The neurophysiological effect of mild hypothermia in gyrencephalic brains submitted to ischemic stroke and spreading depolarizations.

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.

Mild hypothermia reduces spreading depolarizations and infarct size in a swine model.

Spreading depolarizations (SDs) have been linked to infarct volume expansion following ischemic stroke. Therapeutic hypothermia provides a neuroprotective effect after ischemic stroke. This study aimed to evaluate the effect of hypothermia on the propagation of SDs and infarct volume in an ischemic swine model. Through left orbital exenteration, middle cerebral arteries were surgically occluded (MCAo) in 16 swine. Extensive craniotomy and durotomy were performed. Six hypothermic and five normothermic animals were included in the analysis. An intracranial temperature probe was placed right frontal subdural. One hour after ischemic onset, mild hypothermia was induced and eighteen hours of electrocorticographic (ECoG) and intrinsic optical signal (IOS) recordings were acquired. Postmortem, 4 mm-thick slices were stained with 2,3,5-triphenyltetrazolium chloride to estimate the infarct volume. Compared to normothermia (36.4 ± 0.4°C), hypothermia (32.3 ± 0.2°C) significantly reduced the frequency and expansion of SDs (ECoG: 3.5 ± 2.1, 73.2 ± 5.2% vs. 1.0 ± 0.7, 41.9 ± 21.8%; IOS 3.9 ± 0.4, 87.6 ± 12.0% vs. 1.4 ± 0.7, 67.7 ± 8.3%, respectively). Further, infarct volume among hypothermic animals (23.2 ± 1.8% vs. 32.4 ± 2.5%) was significantly reduced. Therapeutic hypothermia reduces infarct volume and the frequency and expansion of SDs following cerebral ischemia.

Spatial and temporal frequency band changes during infarct induction, infarct progression, and spreading depolarizations in the gyrencephalic brain.

Aim: To describe the spatial and temporal electrocorticographic (ECoG) changes after middle cerebral artery occlusion (MCAo), including those caused by spreading depolarization (SD) in the pig brain. Methods: The left middle cerebral arteries (MCAs) were clipped in six pigs. The clipping procedure lasted between 8 and 12 min, achieving a permanent occlusion (MCAo). Five-contact ECoG stripes were placed bilaterally over the frontoparietal cortices corresponding to the irrigation territory of the MCA and anterior cerebral artery (ACA). ECoG recordings were performed around 24 h: 1 h before and 23 h after the MCAo, and SDs were quantified. Five-minute ECoG signal segments were sampled before, 5 min, and 4, 8, and 12 h after cerebral artery occlusion and before, during, and after the negative direct current shift of the SDs. The power spectrum of the signals was decomposed into delta, theta, alpha, beta, and gamma bands. Descriptive statistics, Wilcoxon matched-pairs signed-rank tests, and Friedman tests were performed. Results: Electrodes close to the MCAo showed instant decay in all frequency bands and SD onset during the first 5 h. Electrodes far from the MCAo exhibited immediate loss of fast frequencies and progressive decline of slow frequencies with an increased SD incidence between 6 and 14 h. After 8 h, the ACA electrode reported a secondary reduction of all frequency bands except gamma and high SD incidence within 12-17 h. During the SD, all electrodes showed a decline in all frequency bands. After SD passage, frequency band recovery was impaired only in MCA electrodes. Conclusion: ECoG can identify infarct progression and secondary brain injury. Severe disturbances in all the frequency bands are generated in the cortices where the SDs are passing by.

Eighteen-hour inhibitory effect of s-ketamine on potassium- and ischemia-induced spreading depolarizations in the gyrencephalic swine brain.

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.

Oral Preconditioning of Donors After Brain Death With Calcineurin Inhibitors vs. Inhibitors of Mammalian Target for Rapamycin in Pig Kidney Transplantation.

