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The ability to nondestructively assess cell invasion dynamically in a full 3D volume would improve the quality and quantity of information available from both in vivo and in vitro experiments. The purpose of this study was to observe glioma cell invasion in a 3D in vitro model using a microimaging protocol at 1.5 tesla and to assess the uptake of micron-sized particles of iron oxide (MPIO) and the consequent effects on cell function.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\n\u003Cjats:sec>\n\u003Cjats:title>Methods\u003C\u002Fjats:title>\n\u003Cjats:p>Rat C6 glioma cells were labeled with MPIO to a sufficient extent to allow single cell detection in vitro without significant effects on cell proliferation or plating efficiency. When placed on agar-coated plates, the cells formed stable multicellular tumor spheroids (MCTSs), which were embedded in collagen type I gel and serially visualized using magnetic resonance (MR) imaging and phase-contrast microscopy over 8 days. 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content-type=\"fine-print\">✓ Lymphocytic hypophysitis is a rare inflammatory disorder of the pituitary gland. Standard therapy consists of transsphenoidal resection or oral administration of corticosteroid medications. Two patients with symptomatic lymphocytic hypophysitis, which recurred after standard therapy, were treated with low-dose stereotactic radiotherapy. On imaging studies both lesions demonstrated a response to radiation and each patient experienced relief of symptoms. 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2001, Natural course of lymphocytic infundibuloneurohypophysitis., 20, 229",{},{"id":24,"text":794,"url":24,"identifiers":795},"Bitton, 1991, The course of lymphocytic hypophysitis., 36, 40",{},{"id":24,"text":797,"url":24,"identifiers":798},"Buxton, 2001, Lymphocytic and granulocytic hypophysitis: a single centre experience., 15, 242",{},{"id":24,"text":800,"url":24,"identifiers":801},"Cheung, 2001, The spectrum and significance of lymphocytic hypophysitis., 86, 1048",{},{"id":24,"text":803,"url":24,"identifiers":804},"Cosman, 1989, Lymphocytic hypophysitis. Report of 3 new cases and review of the literature., 68, 240",{},{"id":24,"text":806,"url":24,"identifiers":807},"Donaldson, 1980, Treatment of orbital pseudotumor (idiopathic orbital inflammation) by radiation therapy., 6, 79",{},{"id":24,"text":809,"url":24,"identifiers":810},"Feigenbaum, 1991, Lymphocytic adenohypophysitis: a pituitary mass lesion occurring in pregnancy., 164, 1549",{},{"id":24,"text":812,"url":24,"identifiers":813},"Fitzpatrick, 1984, Lymphoreticular tumors of the orbit., 10, 333",{},{"id":24,"text":815,"url":24,"identifiers":816},"Flanagan, 2002, Inflammatory hypophysitis—the spectrum of disease., 144, 47",{},{"id":24,"text":818,"url":24,"identifiers":819},"Goudie, 1962, Anterior hypophysitis and Hashimoto's disease in a young woman., 83, 584",{},{"id":24,"text":821,"url":24,"identifiers":822},"Harris, 1976, Visual complications following irradiation for pituitary adenomas and craniopharyngiomas., 120, 167",{},{"id":24,"text":824,"url":24,"identifiers":825},"Honegger, 1997, Lymphocytic and granulomatous hypophysitis: experience with nine cases., 40, 713",{},{"id":24,"text":827,"url":24,"identifiers":828},"Keleti, 1992, Radiotherapy of lymphoproliferative diseases of the orbit. Surveillance of 65 cases., 15, 422",{},{"id":24,"text":830,"url":24,"identifiers":831},"Kristof, 1999, Lymphocytic hypophysitis: noninvasive diagnosis and treatment by high dose methylprednisolone pulse therapy?, 67, 398",{},{"id":24,"text":833,"url":24,"identifiers":834},"Lanciano, 1990, The results of radiotherapy for orbital pseudotumor., 18, 407",{},{"id":24,"text":836,"url":24,"identifiers":837},"Lee, 1994, Lymphocytic hypophysitis: occurrence in two men., 34, 159",{},{"id":24,"text":839,"url":24,"identifiers":840},"Leksell, 1951\u002F1952, The stereotactic method and radiosurgery of the brain., 102, 316",{},{"id":24,"text":842,"url":24,"identifiers":843},"Mitsumori, 1998, Initial clinical results of linac-based stereotactic radiosurgery and stereotactic radiotherapy for pituitary adenomas., 42, 573",{},{"id":24,"text":845,"url":24,"identifiers":846},"Nussbaum, 1991, Lymphocytic hypophysitis with involvement of the cavernous sinus and hypothalamus., 28, 440",{},{"id":24,"text":848,"url":24,"identifiers":849},"Pestell, 1990, Lymphocytic hypophysitis. The clinical spectrum of the disorder and evidence for an autoimmune pathogenesis., 33, 457",{},{"id":24,"text":851,"url":24,"identifiers":852},"Prasad, 1991, Lymphocytic hypophysitis: can open exploration of the sella be avoided?, 5, 639",{},{"id":24,"text":854,"url":24,"identifiers":855},"Selch, 2002, Initial clinical results of stereotactic radiotherapy for the treatment of craniopharyngiomas., 1, 