Bleich, Stefan

[["dc.bibliographiccitation.firstpage","296"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","299"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Frieling, Helge"],["dc.contributor.author","Hillemacher, Thomas"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:15:16Z"],["dc.date.available","2018-11-07T11:15:16Z"],["dc.date.issued","2008"],["dc.description.abstract","Aims: The individual extent of structural brain tissue changes in patients with alcohol dependence is influenced by genetic factors, gender, age and possibly a dose/duration-effect. Aim of the present study was to investigate different types of alcoholic beverages with regard to hippocampal volume loss in patients suffering from alcoholism. Methods: We included 52 patients with alcohol dependence and divided them according to their preferred type of beverage consumption (beer, wine, and spirits). Hippocampal volumes were determined using volumetric high-resolution MR imaging. Results: There was a significant difference in hippocampal volumes between patients consuming different beverages (ANOVA: F = 7.454; df = 2; P = 0.0015) with the smallest volumes in the wine group, followed by the spirits group. Furthermore, patients with a preferred spirits consumption showed significantly higher plasma homocysteine levels (ANOVA: F = 3.39; df = 2; P = 0.042). Linear regression analyses revealed an association of homocysteine and hippocampal volume only in the group of patients preferring spirits (R(2) = 0.364; P = 0.008). Conclusions: Homocysteine-mediated excitotoxicity may be an important pathophysiological mechanism in ethanol-related brain damage, particularly in patients consuming wine and spirits. The extent of brain atrophy in beer consuming patients seems to be more moderate."],["dc.identifier.doi","10.1093/alcalc/agn002"],["dc.identifier.isi","000255756300008"],["dc.identifier.pmid","18238850"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0735-0414"],["dc.title","Hippocampal volume loss in patients with alcoholism is influenced by the consumed type of alcoholic beverage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Schlautmann, V."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T09:29:24Z"],["dc.date.available","2018-11-07T09:29:24Z"],["dc.date.issued","2000"],["dc.format.extent","369S"],["dc.identifier.doi","10.1016/S0924-9338(00)94588-7"],["dc.identifier.isi","000165731700527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31020"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Editions Scientifiques Medicales Elsevier"],["dc.publisher.place","Paris cedex 15"],["dc.relation.issn","0924-9338"],["dc.title","Thyroid axis alterations in psychoses"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuropsychiatry"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Kern, V."],["dc.contributor.author","Lange, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Emrich, H. M."],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:20:37Z"],["dc.date.available","2018-11-07T11:20:37Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurotoxicity of first-generation antipsychotics: (FGAs) may be involved in lipid peroxidation, which is the pathogenesis of extrapyramidal symptoms, including tardive dyskinesia (TD). Blood samples at day 0, 7, and 21 drawn from patients taking antipsychotics were analyzed for malondialdehyde (MDA) in plasma, a marker of lipid peroxidation, by high-performance liquid chromatography. Of 115 patients enrolled, 92 patients completed the study. Most MDA levels were within normal ranges (<1.0 mu mol/liter). Malondialdehyde levels in patients receiving clozapine (p = 0.002), quetiapine (p = 0.003), amisulpride (p = 0.008), and risperidone (p = 0.008) were significantly lower than within the first generation antipsychotic group. The authors conclude that lipid peroxidation is significantly higher in treatment with FGAs."],["dc.identifier.doi","10.1176/appi.neuropsych.17.2.227"],["dc.identifier.isi","000229541000014"],["dc.identifier.pmid","15939978"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Psychiatric Publishing, Inc"],["dc.publisher.place","Arlington"],["dc.relation.conference","Annual Meeting of the Nordic-Association-for-Psychiatric-Epidemiology"],["dc.relation.eventlocation","REYKJAVIK, ICELAND"],["dc.relation.issn","1545-7222"],["dc.relation.issn","0895-0172"],["dc.title","Oxidative stress during treatment with first- and second-generation antipsychotics"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","466"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","475"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Maler, Manuel"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Rüther, Eckart"],["dc.date.accessioned","2017-09-07T11:44:45Z"],["dc.date.available","2017-09-07T11:44:45Z"],["dc.date.issued","2008"],["dc.description.abstract","The spectrum of action of flupirtine includes analgesic, muscle-relaxant and neuroprotective properties. The substance's mechanism of action has yet to be fully explained. Over the past few years, however, evidence has accumulated that flupirtine interacts with the glutamatergic N-Methyl-D-Aspartate (NMDA) receptor. Although it was not possible to demonstrate a direct effect on the NMDA receptor, all of the findings pointed to an indirect influence on the NMDA receptor in the sense of a functional