Pub Date : 2017-05-19DOI: 10.3109/15622975.2015.1086492
S. Schreiber, M. Bader, V. Rubovitch, C. Pick
Abstract Objectives: Methylphenidate (MPH), a psychostimulant used for treatment of attention deficit hyperactivity disorder (ADHD), is widely used by patients on antidepressants and methadone maintenance treatment (MMT). Preclinical studies showed MPH to exert analgesic effects when given alone or with morphine. Methods: Using the hotplate assay on mice, we studied the interaction of acute doses of MPH with sub-threshold doses of methadone and different antidepressant medications and the interaction of increasing doses of MPH with chronic methadone. Results: Adding a sub-threshold dose of venlafaxine, desipramine or clomipramine to MPH produced significant augmentation of MPH antinociception with each medication (P < 0.05). No such interactions were found between escitalopram and acute methadone. However, addition of increasing doses of MPH to chronic methadone given for 2 weeks using ALZET osmotic mini pumps induced augmentation of the antinociceptive effect of chronic methadone exclusively at high dose of MPH (7.5 mg/kg). Conclusions: These findings may implicate the need of an excessive attention to the administration of MPH to MMT patients. The no interaction found between MPH and escitalopram may hint to the possibly safe co-administration of MPH and selective serotonin reuptake inhibitors (SSRIs) to depressed ADHD patients. Further studies are needed in order to validate these possible clinical implications.
{"title":"Interaction between methylphenidate, methadone and different antidepressant drugs on antinociception in mice, and possible clinical implications","authors":"S. Schreiber, M. Bader, V. Rubovitch, C. Pick","doi":"10.3109/15622975.2015.1086492","DOIUrl":"https://doi.org/10.3109/15622975.2015.1086492","url":null,"abstract":"Abstract Objectives: Methylphenidate (MPH), a psychostimulant used for treatment of attention deficit hyperactivity disorder (ADHD), is widely used by patients on antidepressants and methadone maintenance treatment (MMT). Preclinical studies showed MPH to exert analgesic effects when given alone or with morphine. Methods: Using the hotplate assay on mice, we studied the interaction of acute doses of MPH with sub-threshold doses of methadone and different antidepressant medications and the interaction of increasing doses of MPH with chronic methadone. Results: Adding a sub-threshold dose of venlafaxine, desipramine or clomipramine to MPH produced significant augmentation of MPH antinociception with each medication (P < 0.05). No such interactions were found between escitalopram and acute methadone. However, addition of increasing doses of MPH to chronic methadone given for 2 weeks using ALZET osmotic mini pumps induced augmentation of the antinociceptive effect of chronic methadone exclusively at high dose of MPH (7.5 mg/kg). Conclusions: These findings may implicate the need of an excessive attention to the administration of MPH to MMT patients. The no interaction found between MPH and escitalopram may hint to the possibly safe co-administration of MPH and selective serotonin reuptake inhibitors (SSRIs) to depressed ADHD patients. Further studies are needed in order to validate these possible clinical implications.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"37 1","pages":"300 - 307"},"PeriodicalIF":0.0,"publicationDate":"2017-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86167092","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 : 2017-05-19DOI: 10.1080/15622975.2016.1224928
Kai-Jing Ding, Jianzhong Yang, G. Reynolds, Bing Chen, Jingru Shao, Rui-xiang Liu, Q. Qian, Hua Liu, Runxu Yang, J. Wen, Chuanyuan Kang
Abstract Objectives: To examine the association of the DNA methylation of DAT1 and DRD4 gene with methylphenidate (MPH) response in attention deficit hyperactivity disorder (ADHD). Methods: One hundred and eleven DSM-IV defined ADHD Chinese Han children were recruited. Inattention, hyperactivity–impulsivity and oppositional symptoms were evaluated by the Swanson, Nolan and Pelham–IV–parent rating scale (SNAP-IV-P) at baseline and 6 weeks after MPH treatment. DNA methylation of CpG sites in the promoter sequences of DAT1 and DRD4 was examined for association with treatment response. Results: Greater improvement on the SNAP-IV-P total score and percentage change from baseline score were both significantly correlated with DAT1 methylation (rho =−0.222, P = .019 and rho = −0.203, P = .032, respectively). A secondary analysis demonstrated that the effect of DAT1 methylation on symptom response was primarily related to the percentage change in oppositional symptoms (rho = −0.242; P = .012), with a smaller significant effect on hyperactivity–impulsivity (rho = −0.192; P = .045). No significant correlation was found between the treatment effect on inattention and DAT1 methylation (rho = −0.101; P = .292). No significant correlation was observed between mean DRD4 methylation and measures of treatment outcome or baseline symptoms. Conclusions: Our findings provide initial evidence for the involvement of the epigenetic alterations of DAT1 in modulating the response to MPH treatment in ADHD, primarily on oppositional and hyperactive-impulsive symptoms.
