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Importance: Cognitive behavioral therapy is recommended for anxiety-related disorders, but evidence for its long-term outcome is limited. Objective: This systematic review and meta-analysis aimed to assess the long-term outcomes after cognitive behavioral therapy (compared with care as usual, relaxation, psychoeducation, pill placebo, supportive therapy, or waiting list) for anxiety disorders, posttraumatic stress disorder (PTSD), and obsessive-compulsive disorder (OCD). Data Sources: English-language publications were identified from PubMed, PsycINFO, Embase, Cochrane, OpenGrey (1980 to January 2019), and recent reviews. The search strategy included a combination of terms associated with anxiety disorders (eg, panic or phobi) and study design (eg, clinical trial or randomized controlled trial). Study Selection: Randomized clinical trials on posttreatment and at least 1-month follow-up effects of cognitive behavioral therapy compared with control conditions among adults with generalized anxiety disorder, panic disorder with or without agoraphobia, social anxiety disorder, specific phobia, PTSD, or OCD. Data Extraction and Synthesis: Researchers independently screened records, extracted statistics, and assessed study quality. Data were pooled using a random-effects model. Main Outcomes and Measures: Hedges g was calculated for anxiety symptoms immediately after treatment and at 1 to 6 months, 6 to 12 months, and more than 12 months after treatment completion. Results: Of 69 randomized clinical trials (4118 outpatients) that were mainly of low quality, cognitive behavioral therapy compared with control conditions was associated with improved outcomes after treatment completion and at 1 to 6 months and at 6 to 12 months of follow-up for a generalized anxiety disorder (Hedges g, 0.07-0.40), panic disorder with or without agoraphobia (Hedges g, 0.22-0.35), social anxiety disorder (Hedges g, 0.34-0.60), specific phobia (Hedges g, 0.49-0.72), PTSD (Hedges g, 0.59-0.72), and OCD (Hedges g, 0.70-0.85). After 12-month follow-up, these associations were still significant for generalized anxiety disorder (Hedges g, 0.22; number of studies [k] = 10), social anxiety disorder (Hedges g, 0.42; k = 3), and PTSD (Hedges g, 0.84; k = 5), but not for panic disorder with or without agoraphobia (k = 5) and could not be calculated for specific phobia (k = 1) and OCD (k = 0). Relapse rates after 3 to 12 months were 0% to 14% but were reported in only 6 randomized clinical trials (predominantly for panic disorder with or without agoraphobia). Conclusions and Relevance: The findings of this meta-analysis suggest that cognitive behavioral therapy for anxiety-related disorders is associated with improved outcomes compared with control conditions until 12 months after treatment completion. After 12 months, effects were small to medium for generalized anxiety disorder and social anxiety disorder, large for PTSD, and not significant or not available for other disorders. High-quality randomized clinical trials with more than 12 months of follow-up and reported relapse rates are needed.

Leading biological hypotheses propose that biological changes may underlie major depressive disorder onset and relapse/recurrence. Here, we investigate if there is prospective evidence for biomarkers derived from leading theories. We focus on neuroimaging, gastrointestinal factors, immunology, neurotrophic factors, neurotransmitters, hormones, and oxidative stress. Searches were performed in Pubmed, Embase and PsychInfo for articles published up to 06/2019. References and citations of included articles were screened to identify additional articles. Inclusion criteria were having an MDD diagnosis as outcome, a biomarker as predictor, and prospective design search terms were formulated accordingly. PRISMA guidelines were applied. Meta-analyses were performed using a random effect model when three or more comparable studies were identified, using a random effect model. Our search resulted in 67,464 articles, of which 75 prospective articles were identified on: Neuroimaging (N = 24), Gastrointestinal factors (N = 1), Immunology (N = 8), Neurotrophic (N = 2), Neurotransmitters (N = 1), Hormones (N = 39), Oxidative stress (N = 1). Meta-analyses on brain volumes and immunology markers were not significant. Only cortisol (N = 19, OR = 1.294,p = 0.024) showed a predictive effect on onset/relapse/recurrence of MDD, but not on time until MDD onset/relapse/recurrence. However, this effect disappeared when studies including participants with a baseline clinical diagnosis were removed from the analyses. Other studies were too heterogeneous to compare. Thus, there is a lack of evidence for leading biological theories for onset and maintenance of depression. Only cortisol was identified as potential predictor for MDD, but results are influenced by the disease state. High-quality (prospective) studies on MDD are needed to disentangle the etiology and maintenance of MDD.