51",{},{"id":24,"text":857,"url":24,"identifiers":858},"Shrieve, 1994, Stereotactic radiotherapy: a technique for dose optimization and escalation for intracranial tumors., 62, 118, 10.1007\u002F978-3-7091-9371-6_25",{"doi":859},"10.1007\u002F978-3-7091-9371-6_25",{"id":24,"text":861,"url":24,"identifiers":862},"Thodou, 1995, Clinical case seminar: lymphocytic hypophysitis: clinicopathological findings., 80, 2302",{},{"id":24,"text":864,"url":24,"identifiers":865},"Tishler, 1993, Tolerance of the cranial nerves of the cavernous sinus to radiosurgery., 27, 215",{},{"id":24,"text":867,"url":24,"identifiers":868},"Tubridy, 2001, Infundibulohypophysitis in a man presenting with diabetes insipidus and cavernous sinus involvement., 71, 798",{},{"id":24,"text":870,"url":24,"identifiers":871},"Williams, 2002, Fractionated stereotactic radiotherapy for acoustic neuromas., 54, 500",{},{"id":873,"createTime":874,"updateTime":875,"relativeEntities":876,"slug":877,"properties":878,"entityType":261,"verifyStatus":23,"verifyTime":874,"verifyNote":895,"languages":896,"translateLanguages":897,"viewCount":25,"primaryUrl":899,"fullTextUrl":24,"authors":900,"publicationType":353,"publisherRelationship":958,"citationCount":1013,"citationInfo":1014,"publishDate":1024,"publishYear":1015,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1025,"openAccess":24,"references":1026,"isForceReanalyzing":572},"490fa07a-5996-4b83-89dd-7877fa1a629e","2024-07-19T04:49:56.510+00:00","2025-02-23T01:40:19.901+00:00",[],"The-International-Cooperative-Study-on-the-Timing-of-Aneurysm-Surgery",{"mag":879,"keywords":881,"openalex":883,"abstract":885,"title":888,"pm":891,"doi":893},{"VOID":880},"2729107688",{"VI":882},"",{"VOID":884},"W2729107688",{"EN":886,"VI":887},"\u003Cjats:p content-type=\"fine-print\">✓ A prospective, observational clinical trial was conducted by the International Cooperative Study on the Timing of Aneurysm Surgery to determine the best time in relation to the hemorrhage for surgical treatment of ruptured intracranial aneurysms. Sixty-eight centers contributed 3521 patients in a 2½-year period beginning in December, 1980. Analysis by a prespecified “planned” surgery interval demonstrated that there was no difference in early (0 to 3 days after the bleed) or late surgery (11 to 14 days). Outcome was worse if surgery was performed in the 7 to 10-day post-bleed interval. Surgical results were better for patients operated on after 10 days. Patients alert on admission fared best; however, alert patients had a mortality rate of 10% to 12% when undergoing surgery prior to Day 11 compared with 3% to 5% when surgery was performed after Day 10. Patients drowsy on admission had a 21% to 25% mortality rate when operated on up to Day 11 and 7% to 10% with surgery thereafter. Overall, early surgery was neither more hazardous nor beneficial than delayed surgery. The postoperative risk following early surgery is equivalent to the risk of rebleeding and vasospasm in patients waiting for delayed surgery.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Một thử nghiệm lâm sàng quan sát triển vọng đã được thực hiện bởi Nghiên cứu Hợp tác Quốc tế về Thời điểm Phẫu thuật Phình mạch nhằm xác định thời điểm tốt nhất liên quan đến xuất huyết để điều trị phẫu thuật phình mạch não bị vỡ. Sáu mươi tám trung tâm đã đóng góp 3521 bệnh nhân trong một khoảng thời gian 2½ năm bắt đầu từ tháng 12 năm 1980. Phân tích theo khoảng thời gian phẫu thuật \"đã lên kế hoạch\" đã chỉ ra rằng không có sự khác biệt nào giữa phẫu thuật sớm (0 đến 3 ngày sau khi xuất huyết) hoặc phẫu thuật muộn (11 đến 14 ngày). Kết quả xấu hơn nếu phẫu thuật được thực hiện trong khoảng thời gian từ 7 đến 10 ngày sau khi xuất huyết. Kết quả phẫu thuật tốt hơn cho các bệnh nhân được phẫu thuật sau 10 ngày. Các bệnh nhân tỉnh táo khi nhập viện có kết quả tốt nhất; tuy nhiên, bệnh nhân tỉnh táo có tỷ lệ tử vong từ 10% đến 12% khi trải qua phẫu thuật trước Ngày 11 so với 3% đến 5% khi phẫu thuật được thực hiện sau Ngày 10. Các bệnh nhân buồn ngủ khi nhập viện có tỷ lệ tử vong từ 21% đến 25% khi được phẫu thuật lên đến Ngày 11 và 7% đến 10% khi phẫu thuật diễn ra sau đó. Tổng thể, phẫu thuật sớm không nguy hiểm hơn và cũng không mang lại lợi ích nhiều hơn so với phẫu thuật trì hoãn. Nguy cơ sau phẫu thuật sau phẫu thuật sớm tương đương với nguy cơ tái chảy máu và co thắt mạch máu ở các bệnh nhân chờ phẫu thuật trì hoãn.