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BACKGROUND: Although some studies have already been done on the quality of websites on depression, they have mainly focused on content quality, and were mostly carried out about a decade ago. The main aim of this work was thus to examine the quality of current websites on depression through the use of several indicators. METHODS: Three keywords on depression were entered into a popular search engine. Websites were evaluated on accountability, interactivity, esthetics, readability, and content quality. Moreover, the presence of the "Health on the Net" (HON) quality label and the website's affiliation were checked, and the Brief DISCERN was used as a potential content quality indicator for general consumers. RESULTS: A total of 45 websites were analyzed. The content quality of the depression-related websites was good. Websites with the HON label had significantly higher accountability, content quality, and Brief DISCERN scores. Moreover, websites with a high score on the Brief DISCERN scored significantly higher for accountability and content quality. Finally, the content quality of websites was significantly and positively correlated with the Brief DISCERN score, the presence of the HON label, and affiliation of the websites. CONCLUSION: The overall quality of websites on depression seems to be rather good.

Background Time- and cost-effective self-rating scales of depressive symptoms are particularly valuable for frequent use in large-scale effectiveness trials. The aim of the present study was to examine the psychometric properties of the French version of the self-rated Montgomery–Asberg Depression Rating Scale (MADRS-S) and determine whether it might complement the MADRS in monitoring depression severity and change over time in routine clinical practice. Methods Sixty-three adult outpatients with a current depressive episode completed the MADRS-S and were interviewed with the MADRS on two occasions, within a 1-month interval. Results All patients readily accepted the MADRS-S. It showed good to excellent internal consistency (Cronbach's alpha 0.85 at Time 1; 0.94 at Time 2). Its factor structure revealed that a single component explained a large proportion of variability (47.0% at Time 1; 68.8% at Time 2). Concurrent validity of the self- and clinician-rated versions was good (Pearson's correlation coefficients for total scores 0.81 at Time 1; 0.91 at Time 2). The MADRS-S was sensitive to change over the 4-week observation period (correlation of 0.71 between change scores on self- and clinician-rated instruments). Limitations Generalizability is restricted to outpatients with moderate to severe depression, and the MADRS-S ability to measure treatment effects needs to be examined. Conclusions The present study indicates that the MADRS-S displays favourable psychometric properties and suggests that it might be a valid complement to the MADRS, both in research settings and clinical practice.

BackgroundResidual depressive symptoms are generally documented as a risk factor for recurrence. In the absence of a specific instrument for the assessment of residual symptoms, a new 25-item Depression Residual Symptom Scale (DRSS) was elaborated and tested for recurrence prediction over a 1-year follow-up.Sampling and methodsFifty-nine patients in remission after a major depressive episode (MDE) were recruited in two centres. They were assessed with the DRSS and the Montgomery-Asberg Depression Rating Scale (MADRS) at inclusion and followed for 1 year according to a seminaturalistic design. The DRSS included specific depressive symptoms and subjective symptoms of vulnerability, lack of return to usual self and premorbid level of functioning.ResultsSeverity of residual symptoms was not significantly associated with increased risk of recurrence. However, DRSS score was significantly higher among patients with three or more episodes than one to two episodes. Number of previous episodes and treatment interruption were not identified as significant predictors of recurrence.ConclusionThe proposed instrument is not predictive of depressive recurrence, but is sensitive to increased perception of vulnerability associated with consecutive episodes. Limitations include small sample size, seminaturalistic design (no standardisation of treatment) and content of the instrument.

Exposure is considered to be an essential ingredient of cognitive-behavioral therapy treatment of social phobia and of most anxiety disorders. To assess the impact of the amount of exposure on outcome, 30 social phobic patients were randomly allocated to 1 of 2 group treatments of 8 weekly sessions: Self-Focused Exposure Therapy which is based essentially on prolonged exposure to public speaking combined with positive feedback or a more standard cognitive and behavioral method encompassing psychoeducation, cognitive work, working through exposure hierarchies of feared situations for exposure within and outside the group. The results show that the 2 methods led to significant and equivalent symptomatic improvements which were maintained at 1-year follow-up. There was a more rapid and initially more pronounced decrease in negative cognitions with the Self-Focused Exposure Therapy, which included no formal cognitive work, than with the more standard approach in which approximately a third of the content was cognitive. In contrast, decrease in social avoidance was more persistent with standard cognitive-behavior therapy which involved less exposure. The results indicate that positive cognitive change can be achieved more rapidly with non cognitive methods while avoidance decreases more reliably with a standard approach rather than an approach with an exclusive focus on exposure.

ObjectiveTo evaluate the performance of the French version of the Mood Disorder Questionnaire (MDQ) in patients attending a general psychiatric outpatient service as well as whether MDQ scores are independent of patient mood state at time of completion.Method183 patients completed the MDQ and were assessed with the MADRS and YMRS scales, before being interviewed with the SCID (time 1). MDQ, MADRS and YMRS assessment was repeated four to six weeks later (time 2).ResultsAccording to the SCID, 44 patients were suffering from bipolar spectrum disorder and 102 from unipolar disorder (37 patients dropped out). The MDQ provided high specificity (83.3%). Sensitivity was 63.6%, with better identification of bipolar I (85.0%) than bipolar II patients (45.8%). In the whole sample, test-retest reliability was satisfactory (kappa = 0.64). Modest correlations were observed between the number of endorsed MDQ items and YMRS scores at time 1 (Spearman r = 0.19; p = 0.021) and time 2 (r = 0.26; p = 0.002).ConclusionsDespite some fluctuations over time and a discrete influence of symptom severity, the screening algorithm can be used reliably, whether in the acute or remission phase of a depressive episode.

