Database : MEDLINE
Search on : Depressive and Disorder [Words]
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[PMID]: 29524456
[Au] Autor:Stapelberg NJC; Pratt R; Neumann DL; Shum DHK; Brandis S; Muthukkumarasamy V; Stantic B; Blumenstein M; Headrick JP
[Ad] Address:Bond University Faculty of Health Sciences and Medicine and Gold Coast Hospital and Health Services, 14 University Dr, Robina, Queensland, 4226, Australia. Electronic address: cstapelb@bond.edu.au.
[Ti] Title:From Feedback Loop Transitions to Biomarkers in the Psycho-Immune-Neuroendocrine Network: Detecting the Critical Transition from Health to Major Depression.
[So] Source:Neurosci Biobehav Rev;, 2018 Mar 07.
[Is] ISSN:1873-7528
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Biological pathways underlying major depressive disorder (MDD) can be viewed as systems biology networks. The psycho-immune-neuroendocrine (PINE) network comprises central nervous, immune, endocrine and autonomic systems, integrating biological mechanisms of MDD. Such networks exhibit recurrent motifs with specific functions, including positive and negative feedback loops, and are subject to critical transitions, influenced by feedback loop transitions (FLTs). AIMS: We aim to identify critical feedback loops and their FLTs, as well sentinel network nodes (SNNs), key network nodes that drive FLTs, within the PINE network. Examples of biomarkers are provided which may reflect early warning signs of impending critical transition to MDD. RESULTS: Disruption of homeostatic feedback loops reflects the physiological transition to MDD. Putative FLTs are identified within hypothalamic-pituitary-adrenal (HPA) and sympathetic-parasympathetic axes, the kynurenine pathway, gut function and dysbiosis. CONCLUSIONS: Progression from health to disease is driven by FLTs in the PINE network, which is likely to undergo changes characteristic of system instability. Biomarkers of system instability may effectively predict the critical transition to MDD.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 160823 MEDLINE  
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[PMID]: 29516036
[Au] Autor:Dolzani SD; Baratta MV; Moss JM; Leslie NL; Tilden SG; Sørensen AT; Watkins LR; Lin Y; Maier SF
[Ad] Address:Department of Psychology and Neuroscience and the Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309.
[Ti] Title:Inhibition of a Descending Prefrontal Circuit Prevents Ketamine-Induced Stress Resilience in Females.
[So] Source:eNeuro;5(1), 2018 Jan-Feb.
[Is] ISSN:2373-2822
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Stress is a potent etiological factor in the onset of major depressive disorder and posttraumatic stress disorder (PTSD). Therefore, significant efforts have been made to identify factors that produce resilience to the outcomes of a later stressor, in hopes of preventing untoward clinical outcomes. The NMDA receptor antagonist ketamine has recently emerged as a prophylactic capable of preventing neurochemical and behavioral outcomes of a future stressor. Despite promising results of preclinical studies performed in male rats, the effects of proactive ketamine in female rats remains unknown. This is alarming given that stress-related disorders affect females at nearly twice the rate of males. Here we explore the prophylactic effects of ketamine on stress-induced anxiety-like behavior and the neural circuit-level processes that mediate these effects in female rats. Ketamine given one week prior to an uncontrollable stressor (inescapable tailshock; IS) reduced typical stress-induced activation of the serotonergic (5-HT) dorsal raphe nucleus (DRN) and eliminated DRN-dependent juvenile social exploration (JSE) deficits 24 h after the stressor. Proactive ketamine altered prelimbic cortex (PL) neural ensembles so that a later experience with IS now activated these cells, which it ordinarily would not. Ketamine acutely activated a PL to DRN (PL-DRN) circuit and inhibition of this circuit with Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) at the time of IS one week later prevented stress prophylaxis, suggesting that persistent changes in PL-DRN circuit activity are responsible, at least in part, for mediating long-term effects associated with ketamine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  3 / 160823 MEDLINE  
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[PMID]: 29476894
[Au] Autor:Zhang S; Zhang H; Ku SM; Juarez B; Morel C; Tzavaras N; Montgomery S; Hodes GE; Brancato A; Russo SJ; Cao JL; Han MH
[Ad] Address:Department of Pharmacological Sciences and Institute for Systems Biomedicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China; Department of Anesthesiology, Renji Hospital, S
[Ti] Title:Sex Differences in the Neuroadaptations of Reward-related Circuits in Response to Subchronic Variable Stress.
