One common denominator to the clinical phenotypes of borderline personality disorder (BPD) and major depressive disorder (MDD) is emotion regulation impairment. Although these two conditions have been extensively studied separately, it remains unclear whether their emotion regulation impairments are underpinned by shared or distinct neurobiological alterations.

We contrasted the neural correlates of negative emotion regulation across an adult sample of BPD patients (n = 19), MDD patients (n = 20), and healthy controls (HCs; n = 19). Emotion regulation was assessed using an established functional magnetic resonance imaging cognitive reappraisal paradigm. We assessed both task-related activations and modulations of interregional connectivity.

When compared to HCs, patients with BPD and MDD displayed homologous decreased activation in the right ventrolateral prefrontal cortex (vlPFC) during cognitive reappraisal. In addition, the MDD group presented decreased activations in other prefrontal areas (i.e., left dorsolateral and bilateral orbitofrontal cortices), while the BPD group was characterized by a more extended pattern of alteration in the connectivity between the vlPFC and cortices of the visual ventral stream during reappraisal.

This study identified, for the first time, a shared neurobiological contributor to emotion regulation deficits in MDD and BPD characterized by decreased vlPFC activity, although we also observed disorder-specific alterations. In MDD, results suggest a primary deficit in the strength of prefrontal activations, while BPD is better defined by connectivity disruptions between the vlPFC and temporal emotion processing regions. These findings substantiate, in neurobiological terms, the different profiles of emotion regulation alterations observed in these disorders.

Although deficits in affective processing are a core component of anorexia nervosa (AN), we lack a detailed characterization of the neurobiological underpinnings of emotion regulation impairment in AN. Moreover, it remains unclear whether these neural correlates scale with clinical outcomes.

We investigated the neural correlates of negative emotion regulation in a sample of young women receiving day-hospital treatment for AN (n = 21) and healthy controls (n = 21). We aimed to determine whether aberrant brain activation patterns during emotion regulation predicted weight gain following treatment in AN patients and were linked to AN severity. To achieve this, participants completed a cognitive reappraisal paradigm during functional magnetic resonance imaging. Skin conductance response, as well as subjective distress ratings, were recorded to corroborate task engagement.

Compared to controls, patients with AN showed reduced activation in the dorsolateral prefrontal cortex (dlPFC) during cognitive reappraisal [pFWE<0.05, threshold-free cluster enhancement (TFCE) corrected]. Importantly, psycho–physiological interaction analysis revealed reduced functional connectivity between the dlPFC and the amygdala in AN patients during emotion regulation (pFWE<0.05, TFCE corrected), and dlPFC-amygdala uncoupling was associated with emotion regulation deficits (r = −0.511, p = 0.018) and eating disorder severity (r = −0.565, p = .008) in the AN group. Finally, dlPFC activity positively correlated with increases in body mass index (r = 0.471, p = 0.042) and in body fat mass percentage (r = 0.605, p = 0.008) following 12 weeks of treatment.

Taken together, our findings indicate that individuals with AN present altered fronto-amygdalar response during cognitive reappraisal and that this response may serve as a predictor of response to treatment and be linked to clinical severity.

DSM-5 proposed a new operational system by using the number of fulfilled criteria as an indicator of gambling disorder severity. This method has proven to be controversial among researchers and clinicians alike, due to the lack of studies indicating whether severity, as measured by these criteria, is clinically relevant in terms of treatment outcome. Additionally, numerous studies have highlighted the associations between gambling disorder and impulsivity, though few have examined the impact of impulsivity on long-term treatment outcomes.

In this study, we aimed to assess the predictive value of DSM-5 severity levels on response to cognitive-behavioral therapy (CBT) in a sample of male adults seeking treatment for gambling disorder (n = 398). Furthermore, we explored longitudinal predictors of CBT treatment response at a follow-up, considering UPPS-P impulsivity traits.

Our study failed to identify differences in treatment outcomes between patients categorized by DSM-5 severity levels. Higher baseline scores in negative urgency predicted relapse during CBT treatment, and higher levels of sensation seeking were predictive of drop-out from short-term treatment, as well as of drop-out at 24-months.