Background According to previous research, dysfunctional attitudes and/or scoring extreme on the end-point anchors of questionnaires of dysfunctional thinking predict depressive relapse/recurrence. Evidence that these two methods represent a risk for depressive relapse/recurrence is however mixed, due to differential or poorly defined concepts. The current study aimed to test the two methods. Methods Remitted recurrently depressed patients with low residual depressive symptoms (N = 264) were recruited as part of a randomized controlled trial of the effectiveness of mobile Cognitive Therapy for recurrent depression versus treatment as usual. In the current secondary analysis, Cox regression models were conducted to test dysfunctional attitudes and extreme responding variables (assessed on the Dysfunctional Attitudes Scale [DAS]) as predictors of depressive relapse/recurrence within two years after randomization. Results Data from 255 participants were analyzed. Results showed that DAS total scores at baseline significantly predicted depressive relapse/recurrence (Hazard Ratio [HR] = 1.01, p = .042). An index that reflects endorsement of habitual relative to functional responses was a significant predictor of depressive relapse/recurrence (HR = 2.11, p = .029). Limitations The current study employed a single measure to identify extreme responses and dysfunctional attitudes. Secondly, various statistical analyses were performed without correcting for multiple testing, which in turn increased the likelihood to finding significant results. Conclusions Current study confirmed both methods: People who scored higher on the DAS or had relatively more habitual than functional responses on the extreme positive ends of the DAS had a decreased time to depressive relapse/recurrence.

Contains fulltext : 217004.pdf (Publisher’s version ) (Closed access) Achtergrond: Voorschrijven van antidepressiva (ad) is sinds 1980 sterk toegenomen, vooral selectieve serotonineheropnameremmers (ssri's), en voor steeds langere tijd. Toch worden, vooral buiten de beroepsgroep, ad nog steeds bekritiseerd en betwijfelt men hun nut. Doel: Verklaren van toename en bieden van een perspectief op oorzaken en oplossingen van de controverse, aanzet tot debat. Methode: Essay met genuanceerde en kritische presentatie van feiten en argumenten van voor- en tegenstanders. Resultaten: Toename is het gevolg van 1. toegenomen veiligheid en gebruiksgemak, 2. toegenomen hulpvraag voor en herkenning van depressie in de huisartspraktijk, 3. uitbreiding indicatiecriteria, 4. effectieve marketingstrategieën, en 5. effectiviteit van ad in de acute fase en bij preventie van terugval/recidief in continuerings- en onderhoudsfasen. Critici wijzen op: 1. beperkte meerwaarde van ad in acute fase t.o.v. placebo, 2. veel uitvallers en mensen zonder respons, 3. terugval/recidiefpreventie met ad in continuerings- en onderhoudsfasen werkt alleen bij patiënten met goede respons op ad in acute fase, 4. terugval/recidief na discontinuering ad vaak onthoudingsverschijnselen, en 5. publicatiebias, selectieve rapportage, selectieve patiëntselectie en suboptimale blindering, leidend tot overschatting voordelen en onderschatting nadelen. Factoren die controverse onderhouden, zijn: 1. critici wijzen op de netto-effectiviteit en voorstanders op de bruto-effectiviteit (dus inclusief spontaan herstel en placebo-effect); 2. hardnekkigheid van beschadigd vertrouwen in industriegefinancierde rct's; 3. gebrek aan rct’s met relevante langetermijnuitkomstmetingen; 4. ideologische posities, versterkt door belangenconflicten en selectieve citaties; 5. maatschappelijk klimaat. Conclusie: Hoewel het lastig zal zijn om deels ideologisch ingegeven posities tot elkaar te brengen, zien wij mogelijkheden. Drie factoren zijn daarbij van groot belang: polderen (welke data overtuigen de tegenpartij), responspredictie en rct's met functionele uitkomstdata over de lange termijn. 10 p.

Leading biological hypotheses propose that biological changes may underlie major depressive disorder onset and relapse/recurrence. Here, we investigate if there is prospective evidence for biomarkers derived from leading theories. We focus on neuroimaging, gastrointestinal factors, immunology, neurotrophic factors, neurotransmitters, hormones, and oxidative stress. Searches were performed in Pubmed, Embase and PsychInfo for articles published up to 06/2019. References and citations of included articles were screened to identify additional articles. Inclusion criteria were having an MDD diagnosis as outcome, a biomarker as predictor, and prospective design search terms were formulated accordingly. PRISMA guidelines were applied. Meta-analyses were performed using a random effect model when three or more comparable studies were identified, using a random effect model. Our search resulted in 67,464 articles, of which 75 prospective articles were identified on: Neuroimaging (N = 24), Gastrointestinal factors (N = 1), Immunology (N = 8), Neurotrophic (N = 2), Neurotransmitters (N = 1), Hormones (N = 39), Oxidative stress (N = 1). Meta-analyses on brain volumes and immunology markers were not significant. Only cortisol (N = 19, OR = 1.294, p = 0.024) showed a predictive effect on onset/relapse/recurrence of MDD, but not on time until MDD onset/relapse/recurrence. However, this effect disappeared when studies including participants with a baseline clinical diagnosis were removed from the analyses. Other studies were too heterogeneous to compare. Thus, there is a lack of evidence for leading biological theories for onset and maintenance of depression. Only cortisol was identified as potential predictor for MDD, but results are influenced by the disease state. High-quality (prospective) studies on MDD are needed to disentangle the etiology and maintenance of MDD.

Objective Antidepressant medication is commonly used for the prevention of depression recurrence in the perinatal period, yet it is unknown what vulnerability markers may play a role in recurrence. The objective of the current study was to provide a descriptive overview of the associated characteristics of women who experienced a perinatal recurrence of depression despite ongoing antidepressant use, and further, to identify clinically measurable vulnerability markers associated with recurrence. Methods Eighty-five pregnant women with a history of depression who used antidepressants (e.g. Selective Serotonin Reuptake Inhibitors or Serotonin and Noradrenaline Reuptake Inhibitors) at the start of the study were included. Clinical features, including information on psychiatric history and antidepressant use, were collected throughout the perinatal period (in this study defined as the period between 12 weeks of pregnancy untill three months postpartum). The clinical features of women experiencing recurrence of depression were described in detail. To identify vulnerability markers associated with recurrence of depression, we performed exploratory univariable logistic regression analyses. Results Eight women (9.4%) experienced a recurrence of depression; two during pregnancy and six in the first 12 weeks postpartum. All women with recurrence of depression had first onset of depression during childhood or adolescence and had at least 2 psychiatric co-morbidities. Identification of vulnerability markers associated with recurrence of depression yielded associations with depressive symptoms around 16 weeks of pregnancy (OR 1.28, 95%CI 1.08–1.52), number of psychiatric co-morbidities (OR 1.89, 95%CI 1.16–3.09) and duration of antidepressant use (OR 1.01, 95%CI 1.00–1.02). Conclusion Implementing adequate risk assessment in pregnant women who use antidepressants can help identify predictors for recurrence of depression in future studies and thus ultimately lead to improved care.

Psychological factors hypothesized to account for relapse of major depressive disorder (MDD) roughly originate from five main theories: Cognitive, diathesis-stress, behavioural, psychodynamic, and personality-based. In a meta-analysis we investigated prospective, longitudinal evidence for these leading psychological theories and their factors in relation to depressive relapse. Included studies needed to establish history of MDD and prospective depressive relapse through a clinical interview, have a longitudinal and prospective design, and measure at least one theory-derived factor before relapse. We identified 66 eligible articles out of 43,586 records published up to November 2018. Pooled odds ratios (OR) indicated a significant relationship between the cognitive, behavioural, and personality-based theories and depressive relapse (cognitive: k = 17, OR = 1.24, 95% CI = 1.10–1.40; behavioural, k = 8, OR = 1.15, 95% CI = 1.05–1.25; personality: k = 12, OR = 1.26, 95% CI = 1.02–1.54), but not for the psychodynamic theories (k = 4, OR = 1.29, 95% CI = 0.83–1.99). Pooled hazard ratios of the theories were not significant. There were no articles identified for the diathesis-stress theories. To conclude, there is a restricted number of prospective studies, and some evidence that the cognitive, behavioural, and personality-based theories indeed partially account for depressive relapse.

Item does not contain fulltext Achtergrond: De zorgstandaard Depressieve stoornissen beschrijft het gehele zorgtraject voor patiënten vanaf de leeftijd van 8 jaar met depressieve klachten en stoornissen. Doel: Beschrijven van de belangrijkste aanbevelingen opgenomen in de zorgstandaard Depressieve stoornissen. Methode: De zorgstandaard is een vertaalslag van bestaande richtlijnen voor depressie aangevuld met praktijkkennis van de professional en ervaringskennis van patiënten. Resultaten: Kernelementen in de zorg voor depressie zijn het aanbieden van gepaste zorg en aandacht voor terugvalpreventie. Bij de persisterende depressie is een combinatie van psychotherapie en farmacotherapie geïndiceerd waarbij meer sessies psychotherapie nodig kunnen zijn. Repeterende transcraniële magnetische stimulatie heeft een plaats bij de therapieresistente depressie. Conclusies: De zorgstandaard is een belangrijk instrument om de bestaande zorg voor depressie in een instelling of regio te verbeteren. 9 p.