\u003C\u002Fjats:p>",{"EN":889,"VI":890},"The International Cooperative Study on the Timing of Aneurysm Surgery","Nghiên cứu hợp tác quốc tế về thời điểm phẫu thuật phình mạch",{"VOID":892},"2191091",{"VOID":894},"10.3171\u002Fjns.1990.73.1.0037","Author affiliation is blank",[265],[898],"VI","https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F73\u002F1\u002Farticle-p37.xml",[901,918,929,940,949],{"id":902,"sortIndex":25,"researcher":24,"roles":903,"affiliations":904,"properties":913},"7d316cb4-6a18-4244-8bdf-19bc9cddcdc6",[],[905],{"id":906,"sortIndex":25,"affiliation":907,"properties":24},"6673a150-c0a6-4f06-980f-709772349004",{"id":906,"createTime":24,"updateTime":24,"relativeEntities":908,"slug":24,"properties":909,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":912,"statistic":24},[],{"title":910},{"VI":911},"Department of Neurological Surgery, University of Virginia Health Sciences Center, Charlottesville",[],{"title":914,"openalex":916},{"EN":915},"Neal F. Kassell",{"VOID":917},"A5078044974",{"id":919,"sortIndex":109,"researcher":24,"roles":920,"affiliations":921,"properties":922},"201da96a-7200-41a7-9fb4-36e750564231",[],[],{"orcid":923,"title":925,"openalex":927},{"VOID":924},"https:\u002F\u002Forcid.org\u002F0000-0003-1460-5572",{"EN":926},"James C. Torner",{"VOID":928},"A5103024292",{"id":930,"sortIndex":108,"researcher":24,"roles":931,"affiliations":932,"properties":933},"fec7c97b-4b58-41bb-a22d-0d81a92fd4d1",[],[],{"orcid":934,"title":936,"openalex":938},{"VOID":935},"https:\u002F\u002Forcid.org\u002F0000-0001-6900-1384",{"EN":937},"John C. Flíckinger",{"VOID":939},"A5040507938",{"id":941,"sortIndex":110,"researcher":24,"roles":942,"affiliations":943,"properties":944},"3633d0a4-9c0d-4d07-acea-c58706a85d85",[],[],{"title":945,"openalex":947},{"EN":946},"E. 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Adams",{"VOID":957},"A5017771451",{"url":24,"publisher":959,"properties":1006},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":960,"slug":10,"properties":961,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":966,"manageAffiliations":975,"indexDatabases":986,"url":91,"thumbnailPath":24,"statistic":1001,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":962,"eissn":963,"issn":964,"title":965},{"VOID":13},{"VOID":15},{"VOID":17},{"EN":19},[967,971],{"id":28,"createTime":24,"updateTime":24,"relativeEntities":968,"label":969,"description":970,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":31},{},{"id":34,"createTime":24,"updateTime":24,"relativeEntities":972,"label":973,"description":974,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":37},{},[976,981],{"id":41,"createTime":24,"updateTime":24,"relativeEntities":977,"slug":24,"properties":978,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":980,"statistic":24},[],{"title":979},{"EN":45},[],{"id":48,"createTime":24,"updateTime":24,"relativeEntities":982,"slug":24,"properties":983,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":985,"statistic":24},[],{"title":984},{"EN":52},[],[987,994],{"id":56,"indexDatabase":988,"url":69,"indexYears":24,"academicFieldIds":993,"indexDatabaseRanking":24},{"id":58,"createTime":24,"updateTime":24,"relativeEntities":989,"label":990,"description":991,"key":65,"publicationTags":992,"standard":24},[],{"EN":61,"VI":61},{"EN":63,"VI":64},[67,68],[71,72],{"id":74,"indexDatabase":995,"url":85,"indexYears":86,"academicFieldIds":1000,"indexDatabaseRanking":90},{"id":76,"createTime":24,"updateTime":24,"relativeEntities":996,"label":997,"description":998,"key":82,"publicationTags":999,"standard":24},[],{"EN":79,"VI":79},{"EN":79,"VI":81},[84],[88,89],{"impactFactor":25,"impactFactorByYear":1002,"i10Index":105,"i10IndexLast5Year":101,"totalPublication":106,"totalPublicationByYear":1003,"totalCitation":117,"totalCitationByYear":1004,"totalCitationPerPublication":180,"totalCitationPerPublicationByYear":1005,"hindexLast5Year":235,"hindex":235},{"2012":94,"2013":95,"2014":96,"2015":97,"2016":98,"2017":99,"2018":100,"2019":101,"2020":102,"2021":103,"2022":102,"2023":104},{"1944":108,"1945":109,"1946":109,"1950":109,"1953":109,"1958":110,"1960":109,"1962":110,"1964":111,"1965":110,"1966":108,"1967":109,"1968":110,"1969":101,"1972":112,"1973":109,"1974":108,"1975":110,"1976":110,"1977":112,"1978":108,"1979":108,"1980":111,"1981":111,"1982":111,"1983":110,"1984":112,"1985":111,"1986":110,"1987":110,"1988":111,"1989":104,"1990":101,"1991":113,"1992":101,"1993":104,"1994":112,"1995":110,"1996":104,"1997":114,"1998":115,"1999":101,"2000":115,"2001":104,"2002":114,"2003":116,"2004":113,"2005":111,"2006":112,"2007":113,"2008":101,"2009":101,"2010":112,"2011":111,"2012":101,"2013":101,"2014":111,"2015":112,"2016":101,"2018":109,"2019":109,"2020":111,"2022":109},{"1944":119,"1945":120,"1946":121,"1950":122,"1953":123,"1958":124,"1960":125,"1962":126,"1964":127,"1965":128,"1966":129,"1967":130,"1968":131,"1969":132,"1972":133,"1973":134,"1974":135,"1975":136,"1976":137,"1977":138,"1978":139,"1979":140,"1980":141,"1981":142,"1982":143,"1983":144,"1984":145,"1985":146,"1986":147,"1987":148,"1988":149,"1989":150,"1990":151,"1991":152,"1992":153,"1993":154,"1994":155,"1995":156,"1996":157,"1997":158,"1998":159,"1999":160,"2000":161,"2001":162,"2002":163,"2003":164,"2004":165,"2005":166,"2006":167,"2007":168,"2008":169,"2009":170,"2010":171,"2011":172,"2012":173,"2013":174,