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Wobrock, Thomas
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Wobrock, Thomas
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Wobrock, Thomas
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Wobrock, T.
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2015Journal Article [["dc.bibliographiccitation.firstpage","142"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","170"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Lieberman, Jeffrey"],["dc.contributor.author","Glenthoj, Birte"],["dc.contributor.author","Gattaz, Wagner F."],["dc.contributor.author","Thibaut, Florence"],["dc.contributor.author","Moeller, Hans-Juergen"],["dc.date.accessioned","2018-11-07T09:59:10Z"],["dc.date.available","2018-11-07T09:59:10Z"],["dc.date.issued","2015"],["dc.description.abstract","These updated guidelines are based on the first edition of the World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of schizophrenia published in the years 2005 and 2006. For this 2015 revision, all available publications pertaining to the biological treatment of schizophrenia were reviewed systematically to allow for an evidence-based update. These guidelines provide evidence-based practice recommendations which are clinically and scientifically relevant. They are intended to be used by all physicians diagnosing and treating patients with schizophrenia. Based on the first version of these guidelines a systematic review, as well as a data extraction from national guidelines have been performed for this update. The identified literature was evaluated with respect to the strength of evidence for its efficacy and subsequently categorised into six levels of evidence (A-F) and five levels of recommendation (1-5). This third part of the updated guidelines covers the management of the following specific treatment circumstances: comorbid depression, suicidality, various comorbid substance use disorders (legal and illegal drugs), and pregnancy and lactation. These guidelines are primarily concerned with the biological treatment (including antipsychotic medication and other pharmacological treatment options) of patients with schizophrenia."],["dc.identifier.doi","10.3109/15622975.2015.1009163"],["dc.identifier.isi","352078300002"],["dc.identifier.pmid","25822804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37530"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1814-1412"],["dc.relation.issn","1562-2975"],["dc.title","World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia. Part 3: Update 2015 Management of special circumstances: Depression, Suicidality, substance use disorders and pregnancy and lactation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2020Journal Article [["dc.bibliographiccitation.firstpage","397"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","407"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Takahashi, Shun"],["dc.contributor.author","Keeser, Daniel"],["dc.contributor.author","Rauchmann, Boris-Stephan"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Keller-Varady, Katriona"],["dc.contributor.author","Maurus, Isabel"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Ertl-Wagner, Birgit"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2021-04-14T08:27:38Z"],["dc.date.available","2021-04-14T08:27:38Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.schres.2019.11.004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82355"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0920-9964"],["dc.title","Effect of aerobic exercise combined with cognitive remediation on cortical thickness and prediction of social adaptation in patients with schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2019Journal Article [["dc.bibliographiccitation.firstpage","26"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Lehmann, Isabel"],["dc.contributor.author","Janssen, Birgit"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Zielasek, Jürgen"],["dc.contributor.author","Gaebel, Wolfgang"],["dc.date.accessioned","2020-12-10T14:08:38Z"],["dc.date.available","2020-12-10T14:08:38Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00115-019-00813-y"],["dc.identifier.eissn","1433-0407"],["dc.identifier.issn","0028-2804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70501"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Die aktualisierte S3-Leitlinie Schizophrenie"],["dc.title.alternative","Revised S3 guidelines on schizophrenia. Developmental process and selected recommendations"],["dc.title.subtitle","Entwicklungsprozess und ausgewählte Empfehlungen"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2015Journal Article [["dc.bibliographiccitation.firstpage","127"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","136"],["dc.bibliographiccitation.volume","265"],["dc.contributor.author","Kittel-Schneider, Sarah"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Zilles, David"],["dc.contributor.author","Wolf, C."],["dc.contributor.author","Schmitt, A."],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Reif, A."],["dc.date.accessioned","2018-11-07T10:00:31Z"],["dc.date.available","2018-11-07T10:00:31Z"],["dc.date.issued","2015"],["dc.description.abstract","The diacylglycerol kinase eta (DGKH) gene, first identified in a genome-wide association study, is one of the few replicated risk genes of bipolar affective disorder (BD). Following initial positive studies, it not only was found to be associated with BD but also implicated in the etiology of other psychiatric disorders featuring affective symptoms, rendering DGKH a cross-disorder risk gene. However, the (patho-)physiological role of the encoded