Journal of Psychiatry & Neuroscience最新文献

{"title":"Thalamocortical functional connectivity in youth with attention-deficit/hyperactivity disorder.","authors":"Soon-Beom Hong","doi":"10.1503/jpn.220109","DOIUrl":"https://doi.org/10.1503/jpn.220109","url":null,"abstract":"<p><strong>Background: </strong>Few studies have empirically tested the relationships between anatomically defined thalamic nuclei and functionally defined cortical networks, and little is known about their implications in attention-deficit/hyperactivity disorder (ADHD). This study aimed to investigate the functional connectivity of the thalamus in youth with ADHD, using both anatomically and functionally defined thalamic seed regions.</p><p><strong>Methods: </strong>Resting-state functional MRIs obtained from the publicly available ADHD-200 database were analyzed. Thalamic seed regions were defined functionally and anatomically based on Yeo's 7 resting-state-network parcellation atlas and the AAL3 atlas, respectively. Functional connectivity maps of the thalamus were extracted, and thalamocortical functional connectivity was compared between youth with and without ADHD.</p><p><strong>Results: </strong>Using the functionally defined seeds, significant group differences in thalamocortical functional connectivity and significant negative correlations between thalamocortical connectivity and ADHD symptom severity were observed within the boundaries of corresponding large-scale networks. However, in the analysis using the anatomically defined thalamic seeds, significant group differences in connectivity and significant positive correlations were observed outside the expected boundaries of major anatomic projections. The thalamocortical connectivity originating from the lateral geniculate nuclei of the thalamus was significantly correlated with age in youth with ADHD.</p><p><strong>Limitations: </strong>The small sample size and smaller proportion of girls were limiting factors.</p><p><strong>Conclusion: </strong>Thalamocortical functional connectivity based on the intrinsic network architecture of the brain appears to be clinically relevant in ADHD. The positive association between thalamocortical functional connectivity and ADHD symptom severity may represent a compensatory process recruiting an alternative neural network.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"48 1","pages":"E50-E60"},"PeriodicalIF":4.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/56/fc/48-1-E50.PMC9943548.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10846165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Utilizing pharmacogenetics when treating first episode psychosis.","authors":"Theo Korchia,&nbsp;Ridha Joober,&nbsp;Raphaelle Richieri,&nbsp;Priyadharshini Sabesan,&nbsp;Lena Palaniyappan","doi":"10.1503/jpn.220154","DOIUrl":"https://doi.org/10.1503/jpn.220154","url":null,"abstract":"The parents of a 21-year-old man brought him to an emergency psychiatric clinic for disturbed behaviour. He displayed significant hallucinatory behaviour, prominent delusions of persecution involving “special forces” and notable disorganization of speech, and had experienced more than 8 months of sociooccupational dysfunction. Upon admission, neurologic examination was unremarkable and results of routine metabolic, endocrine, liver and renal screening were within normal limits. He met the diagnostic criteria for schizophrenia, with a first episode of untreated psychosis. He was prescribed 10 mg aripiprazole for 4 days, but quickly developed adverse effects with disabling extrapyramidal rigidity. He then was switched to 2 mg risperidone, but after 1 week, he presented hypersalivation and debilitating daytime sleepiness. Despite ongoing hallucinations and persecutory fears, he refused the options of clozapine, olanzapine and quetiapine owing to concerns about weight gain, but he accepted haloperidol. He was put on 5 mg haloperidol, but he soon reported tremors, stiffness and a notable anhedonia. At this stage, we sought a cytochrome P450 (CYP450) genotype assay for 2C19 and 2D6. The patient was found to be a normal (extensive) metaboliser for 2C19 but a poor metaboliser (PM) for CYP2D6. Haloperidol, aripiprazole and risperidone are likely to be degraded too slowly in patients who are CYP2D6 PM, leading to treatment failure, and risperidone is likely to be too slowly converted to its active metabolite, leading to a greater risk of adverse effects. The patient consented to be switched to paliperidone, and a rapid antipsychotic response followed over the next 10 days. The patient was discharged on 6 mg/d paliperidone and had a score of 2 on the Clinical Global Impressions Scale of Severity at 6 months. Most antipsychotics are hepatically metabolized by several CYP450 enzymes, but some, like paliperidone or amisulpride, are less metabolized than others.1 In clinical practice, pharmacogenomic testing of CYP2D6 and CYP2C19 is seldom done, likely because many prescribers do not