Paroxetine is characterized by large interindividual pharmacokinetic variability and heterogeneous response patterns. The present study investigates plasma concentration and therapeutic response to paroxetine for the influence of age, sex, and CYP2D6 and ABCB1 polymorphisms, the latter gene encoding for the permeability glycoprotein. Genotyping for CYP2D6 (alleles *3, *4, *5, *6, and *xN) and ABCB1 polymorphisms (61A>G, 2677G>T, and 3435C>T) was performed in 71 depressed patients who started 20 mg paroxetine per day and had plasma concentration measured after 2 weeks at a fixed dose. A dose increase to 30 mg per day was possible starting at week 2. For 63 patients, severity of depression (Montgomery-Asberg Depression Rating Scale) was assessed at weeks 0, 2, and 4 and every 2 weeks thereafter until discontinuation. Persistent response was defined as 50% improvement from baseline score sustained from the first occurrence to study end point. Paroxetine concentration significantly differed between female and male patients (median, 28 versus 16 ng/mL; P = 0.001). Differences were not significant between CYP2D6 heterozygous and homozygous extensive metabolizers (median, 27 versus 22 ng/mL; P = 0.074) and between ABCB1 genotypes (P > 0.10). When considered in a multivariate model, CYP2D6 heterozygous extensive metabolizer phenotype (P = 0.062) and female gender (P = 0.001) predicted 1.3-fold and 1.6-fold higher paroxetine concentration, respectively, but fraction of explained variability was modest (21%). Frequency of persistent response at study end point did not significantly differ according to CYP2D6 heterozygous extensive metabolizer versus homozygous extensive metabolizer phenotype and ABCB1 polymorphisms in univariate analyses. After adjusting for age, sex, paroxetine concentration at week 2, and daily dose at study end point, ABCB1 genotype contributed to improving the model significantly for 61A>G (P = 0.043), but not 2677G>T (P = 0.068) and 3435C>T (P = 0.11). None of two poor metabolizers and four ultrarapid metabolizers showed persistent response to paroxetine. The hypothesis that permeability glycoprotein activity might be a relevant predictor of therapeutic response deserves to be further investigated while controlling for pharmacokinetic variability.

The present study aims to evaluate the quality of web-based information on gambling and to investigate potential content quality indicators. The following key words: gambling, pathological gambling, excessive gambling, gambling problem and gambling addiction were entered into two popular search engines: Google and Yahoo. Websites were assessed with a standardized proforma designed to rate sites on the basis of "accountability", "presentation", "interactivity", "readability" and "content quality". "Health on the Net" (HON) quality label, and DISCERN scale scores aiding people without content expertise to assess quality of written health publication were used to verify their efficiency as quality indicators. Of the 200 links identified, 75 websites were included. The results of the study indicate low scores on each of the measures. A composite global score appeared as a good content quality indicator. While gambling-related education websites for patients are common, their global quality is poor. There is a need for useful evidence-based information about gambling on the web. As the phenomenon has greatly increased, it could be relevant for Internet sites to improve their content by using global score as a quality indicator.

Early improvement of depression severity is considered an important therapeutic goal, predictive of later remission. The present study aimed at testing the hypothesis that plasma concentration might influence the time course of response to paroxetine. Eighty-four patients with a severe depressive episode started paroxetine 20 mg/day, with a possible dose adjustment to 30 mg/day after 2 weeks. Severity of depression (Montgomery-Asberg Depression Rating Scale) was assessed at weeks 0, 2 and 4 for all patients, and every 2 weeks thereafter until discontinuation. Median duration on paroxetine was 6 weeks (range 4-18 weeks). Plasma concentration was measured at steady-state after 2 weeks at 20 mg/day. In a first stage, pattern analysis led to distinguish patients with non-response, non-persistent response, early persistent response (obtained at week 2) and delayed persistent response (week 4 or later). Comparison of patients with (n=29, 34.5%) and without persistent response (n=55, 65.5%) did not reveal any significant difference, whereas focus on patients with persistent response indicated that shorter time to response was significantly associated with shorter duration of current episode (r(S)=0.54, p=0.003) and higher plasma level (r(S)=-0.47, p=0.011). In a second stage, a sigmoid mixed effects model was developed that adequately fitted depression severity versus time profiles among patients with persistent response (n=157 data for 29 patients). Estimated median time to response was 3.2 weeks (range 0.9-6.6). Higher paroxetine concentration, younger age and shorter episode duration were confirmed as significant determinants of a shorter time to response (likelihood ratio tests, p0.005). The present study supports the hypothesis that higher paroxetine concentration might contribute to hasten relief of depressive symptoms in severely depressed patients.

Hypothalamo–pituitary–adrenal (HPA) system dysfunction is the most characteristic biological alteration found in a majority of depressed patients. Accumulating evidence suggests that the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH) test is highly sensitive to detect HPA system abnormalities. The aim of this study was to evaluate whether the DEX/CRH test has a predictive value for the risk of depressive relapse in outpatients who are in clinical remission from a major depressive episode. Thirty-eight depressed outpatients (23 women, 15 men) in remission (MADRS score ⩽8) underwent the DEX/CRH test and were followed up for 12 months regarding the occurrence of a new depressive episode. In parallel we recruited 24 controls (13 men and 11 women). The main result is a statistically significant difference concerning the delta and AUC numbers for cortisol plasmatic values between the group of patients who relapsed during the 1-year follow-up and control subjects, but not between the group of patients with prolonged remission and controls. These results suggest that in outpatients who are in clinical remission from a major depressive episode, high delta and AUC values in the DEX/CRH test compared to controls subjects can be associated with a higher risk of relapse.

Dans cet article nous considerons la formation a la psychotherapie cognitivo-comportementale sous l’angle du developpement considerable qu’elle a connu ces trente dernieres annees. Les principales donnees publiees dans le domaine de la formation en psychotherapie cognitivo-comportementale indiquent que l’amelioration des programmes de formation necessite : une definition claire des pre-requis des participants, une adequation du contenu aux developpements recents et leur evaluation. La situation de la formation en psychotherapie cognitivo-comportementale est ensuite discutee par rapport aux exigences de formation en Europe et a quelques programmes de formation en Europe et en Suisse.

Body dysmorphic disorder is described in the DSM-IV as a single clinical entity, but an additional diagnosis of delusional disorder, somatic type, is allowed when the preoccupation concerning an imaginary defect in appearance is held with delusional intensity. The existence of two clinical forms is implicitly recognized, depending on the presence or absence of psychotic symptoms. Several studies have suggested that these two forms make up a single illness, characterized by different degrees of insight. This supposition is supported by the fact that the symptomatology and the clinical response to the SSRIs are thought to be similar for the two forms. Moreover, certain authors have suggested that categorical nosography (as used by the DSM-IV) should not be the point of reference and that a ‘dimensional’ point of view is preferable, meaning that the presence of psychotic symptoms would constitute merely a simple phenomenon or state of the same illness.

Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive experimental technique which has mostly been investigated in the treatment of mood disorders with possible efficacy in depression. Among its potential side effects, there have been some reports of rTMS-induced (hypo)mania in the literature but none for rTMS-induced mixed episodes. We report the case of a 39-year-old woman suffering from refractory chronic major depression who developed a depressive mixed episode associated with a mild serotonin syndrome during her second week of rTMS treatment. She was receiving a combination of antidepressants, the doses of which were kept unchanged during rTMS treatment. Mixed as well as manic episodes may be induced by transcranial magnetic stimulation, complications already observed with antidepressants and electroconvulsive therapy. Therefore, caution should be exercised among clinicians using this experimental procedure, particularly in the treatment of bipolar depressed patients.