Background: The systemic inflammatory cascade triggered in donors after brain death enhances the ischemia-reperfusion injury after organ transplantation. Intravenous steroids are routinely used in the intensive care units for the donor preconditioning. Immunosuppressive medications could be potentially used for this purpose as well. Data regarding donor preconditioning with calcineurin inhibitors or inhibitors of mammalian target for Rapamycin is limited. The aim of this project is to investigate the effects of (oral) donor preconditioning with a calcineurin inhibitor (Cyclosporine) vs. an inhibitor of mammalian target for Rapamycin (Everolimus) compared to the conventional administration of steroid in the setting of donation after brain death in porcine renal transplantation. Methods: Six hours after the induction of brain death, German landrace donor pigs (33.2 ± 3.9 kg) were randomly preconditioned with either Cyclosporine (n = 9) or Everolimus (n = 9) administered via nasogastric tube with a repeated dose just before organ procurement. Control donors received intravenous Methylprednisolone (n = 8). Kidneys were procured, cold-stored in Histidine-Tryptophane-Ketoglutarate solution at 4°C and transplanted in nephrectomized recipients after a mean cold ischemia time of 18 h. No post-transplant immunosuppression was given to avoid confounding bias. Blood samples were obtained at 4 h post reperfusion and daily until postoperative day 5 for complete blood count, blood urea nitrogen, creatinine, and electrolytes. Graft protocol biopsies were performed 4 h after reperfusion to assess early histological and immunohistochemical changes. Results: There was no difference in the hemodynamic parameters, hemoglobin/hematocrit and electrolytes between the groups. Serum blood urea nitrogen and creatinine peaked on postoperative day 1 in all groups and went back to the preoperative levels at the conclusion of the study on postoperative day 5. Histological assessment of the kidney grafts revealed no significant differences between the groups. TNF-α expression was significantly lower in the study groups compared with Methylprednisolone group (p = 0.01) Immunohistochemistry staining for cytochrome c showed no difference between the groups. Conclusion: Oral preconditioning with Cyclosporine or Everolimus is feasible in donation after brain death pig kidney transplantation and reduces the expression of TNF-α. Future studies are needed to further delineate the role of oral donor preconditioning against ischemia-reperfusion injury.

Detection of spreading depolarizations in a middle cerebral artery occlusion model in swine.

BACKGROUND: The main objective of this study was to generate a hemodynamically stable swine model to detect spreading depolarizations (SDs) using electrocorticography (ECoG) and intrinsic optical signal (IOS) imaging and laser speckle flowmetry (LSF) after a 30-h middle cerebral artery (MCA) occlusion (MCAo) in German Landrace Swine. METHODS: A total of 21 swine were used. The study comprised a training group (group 1, n = 7), a group that underwent bilateral craniectomy and MCAo (group 2, n = 10) and a group used for 2,3,5-triphenyltetrazolium (TTC) staining (group 3, n = 5). RESULTS: In group 2, nine animals that underwent MCAo survived for 30 h, and one animal survived for 12 h. We detected MCA variants with 2 to 4 vessels. In all cases, all of the MCAs were occluded. The intensity changes exhibited by IOS and LSF after clipping were closely correlated and indicated a lower blood volume and reduced blood flow in the middle cerebral artery territory. Using IOS, we detected a mean of 2.37 ± (STD) 2.35 SDs/h. Using ECoG, we detected a mean of 0.29 ± (STD) 0.53 SDs/h. Infarctions were diagnosed using histological analysis. TTC staining in group 3 confirmed that the MCA territory was compromised and that the anterior and posterior cerebral arteries were preserved. CONCLUSIONS: We confirm the reliability of performing live monitoring of cerebral infarctions using our MCAo protocol to detect SDs.

Lasting s-ketamine block of spreading depolarizations in subarachnoid hemorrhage: a retrospective cohort study.

