von Patrick Dömer ; Simeon Helgers ; Franziska Meinert ; Renán Sánchez-Porras ; Christian Mathys ; Karsten Witt ; Peter Vajkoczy ; Nils Nicholas Hecht ; Johannes Woitzik
von Roberto Díaz-Peregrino ; Modar Kentar ; Carlos Alberto Trenado Colin ; Renán Sánchez-Porras ; Pablo Albiña-Palmarola ; Francisco L. Ramírez-Cuapio ; Daniel San-Juan ; Andreas Unterberg ; Johannes Woitzik ; Edgar Santos
ECoG recording; Mild hypothermia; power spectrum of frequency bands; Spreading depolarization; Stroke progression
Objective: Characterize the neurophysiological effects of mild hypothermia on stroke and spreading depolarizations (SDs) in gyrencephalic brains. Methods: Left middle cerebral arteries (MCAs) of six hypothermic and six normothermic pigs were permanently occluded (MCAo). Hypothermia began 1 h after MCAo and continued throughout the experiment. ECoG signals from both frontoparietal cortices were recorded. Five-minute ECoG epochs were collected 5 min before, at 5 min, 4, 8, 12, and 16 h after MCAo, and before, during, and after SDs. Power spectra were decomposed into fast (alpha, beta, and gamma) and slow (delta and theta) frequency bands. Results: In the vascular insulted hemisphere under normothermia, electrodes near the ischemic core exhibited power decay across all frequency bands at 5 min and the 4th hour after MCAo. The same pattern was registered in the two furthest electrodes at the 12th and 16th hour. When mild hypothermia was applied in the vascular insulted hemispheres, the power decay was generalized and seen even in electrodes with uncompromised blood flow. During SD analysis, hypothermia maintained increased delta and beta power during the three phases of SDs in the furthest electrode from the ischemic core, followed by the second furthest and third electrode in the beta band during preSD and postSD segments. However, in hypothermic conditions, the third electrode showed lower delta, theta, and alpha power. Conclusion: Mild hypothermia attenuates all frequency bands in the vascularly compromised hemisphere, irrespective of the cortical location. During SD formation, it preserves power spectra more significantly in electrodes further from the ischemic core.
Frontiers in neuroscience Lausanne : Frontiers Research Foundation, 2007 18(2024), Artikel-ID 1302767, Seite 1-15 Online-Ressource
von Thomas van Essen ; Inge A. M. van Erp ; Hester F. Lingsma ; Dana Pisică ; John K. Yue ; Ranjit D. Singh ; Jeroen T. J. M. van Dijck ; Victor Volovici ; Alexander Younsi ; Angelos Kolias ; Lianne D. Peppel ; Majanka Heijenbrok-Kal ; Gerard M. Ribbers ; David K. Menon ; Peter J. A. Hutchinson ; Geoffrey T. Manley ; Bart Depreitere ; Ewout W. Steyerberg ; Andrew I. R. Maas ; Godard C. W. de Ruiter ; Wilco C. Peul ; Renán Sánchez-Porras
Background - Limited evidence existed on the comparative effectiveness of decompressive craniectomy (DC) versus craniotomy for evacuation of traumatic acute subdural hematoma (ASDH) until the recently published randomised clinical trial RESCUE-ASDH. In this study, that ran concurrently, we aimed to determine current practice patterns and compare outcomes of primary DC versus craniotomy. - Methods - We conducted an analysis of centre treatment preference within the prospective, multicentre, observational Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (known as CENTER-TBI) and NeuroTraumatology Quality Registry (known as Net-QuRe) studies, which enrolled patients throughout Europe and Israel (2014-2020). We included patients with an ASDH who underwent acute neurosurgical evacuation. Patients with severe pre-existing neurological disorders were excluded. In an instrumental variable analysis, we compared outcomes between centres according to treatment preference, measured by the case-mix adjusted proportion DC per centre. The primary outcome was functional outcome rated by the 6-months Glasgow Outcome Scale Extended, estimated with ordinal regression as a common odds ratio (OR), adjusted for prespecified confounders. Variation in centre preference was quantified with the median odds ratio (MOR). CENTER-TBI is registered with ClinicalTrials.gov, number NCT02210221, and the Resource Identification Portal (Research Resource Identifier SCR_015582). - Findings - Between December 19, 2014 and December 17, 2017, 4559 patients with