Pub Date : 2016-04-01DOI: 10.3109/15622975.2015.1112033
Judith Buse, C. Beste, Elisabeth Herrmann, V. Roessner
Abstract Objectives: It has been hypothesised that altered sensorimotor gating might be a core problem in Tourette Syndrome (TS). However, the underlying neurophysiological mechanisms are elusive. Methods: We applied functional magnetic resonance imaging (fMRI) to investigate the neural correlates of altered sensorimotor gating by means of prepulse inhibition (PPI) in 22 boys with TS and 22 healthy boys using tactile PPI. The electromyography of the startle response was recorded simultaneously to the acquisition of the fMRI images. Results: As expected, PPI of the startle response was reduced in boys with TS compared to the healthy boys. We found decreased PPI-related blood oxygen level-dependent (BOLD) activity in boys with TS in the middle frontal gyrus, postcentral gyrus, superior parietal cortex, cingulate gyrus and caudate body. In boys with TS PPI of the startle response was positively correlated to PPI-related BOLD activity in the superior parietal cortex. Conclusions: Our findings indicate that deficient sensorimotor gating in boys with TS is associated with reduced recruitment of brain regions responsible for the higher-order integration of somatosensory stimuli. Due to our strict sample selection we were able to reduce confounding by neural adaptation processes, long-term medication, gender or comorbidities.
{"title":"Neural correlates of altered sensorimotor gating in boys with Tourette Syndrome: A combined EMG/fMRI study","authors":"Judith Buse, C. Beste, Elisabeth Herrmann, V. Roessner","doi":"10.3109/15622975.2015.1112033","DOIUrl":"https://doi.org/10.3109/15622975.2015.1112033","url":null,"abstract":"Abstract Objectives: It has been hypothesised that altered sensorimotor gating might be a core problem in Tourette Syndrome (TS). However, the underlying neurophysiological mechanisms are elusive. Methods: We applied functional magnetic resonance imaging (fMRI) to investigate the neural correlates of altered sensorimotor gating by means of prepulse inhibition (PPI) in 22 boys with TS and 22 healthy boys using tactile PPI. The electromyography of the startle response was recorded simultaneously to the acquisition of the fMRI images. Results: As expected, PPI of the startle response was reduced in boys with TS compared to the healthy boys. We found decreased PPI-related blood oxygen level-dependent (BOLD) activity in boys with TS in the middle frontal gyrus, postcentral gyrus, superior parietal cortex, cingulate gyrus and caudate body. In boys with TS PPI of the startle response was positively correlated to PPI-related BOLD activity in the superior parietal cortex. Conclusions: Our findings indicate that deficient sensorimotor gating in boys with TS is associated with reduced recruitment of brain regions responsible for the higher-order integration of somatosensory stimuli. Due to our strict sample selection we were able to reduce confounding by neural adaptation processes, long-term medication, gender or comorbidities.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"1 1","pages":"187 - 197"},"PeriodicalIF":0.0,"publicationDate":"2016-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75623703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.3109/15622975.2016.1142608
G. Rivero, I. Martín-Guerrero, Elena de Prado, A. Gabilondo, L. Callado, J. García-Sevilla, A. García-Orad, J. Meana
Abstract Objectives α2C-adrenoceptors (α2C-AR) are involved in behavioural responses relevant to psychiatric disorders and suicide completion. The genetic polymorphism α2CDel322-325-AR confers a loss-of-function phenotype. Functional human studies have associated α2CDel322-325-AR polymorphism with major depression pathophysiology. The aim of this study was to analyse, for the first time, the association of α2CDel322-325-AR polymorphism with suicide completion and with related psychiatric disorders: major depression, schizophrenia, opiate and alcohol abuse and dependence. Methods Post-mortem brain DNA was extracted (n = 516) and genotyping performed by HaeIII restriction endonuclease digestion of PCR products and DNA fragment analysis on capillary sequencer. Amplified products were sequenced to confirm the presence of the polymorphism. Results The frequency of α2CDel322-325-AR in suicide (9%, n = 236) and non-suicide victims (11%, n = 280) was similar. Genotype frequencies for the α2CDel322-325-AR polymorphism in depressed (15%, n = 39) and schizophrenic subjects (18%, n = 39) were higher than in controls (7%, n = 187), but these differences did not reach statistical significance (P = 0.125 and P = 0.063, respectively). A selective and significant association of α2CDel322-325-AR polymorphism with opiate abuse and dependence was found (23%, n = 35, P = 0.011). Conclusions Our results indicate that α2CDel322-325-AR may play a role in the pathophysiology of opiate abuse and dependence and raise the interest for larger genetic associative studies.
