Steinhoff, Bernhard Jochen

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","AKTUELLE NEUROLOGIE"],["dc.bibliographiccitation.lastpage","87"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Baumgartner, C."],["dc.contributor.author","Elger, Christian E."],["dc.contributor.author","Hufnagel, A."],["dc.contributor.author","Oppel, F."],["dc.contributor.author","Runge, Ullrich"],["dc.contributor.author","Schramm, J."],["dc.contributor.author","Stefan, H."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Wieser, H. G."],["dc.contributor.author","Zentner, J."],["dc.date.accessioned","2018-11-07T08:50:19Z"],["dc.date.available","2018-11-07T08:50:19Z"],["dc.date.issued","2000"],["dc.description.abstract","Presurgical epilepsy diagnosis and surgical treatment of the various types of epilepsy represent diagnostic and therapeutic procedures that require special training and expertise in the following areas: neurology/paediatric (epileptology), neurosurgery, neuroradiology, neuropsychology, medical technical personnel/EEC technicians. Therefore the Working Group of Presurgical Epilepsy Diagnosis and Surgical Treatment of Epilepsy in the German-speaking countries defined a certificate for presurgical epilepsy diagnosis and surgical treatment of the various forms of epilepsy. The requirements for this certificate in the areas mentioned above are detailed in the following article."],["dc.identifier.doi","10.1055/s-2007-1017524"],["dc.identifier.isi","000086559200007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21668"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag"],["dc.relation.issn","0302-4350"],["dc.title","Certificate of the Working Group for Presurgical Epilepsy Diagnosis and Surgical Treatment of Epilepsy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1030"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1033"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Gilliam, Frank S."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Bittermann, H. J."],["dc.contributor.author","Kuzniecky, R."],["dc.contributor.author","Faught, E."],["dc.contributor.author","Abou-Khalil, B."],["dc.date.accessioned","2018-11-07T09:11:13Z"],["dc.date.available","2018-11-07T09:11:13Z"],["dc.date.issued","2000"],["dc.description.abstract","The authors present 11 cases of idiopathic generalized epilepsy that began in adulthood at a mean age of 39 years. All patients had myoclonic jerks, five had absence seizures, and nine had infrequent generalized tonic-clonic seizures. A majority had a family history of seizures. EEG in all patients showed generalized epileptiform abnormalities, whereas neuroimaging and neurologic examination results were normal. This series appears to represent a previously undescribed idiopathic generalized epilepsy syndrome of adult myoclonic epilepsy."],["dc.description.sponsorship","NINDS NIH HHS [NS01794-01]"],["dc.identifier.isi","000089696500024"],["dc.identifier.pmid","11061264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26669"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Adult myoclonic epilepsy: A distinct syndrome of idiopathic generalized epilepsy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","713"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.lastpage","718"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Herrendorf, Gregor"],["dc.contributor.author","Mogge, Sebastian"],["dc.contributor.author","Steinhoff, Bernhard J."],["dc.date.accessioned","2017-09-07T11:44:34Z"],["dc.date.available","2017-09-07T11:44:34Z"],["dc.date.issued","1999"],["dc.description.abstract","Summary: Purpose: To investigate and compare the temporal profile of serial levels of neuron-specific enolase (NSE) and prolactin in serum from patients after single epileptic seizures.Methods: Measurement of NSE and prolactin by sensitive immunoassays in 21 patients with complex partial seizure (CPSs; n = 11) and secondarily generalized tonic-clonic seizures (SGTCSs; n = 10) during continuous video-EEG monitoring at four different time points (1, 3, 6, and 24 h after ictal event). Statistical analysis was performed by using a repeated-measures analysis of variance (ANOVA) model.Results: Mean ± SD values for NSE levels (ng/ml) were 12.5 ± 4.4 (1 h), 10.8 ± 3.8 (3 h), 11.1 ± 4.9 (6 h), and 8.2 ± 1.9 (24 h). The corresponding prolactin levels (mU/L) were 1,311 ± 1,034, 232 ± 158, 237 ± 175, and 251 ± 98. There was a significant decrease of NSE and prolactin levels over time (p < 0.001). The pair-wise comparison of NSE levels showed significant differences between the time points 1 vs. 24 h (p < 0.001), 3 vs. 24 h (p = 0.007), and 6 vs. 24 h (p = 0.009). In contrast, serum prolactin levels showed a significant difference between 1 vs. 3 h (p < 0.001) only. Most of the NSE levels remained normal after CPSs and SGTCSs. At 1 h after the seizure, only 33% of the subjects had increased NSE, whereas abnormal prolactin levels occurred with a sensitivity of 80%.Conclusions: In