[So] Source:Neuroscience;376:108-116, 2018 Feb 22.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Women are twice as likely to be diagnosed with major depressive disorder. However, fewer studies in rodent models of depression have used female animals, leading to a relative lack of understanding of the female brain's response to stress, especially at a neural circuit level. In this study, we utilized a 6-day subchronic variable stress (SCVS) mouse model and measured novelty suppressed feeding as behavioral criteria to evaluate susceptibility to SCVS in male and female mice. First, we showed that SCVS induced a decrease in latency to eat (susceptible phenotype) in female mice, but not in males (resilient phenotype). After determining behavioral phenotypes, we investigated the firing activities of dopamine (DA) neurons in the ventral tegmental area (VTA), as well as the neurons that project from lateral habenula (LHb) to the VTA and from locus coeruleus (LC) to the VTA. Utilizing retrograding lumafluor fluorescent tracers and electrophysiology techniques, we performed cell type- and circuit-specific measures of neuronal firing rates. Our data show that SCVS significantly increased the firing rate of LHb-VTA circuit neurons in female mice when compared to that of their female controls, an effect that was absent in SCVS-exposed males. Interestingly, SCVS did not induce significant firing alterations in VTA DA neurons and LC-VTA circuit neurons in either female mice or male mice when compared to their stress-naïve controls. Overall, our data show sex differences in the LHb-VTA circuit responses to SCVS, and implicates a potential role of this projection in mediating vulnerability of female mice to stress-induced depression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 160823 MEDLINE  
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[PMID]: 29466722
[Au] Autor:Yao X; Yin Z; Liu F; Wei S; Zhou Y; Jiang X; Wei Y; Xu K; Wang F; Tang Y
[Ad] Address:Department of Psychiatry, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China; The 7th People's Hospital, Dalian, Liaoning, PR China.
[Ti] Title:Shared and distinct regional homogeneity changes in bipolar and unipolar depression.
[So] Source:Neurosci Lett;673:28-32, 2018 Feb 18.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:BACKGROUND: Bipolar depression (BD) is easily misdiagnosed as unipolar depression (UD) or major depressive disorder (MDD) because the depressive symptoms can overlap. Regional homogeneity (ReHo), a measure commonly used for analyzing resting-state fMRI data, has been applied to the study of various neuropsychiatric disorders. However, to date, studies directly comparing BD and UD using ReHo have been relatively scarce. Further investigation is needed to study the latent pathophysiological mechanisms of BD and UD. METHODS: Fifty-five patients with BD and 76 patients with UD, as well as 113 healthy controls (HC), underwent resting-state functional magnetic resonance imaging (fMRI). We compared the voxel-wise ReHo across the whole brain for subjects in each of the three groups. RESULTS: Significant differences were found in the left frontal cluster (LFC) across the three groups. There were differences between BD and UD in the LFC and left temporal cluster (LTC). In addition, differences between UD and HC existed in the LFC and the occipital cluster (OC). When comparing BD subjects with HC subjects, significant differences were found in all three clusters. No correlations were observed between the 17-item Hamilton Depression Rating Scale (HDRS-17) scores or sub-scores and the ReHo values of BD or UD patients. CONCLUSION: ReHo values in the LFC differed significantly among BD, UD, and HC subjects. ReHo in the LTC showed significant differences between BD and UD that might serve as neuroimaging markers of BD. Further, BD and UD shared ReHo changes in the cuneus, suggesting that the cuneus might provide a depressive state neuroimaging marker of BD and UD patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 160823 MEDLINE  
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[PMID]: 29408968
[Au] Autor:Qi S; Yang X; Zhao L; Calhoun VD; Perrone-Bizzozero N; Liu S; Jiang R; Jiang T; Sui J; Ma X
[Ad] Address:Brainnetome Center and National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, China.
[Ti] Title:MicroRNA132 associated multimodal neuroimaging patterns in unmedicated major depressive disorder.