{"title":"Alpha2C-adrenoceptor Del322-325 polymorphism and risk of psychiatric disorders: significant association with opiate abuse and dependence","authors":"G. Rivero, I. Martín-Guerrero, Elena de Prado, A. Gabilondo, L. Callado, J. García-Sevilla, A. García-Orad, J. Meana","doi":"10.3109/15622975.2016.1142608","DOIUrl":"https://doi.org/10.3109/15622975.2016.1142608","url":null,"abstract":"Abstract Objectives α2C-adrenoceptors (α2C-AR) are involved in behavioural responses relevant to psychiatric disorders and suicide completion. The genetic polymorphism α2CDel322-325-AR confers a loss-of-function phenotype. Functional human studies have associated α2CDel322-325-AR polymorphism with major depression pathophysiology. The aim of this study was to analyse, for the first time, the association of α2CDel322-325-AR polymorphism with suicide completion and with related psychiatric disorders: major depression, schizophrenia, opiate and alcohol abuse and dependence. Methods Post-mortem brain DNA was extracted (n = 516) and genotyping performed by HaeIII restriction endonuclease digestion of PCR products and DNA fragment analysis on capillary sequencer. Amplified products were sequenced to confirm the presence of the polymorphism. Results The frequency of α2CDel322-325-AR in suicide (9%, n = 236) and non-suicide victims (11%, n = 280) was similar. Genotype frequencies for the α2CDel322-325-AR polymorphism in depressed (15%, n = 39) and schizophrenic subjects (18%, n = 39) were higher than in controls (7%, n = 187), but these differences did not reach statistical significance (P = 0.125 and P = 0.063, respectively). A selective and significant association of α2CDel322-325-AR polymorphism with opiate abuse and dependence was found (23%, n = 35, P = 0.011). Conclusions Our results indicate that α2CDel322-325-AR may play a role in the pathophysiology of opiate abuse and dependence and raise the interest for larger genetic associative studies.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"288 1","pages":"308 - 315"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74951348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-16DOI: 10.3109/15622975.2016.1139747
M. D. Cooper, J. Rosenblat, D. Cha, Yena Lee, Ron Kakar, R. McIntyre
Abstract Objectives Replicated evidence has demonstrated that ketamine exerts rapid-acting and potent antidepressant effects. Notwithstanding, its promise to mitigate depressive symptoms and suicidality in antidepressant-resistant populations, several limitations and safety concerns accompany ketamine including, but not limited to, the potential for abuse and psychotomimetic/dissociative experiences. The focus of the current narrative review is to synthesise available evidence of strategies that may mitigate and fully prevent treatment-emergent psychotomimetic and dissociative effects associated with ketamine administration. Methods PubMed, Google Scholar and ClinicalTrials.gov were searched for relevant articles. Results Potential avenues investigated to minimise psychotomimetic effects associated with ketamine administration include the following: (1) altering dosing and infusion rates; (2) route of administration; (3) enantiomer choice; (4) co-administration with mood stabilisers of antipsychotics; and (5) use of alternative N-methyl-d-aspartate (NMDA)-modulating agents. Emerging evidence indicates that dissociative experiences can be significantly mitigated by using an intranasal route of administration, lower dosages, or use of alternative NMDA-modulating agents, namely lanicemine (AZD6765) and GLYX-13. Conclusions Currently, intranasal administration presents as the most promising strategy to mitigate dissociative and psychotomimetic effects; however, studies of strategies to mitigate the adverse events of ketamine are limited in number and quality and thus further investigation is still needed.