{"title":"DAT1 methylation is associated with methylphenidate response on oppositional and hyperactive-impulsive symptoms in children and adolescents with ADHD","authors":"Kai-Jing Ding, Jianzhong Yang, G. Reynolds, Bing Chen, Jingru Shao, Rui-xiang Liu, Q. Qian, Hua Liu, Runxu Yang, J. Wen, Chuanyuan Kang","doi":"10.1080/15622975.2016.1224928","DOIUrl":"https://doi.org/10.1080/15622975.2016.1224928","url":null,"abstract":"Abstract Objectives: To examine the association of the DNA methylation of DAT1 and DRD4 gene with methylphenidate (MPH) response in attention deficit hyperactivity disorder (ADHD). Methods: One hundred and eleven DSM-IV defined ADHD Chinese Han children were recruited. Inattention, hyperactivity–impulsivity and oppositional symptoms were evaluated by the Swanson, Nolan and Pelham–IV–parent rating scale (SNAP-IV-P) at baseline and 6 weeks after MPH treatment. DNA methylation of CpG sites in the promoter sequences of DAT1 and DRD4 was examined for association with treatment response. Results: Greater improvement on the SNAP-IV-P total score and percentage change from baseline score were both significantly correlated with DAT1 methylation (rho =−0.222, P = .019 and rho = −0.203, P = .032, respectively). A secondary analysis demonstrated that the effect of DAT1 methylation on symptom response was primarily related to the percentage change in oppositional symptoms (rho = −0.242; P = .012), with a smaller significant effect on hyperactivity–impulsivity (rho = −0.192; P = .045). No significant correlation was found between the treatment effect on inattention and DAT1 methylation (rho = −0.101; P = .292). No significant correlation was observed between mean DRD4 methylation and measures of treatment outcome or baseline symptoms. Conclusions: Our findings provide initial evidence for the involvement of the epigenetic alterations of DAT1 in modulating the response to MPH treatment in ADHD, primarily on oppositional and hyperactive-impulsive symptoms.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"87 1","pages":"291 - 299"},"PeriodicalIF":0.0,"publicationDate":"2017-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81232029","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 : 2017-05-19DOI: 10.3109/15622975.2015.1102325
Koji Shimada, T. Fujisawa, Shinichiro Takiguchi, Hiroaki Naruse, H. Kosaka, H. Okazawa, A. Tomoda
Abstract Objectives: Attention deficit/hyperactivity disorder (ADHD) is associated with deficits in the dopaminergic fronto-striatal systems mediating higher-level cognitive functions. We hypothesised that a dopamine-regulating gene, catechol-O-methyltransferase (COMT), would have differential effects on the neural systems of different ethnic samples with ADHD. In Caucasian children with ADHD, the COMT Val-homozygotes have been previously shown to be associated with striatal grey matter volume (GMV) alterations. By using voxel-based morphometry, we examined whether Asian children with ADHD would exhibit a pattern opposite to that found in Caucasian samples. Methods: Structural brain images were obtained for Japanese children with ADHD (n = 17; mean age = 10.3 years) and typically developing (TD) children (n = 15; mean age = 12.8 years). COMT Val158Met genotype data were also obtained for the ADHD group. Results: Reduced GMV in the left striatum was observed in the ADHD group versus the TD group. This reduced GMV was modulated by COMT polymorphism; Met-carriers exhibited smaller striatal GMV than the Val/Val genotype. Conclusions: Contrasting with previous findings in Caucasians, the COMT Met allele was associated with striatal GMV alterations in Japanese children with ADHD. These results suggest the existence of ethnic differences in the COMT genetic effect on ADHD-related striatal abnormalities.
