Intracranial pressure (ICP) monitoring and monitoring of brain tissue oxygenation (PbtO2) in addition to ICP have been used in the management of traumatic brain injury (TBI). However, the optimal monitoring method is inconclusive. We searched four databases with no language restrictions through January 2024 for peer-reviewed randomized controlled trials (RTCs) comparing ICP monitoring with combined Pbto2 and ICP monitoring in patients with TBI. A favorable neurological outcome was the primary outcome, and the secondary outcome was survival. Two reviewers screened manuscripts, extracted data, and assessed the risk of bias. We then performed a meta-analysis to assess efficacy using the Grading of Recommendations, Assessment, Development, and Evaluation working group approach. We included five trials comprising 522 patients. There was no difference in favorable neurological outcome (Risk Ratio [RR]: 1.16; 95% Confidence Interval [CI]: 0.98, 1.37; I2: 28%; 5 RCTs: 522 patients; moderate low certainty) and survival (RR: 1.10; 95% CI: 0.99, 1.21; I2: 13%; 5 RCTs: 522 patients; moderate low certainty). We found no evidence that the combination of Pbt2o and ICP is more useful than ICP. The included RCTs are few and small, and further study is needed to draw conclusions.

BACKGROUND: Continuous bedside monitoring of brain tissue oxygen levels is a crucial component in the management of comatose patients suffering from acute brain injury on neurointensive care units. Ensuring sufficient brain oxygenation is recognized as an essential objective within neurocritical care, aimed at safeguarding patients from secondary ischemia. Hypoperfusion in occipital and the posterior watershed regions often remains undetected, as the placement of probes in these areas is challenging. A major concern is that patients would have to lie on the traditionally used implanted bolts due to the occipital entry point of the probes. Therefore, we present a novel technique compatible with magnetic resonance imaging that enables bedside placement of brain tissue oxygen probes without the use of a bolt in these areas.
METHODS: We conducted bedside implantations of Licox brain tissue oxygenation probes through Frazier\'s point utilizing peripheral venous cannulas on burr holes eliminating the need for bolts.
RESULTS: A novel approach was successfully established for the bedside implantation of a Licox brain tissue oxygenation probe for occipital regions.
CONCLUSIONS: This technical note describes the feasibility of a novel, simple, and straightforward bedside technique for boltless implantation of Licox brain tissue oxygen probes leading to rigid fixation and compatibility with magnetic resonance imaging.

This study measured the relationship between pial collateral (leptomeningeal anastomoses, LMA) flow, intraparenchymal cortical cerebral blood flow (cCBF) and brain tissue oxygenation (btO2) during acute ischemic stroke to investigate how pial flow translates to downstream cCBF and btO2 and examined how this relationship is altered in hypertension. Proximal transient middle cerebral artery occlusion (tMCAO) was performed in male Wistar (n = 8/group) and Spontaneously Hypertensive Rats (SHR, n = 8/group). A combination laser Doppler-oxygen probe was placed within the expected cortical peri-infarct in addition to a surface laser doppler probe which measured LMA flow. Phenylephrine (PE) was infused 30 minutes into tMCAO to increase blood pressure (BP) by 30% for 10 minutes and assessed CBF autoregulation. During the initial 30-minute period of tMCAO, btO2 and cCBF were lower in SHR compared to Wistar rats (btO2: 11.5 ± 10.5 vs 17.5 ± 10.8 mmHg and cCBF: -29.7 ± 23.3% vs -17.8 ± 41.9%); however, LMA flow was similar between groups. The relationship between LMA flow, cCBF and btO2 were interdependent in Wistar rats. However, this relationship was disrupted in SHR rats and partially restored by induced hypertension. This study provides evidence that cCBF and btO2 were diminished during tMCAO in chronic hypertension, and that induced hypertension was beneficial regardless of hypertensive status.

OBJECTIVE: The clinical condition of a brain abscess is a potentially life-threatening disease. The combination of MRI-based imaging, surgical therapy and microbiological analysis is critical for the treatment and convalescence of the individual patient. The aim of this study was to evaluate brain tissue oxygenation measured with dynamic susceptibility contrast perfusion weighted imaging (DSC-PWI) in patients with brain abscess and its potential benefit for a better understanding of the environment in and around brain abscesses.
METHODS: Using a local database, 34 patients (with 45 abscesses) with brain abscesses treated between January 2013 and March 2021 were retrospectively included in this study. DSC-PWI imaging and microbiological work-up were key inclusion criteria. These data were analysed regarding a correlation between DSC-PWI and microbiological result by quantifying brain tissue oxygenation in the abscess itself, the abscess capsula and the surrounding oedema and by using six different parameters (CBF, CBV, CMRO2, COV, CTH and OEF).
RESULTS: Relative cerebral blood flow (0.335 [0.18-0.613] vs. 0.81 [0.49-1.08], p = 0.015), relative cerebral blood volume (0.44 [0.203-0.72] vs. 0.87 [0.67-1.2], p = 0.018) and regional cerebral metabolic rate for oxygen (0.37 [0.208-0.695] vs. 0.82 [0.55-1.19], p = 0.022) were significantly lower in the oedema around abscesses without microbiological evidence of a specific bacteria in comparison with microbiological positive lesions.
CONCLUSIONS: The results of this study indicate a relationship between brain tissue oxygenation status in DSC-PWI and microbiological/inflammatory status. These results may help to better understand the in vivo environment of brain abscesses and support future therapeutic decisions.

