Globally, stigma associated with mental, neurological and substance use (MNS) disorders is rampant and a barrier to good health and overall well-being of people with these conditions. Person-centred digital approaches such as participatory video may reduce stigma, but evidence on their effectiveness in Africa is absent.

To evaluate the effectiveness of participatory video in reducing mental health-related stigma in a resource-limited setting.

We evaluated the effectiveness of using participatory video and face-to-face interaction between people with MNS disorders and a target audience in lowering stigma among 420 people living in Kilifi, Kenya. Changes in knowledge, attitudes and behaviour (KAB) were measured by comparing baseline scores with scores immediately after watching the participatory videos and 4 months after the intervention. Sociodemographic correlates of stigma scores were examined using multivariable linear regression models.

Compared with baseline, KAB scores significantly improved at both time points, suggesting reduced stigma levels. At 4 months, the changes in scores were: knowledge (β = 0.20, 95% CI 0.16–0.25; P < 0.01), liberal attitude (β = 1.08, 95% CI 0.98–1.17; P < 0.01), sympathetic attitude (β = 0.52, 95% CI 0.42–0.62; P < 0.01), tolerant attitude (β = 0.72, 95% CI 0.61–0.83; P < 0.01) and behaviour (β = 0.37, 95% CI 0.31–0.43; P < 0.01). Sociodemographic variables were significantly correlated with KAB scores; the correlations were not consistent across the domains.

Participatory video is a feasible and effective strategy in improving knowledge, attitudes and intended behaviour in a resource-limited setting. Further studies are required to understand the mechanisms through which it lowers stigma and to examine long-term sustainability and the effectiveness of multicomponent interventions.

Cocaine is a highly addictive psychostimulant that affects synaptic activity with structural and functional adaptations of neurons. The transmembrane synaptic vesicle glycoprotein 2A (SV2A) of pre-synaptic vesicles is commonly used to measure synaptic density, as a novel approach to the detection of synaptic changes. We do not know if a single dose of cocaine suffices to affect pre-synaptic SV2A density, especially during adolescence when synapses undergo intense maturation. Here, we explored potential changes of pre-synaptic SV2A density in target brain areas associated with the cocaine-induced boost of dopaminergic neurotransmission, specifically testing if the effects would last after the return of dopamine levels to baseline.

We administered cocaine (20 mg/kg i.p.) or saline to rats in early adolescence, tested their activity levels and removed the brains 1 hour and 7 days after injection. To evaluate immediate and lasting effects, we did autoradiography with [3H]UCB-J, a specific tracer for SV2A, in medial prefrontal cortex, striatum, nucleus accumbens, amygdala, and dorsal and ventral areas of hippocampus. We also measured the striatal binding of [3H]GBR-12935 to test cocaine’s occupancy of the dopamine transporter at both times of study.

We found a significant increase of [3H]UCB-J binding in the dorsal and ventral sections of hippocampus 7 days after the cocaine administration compared to saline-injected rats, but no differences 1 hour after the injection. The [3H]GBR-12935 binding remained unchanged at both times.

Cocaine provoked lasting changes of hippocampal synaptic SV2A density after a single exposure during adolescence

For many years, biofeedback and neurofeedback have been implemented in the treatment of depression. However, the effectiveness of these techniques on depressive symptomatology is still controversial. Hence, we conducted a meta-analysis of studies extracted from PubMed, Scopus, Web of Science and Embase.

Two different strings were considered for each of the two objectives of the study: A first group comprising studies patients with major depressive disorder (MDD) and a second group including studies targeting depressive symptomatology reduction in other mental or medical conditions.

In the first group of studies including patients with MDD, the within-group analyses yielded an effect size of Hedges' g = 0.717, while the between-group analysis an effect size of Hedges' g = 1.050. Moderator analyses indicate that treatment efficacy is only significant when accounting for experimental design, in favor of randomized controlled trials (RCTs) in comparison to non RCTs, whereas the type of neurofeedback, trial design, year of publication, number of sessions, age, sex and quality of study did not influence treatment efficacy. In the second group of studies, a small but significant effect between groups was found (Hedges' g = 0.303) in favor of bio- and neurofeedback against control groups. Moderator analyses revealed that treatment efficacy was not moderated by any of the sociodemographic and clinical variables.

Heart rate variability (HRV) biofeedback and neurofeedback are associated with a reduction in self-reported depression. Despite the fact that the field has still a large room for improvement in terms of research quality, the results presented in this study suggests that both modalities may become relevant complementary strategies for the treatment of MDD and depressive symptomatology in the coming years.

The relevance of inflammation to psychiatric disorders is well established. While inflammation was broadly investigated in mood disorders, obsessive-compulsive disorder (OCD) received little attention. C-reactive protein (CRP) is an inflammatory marker commonly assessed in clinical practice. Studies comparing CRP levels across mood disorders and OCD are lacking.