NMDA antagonism. It was thus postulated that a site of action \"up- or downstream\" of the NMDA receptor is influenced. Such a site of action proved to be the G-protein-activated inwardly rectifying K+ channels (GIRK), the opening of which leads to a stabilisation of the resting membrane potential of neuronal cells and thus causes an indirect inhibition of the NMDA receptor. At therapeutically relevant concentrations, flupirtine is a neuronal potassium channel opener. This mechanism may explain the spectrum of action of flupirtine. Selective neuronal potassium channel opening (SNEPCO) thus proves to be a new principle of action, making flupirtine the prototype of a new substance class with analgesic, muscle-relaxant and neuroprotective properties. The experimental basis for this working hypothesis and the resulting model concepts are presented from the perspective of a four-stage approach."],["dc.description.abstract","Das Wirkspektrum von Flupirtin umfaßt analgetische, muskelentspannende und neuroprotektive Eigenschaften. Der Wirkmechanismus der Substanz war bislang unzureichend bekannt. In den letzten Jahren verdichteten sich jedoch Hinweise auf eine Interaktion von Flupirtin mit dem glutamatergen N-Methyl-D-Aspartat (NMDA)-Rezeptor. Obwohl eine direkte Wirkung am NMDA-Rezeptor nicht nachweisbar war. sprachen alle Befunde für eine indirekte Beeinflussung des NMDA-Rezeptors im Sinne eines funktionellen NMDA-Antagonismus. Es wurde somit postuliert, daß ein Wirkort ,,up- oder downstream\" vom NMDA-Rezeptor beeinflußt wird. Als solcher erwiesen sich die G-Protein gesteuerten einwärts gleichrichtenden K\"-Kanale (GIRK), deren Öffnung zu einer Stabilisierung des Ruhemembranpotentials neuronaler Zellen führt und dadurch eine indirekte Hemmung des NMDA-Rezeptors bewirkt. Flupirtin ist in therapeutisch relevanten Konzentrationen ein neuronaler K'-Kanalöffner (neuronal potassium Channel opener). Dieser Mechanismus vermag das Wirkspektrum von Flupirtin zu erklären. Damit erweist sich die selektive neuronale K+-Kanaloffnung (SNEPCO) als ein neues Wirkprinzip und Flupirtin als Prototyp einer neuen Substanzklasse mit analgetischen, muskelrelaxierenden und neuroprotektiven Eigenschaften. Die experimentellen Grundlagen dieser Arbeitshypothese und der daraus resultierenden Modellvorstellungen werden in einer vierstufigen Betrachtungsebene vorgestellt."],["dc.identifier.doi","10.1055/s-2007-994997"],["dc.identifier.gro","3151740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8561"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0720-4299"],["dc.title","Neuronale Kaliumkanalöffnung durch Flupirtin"],["dc.title.subtitle","Opening of Neuronal K+ Channels by Flupirtine"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","857"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Bleich, S."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Maler, M."],["dc.contributor.author","Parsons, C. G."],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","2002"],["dc.description.abstract","The spectrum of action of flupirtine includes analgesia, muscle relaxation and neuroprotection. N-methyl-D-aspartate (NMDA) receptor antagonism has been discussed as a possible mechanism of action of this compound with little direct evidence. The objective of the present study was to develop a plausible model to explain flupirtine's spectrum of action. A four-stage strategy was selected for this purpose: Firstly, the serum concentration of flupirtine under therapeutic conditions was determined on the basis of the current literature. The second stage involved assessing the known in-vitro effects in light of the therapeutic active concentration. Using whole cell patch clamp recordings from cultured rat superior colliculus neurones interactions between flupirtine and NMDA receptors were assessed. Only very high concentrations of flupirtine antagonized inward currents to NMDA (200 μM) at −70 mV with an lC50 against steady-state responses of 182.1 ± 12.1 μM. The effects of flupirtine were voltage-independent and not associated with receptor desensitization making actions within the NMDA receptor channel or at the glycine modulatory site unlikely. NMDA receptor antagonism probably has little relevance for the clinical efficacy of flupirtine as the concentrations needed were far higher than those achieved in clinical practice. However, the activation of a G-protein-regulated inwardly rectifying K+ channel was identified as an interesting molecular target site of flupirtine. In the next stage, the central nervous spectrum of action of experimental K+ channel openers (PCO) was considered. As far as they have been studied, experimental K+ channel openers display a spectrum of action comparable to that of flupirtine. In the final stage, a global model was developed in which flupirtine stabilizes the resting membrane potential by activating inwardly rectifying K+ channels, thus indirectly inhibiting the activation of NMDA receptors. The model presented here reconciles the known functional NMDA receptor antagonism of flupirtine with the activation of K+ channels that occurs at therapeutic concentrations, thus providing an understanding of flupirtine's spectrum of action. This makes flupirtine the prototype of a clinically applicable substance group with analgesic, muscle-relaxant and neuroprotective