LAUSR

Brain tsunamis, or spreading depolarizations (SDs), are abrupt, massive, and self-propagating waves of depolarization in neurons and astrocytes that slowly travel across the brain’s gray matter and often lead to the depression of cortical activity. This phenomenon, and the association of the nearly complete breakdown of transmembrane ionic gradient with regional blood flow, were first described in the 1940s by the Brazilian physiologist, Aristides Leão [1, 2]. It took 40 years for the recognition of the potential implications of brain tsunamis in acute brain disorders [3], but it was only in the early 2000s that traction emerged among the scientific community, when early electrocorticographic recordings demonstrated their surprisingly frequent occurrence in the acutely injured human brain [4]. Slow, steady scientific progress has been made since the recognition of the direct current (DC) shift—the characteristic electrophysiologic signature of SD—as a physiologic phenomenon and not as a mere artifact from experiments. We now know so much more about neurovascular coupling, uncoupling, SD triggers and their modulation by medications, a distinct susceptibility of various brain regions, the metabolic toll, propagation behavior, and the interplay of these factors with age, sex, and nuances across different species. Thus far, our understanding of the link between the systemic circulation and SDs has been rather simplistic: drops in cerebral perfusion pressure resulting in global and/or focal ischemia usually precede, and thus have been thought to be triggers for, brain tsunamis [5]. Although SDs and their effects on cerebral hemodynamics and metabolism have been extensively studied using multimodal experimental paradigms [6], Han et al. [7] take a closer look on blood pressure and heart rate while anoxic depolarizations were happening, hence unveiling for the first time a potential systemic shockwave effect from brain tsunamis. The main hypothesis driving this study was that anoxic depolarizations—a subtype of transient SDs triggered by ischemia or anoxia [5], often in the setting of cardiac arrest—may have effects on the systemic circulation. Hence, the goal of this study was to analyze the peripheral downstream effects on blood pressure and heart rate from SDs in an established murine model of asphyxia-induced cardiac arrest. The investigators used well-accepted methods to study SD: two contiguous DC cortical electrodes to capture DC potential shift and electrocorticography in 14 animals (electrophysiologic monitoring only cohort) and laser speckle imaging and spatial frequency domain imaging via right parietal craniectomy in 10 animals (optical imaging plus electrophysiologic cohort). Optical imaging in the latter cohort also allowed for the concurrent characterization of cerebral blood flow, cerebral metabolic rate of oxygen consumption, and cerebral vascular resistance. Electrocorticography using alternating current electrodes was also employed in both cohorts, which allowed for the measurement of time to burst activity and burst suppression ratio. By virtue of using different DC cortical electrodes, the investigators were able to analyze delays on the detection of wave fronts between the electrodes, termed ΔSD1-2 period, which the authors interpreted as the period during which asynchronous SDs arose from different foci in the brain. The authors then took a deeper dive on what was going *Correspondence: [email protected] 1 Division of Neurocritical Care, Department of Neurology, McKnight Brain Institute, University of Florida College of Medicine, 1149 Newell Dr/ L3‐100, Gainesville, FL 32610, USA Full list of author information is available at the end of the article