In the last two decades much progress has been made in the neurobiological, pharmacological and neuro-imaging research of sexual dysfunctions.

to present an overview of current treatment options

to provide better understanding of underlying (neuro)biological mechanisms

use of evidence-based research articles

Erectile dysfunction and lifelong premature ejaculation, previously regarded as pure psychological disorders, are currently regarded as (neuro)biologically and even genetically influenced dysfunctions. On the other hand, vaginismus and a substantial part of dyspareunia remain to have mainly psychological causes. Antidepressant and antipsychotic induced sexual side effects remain difficult to be treated. Switching to another drug with less sexual side effect remains the first option of treatment, but may negatively interfere with the underlying psychiatric disorder. Although antidepressant-induced sexual side effects are reversible, SSRI-induced sexual side effect may persist for a very long time after SSRI discontinuation. This so called, post SSRI sexual dysfunction (PSSD) is probably the most serious side effect of SSRI treatment. A new libido-increasing drug is currently investigated in multi-centered trials. Its mechanism of action is totally new in neuropharmacology. In addition, a new antidepressant with a complex neuropharmacological underlying mechanism of action, may be the first manifestation of the advent of newly produced antidepressants without sexual side effects.

evidence-based drug treatment of a number of sexual dysfunctions has replaced non-evidence based psychotherapies. Still, psycho-education and counseling remain essential for an effective treatment of sexual disorders.

There is debate as to whether maternal tobacco use in pregnancy is related to offspring behaviour later on. We tested this association examining multiple aspects of children's behaviour at age 5 and accounting for parental smoking outside of pregnancy, as well as child and family characteristics.

Data come from a prospective community based birth cohort study (EDEN; n = 1113 families in France followed since pregnancy in 2003–2005 until the child's 5th birthday). Maternal tobacco use in pregnancy was self-reported. Children's socio-emotional development (emotional symptoms, conduct problems, symptoms of hyperactivity/inattention, peer relationship problems, prosocial behaviour) was assessed by mothers using the Strengths and Difficulties Questionnaire (SDQ) at age 5 years. Logistic regression analyses controlled for Inverse Probability Weights (IPW) of maternal tobacco use calculated based on study center, children's characteristics (sex, premature birth, low birth weight, breastfeeding), maternal characteristics (age at the child's birth, psychological difficulties and alcohol use in pregnancy, post-pregnancy depression, and smoking), paternal smoking in and post-pregnancy, parental educational attainment, family income, parental separation, and maternal negative life events.

Maternal smoking in pregnancy only predicted children's high symptoms of hyperactivity/inattention (sex and study center-adjusted ORs: maternal smoking in the 1st trimester: 1.95, 95%CI: 1.13–3.38; maternal smoking throughout pregnancy: OR = 2.11, 95%CI: 1.36–3.27). In IPW-controlled regression models, only children of mothers who smoked throughout pregnancy had significantly elevated levels of hyperactivity/inattention (OR = 2.20, 95%CI: 1.21–4.00).

Maternal tobacco smoking in pregnancy may contribute directly or through epigenetic mechanisms to children's symptoms of hyperactivity/inattention.

Randomized trials with antidepressants are often run under double blind placebo-controlled conditions, whereas those with psychotherapies are mostly unblinded. This can introduce bias in favor of psychotherapy when the treatments are directly compared. In this meta-analysis, we examine this potential source of bias.

We searched Pubmed, PsycInfo, Embase and the Cochrane database (1966 to January 2014) by combining terms indicative of psychological treatment and depression, and limited to randomized trials. We included 35 trials (with 3721 patients) in which psychotherapy and pharmacotherapy for adult depression were directly compared with each other. We calculated effect sizes for each study indicating the difference between psychotherapy and pharmacotherapy at post-test. Then, we examined the difference between studies with a placebo condition and those without in moderator analyses.

We did not find a significant difference between the studies with and those without a placebo condition. The studies in which a placebo condition was included indicated no significant difference between psychotherapy and pharmacotherapy (g = −0.07; NNT = 25). Studies in which no placebo condition was included (and patients and clinicians in both conditions were not blinded), resulted in a small, but significant difference between psychotherapy and pharmacotherapy in favor of pharmacotherapy (g = −0.13; NNT = 14).