{"title":"Strategies to mitigate dissociative and psychotomimetic effects of ketamine in the treatment of major depressive episodes: a narrative review","authors":"M. D. Cooper, J. Rosenblat, D. Cha, Yena Lee, Ron Kakar, R. McIntyre","doi":"10.3109/15622975.2016.1139747","DOIUrl":"https://doi.org/10.3109/15622975.2016.1139747","url":null,"abstract":"Abstract Objectives Replicated evidence has demonstrated that ketamine exerts rapid-acting and potent antidepressant effects. Notwithstanding, its promise to mitigate depressive symptoms and suicidality in antidepressant-resistant populations, several limitations and safety concerns accompany ketamine including, but not limited to, the potential for abuse and psychotomimetic/dissociative experiences. The focus of the current narrative review is to synthesise available evidence of strategies that may mitigate and fully prevent treatment-emergent psychotomimetic and dissociative effects associated with ketamine administration. Methods PubMed, Google Scholar and ClinicalTrials.gov were searched for relevant articles. Results Potential avenues investigated to minimise psychotomimetic effects associated with ketamine administration include the following: (1) altering dosing and infusion rates; (2) route of administration; (3) enantiomer choice; (4) co-administration with mood stabilisers of antipsychotics; and (5) use of alternative N-methyl-d-aspartate (NMDA)-modulating agents. Emerging evidence indicates that dissociative experiences can be significantly mitigated by using an intranasal route of administration, lower dosages, or use of alternative NMDA-modulating agents, namely lanicemine (AZD6765) and GLYX-13. Conclusions Currently, intranasal administration presents as the most promising strategy to mitigate dissociative and psychotomimetic effects; however, studies of strategies to mitigate the adverse events of ketamine are limited in number and quality and thus further investigation is still needed.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"33 1","pages":"410 - 423"},"PeriodicalIF":0.0,"publicationDate":"2016-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74698105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.3109/15622975.2015.1083616
M. Dold, M. Tardy, M. Samara, Chunbo Li, S. Kasper, S. Leucht
Abstract Objectives: Narrative, unsystematic reviews revealed no differences in efficacy between the various first-generation antipsychotics (FGAs) resulting in the psychopharmacological assumption of comparable efficacy between the different FGAs. We sought to determine if the assumption of comparable efficacy of all FGAs can be regarded as evidence-based using meta-analytic statistics. Methods: A systematic literature survey (Cochrane Schizophrenia Group trial register) was applied to identify all RCTs that compared oral haloperidol with another oral FGA in schizophrenia. Primary outcome was dichotomous treatment response. Secondary outcomes were symptom severity measured by rating scales, discontinuation rates, and specific adverse effects. Results: Altogether, 79 RCTs with 4343 participants published between 1962 and 1999 were included. We found a significant between-group difference only between haloperidol and nemonapride, but not for the remaining 19 investigated FGAs. There were no significant differences for discontinuation rates. Conclusions: As most of the single meta-analytic comparisons can be regarded as underpowered, the evidence for the assumption of comparable efficacy of all FGAs is inconclusive. We therefore cannot confirm or reject the statements of previous narrative, unsystematic reviews in this regard. Our findings were limited by the small sample size in the individual comparisons and the low methodological quality in many included studies.
