{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T14:42:14Z","timestamp":1777300934655,"version":"3.51.4"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2003,3]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background and Purpose\u2014<\/jats:italic>\n            <\/jats:bold>\n            The goals of this study were to investigate (1) whether the concentrations of choline, creatine, and\n            <jats:italic>N<\/jats:italic>\n            -acetyl aspartate (NAA) in cerebral white matter are changed in patients with symptomatic occlusion of the internal carotid artery (ICA) and (2) whether possible changes in metabolite concentration are related to regional cerebral perfusion or cerebral vasoreactivity.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods\u2014<\/jats:italic>\n            <\/jats:bold>\n            In 19 patients (mean\u00b1SD age, 60\u00b19 years), white matter metabolite concentrations were measured with proton MR spectroscopic imaging on average 4\u00b12 months after symptoms occurred. In selected voxels, corresponding cerebral blood flow and volume, mean transit time, and time-to-bolus peak were determined with dynamic susceptibility contrast MRI. Cerebral CO\n            <jats:sub>2<\/jats:sub>\n            reactivity was determined with transcranial Doppler sonography.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            No significant changes in choline and creatine concentrations were observed. NAA concentration was significantly reduced in the hemisphere on the side of the symptomatic ICA (9.1\u00b11.7 mmol\/L) compared with the contralateral hemisphere (10.5\u00b11.7 mmol\/L,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.005) and control subjects (10.5\u00b10.9 mmol\/L,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01). Although no significant interhemispheric difference in NAA concentration was found in patients who presented with retinal ischemia, patients with cerebral ischemia had a significantly lower NAA concentration in the symptomatic hemisphere (9.0\u00b11.7 mmol\/L) compared with the asymptomatic hemisphere (10.4\u00b11.6 mmol\/L,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). In all patients, NAA concentration was not significantly correlated with quantitative cerebral perfusion parameters or CO\n            <jats:sub>2<\/jats:sub>\n            reactivity.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions\u2014<\/jats:italic>\n            <\/jats:bold>\n            Patients with symptomatic ICA occlusion may show chronic neuronal damage in cerebral white matter as evidenced by reduced NAA concentration. This seems to be related to previous symptomatology rather than to the cerebral hemodynamic status in a chronic stage.\n          <\/jats:p>","DOI":"10.1161\/01.str.0000058158.41581.41","type":"journal-article","created":{"date-parts":[[2003,3,6]],"date-time":"2003-03-06T21:44:28Z","timestamp":1046987068000},"page":"648-652","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":16,"title":["Cerebral Hemodynamics and Metabolism in Patients With Symptomatic Occlusion of the Internal Carotid Artery"],"prefix":"10.1161","volume":"34","author":[{"given":"D.R.","family":"Rutgers","sequence":"first","affiliation":[{"name":"From the Department of Radiology (D.R.R., W.P.T.M.M., J. vd G.), Image Sciences Institute (M.J.P. v O.), and Department of Neurology (L.J.K.), University Medical Center Utrecht, Utrecht, the Netherlands."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.J.P.","family":"van Osch","sequence":"additional","affiliation":[{"name":"From the Department of Radiology (D.R.R., W.P.T.M.M., J. vd G.), Image Sciences Institute (M.J.P. v O.), and Department of Neurology (L.J.K.), University Medical Center Utrecht, Utrecht, the Netherlands."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.J.","family":"Kappelle","sequence":"additional","affiliation":[{"name":"From the Department of Radiology (D.R.R., W.P.T.M.M., J. vd G.), Image Sciences Institute (M.J.P. v O.), and Department of Neurology (L.J.K.), University Medical Center Utrecht, Utrecht, the Netherlands."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W.P.T.M.","family":"Mali","sequence":"additional","affiliation":[{"name":"From the Department of Radiology (D.R.R., W.P.T.M.M., J. vd G.), Image Sciences Institute (M.J.P. v O.), and Department of Neurology (L.J.K.), University Medical Center Utrecht, Utrecht, the Netherlands."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"van der Grond","sequence":"additional","affiliation":[{"name":"From the Department of Radiology (D.R.R., W.P.T.M.M., J. vd G.), Image Sciences Institute (M.J.P. v O.), and Department of Neurology (L.J.K.), University Medical Center Utrecht, Utrecht, the Netherlands."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1159\/000108851"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.28.10.2084"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.280.12.1055"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.31.12.3001"},{"key":"e_1_3_2_5_2","first-page":"1357","volume":"41","year":"2000","unstructured":"Tsuchida C, Kimura H, Sadato N, Tsuchida T, Tokuriki Y, Yonekura Y. 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