We compared the prevalence of CRP-based low-grade inflammation (LGI) across major depressive disorder (MDD), bipolar disorder (BD) and OCD, taking into account multiple individual variables that may affect CRP levels.

Retrospective, observational cross-sectional study in a naturalistic sample of hospitalized patients with MDD or BD or OCD. Information was collected from electronic medical records. Based on serum CRP levels at admission, the following were defined: CRP: >3 mg/L and ≤10 mg/l, “yes” LGI; ≤3 mg/L, “no” LGI. Logistic regression models were applied.

We included 156 patients with MDD, 135 with BD, and 97 with OCD. We found prevalence rates of CRP-LGI of 29.9%, 36.5%, and 47.4% in patients with OCD, MDD, and BD, respectively, without significant differences between groups. The entire set of individual variables considered (e.g., sex, body mass index, medication) explained only one-third of the observed variations in CRP-LGI.

CRP-LGI may be a transdiagnostic feature of a substantial portion of patients with MDD or BD or OCD, rather than being exclusive to a specific psychiatric disorder. The presence of LGI was not fully explained by individual confounding factors. Given the relevance of inflammation to psychiatric and medical outcome, routine measurements of CRP in psychiatric settings may be valuable.

No significant relationships.

The objective is to describe the prevalence and nature of painful symptoms among depressive outpatients and how are they related with depressive symptoms and somatic non painful symptoms at baseline.

The FINDER study, conducted in 12 European countries in depressed outpatients in routine primary and specialist care settings provides a unique opportunity to answer these questions.

Painful symptoms were evaluated among 3468 patients enrolled by 437 investigators, using the 28-item Somatic Symptom Inventory (SSI-28) and 6 Visual Analogue Scales (1 item on overall pain and 5 items on pain characteristics: headaches, back pain, shoulder pain, interferences with daily activities and pain while awake). There was a strong correlation between the VAS overall pain score and the pain sub score of the SSI-28. The threshold score of 30 mm on the overall pain severity in combination with selected comorbidities was used to divide patients in three pain cohorts: (1) those with no/mild pain; (2) those with moderate/severe œmedically explained pain and (3) those with moderate/severe medically unexplained pain.

Results showed that 1447 (43.7%) patients had no/mild pain, 550 (16,6%) had moderate/severe medically explained pain, and 1311 (39,6%) had moderate/severe medically unexplained pain. Of the different locations of pain symptoms (from the SSI-28), headaches were the most common, followed by muscle soreness and lower back pain. The mean depression score (HADS-D) was higher in patients with pain-related symptoms.

We studied the correlations between the measures of pain and depression. These results and their implications will be discussed.

The aim of this pilot study is to assess, in a sample of patients with chemical (alcohol) and behavioural (gambling) dependence, the specifical association between core symptoms and Separation Anxiety Disorder, both in Childhood and in Adulthood.

After a stabilization period of three months, outpatients with alcohol dependence (n = 30), patological gambling (n = 30) and a control group of anxiety disorders (n = 30) will be assessed with the following psychometric battery:

1. • SCI-SAS (Structured Clinical Interview for Separation Anxiety) Child and Adult

2. • SASI (Separation Anxiety Symptom Inventory)

3. • ASA-27 (Adult Separation Anxiety Questionnaire)

4. • TCI-R (Temperament anc Character Inventory Revised)

5. • GAF (Global Assess of Functioning)

6. • SCL-90-R (Symptom Checklist Revised)

7. • SOGS (South Oaks Gambling Scale)

8. • ADS (Alcohol Dependence Scale)

9. • HAM-A (Hamilton Anxiety Rating Scale)

A preliminary analisys of collected datas (n = 33) shows a strong inter-reliability of the Separation Anxiety Scales (SCI-SAS, SASI and ASA-27) with a p = 0.001 and an association between levels of functioning (GAF) and ASA-27 and SASI scores (p = 0.010 and p = 0,001).

It shows a statistical correlation between ASA-27 and TCI-R: inverse proportion with Self Directness (SD) (p = 0.004) and direct relation with Self Trascendency (ST) (p = 0.003).

Even if the sample is still limited we found an interesting trend between Separation Anxiety symptoms, TCI-R dimensions and core symptoms of dependance. We should focus better, when the study will be over, on narrow and specific sub-analisys that should lead us to a better understanding of the disorders.

A recent meta-analyses by our team found baseline respiratory abnormalities in subjects with Panic Disorder (PD) compared to subjects without PD. However, it is still open the question whether these abnormalities are intrinsic to pathophysiology of PD or may be shared with other psychiatric populations with high trait and state anxiety levels, such as subjects suffering from other anxiety disorders.