properties."],["dc.identifier.doi","10.1007/s007020050206"],["dc.identifier.gro","3151702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8521"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0300-9564"],["dc.title","Flupirtine shows functional NMDA receptor antagonism by enhancing Mg 2+ block via activation of voltage independent potassium channels"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","65"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gerontology"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Hüther, Gerald"],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2017-09-07T11:44:43Z"],["dc.date.available","2017-09-07T11:44:43Z"],["dc.date.issued","2001"],["dc.description.abstract","Over the past few years, molecular biological research has considerably deepened our understanding of the pathophysiological basis of Alzheimer’s dementia (AD). Although different genetic origins of the disease have been identified, all of the findings point to a common terminal sequence in familial AD. This consists of an increased production of β-amyloid peptides from β-amyloid precursor protein. For the cases of sporadic AD, which far outweigh the number of cases of familial AD, an impaired catabolism of the β-amyloid peptides may also be pathophysiologically decisive according to the latest findings. Research into the molecular level of AD makes it possible to identify points of attack for rational drug treatment of the disease, while molecular markers of AD are increasingly being used as a part of early and differential neurochemical diagnostics."],["dc.identifier.doi","10.1159/000052775"],["dc.identifier.gro","3151719"],["dc.identifier.pmid","11287729"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8539"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0304-324X"],["dc.title","Molecular Biology of Alzheimer’s Dementia and Its Clinical Relevance to Early Diagnosis and New Therapeutic Strategies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1282"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Alcoholism Clinical and Experimental Research"],["dc.bibliographiccitation.lastpage","1287"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Schmidt, Lutz G."],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Boening, J."],["dc.contributor.author","Buehringer, G."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Weijers, H. G."],["dc.contributor.author","Wiesbeck, G. A."],["dc.contributor.author","Wolfgramm, J."],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.date.accessioned","2018-11-07T08:47:47Z"],["dc.date.available","2018-11-07T08:47:47Z"],["dc.date.issued","2005"],["dc.description.abstract","This article presents the proceedings of a symposium at the 2004 International Society for Biomedical Research on Alcoholism meeting in Heidelberg/Mannheim, Germany, put together by the German Society of Addiction Therapy and Research (DG-Sucht e.V.). The aim was to give an overview on recent findings from animal to human studies that were conducted by several research groups engaged in the alcoholism field in Germany for longer periods. Results of his animal studies were presented by J. Wolfgramm; G. Buehringer reported on epidentiologic and psychotherapeutic research advances on alcohol-related disorders in Germany. L. G. Schmidt summarized results of novel diagnostic and therapeutic approaches in alcohol dependence, and J. Boening focused on biopsychological personality traits as predictors for relapse in alcoholism. Data relating hyperhomocysteinernia and brain shrinkage in patients with alcoholism were presented by J. Kornhuber. Four addiction research networks federally funded represented their results in separate symposia and were therefore deliberately excluded from this symposium."],["dc.identifier.doi","10.1097/01.ALC.0000171897.16149.E7"],["dc.identifier.isi","000230860500020"],["dc.identifier.pmid","16088985"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21046"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","12th International Congress of the International-Society-for-Biomedical-Research-on-Alcoholism"],["dc.relation.eventlocation","Heidelberg, GERMANY"],["dc.relation.issn","0145-6008"],["dc.title","Advances in Alcoholism Research in Germany"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","871"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Psychiatric Research"],["dc.bibliographiccitation.lastpage","875"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Hillemacher, Thomas"],["dc.contributor.author","Bayerlein, Kristina"],["dc.contributor.author","Frieling, Helge"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T10:57:13Z"],["dc.date.available","2018-11-07T10:57:13Z"],["dc.date.issued","2007"],["dc.description.abstract","Aim of this study was to investigate the possible association of apolipoprotein E (ApoE) gene polymorphism with a history of alcohol withdrawal seizures. We included 194 patients with alcohol dependence who were divided into patients with (SZ+) and without (SZ-) previous alcohol withdrawal seizures. ApoE genotypes were deter-mined using PCR. For statistical analysis we examined the number of ApoE alleles (ApoE2: n = 36; ApoE3: n = 311; ApoE4: n = 41). A significant positive association with a positive history of withdrawal seizures (SZ+) was found in the ApoE3 allele group (Fisher's exact test: p = 0.006) while a significant