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Effective suicide prevention is hindered by a limited understanding of the natural progression and neurobiology of the suicidal process. Our objective was to characterize the duration of the suicidal process and its relation to possible determinants: time judgment and cognitive impulsivity. In four groups of adults of both sexes including recent suicide attempters (n = 57), suicidal ideators (n = 131), non-suicidal depressed controls (n = 51) and healthy controls (n = 48) we examined time estimation and production, impulsivity and other cognitive variables. Duration of the suicidal process was recorded in suicide attempters. The suicide process duration, suicide contemplation and action intervals, had a bimodal distribution, ∼40% of attempters took less than 5 min from decision to attempt. Time slowing correlated negatively with the suicidal action interval (time from the decision to kill oneself to suicide attempt) (p = .003). Individuals with suicide contemplation interval shorter than three hours showed increased time slowing, measured as shorter time production at 35 s (p = .011) and 43 s (p = .036). Delay discounting for rewards correlated with time estimation at 25 min (p = .02) and 90 s (p = .01). Time slowing correlated positively with suicidal ideation severity, independently of depression severity (p < .001). Perception of time slowing may influence both the intensity and the duration of the suicidal process. Time slowing may initially be triggered by intense psychological pain, then worsen the perception of inescapability in suicidal patients., (Published by Elsevier B.V.)

Purpose/background: In addition to clozapine, other atypical antipsychotic drugs pharmacologically similar to clozapine, for example, olanzapine, risperidone, and melperone, are also effective in a similar proportion of treatment-resistant schizophrenia (TRS) patients, ~40%. The major goal of this study was to compare 2 doses of lurasidone, another atypical antipsychotic drug, and time to improvement in psychopathology and cognition during a 6-month trial in TRS patients., Methods/procedures: The diagnosis of TRS was based on clinical history and lack of improvement in psychopathology during a 6-week open trial of lurasidone 80 mg/d (phase 1). This was followed by a randomized, double-blind, 24-week trial of lurasidone, comparing 80- and 240-mg/d doses (phase 2)., Findings/results: Significant non-dose-related improvement in the Positive and Negative Syndrome Scale-Total and subscales and in 2 of 7 cognitive domains, speed of processing and executive function, were noted. Twenty-eight (41.8%) of 67 patients in the combined sample improved ≥20% in the Positive and Negative Syndrome Scale-Total. Of the 28 responders, 19 (67.9%) first reached ≥20% improvement between weeks 6 and 24 during phase 2, including some who had previously failed to respond to clozapine., Implications/conclusions: Improvement with lurasidone is comparable with those previously reported for clozapine, melperone, olanzapine, and risperidone in TRS patients. In addition, this study demonstrated that 80 mg/d lurasidone, an effective and tolerable dose for non-TRS patients, was also effective in TRS patients but required longer duration of treatment. Direct comparison of lurasidone with clozapine in TRS patients is indicated.

Constantly shifting cultural views influence public perceptions of psychiatric diagnoses, sometimes accommodated by changes in diagnostic terminology. Evolving scientific knowledge of the era is at times used to justify and support mental illnesses. Too often, however, remasked nomenclatures fail to alter social stigma, in part because political arguments are used. Scientific validations of variant behaviors as symptoms with a pathologic status are unfortunately overshadowed. Examples of cultural bias effects on recurring diagnostic challenges illustrate a need for scientific validation. Renaming fails to improve stigma or diagnostic clarity. For example, neurasthenia, or nervous exhaustion, was attributed to fast-paced urban life through the late 1970s. Its symptoms are now largely, to no real advantage, retitled as chronic fatigue syndrome. Diagnoses like "hysteria" have evolved into histrionic personality disorder and somatoform spectrum disorders, although less as a result of demonic possession or a "wandering uterus." Decriminalized and depathologized homosexuality remains a political football, where religious "sin" conceptualizations have not been displaced by studies documenting healthy adjustments among groups with diverse sexual orientations and preferences. Each of these remains severely socially stigmatized. The pseudoscience of "drapetomania," once used to rationalize and pathologize a slave's freedom, is perceived now as psychiatric incarcerations of mentally healthy individuals, more commonly in totalitarian regimes-a politicization of stigma. Research reviews and funding efforts need to emphasize a sound basis for individuals caught in perpetuated diagnostic challenges, not remedied by simple shifts in nomenclature.