"2014":175,"2015":146,"2016":176,"2018":125,"2019":177,"2020":178,"2022":179},{"1944":182,"1945":120,"1946":121,"1950":122,"1953":123,"1958":183,"1960":125,"1962":184,"1964":185,"1965":186,"1966":187,"1967":130,"1968":188,"1969":189,"1972":190,"1973":134,"1974":191,"1975":192,"1976":193,"1977":194,"1978":195,"1979":196,"1980":197,"1981":198,"1982":199,"1983":200,"1984":201,"1985":202,"1986":203,"1987":204,"1988":205,"1989":206,"1990":207,"1991":208,"1992":209,"1993":210,"1994":211,"1995":212,"1996":213,"1997":214,"1998":215,"1999":216,"2000":217,"2001":218,"2002":219,"2003":220,"2004":221,"2005":222,"2006":223,"2007":224,"2008":225,"2009":226,"2010":227,"2011":228,"2012":229,"2013":230,"2014":231,"2015":232,"2016":233,"2018":125,"2019":177,"2020":234,"2022":179},{"issue":1007,"pages":1009,"volume":1011},{"VOID":1008},"1",{"VOID":1010},"37-47",{"VOID":1012},"73",908,{"total":1013,"publishYear":1015,"statisticByYear":1016},1990,{"2012":1017,"2013":1018,"2014":1019,"2015":1020,"2016":1021,"2017":122,"2018":122,"2019":1022,"2020":1021,"2021":179,"2022":1023,"2023":177,"2024":115},31,24,26,18,20,14,25,"1990-07-01",[67,90],[1027,1031,1035,1039,1043,1047,1050,1054,1057,1061,1065,1069,1073,107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1976, Intracranial aneurysms: analysis of results of microneurosurgery., 2, 607, 10.1136\u002Fbmj.2.6036.607",{"doi":1030},"10.1136\u002Fbmj.2.6036.607",{"id":24,"text":1032,"url":24,"identifiers":1033},"Adams, 1981, Early management of aneurysmal subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study., 54, 141, 10.3171\u002Fjns.1981.54.2.0141",{"doi":1034},"10.3171\u002Fjns.1981.54.2.0141",{"id":24,"text":1036,"url":24,"identifiers":1037},"Alvord, 1972, Subarachnoid hemorrhage due to ruptured aneurysms. A simple method of estimating prognosis., 27, 273, 10.1001\u002Farchneur.1972.00490160001001",{"doi":1038},"10.1001\u002Farchneur.1972.00490160001001",{"id":24,"text":1040,"url":24,"identifiers":1041},"Bohm, 1970, Results of surgical treatment of 200 consecutive cerebral arterial aneurysms., 46, 43, 10.1111\u002Fj.1600-0404.1970.tb05603.x",{"doi":1042},"10.1111\u002Fj.1600-0404.1970.tb05603.x",{"id":24,"text":1044,"url":24,"identifiers":1045},"Bolander, 1984, Retrospective analysis of 162 consecutive cases of ruptured intracranial aneurysms. Total mortality and early surgery., 70, 31, 10.1007\u002FBF01406040",{"doi":1046},"10.1007\u002FBF01406040",{"id":24,"text":1048,"url":24,"identifiers":1049},"Cox, 1972, Regression models and life-tables., 34, 187",{},{"id":24,"text":1051,"url":24,"identifiers":1052},"Dorsch, 1984, Surgery for cerebral aneurysms, an eight year experience., 141, 18, 10.5694\u002Fj.1326-5377.1984.tb132661.x",{"doi":1053},"10.5694\u002Fj.1326-5377.1984.tb132661.x",{"id":24,"text":1055,"url":24,"identifiers":1056},"Drake, 1976, Cerebral aneurysm surgery: an update, 289",{},{"id":24,"text":1058,"url":24,"identifiers":1059},"Drake, 1981, Management of cerebral aneurysm., 12, 273, 10.1161\u002F01.STR.12.3.273",{"doi":1060},"10.1161\u002F01.STR.12.3.273",{"id":24,"text":1062,"url":24,"identifiers":1063},"Fisher, 1980, Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning., 6, 1, 10.1227\u002F00006123-198001000-00001",{"doi":1064},"10.1227\u002F00006123-198001000-00001",{"id":24,"text":1066,"url":24,"identifiers":1067},"Fisher, 1977, Cerebral vasospasm with ruptured saccular aneurysm — the clinical manifestations., 1, 245, 10.1227\u002F00006123-197711000-00004",{"doi":1068},"10.1227\u002F00006123-197711000-00004",{"id":24,"text":1070,"url":24,"identifiers":1071},"Flamm, 1977, Parasurgical treatment of aneurysms., 24, 240, 10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.240",{"doi":1072},"10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.240",{"id":24,"text":1074,"url":24,"identifiers":1075},"Fleischer, 1980, Cerebral vasospasm following aneurysm rupture. A protocol for therapy and prophylaxis., 52, 149, 10.3171\u002Fjns.1980.52.2.0149",{"doi":1076},"10.3171\u002Fjns.1980.52.2.0149",{"id":24,"text":1078,"url":24,"identifiers":1079},"Graf, 1974, Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage. Report of a randomized treatment study. III. Intracranial surgery., 5, 559",{},{"id":24,"text":1081,"url":24,"identifiers":1082},"Hamby, 1970, Remarks concerning intracranial aneurysm surgery., 17, 1, 10.1093\u002Fneurosurgery\u002F17.CN_suppl_1.1",{"doi":1083},"10.1093\u002Fneurosurgery\u002F17.CN_suppl_1.1",{"id":24,"text":1085,"url":24,"identifiers":1086},"Hashi, 1982, Surgery in the prevasospastic interval., 63, 141, 10.1007\u002FBF01728866",{"doi":1087},"10.1007\u002FBF01728866",{"id":24,"text":1089,"url":24,"identifiers":1090},"Hollin, 1973, Effectiveness of microsurgery for intracranial aneurysms. Postoperative angiographic study of 50 cases., 39, 690, 10.3171\u002Fjns.1973.39.6.0690",{"doi":1091},"10.3171\u002Fjns.1973.39.6.0690",{"id":24,"text":1093,"url":24,"identifiers":1094},"Hunt, 