Four studies have found a smaller amygdalar volume in patients with borderline personality disorder (BPD) relative to controls, whereas four other studies have found similar amygdalar volume in BPD patients relative to controls. This study aims to compare amygdalar volumes of BPD patients with controls, and also to compare BPD patients with and without post-traumatic stress disorder (PTSD) with controls in order to determine whether PTSD can explain the heterogeneity of findings.

Systematic review and meta-analysis of magnetic resonance imaging studies that measured amygdalar volumes in BPD patients and healthy controls.

A significant reduction of amygdalar volumes in BPD patients was confirmed (p < .001). However, data from the studies that discriminated BPD patients with and without PTSD indicated that amygdalar volumes were significantly smaller in BPD patients without PTSD relative to controls (left: p = .02; right: p = .05), but not in BPD patients with PTSD relative to controls (left: p = .08; right: p = .20).

This meta-analysis suggests that amygdalar volumes are reduced in patients with BPD. This pattern is confirmed in BPD patients without PTSD, but not in BPD patients with PTSD, raising the possibility that reduced amygdalar volume in BPD patients cannot be explained by comorbid PTSD.

To examine the prevalence of the C677T polymorphism of the methylene tetrahydrofolate reductase (MTHFR) gene and the A2756G polymorphism of methionine synthase (MS), and their impact on antidepressant response.

We screened 224 subjects (52% female, mean age 39 ± 11 years) with SCID-diagnosed major depressive disorder (MDD), and obtained 194 genetic samples. 49 subjects (49% female, mean age 36 ± 11 years) participated in a 12-week open clinical trial of fluoxetine 20–60 mg/day. Association between clinical response and C677T and A2756G polymorphisms, folate, B12, and homocysteine was examined.

Prevalence of the C677T and A2756G polymorphisms was consistent with previous reports (C/C = 41%, C/T = 47%, T/T = 11%, A/A = 66%, A/G = 29%, G/G = 4%). In the fluoxetine-treated subsample (n = 49), intent-to-treat (ITT) response rates were 47% for C/C subjects and 46% for pooled C/T and T/T subjects (nonsignificant). ITT response rates were 38% for A/A subjects and 60% for A/G subjects (nonsignificant), with no subjects exhibiting the G/G homozygote. Mean baseline plasma B12 was significantly lower in A/G subjects compared to A/A, but folate and homocysteine levels were not affected by genetic status. Plasma folate was negatively associated with treatment response.

The C677T and A2756G polymorphisms did not significantly affect antidepressant response. These preliminary findings require replication in larger samples.

This study investigated the safety and efficacy of long-term treatment with high-dose desvenlafaxine (administered as desvenlafaxine succinate) in major depressive disorder (MDD).

In this multicenter, open-label study, adult outpatients with MDD aged 18–75 were treated with flexible doses of desvenlafaxine (200–400 mg/d) for ≤ 1 year. Safety assessments included monitoring of treatment-emergent adverse events (TEAEs), patient discontinuations due to adverse events, electrocardiograms, vital signs, and laboratory determinations. The primary efficacy measure was mean change from baseline in the 17-item Hamilton Rating Scale for Depression [HAM-D(17)] total score.

The mean daily desvenlafaxine dose range over the duration of the trial was 267–356 mg (after titration). The most frequent TEAEs in the safety population (n = 104) were nausea (52%) and headache (41%), dizziness (31%), insomnia (29%), and dry mouth (27%). All TEAEs were mild or moderate in severity. Thirty-four (33%) patients discontinued from the study because of TEAEs; nausea (12%) and dizziness (9%) were the most frequently cited reasons. The mean change in HAM-D(17) total score for the intent-to-treat population (n = 99) was −9.9 at the last on-therapy visit in the last-observation-carried-forward analysis and −14.0 at month 12 in the observed cases analysis.

High-dose desvenlafaxine (200–400 mg/d) was generally safe and effective in the long-term treatment of MDD.

Risk for post-traumatic stress disorder (PTSD) varies in part due to the nature of the traumatic event involved. Both injury and return from combat pose high risk of PTSD symptoms. How different injuries may predispose towards PTSD is less well understood.

A retrospective record review was conducted from 1402 service members who had returned to Naval Medical Center San Diego from Iraq or Afghanistan and who had completed the PTSD Checklist as part of their post-deployment screening. Rates of PTSD were examined in relation to mechanism of injury.

Of those without injury, 8% met Diagnostic and Statistical Manual criteria for PTSD. Thirteen percent of those with a penetrating injury, 29% with blunt trauma, and 33% with combination injuries met criteria for PTSD. PTSD severity scores varied significantly according to type of injury.

The World War I concept of “shell shock” implied that blast-related injuries were more likely to result in psychological symptoms than were other injuries. These data may support that idea. Circumstance of injury, population differences, and reporting bias could also have influenced the results.

These results suggest that service members with blunt or combination injuries merit particular attention when screening for PTSD.

This meta-analysis compared the efficacy and safety of desvenlafaxine and venlafaxine at the Australian approved doses.

A systematic literature search was conducted to identify all placebo-controlled studies of desvenlafaxine and venlafaxine in the treatment of major depression. The pivotal outcome measure used to assess comparative efficacy was the mean change in Hamilton Rating Scale for Depression-17 score from baseline. Tolerability and safety were compared by an evaluation of reported adverse events. Standard and Bayesian methods were used to conduct the indirect comparisons.