{"title":"Ethnic differences in COMT genetic effects on striatal grey matter alterations associated with childhood ADHD: A voxel-based morphometry study in a Japanese sample","authors":"Koji Shimada, T. Fujisawa, Shinichiro Takiguchi, Hiroaki Naruse, H. Kosaka, H. Okazawa, A. Tomoda","doi":"10.3109/15622975.2015.1102325","DOIUrl":"https://doi.org/10.3109/15622975.2015.1102325","url":null,"abstract":"Abstract Objectives: Attention deficit/hyperactivity disorder (ADHD) is associated with deficits in the dopaminergic fronto-striatal systems mediating higher-level cognitive functions. We hypothesised that a dopamine-regulating gene, catechol-O-methyltransferase (COMT), would have differential effects on the neural systems of different ethnic samples with ADHD. In Caucasian children with ADHD, the COMT Val-homozygotes have been previously shown to be associated with striatal grey matter volume (GMV) alterations. By using voxel-based morphometry, we examined whether Asian children with ADHD would exhibit a pattern opposite to that found in Caucasian samples. Methods: Structural brain images were obtained for Japanese children with ADHD (n = 17; mean age = 10.3 years) and typically developing (TD) children (n = 15; mean age = 12.8 years). COMT Val158Met genotype data were also obtained for the ADHD group. Results: Reduced GMV in the left striatum was observed in the ADHD group versus the TD group. This reduced GMV was modulated by COMT polymorphism; Met-carriers exhibited smaller striatal GMV than the Val/Val genotype. Conclusions: Contrasting with previous findings in Caucasians, the COMT Met allele was associated with striatal GMV alterations in Japanese children with ADHD. These results suggest the existence of ethnic differences in the COMT genetic effect on ADHD-related striatal abnormalities.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"11 1","pages":"322 - 328"},"PeriodicalIF":0.0,"publicationDate":"2017-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80454105","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 : 2017-04-01DOI: 10.1080/15622975.2016.1224926
S. Ivanova, D. Osmanova, M. Freidin, O. Fedorenko, A. Boiko, I. Pozhidaev, A. Semke, N. Bokhan, A. Agarkov, B. Wilffert, A. Loonen
Abstract Objectives: Hyperprolactinaemia (HPRL) is a classical side effect of antipsychotic drugs primarily attributed to blockade of dopamine D2 subtype receptors in the pituitary gland. Although dopamine is considered the primary factor inhibiting prolactin release, the activity of prolactin-producing lactotrophs is also regulated by the secretagogues thyrotrophin releasing hormone, vasoactive intestinal polypeptide and serotonin (5-hydroxytryptamine; 5-HT). Methods: We describe the association between HPRL and a set of 29 SNPs from 5-HT receptor genes HTR1A, HTR1B, HTR2A, HTR2C, HTR3A, HTR3B and HTR6 in a population of 446 Caucasians (221 males/225 females) with a clinical diagnosis of schizophrenia (according to ICD-10: F20) who were treated with classical and/or atypical antipsychotic drugs. Results: None of the studied autosomal markers were found to be associated with HPRL. However, a significant association was established between various HTR2C polymorphisms and HPRL. Conclusions: This study revealed an association between HPRL and X-chromosome haplotypes comprised of the rs569959 and rs17326429 polymorphisms.