contrast to prolactin, serum NSE is not a sensitive marker of individual seizures. Only some individuals showed an increase of NSE beyond the prolactin-sensitive time frame after a single seizure, and mean NSE levels were not significantly increased compared with those of normal controls."],["dc.identifier.doi","10.1111/j.1528-1157.1999.tb00768.x"],["dc.identifier.gro","3151700"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8519"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0013-9580"],["dc.title","Kinetics of Serum Neuron-Specific Enolase and Prolactin in Patients After Single Epileptic Seizures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","67"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Epilepsy Research"],["dc.bibliographiccitation.lastpage","77"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Wischer, S."],["dc.contributor.author","Somal, H. S."],["dc.contributor.author","Nitsche, M. A."],["dc.contributor.author","Mercer, A. J."],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Steinhoff, B. J."],["dc.date.accessioned","2018-11-07T10:36:26Z"],["dc.date.available","2018-11-07T10:36:26Z"],["dc.date.issued","2003"],["dc.description.abstract","The antiepileptic drug lamotrigine (LTG) is known to reduce cortical excitability evaluated by transcranial magnetic stimulation (TMS). We investigated the relationship between LTG oral dosages, serum levels and inhibitory effects on resting motor threshold (RMT), a parameter of motor system excitability assessed by TMS. In a randomized, placebo-controlled crossover study 16 male volunteers received 325 mg LTG as a single dose, as bi-hourly graded cumulative dose, or placebo. RMT and serum levels were measured before and after 2-8 h. With single dose, RMT elevation showed a poor but significant correlation to serum levels. With graded dose, serum levels as well as RMT increased dose-dependently with significant (P < 0.0001) linear correlation. However, detailed comparison showed a high inter-individual variability in the relationship resembling a sigmoid correlation. Different mechanisms besides the sodium-channel blockage as the main mode of action of LTG are discussed to explain the diversity of individual dose-response relationships. Provided that the RMT elevation reflects the antiepileptic potential of LTG, TMS may be developed as a tool to monitor interindividual response of epilepsy patients to LTG treatment as well as to explore efficacy of other antiepileptic drugs with similar mode of action. (C) 2003 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.eplepsyres.2003.08.006"],["dc.identifier.isi","000185951300007"],["dc.identifier.pmid","14529954"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45323"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0920-1211"],["dc.title","Relationship between lamotrigine oral dose, serum level and its inhibitory effect on CNS: insights from transcranial magnetic stimulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1362"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Annals of Biomedical Engineering"],["dc.bibliographiccitation.lastpage","1369"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Kurth, C."],["dc.contributor.author","Gillam, F."],["dc.contributor.author","Steinhoff, B. J."],["dc.date.accessioned","2018-11-07T11:06:46Z"],["dc.date.available","2018-11-07T11:06:46Z"],["dc.date.issued","2000"],["dc.description.abstract","Artificial neural networks are widely used for pattern recognition tasks. For spike detection in electroencephalography (EEC;), feedforward networks trained by the back-propagation algorithm are preferred by most authors. Opposed to this. we examined the off-line spike detection abilities of a Kohonen feature map (KFM), which is different from feedforward networks in certain aspects. The EEG data for the training set were obtained from patients with intractable partial epilepsies of mesiotemporal (n=2) or extratemporal (n=2) origin. For each patient the training set for the KFM included the same patterns of background activity and artifacts as well as the typical individual spike patterns. Three different-sized networks were examined ( 15X15 cells, 25X25 cells, and 60X60 cells in the Kohonen layer). To investigate the quality of spike detection the results obtained with the KFM were compared with the findings of two board-certified electroencephalographers. Application of a threshold based on the partial invariance of spike recognition against translation of the EEG provided an average sensitivity and selectivity of 80.2% at crossover threshold (71%-86%) depending on the networksize and noise. Multichannel EEG processing in real time will be available soon. In conclusion, pattern-based automated spike detection with a KFM is a promising approach in clinical epileptology and stems to be at least as accurate as other more-established methods of spike detection. (C) 2000 Biomedical Engineering Society. [S0090-6964(00)01011-0]."],["dc.identifier.doi","10.1114/1.1331312"],["dc.identifier.isi","000166492500008"],["dc.identifier.pmid","11212954"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52396"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Inst Physics"],["dc.relation.issn","0090-6964"],["dc.title","EEG spike detection with a Kohonen feature map"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","133"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","FUNCTIONAL NEUROLOGY"],["dc.bibliographiccitation.lastpage","136"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Mursch, K."],["dc.contributor.author","Schafer, M."