1968, Surgical risk as related to time of intervention in the repair of intracranial aneurysms., 28, 14, 10.3171\u002Fjns.1968.28.1.0014",{"doi":1095},"10.3171\u002Fjns.1968.28.1.0014",{"id":24,"text":1097,"url":24,"identifiers":1098},"Hunt, 1974, Timing and perioperative care in intracranial aneurysm surgery., 21, 79, 10.1093\u002Fneurosurgery\u002F21.CN_suppl_1.79",{"doi":1099},"10.1093\u002Fneurosurgery\u002F21.CN_suppl_1.79",{"id":24,"text":1101,"url":24,"identifiers":1102},"Hunt, 1977, The results of early operation for aneurysm., 24, 208, 10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.208",{"doi":1103},"10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.208",{"id":24,"text":1105,"url":24,"identifiers":1106},"Jane, 1977, The natural history of intracranial aneurysms. Rebleeding rates during the acute and long-term period and implications for surgical management., 24, 176, 10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.176",{"doi":1107},"10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.176",{"id":24,"text":1109,"url":24,"identifiers":1110},"Jennett, 1975, Assessment of outcome after severe brain damage. A practical scale., 1, 480",{},{"id":24,"text":1112,"url":24,"identifiers":1113},"Kassell, 1981, Overall management of ruptured aneurysm: comparison of early and late operation., 9, 120, 10.1227\u002F00006123-198108000-00002",{"doi":1114},"10.1227\u002F00006123-198108000-00002",{"id":24,"text":1116,"url":24,"identifiers":1117},"Kassell, 1982, Timing of aneurysm surgery., 10, 514, 10.1227\u002F00006123-198204000-00019",{"doi":1118},"10.1227\u002F00006123-198204000-00019",{"id":24,"text":1120,"url":24,"identifiers":1121},"Kassell, 1990, The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results., 73, 000",{},{"id":24,"text":1123,"url":24,"identifiers":1124},"Koos, 1982, Timing of surgery for ruptured aneurysms — experience from 800 consecutive cases., 63, 125, 10.1007\u002FBF01728864",{"doi":1125},"10.1007\u002FBF01728864",{"id":24,"text":1127,"url":24,"identifiers":1128},"Ljunggren, 1981, Results of early operations for ruptured aneurysms., 54, 473, 10.3171\u002Fjns.1981.54.4.0473",{"doi":1129},"10.3171\u002Fjns.1981.54.4.0473",{"id":24,"text":1131,"url":24,"identifiers":1132},"Ljunggren, 1983, Causes of unfavorable outcome after early aneurysm operation., 13, 629, 10.1227\u002F00006123-198312000-00001",{"doi":1133},"10.1227\u002F00006123-198312000-00001",{"id":24,"text":1135,"url":24,"identifiers":1136},"Lougheed, 1969, Selection, timing, and technique of aneurysm surgery of the anterior circle of Willis., 16, 95, 10.1093\u002Fneurosurgery\u002F16.CN_suppl_1.95",{"doi":1137},"10.1093\u002Fneurosurgery\u002F16.CN_suppl_1.95",{"id":24,"text":1139,"url":24,"identifiers":1140},"Mullan, 1978, Management of 136 consecutive supratentorial berry aneurysms., 49, 794, 10.3171\u002Fjns.1978.49.6.0794",{"doi":1141},"10.3171\u002Fjns.1978.49.6.0794",{"id":24,"text":1143,"url":24,"identifiers":1144},"Nishimoto, 1985, Nationwide Cooperative Study of intracranial aneurysm surgery in Japan., 16, 48, 10.1161\u002F01.STR.16.1.48",{"doi":1145},"10.1161\u002F01.STR.16.1.48",{"id":24,"text":1147,"url":24,"identifiers":1148},"Öhman, 1989, Timing of operation for ruptured supratentorial aneurysms: a prospective randomized study., 70, 55, 10.3171\u002Fjns.1989.70.1.0055",{"doi":1149},"10.3171\u002Fjns.1989.70.1.0055",{"id":24,"text":1151,"url":24,"identifiers":1152},"Pool, 1962, Timing and techniques in the intracranial surgery of ruptured aneurysms of the anterior communicating artery., 19, 378, 10.3171\u002Fjns.1962.19.5.0378",{"doi":1153},"10.3171\u002Fjns.1962.19.5.0378",{"id":24,"text":1155,"url":24,"identifiers":1156},"Post, 1977, Ruptured intracranial aneurysms. Case morbidity and mortality., 46, 290, 10.3171\u002Fjns.1977.46.3.0290",{"doi":1157},"10.3171\u002Fjns.1977.46.3.0290",{"id":24,"text":1159,"url":24,"identifiers":1160},"Richardson, 1966, The prediction of morbidity and mortality in anterior communicating aneurysms treated by proximal anterior cerebral ligation., 25, 280, 10.3171\u002Fjns.1966.25.3.0280",{"doi":1161},"10.3171\u002Fjns.1966.25.3.0280",{"id":24,"text":1163,"url":24,"identifiers":1164},"Richardson, 1966, Prognostic factors in the untreated course of posterior communicating aneurysms., 14, 172, 10.1001\u002Farchneur.1966.00470080056008",{"doi":1165},"10.1001\u002Farchneur.1966.00470080056008",{"id":24,"text":1167,"url":24,"identifiers":1168},"Saito, 1973, Surgical treatment of intracranial aneurysms in the acute stage, with special reference to pre- and postoperative vasospasm, 160",{},{"id":24,"text":1170,"url":24,"identifiers":1171},"Saito, 1977, Significance of vasospasm in the treatment of ruptured intracranial aneurysms., 47, 412, 10.3171\u002Fjns.1977.47.3.0412",{"doi":1172},"10.3171\u002Fjns.1977.47.3.0412",{"id":24,"text":1174,"url":24,"identifiers":1175},"Samson, 