enzyme is still elusive. In the present study, we investigated primarily the influence of a risk haplotype on amygdala volume in patients suffering from schizophrenia or BD as well as healthy controls and four single nucleotide polymorphisms conveying risk. There was a significant association of the DGKH risk haplotype with increased amygdala volume in BD, but not in schizophrenia or healthy controls. These findings add to the notion of a role of DGKH in the pathogenesis of BD."],["dc.description.sponsorship","DFG [RTG 1253/1, RE1632/5-1]; BMBF (DZHI) [01EO1004]; IZKF [Z3-24]"],["dc.identifier.doi","10.1007/s00406-014-0513-9"],["dc.identifier.isi","000350305500005"],["dc.identifier.pmid","24958494"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1433-8491"],["dc.relation.issn","0940-1334"],["dc.title","Influence of DGKH variants on amygdala volume in patients with bipolar affective disorder and schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2015Journal Article [["dc.bibliographiccitation.firstpage","589"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","600"],["dc.bibliographiccitation.volume","265"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Wolff-Menzler, Claus"],["dc.contributor.author","Pfeiffer, Sebastian"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Weidinger, Elif"],["dc.contributor.author","Jobst, Andrea"],["dc.contributor.author","Hoell, Imke"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Yeganeh-Doost, Peyman"],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Quast, Silke"],["dc.contributor.author","Mueller, Norbert"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2018-11-07T09:51:15Z"],["dc.date.available","2018-11-07T09:51:15Z"],["dc.date.issued","2015"],["dc.description.abstract","Despite many pharmacological and psychosocial treatment options, schizophrenia remains a debilitating disorder. Thus, new treatment strategies rooted in the pathophysiology of the disorder are needed. Recently, vagus nerve stimulation (VNS) has been proposed as a potential treatment option for various neuropsychiatric disorders including schizophrenia. The objective of this study was to investigate for the first time the feasibility, safety and efficacy of transcutaneous VNS in stable schizophrenia. A bicentric randomized, sham-controlled, double-blind trial was conducted from 2010 to 2012. Twenty schizophrenia patients were randomly assigned to one of two treatment groups. The first group (active tVNS) received daily active stimulation of the left auricle for 26 weeks. The second group (sham tVNS) received daily sham stimulation for 12 weeks followed by 14 weeks of active stimulation. Primary outcome was defined as change in the Positive and Negative Symptom Scale total score between baseline and week 12. Various other secondary measures were assessed to investigate safety and efficacy. The intervention was well tolerated with no relevant adverse effects. We could not observe a statistically significant difference in the improvement of schizophrenia psychopathology during the observation period. Neither psychopathological and neurocognitive measures nor safety measures showed significant differences between study groups. Application of tVNS was well tolerated, but did not improve schizophrenia symptoms in our 26-week trial. While unsatisfactory compliance questions the feasibility of patient-controlled neurostimulation in schizophrenia, the overall pattern of symptom change might warrant further investigations in this population."],["dc.description.sponsorship","CerboMed GmbH, Erlangen, Germany"],["dc.identifier.doi","10.1007/s00406-015-0618-9"],["dc.identifier.isi","000361397100006"],["dc.identifier.pmid","26210303"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35876"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1433-8491"],["dc.relation.issn","0940-1334"],["dc.title","Transcutaneous noninvasive vagus nerve stimulation (tVNS) in the treatment of schizophrenia: a bicentric randomized controlled pilot study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2015Journal Article [["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Bunse, Tilmann"],["dc.contributor.author","Rein, Bettina"],["dc.contributor.author","Herrmann, Maximiliane"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Nieratschker, Vanessa"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Hasan, Alkomiet"],["dc.date.accessioned","2018-11-07T10:01:13Z"],["dc.date.available","2018-11-07T10:01:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Brain-derived neurotrophic factor (BDNF) has been shown to be a moderator of neuroplasticity. A frequent BDNF-polymorphism (Val66Met) is associated with impairments of cortical plasticity. In patients with schizophrenia, reduced neuroplastic responses following non-invasive brain stimulation have been reported consistently. Various studies have indicated a relationship between the BDNF-Val66Met-polymorphism and motor-cortical plasticity in healthy individuals, but schizophrenia patients have yet to be investigated. The aim of this proof-of-concept study was, therefore, to test the impact of the BDNF-Val66Met-polymorphism on inhibitory and facilitatory cortical plasticity in schizophrenia patients. Methods: Cortical plasticity was investigated in 22 schizophrenia patients and 35 healthy controls using anodal and cathodal transcranial direct-current stimulation (tDCS) applied to the left primary motor cortex. Animal and human research indicates that excitability shifts following anodal and cathodal tDCS are related to molecular long-term potentiation and long-term depression. To test motor-cortical excitability before and after tDCS, well-established