{"title":"Are all first-generation antipsychotics equally effective in treating schizophrenia? A meta-analysis of randomised, haloperidol-controlled trials","authors":"M. Dold, M. Tardy, M. Samara, Chunbo Li, S. Kasper, S. Leucht","doi":"10.3109/15622975.2015.1083616","DOIUrl":"https://doi.org/10.3109/15622975.2015.1083616","url":null,"abstract":"Abstract Objectives: Narrative, unsystematic reviews revealed no differences in efficacy between the various first-generation antipsychotics (FGAs) resulting in the psychopharmacological assumption of comparable efficacy between the different FGAs. We sought to determine if the assumption of comparable efficacy of all FGAs can be regarded as evidence-based using meta-analytic statistics. Methods: A systematic literature survey (Cochrane Schizophrenia Group trial register) was applied to identify all RCTs that compared oral haloperidol with another oral FGA in schizophrenia. Primary outcome was dichotomous treatment response. Secondary outcomes were symptom severity measured by rating scales, discontinuation rates, and specific adverse effects. Results: Altogether, 79 RCTs with 4343 participants published between 1962 and 1999 were included. We found a significant between-group difference only between haloperidol and nemonapride, but not for the remaining 19 investigated FGAs. There were no significant differences for discontinuation rates. Conclusions: As most of the single meta-analytic comparisons can be regarded as underpowered, the evidence for the assumption of comparable efficacy of all FGAs is inconclusive. We therefore cannot confirm or reject the statements of previous narrative, unsystematic reviews in this regard. Our findings were limited by the small sample size in the individual comparisons and the low methodological quality in many included studies.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"66 1","pages":"210 - 220"},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90652390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.3109/15622975.2016.1142607
E. Lenze, N. Farber, E. Kharasch, J. Schweiger, Michael D Yingling, J. Olney, J. Newcomer
ABSTRACT Objectives We examined the feasibility of a high-dose, 96-h infusion of ketamine in treatment-resistant depression. Methods Ten participants were randomised to receive a 96-h ketamine infusion, titrated as tolerated to a target rate of 0.6 mg/kg/h, while 10 received a 40-min ketamine infusion (0.5 mg/kg). Both groups received clonidine, titrated to a maximum of 0.6 mg orally daily, during the infusion to mitigate side effects of ketamine. Participants were followed for 8 weeks to examine potential antidepressant effects. Results All 20 participants completed the infusion. Most participants tolerated the infusion well, with minimal psychotomimetic symptoms or blood pressure elevation despite achieving high ketamine concentrations (mean 424 ng/ml for 96-h arm, 156 ng/ml for 40-min arm). There was no rebound hypertension upon discontinuing clonidine. Rapid and sustained improvement in depressive symptoms was observed in both study groups. Higher ketamine concentration was associated with sustained antidepressant response, and was not with greater psychotomimetic side effects, in the 96-h arm. Conclusions This study provides evidence for the feasibility of prolonged ketamine infusions in treatment-resistant depression. Co-administration of clonidine appeared to mitigate ketamine’s psychotomimetic effects. Further study is required to investigate the extent to which prolonged ketamine infusions could provide both rapid and sustained improvements in treatment-resistant depression. Clinicaltrials.gov identifier NCT01179009
{"title":"Ninety-six hour ketamine infusion with co-administered clonidine for treatment-resistant depression: A pilot randomised controlled trial","authors":"E. Lenze, N. Farber, E. Kharasch, J. Schweiger, Michael D Yingling, J. Olney, J. Newcomer","doi":"10.3109/15622975.2016.1142607","DOIUrl":"https://doi.org/10.3109/15622975.2016.1142607","url":null,"abstract":"ABSTRACT Objectives We examined the feasibility of a high-dose, 96-h infusion of ketamine in treatment-resistant depression. Methods Ten participants were randomised to receive a 96-h ketamine infusion, titrated as tolerated to a target rate of 0.6 mg/kg/h, while 10 received a 40-min ketamine infusion (0.5 mg/kg). Both groups received clonidine, titrated to a maximum of 0.6 mg orally daily, during the infusion to mitigate side effects of ketamine. Participants were followed for 8 weeks to examine potential antidepressant effects. Results All 20 participants completed the infusion. Most participants tolerated the infusion well, with minimal psychotomimetic symptoms or blood pressure elevation despite achieving high ketamine concentrations (mean 424 ng/ml for 96-h arm, 156 ng/ml for 40-min arm). There was no rebound hypertension upon discontinuing clonidine. Rapid and sustained improvement in depressive symptoms was observed in both study groups. Higher ketamine concentration was associated with sustained antidepressant response, and was not with greater psychotomimetic side effects, in the 96-h arm. Conclusions This study provides evidence for the feasibility of prolonged ketamine infusions in treatment-resistant depression. Co-administration of clonidine appeared to mitigate ketamine’s psychotomimetic effects. Further study is required to investigate the extent to which prolonged ketamine infusions could provide both rapid and sustained improvements in treatment-resistant depression. Clinicaltrials.gov identifier NCT01179009","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"115 1","pages":"230 - 238"},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86203699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-26DOI: 10.3109/15622975.2016.1142606