1979, Risk of intracranial aneurysm surgery in the good grade patient: early versus late operation., 5, 422, 10.1227\u002F00006123-197910000-00002",{"doi":1176},"10.1227\u002F00006123-197910000-00002",{"id":24,"text":1178,"url":24,"identifiers":1179},"Sano, 1978, Timing and indication of surgery for ruptured intracranial aneurysms with regard to cerebral vasospasm., 41, 49, 10.1007\u002FBF01809136",{"doi":1180},"10.1007\u002FBF01809136",{"id":24,"text":1182,"url":24,"identifiers":1183},"Shephard, 1983, Ruptured cerebral aneurysms: early and late prognosis with surgical treatment. A personal series, 1958–1980., 59, 6, 10.3171\u002Fjns.1983.59.1.0006",{"doi":1184},"10.3171\u002Fjns.1983.59.1.0006",{"id":24,"text":1186,"url":24,"identifiers":1187},"Sundt, 1977, Cerebral vasospasm following subarachnoid hemorrhage: evolution, management, and relationship to timing of surgery., 24, 228, 10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.228",{"doi":1188},"10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.228",{"id":24,"text":1190,"url":24,"identifiers":1191},"Sundt, 1982, Results and complications of surgical management of 809 intracranial aneurysms in 722 cases. Related and unrelated to grade of patient, type of aneurysm, and timing of surgery., 56, 753, 10.3171\u002Fjns.1982.56.6.0753",{"doi":1192},"10.3171\u002Fjns.1982.56.6.0753",{"id":24,"text":1194,"url":24,"identifiers":1195},"Sundt, 1978, Subarachnoid hemorrhage from intracranial aneurysms. Surgical management and natural history of disease., 299, 116, 10.1056\u002FNEJM197807202990303",{"doi":1196},"10.1056\u002FNEJM197807202990303",{"id":24,"text":1198,"url":24,"identifiers":1199},"Suzuki, 1979, Results of early operations on cerebral aneurysms., 11, 407",{},{"id":24,"text":1201,"url":24,"identifiers":1202},"Takaku, 1979, Postoperative complications in 1,000 cases of intracranial aneurysms., 12, 137",{},{"id":24,"text":1204,"url":24,"identifiers":1205},"Taneda, 1983, Biphasic occurrence of delayed ischemia after early aneurysm surgery. Case report., 58, 440, 10.3171\u002Fjns.1983.58.3.0440",{"doi":1206},"10.3171\u002Fjns.1983.58.3.0440",{"id":24,"text":1208,"url":24,"identifiers":1209},"Tucker, 1987, The relationship between timing of surgery and operative complications in aneurysmal subarachnoid hemorrhage., 14, 84, 10.1017\u002FS0317167100026895",{"doi":1210},"10.1017\u002FS0317167100026895",{"id":24,"text":1212,"url":24,"identifiers":1213},"Weir, 1982, Management and postoperative mortality related to time of clipping for supratentorial aneurysms. A personal series., 63, 135, 10.1007\u002FBF01728865",{"doi":1214},"10.1007\u002FBF01728865",{"id":24,"text":1216,"url":24,"identifiers":1217},"Weir, 1981, Management mortality and the timing of surgery for supratentorial aneurysms., 54, 146, 10.3171\u002Fjns.1981.54.2.0146",{"doi":1218},"10.3171\u002Fjns.1981.54.2.0146",{"id":24,"text":1220,"url":24,"identifiers":1221},"Whisnant, 1982, Aneurysmal subarachnoid hemorrhage timing of surgery and mortality., 57, 471",{},{"id":24,"text":1223,"url":24,"identifiers":1224},"Wilkins, 1977, The role of intracranial arterial spasm in the timing of operations for aneurysm., 24, 185, 10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.185",{"doi":1225},"10.1093\u002Fneurosurgery\u002F24.CN_suppl_1.185",{"id":24,"text":1227,"url":24,"identifiers":1228},"Yoshimoto, 1979, An analysis of follow-up results of 1000 intracranial saccular aneurysms with definitive surgical treatment., 50, 152, 10.3171\u002Fjns.1979.50.2.0152",{"doi":1229},"10.3171\u002Fjns.1979.50.2.0152",{"id":1231,"createTime":1232,"updateTime":1233,"relativeEntities":1234,"slug":1235,"properties":1236,"entityType":261,"verifyStatus":23,"verifyTime":1252,"verifyNote":895,"languages":1253,"translateLanguages":1254,"viewCount":25,"primaryUrl":1255,"fullTextUrl":24,"authors":1256,"publicationType":353,"publisherRelationship":1321,"citationCount":1375,"citationInfo":1376,"publishDate":1390,"publishYear":1377,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1391,"openAccess":24,"references":1392,"isForceReanalyzing":572},"9dba89fd-660a-449a-8b53-842ce2da2ea3","2024-07-18T11:26:23.235+00:00","2025-02-23T01:39:24.185+00:00",[],"A-new-model-of-diffuse-brain-injury-in-rats",{"mag":1237,"keywords":1239,"openalex":1240,"abstract":1242,"title":1245,"pm":1248,"doi":1250},{"VOID":1238},"2103044571",{"VI":882},{"VOID":1241},"W2103044571",{"EN":1243,"VI":1244},"\u003Cjats:p content-type=\"fine-print\">✓ This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Báo cáo này mô tả sự phát triển của một mô hình chấn thương đầu thí nghiệm có khả năng gây ra chấn thương não lan tỏa ở loài gặm nhấm. Tổng cộng 161 con chuột trưởng thành được gây mê đã bị thương bằng cách sử dụng một thiết bị rơi trọng lực đơn giản bao gồm một quả nặng bằng đồng phân khúc rơi tự do qua một