consider genetic factors to be critical for treatment choice, dose titration or adverse effect reduction.2 The prevalence of PMs and ultra-rapid metabolizers (UM) is estimated to be less than 5% in Euro peans (with notable variations across other ethnicities4,5); preventive testing is deemed to have low yield in practice. Thus, the maximum daily doses recommended for antipsychotics are based on a genotype-weighted population equilibrium that ignores the clinical relevance of CYP2C19/CYP2D6 metab olizer categories. Nevertheless, several product labels offer dosing recommendations based on metabolizer status,2 and many commercial tests are now available to assist prescribers.5 Of relevance to the present case is a recent large retrospective observational study confirming the higher frequency of treatment failures in PMs.6 CYP2D6 PMs are 2–3 times more frequent than UMs among Euro pea","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"48 1","pages":"E11-E12"},"PeriodicalIF":4.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1d/8b/48-1-E11.PMC9829032.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9636175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is history of abuse predictive of eating disorders with binge-eating episodes through an effect mediated by impulsivity? A French longitudinal study.","authors":"Clémence Cabelguen,&nbsp;Anaïs Saillard,&nbsp;Antoine Vanier,&nbsp;Manuel Laslandes,&nbsp;Juliette Leboucher,&nbsp;Morgane Rousselet,&nbsp;Elsa Thiabaud,&nbsp;Marie Grall-Bronnec,&nbsp;Gaëlle Challet-Bouju","doi":"10.1503/jpn.210218","DOIUrl":"https://doi.org/10.1503/jpn.210218","url":null,"abstract":"<p><strong>Background: </strong>In recent years, many studies have explored the associations among impulsivity, history of abuse, the emergence of eating disorders with episodes of binge eating (EDBE) and their severity. Nevertheless, factors associated with successful clinical outcomes of EDBE are still unknown. Our study aimed to test the hypothesis that a history of abuse is associated with unsuccessful clinical outcomes of EDBE through an effect mediated by impulsivity.</p><p><strong>Methods: </strong>We assessed patients older than 15 years, 3 months with EDBE at inclusion and at 1 year. Recovery was defined as the absence of eating disorders at 1 year. A mediation analysis was performed by means of structural equation modelling.</p><p><strong>Results: </strong>We included 186 patients in our analyses (54% bulimia nervosa, 29% anorexia nervosa binge eating/purging type and 17% binge-eating disorder); 179 (96%) were female. One-third (<i>n</i> = 63) of patients reported a history of abuse, and recovery was observed for 20% of the sample (<i>n</i> = 38). Contrary to our assumption, a history of abuse was not associated with the absence of recovery of EDBE at 1 year. Factors unfavourable for achieving recovery were anxiety disorders (odds ratio [OR] 0.41), vomiting (OR 0.39), physical hyperactivity (OR 0.29), negative urgency and a lack of perseverance (OR 0.85 for both). Only positive urgency was positively associated with recovery (OR 1.25).</p><p><strong>Limitations: </strong>We excluded 219 patients lost to the 1-year follow-up.</p><p><strong>Conclusion: </strong>Our findings may help to deconstruct the empirical belief that traumatic events may interfere with the successful course of treatment for eating disorders. A high level of positive urgency may be associated with more receptivity to care.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"48 1","pages":"E13-E22"},"PeriodicalIF":4.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/64/e9/48-1-E13.PMC9833835.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10673659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippocampal subfield alterations in schizophrenia and major depressive disorder: a systematic review and network meta-analysis of anatomic MRI studies.","authors":"Yuan Sun,&nbsp;Na Hu,&nbsp;Mingqi Wang,&nbsp;Lu Lu,&nbsp;Chunyan Luo,&nbsp;Biqiu Tang,&nbsp;Chenyang Yao,&nbsp;John A Sweeney,&nbsp;Qiyong Gong,&nbsp;Changjian Qiu,&nbsp;Su Lui","doi":"10.1503/jpn.220086","DOIUrl":"https://doi.org/10.1503/jpn.220086","url":null,"abstract":"<p><strong>Background: </strong>Hippocampal disturbances are important in the pathophysiology of both schizophrenia and major depressive disorder (MDD). Imaging studies have shown selective volume deficits across hippocampal subfields in both disorders. We aimed to investigate whether these volumetric alterations in hippocampal subfields are shared or divergent across disorders.</p><p><strong>Methods: </strong>We searched PubMed and Embase from database inception to May 8, 2021. We identified MRI studies in patients with schizophrenia, MDD or both, in which hippocampal subfield volumes were measured. We excluded nonoriginal, animal or postmortem studies, and studies that used other imaging modalities or overlapping data. We conducted a network meta-analysis to estimate and contrast alterations in subfield volumes in the 2 disorders.