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Cerebral autoregulation, spreading depolarization, and implications for targeted therapy in brain injury and ischemia

  • Andrew P. Carlson ORCID logo EMAIL logo , Andrew R. Mayer , Chad Cole , Harm J. van der Horn , Joshua Marquez , Taylor C. Stevenson ORCID logo and C. William Shuttleworth
Published/Copyright: April 8, 2024

Abstract

Cerebral autoregulation is an intrinsic myogenic response of cerebral vasculature that allows for preservation of stable cerebral blood flow levels in response to changing systemic blood pressure. It is effective across a broad range of blood pressure levels through precapillary vasoconstriction and dilation. Autoregulation is difficult to directly measure and methods to indirectly ascertain cerebral autoregulation status inherently require certain assumptions. Patients with impaired cerebral autoregulation may be at risk of brain ischemia. One of the central mechanisms of ischemia in patients with metabolically compromised states is likely the triggering of spreading depolarization (SD) events and ultimately, terminal (or anoxic) depolarization. Cerebral autoregulation and SD are therefore linked when considering the risk of ischemia. In this scoping review, we will discuss the range of methods to measure cerebral autoregulation, their theoretical strengths and weaknesses, and the available clinical evidence to support their utility. We will then discuss the emerging link between impaired cerebral autoregulation and the occurrence of SD events. Such an approach offers the opportunity to better understand an individual patient’s physiology and provide targeted treatments.


Corresponding author: Andrew P. Carlson, Department of Neurosurgery, University of New Mexico School of Medicine, MSC10 5615, 1 UNM, Albuquerque, NM, 87131, USA; and Department of Neurosciences, University of New Mexico School of Medicine, 915 Camino de Salud NE, Albuquerque, NM, 87106, USA, E-mail:

Award Identifier / Grant number: R01 NS128006 (Carlson)

Funding source: National Institutes of General Medical Sciences

Award Identifier / Grant number: P20 GM109089 (Shuttleworth)

  1. Research ethics: Not Applicable.

  2. Author contributions: The authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  3. Competing interests: All other authors state no conflict of interest.

  4. Research funding: This work was supported by the National Institutes of Health R01 NS128006 (Carlson), P20 GM109089 (Shuttleworth).

  5. Data availability: Not applicable.

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Received: 2024-02-22
Accepted: 2024-03-25
Published Online: 2024-04-08
Published in Print: 2024-08-27

© 2024 Walter de Gruyter GmbH, Berlin/Boston

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