{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T12:42:08Z","timestamp":1791031328468,"version":"4.1.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Background<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Cognitive dysfunction is a common and disabling sequela of subarachnoid hemorrhage (SAH). Although several clinical and radiographic findings have been implicated in the pathogenesis of cognitive dysfunction after SAH, few prospective studies have comprehensively and simultaneously evaluated these risk factors.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Methods<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Between July 1996 and March 2000, we prospectively evaluated 113 of 248 consecutively admitted nontraumatic SAH patients alive at 3 months with a comprehensive neuropsychological evaluation. Summary scores for 8 cognitive domains were calculated to express test performance relative to the entire study population. Clinical and radiographic variables associated with domain-specific cognitive dysfunction were identified with forward stepwise multiple regression, with control for the influence of demographic factors.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Results<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            The study participants were younger (\n            <jats:italic>P<\/jats:italic>\n            =0.005), less often white (\n            <jats:italic>P<\/jats:italic>\n            =0.006), and had better 3-month modified Rankin scores (\n            <jats:italic>P<\/jats:italic>\n            =0.001) than those who did not undergo neuropsychological testing. The proportion of subjects who scored in the impaired range (&gt;2 SD below the normative mean) on each neuropsychological test ranged from 10% to 50%. Predictors of cognitive dysfunction in 2 or more domains in the multivariate analysis included global cerebral edema (4 domains), left-sided infarction (3 domains), and lack of a posterior circulation aneurysm (2 domains). Other variables consistently associated with cognitive dysfunction in the univariate analysis included admission Hunt-Hess grade &gt;2 and thick SAH in the anterior interhemispheric and sylvian fissures.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Conclusions<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Global cerebral edema and left-sided infarction are important risk factors for cognitive dysfunction after SAH. Treatment strategies aimed at reducing neurological injury related to generalized brain swelling, infarction, and clot-related hemotoxicity hold the best promise for improving cognitive outcomes after SAH.\n          <\/jats:p>","DOI":"10.1161\/hs0102.101080","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T23:16:47Z","timestamp":1027898207000},"page":"200-209","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":245,"title":["Predictors of Cognitive Dysfunction After Subarachnoid Hemorrhage"],"prefix":"10.1161","volume":"33","author":[{"given":"Kurt T.","family":"Kreiter","sequence":"first","affiliation":[{"name":"From the Departments of Neurology (K.T.K., D.C., G.L.B., J.E.B., S.P., J.C., Y.S., S.A.M) and Neurosurgery (E.S.C., S.A.M.), College of Physicians and Surgeons, the Gertrude H. Sergievsky Center (Y.S.), and the School of Public Health (Y.E.D.), Columbia University, New York, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daphne","family":"Copeland","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (K.T.K., D.C., G.L.B., J.E.B., S.P., J.C., Y.S., S.A.M) and Neurosurgery (E.S.C., S.A.M.), College of Physicians and Surgeons, the Gertrude H. Sergievsky Center (Y.S.), and the School of Public Health (Y.E.D.), Columbia University, New York, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary L.","family":"Bernardini","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (K.T.K., D.C., G.L.B., J.E.B., S.P., J.C., Y.S., S.A.M) and Neurosurgery (E.S.C., S.A.M.), College of Physicians and Surgeons, the Gertrude H. Sergievsky Center (Y.S.), and the School of Public Health (Y.E.D.), Columbia University, New York, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph E.","family":"Bates","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (K.T.K., D.C., G.L.B., J.E.B., S.P., J.C., Y.S., S.A.M) and Neurosurgery (E.S.C., S.A.M.), College of Physicians and Surgeons, the Gertrude H. Sergievsky Center (Y.S.), and the School of Public Health (Y.E.D.), Columbia University, New York, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shelley","family":"Peery","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (K.T.K., D.C., G.L.B., J.E.B., S.P., J.C., Y.S., S.A.M) and Neurosurgery (E.S.C., S.A.M.), College of Physicians and Surgeons, the Gertrude H. 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