Studies comparing psychotherapy and pharmacotherapy in which both groups of patients (and therapists) are not blinded (no placebo condition is included) result in a very small, but significantly higher effect for pharmacotherapy.

The aim of this study was to assess the factor structure of negative symptoms in first-episode schizophrenia (FES), and to examine the relationship of these factors with clinical course and functioning of patients during the two-year follow up.

We assessed 174 drug-naïve patients with FES using Brief Psychiatric Rating Scale-Expanded (BPRS), Scale for the Assessment of Negative Symptoms (SANS), Scale for the Assessment of Positive Symptoms (SAPS), and Global Assessment of Functioning (GAF) and a cognitive battery at admission. The scales were repeated monthly during follow up. We recorded the patients’ functioning levels, remission, and work status after 12 and 24 months.

A two-factor structure was found at the baseline, whereas one factor was found after 12 and 24 months. Expressive deficit (ED) factor consisted of alogia and blunted affect, and motivation-pleasure deficit (MPD) factor consisted of avolition and anhedonia. ED factor was related to earlier onset and remission, and it was negatively correlated with duration of education and cognitive test scores. MPD factor was related to duration of untreated psychosis, family history of schizophrenia, and work status, and it appeared as the only independent variable that contributed to the baseline GAF score in linear regression analysis.

Our findings suggest that the factors have different aetiologies and impacts on the clinical course of schizophrenia and functioning after FES.

Interventions based on the experience sampling method (ESM) are ideally suited to provide insight into personal, contextualized affective patterns in the flow of daily life. Recently, we showed that an ESM-intervention focusing on positive affect was associated with a decrease in symptoms in patients with depression. The aim of the present study was to examine whether ESM-intervention increased patient empowerment.

Depressed out-patients (n = 102) receiving psychopharmacological treatment who had participated in a randomized controlled trial with three arms: (i) an experimental group receiving six weeks of ESM self-monitoring combined with weekly feedback sessions, (ii) a pseudo-experimental group participating in six weeks of ESM self-monitoring without feedback, and (iii) a control group (treatment as usual only). Patients were recruited in the Netherlands between January 2010 and February 2012. Self-report empowerment scores were obtained pre- and post-intervention.

There was an effect of group × assessment period, indicating that the experimental (B = 7.26, P = 0.061, d = 0.44, statistically imprecise) and pseudo-experimental group (B = 11.19, P = 0.003, d = 0.76) increased more in reported empowerment compared to the control group. In the pseudo-experimental group, 29% of the participants showed a statistically reliable increase in empowerment score and 0% reliable decrease compared to 17% reliable increase and 21% reliable decrease in the control group. The experimental group showed 19% reliable increase and 4% reliable decrease.

These findings tentatively suggest that self-monitoring to complement standard antidepressant treatment may increase patients’ feelings of empowerment. Further research is necessary to investigate long-term empowering effects of self-monitoring in combination with person-tailored feedback.

Joint hypermobility syndrome (JHS) has repeatedly been associated with anxiety and anxiety disorders, fibromyalgia, irritable bowel syndrome and temporomandibular joint disorder. However, the neural underpinnings of these associations still remain unclear. This study explored brain responses to facial visual stimuli with emotional cues using fMRI techniques in general population with different ranges of hypermobility.

Fifty-one non-clinical volunteers (33 women) completed state and trait anxiety questionnaire measures, were assessed with a clinical examination for hypermobility (Beighton system) and performed an emotional face processing paradigm during functional neuroimaging.

Trait anxiety scores did significantly correlate with both state anxiety and hypermobility scores. BOLD signals of the hippocampus did positively correlate with hypermobility scores for the crying faces versus neutral faces contrast in ROI analyses. No results were found for any of the other studied ROIs. Additionally, hypermobility scores were also associated with other key affective processing areas (i.e. the middle and anterior cingulate gyrus, fusiform gyrus, parahippocampal region, orbitofrontal cortex and cerebellum) in the whole brain analysis.