ống dẫn Plexiglas. Việc gãy sọ được ngăn chặn bằng cách gắn một đĩa thép không gỉ nhỏ lên xương sọ. Hai nhóm chuột đã được thử nghiệm: Nhóm 1, bao gồm 54 con chuột, để xác định ngưỡng gãy; và Nhóm 2, bao gồm 107 con chuột, để xác định nguyên nhân chính gây tử vong ở mức độ chấn thương nghiêm trọng. Dữ liệu từ nhóm 1 cho thấy rằng một quả nặng 450 gam rơi từ độ cao 2 mét (0,9 kg-m) dẫn đến tỷ lệ tử vong là 44% với tỷ lệ gãy sọ thấp (12,5%). Va chạm được theo sau bởi ngừng thở, co giật, và tăng huyết áp vừa phải. Những con chuột sống sót phát triển biến dạng gập chi trên, với sự trầm cảm hành vi và mất trương lực cơ. Dữ liệu từ nhóm 2 cho thấy rằng nguyên nhân tử vong là do suy hô hấp trung ương; tỷ lệ tử vong giảm đáng kể ở những con vật được thông khí cơ học trong quá trình va chạm. Phân tích các mô hình toán học cho thấy rằng sự kết hợp giữa khối lượng và độ cao này dẫn đến gia tốc não là 900 G và gradient nén não là 0,28 mm. Kết luận rằng mô hình đơn giản này có khả năng gây ra chấn thương não theo độ nặng ở loài gặm nhấm mà không xảy ra hiện tượng tăng huyết áp lớn hay tổn thương thân não quá mức.\u003C\u002Fjats:p>",{"EN":1246,"VI":1247},"A new model of diffuse brain injury in rats","Mô hình mới về chấn thương não lan tỏa ở chuột",{"VOID":1249},"8283269",{"VOID":1251},"10.3171\u002Fjns.1994.80.2.0291","2024-07-18T11:26:23.234+00:00",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F80\u002F2\u002Farticle-p291.xml",[1257,1274,1283,1294,1303,1312],{"id":1258,"sortIndex":25,"researcher":24,"roles":1259,"affiliations":1260,"properties":1269},"cc103a2f-c488-485b-bb34-bacbc59d0713",[],[1261],{"id":1262,"sortIndex":25,"affiliation":1263,"properties":24},"3901af4c-3c3a-467b-863c-d0ff38f45e70",{"id":1262,"createTime":24,"updateTime":24,"relativeEntities":1264,"slug":24,"properties":1265,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1268,"statistic":24},[],{"title":1266},{"EN":1267},"Richard Roland Reynolds Neurosurgical Research Laboratories, Division of Neurosurgery, Medical College of Virginia, Richmond.",[],{"title":1270,"openalex":1272},{"EN":1271},"Anthony Marmarou",{"VOID":1273},"A5001985393",{"id":1275,"sortIndex":109,"researcher":24,"roles":1276,"affiliations":1277,"properties":1278},"2f567f38-d5c8-4881-b82b-0519b9025161",[],[],{"title":1279,"openalex":1281},{"EN":1280},"Mohamed A. 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DL, 1969, Proc Soc Exp Biol Med, 130, 5, 10.3181\u002F00379727-130-33475",{"doi":1402},"10.3181\u002F00379727-130-33475",{"id":24,"text":1404,"url":24,"identifiers":1405},"10.3171\u002Fjns.1987.67.1.0110",{"doi":1404},{"id":24,"text":1407,"url":24,"identifiers":1408},"10.3171\u002Fjns.1994.80.2.0301",{"doi":1407},{"id":24,"text":1410,"url":24,"identifiers":1411},"Gennarelli TA, 1985, Central Nervous System Trauma Status Report., 391",{},{"id":24,"text":1413,"url":24,"identifiers":1414},"10.1002\u002Fana.410120611",{"doi":1413},{"id":24,"text":1416,"url":24,"identifiers":1417},"Gennarelli TA, 1972, Proceedings of the 16th Strapp Car Crash Conference., 295",{},{"id":24,"text":1419,"url":24,"identifiers":1420},"10.3171\u002Fjns.1970.32.3.0320",{"doi":1419},{"id":24,"text":1422,"url":24,"identifiers":1423},"10.1016\u002FS0009-9260(76)80069-4",{"doi":1422},{"id":24,"text":1425,"url":24,"identifiers":1426},"10.1111\u002Fj.1471-4159.1979.tb11710.x",{"doi":1425},{"id":24,"text":1428,"url":24,"identifiers":1429},"Levin HS, 1981, Arch Neurol, 38, 623, 10.1001\u002Farchneur.1981.00510100051007",{"doi":1430},"10.1001\u002Farchneur.1981.00510100051007",{"id":24,"text":1432,"url":24,"identifiers":1433},"10.3171\u002Fjns.1980.53.4.0500",{"doi":1432},{"id":24,"text":1435,"url":24,"identifiers":1436},"Marshall LF, 1991, J Neurosurg, 75, S14, 10.3171\u002Fsup.1991.75.1s.0s14",{"doi":1437},"10.3171\u002Fsup.1991.75.1s.0s14",{"id":24,"text":1439,"url":24,"identifiers":1440},"10.1016\u002F0306-4522(89)90247-9",{"doi":1439},{"id":24,"text":1442,"url":24,"identifiers":1443},"10.3171\u002Fjns.1970.32.3.0304",{"doi":1442},{"id":24,"text":1445,"url":24,"identifiers":1446},"Millen JE, 1980, J Appl Physiol, 49, 856, 10.1152\u002Fjappl.1980.49.5.856",{"doi":1447},"10.1152\u002Fjappl.1980.49.5.856",{"id":24,"text":1449,"url":24,"identifiers":1450},"Nelson SR, 1966, Head Injury. Conference Proceedings., 444",{},{"id":24,"text":1452,"url":24,"identifiers":1453},"10.3171\u002Fjns.1977.47.2.0262",{"doi":1452},{"id":24,"text":1455,"url":24,"identifiers":1456},"10.3171\u002Fjns.1977.47.2.0274",{"doi":1455},{"id":24,"text":1458,"url":24,"identifiers":1459},"10.3171\u002Fjns.1977.47.2.0252",{"doi":1458},{"id":24,"text":1461,"url":24,"identifiers":1462},"10.3171\u002Fjns.1977.47.2.0241",{"doi":1461},{"id":24,"text":1464,"url":24,"identifiers":1465},"10.1093\u002Fbrain\u002F97.1.633",{"doi":1464},{"id":24,"text":1467,"url":24,"identifiers":1468},"Ommaya AK, 1974, Neural Trauma., 