Sofie Dietvorst

Continuous real-time assessment of cerebral blood flow (CBF) and cerebrovascular autoregulation (CA) remains a major unmet clinical need in acute brain injury. Methods such as laser Doppler flowmetry (LDF), transcranial Doppler, or indirect indices lack accuracy and robustness. Functional ultrasound (fUS) is an emerging modality combining high spatiotemporal resolution, large field-of-view, and sensitivity to blood velocity and volume, making it a promising neuromonitoring tool. Piglets were equipped with arterial blood pressure (ABP), intracranial pressure (ICP), and LDF probes, plus cranial windows for fUS and red blood cell (RBC) flux imaging. CA was challenged by non-pharmacological ABP manipulation via intraaortic or intracaval balloon inflation. fUS hemodynamic parameters were compared with other modaliters across a CPP range of 10–150 mmHg. fUS provided continuous, stable intensity- and velocity-derived parameters across vessels types. CBF estimates correlated strongly with RBC flux and showed reproducibility comparable to LDF, with lower inter-animal variability. Autoregulation breakpoints were reliably identified by fUS, particularly the lower limit, while the upper limit was more variable. Parcellation confirmed robustness of fUS across brain regions. fUS images CBF and CA with higher stability and reproducibility than standard approaches, supporting its applicability for bedside neuromonitoring and clinical translation.

Cerebrovascular autoregulation (CA) is the ability to maintain adequate cerebral blood flow (CBF) over a wide range of arterial blood pressures (ABPs). Carbon dioxide (CO₂) is a potent vasodilator, but its precise influence on CA remains incompletely understood. A porcine cranial window model, in which CBF can be measured directly in the pial arterioles while ABP is mechanically manipulated, is used to investigate the effect of partial pressure of CO₂ in arterial blood (PaCO₂) on CA capacity. Hypercapnia and hypocapnia were induced in 12 male piglets each by adjusting the respiratory rate. Once stable PaCO₂ levels of 60 and 25 mm Hg, respectively, were achieved, ABP was gradually increased in half of the animals or decreased in the other half beyond limits of CA by inflating a balloon in the aorta or inferior vena cava. Before ABP manipulation, hypercapnia already induced significant vasodilation (+ 33.9%) and an increase in CBF (+ 20.5%), whereas hypocapnia did not alter diameter or CBF. Both hypercapnia and hypocapnia significantly reduced the ability to adjust arteriolar diameters in response to changes in ABP. During hypocapnia as well as hypercapnia, narrowing of the CA range with a shorter plateau between the upper and lower limit of autoregulation was observed, compared to normocapnia.

Introduction: Cerebrovascular autoregulation (CA) is the ability to maintain adequate cerebral blood flow (CBF) over a wide range of arterial blood pressure (ABP). Carbon dioxide (PaCO₂) is a potent vasodilator, but its precise influence on CA remains incompletely understood. Methods: A porcine cranial window model, in which CBF can be measured directly in the pial arterioles while ABP is mechanically manipulated, is used to investigate the effect of PaCO₂ on CA capacity. Hypercapnia and hypocapnia were induced in 12 male piglets each by adjusting the respiratory rate. Once stable PaCO₂ levels of resp 60 mmHg and 25 mmHg respectively were achieved, ABP was gradually increased in half of the animals or decreased in the other half beyond limits of CA by inflating a balloon in the aorta or inferior caval vein. Results: Before ABP manipulation, hypercapnia already induced a significant vasodilation (+33.9%) and increase in CBF (+20.5%) whereas hypocapnia did not alter diameter or CBF. Both hyper- and hypocapnia significantly reduced the ability to adjust arteriolar diameters in response to changes in ABP. Conclusion: During hypo- as well as hypercapnia, narrowing of the CA range with a shorter plateau between upper and lower limit of autoregulation was observed, compared to normocapnia.

Objective Due to evidence for proton beam therapy (PBT) in pediatric central nervous system (CNS) tumors, compact proton therapy systems became commercially available to allow better integration in a hospital setting. However, these systems have a non-zero magnetic field at the level of the patient. Often, these patients have a cerebrospinal fluid shunt, and most of them are adjustable through a magnet. Whether the induced magnetic fields could interfere with adjustable shunts is unknown. Methods In the first five CNS tumor patients with adjustable shunts who underwent PBT, the shunt setting was controlled before, during, and after treatment with PBT. Additionally, we used an ex vivo adjustable shunt to check if the settings could be altered by the magnetic field. Results We did not observe unintentional changes in shunt settings in vivo during treatment. In ex vivo testing, the shunt settings were altered directly cranial to the exit window of PBT due to the magnetic field. Conclusion Although we did not observe any shunt setting alteration during PBT in this small cohort, caution is warranted. Given the lack of high-volume data, there should be a low threshold for checking the shunt setting at the end of PBT therapy or in a symptomatic patient.

Purpose of review: Severe traumatic brain injury (TBI) remains the most prevalent neurological condition worldwide. Observational and interventional studies provide evidence to recommend monitoring of intracranial pressure (ICP) in all severe TBI patients. Existing guidelines focus on treating elevated ICP and optimizing cerebral perfusion pressure (CPP), according to fixed universal thresholds. However, both ICP and CPP, their target thresholds, and their interaction, need to be interpreted in a broader picture of cerebral autoregulation, the natural capacity to adjust cerebrovascular resistance to preserve cerebral blood flow in response to external stimuli. Recent findings: Cerebral autoregulation is often impaired in TBI patients, and monitoring cerebral autoregulation might be useful to develop personalized therapy rather than treatment of one size fits all thresholds and guidelines based on unidimensional static relationships. Summary: Today, there is no gold standard available to estimate cerebral autoregulation. Cerebral autoregulation can be triggered by performing a mean arterial pressure (MAP) challenge, in which MAP is increased by 10% for 20 min. The response of ICP (increase or decrease) will estimate the status of cerebral autoregulation and can steer therapy mainly concerning optimizing patient-specific CPP. The role of cerebral metabolic changes and its relationship to cerebral autoregulation is still unclear and awaits further investigation.