</p><p><strong>Results: </strong>We identified 45 studies that met the initial criteria for systematic review, of which 15 were eligible for network metaanalysis. Compared to healthy controls, patients with schizophrenia had reduced volumes in the bilateral cornu ammonis (CA) 1, granule cell layer of the dentate gyrus, subiculum, parasubiculum, molecular layer, hippocampal tail and hippocampus-amygdala transition area (HATA); in the left CA4 and presubiculum; and in the right fimbria. Patients with MDD had decreased volumes in the left CA3 and CA4 and increased volumes in the right HATA compared to healthy controls. The bilateral parasubiculum and right HATA were smaller in patients with schizophrenia than in patients with MDD.</p><p><strong>Limitations: </strong>We did not investigate medication effects because of limited information. Study heterogeneity was noteworthy in direct comparisons between patients with MDD and healthy controls.</p><p><strong>Conclusion: </strong>The volumes of multiple hippocampal subfields are selectively altered in patients with schizophrenia and MDD, with overlap and differentiation in subfield alterations across disorders. Rigorous head-to-head studies are needed to validate our findings.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"48 1","pages":"E34-E49"},"PeriodicalIF":4.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/00/ee/48-1-E34.PMC9911126.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10678329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overlap between genetic variants associated with schizophrenia spectrum disorders and intelligence quotient: a systematic review.","authors":"Nancy Murillo-García,&nbsp;Sara Barrio-Martínez,&nbsp;Esther Setién-Suero,&nbsp;Jordi Soler,&nbsp;Sergi Papiol,&nbsp;Mar Fatjó-Vilas,&nbsp;Rosa Ayesa-Arriola","doi":"10.1503/jpn.220026","DOIUrl":"https://doi.org/10.1503/jpn.220026","url":null,"abstract":"<p><strong>Background: </strong>To study whether there is genetic overlap underlying the risk for schizophrenia spectrum disorders (SSDs) and low intelligence quotient (IQ), we reviewed and summarized the evidence on genetic variants associated with both traits.</p><p><strong>Methods: </strong>We performed this review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and preregistered it in PROSPERO. We searched the Medline databases via PubMed, PsycInfo, Web of Science and Scopus. We included studies in adults with a diagnosis of SSD that explored genetic variants (single nucleotide polymorphisms [SNPs], copy number variants [CNVs], genomic insertions or genomic deletions), estimated IQ and studied the relationship between genetic variability and both traits (SSD and IQ). We synthesized the results and assessed risk of bias using the Quality of Genetic Association Studies (Q-Genie) tool.</p><p><strong>Results: </strong>Fifty-five studies met the inclusion criteria (45 case-control, 9 cross-sectional, 1 cohort), of which 55% reported significant associations for genetic variants involved in IQ and SSD. The SNPs more frequently explored through candidate gene studies were in <i>COMT</i>, <i>DTNBP1</i>, <i>BDNF</i> and <i>TCF4</i>. Through genome-wide association studies, 2 SNPs in <i>CHD7</i> and <i>GATAD2A</i> were associated with IQ in patients with SSD. The studies on CNVs suggested significant associations between structural variants and low IQ in patients with SSD.</p><p><strong>Limitations: </strong>Overall, primary studies used heterogeneous IQ measurement tools and had small samples. Grey literature was not screened.</p><p><strong>Conclusion: </strong>Genetic overlap between SSD and IQ supports the neurodevelopmental hypothesis of schizophrenia. Most of the risk polymorphisms identified were in genes relevant to brain development, neural proliferation and differentiation, and synaptic plasticity.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"47 6","pages":"E393-E408"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/88/9d/47-6-E393.PMC9710545.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10351250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An fMRI study of cognitive planning before and after symptom provocation in pediatric obsessive-compulsive disorder.","authors":"Fern Jaspers-Fayer,&nbsp;Sarah Yao Lin,&nbsp;John R Best,&nbsp;Anders Lillevik Thorsen,&nbsp;Juliana Negreiros,&nbsp;Elaine Chan,&nbsp;Rhonda Ellwyn,&nbsp;Boyee Lin,&nbsp;Stella de Wit,&nbsp;Odile A van den Heuvel,&nbsp;S Evelyn Stewart","doi":"10.1503/jpn.220064","DOIUrl":"https://doi.org/10.1503/jpn.220064","url":null,"abstract":"<p><strong>Background: </strong>Pediatric obsessive-compulsive disorder (OCD) has been associated with poorer planning in laboratory, school and home settings. It is unclear whether this impairment is a standalone cognitive issue or the result of OCD symptoms. No study has examined the influence of provoked distress on planning performance and neural correlates in pediatric OCD.