A systematic review on the assessment of cerebral autoregulation in patients with Large Vessel Occlusion

Abstract

As the majority of large vessel occlusion (LVO) patients are not treated with revascularization therapies or efficiently revascularized, complementary management strategies are needed. In this article we explore the importance of cerebral autoregulation (CA) assessment in the prediction and/or modification of infarct growth and hemorrhagic transformation. In patients with LVO, these are important factors that affect prognosis. A systematic search of the PubMed, EMBASE databases and a targeted Google search was conducted, resulting in the inclusion of 34 relevant articles. There is an agreement that CA is impaired in patients with LVO; several factors have been identified such as time course, revascularization status, laterality, disease subtype and location, some of which may be potentially modifiable and affect outcomes. The personalized CA assessment of these patients suggests potential for better understanding of the inter-individual variability. Further research is needed for the development of more accurate, noninvasive techniques for continuous monitoring and personalized thresholds for CA.

Keywords: acute ischemic stroke; cerebral autoregulation; cerebral blood flow; large vessel occlusion; mechanical thrombectomy.

Figure 1

Depiction of cerebral autoregulation processes: (A) Myogenic response adjusts arterial size based on transmural pressure via muscle activity. (B) Metabolic response modulates small artery size based on carbon dioxide (CO₂) levels from oxidative phosphorylation. (C) Endothelial response involves secretion of agents like nitric oxide and endothelin-1 that act on smooth muscle. (D) Neurogenic response involves neuroglial cells regulating vessel diameter through various vasoactive neurotransmitters. Reproduced with permission from the publisher Walters Kluwer Health, Inc., for the original article by Rivera-Lara et al. (2).

Figure 2

PRISMA diagram.

Figure 3

Analysis of Transfer Functions: This figure provides a visual interpretation of transfer function analysis using two sinusoidal waves with identical periods (T). The frequency (F) of these waveforms is determined as 1/T. (A) Illustrates Waveform 1 (W1), shown as a solid line, with its amplitude. (B) Depicts Waveform 2 (W2), indicated by a dashed line, and its amplitude. The concept of gain in this context refers to the reduction effect observed from W1 to W2, while the phase shift indicates the time lag between W1 and W2. In this scenario, W1 serves as the input and W2 as the output in the transfer function. The system’s controller reduces the amplitude of the input, resulting in a diminished amplitude (gain) in W2. The temporal displacement of W2 compared to W1 is depicted through the phase shift. Reproduced with permission from the publisher SAGE Publications for the original article by van Beek et al. (5).

Figure 4

Summary of factors affecting CA/Neurovascular coupling and monitoring in LVO. BP, Blood Pressure; CBF, Cerebral Blood Flow; CA, Cerebral Autoregulation; DCS, Diffuse Correlation Spectroscopy; ETC02, End-Tidal Carbon Dioxide; ICAD, Intracranial Atherosclerotic Disease; IVT, Intravenous Thrombolysis; LVO, large vessel occlusion; MMO, Moyamoyo Disease; MT, Mechanical Thrombectomy; NIRS, Near-Infrared Spectroscopy; PaCO2, Partial Pressure of Carbon Dioxide in Arterial Blood; TCD, Transcranial Doppler Ultrasound.