Defects in experiencing disgust may contribute to obesity by allowing for the overconsumption of food. However, the relationship of disgust proneness and its associated neural locus has yet to be explored in the context of obesity. Thirty-three participants (17 obese, 16 lean) completed the Disgust Propensity and Sensitivity Scale-Revised and a functional magnetic resonance imaging paradigm where images from 4 categories (food, contaminates, contaminated food or fixation) were randomly presented. Independent two-sample t-tests revealed significantly lower levels of Disgust Sensitivity for the obese group (mean score = 14.7) compared with the lean group (mean score = 17.6, P = 0.026). The obese group had less activation in the right insula than the lean group when viewing contaminated food images. Multiple regression with interaction analysis revealed one left insula region where the association of Disgust Sensitivity scores with activation differed by group when viewing contaminated food images. These interaction effects were driven by the negative correlation of Disgust Sensitivity scores with beta values extracted from the left insula in the obese group (r = -0.59) compared with a positive correlation in the lean group (r = 0.65). Given these body mass index-dependent differences in Disgust Sensitivity and neural responsiveness to disgusting food images, it is likely that altered Disgust Sensitivity may contribute to obesity., (© The Author (2015). Published by Oxford University Press. For Permissions, please email: journals.permissions@oup.com.)

Depression remains a great societal burden and a major treatment challenge. Most antidepressant medications target serotonergic raphé nuclei. Acute tryptophan depletion (ATD) modulates serotonin function. To better understand the raphé's role in mood networks, we studied raphé functional connectivity in depression. Fifteen depressed patients were treated with sertraline for 12 weeks and scanned during ATD and sham conditions. Based on our previous findings in a separate cohort, resting state MRI functional connectivity between raphé and other depression-related regions (ROIs) was analyzed in narrow frequency bands. ATD decreased raphé functional connectivity with the bilateral thalamus within 0.025-0.05 Hz, and also decreased raphé functional connectivity with the right pregenual anterior cingulate cortex within 0.05-0.1 Hz. Using the control broadband filter 0.01-0.1 Hz, no significant differences in raphé-ROI functional connectivity were observed. Post-hoc analysis by remission status suggested increased raphé functional connectivity with left pregenual anterior cingulate cortex in remitters (n=10) and decreased raphé functional connectivity with left thalamus in non-remitters (n=5), both within 0.025-0.05 Hz. Reducing serotonin function appears to alter coordination of these mood-related networks in specific, low frequency ranges. For examination of effects of reduced serotonin function on mood-related networks, specific low frequency BOLD fMRI signals can identify regions implicated in neural circuitry and may enable clinically-relevant interpretation of functional connectivity measures. The biological significance of these low frequency signals detected in the raphé merits further study., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Background: Deep brain stimulation (DBS) is an effective treatment for patients with advanced Parkinson's disease (PD) and motor symptom complications. Recently, attention has been focused on whether offering DBS earlier in the course of PD is beneficial., Objective: The purpose of this study was to determine the effects of DBS on neuropsychological functioning in subjects with early stage PD., Methods: Thirty subjects with early PD (Hoehn & Yahr Stage II off medication) were randomized to optimal drug therapy (ODT) (n = 15) or bilateral subthalamic nucleus (STN) DBS+ODT (n = 15) after completing an expanded informed consent process specially designed for the study and administered by a medical ethicist and the study team. Comprehensive neuropsychological testing was completed in the treatment-withdrawn state at baseline and at 12 month and 24 month follow-ups., Results: Two serious adverse events occurred in the DBS+ODT group. One subject experienced a stroke and another developed infected hardware that contributed to specific declines in cognitive functioning. However, compared to the ODT group, the remaining subjects in the DBS+ODT group exhibited modest reductions on a few measures of attention, executive function, and word fluency at 12 months. These differences were largely diminished at 24 months, especially when those with the adverse events were excluded., Conclusions: The results of this trial provide novel data regarding the effects of DBS on cognitive function in early PD. We believe that the findings and insights from this trial can help guide the safety analysis and risk-benefit evaluations in future discussions of DBS in early stage PD.