[So] Source:Brain;, 2018 Feb 02.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:There is compelling evidence that epigenetic factors contribute to the manifestation of depression, in which microRNA132 (miR-132) is suggested to play a pivotal role in the pathogenesis and neuronal mechanisms underlying the symptoms of depression. Additionally, several depression-associated genes [MECP2, ARHGAP32 (p250GAP), CREB, and period genes] were experimentally validated as miR-132 targets. However, most studies regarding miR-132 in major depressive disorder are based on post-mortem, animal models or genetic comparisons. This work will be the first attempt to investigate how miR-132 dysregulation may impact covariation of multimodal brain imaging data in 81 unmedicated major depressive patients and 123 demographically-matched healthy controls, as well as in a medication-naïve subset of major depressive patients. MiR-132 values in blood (patients > controls) was used as a prior reference to guide fusion of three MRI features: fractional amplitude of low frequency fluctuations, grey matter volume, and fractional anisotropy. The multimodal components correlated with miR-132 also show significant group difference in loadings. Results indicate that (i) higher miR-132 levels in major depressive disorder are associated with both lower fractional amplitude of low frequency fluctuations and lower grey matter volume in fronto-limbic network; and (ii) the identified brain regions linked with increased miR-132 levels were also associated with poorer cognitive performance in attention and executive function. Using a data-driven, supervised-learning method, we determined that miR-132 dysregulation in major depressive disorder is associated with multi-facets of brain function and structure in fronto-limbic network (the key network for emotional regulation and memory), which deepens our understanding of how miR-132 dysregulation in major depressive disorders contribute to the loss of specific brain areas and is linked to relevant cognitive impairments.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1093/brain/awx366

  6 / 160823 MEDLINE  
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[PMID]: 29524099
[Au] Autor:Lopez KC; Luby JL; Belden AC; Barch DM
[Ad] Address:Department of Psychological & Brain Sciences, Washington University, St. Louis, MO, USA.
[Ti] Title:Emotion dysregulation and functional connectivity in children with and without a history of major depressive disorder.
[So] Source:Cogn Affect Behav Neurosci;, 2018 Mar 09.
[Is] ISSN:1531-135X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Recent interest has emerged in understanding the neural mechanisms by which deficits in emotion regulation (ER) early in development may relate to later depression. Corticolimbic alterations reported in emotion dysregulation and depression may be one possible link. We examined the relationships between emotion dysregulation in school age, corticolimbic resting-state functional connectivity (rs-FC) in preadolescence, and depressive symptoms in adolescence. Participants were 143 children from a longitudinal preschool onset depression study who completed the Children Sadness Management Scale (CSMS; measuring ER), Child Depression Inventory (CDI-C; measuring depressive symptoms), and two resting-state MRI scans. Rs-FC between four primary regions of interest (ROIs; bilateral dorsolateral prefrontal cortex [dlPFC] and amygdala) and six target ROIs thought to contribute to ER were examined. Findings showed that ER in school age did not predict depressive symptoms in adolescence, but did predict preadolescent increases in dlPFC-insula and dlPFC-ventromedial PFC rs-FC across diagnosis, as well as increased dlPFC-dorsal anterior cingulate cortex (dACC) rs-FC in children with a history of depression. Of these profiles, only dlPFC-dACC rs-FC in preadolescence predicted depressive symptoms in adolescence. However, dlPFC-dACC connectivity did not mediate the relationship between ER in school age and depressive symptoms in adolescence. Despite the absence of a direct relationship between ER and depressive symptoms and no significant rs-FC mediation, the rs-FC profiles predicted by ER are consistent with the hypothesis that emotion dysregulation is associated with abnormalities in top-down control functions. The extent to which these relationships might confer greater risk for later depression, however, remains unclear.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.3758/s13415-018-0564-x

  7 / 160823 MEDLINE  
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[PMID]: 29524021
[Au] Autor:Mocking RJT; Assies J; Ruhé HG; Schene AH
[Ad] Address:Department of Psychiatry, Academic Medical Center, University of Amsterdam, Meibergdreef 5, Amsterdam, 1105 AZ, The Netherlands. R.J.Mocking@amc.uva.nl.
[Ti] Title:Focus on fatty acids in the neurometabolic pathophysiology of psychiatric disorders.
[So] Source:J Inherit Metab Dis;, 2018 Mar 09.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Continuous research into the pathophysiology of psychiatric disorders, such as major depressive disorder (MDD), posttraumatic stress disorder (PTSD), and schizophrenia, suggests an important role for metabolism. This narrative review will provide an up-to-date summary of how metabolism is thought to be involved in the pathophysiology of these psychiatric disorders. We will focus on (I) the important role of fatty acids in these metabolic alterations, (II) whether fatty acid alterations represent epiphenomena or risk factors, and (III) similarities and dissociations in fatty acid alterations between different psychiatric disorders. (Historical) epidemiological evidence links fatty acid intake to psychiatric disorder prevalence, corroborated by altered fatty acid concentrations measured in psychiatric patients. These fatty acid alterations are connected with other concomitant pathophysiological mechanisms, including biological stress (hypothalamic-pituitary-adrenal (HPA)-axis and oxidative stress), inflammation, and brain network structure and function. Metabolomics and lipidomics studies are underway to more deeply investigate this complex network of associated neurometabolic alterations. Supplementation of fatty acids as disease-modifying nutraceuticals has clinical potential, particularly add-on eicosapentaenoic acid (EPA) in depressed patients with markers of increased inflammation. However, by interpreting the observed fatty acid alterations as partly (mal)adaptive phenomena, we attempt to nuance translational expectations and provide new clinical applications for these novel neurometabolic insights, e.g., to predict treatment response or depression recurrence. In conclusion, placing fatty acids in context can contribute to further understanding and optimized treatment of psychiatric disorders, in order to diminish their overwhelming burden of disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s10545-018-0158-3

  8 / 160823 MEDLINE  
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[PMID]: 29523295
[Au] Autor:Peter-Ross EM
[Ad] Address:Department of Psychiatry and Mental Health, University of Cape Town, Neurogenetic Psychiatric Outpatients Clinic, Groote Schuur Hospital, Main Road, Observatory 7935, Cape Town, South Africa; Life Vincent Pallotti Hospital, Suite 116, Alexandra Road, Pinelands 7405, Cape Town, South Africa. Electronic address: peterem@mweb.co.za.