To meta-analyze the results from all of the studies that compared baseline respiratory parameters between subjects with PD and subjects with other anxiety disorders.

A literature research in bibliographic databases was performed. Only fixed-effects models were applied due to the small number of studies available for each parameter. Several moderator analyses and publication bias diagnostics were performed.

Subjects with PD showed a lower end-tidal CO2 pressure and a higher mean respiration rate at baseline compared to patients with both Generalized Anxiety Disorders and Social Phobia. Furthermore, also a significantly lower venous CO2 pressure and a higher venous HCO3- (bicarbonate ion) concentrations in PD than Social Phobia was found. Moderator analyses suggested that these differences between groups are not explained by differences in the state anxiety levels experienced during the assessment procedure. No evidence of publication bias was found.

Results suggest that peculiar baseline respiratory abnormalities and particularly a chronic hyperventilation may be specific of PD pathophysiology also when compared to other anxiety disorders.

A connection between balance system dysfunction and Agoraphobia (AG) in Panic Disorder (PD) has been found. Balance control of many patients with PD and AG rely mainly on visual cues (visual dependence) and moving visual stimuli in their peripheral visual field induce postural instability and anxiety. These features may maintain agoraphobic symptoms after standard treatments.

To study whether balance rehabilitation with moving peripheral visual stimuli would benefit patients with PD and AG not fully responders to standard treatments.

Six patients with PD and AG were included. Inclusion criteria: 1) panic-phobic symptoms despite adequate treatments (SSRIs for at least 3 months; cognitive behavioral therapy) and 2) balance dysfunction with instability during peripheral visual stimuli (posturography with and without peripheral visual stimulation).

The patients went through 10 sessions (3 sessions/week) of balance rehabilitation: static and dynamic exercises, with movements of eyes and head, during projection of peripheral visual stimuli (video-films, 32 times-accelerated, on large lateral screens). Descriptive and non-parametric analyses were applied.

After rehabilitation, the patients showed significant improvement both in panic-phobic symptoms (specific psychometric scale scores) (p < 0.05) and in balance performance (post-rehabilitation posturography with and without peripheral visual stimulation) (p < 0.05).

Balance rehabilitation with peripheral visual stimuli may increase the efficacy of standard treatments in patients with PD and AG and visual-balance dysfunction. Mechanisms of physical and emotional habituation to environmental destabilizing stimuli may be involved. Further larger and controlled studies are warranted.

In patients with Schizophrenia an association between smoking and improvement in cognitive deficits was found. Patients with Major Depressive Disorder (MDD) and Bipolar Disorder (BD) have shown a high prevalence of smoking habit and cognitive deficits but only a few studies have investigated the effect of smoking on their cognitive functions.

To study the effect of nicotine assumption on cognitive function in MDD and BD.

50 inpatients with MDD and 50 with BD (Major Depressive Episode) underwent a neuropsychological test battery (Anna Pesenti test, Attentive Matrices, Rey-Osterrieth Complex Figure, Phonemic/Semantic Fluency tests, Token test) at the beginning of their hospitalization. Smoking habit (current, lifetime) was investigated by specific questionnaires. Factorial ANOVA models were applied, with cognitive test scores as dependent variables and smoking (smoker/non-smoker) and diagnosis (MDD/BD) as factors.

Smokers showed significantly better performance in verbal memory (p < 0.001) and fluency tests (phonemic p = 0.012; semantic p = 0.023) than non-smokers. Significant and positive correlations were found between the scores of these tests and the number of cigarettes smoked in the 24 hours before, while no associations with the years of smoking habit were found. No effects of diagnosis or interaction between smoking and diagnosis on the cognitive performance were found.

Animal models show that nicotine can increase the monoamine levels in brain areas involved in memory and language functions. Our results suggest that the positive effect of smoking on cognitive functions may contribute to increase the smoking habit in patients with Mood Disorders as a self-medication strategy.

Despite the growing literature on the co-occurrence of obsessive-compulsive disorder (OCD) and schizophrenia, there is a lack of studies addressing the co-occurrence of OCD spectrum disorders, such as hypochondriasis, and schizophrenia.

The aim of the study was to investigate the prevalence rates of OCD and Hypochondriasis in schizophrenic patients treated with clozapine versus other atypical antipsychotics (AAPs).

We enrolled 24 consecutive schizophrenic patients treated with clozapine attending the ‘Clozapine Clinic’ of the University of Florence and 24 consecutive schizophrenic patients treated with other AAPs. Patient’s assessment was performed with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), the Hypochondriasis Y-BOCS (HY-BOCS) and the Global Assessment of Functioning Scale (GAF).