UNASSIGNED: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the CNS with a variety of clinical manifestations, including cerebral edema.
UNASSIGNED: A 7-year-old boy presented with headaches, nausea, and somnolence. He was found to have cerebral edema that progressed to brainstem herniation. Invasive multimodality neuromonitoring was initiated to guide management of intracranial hypertension and cerebral hypoxia while he received empiric therapies for neuroinflammation. Workup revealed serum myelin oligodendrocyte glycoprotein antibodies. He survived with a favorable neurologic outcome.
UNASSIGNED: We describe a child who presented with cerebral edema and was ultimately diagnosed with MOGAD. Much of his management was guided using data from invasive multimodality neuromonitoring. Invasive multimodality neuromonitoring may have utility in managing life-threatening cerebral edema due to neuroinflammation.

Localized increases in neuronal activity are supported by the hemodynamic response, which delivers oxygen to the brain tissue to support synaptic functions, action potentials and other neuronal processes. However, it remains unknown if changes in baseline neuronal activity, which are expected to reflect neuronal metabolic demand, alter the relationship between the local hemodynamic and oxygen behaviour. In order to better characterize this system, we examine here the relationship between brain tissue oxygen (PO2) and hemodynamic responses (BOLD functional MRI) under different levels of neuronal activity. By comparing the stimulus-evoked responses during different levels of baseline neuronal activity, the awake state vs isoflurane anesthesia, we were able to measure how a known change in neuronal demand affected tissue PO2 as well as the hemodynamic response to stimulation. We observed a high correlation between stimulus-evoked PO2 and BOLD responses in the awake state. Moreover, we found that the evoked PO2 and BOLD responses were still present despite the elevated tissue oxygen baseline and decreased baseline of neuronal activity under low concentration isoflurane, and that the magnitudes of these responses decreased by similar proportions but the relationship between these signals was distorted. Our findings point to distortion of the BOLD-PO2 relationship due to anesthesia. The feedback mechanism to adjust the level of brain tissue oxygen, as well as the correlation between BOLD and PO2 responses, are impaired even by a small dose of anesthetics.

The primary aim was to explore the concept of isolated and combined threshold-insults for brain tissue oxygenation (pbtO2) in relation to outcome in traumatic brain injury (TBI).
A total of 239 TBI patients with data on clinical outcome (GOS) and intracranial pressure (ICP) and pbtO2 monitoring for at least 12 h, who had been treated at the neurocritical care unit, Addenbrooke\'s Hospital, Cambridge, UK, between 2002 and 2022 were included. Outcome was dichotomised into favourable/unfavourable (GOS 4-5/1-3) and survival/mortality (GOS 2-5/1). PbtO2 was studied over the entire monitoring period. Thresholds were analysed in relation to outcome based on median and mean values, percentage of time and dose per hour below critical values and visualised as the combined insult intensity and duration.
Median pbtO2 was slightly, but not significantly, associated with outcome. A pbtO2 threshold at 25 and 20 mmHg, respectively, yielded the highest x2 when dichotomised for favourable/unfavourable outcome and mortality/survival in chi-square analyses. A higher dose and higher percentage of time spent with pbtO2 below 25 mmHg as well as lower thresholds were associated with unfavourable outcome, but not mortality. In a combined insult intensity and duration analysis, there was a transition from favourable towards unfavourable outcome when pbtO2 went below 25-30 mmHg for 30 min and similar transitions occurred for shorter durations when the intensity was higher. Although these insults were rare, pbtO2 under 15 mmHg was more strongly associated with unfavourable outcome if, concurrently, ICP was above 20 mmHg, cerebral perfusion pressure below 60 mmHg, or pressure reactivity index above 0.30 than if these variables were not deranged. In a multiple logistic regression, a higher percentage of monitoring time with pbtO2 < 15 mmHg was associated with a higher rate of unfavourable outcome.
Low pbtO2, under 25 mmHg and particularly below 15 mmHg, for longer durations and in combination with disturbances in global cerebral physiological variables were associated with poor outcome and may indicate detrimental ischaemic hypoxia. Prospective trials are needed to determine if pbtO2-directed therapy is beneficial, at what individualised pbtO2 threshold therapies are warranted, and how this may depend on the presence/absence of concurrent cerebral physiological disturbances.