Clozapine, an atypical antipsychotic, depends mainly on cytochrome P4501A2 (CYP1A2) for its metabolic clearance. CYP1A2 is inducible by smoking, and lower plasma concentrations of clozapine are measured in smokers than in nonsmokers. Case reports have been published on the effects of discontinuing smoking in patients receiving clozapine, which might lead to elevated plasma concentrations and severe side effects. We present 2 cases on the consequences of smoking cessation in patients receiving this drug. In the first patient, smoking cessation resulted, within 2 weeks, in severe sedation and fatigue, with an approximately 3-fold increase of plasma clozapine concentrations. In the second patient, a very high plasma concentration of clozapine (3004 ng/mL) was measured 6 days following a 16-day stay in a general hospital, during which smoking was prohibited. In the latter patient, the replacement of omeprazole, a strong CYP1A2 inducer, by pantoprazole, a weaker CYP1A2 inducer, could have contributed, in addition to smoking cessation, to the observed strong increase of plasma clozapine concentrations. Genotyping of the 2 patients revealed that they were carriers of the AA genotype for the -164C>A polymorphism (CYP1A2*1F) in intron 1 of CYP1A2 gene, which has previously been shown to confer a high inducibility of CYP1A2 by smoking. Thus, at the initiation of clozapine treatment, smoking patients should be informed that, if they decide to stop smoking, they are encouraged to do so but must inform their prescriber beforehand. Also, because of the increased use of no-smoking policies in many hospitals, studies examining the consequences of such policies on the pharmacokinetics/pharmacodynamics of drugs metabolized by CYP1A2, taking into account different CYP1A2 genotypes, are needed.

Background Recent reports have suggested a role for brain-derived neurotrophic factor (BDNF) in psychiatric disorders. Decreased serum BDNF levels have been reported in major depression, but the cause of this decrease has not yet been investigated. The goal of this study was to assess blood BDNF and a platelet activation index, PF4. Methods Forty-three drug-free patients (27 female, 16 male) diagnosed with major depression and 35 healthy control subjects (18 female, 17 male) were assessed for plasma, serum, and blood BDNF content. Brain-derived neurotrophic factor and PF4 were assayed with enzyme-linked immunosorbent assay methods, and severity of depression was evaluated with the Montgomery-Asberg Depression Rating Scale. Results Serum and plasma BDNF levels were decreased in depressed patients compared with control subjects. In whole blood, BDNF levels were unaltered in the depressed subjects compared with control subjects. The serum/blood BDNF ratio was lower in patients with major depression. Increased plasma but not serum PF4 levels were observed in depressed subjects compared with control subjects. Conclusions Our results suggest that an alteration of serum or plasma BDNF is not due to the change in blood BDNF but rather is probably related to mechanisms of BDNF release. Secretion of BDNF seems to be independent of platelet reactivity; other mechanisms are therefore probably involved and need to be elucidated.

We had previously reported decreased serum brain-derived neurotrophic factor (BDNF) levels in depressed patients. In the present study, we tested the hypothesis that antidepressant treatment would normalize serum BDNF levels, at least in a subgroup of patients. Major depressed patients (15 females and 11 males) diagnosed according to DSM-IV criteria and healthy controls (13 females and 13 males) participated in this study. Serum BDNF was assayed with the ELISA method for depressed and remitted patients and the severity of depression was evaluated with the Montgomery-Asberg Depression Rating Scale. An analysis of variance showed that treatment had an effect [F(1, 24) = 4.46, p = 0.045] on the normalization of serum BDNF levels. We also found a correlation between the severity of depression (r = 0.51, p = 0.008), the pretreatment BDNF levels (r = 0.62, p = 0.001) and the difference in serum BDNF levels after antidepressant treatment. These results suggest that antidepressant treatment has a positive effect on serum BDNF levels and support the hypothesis of neurotrophic factor involvement in affective disorders.

Background Atypical antipsychotics are widely used in clinical practice for several psychiatric disorders. Between 1994 and 1999, 26 cases of manic and hypomanic syndromes were reported with olanzapine and risperidone and were described in a previous review article. Method An updated MEDLINE search (1999-2003) using the terms atypical antipsychotics, amisulpride, aripiprazole, clozapine, flupenthixol, olanzapine, quetiapine, risperidone, sertindole, ziprasidone, zotepine, hypomania, and mania showed that 34 new cases of induced hypomanic or manic syndromes have been published, not only with olanzapine (N = 5) and risperidone (N = 6), but also with quetiapine (N = 5) and ziprasidone (N = 11) treatment. Six cases have been reported with flupenthixol and 1 with amisulpride, two antipsychotics considered as "partial" atypicals. Results A critical analysis of these case reports revealed that the effects on mood were insufficiently documented in some of the reports but that for 20 of them, evidence is highly suggestive of a causative role of atypical antipsychotics in the induction of manic/hypomanic symptomatology. Conclusion This updated review continues and extends the results of the initial review and suggests that atypical antipsychotics have some intriguing effects on mood. Such effects have never been reported with conventional antipsychotics. The mechanisms involved in this phenomenon of mood switch remain to be elucidated.

The DEX/CRH test is now a well established method to test the hypothalamic-pituitary-adrenal (HPA) axis for depressed patients in an inpatient setting. The aim of this study was to evaluate this test in an outpatient population suffering from major depression compared to a healthy control group. The main result is a statistically significant difference concerning the delta value for cortisol plasma value on the DEX/CRH test for depressed patients with two or more previous episodes compared to healthy controls. On the contrary, the difference was not statistically significant for patients with only one or no previous episodes. In future studies, it could be interesting to use this test more specifically by dividing ambulatory patients into subgroups according to their past depressive history. It could also be interesting to measure the ACTH level.