single-and paired-pulse transcranial magnetic stimulation protocols were applied. Results: Our analysis revealed increased glutamate-mediated intracortical facilitation in met-heterozygotes compared to val-homozygotes at baseline. Following cathodal tDCS, schizophrenia met-heterozygotes had reduced gamma-amino-butyric-acid-mediated short-interval intracortical inhibition, whereas healthy met-heterozygotes displayed the opposite effect. The BDNF-Val66Met-polymorphism did not influence single-pulse motor-evoked potential amplitudes after tDCS. Conclusions: These preliminary findings support the notion of an association of the BDNF-Val66Met-polymorphism with observable alterations in plasticity following cathodal tDCS in schizophrenia patients. This indicates a complex interaction between inhibitory intracortical interneuron-networks, cortical plasticity, and the BDNF-Val66Met-polymorphism. Further replication and validation need to be dedicated to this question to confirm this relationship."],["dc.description.sponsorship","AstraZeneca; I3G; AOK"],["dc.identifier.doi","10.1093/ijnp/pyu040"],["dc.identifier.isi","000352536800005"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11781"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37969"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1469-5111"],["dc.relation.issn","1461-1457"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","BDNF-Val66Met-Polymorphism Impact on Cortical Plasticity in Schizophrenia Patients: A Proof-of-Concept Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI WOS2019Journal Article [["dc.bibliographiccitation.firstpage","370"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","376"],["dc.bibliographiccitation.volume","208"],["dc.contributor.author","Wagner, Elias"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Kunze, Birgit"],["dc.contributor.author","Langguth, Berthold"],["dc.contributor.author","Landgrebe, Michael"],["dc.contributor.author","Eichhammer, Peter"],["dc.contributor.author","Frank, Elmar"],["dc.contributor.author","Cordes, Joachim"],["dc.contributor.author","Wölwer, Wolfgang"],["dc.contributor.author","Winterer, Georg"],["dc.contributor.author","Gaebel, Wolfgang"],["dc.contributor.author","Hajak, Göran"],["dc.contributor.author","Ohmann, Christian"],["dc.contributor.author","Verde, Pablo E."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Ahmed, Raees"],["dc.contributor.author","Honer, William G."],["dc.contributor.author","Siskind, Dan"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Hasan, Alkomiet"],["dc.date.accessioned","2020-12-10T15:21:10Z"],["dc.date.available","2020-12-10T15:21:10Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.schres.2019.01.021"],["dc.identifier.issn","0920-9964"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72938"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Efficacy of high-frequency repetitive transcranial magnetic stimulation in schizophrenia patients with treatment-resistant negative symptoms treated with clozapine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2013Journal Article [["dc.bibliographiccitation.firstpage","821"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Brain Stimulation"],["dc.bibliographiccitation.lastpage","829"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Misewitsch, Kristina"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Padberg, Frank"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2018-11-07T09:20:31Z"],["dc.date.available","2018-11-07T09:20:31Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Schizophrenia has recently been described as a disorder of impaired plasticity and dys-connectivity. Several lines of evidence suggest that alterations in glutamatergic neurotransmission underlie different symptom domains of schizophrenia. Little is known about the impact of genetic liability on cortical plasticity and connectivity in schizophrenia. Objective: To compare N-methyl-D-aspartate receptor (NMDAR)-dependent cortical plasticity and connectivity in schizophrenia patients and unaffected first-degree relatives to that in healthy subjects. Methods: Cortical plasticity can be induced in the motor cortex with cathodal transcranial direct current stimulation (tDCS). Animal and human research indicates that this long-term depression-like plasticity (LTD-like) is NMDAR dependent, and that these plasticity shifts can last for several hours. tDCS-induced plasticity was assessed by measuring motor-evoked potentials (MEPs) generated by applying transcranial magnetic stimulation (TMS) to both hemispheres in healthy controls, chronically ill schizophrenia patients and unaffected first-degree relatives. Results: Compared to healthy controls, both first-degree relatives and schizophrenia patients showed abolished motor-cortical LTD-like plasticity of the stimulated hemisphere. On the non-stimulated hemisphere, plasticity was again abolished in schizophrenia patients, whereas first-degree relatives had a reversed plasticity. Conclusions: Non-psychotic and clinically unaffected first-degree relatives showed an alteration and a reversal of LTD-like cortical plasticity, indicating functional alterations of glutamatergic transmission as a result of a genetic liability for developing schizophrenia. These results provide new evidence for the association between plasticity dysregulation and functional cortical connectivity, and the importance of these networks in the pathophysiology of schizophrenia. (C) 2013 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Faculty of Medicine Goettingen (Georg-August-University