Exposure-based treatment for anxiety disorders is effective for many patients, but relapse is not uncommon. One predictor of the return of fear is the negative valence of fear-relevant stimuli. The aim of the current experiments was to examine whether counterconditioning with positive film clips reduces this negative stimulus valence as well as the return of fear, compared to standard extinction training and to an extinction training with non-contingent exposure to the positive film clips. Participants were 87 students in Experiment 1 (three-day paradigm), and 90 students in Experiment 2 (one-day paradigm). They first underwent a differential acquisition phase, in which one of three pictures was paired with an electric shock. They were then randomly allocated to one of the three intervention groups. Afterwards, they underwent a test phase in which pictures were presented without shock (to measure spontaneous recovery of fear), which was followed by unsignaled shocks to induce reinstatement of extinguished fear. Outcome variables were self-reported stimulus valence, shock expectancy, skin conductance, and fear-potentiated startle. In both experiments, counterconditioning decreased negative stimulus valence, relative to the other interventions, but it did not reduce spontaneous fear recovery or fear reinstatement. Overall, our findings do not support the notion that counterconditioning reduces return of fear.

In het recent verschenen rapport over de bekostiging van de curatieve ggz concludeert de Algemene Rekenkamer (2017): ‘informatie die met rom [routine outcome monitoring] wordt verkregen, heeft beperkingen en is van onvoldoende kwaliteit om te dienen als sturingsinformatie bij de zorginkoop’ (p. 14). Dit rapport is door een groep psychiaters en psychologen aangegrepen om de petitie ‘Stop benchmark met rom ’ (www.stoprom.com) in het leven te roepen, die inmiddels door ruim 6000 mensen getekend is. In dit artikel reageren wij op deze petitie. Wij onderschrijven dat rom geen basis mag zijn voor zorginkoop, maar vinden dat rom en benchmarking van grote waarde kunnen zijn voor het verbeteren van de kwaliteit van de behandeling en pleiten daarom voor inhoudelijke doorontwikkeling van benchmarking in plaats van deze te stoppen.

Exposure-based treatment for anxiety disorders is effective for many patients, but relapse is not uncommon. One predictor of the return of fear is the negative valence of fear-relevant stimuli. The aim of the current experiments was to examine whether counterconditioning with positive film clips reduces this negative stimulus valence as well as the return of fear, compared to standard extinction training and to an extinction training with non-contingent exposure to the positive film clips. Participants were 87 students in Experiment 1 (three-day paradigm), and 90 students in Experiment 2 (one-day paradigm). They first underwent a differential acquisition phase, in which one of three pictures was paired with an electric shock. They were then randomly allocated to one of the three intervention groups. Afterwards, they underwent a test phase in which pictures were presented without shock (to measure spontaneous recovery of fear), which was followed by unsignaled shocks to induce reinstatement of extinguished fear. Outcome variables were self-reported stimulus valence, shock expectancy, skin conductance, and fear-potentiated startle. In both experiments, counterconditioning decreased negative stimulus valence, relative to the other interventions, but it did not reduce spontaneous fear recovery or fear reinstatement. Overall, our findings do not support the notion that counterconditioning reduces return of fear.

Background It is presumed that pharmacological and non-pharmacological treatment of prenatal common mental disorders can mitigate associated adverse effects in offspring, yet strong evidence for the prophylactic benefits of treatment is lacking. We therefore examined the effect of prenatal treatments for common mental disorders on offspring outcomes. Methods For this meta-analysis, articles published up to August 31, 2017, were obtained from PubMed, PsycInfo, Embase, and Cochrane databases. Included studies needed to be randomized controlled trials (RCTs) on the effect of treatment of prenatal common mental disorders comparing an intervention to a control condition, including offspring outcome(s). Random effects models were used to calculate Hedges’ g in the program Comprehensive Meta-Analysis© (version 3.0). Results Sixteen randomized controlled trials among 2778 pregnant women compared offspring outcomes between prenatal interventions and control groups. There were zero pharmacological, 13 psychological, and three other interventions (homeopathy, relaxation interventions, and short psycho-education). Birth weight (mean difference 42.88 g, g = 0.08, 95% CI −0.06 to 0.22, p = 0.27, n = 11), Apgar scores (g = 0.13, 95% CI −0.28 to 0.54, p = 0.53, n = 4), and gestational age (g = 0.03, 95% CI −0.06 to 0.54, p = 0.49, n = 10) were not significantly affected. Other offspring outcomes could not be meta-analyzed due to the inconsistent reporting of offspring outcomes and an insufficient number of studies. Conclusions Non-pharmacological interventions had no significant effect on birth outcomes, although this outcome should be considered with caution due to the risk of biases. No randomized controlled trial examined the effects of prenatal pharmacological treatments as compared to treatment as usual for common mental disorders on offspring outcomes. Present clinical guidelines may require more research evidence on offspring outcomes, including child development, in order to warrant the current recommendation to routinely screen and subsequently treat prenatal common mental disorders. Trial registration PROSPERO CRD42016047190 Electronic supplementary material The online version of this article (10.1186/s12916-018-1192-6) contains supplementary material, which is available to authorized users.