La mindfulness (en français pleine conscience) représente le dénominateur commun qui est à la base des différents courants de pratique de méditation bouddhiste. Par pleine conscience, on entend le fait de porter son attention d’une manière particulière, délibérément, au moment présent et sans jugement de valeur. Au cours de ces dernières années, plusieurs approches thérapeutiques intégrant la pratique de la méditation (Mindfulness Based Stress Reduction ; Dialectical Behavior Therapy ; Mindfulness Based Cognitive Therapy) ont été développées et évaluées. Dans cet article nous examinons les mécanismes pouvant expliquer pourquoi cette pratique peut conduire à une réduction symptomatique et/ou à un changement comportemental dans le cadre de divers troubles émotionnels et plus particulièrement dans le traitement des troubles anxieux., Mindfulness is the fundamental attentional stance underlying all streams of Buddhist meditative practice. It has been described as “paying attention in a particular way: on purpose, in the present moment, and nonjudgmentally.” During the last years, mindfulness practice has been evaluated and introduced into several mental health treatments (Mindfulness Based Stress Reduction; Dialectical Behavior Therapy; Mindfulness Based Cognitive Therapy). In this paper, the author considers the mechanisms that may explain how mindfulness skills can lead to symptom reduction and behavior change in different emotional disorders and in anxiety disorders., La mindfulness (en español consciencia plena) representa el denominador común en la base de las diferentes corrientes de práctica de meditación budista. Por consciencia plena entendemos el hecho de concentrar la atención de una forma particular, deliberada, en el presente y sin juicios de valor. En el curso de los últimos años, se han desarrollado y evaluado varios enfoques terapéuticos que integran la práctica de la meditación (Mindfulness Based Stress Reduction; Dialectical Behavior Therapy; Mindfulness Based Cognitive Therapy). En este artículo examinamos los mecanismos que pueden explicar por qué esta práctica puede conducir a una reducción sintomática y/o a un cambio de comportamiento en el marco de diversos trastornos emocionales y, en particular, en el tratamiento de los trastornos de ansiedad., A “mindfulness” (em português “consciência plena”) representa o denominador comum que é a base de diferentes correntes de prática de meditação budista. Por consciência plena entende-se o fato de levar sua atenção de uma maneira especial, deliberadamente, ao momento presente e sem julgamento de valor. Durante os últimos anos, várias abordagens terapêuticas integrando a prática da meditação (Mindfulness Based Stress Reduction; Dialectical Behavior Therapy; Mindfulness Based Cognitive Therapy) foram desenvolvidas e avaliadas. Neste artigo examinamos os mecanismos que podem explicar porque esta prática pode conduzir a uma redução sintomática e ou a uma mudança comportamental no caso de diversos transtornos emocionais e, mais especificamente, no tratamento de transtornos de ansiedade.

In this open, 30-day trial, the pharmacokinetics, safety and tolerability of a combination therapy of risperidone (4 or 6 mg/day) and fluoxetine (20 mg/day from day 6) were evaluated in I I psychotic inpatients. CYP2D6 genotyping revealed that 3 and 8 patients were poor metabolizers (PMs) and extensive metabolizers (EMS) of debrisoquine, respectively. The mean (+/- SD) AUC of risperidone increased from 83.1 +/- 46.8 ng.h/ml and 398.3 +/- 33.2 ng.h/ml (monotherapy) to 345.1 +/- 158.0 ng.h/ml (p < 0.05) and 514.0 +/- 144.2 ng.h/ml (p < 0.001) when coadministered with fluoxetine in EMs and PMs, respectively. The AUC of the active moiety (risperidone plus 9-hydroxy-risperidone) increased from 470.0 +/- 170.0 ng.h/ml to 663.0 +/- 243.3 ng.h/ml (p < 0.05) and from 576.3 +/- 19.6 ng.h/ml to 788.0 +/- 89.1 ng.h/ml (ns) in EMs and PMs, respectively. In EMs, the AUC of 9-hydroxy-risperidone remained similar (monotherapy vs. combination therapy: 386.8 +/- 153.0 ng.h/ml vs. 317.7 +/- 125.2 ng.h/ml, ns), whereas it increased in PMs (178.3 +/- 23.5 ng.h/ml vs. 274.0 +/- 55.1 ng.h/ml (p < 0.05)). Ten of the I I patients showed a clinical improvement (reduction of 20% or more in total PANSS score and 70% on the mean MADRS score compared to baseline). The severity and incidence of extrapyramidal symptoms and adverse events did not significantly increase when fluoxetine was added.

Recent findings with animal models have suggested a possible role for brain-derived neurotrophic factor (BDNF) in depression. We have therefore hypothesized that depression could be characterized by low levels of serum BDNF. Major depressed patients (15F + 15M) diagnosed according to DSM-IV criteria and healthy controls (15F + 15M) participated in the study. Serum BDNF was assayed with the ELISA method and the severity of depression was evaluated with Montgomery-Asberg-Depression Rating Scale (MADRS). BDNF levels were significantly lower in patients than in controls: 22.6 +/- 3 and 26.5 +/- 7 ng/ml (t-test = 2.7; d.f. = 58; P < 0.01). They were negatively correlated to the MADRS scores (r = -0.55; P < 0.02). Female patients were more depressed and released less BDNF than men. Analysis of covariance (MADRS and gender as independent variable vs. BDNF as dependent variable) indicated that depression severity mainly accounted for the negative correlation. These results suggest that major depression is characterized by low serum BDNF levels and support the hypothesis of neurotrophic factor involvement in affective disorders.

Negative symptoms of schizophrenia are often difficult to treat and may be associated with poorer long-term outcome. As depressive and negative symptoms show some overlap, augmentation of neuroleptics by antidepressants has repeatedly been investigated for efficacy against negative symptoms in schizophrenic patients. Studies on SSRI augmentation of neuroleptic medication reveal some evidence for increased efficacy of conventional antipsychotics in negative symptoms after addition of SSRIs. Since no correlation could be found between improvement of negative symptoms on the one hand and positive, depressive or extrapyramidal motor symptoms on the other, a direct effect seems likely. SSRIs may therefore be an alternative to clozapine, especially in patients for whom there are contraindications against clozapine treatment. As yet, there is no convincing rationalization for the paradox that both serotonergic and antiserotonergic substances, e.g. atypical antipsychotics, may improve negative symptoms.

It would be beneficial to find genetic predictors of antidepressant response to help personalise treatment of major depressive disorder (MDD). Rare copy number variants (CNVs) have been implicated in several psychiatric disorders, including MDD, but their role in antidepressant response has yet to be investigated. CNV data were available for 1565 individuals with MDD from the NEWMEDS (Novel Methods leading to New Medications in Depression and Schizophrenia) consortium with prospective data on treatment outcome with either a serotonergic or noradrenergic antidepressant. No association was seen between the presence of CNV (rare or common), the overall number of CNVs or genomic CNV 'burden' and antidepressant response. Specific CNVs were nominally associated with antidepressant response, including 15q13.3 duplications and exonic NRXN1 deletions. These were associated with poor response to antidepressants. Overall burden of CNVs is unlikely to contribute to personalising antidepressant treatment. Specific CNVs associated with antidepressant treatment require replication and further study to confirm their role in the therapeutic action of antidepressant.