BACKGROUND: Cerebral hypoxia is a frequent cause of secondary brain damage in patients with acute brain injury. Although hypercapnia can increase intracranial pressure, it may have beneficial effects on tissue oxygenation. We aimed to assess the effects of hypercapnia on brain tissue oxygenation (PbtO2).
METHODS: This single-center retrospective study (November 2014 to June 2022) included all patients admitted to the intensive care unit after acute brain injury who required multimodal monitoring, including PbtO2 monitoring, and who underwent induced moderate hypoventilation and hypercapnia according to the decision of the treating physician. Patients with imminent brain death were excluded. Responders to hypercapnia were defined as those with an increase of at least 20% in PbtO2 values when compared to their baseline levels.
RESULTS: On a total of 163 eligible patients, we identified 23 (14%) patients who underwent moderate hypoventilation (arterial partial pressure of carbon dioxide [PaCO2] from 44 [42-45] to 50 [49-53] mm Hg; p < 0.001) during the study period at a median of 6 (4-10) days following intensive care unit admission; six patients had traumatic brain injury, and 17 had subarachnoid hemorrhage. A significant overall increase in median PbtO2 values from baseline (21 [19-26] to 24 [22-26] mm Hg; p = 0.02) was observed. Eight (35%) patients were considered as responders, with a median increase of 7 (from 4 to 11) mm Hg of PbtO2, whereas nonresponders showed no changes (from - 1 to 2 mm Hg of PbtO2). Because of the small sample size, no variable independently associated with PbtO2 response was identified. No correlation between changes in PaCO2 and in PbtO2 was observed.
CONCLUSIONS: In this study, a heterogeneous response of PbtO2 to induced hypercapnia was observed but without any deleterious elevations of intracranial pressure.

The primary aim was to explore the association of global cerebral physiological variables including intracranial pressure (ICP), cerebrovascular reactivity (PRx), cerebral perfusion pressure (CPP), and deviation from the PRx-based optimal CPP value (∆CPPopt; actual CPP-CPPopt) in relation to brain tissue oxygenation (pbtO2) in traumatic brain injury (TBI).
A total of 425 TBI patients with ICP- and pbtO2 monitoring for at least 12 h, who had been treated at the neurocritical care unit, Addenbrooke\'s Hospital, Cambridge, UK, between 2002 and 2022 were included. Generalized additive models (GAMs) and linear mixed effect models were used to explore the association of ICP, PRx, CPP, and CPPopt in relation to pbtO2. PbtO2 < 20 mmHg, ICP > 20 mmHg, PRx > 0.30, CPP < 60 mmHg, and ∆CPPopt < - 5 mmHg were considered as cerebral insults.
PbtO2 < 20 mmHg occurred in median during 17% of the monitoring time and in less than 5% in combination with ICP > 20 mmHg, PRx > 0.30, CPP < 60 mmHg, or ∆CPPopt < - 5 mmHg. In GAM analyses, pbtO2 remained around 25 mmHg over a large range of ICP ([0;50] mmHg) and PRx [- 1;1], but deteriorated below 20 mmHg for extremely low CPP below 30 mmHg and ∆CPPopt below - 30 mmHg. In linear mixed effect models, ICP, CPP, PRx, and ∆CPPopt were significantly associated with pbtO2, but the fixed effects could only explain a very small extent of the pbtO2 variation.
PbtO2 below 20 mmHg was relatively frequent and often occurred in the absence of disturbances in ICP, PRx, CPP, and ∆CPPopt. There were significant, but weak associations between the global cerebral physiological variables and pbtO2, suggesting that hypoxic pbtO2 is often a complex and independent pathophysiological event. Thus, other variables may be more crucial to explain pbtO2 and, likewise, pbtO2 may not be a suitable outcome measure to determine whether global cerebral blood flow optimization such as CPPopt therapy is successful.

The cerebral oxygen cascade includes three key stages: (a) convective oxygen delivery representing the bulk flow of oxygen to the cerebral vascular bed; (b) diffusion of oxygen from the blood into brain tissue; and (c) cellular utilisation of oxygen for aerobic metabolism. All three stages may become dysfunctional after resuscitation from cardiac arrest and contribute to hypoxic-ischaemic brain injury (HIBI). Improving convective cerebral oxygen delivery by optimising cerebral blood flow has been widely investigated as a strategy to mitigate HIBI. However, clinical trials aimed at optimising convective oxygen delivery have yielded neutral results. Advances in the understanding of HIBI pathophysiology suggest that impairments in the stages of the oxygen cascade pertaining to oxygen diffusion and cellular utilisation of oxygen should also be considered in identifying therapeutic strategies for the clinical management of HIBI patients. Culprit mechanisms for these impairments may include a widening of the diffusion barrier due to peri-vascular oedema and mitochondrial dysfunction. An integrated approach encompassing both intra-parenchymal and non-invasive neuromonitoring techniques may aid in detecting pathophysiologic changes in the oxygen cascade and enable patient-specific management aimed at reducing the severity of HIBI.