</p><p><strong>Methods: </strong>Before and after a symptom provocation task, youth with OCD (<i>n</i> = 23; 9 boys; mean age ± standard deviation 15.1 ± 2.6 years) and matched healthy controls (<i>n</i> = 23) completed the Tower of London task during functional MRI scanning.</p><p><strong>Results: </strong>During planning, participants with OCD recruited the left superior frontal gyrus to a greater extent than healthy controls after symptom provocation (group × time point interaction; <i>t</i> ₄₄ = 5.22, <i>p <</i> 0.001). In a seeded, region of interest-constrained, functional connectivity analysis, we identified greater connectivity between the left superior frontal gyrus and the right middle frontal gyrus, left precuneus and left inferior parietal lobule in participants with OCD than healthy controls. We also identified greater connectivity between the right amygdala and right medial frontal gyrus in patients with OCD than healthy controls, but only before symptom provocation.</p><p><strong>Limitations: </strong>The fixed-order design of the study and the number of participants taking medication (<i>n</i> = 20) should be noted.</p><p><strong>Conclusion: </strong>Participants with OCD demonstrated greater amygdalar-cortical connectivity before symptom provocation, while sustaining greater recruitment and connectivity of task-related planning areas throughout the task. These results suggest that brain activity and connectivity is altered after symptom provocation, in the absence of impaired planning performance.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"47 6","pages":"E409-E420"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bc/80/47-6-E409.PMC9710544.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10351251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>RGS3</i> and <i>IL1RAPL1</i> missense variants implicate defective neurotransmission in early-onset inherited schizophrenias.","authors":"Ambreen Kanwal,&nbsp;José V Pardo,&nbsp;Sadaf Naz","doi":"10.1503/jpn.220070","DOIUrl":"https://doi.org/10.1503/jpn.220070","url":null,"abstract":"<p><strong>Background: </strong>Schizophrenia is characterized by hallucinations, delusions and disorganized behaviour. Recessive or X-linked transmissions are rarely described for common psychiatric disorders. We examined the genetics of psychosis to identify rare large-effect variants in patients with extreme schizophrenia.</p><p><strong>Methods: </strong>We recruited 2 consanguineous families, each with patients affected by early-onset, severe, treatment-resistant schizophrenia. We performed exome sequencing for all participants. We checked variant rarity in public databases and with ethnically matched controls. We performed in silico analyses to assess the effects of the variants on proteins.</p><p><strong>Results: </strong>Structured clinical evaluations supported diagnoses of schizophrenia in all patients and phenotypic absence in the unaffected individuals. Data analyses identified multiple variants. Only 1 variant per family was predicted as pathogenic by prediction tools. A homozygous c.649C > T:p.(Arg217Cys) variant in <i>RGS3</i> and a hemizygous c.700A > G:p.(Thr234Ala) variant in <i>IL1RAPL1</i> affected evolutionary conserved amino acid residues and were the most likely causes of phenotype in the patients of each family. Variants were ultra-rare in publicly available databases and absent from the DNA of 400 ethnically matched controls. <i>RGS3</i> is implicated in modulating sensory behaviour in <i>Caenorhabditis elegans</i>. Variants of <i>IL1RAPL1</i> are known to cause nonsyndromic X-linked intellectual disability with or without human behavioural dysfunction.</p><p><strong>Limitations: </strong>Each variant is unique to a particular family's patients, and findings may not be replicated.</p><p><strong>Conclusion: </strong>Our work suggests that some rare variants may be involved in causing inherited psychosis or schizophrenia. Variant-specific functional studies will elucidate the pathophysiology relevant to schizophrenias and motivate translation to personalized therapeutics.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"47 6","pages":"E379-E390"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5e/3a/47-6-E379.PMC9633053.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9408457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered coordination between frontal delta and parietal alpha networks underlies anhedonia and depressive rumination in major depressive disorder.","authors":"Zenas C Chao,&nbsp;Daniel G Dillon,&nbsp;Yi-Hung Liu,&nbsp;Elyssa M Barrick,&nbsp;Chien-Te Wu","doi":"10.1503/jpn.220046","DOIUrl":"https://doi.org/10.1503/jpn.220046","url":null,"abstract":"<p><strong>Background: </strong>A hyperactive default mode network (DMN) has been observed in people with major depressive disorder (MDD), and weak DMN suppression has been linked to depressive symptoms. However, whether dysregulation of the DMN contributes to blunted positive emotional experience in people with MDD is unclear.