Two published case reports showed that addition of risperidone (1 and 2 mg/d) to a clozapine treatment resulted in a strong increase of clozapine plasma levels. As clozapine is metabolized by cytochrome P450 isozymes, a study was initiated to assess the in vivo interaction potential of risperidone on various cytochrome P450 isozymes. Eight patients were phenotyped with dextromethorphan (CYP2D6), mephenytoin (CYP2C19), and caffeine (CYP1A2) before and after the introduction of risperidone. Before risperidone, all eight patients were phenotyped as being extensive metabolizers of CYP2D6 and CYP2C19. Risperidone at dosages between 2 and 6 mg/d does not appear to significantly inhibit CYP1A2 and CYP2C19 in vivo (median plasma paraxanthine/caffeine ratios before and after risperidone: 0.65, 0.69; p = 0.89; median urinary (S)/(R) mephenytoin ratios before and after risperidone:0.11, 0.12; p = 0.75). Although dextromethorphan metabolic ratio is significantly increased by risperidone (median urinary dextromethorphan/dextrorphan ratios before and after risperidone: 0.010, 0.018; p = 0.042), risperidone can be considered a weak in vivo CYP2D6 inhibitor, as this increase is modest and none of the eight patients was changed from an extensive to a poor metabolizer. The reported increase of clozapine concentrations by risperidone can therefore not be explained by an inhibition of CYP1A2, CYP2D6, CYP2C19 or by any combination of the three.

OBJECTIVE: The purpose of this study was to compare the short-term efficacy and safety of risperidone and clozapine in treatment-resistant chronic schizophrenic patients. METHOD: In a controlled double-blind, multicenter study, 86 inpatients with chronic schizophrenia (DSM-III-R), who were resistant to or intolerant of conventional neuroleptics, were randomly assigned to receive risperidone or clozapine for 8 weeks after a 7-day washout period. After a 1-week dose-titration phase, doses were fixed at 6 mg/day of risperidone and 300 mg/day of clozapine for 1 week and then adjusted according to each patient's response. The final mean doses were 6.4 mg/day of risperidone and 291.2 mg/day of clozapine. Treatment efficacy and safety were evaluated with several well-known rating scales. RESULTS: Both risperidone and clozapine significantly reduced the severity of psychotic symptoms (scores on the Positive and Negative Syndrome Scale and the Clinical Global Impression scale) from baseline, with no significant be...

Our clinic has fortuitously developed the therapeutic use of the association of mianserin (maximum daily dose 90 mg) and carbamazepine (maximum daily dose 400 mg) in opiate withdrawal management. If animal studies have suggested efficacy of mianserin in such indication, no human studies have been performed. To test the efficacy of such an association, a comparison was made to clonidine (maximum daily dose 0.600 mg) in a one week treatment period according to a double blind pilot study design. Thirty-two patients were included (16 in each treatment group). The two treatments did not differ in the intensity of the withdrawal, according to the rate of retention in treatment and symptoms, and the psychic distress which were auto-evaluated every other day with the Opiate Withdrawal Questionnaire and several Visual Analog Scales (VAS). The clonidine group, however, scored significantly higher (P0.05) on the VAS rating of the global feeling of satisfaction on the last day. The patients in the mianserin group fortuitously had a moderately lower number of daily heroin intakes but there was no significant correlation between this variable and the global OWQ scores on Days 1, 3, 5 and 7. Given the size of the groups, we cannot conclude that the association carbamazepine-mianserin is as effective as clonidine, but a real effectiveness is probable. A study versus placebo would be necessary to draw more definitive conclusions.

Unipolar depression is among the leading causes of invalidity and disability-adjusted life-years. General practitioners frequently encounter patients suffering from depressive syndromes and very often, it's they, who make the initial diagnosis, take care of these patients, eventually prescribe an antidepressant treatment, identify difficult cases and address them to the specialists of mental health. In this article, we present concepts of diagnosis and differential diagnoses of depression, its therapy and the collaboration between the general practitioner and the psychiatrist/psychotherapist.

Mindfulness-Based Cognitive Therapy (MBCT) is a promising intervention to prevent depressive relapse. Yet beyond efficacy studies, little is known regarding the mechanisms that could be modified through MBCT. Objectives of the present study were twofold: determine whether cognitive functioning was altered among patients remitted from depression at admission in a MBCT trial; and document possible changes during the trial and follow-up. In a cross-sectional perspective, cognitive functioning (autobiographical memory, shifting capacities, dysfunctional attitudes, mindful attention awareness and rumination habits) was first compared between 36 patients remitted from depression, 20 acutely depressed patients and 20 control participants. In a longitudinal perspective, changes in the remitted sample were explored during a MBCT plus Treatment As Usual versus Treatment As Usual randomized controlled trial and 9-month follow-up. Performances of remitted patients were similar to the ones of control participants for autobiographical memories, shifting capacities, and mindful attention awareness, whereas levels of rumination and dysfunctional attitudes were significantly elevated. Participation in the MBCT program was accompanied with a significant decrease of dysfunctional attitudes that continued up to 9-month postintervention. No other change was observed that was specific to MBCT. Results suggest that MBCT might help people to identify dysfunctional attitudes at a very early stage and to avoid engaging further in these attitudes.

There was an error in affiliations of the seventh author, Giampiero Arciero. This author's affiliations should only be: Institute of Post-Rationalist Psychology (IPRA), Rome, Italy Department of Mental Health and Psychiatry, University Hospital of Geneva, Geneva, Switzerland

Approximately 20-30% of patients with schizophrenia are resistant to conventional neuroleptics (i.e. are treatment-resistant). Clozapine has been shown to be effective in a proportion of treatment-resistant cases and to have a low side effect profile. However, it can cause agranulocytosis, is sedative and has marked anticholinergic properties. Risperidone, which is effective in chronic schizophrenia and has a low side effect profile and does not require routine blood monitoring, was compared with clozapine in a double-blind comparative study in 86 treatment-resistant patients. Preliminary findings indicate that, at endpoint, risperidone and clozapine were almost equieffective (total PANSS, PANSS subscales and CGI). Both drugs caused few adverse effects, and the severity of extrapyramidal symptoms was no different in the two groups. It is concluded that risperidone could be another drug effective in treatment-resistant schizophrenia. Further, larger trials will be needed to confirm this.

Chronic diseases and their associated biopsychosocial adjustements tax the limits of modern conventional medicine, with the need then to turn towards new resources. Among these, Mindfulness-Based Stress Reduction (MBSR) is a therapeutic approach developed more than 30 years ago. Designed as an adjuvant to medical care, in particular in the case of chronic pain which is the scope of our article, MBSR is usually provided in group format and based on a meditative practice. Simple, brief and cost-limited, MBSR can potentially be offered to a wide variety of chronic diseases and is part of participatory medicine. After having presented this approach, several results from studies confirming the legitimacy of MBSR as a nonreligious and nonesoteric scientific approach for the treatment of various diseases will be reported.

