials.gov identifier for primary study: NCT02389816.

Shoko Sakamoto,1,2 Dai Miyawaki,1,3 Ayako Goto,1 Kaoru Hirai,1,4 Hiroki Hama,1,2 Shin Kadono,1,2 Sayaka Nishiura,1,2 Koki Inoue1 1Department of Neuropsychiatry, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan; 2Department of Neuropsychiatry, Osaka City University Graduate School of Medicine, Osaka, Japan; 3Department of Child and Adolescent Psychiatry, Osaka City General Hospital, Osaka, Japan; 4Department of Pediatrics, Osaka Metropolitan University Graduate School of Medicine, Osaka, JapanCorrespondence: Dai Miyawaki, Department of Child and Adolescent Psychiatry, Osaka City General Hospital, Osaka, Japan, Email miyawakidai@omu.ac.jp

We aimed to explore the prevalence of probable sleep and mood disorders in eye clinic visitors. This was a cross-sectional study. The participants were outpatients at six eye clinics from January through March, 2014. Outpatients were invited to complete a questionnaire containing the Pittsburgh Sleep Quality Index (PSQI) and Hospital Anxiety and Depression Scale (HADS). A final diagnosis was made, and patients were classified into six diagnostic groups. The main outcome measures were the scores of the PSQI and HADS among the diagnostic groups. A total 1,000 outpatients participated, and 730 patients (mean age 59.5±19.0 years; 487 females) were analyzed after exclusion of children and patients diagnosed with healthy eyes, acute injury, or unilateral pseudophakia. The mean PSQI and HADS scores across all patients were 5.3±3.1 and 9.2±6.2, respectively. For the diagnostic groups, the mean PSQI and HADS scores, respectively, were 5.7±3.3 and 10.2±6.0 for dry eye (n=247), 5.4±3.2 and 9.2±5.7 for bilateral cataracts (n=159), 5.3±3.3 and 8.0±5.3 for bilateral pseudophakia (n=99), and, 5.0±3.1 and 9.8±6.6 for glaucoma (n=109). Overall, 37.3% of patients were poor sleepers (PSQI ≥6), and 45.5% had possible mood disorders (HADS ≥10). Stepwise regression analysis revealed that the PSQI and HADS scores were significantly correlated with both age (P<0.05) and the presence of dry eye (P<0.05). The prevalence of sleep and mood disorders was significantly higher in patients with dry eye. The present results suggest consultation-liaison psychiatry services may be beneficial among eye disease patients.

Purpose: Originally developed in English, the Oxford Depression Questionnaire (ODQ) is a patient-reported scale specifically developed for assessing emotional blunting in people with major depressive disorder (MDD). We aimed to examine the reliability and validity of the Japanese version of the ODQ. Patients and methods: This was a prespecified analysis of a prospective, 24-week, multicenter, observational cohort study of employed Japanese outpatients with MDD initiating treatment with vortioxetine according to the Japanese label (JRCT1031210200). Participants were assessed using the Japanese version of the ODQ and other clinical rating scales at baseline and Weeks 8, 12 and 24. Results: One hundred and sixteen patients initiated vortioxetine and had [greater than or equal to]1 post-baseline visit. Directionally, the associations between ODQ scores and other clinical measures were as expected and demonstrated good concurrent validity. Factor analysis shows that the scale has a good fit for three factors. The Cronbach's [alpha] coefficient was 0.912, and the scale also showed good test-retest reliability with intraclass correlation coefficients for the ODQ total score and domains ranging between 0.69 and 0.82. ODQ scores had strong positive correlations with symptom severity assessed using the Montgomery and Asberg Depression Rating Scale and were moderately correlated with work productivity, overall functioning, and quality of life scales. Conclusion: Data from this prospective analysis confirm that the Japanese version of the ODQ retains the good validity and reliability of the original English scale and is suitable for use in prospective studies wanting to capture treatment effects on emotional blunting in MDD. Keywords: emotional blunting, major depressive disorder, Oxford depression questionnaire, MADRS-emotional blunting, validation, vortioxetine

Epidemiology research has demonstrated that magnesium (Mg) deficiency is associated with a high incidence of Parkinson's disease (PD). It is known that the systemic administration of MgSO is not able to elevate the Mg concentration in cerebrospinal fluid (CSF). This study aims to verify the protective effect of magnesium-L-threonate (MgT) in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) mouse model. C57BL/6J mice were orally administered MgT or MgSO for 4 weeks, and received MPTP in the third week. After analysis of open-field and rotarod tests on the last day, tyrosine hydroxylase (TH) immunopositive cells and protein levels were quantified in the substantia nigra pars compacta (SNpc) and striatum. The expression of inducible nitric oxide synthase (iNOS) level was evaluated. Mg concentration in serum and CSF was measured after oral administration of MgSO or MgT in normal mice. Mg concentration in the CSF was increased in the mice treated with MgT but not MgSO . The total distance and mean speed in open-field tests, and the time spent on rotarod in the MgT group were increased, compared with MPTP group. The MgT treatment but not MgSO dose-dependently attenuated the loss of TH-positive neurons, and the reduction of the TH expression in the SNpc. The MgT treatment also inhibited the expression of iNOS as measured by immunohistochemistry and Western blots. Double-immunofluorescence staining of TH and iNOS showed iNOS-positive cells were collocalized for TH-positive cells. The treatment with MgT is associated with an increase of Mg in the CSF. MgT, rather than MgSO4, can significantly attenuate MPTP-induced motor deficits and dopamine (DA) neuron loss.

Psychiatric non-epileptic seizure (PNES), also known as a form of functional neurological disorders (FND), is a common but still underrecognized disorder presenting seizure-like symptoms and no electrophysiological abnormality. Despite the significant burden of this disorder, the neurobiological mechanisms are not clearly understood, which hinders the development of better diagnosis and treatment. In the recent neuroimaging research on PNES, brain network analysis has become a relevant topic beyond conventional methodologies. The human brain is a highly intricate system of interconnected regions that collaborate to facilitate a wide range of cognitive and behavioral functions. White matter tracts, which are comprised of bundles of axonal fibers, are the primary means by which information is transmitted between different brain regions. As such, comprehending the organization and structure of the brain's white matter network is critical for gaining insight into its functional architecture. This review article aims to provide an overview of the brain mechanisms underlying PNES, with a special focus on analyzing brain networks.