Considering the whole group (n = 48), we found an OCD prevalence rate of 29.2% (n = 14) and a hypochondriasis prevalence rate of 22.9% (n = 11). We found a significant correlation between Y-BOCS and HY-BOCS scores (p = .007) suggesting an association between OCD and hypochondriasis in these patients. We also found a significant negative correlation between H-YBOCS scores and GAF scores (p = .006). Clozapine-treated patients had a higher rate of OCD (37.5% vs 20.8%). and hypochondriasis (37.5% vs 8.3%) than other AAP-treated patients.

We found a higher prevalence rate of OCD and hypochondriasis comorbidity in schizophrenic patients than in general population. The prevalence rate of OCD and hypochondriasis was higher in clozapine-treated patients versus other AAP-treated patients. Furthermore, the severity of hypochondriasis symptoms was correlated to a lower level of global functioning.

Previous studies suggested that cognitive enhancement associated with nicotine may be a form of “selfmedication” explaining high rates of smokers among patients with Schizophrenia or Mood Disorders. On the contrary, patients with Obsessive-Compulsive Disorder (OCD), though are characterized by cognitive impairment, do not show a higher tendency to smoking than general population and show a lower tendency to smoking than other psychiatric patients.

Our pilot study aims to investigate the effect of cigarette smoking on cognitive performance in patients with OCD. No published studies investigated this issue.

Fifty-nine inpatients suffering from OCD (22 smokers and 37 non-smokers) were recruited. At the beginning of the hospitalization, we assessed different cognitive domains using a standard non-computerized neuropsychological battery (memory, attention and verbal fluency). In addition, 28 patients out of the 59 (12 smokers and 16 non-smokers) underwent a computerized neuropsychological evaluation specific for executive functions (CANTAB software). OCD-clinical symptoms were evaluated by Y-BOCS.

Smokers and non-smokers did not differ for demographic (age, schooling) and clinical variables (Y-BOCS scores). Compared to non-smokers, smokers showed worse performances on the phonemic fluency test (non-computerized battery) and a tendency to risk higher amount of money on a decision making task (CANTAB).

Smoking does not seem to improve cognitive performances of patients with OCD, whereas it seems to affect impulsivity, thus worsening decision making ability and flexibility, possibly by an effect of nicotine on dopaminergic neurotransmission in orbito-frontal cortex. This may explain the low rate of smokers in patients with OCD.

The screen for cognitive impairment in psychiatry (SCIP) is a brief, accessible scale designed for detecting cognitive deficits in psychiatric disorders.

The objective of this study is to test the SCIP's validity as a cognitive test by comparison with standard neuropsychological scale using the Pearson's correlation.

Aims Test the convergent and discriminant validity of the SCIP within the Italian SCIP validation project.

Patients between 18 and 65 years who are in a stable phase of the disease, diagnosed with schizophrenia, schizoaffective disorder or bipolar I disorder were enrolled in this study, from the community mental health department of Ferrara.

The tests were administered to 110 patients (mean age: 45 ± 11,4) and to 86 controls (mean age: 35 ± 12,6) of both sex. SCIP presents high correlation with the R-BANS total score (P < 0.01) and the subscales (verbal learning test-immediate, working memory, verbal fluency test, verbal learning test-delayed, processing speed test, P < 0.01). There are significant differences (P < 0.01) in all SCIP dimensions between patient and control group (Table 1).

Our analysis confirm the results of the English, French and Spanish version of the SCIP regarding convergent and discriminant validity. The SCIP represents a valid, simple and brief screening tool for the cognitive evaluation of patients with schizophrenia-spectrum disorders.

The authors have not supplied their declaration of competing interest.

Mental disorders can have a major impact on brain development. Peripheral blood concentrations of brain-derived neurotrophic factor (BDNF) are lower in adult psychiatric disorders. Serum BDNF concentrations and BDNF genotype have been associated with cortical maturation in children and adolescents. In 2 large independent samples, this study tests associations between serum BDNF concentrations, brain structure, and psychopathology, and the effects of BDNF genotype on BDNF serum concentrations in late childhood and early adolescence.

Children and adolescents (7-14 years old) from 2 cities (n = 267 in Porto Alegre; n = 273 in São Paulo) were evaluated as part of the Brazilian high-risk cohort (HRC) study. Serum BDNF concentrations were quantified by sandwich ELISA. Genotyping was conducted from blood or saliva samples using the SNParray Infinium HumanCore Array BeadChip. Subcortical volumes and cortical thickness were quantified using FreeSurfer. The Development and Well-Being Behavior Assessment was used to identify the presence of a psychiatric disorder.

Serum BDNF concentrations were not associated with subcortical volumes or with cortical thickness. Serum BDNF concentration did not differ between participants with and without mental disorders, or between Val homozygotes and Met carriers.

No evidence was found to support serum BDNF concentrations as a useful marker of developmental differences in brain and behavior in early life. Negative findings were replicated in 2 of the largest independent samples investigated to date.

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.