E. Real, M. Subirà, P. Alonso, C. Segalàs, J. Labad, C. Orfila, C. López-Solà, I. Martínez-Zalacaín, E. Via, N. Cardoner, S. Jiménez-Murcia, C. Soriano-Mas, J. Menchón
Abstract Objectives There is growing evidence supporting a role for stressful life events (SLEs) at obsessive–compulsive disorder (OCD) onset, but neurobiological correlates of such effect are not known. We evaluated regional grey matter (GM) changes associated with the presence/absence of SLEs at OCD onset. Methods One hundred and twenty-four OCD patients and 112 healthy controls were recruited. Patients were split into two groups according to the presence (n = 56) or absence (n = 68) of SLEs at disorder’s onset. A structural magnetic resonance image was acquired for each participant and pre-processed with Statistical Parametric Mapping software (SPM8) to obtain a volume-modulated GM map. Between-group differences in sociodemographic, clinical and whole-brain regional GM volumes were assessed. Results SLEs were associated with female sex, later age at disorder’s onset, more contamination/cleaning and less hoarding symptoms. In comparison with controls, patients without SLEs showed GM volume increases in bilateral dorsal putamen and the central tegmental tract of the brainstem. By contrast, patients with SLEs showed specific GM volume increases in the right anterior cerebellum. Conclusions Our findings support the idea that neuroanatomical alterations of OCD patients partially depend on the presence of SLEs at disorder’s onset.
{"title":"Brain structural correlates of obsessive–compulsive disorder with and without preceding stressful life events","authors":"E. Real, M. Subirà, P. Alonso, C. Segalàs, J. Labad, C. Orfila, C. López-Solà, I. Martínez-Zalacaín, E. Via, N. Cardoner, S. Jiménez-Murcia, C. Soriano-Mas, J. Menchón","doi":"10.3109/15622975.2016.1142606","DOIUrl":"https://doi.org/10.3109/15622975.2016.1142606","url":null,"abstract":"Abstract Objectives There is growing evidence supporting a role for stressful life events (SLEs) at obsessive–compulsive disorder (OCD) onset, but neurobiological correlates of such effect are not known. We evaluated regional grey matter (GM) changes associated with the presence/absence of SLEs at OCD onset. Methods One hundred and twenty-four OCD patients and 112 healthy controls were recruited. Patients were split into two groups according to the presence (n = 56) or absence (n = 68) of SLEs at disorder’s onset. A structural magnetic resonance image was acquired for each participant and pre-processed with Statistical Parametric Mapping software (SPM8) to obtain a volume-modulated GM map. Between-group differences in sociodemographic, clinical and whole-brain regional GM volumes were assessed. Results SLEs were associated with female sex, later age at disorder’s onset, more contamination/cleaning and less hoarding symptoms. In comparison with controls, patients without SLEs showed GM volume increases in bilateral dorsal putamen and the central tegmental tract of the brainstem. By contrast, patients with SLEs showed specific GM volume increases in the right anterior cerebellum. Conclusions Our findings support the idea that neuroanatomical alterations of OCD patients partially depend on the presence of SLEs at disorder’s onset.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"3 1","pages":"366 - 377"},"PeriodicalIF":0.0,"publicationDate":"2016-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85337679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-19DOI: 10.3109/15622975.2015.1126675
Marco Solmi, D. Gallicchio, E. Collantoni, Christoph U. Correll, Maurizio Clementi, C. Pinato, M. Forzan, Matteo Cassina, F. Fontana, Valeria Giannunzio, I. Piva, R. Siani, P. Salvo, P. Santonastaso, E. Tenconi, N. Veronese, A. Favaro
Objectives Growing interest focuses on the association between 5-HTTLPR polymorphism and eating disorders (ED), but published findings have been conflicting. Methods The Italian BIO.VE.D.A. biobank provided 976 samples (735 ED patients and 241 controls) for genotyping. We conducted a literature search of studies published up to 1 April 2015, including studies reporting on 5HTTLPR genotype and allele frequencies in obesity and/or ED. We ran a meta-analysis, including data from BIO.VE.D.A. – comparing low and high-functioning genotype and allele frequencies in ED vs. controls. Results Data from 21 studies, plus BIO.VE.D.A., were extracted providing information from 3,736 patients and 2,707 controls. Neither low- nor high-functioning genotype frequencies in ED patients, with both bi- and tri-allelic models, differed from controls. Furthermore, neither low- nor high-functioning allele frequencies in ED or in BN, in both bi- and triallelic models, differed from control groups. After sensitivity analysis, results were the same in AN vs. controls. Results remained unaltered when investigating recessive and dominant models. Conclusions 5HTTLPR does not seem to be associated with ED in general, or with AN or BN in particular. Future studies in ED should explore the role of ethnicity and psychiatric comorbidity as a possible source of bias.