Background Football (soccer) is one of the most popular sports in the world, including Europe. It is associated with important betting activities. A common belief, widely spread among those who participate in gambling activities, is that knowledge and expertise on football lead to better prediction skills for match outcomes. If unfounded, however, this belief should be considered as a form of “illusion of control.” The aim of this study was to examine whether football experts are better than nonexperts at predicting football match scores. Methods Two hundred and fifty-eight persons took part in the study: 21.3% as football experts, 54.3% as laypersons (non-initiated to football), and 24.4% as football amateurs. They predicted the scores of the first 10 matches of the 2008 UEFA European Football Championship. Logistic regressions were carried out to assess the link between the accuracy of the forecasted scores and the expertise of the participants (expert, amateur, layperson), controlling for age and gender. Results The variables assessed did not predict the accuracy of scoring prognosis (R2 ranged from 1% to 6%). Conclusions Expertise, age, and gender did not appear to have an impact on the accuracy of the football match prognoses. Therefore, the belief that football expertise improves betting skills is no more than a cognitive distortion called the “illusion of control.” Gamblers may benefit from psychological interventions that target the illusion of control related to their believed links between betting skills and football expertise. Public health policies may need to consider the phenomenon in order to prevent problem gambling related to football betting.

Few studies have examined changes of diurnal cortisol profiles prospectively, in relation to non-pharmacological interventions such as mindfulness-based cognitive therapy (MBCT). Fifty-six patients remitted from recurrent depression (≥3 episodes) were included in an 8-week randomized controlled trial comparing MBCT plus treatment as usual (TAU) with TAU for depression relapse prophylaxis. Saliva samples (0, 15, 30, 45, 60 min post-awakening, 3 PM, 8 PM) were collected on six occasions (pre- and post-intervention, 3-, 6-, 9-, 12-month follow-up). Cortisol awakening response (CAR), average day exposure (AUCday) and diurnal slope were analyzed with mixed effects models (248 profiles, 1-6 per patient). MBCT (n = 28) and TAU groups (n = 28) did not significantly differ with respect to baseline variables. Intra-individual variability exceeded inter-individual variability for the CAR (62.2% vs. 32.5%), AUC(day) (30.9% vs. 23.6%) and diurnal slope (51.0% vs. 34.2%). No time, group and time by group effect was observed for the CAR and diurnal slope. A significant time effect (p = 0.003) was detected for AUCday, which was explained by seasonal variations (p = 0.012). Later wake-up was associated with lower CAR (-11.7% per 1-hour later awakening, p < 0.001) and lower AUCday (-4.5%, p = 0.014). Longer depression history was associated with dampened CAR (-15.2% per 10-year longer illness, p = 0.003) and lower AUCday (-8.8%, p = 0.011). Unchanged cortisol secretion patterns following participation in MBCT should be interpreted with regard to large unexplained variability, similar relapse rates in both groups and study limitations. Further research is needed to address the scar hypothesis of diminished HPA activity with a longer, chronic course of depression.

Testing whether genetic information could inform the selection of the best drug for patients with depression, Rudolf Uher and colleagues searched for genetic variants that could predict clinically meaningful responses to two major groups of antidepressants., Background It has been suggested that outcomes of antidepressant treatment for major depressive disorder could be significantly improved if treatment choice is informed by genetic data. This study aims to test the hypothesis that common genetic variants can predict response to antidepressants in a clinically meaningful way. Methods and Findings The NEWMEDS consortium, an academia–industry partnership, assembled a database of over 2,000 European-ancestry individuals with major depressive disorder, prospectively measured treatment outcomes with serotonin reuptake inhibiting or noradrenaline reuptake inhibiting antidepressants and available genetic samples from five studies (three randomized controlled trials, one part-randomized controlled trial, and one treatment cohort study). After quality control, a dataset of 1,790 individuals with high-quality genome-wide genotyping provided adequate power to test the hypotheses that antidepressant response or a clinically significant differential response to the two classes of antidepressants could be predicted from a single common genetic polymorphism. None of the more than half million genetic markers significantly predicted response to antidepressants overall, serotonin reuptake inhibitors, or noradrenaline reuptake inhibitors, or differential response to the two types of antidepressants (genome-wide significance p, Editors' Summary Background Genetic and environmental factors can influence a person's response to medications. Taking advantage of the recent advancements in genetics, scientists are working to match specific gene variations with responses to particular medications. Knowing whether a patient is likely to respond to a drug or have serious side effects would allow doctors to select the best treatment up front. Right now, there are only a handful of examples where a patient's version of a particular gene predicts their response to a particular drug. Some scientists believe that there will be many more such matches between genetic variants and treatment responses. Others think that because the action of most drugs is influenced by many different genes, a variant in one of those genes is unlikely to have measurable effect in most cases. Why Was This Study Done? One of the areas where patients' responses to available drugs vary widely is severe depression (or major depressive disorder). Prescription of an antidepressant is often the first step in treating the disease. However, less than half of patients get well taking the first antidepressant prescribed. Those who don't respond to the first drug need to, together with their doctors, try multiple courses of treatment to find the right drug and the right dose for them. For some patients none of the existing drugs work well. To see whether genetic information could help improve the choice of antidepressant, researchers from universities and the pharmaceutical industry joined forces in this large study. They examined two ways to use genetic information to improve the treatment of depression. First, they searched all genes for common genetic variants that could predict which patients would not respond to the two major groups of antidepressants (serotonin reuptake inhibitors, or SRIs, and noradrenaline reuptake inhibitors, or NRIs). They hoped that this would help with the development of new drugs that could help these patients. Second, they looked for common genetic variants in all genes that could identify patients who responded to one of the two major groups of antidepressants. Such predictors would make it possible to know which drug to prescribe for which patient. What Did the Researchers Do and Find? The researchers selected 1,790 patients with severe depression who had participated in one of several research studies; 1,222 of the patients had been treated with an SRI, the remaining 568 with an NRI, and it was recorded how well the drugs worked for each patient. The researchers also had a detailed picture of the genetic make-up of each patient, with information for over half a million genetic variants. They then looked for an association between genetic variants and responses to drugs. They found not a single genetic variant that could predict clearly whether a person would respond to antidepressants in general, to one of the two main groups (SRIs and NRIs), or much better to one than the other. They also didn't find any combination of variants in groups of genes that work together that could predict responses. Combining their data with those from another large study did not yield any robust predictors either. What Do These Findings Mean? This study was large enough that it should have been possible to find common genetic variants that by themselves could predict a clinically meaningful response to SRIs and/or NRIs, had such variants existed. The fact that the study failed to find such variants suggests that such variants do not exist. It is still possible, however, that variants that are less common could predict response, or that combinations of variants could. To find those, if they do exist, even larger studies will need to be done. Additional Information Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001326 The National Institute of General Medical Sciences at the US National Institutes of Health has a fact sheet on personalized medicine PubMed Health at the US National Library of Medicine has a page on major depressive disorder Wikipedia has pages on major depressive disorder and pharmacogenetics, the study of how genetic variation affects response to certain drugs (note that Wikipedia is a free online encyclopedia that anyone can edit) The UK National Health Service has comprehensive information pages on depression