Hypermobility scores are associated with trait anxiety and higher brain responses to emotional faces in emotion processing brain areas (including hippocampus) described to be linked to anxiety and somatic symptoms. These findings increase our understanding of emotion processing in people bearing this heritable variant of collagen and the mechanisms through which vulnerability to anxiety and somatic symptoms arises in this population.

Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) have essential roles in synaptic plasticity which is involved in pathogenesis and treatment of psychiatric disorders. However, it is not clear whether they act simultaneously during illness states in major psychiatric disorders.

BDNF and GDNF serum levels were measured concomitantly by enzyme-linked immunosorbent assay (ELISA) method in 171 patients diagnosed with schizophrenia (n = 33), bipolar disorder-manic episode (n = 39), bipolar/unipolar depression (n = 64, 24/40) and obsessive-compulsive disorder (n = 35) according to DSM-IV, and 78 healthy volunteers. SCID-I and SCID non-patient version were used for clinical evaluation of the patients and healthy volunteers, respectively. Correlations between the two trophic factor levels, and illness severity scores, duration of illness and medication dosages were studied across different illnesses.

While patients had equally lower BDNF levels in all diagnoses, GDNF levels were significantly higher in mania and lower in schizophrenia compared to healthy controls. BDNF levels were negatively correlated to illness severity scores in affective episodes (mania and depression). Longer duration of illness (> 5 years) had an impact on lower GDNF levels in schizophrenia. BDNF levels and antipsychotic drug dosages in schizophrenia, and GDNF levels and antidepressant drug dosages in obsessive-compulsive disorder were positively correlated.

Our data confirmed the evidence of equally deficient neuronal support by BDNF in all major psychiatric illnesses, but suggested a diverse glial functioning between schizophrenia and mania.

Autoantibodies have been implicated in the etiologic pathway of depressive disorders. Here, we determine the association between the presence of a panel of autoantibodies at baseline and change in depression symptom score over 5-year follow-up in a cohort of healthy elderly Australians.

Serum samples from 2049 randomly selected subjects enrolled in the Hunter Community Study (HCS) aged 55–85 years were assayed for a range of autoimmune markers (anti-nuclear autoantibodies, extractable nuclear antigen autoantibodies, anti-neutrophil cytoplasmic autoantibodies, thyroid peroxidase autoantibodies, tissue transglutaminase autoantibodies, anti-cardiolipin autoantibodies, rheumatoid factor and cyclic citrullinated peptide autoantibodies) at baseline. Depression symptom score was assessed using the Centre for Epidemiological Study (CES-D) scale at baseline and 5 years later.

Autoantibody prevalence varied amongst our sample with ANA being the most prevalent; positive in 16% and borderline in 36% of study population. No evidence for a relationship was found between change in CES-D score over time and any autoimmune marker. Statins and high cholesterol were significantly associated with change in CES-D score over time in univariate analysis; however, these were probably confounded since they failed to remain significant following multivariable analysis.

Autoantibodies were not associated with change in CES-D score over time. These findings point to an absence of autoimmune mechanisms in the general population or in moderate cases of depression.

The aims of the study were: (1) to evaluate longitudinally symptomatic remission in first-episode (FE) schizophrenia, (2) to describe symptoms, social functioning and quality of life (Qol) in relation to remission status, and (3) to determine the long-term outcome of schizophrenia and its early predictors.

Sixty-four patients were assessed 1 month after a first hospitalization (T1), 12 months (T2), 4–6 years (T3), and 7–11 years (T4) after T1. The patients were allocated to three remission groups according to their remission status over the whole observation period, e.g. stable remission (SR), unstable remission (UR) and non-remission (NR). The PANSS, Social Functioning Scale and WHOQoL were used to evaluate the patients’ psychosocial functioning levels, symptomatic and functional remissions and satisfying QoL. A good outcome was defined as meeting, simultaneously, the criteria of symptomatic and functional remissions and satisfying QoL at T4, while failure to meet all of these criteria was defined as a poor outcome.