traumatic brain injury were enrolled in CENTER-TBI of whom 336 (7%) underwent acute surgery for ASDH evacuation; 91 (27%) underwent DC and 245 (63%) craniotomy. The proportion primary DC within total acute surgery cases ranged from 6 to 67% with an interquartile range (IQR) of 12-26% among 46 centres; the odds of receiving a DC for prognostically similar patients in one centre versus another randomly selected centre were trebled (adjusted median odds ratio 2.7, p < 0.0001). Higher centre preference for DC over craniotomy was not associated with better functional outcome (adjusted common odds ratio (OR) per 14% [IQR increase] more DC in a centre = 0.9 [95% CI 0.7-1.1], n = 200). Primary DC was associated with more follow-on surgeries and complications [secondary cranial surgery 27% vs. 18%; shunts 11 vs. 5%]; and similar odds of in-hospital mortality (adjusted OR per 14% IQR more primary DC 1.3 [95% CI (1.0-3.4), n = 200]). - Interpretation - We found substantial practice variation in the employment of DC over craniotomy for ASDH. This variation in treatment strategy did not result in different functional outcome. These findings suggest that primary DC should be restricted to salvageable patients in whom immediate replacement of the bone flap is not possible due to intraoperative brain swelling. - Funding - Hersenstichting Nederland for the Dutch NeuroTraumatology Quality Registry and the European Union Seventh Framework Program.
von Renán Sánchez-Porras ; Francisco L. Ramírez‑Cuapio ; Nils Hecht ; Martin Seule ; Roberto Díaz‑Peregrino ; Andreas Unterberg ; Johannes Woitzik ; Jens P. Dreier ; Oliver W. Sakowitz ; Edgar Santos
Online veröffentlicht am 28. Dezember 2022 ; Gesehen am 28.11.2023
Mild traumatic brain injury (mTBI) can be accompanied by structural damage to the brain. Here, we investigated how the presence of intracranial traumatic computed tomography (CT) pathologies relates to the global functional outcome in young patients one year after mTBI. ...
Journal of neurotrauma Larchmont, NY : Liebert, 1988 40(2023), 11/12 vom: Juni, Seite 1243-1254 Online-Ressource
von Modar Kentar ; Francisco L. Ramirez-Cuapio ; Mildred A. Gutiérrez-Herrera ; Renán Sánchez-Porras ; Roberto Díaz-Peregrino ; Niklas Holzwarth ; Lena Maier-Hein ; Johannes Woitzik ; Edgar Santos
von Renán Sánchez-Porras ; Modar Kentar ; Roland Zerelles ; Martina Geyer ; Carlos Alberto Trenado Colin ; Jed A. Hartings ; Johannes Woitzik ; Jens P. Dreier ; Edgar Santos
Spreading depolarizations (SDs) are characterized by near-complete breakdown of the transmembrane ion gradients, cytotoxic edema, and glutamate release. SDs are associated with poor neurological outcomes in cerebrovascular diseases and brain trauma. Ketamine, a N-methyl-d-aspartate receptor antagonist, has shown to inhibit SDs in animal models and in humans. However, little is known about its SD-inhibitory effect during long-term administration. Lissencephalic animal models have shown that ketamine loses its SD-blocking effect after some minutes to hours. Physio-anatomical differences between lissencephalic and the more evolved gyrencephalic animals may affect their SDs-blocking effect. Therefore, information from the last may have more translational potential. Therefore, the aim of this study was to investigate the 18 h-effect of s-ketamine as a basis for its possible long-term clinical use for neuroprotection. For this purpose, two gyrencephalic swine brain models were used. In one, SDs were elicited through topical application of KCl; in the other model, SDs were spontaneously induced after occlusion of the middle cerebral artery. S-ketamine was administered at therapeutic human doses, 2, 4 and 5 mg/kg BW/h for up to 18 h. Our findings indicate that s-ketamine significantly reduces SD incidence and expansion without clear evidence of loss of its efficacy. Pharmacological susceptibility of SDs to s-ketamine in both the ischemic gyrencephalic brain and well-perfused brain was observed. SDs were most potently inhibited by s-ketamine doses that are above the clinically recommended (4 mg/kg BW/h and 5 mg/kg BW/h). Nonetheless, such doses are given by neurointensivists in individual cases. Our results give momentum to further investigate the feasibility of a multicenter, neuromonitoring-guided, proof-of-concept clinical trial.