{"title":"Identification of 5-hydroxytryptamine receptor gene polymorphisms modulating hyperprolactinaemia in antipsychotic drug-treated patients with schizophrenia","authors":"S. Ivanova, D. Osmanova, M. Freidin, O. Fedorenko, A. Boiko, I. Pozhidaev, A. Semke, N. Bokhan, A. Agarkov, B. Wilffert, A. Loonen","doi":"10.1080/15622975.2016.1224926","DOIUrl":"https://doi.org/10.1080/15622975.2016.1224926","url":null,"abstract":"Abstract Objectives: Hyperprolactinaemia (HPRL) is a classical side effect of antipsychotic drugs primarily attributed to blockade of dopamine D2 subtype receptors in the pituitary gland. Although dopamine is considered the primary factor inhibiting prolactin release, the activity of prolactin-producing lactotrophs is also regulated by the secretagogues thyrotrophin releasing hormone, vasoactive intestinal polypeptide and serotonin (5-hydroxytryptamine; 5-HT). Methods: We describe the association between HPRL and a set of 29 SNPs from 5-HT receptor genes HTR1A, HTR1B, HTR2A, HTR2C, HTR3A, HTR3B and HTR6 in a population of 446 Caucasians (221 males/225 females) with a clinical diagnosis of schizophrenia (according to ICD-10: F20) who were treated with classical and/or atypical antipsychotic drugs. Results: None of the studied autosomal markers were found to be associated with HPRL. However, a significant association was established between various HTR2C polymorphisms and HPRL. Conclusions: This study revealed an association between HPRL and X-chromosome haplotypes comprised of the rs569959 and rs17326429 polymorphisms.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"1 1","pages":"239 - 246"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88029850","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 : 2017-02-17DOI: 10.1080/15622975.2016.1234069
H. Yoo, Mira Park, Soon-Ae Kim
Abstract Objectives: Several reports suggest that mitochondrial dysfunction is involved in the pathophysiology of autism spectrum disorders (ASD). Therefore, mitochondrial DNA (mtDNA) copy number, a common biomarker for mitochondrial dysfunction, might be associated with ASD phenotypes. Methods: Relative mtDNA copy number in the peripheral blood cells of 100 Korean ASD patients and their unaffected sib-pairs was measured by quantitative polymerase chain reaction (qPCR). Results: ASD patients had significantly higher relative mtDNA copy numbers than their unaffected sibs (P = .042). In addition, there were statistically significant correlations between mtDNA copy number and clinical phenotypes for language and communication in ASD. Conclusions: Our findings suggest that mitochondrial dysfunction and elevated mtDNA copy number may be a biological subtype of ASD that is related to the phenotype for communication.
{"title":"Difference in mitochondrial DNA copy number in peripheral blood cells between probands with autism spectrum disorders and their unaffected siblings","authors":"H. Yoo, Mira Park, Soon-Ae Kim","doi":"10.1080/15622975.2016.1234069","DOIUrl":"https://doi.org/10.1080/15622975.2016.1234069","url":null,"abstract":"Abstract Objectives: Several reports suggest that mitochondrial dysfunction is involved in the pathophysiology of autism spectrum disorders (ASD). Therefore, mitochondrial DNA (mtDNA) copy number, a common biomarker for mitochondrial dysfunction, might be associated with ASD phenotypes. Methods: Relative mtDNA copy number in the peripheral blood cells of 100 Korean ASD patients and their unaffected sib-pairs was measured by quantitative polymerase chain reaction (qPCR). Results: ASD patients had significantly higher relative mtDNA copy numbers than their unaffected sibs (P = .042). In addition, there were statistically significant correlations between mtDNA copy number and clinical phenotypes for language and communication in ASD. Conclusions: Our findings suggest that mitochondrial dysfunction and elevated mtDNA copy number may be a biological subtype of ASD that is related to the phenotype for communication.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"36 1","pages":"151 - 156"},"PeriodicalIF":0.0,"publicationDate":"2017-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81615766","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 : 2017-02-17DOI: 10.1080/15622975.2016.1249952
Kimberly Goodyear, Mary R. Lee, M. Schwandt, C. Hodgkinson, L. Leggio
Abstract Objectives: Alcohol dependence represents a leading cause of mortality and morbidity. Understanding the variables that contribute to this diagnosis and its severity is critical. An overlap between factors that may predispose people to become obese and those that may increase the risk of alcohol dependence may exist. However, data in the literature are not conclusive. Therefore, this study aimed to identify the association between alcohol dependence and obesity-related factors, including biochemical and genetic factors. Methods: In a case–control study with 829 participants, factors involved with metabolism and obesity were assessed, including biochemical lipid and liver markers, and the fat mass and obesity-associated (FTO) single nucleotide polymorphism (SNP) rs8050136. Results: Increased triglycerides, having one or two minor A alleles for rs8050136 and being a smoker were associated with increased risk of alcohol dependence, while increased low-density lipoprotein cholesterol was associated with decreased risk. In addition, having abnormal gamma-glutamyl transferase and being female were factors associated with an increased severity of alcohol dependence. Conclusions: Our preliminary findings suggest a link between alcohol dependence and obesity-related biochemical and genetic factors. Future studies are needed to better understand if these factors may play a predictive role and/or may act as biomarkers for treatment response.