5-HTTLPR多态性与饮食失调(ED)之间的关系越来越受到关注，但已发表的研究结果却相互矛盾。方法意大利BIO.VE.D.A。生物库提供976份样本(735例ED患者和241例对照组)进行基因分型。我们对截至2015年4月1日发表的研究进行了文献检索，包括报告肥胖和/或ED中5HTTLPR基因型和等位基因频率的研究。我们进行了荟萃分析，包括来自BIO.VE.D.A的数据。-比较ED患者与对照组的低功能和高功能基因型和等位基因频率。数据来自21项研究，外加bio . ve . da。，提供了3736名患者和2707名对照者的信息。无论是双等位基因模型还是三等位基因模型，ED患者的低功能基因型频率和高功能基因型频率与对照组都没有差异。此外，在双等位基因和试验等位基因模型中，ED或BN的低功能和高功能等位基因频率与对照组没有差异。经过敏感性分析，AN组与对照组的结果相同。当研究隐性和显性模型时，结果保持不变。结论5HTTLPR似乎与ED无关，特别是与AN或BN无关。未来的ED研究应该探索种族和精神共病作为可能的偏倚来源的作用。
{"title":"Serotonin transporter gene polymorphism in eating disorders: Data from a new biobank and META-analysis of previous studies","authors":"Marco Solmi, D. Gallicchio, E. Collantoni, Christoph U. Correll, Maurizio Clementi, C. Pinato, M. Forzan, Matteo Cassina, F. Fontana, Valeria Giannunzio, I. Piva, R. Siani, P. Salvo, P. Santonastaso, E. Tenconi, N. Veronese, A. Favaro","doi":"10.3109/15622975.2015.1126675","DOIUrl":"https://doi.org/10.3109/15622975.2015.1126675","url":null,"abstract":"Objectives Growing interest focuses on the association between 5-HTTLPR polymorphism and eating disorders (ED), but published findings have been conflicting. Methods The Italian BIO.VE.D.A. biobank provided 976 samples (735 ED patients and 241 controls) for genotyping. We conducted a literature search of studies published up to 1 April 2015, including studies reporting on 5HTTLPR genotype and allele frequencies in obesity and/or ED. We ran a meta-analysis, including data from BIO.VE.D.A. – comparing low and high-functioning genotype and allele frequencies in ED vs. controls. Results Data from 21 studies, plus BIO.VE.D.A., were extracted providing information from 3,736 patients and 2,707 controls. Neither low- nor high-functioning genotype frequencies in ED patients, with both bi- and tri-allelic models, differed from controls. Furthermore, neither low- nor high-functioning allele frequencies in ED or in BN, in both bi- and triallelic models, differed from control groups. After sensitivity analysis, results were the same in AN vs. controls. Results remained unaltered when investigating recessive and dominant models. Conclusions 5HTTLPR does not seem to be associated with ED in general, or with AN or BN in particular. Future studies in ED should explore the role of ethnicity and psychiatric comorbidity as a possible source of bias.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"22 1","pages":"244 - 257"},"PeriodicalIF":0.0,"publicationDate":"2016-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89705279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-17DOI: 10.3109/15622975.2016.1150090
{"title":"Reviewers of the year 2015","authors":"","doi":"10.3109/15622975.2016.1150090","DOIUrl":"https://doi.org/10.3109/15622975.2016.1150090","url":null,"abstract":"","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"31 1","pages":"171 - 172"},"PeriodicalIF":0.0,"publicationDate":"2016-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88536050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-17DOI: 10.3109/15622975.2015.1132007
M. Garriga, I. Pacchiarotti, S. Kasper, S. Zeller, M. Allen, G. Vázquez, L. Baldaçara, L. San, R. H. McAllister-Williams, K. Fountoulakis, P. Courtet, D. Naber, Esther W. Chan, A. Fagiolini, H. Möller, H. Grunze, P. Llorca, R. Jaffe, L. Yatham, D. Hidalgo-Mazzei, M. Passamar, T. Messer, M. Bernardo, E. Vieta