OBJECTIVE: Spreading depolarizations (SD) are characterized by breakdown of transmembrane ion gradients and excitotoxicity. Experimentally, N-methyl-D-aspartate receptor (NMDAR) antagonists block a majority of SDs. In many hospitals, the NMDAR antagonist s-ketamine and the GABAA agonist midazolam represent the current second-line combination treatment to sedate patients with devastating cerebral injuries. A pressing clinical question is whether this option should become first-line in sedation-requiring individuals in whom SDs are detected, yet the s-ketamine dose necessary to adequately inhibit SDs is unknown. Moreover, use-dependent tolerance could be a problem for SD inhibition in the clinic. METHODS: We performed a retrospective cohort study of 66 patients with aneurysmal subarachnoid hemorrhage (aSAH) from a prospectively collected database. Thirty-three of 66 patients received s-ketamine during electrocorticographic neuromonitoring of SDs in neurointensive care. The decision to give s-ketamine was dependent on the need for stronger sedation, so it was expected that patients receiving s-ketamine would have a worse clinical outcome. RESULTS: S-ketamine application started 4.2 ± 3.5 days after aSAH. The mean dose was 2.8 ± 1.4 mg/kg body weight (BW)/h and thus higher than the dose recommended for sedation. First, patients were divided according to whether they received s-ketamine at any time or not. No significant difference in SD counts was found between groups (negative binomial model using the SD count per patient as outcome variable, p = 0.288). This most likely resulted from the fact that 368 SDs had already occurred in the s-ketamine group before s-ketamine was given. However, in patients receiving s-ketamine, we found a significant decrease in SD incidence when s-ketamine was started (Poisson model with a random intercept for patient, coefficient - 1.83 (95% confidence intervals - 2.17; - 1.50), p < 0.001; logistic regression model, odds ratio (OR) 0.13 (0.08; 0.19), p < 0.001). Thereafter, data was further divided into low-dose (0.1-2.0 mg/kg BW/h) and high-dose (2.1-7.0 mg/kg/h) segments. High-dose s-ketamine resulted in further significant decrease in SD incidence (Poisson model, - 1.10 (- 1.71; - 0.49), p < 0.001; logistic regression model, OR 0.33 (0.17; 0.63), p < 0.001). There was little evidence of SD tolerance to long-term s-ketamine sedation through 5 days. CONCLUSIONS: These results provide a foundation for a multicenter, neuromonitoring-guided, proof-of-concept trial of ketamine and midazolam as a first-line sedative regime.

Large field-of-view movement-compensated intrinsic optical signal imaging for the characterization of the haemodynamic response to spreading depolarizations in large gyrencephalic brains.

Haemodynamic responses to spreading depolarizations (SDs) have an important role during the development of secondary brain damage. Characterization of the haemodynamic responses in larger brains, however, is difficult due to movement artefacts. Intrinsic optical signal (IOS) imaging, laser speckle flowmetry (LSF) and electrocorticography were performed in different configurations in three groups of in total 18 swine. SDs were elicited by topical application of KCl or occurred spontaneously after middle cerebral artery occlusion. Movement artefacts in IOS were compensated by an elastic registration algorithm during post-processing. Using movement-compensated IOS, we were able to differentiate between four components of optical changes, corresponding closely with haemodynamic variations measured by LSF. Compared with ECoG and LSF, our setup provides higher spatial and temporal resolution, as well as a better signal-to-noise ratio. Using IOS alone, we could identify the different zones of infarction in a large gyrencephalic middle cerebral artery occlusion pig model. We strongly suggest movement-compensated IOS for the investigation of the role of haemodynamic responses to SDs during the development of secondary brain damage and in particular to examine the effect of potential therapeutic interventions in gyrencephalic brains.

Perihemorrhagic ischemia occurs in a volume-dependent manner as assessed by multimodal cerebral monitoring in a porcine model of intracerebral hemorrhage.