Goettingen)"],["dc.identifier.doi","10.1016/j.brs.2013.03.001"],["dc.identifier.isi","000325046600017"],["dc.identifier.pmid","23545473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28897"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1935-861X"],["dc.title","Impaired Motor Cortex Responses in Non-Psychotic First-Degree Relatives of Schizophrenia Patients: A Cathodal tDCS Pilot Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2013Journal Article [["dc.bibliographiccitation.artnumber","121"],["dc.bibliographiccitation.journal","Frontiers in psychiatry"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Bergener, Theresa"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Bunse, Tilmann"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2019-07-09T11:40:09Z"],["dc.date.available","2019-07-09T11:40:09Z"],["dc.date.issued","2013"],["dc.description.abstract","Transcranial direct current stimulation (tDCS) is a non-invasive stimulation technique that can be applied to modulate cortical activity through induction of cortical plasticity. Since various neuropsychiatric disorders are characterized by fluctuations in cortical activity levels (e.g., schizophrenia), tDCS is increasingly investigated as a treatment tool. Several studies have shown that the induction of cortical plasticity following classical, unilateral tDCS is reduced or impaired in the stimulated and non-stimulated primary motor cortices (M1) of patients with schizophrenia. Moreover, an alternative, bilateral tDCS setup has recently been shown to modulate cortical plasticity in both hemispheres in healthy subjects, highlighting another potential treatment approach. Here we present the first study comparing the efficacy of unilateral tDCS (cathode left M1, anode right supraorbital) with simultaneous bilateral tDCS (cathode left M1, anode right M1) in patients with schizophrenia. tDCS-induced cortical plasticity was monitored by investigating motor-evoked potentials induced by single-pulse transcranial magnetic stimulation applied to both hemispheres. Healthy subjects showed a reduction of left M1 excitability following unilateral tDCS on the stimulated left hemisphere and an increase in right M1 excitability following bilateral tDCS. In schizophrenia, no plasticity was induced following both stimulation paradigms. The pattern of these results indicates a complex interplay between plasticity and connectivity that is impaired in patients with schizophrenia. Further studies are needed to clarify the biological underpinnings and clinical impact of these findings."],["dc.identifier.doi","10.3389/fpsyt.2013.00121"],["dc.identifier.fs","598800"],["dc.identifier.pmid","24109457"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58101"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1664-0640"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Impairments of motor-cortex responses to unilateral and bilateral direct current stimulation in schizophrenia."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2012Journal Article [["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Brain Research"],["dc.bibliographiccitation.lastpage","23"],["dc.bibliographiccitation.volume","217"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Hamada, Masashi"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Ruge, Diane"],["dc.contributor.author","Galea, Joseph Michael"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Rothwell, John C."],["dc.date.accessioned","2018-11-07T09:13:07Z"],["dc.date.available","2018-11-07T09:13:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Animal studies using polarising currents have shown that induction of synaptic long-term potentiation (LTP) and long-term depression (LTD) by bursts of patterned stimulation is affected by the membrane potential of the postsynaptic neurone. The aim of the present experiments was to test whether it is possible to observe similar phenomena in humans with the aim of improving present protocols of inducing synaptic plasticity for therapeutic purposes. We tested whether the LTP/LTD-like after effects of transcranial theta-burst stimulation (TBS) of human motor cortex, an analogue of patterned electrical stimulation in animals, were affected by simultaneous transcranial direct-current stimulation (tDCS), a non-invasive method of polarising cortical neurones in humans. Nine healthy volunteers were investigated in a single-blind, balanced cross-over study; continuous TBS (cTBS) was used to introduce LTD-like after effects, whereas intermittent TBS (iTBS) produced LTP-like effects. Each pattern was coupled with concurrent application of tDCS (<200 s, anodal, cathodal, sham). Cathodal tDCS increased the response to iTBS and abolished the effects of cTBS. Anodal tDCS changed the effects of cTBS towards facilitation, but had no impact on iTBS. Cortical motor thresholds and intracortical inhibitory/facilitatory networks were not altered by any of the stimulation protocols. We conclude that the after effects of TBS can be modulated by concurrent tDCS. We hypothesise that tDCS changes the membrane potential of the apical dendrites of cortical pyramidal neurones and that this changes the response to patterned synaptic input evoked by TBS. The data show that it may be possible to enhance LTP-like plasticity after TBS in the human cortex."],["dc.identifier.doi","10.1007/s00221-011-2968-5"],["dc.identifier.isi","000300580400003"],["dc.identifier.pmid","22143872"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27099"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0014-4819"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Direct-current-dependent shift of theta-burst-induced plasticity in the human motor cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS