Fibromyalgia (FM) is a chronic pain syndrome with a controversial etiopathogenesis. Patients with FM usually complain of cognitive symptoms, which are described as “fibrofog.” These cognitive complaints might be caused partially by dissociative disorders (DD). The aim of this research is to determine the association between FM and DD.

The authors conducted a case-control study for this purpose, integrated by 3 groups: control (C), patients with rheumatic disorders (R), and patients with FM (FM), who were compared through the Dissociative Experiences Scale (DES).

The findings are as follows: 42% were taking medications in the FM group, and their differences in scores with those who were not under medications were then considered. In terms of the results, the FM group showed higher scores than both C and R groups (p < 0.05). Patients with FM who were taking antidepressants had lower scores than those who were not (Z-score –8.03; p < 0.05); and finally, 5.71% had a score over 30 (χ2 = 3.73, p = 0.15).

Patients with FM had higher scores, which might be related to the association of dissociative experiences, lifetime trauma, and victimization. Antidepressants might have some role on dissociative symptoms as well.

Numerous studies shown that structural hippocampal alterations are present in subjects at high risk of developing psychosis or schizophrenia. These findings indicate that in a subset of patients undergoing first-psychosis episode (FPE), hippocampal volume alterations are accompanied by associated cognitive and neuropsychological deficits. The combination of psychological deficits and neuroanatomical alterations, in turn, appears to increase treatment complexity and worsen clinical outcomes.

We aim to determine whether cognitive and neuropsychological functioning deficits precede or follow hippocampal alterations during early onset psychosis.

This cross-sectional study describes 3 case-studies of adolescent subjects, ages 16–17, admitted at the child and adolescent inpatient psychiatric unit in lieu of first psychotic episode. We conducted detailed structured clinical psychiatric interviews, anatomical-structural magnetic resonance imaging (MRI), sleep-deprived electroencephalogram (EEG) recordings, laboratory testing, and a comprehensive battery of psychological testing to better understand their clinical pictures.

Psychological testing in each patient demonstrated the presence of low to borderline intellectual functioning coupled with neuropsychological deficits in different psychiatric domains. Interestingly, these changes coincided with structural MRI alterations in the hippocampal area.

Our case report adds to the armamentarium of literature signifying that radiologically detectable alterations of the hippocampus may occur either concomitantly or closely following the development of early cognitive deficits in patients with FPE.

Our aim was to summarize the efficacy and safety of atomoxetine, amphetamines, and methylphenidate in schizophrenia.

We undertook a systematic review, searching PubMed/Scopus/Clinicaltrials.gov for double-blind, randomized, placebo-controlled studies of psychostimulants or atomoxetine in schizophrenia published up to 1 January 2017. A meta-analysis of outcomes reported in two or more studies is presented.

We included 22 studies investigating therapeutic effects of stimulants (k=14) or measuring symptomatic worsening/relapse prediction after stimulant challenge (k=6). Six studies of these two groups plus one additional study investigated biological effects of psychostimulants or atomoxetine. No effect resulted from interventional studies on weight loss (k=1), smoking cessation (k=1), and positive symptoms (k=12), and no improvement was reported with atomoxetine (k=3) for negative symptoms, with equivocal findings for negative (k=6) and mood symptoms (k=2) with amphetamines. Attention, processing speed, working memory, problem solving, and executive functions, among others, showed from no to some improvement with atomoxetine (k=3) or amphetamines (k=6). Meta-analysis did not confirm any effect of stimulants in any symptom domain, including negative symptoms, apart from atomoxetine improving problem solving (k=2, standardized mean difference (SMD)=0.73, 95% CI=0.10–1.36, p=0.02, I2=0%), and trending toward significant improvement in executive functions with amphetamines (k=2, SMD=0.80, 95% CI=−1.68 to +0.08, p=0.08, I2=66%). In challenge studies, amphetamines (k=1) did not worsen symptoms, and methylphenidate (k=5) consistently worsened or predicted relapse. Biological effects of atomoxetine (k=1) and amphetamines (k=1) were cortical activation, without change in β-endorphin (k=1), improved response to antipsychotics after amphetamine challenge (k=2), and an increase of growth hormone–mediated psychosis with methylphenidate (k=2). No major side effects were reported (k=6).