To describe the weight gain-related side-effects of psychotropic drugs and their consequences on metabolic complications (hypercholesterolemia, obesity) in a Swiss cohort of psychiatric patients.This cross-sectional observational study was performed in an out-patient psychiatric division with patients having received for more than 3 months the following drugs: clozapine, olanzapine, quetiapine, risperidone, lithium, and/or valproate. Clinical measures and lifestyle information (smoking behaviour, physical activity) were recorded.196 inclusions were completed. Weight gain (≥10% of initial weight) following drug treatment was reported in 47% of these patients. Prevalence of obesity (BMI ≥ 30), hypercholesterolemia (≥6.2 mmol/L) and low HDL-cholesterol (1.0 mmol/L in men,1.3 mmol/L in women) were present in 38%, 21%, and 27% of patients, respectively. A higher standardised dose, an increase of appetite following medication introduction, the type of medication (clozapine or olanzapine quetiapine or risperidone lithium or valproate), and the gender were shown to be significantly associated with evolution of BMI.High prevalence of obesity and hypercholesterolemia was found in an out-patient psychiatric population and confirms drug-induced weight gain complications during long-term treatment. The results support the recently published recommendations of monitoring of metabolic side-effects during treatment with atypical antipsychotics. Moreover, the weight gain predictors found in the present study could help to highlight patients with special health care management requirement.

Diese Behandlungsempfehlung orientiert sich an der internationalen Leitlinie der World Federation of Societies of Biological Psychiatry (WFSBP) [1] und der S3-Leitlinie / Nationalen Versorgungsleitlinie der Deutschen Gesellschaft fur Psychiatrie, Psychotherapie und Nervenheilkunde (DGPPN) [2] und fasst die evidenzbasierten Therapiestrategien (neuester Stand der wissenschaftlichen Erkenntnisse nach den Kriterien der evidenzbasierten Medizin) zur akuten Behandlung der depressiven Episoden nach den Kriterien der «International Classification of Diseases» (ICD-10, WHO 1992) sowie des «Diagnostic and Statistical Manual of Mental Disorders» (DSM-IV) zusammen. Die Behandlungsempfehlung setzt eine grundliche diagnostische Abklarung durch eine arztliche Fachperson voraus, wobei andere psychische sowie somatische Erkrankungen ausgeschlossen und depressionsauslosende Faktoren (z.B. Medikamente, psychosoziale Stressfaktoren usw.) berucksichtigt werden mussen. Die vier Grundelemente der psychiatrischen Behandlung (aktiv abwartende Begleitung, medikamentose und psychotherapeutische Behandlungen sowie Kombinationstherapie) sollten wahrend der gesamten Behandlung angemessen unter Berucksichtigung von klinischen Faktoren wie Symptomschwere, Erkrankungsverlauf und Patientenpraferenz eingesetzt werden. Der Behandlungsplan richtet sich in erster Linie nach dem Schweregrad der Depression (Abb. 1 x). Eine aktiv abwartende Begleitung (watchful waiting) kann bei Patienten mit leichter depressiver Episode genugen. Jedoch sollte die Besserung der Symptomatik innerhalb der ersten beiden Wochen uberpruft werden. Antidepressiva sollten nicht generell zur Erstbehandlung von leichten depressiven Episoden eingesetzt werden, sondern nur nach kritischer Abwagung des Nutzen-Risiko-Verhaltnisses. Das berucksichtigt u.a. den Wunsch des Patienten, positives Ansprechen in der Vergangenheit, Fortbestehen von Symptomen nach anderen Interventionen sowie mittelgradige oder schwere Depressionen in der Vorgeschichte. Zur Behandlung von leichten bis mittelschweren Depressionen soll eine angemessene Psychotherapie angeboten werden. Der Einsatz von Antidepressiva ist insbesondere bei mittelgradigen und schweren depressiven Episoden indiziert. Ein wesentliches Behandlungsmoment ist die vertrauensvolle Beziehung zwischen Patient und Behandler, weshalb jede Pharmakotherapie in ein entsprechendes Gesprachsangebot eingebettet gehort. Der Evidenzgrad der einzelnen Therapien wird in Stufen (Level A bis D) angegeben (Tab. 1 p). Methodische Kriterien bestimmen die Evidenz, d.h. die Bewertung der Wirksamkeit einer Intervention basiert in der Regel auf randomisierten klinischen Studien (RCT). Aus dem Fehlen von RCT fur einzelne Behandlungen kann aber nicht der Ruckschluss gezogen werden, dass diese Verfahren nicht wirksam sind. Die psychiatrische Theorie und Praxis beruht in der Schweiz auf einem biopsychosozialen Ansatz in der Diagnostik und Behandlung psychischer Storungen (vgl. Weiterbildungsprogramm und Leitbild der SGPP). Entsprechend werden erganzend zu den vorliegenden evidenzbasierten somatischen Behandlungsempfehlungen auch Empfehlungen fur die Psychotherapie der Depression inklusive dem sozialen Blickwinkel (soziales Netz, Arbeitsfahigkeit usw.) mit der SGPP als Herausgeberin erarbeitet und veroffentlicht.

This article explores mindfulness skills in community and borderline personality disorder (BPD) samples. Study 1 includes 173 community volunteers and explores the psychometric properties of the French version of the Kentucky Inventory of Mindfulness Skills (KIMS). Study 2 explores the KIMS factor structure in 130 BPD patients and compares KIMS scores of this sample with those of the community sample from Study 1. Study 3 investigates the changes in KIMS scores in a BPD sample ( n = 82) treated with Intensive Dialectical Behavior Therapy (I-DBT). Results suggest that the psychometric properties of the French KIMS are comparable with those of the original version in the community and the BPD samples. Moreover, fewer mindfulness skills were found in BPD patients than in control participants. It was also observed that the ability to describe and to act with awareness increased in BPD patients after I-DBT. The present work makes a French instrument measuring mindfulness in daily activities available for clinical practice and research.

