Spreading depolarization in neurocritical care: a review of SD'S pathophysiological continuum and clinical translation.

Patients in neurocritical care are often vulnerable to secondary brain injury, wherein spreading depolarization (SD) is identified as a pivotal electrophysiological catalyst. This study consolidates current advancements in SD research, focusing on its clinical translation into neurointensive care. A primary emphasis is the revised and accurate terminology, differentiating the depolarization event (SD) from the concomitant electrophysiological suppression termed cortical spreading depression (CSD), a distinction crucial for interpreting both fundamental and clinical data. Notable advancements in non-invasive detection, especially using full-band scalp electroencephalography (EEG) enhanced by machine learning, currently attain sensitivities of over 85%, with the potential to broaden SD monitoring outside specialized facilities. The integration of SD data with multimodal parameters-such as cerebral microdialysis (which reveals distinctive glutamate surges and metabolic crises) and tissue oxygenation-provides a more comprehension understanding of the underlying pathophysiology. The review highlights dose-dependent treatment strategies, indicating that preliminary clinical studies suggest ketamine's effectiveness in suppressing SD may rely on maintenance dosages beyond approximately 1.15 mg/kg/h. These converging research fronts establish SD not merely as an epiphenomenon but as a dynamic, actionable biomarker for real-time precision management in brain injury.