Using a mixed model repeated measures analysis, the pooled weighted mean difference for the mean change in Hamilton Rating Scale for Depression-17 score from baseline was −2.81 (−3.72, −1.91; p < 0.001) for desvenlafaxine and −2.61 (−3.17, −2.05; p < 0.001) for venlafaxine. An indirect Bayesian analysis adjusted for baseline Hamilton Rating Scale for Depression-17 score showed no significant difference between the two treatments (weighted mean difference −0.27; −1.17, 0.65). A standard indirect comparison of any adverse events showed no significant difference between desvenlafaxine and venlafaxine (relative risk 1.01; 0.96, 1.06; p = 0.70 and risk difference −0.01; −0.05, 0.03; p = 0.59). Standard indirect comparisons of both nausea and drop-outs identified potential differences between treatments, with the risk difference analyses suggesting a trend in favor of desvenlafaxine (nausea: relative risk 0.97; 0.77, 1.22; p = 0.80/RD −0.07; −0.12, −0.01; p = 0.02; and drop-outs due to adverse events: RR 0.86; 0.58, 1.29; p = 0.48/RD −0.04; −0.08, 0.00; p = 0.06).

Based on the results of this meta-analysis, desvenlafaxine was shown to be non-inferior to venlafaxine in terms of efficacy, and has an advantage in terms of less nausea.

The best prevention against relapse results when patients are taught to restructure negative core beliefs (CBs). Efficacy of the trial-based thought record (TBTR) in decreasing the credit given by patients to negative CBs and corresponding emotions was evaluated.

Patients (n = 166) were submitted to a simulation of a legal trial to assess their adherence to negative CBs and corresponding emotions after each cognitive therapy technique incorporated by TBTR.

Significant reductions existed in percent values after the first and second defense attorney pleas, as well as after jury's verdict and initial preparation for the appeal (p < 0.001), relative to the investigation phase. Significant differences also emerged between the defense attorney's first and second pleas and between the defense attorney's second plea and jury's verdict, as well as preparation for the appeal (p < 0.001). There was no significant difference between percentages presented by patients submitted to TBTR used in the empty chair format relative to the conventional format. Similarly, there was no difference between outcomes, regardless of therapists’ level of exposure to TBTR.

TBTR may help patients reduce attachment to negative CBs and corresponding emotions. Outcomes were significantly favorable regardless of the format use and therapists’ level of exposure to TBTR.

Pathological gambling (PG) is a severe and persistent pattern of problem gambling that has been aligned with obsessive-compulsive disorder (OCD). However, no study has compared the neurocognitive profiles of individuals with PG and OCD.

We compared neurocognitive functioning, including executive function, verbal learning and memory, and visual–spatial organization and memory among 16 pathological gamblers, 31 drug-naïve OCD subjects, and 52 healthy controls.

The only neurocognitive marker common to both groups was increased fragmentation errors on the Rey–Osterrieth Complex Figure Test (ROCF). The PG subjects showed increased nonperseverative error on the Wisconsin Card Sorting Test and organization difficulties in the ROCF, whereas the OCD subjects revealed longer response times on the Stroop test and retention difficulties on the immediate recall scale of the ROCF.

A more careful approach is required in considering whether PG is a part of the OCD spectrum, as little evidence of neurocognitive overlap between PG and OCD has been reported.

To evaluate the clinical features of obsessive-compulsive disorder (OCD) patients with comorbid tic disorders (TD) in a large, multicenter, clinical sample.

A cross-sectional study was conducted that included 813 consecutive OCD outpatients from the Brazilian OCD Research Consortium and used several instruments of assessment, including the Yale-Brown Obsessive-Compulsive Scale, the Dimensional Yale-Brown Obsessive-Compulsive Scale, the Yale Global Tic Severity Scale (YGTSS), the USP Sensory Phenomena Scale, and the Structured Clinical Interview for DSM-IV Axis I Disorders.

The sample mean current age was 34.9 years old (SE 0.54), and the mean age at obsessive-compulsive symptoms (OCS) onset was 12.8 years old (SE 0.27). Sensory phenomena were reported by 585 individuals (72% of the sample). The general lifetime prevalence of TD was 29.0% (n = 236), with 8.9% (n = 72) presenting Tourette syndrome, 17.3% (n = 141) chronic motor tic disorder, and 2.8% (n = 23) chronic vocal tic disorder. The mean tic severity score, according to the YGTSS, was 27.2 (SE 1.4) in the OCD + TD group. Compared to OCD patients without comorbid TD, those with TD (OCD + TD group, n = 236) were more likely to be males (49.2% vs. 38.5%, p < .005) and to present sensory phenomena and comorbidity with anxiety disorders in general: separation anxiety disorder, social phobia, specific phobia, generalized anxiety disorder, post-traumatic stress disorder, attention-deficit hyperactivity disorder, impulse control disorders in general, and skin picking. Also, the “aggressive,” “sexual/religious,” and “hoarding” symptom dimensions were more severe in the OCD + TD group.

Tic-related OCD may constitute a particular subgroup of the disorder with specific phenotypical characteristics, but its neurobiological underpinnings remain to be fully disentangled.