BACKGROUND: Changes in the perihemorrhagic zone (PHZ) of intracerebral hemorrhage (ICH) are variable. Different mechanisms contribute to secondary neuronal injury after ICH. This multimodal monitoring study investigated early changes in the PHZ of ICH. METHODS: Twenty-four swine were anesthetized, ventilated, and underwent monitoring of vital parameters. Next to an intracranial pressure-probe (ICP), microdialysis (MD), thermodiffusion cerebral blood flow (td-CBF), and oxygen probes (PbrO2) were placed into the gray white matter junction for 12 h of monitoring. ICH was induced using the autologous blood injection model. Pre-defined volumes were 0 ml (sham), 1.5 ml ipsilateral (1.5 ml), 3.0 ml ipsilateral (3.0 ml), and 3.0 ml contralateral (3.0 ml contra). RESULTS: ICP equally increased in all groups after ICH. In the 3.0 ml group tissue oxygenation decreased to ischemic values of 9 ± 7 mmHg early after 6 h of monitoring. This decrease was associated with a significant perfusion reduction from 36 ± 8 ml/100 g/min to 20 ± 10 ml/100 g/min. MD correlated with a threefold lactate/pyruvate ratio increase. Measurements in all other groups were unchanged. CONCLUSION: Multimodal monitoring demonstrates volume-dependent changes of tissue oxygenation, blood flow, and ischemic MD markers in the PHZ independent of increased ICP suggesting early moderate ischemia. No evidence was found for the existence of a perihemorrhagic ischemia in the small hematoma groups.

Decompressive craniectomy in patients with aneurysmal subarachnoid hemorrhage: a single-center matched-pair analysis.

BACKGROUND: The role of decompressive craniectomy (DC) in aneurysmal subarachnoid hemorrhage (aSAH) patients is still controversial. In this study we evaluated the effect of DC for aSAH patients. METHODS: A matched-pair analysis was performed to compare the outcomes of patients with DC to those of patients without DC. Among 295 consecutive aSAH patients, 56 required DC. Of the remaining group, 56 matched controls were found. The match was conducted on the basis of epidemiological and potential prognostic factors, such as age, gender, World Federation of Neurosurgical Societies (WFNS) grade, Fisher group and occurrence of vasospasm. RESULTS: Fifty-four of 56 (96.4%) patients with DC were dependent or dead at 1 month, compared with 49 of 56 (87.5%) without DC. There was no significant difference between the groups (p = 0.16). One-year outcomes were available for 108 patients (96.4%). Thirty-nine of 54 (72.2%) patients treated with DC were dependent or dead at 1 year, compared with 30 of 54 (55.6%) patients in the control group. There was no significant difference between the groups (p = 0.11). This result was unaffected by age, sex and WFNS grade. Subgroup analyses whether DC was performed primarily or delayed, and whether DC was performed due to spasm, hematoma or vessel occlusion failed to detect any significant difference. CONCLUSION: There was no significant advantage for patients treated with DC, but more than 25% achieved a good long-term outcome. While the value of DC is deemed uncertain, it may be effective for a very specific subset of aSAH patients. Further comparative studies are needed to resolve this matter.

Cortical spreading depression dynamics can be studied using intrinsic optical signal imaging in gyrencephalic animal cortex.

OBJECTIVE: The aim of this study was to co-record electrical changes using electrocorticography (ECoG) and blood volume changes using intrinsic optical signal (IOS) imaging during the induction, propagation, and termination of cortical spreading depolarizations (CSDs). METHODS: Anesthetized male swine were craniotomized and monitored over 16-20 h. A ten-contact electrode strip was placed on the cortex of one hemisphere for ECoG. An optical imaging recording was implemented using a camera with an optical bandpass filter (564 nm, FWHM:15 nm) and a full spectrum light source. CSDs were induced by mechanical and KCl stimulation. Co-occurrences of ECoG baseline shifts and blood volume changes around electrodes were identified. RESULTS: A mean of 3 CSDs per hour were induced, in a total of 4 swine during 80 h of recording. The propagation of the CSDs increased progressively over the monitoring time. IOS enabled us to clearly visualize the induction, propagation, and termination of CSDs with a spatial resolution within the sub-millimeter range. Every CSD recorded using ECoG could also be observed in IOS imaging, although some blood volume changes of CSDs were observed that terminated before reaching any of the ECoG electrodes. CONCLUSION: IOS imaging enables an in vivo evaluation of CSD dynamics over a large surface of gyrencephalic brain.

Intracranial pressure telemetry: first experience of an experimental in vivo study using a new device.