Abstract Background Psychomotor agitation is associated with different psychiatric conditions and represents an important issue in psychiatry. Current recommendations on agitation in psychiatry are not univocal. Actually, an improper assessment and management may result in unnecessary coercive or sedative treatments. A thorough and balanced review plus an expert consensus can guide assessment and treatment decisions. Methods An expert task force iteratively developed consensus using the Delphi method. Initial survey items were based on systematic review of the literature. Subsequent surveys included new, re-worded or re-rated items. Results Out of 2175 papers assessing psychomotor agitation, 124 were included in the review. Each component was assigned a level of evidence. Integrating the evidence and the experience of the task force members, a consensus was reached on 22 statements on this topic. Conclusions Recommendations on the assessment of agitation emphasise the importance of identifying any possible medical cause. For its management, experts agreed in considering verbal de-escalation and environmental modification techniques as first choice, considering physical restraint as a last resort strategy. Regarding pharmacological treatment, the “ideal” medication should calm without over-sedate. Generally, oral or inhaled formulations should be preferred over i.m. routes in mildly agitated patients. Intravenous treatments should be avoided.
{"title":"Assessment and management of agitation in psychiatry: Expert consensus","authors":"M. Garriga, I. Pacchiarotti, S. Kasper, S. Zeller, M. Allen, G. Vázquez, L. Baldaçara, L. San, R. H. McAllister-Williams, K. Fountoulakis, P. Courtet, D. Naber, Esther W. Chan, A. Fagiolini, H. Möller, H. Grunze, P. Llorca, R. Jaffe, L. Yatham, D. Hidalgo-Mazzei, M. Passamar, T. Messer, M. Bernardo, E. Vieta","doi":"10.3109/15622975.2015.1132007","DOIUrl":"https://doi.org/10.3109/15622975.2015.1132007","url":null,"abstract":"Abstract Background Psychomotor agitation is associated with different psychiatric conditions and represents an important issue in psychiatry. Current recommendations on agitation in psychiatry are not univocal. Actually, an improper assessment and management may result in unnecessary coercive or sedative treatments. A thorough and balanced review plus an expert consensus can guide assessment and treatment decisions. Methods An expert task force iteratively developed consensus using the Delphi method. Initial survey items were based on systematic review of the literature. Subsequent surveys included new, re-worded or re-rated items. Results Out of 2175 papers assessing psychomotor agitation, 124 were included in the review. Each component was assigned a level of evidence. Integrating the evidence and the experience of the task force members, a consensus was reached on 22 statements on this topic. Conclusions Recommendations on the assessment of agitation emphasise the importance of identifying any possible medical cause. For its management, experts agreed in considering verbal de-escalation and environmental modification techniques as first choice, considering physical restraint as a last resort strategy. Regarding pharmacological treatment, the “ideal” medication should calm without over-sedate. Generally, oral or inhaled formulations should be preferred over i.m. routes in mildly agitated patients. Intravenous treatments should be avoided.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"98 1","pages":"128 - 86"},"PeriodicalIF":0.0,"publicationDate":"2016-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75938012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-02-17DOI: 10.3109/15622975.2015.1093658
M. Fatjó-Vilas, C. Prats, E. Pomarol-Clotet, L. Lázaro, C. Moreno, I. Gonzalez-ortega, S. Lera-Miguel, S. Miret, M. J. Muñoz, I. Ibáñez, S. Campanera, M. Giralt-López, M. Cuesta, V. Peralta, G. Ortet, M. Parellada, A. González-Pinto, P. McKenna, L. Fañanás