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Behnke-Mursch, J."],["dc.date.accessioned","2018-11-07T10:20:58Z"],["dc.date.available","2018-11-07T10:20:58Z"],["dc.date.issued","2002"],["dc.description.abstract","Trigeminal evoked potentials (TEPs) and sensory deficits in eighty-three patients admitted for first surgical treatment of facial pain were retrospectively analysed. Thirty-seven patients suffered from trigeminal neuralgia (TN), 10 from symptomatic TN (sTN), and 36 from atypical facial pain (AFP). Eighteen percent of the TN patients reported sensory deficits on the pain side, but 35% had delayed ipsilateral N13 waves. Of the sTN patients, 60% had either sensory deficits or a pathological corneal reflex and 62.5% a pathological N13. Of the AFP patients, 61% complained of sensory deficits, but only 31% had a pathological N13. The percentage of pathological P19 waves was slightly lower (20%, 50%, and 11%, respectively), but showed a similar trend. Normal TEPs were found even in the presence of a sensory deficit (reported only in the AFP group). These findings may add weight to the hypothesis of underlying psychiatric disorders in AFP."],["dc.identifier.isi","000180533800005"],["dc.identifier.pmid","12549718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41993"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","C I C-edizioni Internazionali Srl"],["dc.relation.issn","0393-5264"],["dc.title","Trigeminal evoked potentials and sensory deficits in atypical facial pain - a comparison with results in trigeminal neuralgia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1292"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Stefan, H."],["dc.contributor.author","Schulze-Bonhage, Andreas"],["dc.contributor.author","Hueber, R."],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Wangemann, M."],["dc.contributor.author","Elger, Christian E."],["dc.date.accessioned","2018-11-07T09:05:04Z"],["dc.date.available","2018-11-07T09:05:04Z"],["dc.date.issued","2012"],["dc.description.abstract","The aim of the study was an assessment of the tolerability and efficacy of slow release oxcarbazepine (OXC-MR) versus immediate release OXC (OXC-IR) after forced titration in patients with focal epileptic seizures with and without secondary generalization who had previously not become seizure-free under OXC-IR with or without concomitant antiepileptic drugs. The primary study variable was to assess the maximum tolerated dosage with OXC-MR and OXC-IR. This was designed as a multicenter, randomized, open, controlled, parallel group phase III study. After randomization patients received OXC-MR or OXC-IR for a study period of 26 days. The initial dosage of 900 mg, 1,200 mg or 1,500 mg OXC was increased every 5 days by 300 mg up to a maximum daily dosage of 2,700 mg. In cases of intolerable adverse events dosage could be reduced by 150 mg 2 days after an increase. Adverse events and executive abilities were assessed with the questionnaire \"Adverse Event Profile plus\" and with the EpitrackA (R) test protocol. Serum concentrations of OXC and its active metabolite were measured in a part of the patient group. The 71 patients (54% male, age: 19-70 years) enrolled in the study were randomized. The maximum mean daily OXC dosage at the end of the study period was 1,950 mg with OXC-MR and thus statistically significantly higher than in OXC-IR group (1,650 mg, p = 0.022). The number of causally related adverse events was lower in the OXC-MR group (n = 104 versus n = 138 with OXC-IR) and CNS-related adverse events such as dizziness, tremor, somnolence and headache occurred significantly less often with OXC-MR (OXC-MR 65.7%, OXC-IR 88.9%, p = 0.01). Fluctuations of serum concentrations of the active metabolite were less pronounced under the OXC-MR regimen. Due to better tolerability OXC-MR allowed higher maintenance dosages to be reached than OXC-IR. In spite of a higher mean daily dosage adverse events and especially CNS-related adverse events occurred less often than with OXC-IR."],["dc.identifier.doi","10.1007/s00115-012-3598-2"],["dc.identifier.isi","000309867700008"],["dc.identifier.pmid","22850688"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25241"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Slow release versus immediate release oxcarbazepine in difficult-to-treat focal epilepsy. A multicenter, randomized, open, controlled, parallel group phase III study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","231"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuropsychologia"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Boucsein, K."],["dc.contributor.author","Weniger, Godehard"],["dc.contributor.author","Mursch, K."