Among them, 17.2% patients were in stable remission, 57.8% in unstable remission and 25.0% were unremitted at all time points. The SR group had lower levels of psychopathological symptoms and reported better social functioning and QoL than the NR group. During the follow-up, the symptoms increased, social functioning slightly improved and QoL did not change. At T4, 53% of the sample had a poor outcome, which was independently predicted by the longer duration of untreated psychosis and a lack of satisfying QoL at T1.

Our results demonstrate that: (1) the long-term course in schizophrenia is heterogeneous and that three illness trajectories exist, (2) social functioning and QoL are only partially connected with symptomatic remission (3), the risk of a poor outcome may potentially be reduced by appropriate interventions at an early stage of the illness.

This study investigated the association between the religiosity of parents and pre-adolescents, and pre-adolescents’ psychiatric problems.

In a clinic-referred cohort of 543 pre-adolescents at least once referred to a mental health outpatient clinic mental health problems were assessed using self-reports (Youth Self-Report; YSR), parent reports (Child Behavior Checklist; CBCL), and teacher reports (Teacher's Report Form; TRF) of child behavioral and emotional problems. Paternal, maternal, and pre-adolescent religiosity were assessed by self-report. MANCOVAs were performed for internalizing and externalizing problems as dependent variables, with maternal religiosity, paternal religiosity, pre-adolescent religiosity, parental religious harmony, and gender as independent variables, and socioeconomic status and divorce as covariates.

Internalizing problems. Pre-adolescents of actively religious mothers had more internalizing symptoms than pre-adolescents of nonreligious mothers. Harmony and gender did not significantly affect the association between maternal religiosity and internalizing problems. Externalizing problems. No associations between religiosity of pre-adolescents, religiosity of mothers, religiosity of fathers and/or harmony of parents and externalizing problem behavior have been found.

Overall, associations between mental health and religiosity were modest to absent. Results are discussed in the context of a clinic-referred cohort, the quest phase of internalizing religious beliefs and role modeling of parents.

In cognitive models of adult psychosis, schematic beliefs about the self and others are important vulnerability and maintaining factors, and are therefore targets for psychological interventions. Schematic beliefs have not previously been investigated in children with distressing unusual, or psychotic-like, experiences (UEDs). The aim of this study was firstly to investigate whether a measure of schematic beliefs, originally designed for adults with psychosis, was suitable for children; and secondly, to examine the association of childhood schematic beliefs with internalising and externalising problems and with UEDs.

Sixty-seven children aged 8–14 years, with emotional and behavioural difficulties, completed measures of UEDs, internalising (depression and anxiety), and externalising (conduct and hyperactivity-inattention) problems, together with the Brief Core Schema Scales (BCSS).

The BCSS was readily completed by participants, and scale psychometric properties were good. Children tended to view themselves and others positively. Internalising and externalising problems and UEDs were all associated with negative schematic beliefs; effect sizes were small to medium.

Schematic beliefs in young people can be measured using the BCSS, and negative schematic beliefs are associated with childhood psychopathology and with UEDs. Schematic beliefs may therefore form a useful target in psychological interventions for young people with UEDs.

Alcohol dependence (AD) is associated with an increase in physical comorbidities. The effects of these diseases on general hospital-based mortality are unclear. Consequently, we conducted a mortality study in which we investigated if the burden of physical comorbidities and their relevance on general hospital-based mortality differs between individuals with and without AD during a 12.5-year observation period in general hospital admissions.

During 1 January 2000 and 30 June 2012, 23,371 individuals with AD were admitted at least once to seven General Manchester Hospitals. Their physical comorbidities with a prevalence ≥ 1% were compared to those of 233,710 randomly selected hospital controls, group-matched for age and gender (regardless of primary admission diagnosis or specialized treatments). Physical comorbidities that increased the risk of hospital-based mortality (but not outside of the hospital) during the observation period were identified using multiple logistic regression analyses.