Cette recommandation de traitement suit les lignes directrices internationales de la World Federation of Societies of Biological Psychiatry (WFSBP) [1] et nationale S3 de la Deutsche Gesellschaft fur Psychiatrie, Psychotherapie und Nervenheilkunde (DGPPN) [2]. Elle reprend les strategies basees sur des preuves (l’ensemble des dernieres connaissances scientifiques selon les criteres de la medecine basee sur des preuves) du traitement aigu des episodes depressifs selon les criteres de l’«International Classification of Diseases» (ICD-10, OMS 1992) et du «Diagnostic and Statistical Manual of Mental Disorders» (DSM-IV). Cette recommandation de traitement presuppose un diagnostic approfondi par un medecin, avec exclusion d’autres maladies psychiques et somatiques, et en tenant compte des facteurs declenchant une depression (par ex. medicaments, stress psychosocial, etc.). Les quatre elements fondamentaux du traitement psychiatrique (accompagnement expectatif actif, traitements medicamenteux, psychotherapeutiques et combines) doivent etre exploites de maniere appropriee pendant toute la duree du traitement et en tenant compte de facteurs cliniques tels que la gravite des symptomes, l’evolution de la maladie et la preference du patient. Le plan de traitement est fait en fonction d’abord de la gravite de la depression (fig. 1 x). Un accompagnement expectatif actif (watchful waiting) peut suffire pour des patients presentant des episodes depressifs legers. Mais l’amelioration de la symptomatologie doit se confirmer au cours des deux premieres semaines. Les antidepresseurs ne doivent pas etre utilises de maniere generale pour le premier traitement d’episodes depressifs legers mais uniquement apres avoir soigneusement pese le rapport beneficerisque. Cela tient compte notamment du souhait du patient, d’une reponse positive anterieure, de la persistance de symptomes apres d’autres interventions et de l’anamnese de depressions moderees ou graves. Une psychotherapie adequate doit etre proposee pour le traitement de depressions legeres a moderees. Les antidepresseurs sont particulierement indiques dans les episodes depressifs moderes et graves. Un moment therapeutique essentiel est la relation de confiance entre le patient et le soignant, raison pour laquelle toute pharmacotherapie doit etre englobee dans une proposition adequate de discussion. Le niveau d’evidence de chaque traitement est donne en paliers (level A a D) (tab. 1 p). Les criteres methodologiques determinent l’evidence, c’est-a-dire que l’evaluation de l’efficacite d’une intervention se base generalement sur des etudes cliniques randomisees (RCT). Il ne faut toutefois pas conclure de l’absence de RCT pour tel ou tel traitement qu’il n’est pas efficace. La theorie et la pratique psychiatriques reposent en Suisse sur une evaluation biopsychosociale dans le diagnostic et le traitement des troubles psychiques (c.f. programme de formation postgraduee et modele de la SSPP). En complement de ces recommandations de traitement somatique basees sur des preuves sont redigees et publiees des recommandations pour la psychotherapie de la depression sous l’angle social (reseau social, capacite de travail, etc.) avec la SSPP comme editrice.

BackgroundThe present open study investigates the feasibility of Mindfulness-based cognitive therapy (MBCT) in groups solely composed of bipolar patients of various subtypes. MBCT has been mostly evaluated with remitted unipolar depressed patients and little is known about this treatment in bipolar disorder.MethodsBipolar outpatients (type I, II and NOS) were included and evaluated for depressive and hypomanic symptoms, as well as mindfulness skills before and after MBCT. Patients’ expectations before the program, perceived benefit after completion and frequency of mindfulness practice were also recorded.ResultsOf 23 included patients, 15 attended at least four MBCT sessions. Most participants reported having durably, moderately to very much benefited from the program, although mindfulness practice decreased over time. Whereas no significant increase of mindfulness skills was detected during the trial, change of mindfulness skills was significantly associated with change of depressive symptoms between pre- and post-MBCT assessments.ConclusionsMBCT is feasible and well perceived among bipolar patients. Larger and randomized controlled studies are required to further evaluate its efficacy, in particular regarding depressive and (hypo)manic relapse prevention. The mediating role of mindfulness on clinical outcome needs further examination and efforts should be provided to enhance the persistence of meditation practice with time.

Alors que des prises en charge psychologiques efficaces sont disponibles pour traiter les joueurs excessifs, la plupart de ces patients ne cherchent pas d’aide par rapport a leurs problemes. Plusieurs freins a la recherche d’aide ont ete mis en evidence, comme la honte, la stigmatisation, le cout ou encore l’accessibilite des traitements. Dans ce contexte, un traitement sur Internet, facilement accessible et disponible a toute heure de la journee, impliquant une stigmatisation moins importante et des couts moins eleves, pourrait etre une alternative utile pour traiter des joueurs qui n’auraient normalement pas entrepris de therapie. Dans cet article, apres avoir decrit les benefices que pourrait permettre ce type de traitement, nous presentons le travail que nous menons actuellement pour valider un programme francophone de traitement du jeu par internet.

BACKGROUND: The article addresses the hypothesis that early telephone intervention for psychiatric outpatients starting antidepressant treatment would increase compliance with pharmacological treatment and retention time in the study, and thus allow for a more favourable clinical outcome. METHODS: The study focuses on 131 depressed outpatients who participated in a study aiming to obtain full remission. Patients who benefited from three early structured telephone interventions (n=81) were compared with participants who benefited from the usual care (n=50) with no clinical contact before the first clinical assessment at 2 weeks. RESULTS: The intervention proved to have no significant effect on treatment adherence, attrition rate, exclusion rate for adverse events or improvement of depression severity. It was nevertheless associated with increased retention time in the present study. CONCLUSIONS: These results suggest that motivational phone calls may reinforce adhesion in psychiatric patients and provide early opportunities to adapt treatment to individual needs. CLINICAL IMPLICATION: These results suggest that motivational phone calls may reinforce adhesion in psychiatric patients and provide early opportunities to adapt treatment to individual needs.

Objective: The purpose of this study was to evaluate the prevalence of pathological gambling in the Swiss adult population before the introduction of new forms of gambling, and the link between pathological gambling and alcohol abuse. Method: 2526 telephone interviews were completed using standardized assessment instruments for identifying potential and probable pathological gamblers (SOGS) and alcohol abuse (CAGE). Results: The current prevalence of probable and potential pathological gamblers were estimated to be 0.8% and 2.2%, respectively. The results also show a clear correlation between alcohol abuse and gambling behaviours. Conclusion: For the first time estimations are available of the Swiss prevalence rates of pathological gambling. Considering the link between gambling availability and increases in the prevalence of pathological gambling and the correlation between alcohol abuse and pathological gambling, the implications of these results for the prevention and treatment of this debilitating disorder are discussed.