{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T07:16:35Z","timestamp":1791357395818,"version":"4.3.1"},"reference-count":18,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1995,6]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            \u201cCrack\u201d cocaine (alkaloidal cocaine) induces ischemic stroke. However, the mechanisms by which this occurs are not well documented in humans. We present pertinent information on three patients whose ischemic strokes involved the territory of the internal carotid artery and were associated with crack use.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Case Descriptions<\/jats:italic>\n            These patients were investigated clinically, radiologically, intraoperatively, and\/or histopathologically at the same institution, and the diagnostic evaluations did not reveal a definite cardiac or hematologic cause for stroke. Large filling defects were noted on conventional carotid angiography in two of these patients; in the third patient, the histopathological changes were compatible with vasospasm. To our knowledge, these changes have not been previously documented in human arteries.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            We suggest that some brain infarcts among crack cocaine users may result from vasospasm of large arteries and secondary intravascular thrombosis.\n          <\/jats:p>","DOI":"10.1161\/01.str.26.6.1114","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"1114-1118","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":105,"title":["Vasospasm and Thrombus Formation as Possible Mechanisms of Stroke Related to Alkaloidal Cocaine"],"prefix":"10.1161","volume":"26","author":[{"given":"Jon P.","family":"Konzen","sequence":"first","affiliation":[{"name":"From the Center for Stroke Research, Departments of Neurology (J.P.K., S.R.L.) and Pathology (Neuropathology) (J.H.G.), Henry Ford Hospital and Health Sciences Center, Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven R.","family":"Levine","sequence":"additional","affiliation":[{"name":"From the Center for Stroke Research, Departments of Neurology (J.P.K., S.R.L.) and Pathology (Neuropathology) (J.H.G.), Henry Ford Hospital and Health Sciences Center, Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julio H.","family":"Garcia","sequence":"additional","affiliation":[{"name":"From the Center for Stroke Research, Departments of Neurology (J.P.K., S.R.L.) and Pathology (Neuropathology) (J.H.G.), Henry Ford Hospital and Health Sciences Center, Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"669","volume":"323","year":"1990","unstructured":"Levine SR, Brust JCM, Futrell N, Ho K-L, Blake D, Millikan CH, Brass LB, Fayad P, Schultz LR, Selwa JF, Welch KMA. 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