Herrendorf, Gregor

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neuroimaging"],["dc.bibliographiccitation.lastpage","161"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Mursch, K."],["dc.contributor.author","Bransi, A."],["dc.contributor.author","Vatter, H."],["dc.contributor.author","Herrendorf, G."],["dc.contributor.author","Behnke-Mursch, J."],["dc.contributor.author","Kolenda, H."],["dc.date.accessioned","2018-11-07T10:41:57Z"],["dc.date.available","2018-11-07T10:41:57Z"],["dc.date.issued","2000"],["dc.description.abstract","In a prospective study, 55 patients were examined by transcranial duplex sonography (TCCS) after subarachnoid hemorrhage (SAH) to determine whether additional transcranial duplex examination on the middle cerebral artery M2 segments would aid in the examination of the-MCA stem segment. The mean;blood flow velocities and pulsatility index were correlated to the occurrence of delayed ischemic neurologic deficits (DIND). Out: of 47 patients included, 21 did not experience any delayed deficit (group 1), 15 did (group II), and in 11 the extent to which vasospasm contributed to a neurologic deficit was unclear (group III). The highest blood flow velocity and the greatest increase of mean blood flow velocity on 1 day were significantly higher in groups II and III both in M1 and in M2. In 10 patients in group II, where the onset day of DIND was known exactly, Doppler data indicating ischemia before or at the time of DIND were observed in nine. In eight patients, Doppler of the MCA stem alone would have provided enough information to recognize the risk of symptomatic vasospasm; in one patient, only the M2 Doppler gave an indication of ischemic complication. Transcranial duplex sonography may provide additional information to TCD by accurate delineation of M1/M2 vasospasm and therefore may help plan cerebral angiography and neurointerventional treatment."],["dc.identifier.isi","000088276600005"],["dc.identifier.pmid","10918742"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46662"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1051-2284"],["dc.title","Blood flow velocities in middle cerebral artery branches after subarachnoid hemorrhage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1254"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","1255"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Herrendorf, Gregor"],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Obermann, Mark"],["dc.date.accessioned","2018-11-07T10:06:16Z"],["dc.date.available","2018-11-07T10:06:16Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1136/jnnp-2016-313091"],["dc.identifier.isi","000389151200017"],["dc.identifier.pmid","27071645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","1468-330X"],["dc.relation.issn","0022-3050"],["dc.title","Late progression of neurological symptoms and MRI T2 hyperintensities in Parry-Romberg syndrome"],["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"]]

[["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","71"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Herrendorf, G."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Kolle, R."],["dc.contributor.author","Baudewig, Juergen"],["dc.contributor.author","Waberski, T. D."],["dc.contributor.author","Buchner, Helmut"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T11:03:40Z"],["dc.date.available","2018-11-07T11:03:40Z"],["dc.date.issued","2000"],["dc.description.abstract","Purpose: By the use of three different head models in EEG dipole analysis, we tried to model the origin of interictal and ictal epileptic activity as precisely as possible. Further, as a control, a second evaluation was made by an independent group to control for interindividual reliability of the dipole source analysis. With the realistic head model (CURRY) considering cortex, skull, and skin segmentation, the spike source was located. Methods: In five patients with mesial temporal epileptogenesis, confirmed by successful epilepsy surgery, the spike source was close to the hippocampus, with a mean distance of the dipole source from the hippocampus of 13.6 mm (range, 9-17.2 mm). In one case the ictal EEG also could be analyzed and resulted in a dipole-source localization comparable to the interictal source. Results: In both head models using either pure cortex segmentation only or a concentric three-shell model, the dipole source was systematically dislocated in a more superior position. Data analysis by a second group with independently chosen EEG samples and identical individual head model resulted in deviations of <5.3 mm. Data analysis using independently selected spikes and independently segmented head models resulted in deviations less than or equal to 16.7 mm. Conclusions: In four cases of extratemporal epileptogenesis, the origin of interictal epileptiform discharges was localized to the suspected primary epileptogenic zone."],["dc.identifier.doi","10.1111/j.1528-1157.2000.tb01508.x"],["dc.identifier.isi","000084703400013"],["dc.identifier.pmid","10643927"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51667"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0013-9580"],["dc.title","Dipole-source analysis in a realistic head model in patients with focal epilepsy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","75"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Epilepsy Research"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Steinhoff, Bernhard J."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Mursch, Kay"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Herrendorf, Gregor"],["dc.contributor.author","Bittermann, Hans-Joachim"],["dc.contributor.author","Felgenhauer, Klaus"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Markakis, Evangelos"],["dc.date.accessioned","2017-09-07T11:44:24Z"],["dc.date.available","2017-09-07T11:44:24Z"],["dc.date.issued","2002"],["dc.description.abstract","In the brain, S100 protein and neuron-specific enolase (NSE) are mainly found in glial cells and neurons, respectively. We investigated concentrations of S100 protein and NSE in cisternal cerebrospinal fluid obtained during implantation of foramen ovale electrodes in eight patients with temporal lobe epilepsy (TLE). In addition, the meningeal markers cystatin-C and β-trace as well as total protein were measured. Patients with trigeminal neuralgia (TN) undergoing glycerol rhizotomy served as controls. S100 protein and NSE levels ipsilateral to the site of seizure onset were significantly higher than in TN. Contralateral TLE values were also markedly but not significantly elevated. The meningeal markers cystatin-C and β-trace protein as well as total protein did not differ in TLE and TN. We conclude that interictal temporal lobe dysfunction corresponds with neuronal and glial marker elevations in the extracellular space and that site-specific elevations may predict the site of seizure origin biochemically."],["dc.identifier.doi","10.1016/s0920-1211(99)00026-1"],["dc.identifier.gro","3151649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8466"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0920-1211"],["dc.title","Cisternal S100 protein and neuron-specific enolase are elevated and site-specific markers in intractable temporal lobe epilepsy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]