Background: It is presumed that pharmacological and non-pharmacological treatment of prenatal common mental disorders can mitigate associated adverse effects in offspring, yet strong evidence for the prophylactic benefits of treatment is lacking. We therefore examined the effect of prenatal treatments for common mental disorders on offspring outcomes. Methods: For this meta-analysis, articles published up to August 31, 2017, were obtained from PubMed, PsycInfo, Embase, and Cochrane databases. Included studies needed to be randomized controlled trials (RCTs) on the effect of treatment of prenatal common mental disorders comparing an intervention to a control condition, including offspring outcome(s). Random effects models were used to calculate Hedges' g in the program Comprehensive Meta-Analysis © (version 3.0). Results: Sixteen randomized controlled trials among 2778 pregnant women compared offspring outcomes between prenatal interventions and control groups. There were zero pharmacological, 13 psychological, and three other interventions (homeopathy, relaxation interventions, and short psycho-education). Birth weight (mean difference 42.88 g, g = 0.08, 95% CI -0.06 to 0.22, p = 0.27, n = 11), Apgar scores (g = 0.13, 95% CI -0.28 to 0.54, p = 0.53, n = 4), and gestational age (g = 0.03, 95% CI -0.06 to 0.54, p = 0.49, n = 10) were not significantly affected. Other offspring outcomes could not be meta-analyzed due to the inconsistent reporting of offspring outcomes and an insufficient number of studies. Conclusions: Non-pharmacological interventions had no significant effect on birth outcomes, although this outcome should be considered with caution due to the risk of biases. No randomized controlled trial examined the effects of prenatal pharmacological treatments as compared to treatment as usual for common mental disorders on offspring outcomes. Present clinical guidelines may require more research evidence on offspring outcomes, including child development, in order to warrant the current recommendation to routinely screen and subsequently treat prenatal common mental disorders. Trial registration: PROSPERO CRD42016047190.

Item does not contain fulltext 181 p.

In het recent verschenen rapport over de bekostiging van de curatieve ggz concludeert de Algemene Rekenkamer (2017): ‘informatie die met ROM [routine outcome monitoring] wordt verkregen, heeft beperkingen en is van onvoldoende kwaliteit om te dienen als sturingsinformatie bij de zorginkoop’ (p. 14). Dit rapport is door een groep psychiaters en psychologen aangegrepen om de petitie ‘Stop benchmark met ROM’ (www.stoprom.com) in het leven te roepen, die inmiddels door ruim 6000 mensen getekend is. In dit artikel reageren wij op deze petitie. Wij onderschrijven dat ROM geen basis mag zijn voor zorginkoop, maar vinden dat ROM en benchmarking van grote waarde kunnen zijn voor het verbeteren van de kwaliteit van de behandeling en pleiten daarom voor inhoudelijke doorontwikkeling van benchmarking in plaats van deze te stoppen.

Depression is a heterogeneous condition with significant variations in both course and response to treatment. The diverse needs of depressed individuals suggest that treatment should be organized systematically, with multiple efficacious treatment modalities such as psychotherapy and pharmacotherapy available and delivered in a manner and sequence consistent with the best available evidence. Moreover, these systems must be cost-conscious, implementable in regular practice, and accessible to those who require treatment. We term such structures “rational” systems of care. In this chapter, we provide a review of essential components of a rational system, including (1) identifying individuals in need of services, (2) selecting treatment(s), (3) monitoring response and supporting clinical decisions, (4) adapting treatment strategies, (5) maintaining the treatment response, and (6) maximizing access. Case examples of national efforts to implement systems of depression care are provided and discussed, followed by a review of implementation and research issues.