[Ti] Title:Molecular hypotheses to explain the shared pathways and underlying pathobiological causes in catatonia and in catatonic presentations in neuropsychiatric disorders.
[So] Source:Med Hypotheses;113:54-64, 2018 Apr.
[Is] ISSN:1532-2777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The pathobiological causes, the shared cellular and molecular pathways in catatonia and in catatonic presentation in neuropsychiatric disorders are yet to be determined. The hypotheses in this paper have been deduced from the latest scientific research findings and clinical observations of patients with genetic disorders, behavioral phenotypes and other family members suffering mental disorders. The first hypothesis postulates that catatonia and the heterogeneity of catatonic signs and symptoms involve nucleolar dysfunction arising from abnormalities of the brain-specific, non-coding micro-RNA, SNORD115 genes (either duplications or deletions) which result in pathobiological dysfunction of various combinations in the downstream pathways (possibly along with other genes in these shared pathways). SNORD115 controls five genes CRHR1, PBRM1, TAF1, DPM2, and RALGPS1 as well as the alternative splicing of serotonin 2C receptor. SNORD115 abnormalities with varying downstream multigene involvement would account for catatonia across the life span within some subtypes of autism spectrum disorders, schizophrenia, bipolar and major depressive disorder, psychosis, genetic disorders, and in immune disorders such as anti-N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis as well as the susceptibility to the neuroleptic malignant syndrome (NMS) if environmentally triggered. Furthermore, SNORD115 genes may underlie a genetic vulnerability when environmental triggers result in excess serotonin producing the serotonin syndrome, a condition similar to NMS in which catatonia may occur. Dysfunction of SNORD115-PBRM1 connecting with SMARCA2 as well as other proven schizophrenia-associated genes might explain why traditionally catatonia has been classified with schizophrenia. SNORD115-TAF1 and SNORD-DPM2 dysfunction introduce possible clues to the parkinsonism and increased creatinine phosphokinase in NMS, while abnormalities of SNORD115-RALGPS1 suggest links to both anti-NMDAR encephalitis and the proven predisposing catatonic SHANK3 gene. The second hypothesis postulates that periodic catatonia (PC) on 15q15 involves abnormalities of vacuolar protein sorting 39 (VPS39), a proven de novo schizophrenic gene in this chromosomal locus and part of the HOPS complex. These will impact the autophagic and endocytic pathways, thereby lowering lysosomal degradation. VPS39 mutations may be considered also to disrupt lysosome-mitochondria tethering and transport of lipids and calcium through membrane contact sites (MCSs). To account for the periodicity in PC it is speculated that the mammalian equivalent of the vacuole and mitochondria patch (vCLAMP) would be altered by VPS39 mutations and subsequently followed by the mammalian equivalent of endoplasmic reticulum mitochondria encounter structure (ERMES) restoring mitochondrial homeostasis. Future precision psychiatry will require accurate pathophysiologically-defined psychiatric diagnoses to accelerate the discovery of specific molecular-targeted medications to improve therapeutic outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  9 / 160823 MEDLINE  
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[PMID]: 29523117
[Au] Autor:Taylor SS; Hughes JM; Coffman CJ; Jeffreys AS; Ulmer CS; Oddone EZ; Bosworth HB; Yancy WS; Allen KD
[Ad] Address:University of South Carolina School of Medicine Greenville, 607 Grove Rd, Greenville, SC, 29605, USA. shannonlstark@gmail.com.
[Ti] Title:Prevalence of and characteristics associated with insomnia and obstructive sleep apnea among veterans with knee and hip osteoarthritis.
[So] Source:BMC Musculoskelet Disord;19(1):79, 2018 Mar 09.