{"title":"Hepatic, lipid and genetic factors associated with obesity: crosstalk with alcohol dependence?","authors":"Kimberly Goodyear, Mary R. Lee, M. Schwandt, C. Hodgkinson, L. Leggio","doi":"10.1080/15622975.2016.1249952","DOIUrl":"https://doi.org/10.1080/15622975.2016.1249952","url":null,"abstract":"Abstract Objectives: Alcohol dependence represents a leading cause of mortality and morbidity. Understanding the variables that contribute to this diagnosis and its severity is critical. An overlap between factors that may predispose people to become obese and those that may increase the risk of alcohol dependence may exist. However, data in the literature are not conclusive. Therefore, this study aimed to identify the association between alcohol dependence and obesity-related factors, including biochemical and genetic factors. Methods: In a case–control study with 829 participants, factors involved with metabolism and obesity were assessed, including biochemical lipid and liver markers, and the fat mass and obesity-associated (FTO) single nucleotide polymorphism (SNP) rs8050136. Results: Increased triglycerides, having one or two minor A alleles for rs8050136 and being a smoker were associated with increased risk of alcohol dependence, while increased low-density lipoprotein cholesterol was associated with decreased risk. In addition, having abnormal gamma-glutamyl transferase and being female were factors associated with an increased severity of alcohol dependence. Conclusions: Our preliminary findings suggest a link between alcohol dependence and obesity-related biochemical and genetic factors. Future studies are needed to better understand if these factors may play a predictive role and/or may act as biomarkers for treatment response.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"19 1","pages":"120 - 128"},"PeriodicalIF":0.0,"publicationDate":"2017-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75325563","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 : 2017-02-17DOI: 10.1080/15622975.2017.1286028
I. Guimarães, Joao M. Fond, G. Fontenelle, L. Forero, Diego Frangou, Sophia Fullana, Miquel A. Funda Sener, Elif Gaedigk
{"title":"Reviewers of the year 2016","authors":"I. Guimarães, Joao M. Fond, G. Fontenelle, L. Forero, Diego Frangou, Sophia Fullana, Miquel A. Funda Sener, Elif Gaedigk","doi":"10.1080/15622975.2017.1286028","DOIUrl":"https://doi.org/10.1080/15622975.2017.1286028","url":null,"abstract":"","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"5 1","pages":"157 - 159"},"PeriodicalIF":0.0,"publicationDate":"2017-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91347559","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 : 2017-02-17DOI: 10.1080/15622975.2016.1246752
M. Soyka, H. Kranzler, V. Hesselbrock, S. Kasper, J. Mutschler, H. Möller
Abstract These practice guidelines for the biological treatment of alcohol use disorders are an update of the first edition, published in 2008, which was developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBP). For this 2016 revision, we performed a systematic review (MEDLINE/PUBMED database, Cochrane Library) of all available publications pertaining to the biological treatment of alcoholism and extracted data from national guidelines. The Task Force evaluated the identified literature with respect to the strength of evidence for the efficacy of each medication and subsequently categorised it into six levels of evidence (A–F) and five levels of recommendation (1–5). Thus, the current guidelines provide a clinically and scientifically relevant, evidence-based update of our earlier recommendations. These guidelines are intended for use by clinicians and practitioners who evaluate and treat people with alcohol use disorders and are primarily concerned with the biological treatment of adults with such disorders.