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Irle, Eva"],["dc.date.accessioned","2018-11-07T09:36:58Z"],["dc.date.available","2018-11-07T09:36:58Z"],["dc.date.issued","2001"],["dc.description.abstract","To investigate the role of unilateral amygdala lesions on processing emotions, 22 drug-resistant temporal lobe epilepsy (TLE) subjects (12 with left-sided and ten with right-sided focus) were tested, after anterior temporal lobectomy or selective amygdalo-hippocampectomy on two associative learning tasks containing emotional and neutral facial expressions, respectively. Volumetric lesion analysis was performed on the basis of 3-D MR images. No effects of lesion side were found in TLE subjects. Taken thr extent of amygdala damage into account, an interaction effect could be shown between task (learning of neutral facial expressions versus emotional facial expressions) acid group (subjects with little versus considerable amygdala damage), indicating worse performance of subjects with considerable amygdala damage in learning emotional facial expressions. Subjects with considerable amygdala damage were also significantly impaired in learning emotional facial expressions when compared with control subjects. (C) 2001 Elsevier Science Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0028-3932(00)00117-2"],["dc.identifier.isi","000166687100002"],["dc.identifier.pmid","11163602"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32732"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0028-3932"],["dc.title","Amygdala lesion in temporal lobe epilepsy subjects impairs associative learning of emotional facial expressions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2558"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2566"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Herms, J. W."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Jastrow, U."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T09:51:28Z"],["dc.date.available","2018-11-07T09:51:28Z"],["dc.date.issued","2002"],["dc.description.abstract","The pathogenesis underlying the typical findings in Creutzfeldt-Jakob disease (CJD) such as periodic EEG changes or myoclonus is not fully understood. The thalamus possesses a high density of inhibitory neurones and serves as a crucial pacemaker of rhythmic EEG activity. As inhibitory neurones expressing parvalbumin (PV) are reduced in the cerebral cortex and hippocampus in sporadic CJD (sCJD), we studied the distribution and number of PV-immunoreactive neurones in sCJD thalami in order to determine whether damage to them could account for certain clinical findings. Immuno histochemical analysis was performed on the thalami from 21 sCJD patients and five controls. The number of PV+ neurones was counted in the thalamic nuclei and compared with clinical and molecular findings. In sCJD patients, PV+ neurones were significantly reduced in the ventrolateral posterior (VLp), ventrolateral anterior (VLa), anteroventral (AV), lateral dorsal (LD), mediodorsal (MD) and reticular (Re) thalamic nuclei (P < 0.05). The VLp was especially damaged in sCJD patients with homozygosity for methionine at codon 129 and scrapie prion protein (PrPSc) type 1. Patients with typical EEG changes [periodic sharp wave complexes (PSWCs)] and myoclonus had a predominant loss of PV+ cells in the reticular thalamic nucleus. In conclusion, our data support the hypothesis that the damage to PV-immunoreactive neurones determines the generation of certain typical clinical features of CJD, i.e. PSWCs associated with myoclonus."],["dc.identifier.doi","10.1093/brain/awf253"],["dc.identifier.isi","000178834400016"],["dc.identifier.pmid","12390980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35920"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical findings in sporadic Creutzfeldt-Jakob disease correlate with thalamic pathology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","629"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","630"],["dc.bibliographiccitation.volume","250"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Serafin, S."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Scherer, M."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:39:18Z"],["dc.date.available","2018-11-07T10:39:18Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1007/s00415-003-1059-3"],["dc.identifier.isi","000183063300023"],["dc.identifier.pmid","12814120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46011"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Diagnostic problems during late course in Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]