OBJECTIVE: To test two new telemetric intracranial pressure (ICP) probes (NEUROVENT(®)-P-tel, NEUROVENT(®)-S-tel) in a porcine model. We aimed to intraoperatively correlate the telemetric probes to parenchymal ICP probes and study their reliability in the first hours after implantation. The experimental set-up, new telemetric technology and first data will be presented. METHODS: We implanted a right parietal (parenchymal) and left parietal (subdural) telemetric ICP probe in 13 Göttingen mini-pigs under general anaesthesia. Through the left parietal burr hole a parenchymal ICP probe (Neurovent(®) ICP) was introduced. Intraoperatively, the head position was changed to provoke ICP changes every 10 min. The telemetric probes were left in situ and finally the parenchymal ICP probe was removed. We correlated mean differences between each telemetric probe and the conventional ICP measurement and Bland-Altman plots were generated for statistical analysis. RESULTS: We present first data containing intraoperative measurements of 26 telemetric probes after implantation. Intraoperatively, mean differences of 2.48 ± 1.52 mmHg SD (NEUROVENT(®)-P-tel) and 2.64 ± 1.79 mmHg (NEUROVENT(®)-S-tel) were observed. The Bland-Altman plot demonstrates good correlation of the telemetric probes compared with parenchymal ICP probes. CONCLUSION: We present a new telemetric technology that was experimentally compared with a parenchymal ICP probe. We provide data that the new telemetric probes will comparably measure ICP vs an external ICP probe. This stand-alone ICP tool may allow permanent measurement of ICP in hydrocephalus patients. Further continuation of our study will demonstrate whether this system guarantees acceptable long-term reliability.

Pressure reactivity index correlates with metabolic dysfunction in a porcine model of intracerebral hemorrhage.

OBJECTIVE: We correlated oxygen, flow, and pressure indices of cerebrovascular reactivity (CR) with extracellular cerebral metabolite concentrations in a porcine model of intracerebral hemorrhage (ICH). METHODS: Continuous advanced multimodal monitoring including microdialysis, cerebral blood flow and P(br)O(2) probes were placed 1 cm in front of the coronal suture in the grey/white matter junction. Following a period of 1 h of monitoring, an autologous arterial ICH with defined volumes (3 mL) was induced. Pressure-, oxygen-, and flow-related autoregulation indices (PRx, ORx, and FRx) were simultaneously calculated and correlated hourly with extracellular cerebral metabolites, including glucose, lactate, pyruvate, and glutamate. RESULTS: Seventeen swine were monitored on average 12 continuous hours per animal. FRx correlated highly with ORx (0.96, P = <0.001), but values of both FRx and ORx > 0.2 did not correlate with any microdialysis metabolite. Values of PRx > 0.2 correlated highly (0.65, P < 0.001) with the lactate/pyruvate ratio, values of PRx > 0.3 correlated with glutamate (0.67, P < 0.05), the lactate/pyruvate ratio (0.60, P < 0.01), and P(br)O(2) (-0.65, P < 0.01). CONCLUSIONS: We found evidence for impaired CR in a porcine model of ICH. The findings suggest that, among other parameters of CR, positive PRx coefficients have the highest significance and could be associated with microdialysis alterations during hypoxic events.

Evidence of spreading depolarizations in a porcine cortical intracerebral hemorrhage model.

OBJECTIVES: To evaluate whether cortical spreading depolarizations (CSD) occur in the early stage after cortical intracerebral hemorrhage (ICH). METHODS: Ten anesthetized male swine were examined over 19 h. Two cerebral probes were inserted around the ICH (microdialysis and thermodiffusion cerebral blood flow), ICP was monitored contralaterally and up to two electrocorticographic grid electrodes were positioned over the hemisphere after hemicraniectomy and dural opening. A right frontal autologous, arterial ICH (3.0 mL) was induced in all the animals studied. RESULTS: Using a modified injection technique an 80% success rate in ICH formation could be achieved. Eight animals with cortical ICH could be analyzed finally. After induction of ICH, ICP increased non-significantly. Overall, six out of eight animals had CSDs, of either single type or clusters. In one animal a CSD occurred as early as 2 h after ICH; in all other animals the first CSD did not occur before 5 h after onset. CONCLUSION: CSD's occur in cortical experimental ICH. As ICP remained stable owing to the hemicraniectomy we cannot argue in favor of ICP-related triggering of CSD. Modifications of the experimental setup avoiding hemicraniectomy may better describe the pathophysiology of CSD related to ICH in future studies.