{"title":"Guidelines for biological treatment of substance use and related disorders, part 1: Alcoholism, first revision","authors":"M. Soyka, H. Kranzler, V. Hesselbrock, S. Kasper, J. Mutschler, H. Möller","doi":"10.1080/15622975.2016.1246752","DOIUrl":"https://doi.org/10.1080/15622975.2016.1246752","url":null,"abstract":"Abstract These practice guidelines for the biological treatment of alcohol use disorders are an update of the first edition, published in 2008, which was developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBP). For this 2016 revision, we performed a systematic review (MEDLINE/PUBMED database, Cochrane Library) of all available publications pertaining to the biological treatment of alcoholism and extracted data from national guidelines. The Task Force evaluated the identified literature with respect to the strength of evidence for the efficacy of each medication and subsequently categorised it into six levels of evidence (A–F) and five levels of recommendation (1–5). Thus, the current guidelines provide a clinically and scientifically relevant, evidence-based update of our earlier recommendations. These guidelines are intended for use by clinicians and practitioners who evaluate and treat people with alcohol use disorders and are primarily concerned with the biological treatment of adults with such disorders.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"95 1","pages":"119 - 86"},"PeriodicalIF":0.0,"publicationDate":"2017-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86924614","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 : 2017-01-25DOI: 10.1080/15622975.2016.1274053
E. Leroux, N. Delcroix, S. Dollfus
Abstract Objectives: Auditory verbal hallucinations (AVHs) are frequently observed in patients with schizophrenia (SZ) and could be the result of white matter (WM) fibre abnormalities involved in speech production/comprehension and perception. We evaluated WM integrity changes in SZ with (SZ+) and without (SZ–) lifetime AVHs compared to healthy controls (HCs), using diffusion tensor imaging-based tractography, with a novel focus on the structural connectivity within both intra- and interhemispheric fasciculi. Methods: The study included 27 SZ+, 12 SZ– and 34 HCs. Fractional anisotropy (FA) and mean and radial diffusivities (MD and RD) were extracted in each participant in two left interhemispheric fasciculi and in the interhemispheric auditory pathway (IAP) to test integrity differences among groups. Results: SZ– and SZ + compared to HCs presented increased diffusivities and/or decreased FA in the interhemispheric fasciculi. Decreased FA was significant only between SZ + and HCs for the IAP. Conclusions: In this first comparison of integrity changes within both intra- and interhemispheric fasciculi, abnormalities in the intrahemispheric fasciculi were observed in both SZ– and SZ+, but an alteration in the IAP was seen only in SZ+. These results suggest that the IAP may be more involved in patients with AVHs-proneness.
{"title":"Abnormalities of language pathways in schizophrenia patients with and without a lifetime history of auditory verbal hallucinations: A DTI-based tractography study","authors":"E. Leroux, N. Delcroix, S. Dollfus","doi":"10.1080/15622975.2016.1274053","DOIUrl":"https://doi.org/10.1080/15622975.2016.1274053","url":null,"abstract":"Abstract Objectives: Auditory verbal hallucinations (AVHs) are frequently observed in patients with schizophrenia (SZ) and could be the result of white matter (WM) fibre abnormalities involved in speech production/comprehension and perception. We evaluated WM integrity changes in SZ with (SZ+) and without (SZ–) lifetime AVHs compared to healthy controls (HCs), using diffusion tensor imaging-based tractography, with a novel focus on the structural connectivity within both intra- and interhemispheric fasciculi. Methods: The study included 27 SZ+, 12 SZ– and 34 HCs. Fractional anisotropy (FA) and mean and radial diffusivities (MD and RD) were extracted in each participant in two left interhemispheric fasciculi and in the interhemispheric auditory pathway (IAP) to test integrity differences among groups. Results: SZ– and SZ + compared to HCs presented increased diffusivities and/or decreased FA in the interhemispheric fasciculi. Decreased FA was significant only between SZ + and HCs for the IAP. Conclusions: In this first comparison of integrity changes within both intra- and interhemispheric fasciculi, abnormalities in the intrahemispheric fasciculi were observed in both SZ– and SZ+, but an alteration in the IAP was seen only in SZ+. These results suggest that the IAP may be more involved in patients with AVHs-proneness.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"17 1","pages":"528 - 538"},"PeriodicalIF":0.0,"publicationDate":"2017-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81601321","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 : 2017-01-23DOI: 10.1080/15622975.2016.1268715