These noteworthy findings raise questions regarding the clinical utility of DSM-5 severity categories and lend support to the implementation of dimensional approaches for gambling disorder.

Impulsivity and cognitive distortions are hallmarks of gambling disorder (GD) but it remains unclear how they contribute to clinical phenotypes. This study aimed to (1) compare impulsive traits and gambling-related distortions in strategic versus non-strategic gamblers and online versus offline gamblers; (2) examine the longitudinal association between impulsivity/cognitive distortions and treatment retention and relapse.

Participants seeking treatment for GD (n = 245) were assessed for gambling modality (clinical interview), impulsive traits (Urgency, Premeditation, Perseverance and Sensation Seeking [UPPS] scale) and cognitive distortions (Gambling Related Cognitions Scale) at treatment onset, and for retention and relapse (as indicated by the clinical team) at the end of treatment. Treatment consisted of 12-week standardized cognitive behavioral therapy, conducted in a public specialized clinic within a general public hospital.

Strategic gamblers had higher lack of perseverance and gambling-related expectancies and illusion of control than non-strategic gamblers, and online gamblers had generally higher distortions but similar impulsivity to offline gamblers. Lack of perseverance predicted treatment dropout, whereas negative urgency and distortions of inability to stop gambling and interpretative bias predicted number of relapses during treatment.

Individuals with online and strategic GD phenotypes have heightened gambling related biases associated with premature treatment cessation and relapse. Findings suggest that these GD phenotypes may need tailored treatment approaches to reduce specific distortions and impulsive facets.

To estimate trajectories of the gambling disorder (GD) severity for 12 months following a manualized cognitive-behavior-therapy (CBT) program, and to identify the main variables associated with each trajectory.

Latent Class Growth Analysis examined the longitudinal changes of n = 603 treatment-seeking patients with GD.

Five separate empirical trajectories were identified: T1 (n = 383, 63.5%) was characterized by the most highest baseline gambling severity levels and positive progress to recovery during the follow-up period; T2 (n = 154, 25.5%) featured participants with high baseline gambling severity and good progress to recovery; T3 (n = 30, 5.0%) was made up of patients with high gambling baseline severity and slow progress to recovery; T4 (n = 13, 2.2%) and T5 (n = 23, 3.8%) contained participants with high baseline gambling severity and moderate (T4) and poor (T5) progress in GD severity during the follow-up. Psychopathological state and personality traits discriminated between trajectories. Poor compliance with the therapy guidelines and the presence of relapses also differed between the trajectories.

Our findings show that patients seeking treatment for GD are heterogeneous and that trends in progress following treatment can be identified considering sociodemographic features, psychopathological state and personality traits. These results could be useful in developing more efficient interventions for GD patients.

Bipolar disorder (BD) and obsessive compulsive disorder (OCD) are prevalent, comorbid, and disabling conditions, often characterized by early onset and chronic course. When comorbid, OCD and BD can determine a more pernicious course of illness, posing therapeutic challenges for clinicians. Available reports on prevalence and clinical characteristics of comorbidity between BD and OCD showed mixed results, likely depending on the primary diagnosis of analyzed samples.

We assessed prevalence and clinical characteristics of BD comorbidity in a large international sample of patients with primary OCD (n = 401), through the International College of Obsessive–Compulsive Spectrum Disorders (ICOCS) snapshot database, by comparing OCD subjects with vs without BD comorbidity.

Among primary OCD patients, 6.2% showed comorbidity with BD. OCD patients with vs without BD comorbidity more frequently had a previous hospitalization (p < 0.001) and current augmentation therapies (p < 0.001). They also showed greater severity of OCD (p < 0.001), as measured by the Yale–Brown Obsessive Compulsive Scale (Y-BOCS).