Low-frequency sampling for PRx calculation does not reduce prognostication and produces similar CPPopt in intracerebral haemorrhage patients.

BACKGROUND: The cerebral pressure reactivity index (PRx) correlates with the outcome in intracerebral haemorrhage (ICH) patients and has been used to define an autoregulation-oriented "optimal cerebral perfusion pressure" (CPPopt). PRx has been calculated as a moving correlation coefficient between mean arterial pressure (MAP) and intracranial pressure (ICP) averaged over 5-10 s, using a 2.5- to 5-min moving time window, in order to reflect changes in MAP and ICP within a time frame of 20 s to 2 min. We compared PRx with a different calculation method [low-frequency PRx (L-PRx)], where rapid fluctuations of MAP and ICP are cancelled (waves with frequencies greater than 0.01 Hz). METHODS: A total of 548.5 h of artefact-free data (sampling frequency 1 Hz) from 18 patients suffering from non-traumatic ICH were included in the analysis. L-PRx was calculated using minute averages, between both MAP and ICP, in 20-min moving correlation windows. CPPopt was calculated based on PRx and on L-PRx. RESULTS: The averaged PRx values for each patient correlated with L-PRx (P = 0.846, p < 0.001). CPPopt based on standard PRx was identified in eight patients. In contrast, a CPPopt value based on L-PRx could be found in 12 patients. CPPopt values by both methods correlated strongly with each other (P = 0.980, p < 0.001). L-PRx had a similar correlation with the National Institutes of Health Stroke Scale Score (NIHSS) (0.667, p = 0.002) as did PRx (0.563, p = 0.015). CONCLUSIONS: L-PRx correlated with the outcome as good as PRx did. CPPopt could be identified in more patients using L-PRx. Slower MAP and ICP changes (in the range of 1-20 min) can be used for autoregulation assessment and contain important prognostic information.

Evaluation of a novel brain tissue oxygenation probe in an experimental swine model.

BACKGROUND: Cerebral microdialysis, cerebral blood flow, and cerebral oxygenation (PbrO2) measurements using intraparenchymal probes are widely accepted as invasive diagnostic monitoring for early detection of secondary ischemia. OBJECTIVE: To evaluate a novel PbrO2 probe for continuous and quantitative oxygenation assessment compared with the existing gold standard PbrO2 probe. METHODS: In 9 pigs, 2 PbrO2 probes (Neurovent-TO vs Licox) were implanted into the subcortical white matter. An intracranial pressure probe was inserted contralaterally. The PbrO2 probes were tested during (1) baseline measurements followed by (2) hyperoxygenation (fraction of inspired oxygen [Fio2]=1.0), medically induced (3) hypo- and (4) hypertension, (5) hyperventilation, (6) tris-hydroxymethylaminomethane application, and (7) hypoxygenation (Fio2<0.05). For statistical analyses, Bland-Altman plots were used. RESULTS: The Neurovent-TO probe is easy to handle and does not need a specific storage or calibration. Bland-Altman analyses revealed good comparability of both technologies under baseline conditions (meandiff 2.09 mm Hg, standard deviation 0.04 mm Hg, range 1.98-2.20 mm Hg), but measurement dynamics during hyperoxygenation (Fio2=1.0) revealed significantly different profiles, eg Neurovent-TO probe reached up to 1.53-fold higher PbrO2 values than the Licox probe. During hypoxygenation (Fio2<0.05), the Neurovent-TO probe detected the hypoxic level of 8.5 mm Hg 1.5 minutes earlier than did the Licox probe. All other maneuvers showed similar responses in both technologies. CONCLUSION: The Neurovent-TO PbrO2 device comparably measures PbrO2 under most conditions tested compared with the Licox device. The Neurovent-TO is more sensitive to rapid Fio2 changes. Further studies are necessary to clarify these differences. It is questionable whether existing knowledge of Licox tissue oxygenation, ie, hypoxic threshold, can be directly transferred to the Neurovent-TO.