I. Giegling, L. Hosak, R. Mössner, A. Serretti, F. Bellivier, S. Claes, D. Collier, A. Corrales, L. DeLisi, C. Gallo, M. Gill, J. Kennedy, M. Leboyer, W. Maier, M. Márquez, I. Massat, O. Mors, P. Muglia, M. Nöthen, J. Ospina-Duque, M. Owen, P. Propping, Yongyong Shi, D. St. Clair, F. Thibaut, S. Cichon, J. Mendlewicz, M. O’Donovan, D. Rujescu
Abstract Objectives: Schizophrenia is a severe psychiatric disease affecting about 1% of the general population. The relative contribution of genetic factors has been estimated to be up to 80%. The mode of inheritance is complex, non-Mendelian, and in most cases involving the combined action of large numbers of genes. Methods: This review summarises recent efforts to identify genetic variants associated with schizophrenia detected, e.g., through genome-wide association studies, studies on copy-number variants or next-generation sequencing. Results: A large, new body of evidence on genetics of schizophrenia has accumulated over recent years. Many new robustly associated genetic loci have been detected. Furthermore, there is consensus that at least a dozen microdeletions and microduplications contribute to the disease. Genetic overlap between schizophrenia, other psychiatric disorders, and neurodevelopmental syndromes raised new questions regarding the current classification of psychiatric and neurodevelopmental diseases. Conclusions: Future studies will address especially the functional characterisation of genetic variants. This will hopefully open the doors to our understanding of the pathophysiology of schizophrenia and other related diseases. Complementary, integrated systems biology approaches to genomics, transcriptomics, proteomics and metabolomics may also play crucial roles in enabling a precision medicine approach to the treatment of individual patients.
{"title":"Genetics of schizophrenia: A consensus paper of the WFSBP Task Force on Genetics","authors":"I. Giegling, L. Hosak, R. Mössner, A. Serretti, F. Bellivier, S. Claes, D. Collier, A. Corrales, L. DeLisi, C. Gallo, M. Gill, J. Kennedy, M. Leboyer, W. Maier, M. Márquez, I. Massat, O. Mors, P. Muglia, M. Nöthen, J. Ospina-Duque, M. Owen, P. Propping, Yongyong Shi, D. St. Clair, F. Thibaut, S. Cichon, J. Mendlewicz, M. O’Donovan, D. Rujescu","doi":"10.1080/15622975.2016.1268715","DOIUrl":"https://doi.org/10.1080/15622975.2016.1268715","url":null,"abstract":"Abstract Objectives: Schizophrenia is a severe psychiatric disease affecting about 1% of the general population. The relative contribution of genetic factors has been estimated to be up to 80%. The mode of inheritance is complex, non-Mendelian, and in most cases involving the combined action of large numbers of genes. Methods: This review summarises recent efforts to identify genetic variants associated with schizophrenia detected, e.g., through genome-wide association studies, studies on copy-number variants or next-generation sequencing. Results: A large, new body of evidence on genetics of schizophrenia has accumulated over recent years. Many new robustly associated genetic loci have been detected. Furthermore, there is consensus that at least a dozen microdeletions and microduplications contribute to the disease. Genetic overlap between schizophrenia, other psychiatric disorders, and neurodevelopmental syndromes raised new questions regarding the current classification of psychiatric and neurodevelopmental diseases. Conclusions: Future studies will address especially the functional characterisation of genetic variants. This will hopefully open the doors to our understanding of the pathophysiology of schizophrenia and other related diseases. Complementary, integrated systems biology approaches to genomics, transcriptomics, proteomics and metabolomics may also play crucial roles in enabling a precision medicine approach to the treatment of individual patients.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"134 1","pages":"492 - 505"},"PeriodicalIF":0.0,"publicationDate":"2017-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80012407","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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