Hospital-based mortality rates were 20.4% in the AD sample and 8.3% in the control sample. Individuals with AD compared to controls had a higher burden of physical comorbidities, i.e. alcoholic liver and pancreatic diseases, diseases of the conducting airways, neurological and circulatory diseases, diseases of the upper gastrointestinal tract, renal diseases, cellulitis, iron deficiency anemia, fracture neck of femur, and peripheral vascular disease. In contrast, coronary heart related diseases, risk factors of cardiovascular disease, diverticular disease and cataracts were less frequent in individuals with AD than in controls. Thirty-two individual physical comorbidities contributed to the prediction of hospital-based mortality in univariate analyses in the AD sample; alcoholic liver disease (33.7%), hypertension (16.9%), chronic obstructive pulmonary disease (14.1%), and pneumonia (13.3%) were the most frequent diagnoses in deceased individuals with AD. Multiple forward logistic regression analysis, accounting for possible associations of diseases, identified twenty-three physical comorbidities contributing to hospital-based mortality in individuals with AD. However, all these comorbidities had an equal or even lower impact on hospital-based mortality than in the comparison sample.

The excess of in-hospital deaths in general hospitals in individuals with AD is due to an increase of multiple physical comorbidities, even though individual diseases have an equal or even reduced impact on general hospital-based mortality in individuals with AD compared to controls.

The use of antidepressants (AD) in children and adolescents has become controversial due to a possible increased risk of suicide, revised evidence about effectiveness, and growing usage. Several studies have been conducted through healthcare databases, mainly restricted to hospitalized cases.

To evaluate the rate of self-harm among children (10–14 years) and adolescents (15–19 years) who use AD and to compare rates between classes of AD, using a common data model.

A retrospective cohort study was conducted in children and adolescents, age 10–19, members of the Quebec (QC) public drug plan or residents of British Columbia (BC), and who received a new AD treatment in 1997–2008 (QC) and 1997–2006 (BC). Self-harm (fatal or non-fatal) was the main outcome. Data sources consisted of prescription, medical services, and hospitalization databases. AD were categorized into: fluoxetine (only AD approved for paediatric use for depression in Canada), non-fluoxetine SSRIs, TCAs, and others. Multivariate logistic regression analyses were conducted using high dimensional propensity scores.

Were included 51,868 and 28,200 AD users from BC and QC, respectively: 70% were females, and 60% had received a diagnosis of depression. Risk of hospitalization for self-harm was 38.15 and 19.23/1000 person-years in BC and QC, respectively. Rates were higher among adolescents (BC: 47.52; QC: 21.36) than children (BC: 17.00, QC: 12.99). For both hospitalized and non-hospitalized cases, while there was no statistically significant difference in risk associated with fluoxetine relative to non-fluoxetine SSRIs, TCAs were associated with a lower risk in BC (OR = 0.47; 95% CI: 0.31–0.72) and Quebec (OR = 0.41; 95% CI: 0.30–0.46).

In two independent large cohorts, there was no apparent differences in risk across ADs. Lower risk of TCAs may be due to residual confounding by indication.

There is considerable evidence that white matter abnormalities play a key role in the pathogenesis of a number of major psychiatric disorders, including schizophrenia, bipolar affective disorder, and obsessive-compulsive disorder. Few studies, however, have compared white matter abnormalities early in the course of the illness.

A total of 102 children and adolescents participated in the study, including 43 with early-onset schizophrenia, 13 with early-onset bipolar affective disorder, 17 with obsessive-compulsive disorder, and 29 healthy controls. Diffusion tensor imaging scans were obtained on all children and the images were assessed for the presence of non-spatially overlapping regions of white matter differences, a novel algorithm known as the pothole approach.

Patients with early-onset schizophrenia and early-onset bipolar affective disorder had a significantly greater number of white matter potholes compared to controls, but the total number of potholes did not differ between the two groups. The volumes of the potholes were significantly larger in patients with early-onset bipolar affective disorder compared to the early-onset schizophrenia group. Children and adolescents with obsessive-compulsive disorder showed no differences in the total number of white matter potholes compared to controls.

White matter abnormalities in early-onset schizophrenia and bipolar affective disorder are more global in nature, whereas children and adolescents with obsessive-compulsive disorder do not show widespread differences in FA.