No efficacy for stimulants or atomoxetine on negative symptoms is proven. Atomoxetine or amphetamines may improve cognitive symptoms, while methylphenidate should be avoided in patients with schizophrenia. Insufficient evidence is available to draw firm conclusions.

The clinical phenotype of gambling disorder (GD) is suggestive of changes in brain regions involved in reward and impulse suppression, notably the striatum. Studies have yet to characterize striatal morphology (shape) in GD and whether this may be a vulnerability marker.

To characterize the morphology of the striatum in those with disordered gambling (at-risk gambling and GD) versus controls.

Individuals aged 18–29 years were classified a priori into those with some degree of GD symptoms (at-risk gambling and GD) or controls. Exclusion criteria were a current mental disorder (apart from GD), history of brain injury, or taking psychoactive medication within 6 weeks of enrollment. History of any substance use disorder was exclusionary. Participants completed an impulsivity questionnaire and structural brain scan. Group differences in volumes and morphology were characterized in subcortical regions of interest, focusing on the striatum.

Thirty-two people with GD symptoms (14 at-risk and 18 GD participants) and 22 controls completed the study. GD symptoms were significantly associated with higher impulsivity and morphological alterations in the bilateral pallidum and left putamen. Localized contraction in the right pallidum strongly correlated with trait impulsivity in those with GD symptoms.

Morphologic abnormalities of the striatum appear to exist early in the disease trajectory from subsyndromal gambling to GD and thus constitute candidate biological vulnerability markers, which may reflect differences in brain development associated with trait impulsivity. Striatal morphology and associated impulsivity might predispose to a range of problematic repetitive behaviors.

Low-field magnetic stimulation (LFMS) has mood-elevating effect, and the increase of brain-derived neurotrophic factor (BDNF) is associated with antidepressant treatment. We evaluated the effects and association with BDNF of rhythmic LFMS in the treatment of major depressive disorder (MDD).

A total of 22 MDD patients were randomized to rhythmic alpha stimulation (RAS) or rhythmic delta stimulation (RDS), with 5 sessions per week, lasting for 6 weeks. Outcomes assessments included the 17-item Hamilton Depression Rating Scale (HAMD–17), the Hamilton Anxiety Rating Scale (HAMA), and the Clinical Global Impressions–Severity scale (CGI–S) at baseline and at weeks 1, 2, 3, 4, and 6. Serum BDNF level was measured at baseline and at weeks 2, 4, and 6.

HAMD–17, HAMA, and CGI–S scores were significantly reduced with both RAS and RDS. RAS patients had numerically greater reductions in HAMD–17 scores than RDS patients (8.9 ± 7.4 vs. 6.2 ± 6.2, effect size [ES]=0.40), while RDS patients had greater improvement in HAMA scores (8.2 ± 8.0 vs. 5.3 ± 5.8, ES=0.42). RAS was associated with clinically relevant advantages in response (54.5% vs. 18.2%, number-needed-to-treat [NNT]=3) and remission (36.4% vs. 9.1%, NNT=4). BDNF increased significantly during the 6-week study period (p<0.05), with greater increases in RAS at weeks 4 and 6 (ES=0.66—0.76) and statistical superiority at week 2 (p=0.034, ES=1.23). Baseline BDNF in the 8 responders (24.8±9.0 ng/ml) was lower than in the 14 nonresponders (31.1±7.3 ng/ml, p=0.083, ES=–0.79), and BDNF increased more in responders (8.9±7.8 ng/ml) than in nonresponders (1.8±3.5 ng/ml, p=0.044). The change in BDNF at week 2 was the most strongly predicted response (p=0.016).

Rhythmic LFMS was effective for MDD. BDNF may moderate/mediate the efficacy of LFMS.

Two similarly designed extension studies evaluated the long-term safety and tolerability of desvenlafaxine for the treatment of children and adolescents with major depressive disorder (MDD). Efficacy was evaluated as a secondary objective.

