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SD is increasingly recognized as a major cause of injury progression in stroke and brain trauma, where the mechanisms of SD\u2010induced neuronal injury are intimately linked to energetic status and metabolic impairment. Here, I review the established working model of SD initiation and propagation. Then, I summarize the historical and recent evidence for the metabolic impact of SD, transitioning from a descriptive to a mechanistic working model of metabolic signaling and its potential to promote neuronal survival and resilience. I quantify the energetic cost of restoring ionic gradients eroded during SD, and the extent to which ion pumping impacts high\u2010energy phosphate pools and the energy charge of affected tissue. I link energy deficits to adaptive increases in the utilization of glucose and O<jats:sub>2<\/jats:sub>, and the resulting accumulation of lactic acid and CO<jats:sub>2<\/jats:sub> downstream of catabolic metabolic activity. Finally, I discuss the neuromodulatory and vasoactive paracrine signaling mediated by adenosine and acidosis, highlighting these metabolites' potential to protect vulnerable tissue in the context of high\u2010frequency SD clusters.<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc15966-fig-0004-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p>","DOI":"10.1111\/jnc.15966","type":"journal-article","created":{"date-parts":[[2023,10,4]],"date-time":"2023-10-04T08:21:50Z","timestamp":1696407710000},"page":"868-887","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Spreading depolarizations pose critical energy challenges in acute brain 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