[Is] ISSN:1471-2474
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Few studies have examined patterns of specific sleep problems among individuals with osteoarthritis (OA). The primary objective of this study was to examine prevalence of symptoms of insomnia and obstructive sleep apnea (OSA) among Veterans with OA. Secondary objectives were to assess proportions of individuals with insomnia and OSA symptoms who may have been undiagnosed and to examine Veterans' characteristics associated with insomnia and OSA symptoms. METHODS: Veterans (n = 300) enrolled in a clinical trial completed the Insomnia Severity Index (ISI) and the Berlin Questionnaire (BQ) at baseline; proportions of participants with symptoms consistent with insomnia and OSA were calculated, using standard cut-offs for ISI and BQ. For Veterans with insomnia and OSA symptoms, electronic medical records were searched to identify whether there was a diagnosis code for these conditions. Multivariable linear (ISI) and logistic (BQ) regression models examined associations of the following characteristics with symptoms of insomnia and OSA: age, gender, race, self-reported general health, body mass index (BMI), diagnosis of post-traumatic stress disorder (PTSD), pain severity, depressive symptoms, number of joints with arthritis symptoms and opioid use. RESULTS: Symptoms consistent with insomnia and OSA were found in 53 and 66% of this sample, respectively. Among participants screening positive for insomnia and OSA, diagnosis codes for these disorders were present in the electronic medical record for 22 and 51%, respectively. Characteristics associated with insomnia were lower age (ß (SE) = - 0.09 (0.04), 95% confidence interval [CI] = - 0.16, - 0.02), having a PTSD diagnosis (ß (SE) = 1.68 (0.73), CI = 0.25, 3.11), greater pain severity (ß (SE) = 0.36 (0.09), CI = 0.17, 0.55), and greater depressive symptoms (ß (SE) = 0.84 (0.07), CI = 0.70, 0.98). Characteristics associated with OSA were higher BMI (odds ratio [OR] = 1.13, CI = 1.06, 1.21), greater depressive symptoms (OR = 1.12, CI = 1.05, 1.20), and opioid use (OR = 0.51, CI = 0.26, 0.99). CONCLUSIONS: Insomnia and OSA symptoms were very common in Veterans with OA, and a substantial proportion of individuals with symptoms may have been undiagnosed. Characteristics associated with insomnia and OSA symptoms were consistent with prior studies. TRIAL REGISTRATION: NCT01130740 .
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review
[do] DOI:10.1186/s12891-018-1993-y

  10 / 160823 MEDLINE  
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[PMID]: 29522960
[Au] Autor:Leichsenring F; Steinert C
[Ad] Address:Clinic of Psychosomatics and Psychotherapy, Justus-Liebig-University Giessen, Germany. Electronic address: Falk.Leichsenring@psycho.med.uni-giessen.de.
[Ti] Title:Towards an evidence-based unified psychodynamic protocol for emotional disorders.
[So] Source:J Affect Disord;232:400-416, 2017 Nov 11.
[Is] ISSN:1573-2517
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: In psychotherapy research unified, transdiagnostic and modular treatments have emerged. This is true for both cognitive-behavioral therapy and psychodynamic therapy. Recently, two unified psychodynamic protocols were presented, one for anxiety disorders, another for depressive disorders. Integrating the treatment principles for these two highly prevalent disorder groups into one protocol for "emotional disorders" may be useful for both clinical practice and training in psychotherapy. METHODS: After updating the evidence for psychodynamic therapy in anxiety and depressive disorders in terms of randomized controlled trials (RCTs) by a systematic search, the treatment elements applied in those RCTs providing evidence for the efficacy of psychodynamic therapy in depressive or anxiety disorders were reviewed and compared. RESULTS: Twenty-seven RCTs for anxiety or depressive disorders were identified. A review revealed a high overlap between the principles used for the psychodynamic treatment of anxiety and depressive disorders, reflecting the transdiagnostic nature of psychodynamic therapy. The overlap suggested to integrate the identified treatment principles into one unified psychodynamic protocol for "emotional disorders" (UPP-EMO). As a result, seven treatment principles or modules were distilled which can be flexibly applied depending on the patient´s symptoms and needs. In addition, a separate module addresses diagnostic assessment. Across modules, a focus on resources has been included. LIMITATIONS: Despite being based on RCTs, UPP-EMO has not yet been examined in an RCT - which is planned as a next step. CONCLUSIONS: As psychodynamic therapy is transdiagnostic in origin focusing on core underlying processes of mental disorders, acceptability of UPP-EMO among psychodynamic psychotherapists is likely to be high.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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