Abstract Objectives Neuritin 1 gene (NRN1) is involved in neurodevelopment processes and synaptic plasticity and its expression is regulated by brain-derived neurotrophic factor (BDNF). We aimed to investigate the association of NRN1 with schizophrenia-spectrum disorders (SSD) and bipolar disorders (BPD), to explore its role in age at onset and cognitive functioning, and to test the epistasis between NRN1 and BDNF. Methods The study was developed in a sample of 954 SSD/BPD patients and 668 healthy subjects. Genotyping analyses included 11 SNPs in NRN1 and one functional SNP in BDNF. Results The frequency of the haplotype C-C (rs645649–rs582262) was significantly increased in patients compared to controls (P = 0.0043), while the haplotype T-C-C-T-C-A (rs3763180–rs10484320–rs4960155–rs9379002–rs9405890–rs1475157) was more frequent in controls (P = 3.1 × 10−5). The variability at NRN1 was nominally related to changes in age at onset and to differences in intelligence quotient, in SSD patients. Epistasis between NRN1 and BDNF was significantly associated with the risk for SSD/BPD (P = 0.005). Conclusions Results suggest that: (i) NRN1 variability is a shared risk factor for both SSD and BPD, (ii) NRN1 may have a selective impact on age at onset and intelligence in SSD, and (iii) the role of NRN1 seems to be not independent of BDNF.
{"title":"Involvement of NRN1 gene in schizophrenia-spectrum and bipolar disorders and its impact on age at onset and cognitive functioning","authors":"M. Fatjó-Vilas, C. Prats, E. Pomarol-Clotet, L. Lázaro, C. Moreno, I. Gonzalez-ortega, S. Lera-Miguel, S. Miret, M. J. Muñoz, I. Ibáñez, S. Campanera, M. Giralt-López, M. Cuesta, V. Peralta, G. Ortet, M. Parellada, A. González-Pinto, P. McKenna, L. Fañanás","doi":"10.3109/15622975.2015.1093658","DOIUrl":"https://doi.org/10.3109/15622975.2015.1093658","url":null,"abstract":"Abstract Objectives Neuritin 1 gene (NRN1) is involved in neurodevelopment processes and synaptic plasticity and its expression is regulated by brain-derived neurotrophic factor (BDNF). We aimed to investigate the association of NRN1 with schizophrenia-spectrum disorders (SSD) and bipolar disorders (BPD), to explore its role in age at onset and cognitive functioning, and to test the epistasis between NRN1 and BDNF. Methods The study was developed in a sample of 954 SSD/BPD patients and 668 healthy subjects. Genotyping analyses included 11 SNPs in NRN1 and one functional SNP in BDNF. Results The frequency of the haplotype C-C (rs645649–rs582262) was significantly increased in patients compared to controls (P = 0.0043), while the haplotype T-C-C-T-C-A (rs3763180–rs10484320–rs4960155–rs9379002–rs9405890–rs1475157) was more frequent in controls (P = 3.1 × 10−5). The variability at NRN1 was nominally related to changes in age at onset and to differences in intelligence quotient, in SSD patients. Epistasis between NRN1 and BDNF was significantly associated with the risk for SSD/BPD (P = 0.005). Conclusions Results suggest that: (i) NRN1 variability is a shared risk factor for both SSD and BPD, (ii) NRN1 may have a selective impact on age at onset and intelligence in SSD, and (iii) the role of NRN1 seems to be not independent of BDNF.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"3 1","pages":"129 - 139"},"PeriodicalIF":0.0,"publicationDate":"2016-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89642303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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