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Abstract <p>The acute phase of ischemic stroke is accompanied by changesin the electrical activity of the cerebral cortex, reflecting thedynamics of pathophysiological processes in the damaged tissue.The first manifestation of ischemia is the early depression of activityassociated with a sharp suppression of synaptic transmission andan increase in the threshold of action potential generation. Further intensificationof metabolic crisis in cerebral tissue is marked by the emergenceof spreading depolarization (SD) waves—slow waves of massive depolarizationof neurons and glial cells, arising in the area of maximum metabolicdeficit and propagating to surrounding tissues. SD waves are themain pathological mechanism of the necrotic area expansion in ischemicstroke, which makes them the major target for therapeutic exposures.Moreover, SD initiates the development of a negative ultraslow potential(NUP), which represents a high-amplitude (up to –100 mV) shift inthe extracellular potential with an extremely slow dynamic. TheNUP arises only in the area of developing injury, and its amplitude correlateswith the size of the future ischemic focus. The mechanisms of NUPgeneration have not been fully studied to date. Although both SDand NUP are highly informative markers of cerebral ischemic injury,their extremely slow dynamics (frequency &lt; 0.01 Hz) makes themundetectable within the classical EEG range (0.5–45 Hz). This reviewaddresses the mechanisms underlying the early depression of electricalactivity, generation of ultraslow SD and NUP signals in focal stroke,their significance for diagnosis and monitoring of the ischemicprocess, as well as current therapeutic approaches to stroke management.</p>

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Ultraslow Signals in Stroke Diagnostics

  • 期刊论文

  • 发表日期：

    2025年1月1日

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  • D. E. Vinokurova

摘要

Abstract

The acute phase of ischemic stroke is accompanied by changesin the electrical activity of the cerebral cortex, reflecting thedynamics of pathophysiological processes in the damaged tissue.The first manifestation of ischemia is the early depression of activityassociated with a sharp suppression of synaptic transmission andan increase in the threshold of action potential generation. Further intensificationof metabolic crisis in cerebral tissue is marked by the emergenceof spreading depolarization (SD) waves—slow waves of massive depolarizationof neurons and glial cells, arising in the area of maximum metabolicdeficit and propagating to surrounding tissues. SD waves are themain pathological mechanism of the necrotic area expansion in ischemicstroke, which makes them the major target for therapeutic exposures.Moreover, SD initiates the development of a negative ultraslow potential(NUP), which represents a high-amplitude (up to –100 mV) shift inthe extracellular potential with an extremely slow dynamic. TheNUP arises only in the area of developing injury, and its amplitude correlateswith the size of the future ischemic focus. The mechanisms of NUPgeneration have not been fully studied to date. Although both SDand NUP are highly informative markers of cerebral ischemic injury,their extremely slow dynamics (frequency < 0.01 Hz) makes themundetectable within the classical EEG range (0.5–45 Hz). This reviewaddresses the mechanisms underlying the early depression of electricalactivity, generation of ultraslow SD and NUP signals in focal stroke,their significance for diagnosis and monitoring of the ischemicprocess, as well as current therapeutic approaches to stroke management.