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We hypothesize that prolonged oligemia, a consequence of cortical spreading depolarization (CSD) underlying migraine aura, may lead to ischemia\/hypoxia at hemodynamically vulnerable watershed zones fed by long penetrating arteries (PAs). For this, we subjected mice to KCl-triggered single or multiple CSDs. We found that post-CSD oligemia was significantly deeper at medial compared to lateral cortical areas, which induced ischemic\/hypoxic changes at watershed areas between the MCA\/ACA, PCA\/anterior choroidal and at the tip of superficial and deep PAs, as detected by histological and MRI examination of brains 2\u20134\u2009weeks after CSD. BALB-C mice, in which MCA occlusion causes large infarcts due to deficient collaterals, exhibited more profound CSD-induced oligemia and were more vulnerable compared to Swiss mice such that a single CSD was sufficient to induce ischemic lesions at the tip of PAs. In conclusion, CSD-induced prolonged oligemia has potential to cause ischemic\/hypoxic injury at hemodynamically vulnerable brain areas, which may be one of the mechanisms underlying WMLs located at the tip of medullary arteries seen in MA patients.<\/jats:p>","DOI":"10.1177\/0271678x231186959","type":"journal-article","created":{"date-parts":[[2023,7,12]],"date-time":"2023-07-12T05:08:56Z","timestamp":1689138536000},"page":"1951-1966","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":14,"title":["Cortical spreading depolarization-induced constriction of penetrating arteries can cause watershed ischemia: A potential mechanism for white matter lesions"],"prefix":"10.1177","volume":"43","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2101-8061","authenticated-orcid":false,"given":"Buket","family":"D\u00f6nmez-Demir","sequence":"first","affiliation":[{"name":"Institute of Neurological Sciences and Psychiatry, 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