</p><p><strong>Methods: </strong>We recorded 128-channel electroencephalograms (EEGs) from 24 participants with MDD and 31 healthy controls in a resting state (RS) and an emotion-induction state (ES), in which participants engaged with emotionally positive pictures. We combined Granger causality analysis and data-driven decomposition to extract latent brain networks shared among states and groups, and we further evaluated their interactions across individuals.</p><p><strong>Results: </strong>We extracted 2 subnetworks. Subnetwork 1 represented a delta (δ)-band (1~4 Hz) frontal network that was activated more in the ES than the RS (i.e., task-positive). Subnetwork 2 represented an alpha (α)-band (8~13 Hz) parietal network that was suppressed more in the ES than the RS (i.e., task-negative). These subnetworks were anticorrelated in both the healthy control and MDD groups, but with different sensitivities: for participants with MDD to achieve the same level of task-positive (subnetwork 1) activation as healthy controls, more suppression of task-negative (subnetwork 2) activation was necessary. Furthermore, the anticorrelation strength in participants with MDD correlated with the severity of 2 core MDD symptoms: anhedonia and rumination.</p><p><strong>Limitations: </strong>The sample size was small.</p><p><strong>Conclusion: </strong>Our findings revealed altered coordination between 2 functional networks in MDD and suggest that weak suppression of the task-negative α-band parietal network contributes to blunted positive emotional responses in adults with depression. The subnetworks identified here could be used for diagnosis or targeted for treatment in the future.</p>","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"47 6","pages":"E367-E378"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5e/3c/47-6-E367.PMC9633055.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9921153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical management of psychosis in 22q11.2 deletion syndrome.","authors":"Anton Iftimovici,&nbsp;Marie-Odile Krebs,&nbsp;Boris Chaumette","doi":"10.1503/jpn.220091","DOIUrl":"https://doi.org/10.1503/jpn.220091","url":null,"abstract":"","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"47 6","pages":"E391-E392"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f8/cf/47-6-E391.PMC9648635.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10343361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to: \"Updated and rectified meta-analysis shows no effect of propranolol versus placebo on traumatic memory reconsolidation disruption\".","authors":"Alain Brunet,&nbsp;Michelle Lonergan,&nbsp;Sereena Pigeon,&nbsp;Daniel Saumier,&nbsp;Scott Orr,&nbsp;Roger Pitman","doi":"10.1503/jpn.220093","DOIUrl":"https://doi.org/10.1503/jpn.220093","url":null,"abstract":"In their letter to the editor, Steenen and colleagues1 argue that the conclusions of our meta-analysis2 on the clinical efficacy of reconsolidation impairment using propranolol are “incorrect in the context of (...) psychotrauma-related symptomatology.” They claim that we did not assess risk of bias and critique our omission of 3 unpublished studies (Aikins,3 Saladin,4 and Orr5). We are not convinced by their attempt to rectify our analysis. Although this is a matter of debate,6 we were asked during the JPN peer review of our manuscript to omit unpublished data from our meta-analysis because the methodological quality of such studies is difficult to verify. Indeed, we could not verify important methodological information with respect to the unpublished results (n = 6) of Aikins,3 such as the adequacy of blinding methods. Moreover, we verified methodological information in the study by Orr5 with the author himself and concluded that the data from this pre-emptively terminated (rather than unpublished) study with n = 5 randomized participants were not suitable for meta-analytic purposes. The inclusion of studies with very small samples in a meta-analysis (n ≤ 3 per group) is bound to compromise the precision of the overall effect estimate.6 We also could not verify important information such as the outcomes used to compute the effect size for Saladin’s unpublished study of reconsolidation interference in participants with posttraumatic stress disorder (PTSD) and comorbid alcohol dependence.4 Considering that Steenen and colleagues1 argue against including studies of addiction (but see Gisquet-Verrier and colleagues7), it is unclear why they included Saladin’s study in their analysis. But even more problematic, we found","PeriodicalId":50073,"journal":{"name":"Journal of Psychiatry & Neuroscience","volume":"47 5","pages":"E338-E339"},"PeriodicalIF":4.3,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b1/2e/47-5-E338.PMC9507037.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9421755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}