These findings from a large international sample indicate that approximately 1 out of 16 patients with primary OCD may additionally have BD comorbidity along with other specific clinical characteristics, including more frequent previous hospitalizations, more complex therapeutic regimens, and a greater severity of OCD. Prospective international studies are needed to confirm our findings.

with the DSM-5 new eating disorders (EDs) diagnostic subtypes were identified within the Other Specified Feeding or Eating Disorders (OSFED) category, which have so far been under-researched. Objectives of this study were to examine differential features among OSFED subtypes, exploring short-term cognitive-behavioral therapy (CBT) response and identifying clinical predictors of therapy outcome.

the sample included 176 female patients diagnosed with OSFED [82 atypical anorexia nervosa (atypical-AN), 57 purging disorder (PD), and 37 subthreshold bulimia nervosa (sub-BN)]. Assessment included eating-related, psychopathological and personality measures.

results showed similar clinical and personality profiles between the diagnostic subtypes, with hardly any differences, only observable in the core symptoms of each diagnosis. The sub-BN group was the one which showed more social impairment. Regarding treatment outcome, the three groups did not reveal significant differences in remission rates, therapeutic adherence or dropout rates, reaching rates of dropout from 36.8% to 50% (p =.391). However, different ED subtype predictors appear related with full remission or dropout risk, specifically personality traits.

our results suggest that OSFED patients may benefit similarly from the same CBT outpatient group approach. However, high dropout rates and low motivation seems to be an important limitation and challenge for future approaches.

Obsessive-compulsive disorder (OCD) is associated with variable risk of suicide and prevalence of suicide attempt (SA). The present study aimed to assess the prevalence of SA and associated sociodemographic and clinical features in a large international sample of OCD patients.

A total of 425 OCD outpatients, recruited through the International College of Obsessive-Compulsive Spectrum Disorders (ICOCS) network, were assessed and categorized in groups with or without a history of SA, and their sociodemographic and clinical features compared through Pearson’s chi-squared and t tests. Logistic regression was performed to assess the impact of the collected data on the SA variable.

14.6% of our sample reported at least one SA during their lifetime. Patients with an SA had significantly higher rates of comorbid psychiatric disorders (60 vs. 17%, p<0.001; particularly tic disorder), medical disorders (51 vs. 15%, p<0.001), and previous hospitalizations (62 vs. 11%, p<0.001) than patients with no history of SA. With respect to geographical differences, European and South African patients showed significantly higher rates of SA history (40 and 39%, respectively) compared to North American and Middle-Eastern individuals (13 and 8%, respectively) (χ2=11.4, p<0.001). The logistic regression did not show any statistically significant predictor of SA among selected independent variables.

Our international study found a history of SA prevalence of ~15% in OCD patients, with higher rates of psychiatric and medical comorbidities and previous hospitalizations in patients with a previous SA. Along with potential geographical influences, the presence of the abovementioned features should recommend additional caution in the assessment of suicide risk in OCD patients.

The aetiological boundary between obsessive–compulsive related disorders (OCRDs) including obsessive–compulsive disorder (OCD) and anxiety disorders is unclear and continues to generate debate.

To determine the genetic overlap and the pattern of causal relationships among OCRDs and anxiety disorders.

Multivariate twin modelling methods and a new regression analysis to infer causation were used, involving 2495 male and female twins.

The amount of common genetic liability observed for OCD symptoms was higher when considering anxiety disorders and OCRDs in the model v. modelling OCRD symptoms alone. OCD symptoms emerged as risk factors for the presence of generalised anxiety, panic and hoarding symptoms, whereas social phobia appeared as a risk factor for OCD symptoms.

OCD represents a complex phenotype that includes important shared features with anxiety disorders and OCRDs. The novel patterns of risk identified between OCD and anxiety disorder may help to explain their frequent co-occurrence.

Despite knowledge of amygdala involvement in fear and anxiety, its contribution to the pathophysiology of obsessive–compulsive disorder (OCD) remains controversial. In the context of neuroimaging studies, it seems likely that the heterogeneity of the disorder might have contributed to a lack of consistent findings.

To assess the influence of OCD symptom dimensions on amygdala responses to a well-validated emotional face-matching paradigm.

Cross-sectional functional magnetic resonance imaging (fMRI) study of 67 patients with OCD and 67 age-, gender- and education-level matched healthy controls.

The severity of aggression/checking and sexual/religious symptom dimensions were significantly associated with heightened amygdala activation in those with OCD when responding to fearful faces, whereas no such correlations were seen for other symptom dimensions.

Amygdala functional alterations in OCD appear to be specifically modulated by symptom dimensions whose origins may be more closely linked to putative amygdala-centric processes, such as abnormal fear processing.