negative association was observed in the ApoE2 allele group (Fisher's exact test: p = 0.029). For the ApoE4 allele group no significant differences were found regarding a history of withdrawal seizures. Our findings suggest an association between the apolipoprotein E3 gene variant and an elevated risk of alcohol withdrawal seizures. These preliminary results must be validated in further studies. (c) 2006 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.jpsychires.2006.07.011"],["dc.identifier.isi","000247131300008"],["dc.identifier.pmid","16959267"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50189"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0022-3956"],["dc.title","Apolipoprotein E gene polymorphism and previous alcohol withdrawal seizures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","249"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Ophthalmic Research"],["dc.bibliographiccitation.lastpage","256"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Roedl, J. B."],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Schloetzer-Schrehardt, Ursula"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Naumann, G. O. H."],["dc.contributor.author","Kruse, F. E."],["dc.contributor.author","Juenemann, A. G. M."],["dc.date.accessioned","2018-11-07T11:20:31Z"],["dc.date.available","2018-11-07T11:20:31Z"],["dc.date.issued","2008"],["dc.description.abstract","Aims: We assessed homocysteine (Hcy) levels in tear fluid and plasma of patients with primary open-angle glaucoma (POAG). We determined the association between Hcy levels, dry eye syndrome and B vitamin status. Methods: This prospective case-control study included 36 patients with POAG and 36 controls. Hcy concentrations were measured by high-performance liquid chromatography. Results: Patients with POAG had significantly higher mean Hcy levels both in tear fluid (205 +/- 84 nmol/l; p < 0.001, t test) and in plasma (13.43 +/- 3.53 mu mol/l; p = 0.001, t test) than control subjects (130 +/- 53 nmol/l and 10.50 +/- 3.33 mu mol/l, respectively). Hcy in tear fluid was significantly correlated with plasma Hcy in POAG patients (r = 0.459; p = 0.005, Pearson's correlation), but not in controls (r = 0.068; p = 0.695). POAG patients with dry eye disease had significantly higher Hcy levels both in tear fluid and plasma than POAG patients without dry eye disease. There was no association between Hcy levels and B vitamin status in subjects with POAG. Conclusions: The study suggests increased Hcy levels in tear fluid and plasma of patients with POAG. Elevated Hcy levels might be a risk factor for POAG and dry eye syndrome in subjects with glaucoma. Copyright (C) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000127832"],["dc.identifier.isi","000258318600006"],["dc.identifier.pmid","18437035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9359"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55551"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0030-3747"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Increased homocysteine levels in tear fluid of patients with primary open-angle glaucoma"],["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"]]

[["dc.bibliographiccitation.firstpage","40"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Sperling, W."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Graesel, E."],["dc.contributor.author","Bleich, K."],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Javaheripour, K."],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2018-11-07T10:41:49Z"],["dc.date.available","2018-11-07T10:41:49Z"],["dc.date.issued","2003"],["dc.description.abstract","Aims and Methods: Magnetic resonance imaging (MRI) of the hippocampus has been extensively studied in both neurological and psychiatric disorders. Furthermore, hippocampal volume reductions on MRI have been reported in patients with chronic alcoholism. The present volumetric MRI study was undertaken to determine whether an association exists between hippocampal volume reduction and first-onset alcohol withdrawal seizure. Until recently, no data as to whether hippocampal volume reductions in alcoholics might serve as a predictor of withdrawal seizures were available. Results: We found the average hippocampal volumes measured by high resolution MRI to be significantly reduced in 52 alcoholics compared with 30 healthy controls. Besides a decrease of hippocampal volume in patients with chronic alcoholism, we could not find any significant correlation between the occurrence of seizures during alcohol withdrawal and the amount of hippocampal volume reduction in these patients. Conclusions: Thus, the alcoholism-related atrophy within the hippocampal formation in patients suffering from chronic alcoholism does not seem to be the source of convulsive activity in these patients. Neither does the amount of atrophy allow the occurrence of first-onset withdrawal seizures to be predicted."],["dc.identifier.doi","10.1093/alcalc/agg017"],["dc.identifier.isi","000181029400008"],["dc.identifier.pmid","12554606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46628"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0735-0414"],["dc.title","Lack of association between hippocampal volume reduction and first-onset alcohol withdrawal seizure. A volumetric MRI study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]