Both 6-month, open-label, flexible-dose extension studies enrolled children and adolescents who had completed one of two double-blind, placebo-controlled, lead-in studies. One lead-in study included a 1-week transition period prior to the extension study. Patients received 26-week treatment with flexible-dose desvenlafaxine (20–50 mg/d). Safety assessments included comprehensive psychiatric evaluations, vital sign assessments, laboratory evaluations, 12-lead electrocardiogram, physical examination with Tanner assessment, and Columbia-Suicide Severity Rating Scale. Adverse events (AEs) were collected throughout the studies. Efficacy was assessed using the Children’s Depression Rating Scale–Revised (CDRS-R).

A total of 552 patients enrolled (completion rates: 66.4 and 69.1%). AEs were reported by 79.4 and 79.1% of patients in the two studies; 8.9 and 5.2% discontinued due to AEs. Treatment-emergent suicidal ideation or behavior was reported for 16.6 and 14.1% of patients in the two studies. Mean (SD) CDRS-R total score decreased from 33.83 (11.93) and 30.92 (10.20) at the extension study baseline to 24.31 (7.48) and 24.92 (8.45), respectively, at week 26.

Desvenlafaxine 20 to 50 mg/d was generally safe and well tolerated with no new safety signals identified in children and adolescents with MDD who received up to 6 months of treatment in these studies. Patients maintained the reduction in severity of depressive symptoms observed in all treatment groups at the end of the lead-in study.

This post-hoc pooled analysis evaluated categorical change in functional impairment in patients with major depressive disorder (MDD) treated with desvenlafaxine versus placebo and examined whether early improvement in functioning predicted functional outcomes at study endpoint.

Data were pooled from eight randomized, double-blind, placebo-controlled studies of desvenlafaxine for the treatment of MDD, including adults who were randomly assigned to receive desvenlafaxine 50 or 100 mg/d or placebo (N=3,384). Shift tables were generated for categorical changes in functional impairment from baseline based on Sheehan Disability Scale (SDS) subscale scores. The categories were none/mild (0–3), moderate (4–6), and marked/extreme (7–10). Treatment comparisons for prespecified shifts of interest and predictive value of week 2 or 4 improvement in SDS subscale scores for functional outcome at week 8 were assessed using logistic regression.

Greater proportions of patients receiving desvenlafaxine 50 and 100 mg achieved improvement from baseline to week 8 for each prespecified shift endpoint versus placebo (all p ≤ 0.02). Early improvement in SDS subscale scores was a statistically significant predictor of functional outcome at week 8, both overall and for each treatment group (all p<0.0001).

Treatment with desvenlafaxine 50 or 100 mg/d led to significantly greater categorical improvement in functional impairment versus placebo, and improvement in SDS subscale scores significantly predicted functional outcome. Monitoring patient progress early in the course of antidepressant treatment using a functional assessment such as the SDS may help clinicians determine whether or not treatment adjustments are needed.

Despite consistently high discontinuation rates due to withdrawal of consent (WOC) and insufficient therapeutic effect (ITE) in schizophrenia trials, insight into the underlying factors contributing to poor satisfaction with treatment and dropout is limited. A better understanding of these factors could help to improve trial design and completion rates.

Using data from 1,136 trial participants with schizophrenia or schizoaffective disorder, we explored associations between predictor variables with (1) dropout due to WOC and ITE and (2) satisfaction with treatment among patients and investigators by means of hierarchic multiple regression analyses.

ITE was associated with poor clinical improvement, poor investigator satisfaction with treatment, and poor patient insight into their own disease, whereas WOC only showed a meaningful association with poor patient satisfaction with treatment. Investigator satisfaction with treatment appeared most strongly associated with Positive and Negative Syndrome Scale (PANSS) positive factor endpoint scores, whereas patient satisfaction with treatment was best predicted by the endpoint score on the PANSS emotional distress factor. The occurrence of severe side effects showed no meaningful association to satisfaction with treatment among investigators and patients, and neither did a patient’s experienced psychopathology, nor their self-rating of functional impairment.

Whereas trial discontinuation due to ITE is associated with poor treatment effectiveness, a patient’s decision to withdraw from an antipsychotic trial remains unpredictable and may occur even when the investigator observes a global clinical improvement and is satisfied with the treatment.