275",{},{"id":24,"text":1470,"url":24,"identifiers":1471},"Shapira Y, 1988, Crit Care Med, 16, 258, 10.1097\u002F00003246-198803000-00010",{"doi":1472},"10.1097\u002F00003246-198803000-00010",{"id":24,"text":1474,"url":24,"identifiers":1475},"10.3171\u002Fjns.1991.74.2.0270",{"doi":1474},{"id":24,"text":1477,"url":24,"identifiers":1478},"10.3171\u002Fjns.1976.45.5.0520",{"doi":1477},{"id":24,"text":1480,"url":24,"identifiers":1481},"van den Brink W, 1993, Intracranial Pressure VII., 221, 10.1007\u002F978-3-642-77789-9_48",{"doi":1482},"10.1007\u002F978-3-642-77789-9_48",{"id":24,"text":1484,"url":24,"identifiers":1485},"van Dongen KJ, 1980, Neurosurgery, 7, 14, 10.1227\u002F00006123-198007000-00003",{"doi":1486},"10.1227\u002F00006123-198007000-00003",{"id":24,"text":1488,"url":24,"identifiers":1489},"10.1016\u002F0013-4694(82)90023-2",{"doi":1488},{"id":24,"text":1491,"url":24,"identifiers":1492},"10.1089\u002Fneu.1991.8.219",{"doi":1491},{"id":1494,"createTime":1495,"updateTime":1496,"relativeEntities":1497,"slug":1498,"properties":1499,"entityType":261,"verifyStatus":262,"verifyTime":1495,"verifyNote":263,"languages":1515,"translateLanguages":1516,"viewCount":25,"primaryUrl":1517,"fullTextUrl":24,"authors":1518,"publicationType":353,"publisherRelationship":1645,"citationCount":1700,"citationInfo":1701,"publishDate":1706,"publishYear":1702,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1707,"openAccess":24,"references":1708,"isForceReanalyzing":572},"b68c6a09-4d56-453c-9d8d-b9e822b1f3ff","2024-10-08T07:08:06.477+00:00","2025-02-23T01:38:27.951+00:00",[],"Adverse-effects-of-prolonged-hyperventilation-in-patients-with-severe-head-injury-a-randomized-clinical-trial",{"mag":1500,"keywords":1502,"openalex":1503,"abstract":1505,"title":1508,"pm":1511,"doi":1513},{"VOID":1501},"2171906554",{"VI":882},{"VOID":1504},"W2171906554",{"EN":1506,"VI":1507},"\u003Cjats:p content-type=\"fine-print\">✓ There is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a loss of HCO\u003Cjats:sub>3\u003C\u002Fjats:sub>\u003Cjats:sup>−\u003C\u002Fjats:sup> buffer from CSF. The latter disadvantage might be overcome by the addition of the buffer tromethamine (THAM), which has shown some promise in experimental and clinical use. Accordingly, a trial was performed with patients randomly assigned to receive normal ventilation (PaCO\u003Cjats:sub>2\u003C\u002Fjats:sub> 35 ± 2 mm Hg (mean ± standard deviation): control group), hyperventilation (PaCO\u003Cjats:sub>2\u003C\u002Fjats:sub> 25 ± 2 mm Hg: HV group), or hyperventilation plus THAM (PaCO\u003Cjats:sub>2\u003C\u002Fjats:sub> 25 ± 2 mm Hg: HV + THAM group). Stratification into subgroups of patients with motor scores of 1–3 and 4–5 took place. Outcome was assessed according to the Glasgow Outcome Scale at 3, 6, and 12 months. There were 41 patients in the control group, 36 in the HV group, and 36 in the HV + THAM group. The mean Glasgow Coma Scale score for each group was 5.7 ± 1.7, 5.6 ± 1.7, and 5.9 ± 1.7, respectively; this score and other indicators of severity of injury were not significantly different. A 100% follow-up review was obtained. At 3 and 6 months after injury the number of patients with a favorable outcome (good or moderately disabled) was significantly (p &lt; 0.05) lower in the hyperventilated patients than in the control and HV + THAM groups. This occurred only in patients with a motor score of 4–5. At 12 months posttrauma this difference was not significant (p = 0.13). Biochemical data indicated that hyperventilation could not sustain alkalinization in the CSF, although THAM could. Accordingly, cerebral blood flow (CBF) was lower in the HV + THAM group than in the control and HV groups, but neither CBF nor arteriovenous difference of oxygen data indicated the occurrence of cerebral ischemia in any of the three groups. Although mean ICP could be kept well below 25 mm Hg in all three groups, the course of ICP was most stable in the HV + THAM group. It is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4–5. When sustained hyperventilation becomes necessary for ICP control, its deleterious effect may be overcome by the addition of THAM.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Vẫn còn tranh cãi về việc liệu bệnh nhân có nên được thông khí quá mức sau chấn thương não hay không, và một thử nghiệm ngẫu nhiên chưa bao giờ được tiến hành. Lợi ích lý thuyết của thông khí quá mức là tạo sự co mạch não để kiểm soát áp lực nội sọ (ICP) và đảo ngược tình trạng toan trong não và dịch não tủy (CSF). Những bất lợi có thể bao gồm co mạch não đến mức dẫn đến thiếu máu não, và chỉ có hiệu lực ngắn hạn trong việc tăng pH CSF với sự mất đi bộ đệm HCO\u003Cjats:sub>3\u003C\u002Fjats:sub>\u003Cjats:sup>−\u003C\u002Fjats:sup> từ CSF. Bất lợi cuối cùng này có thể được khắc phục bằng cách thêm vào bộ đệm tromethamine (THAM), đã cho thấy một số hứa hẹn trong thực nghiệm và lâm sàng. Do đó, một thử nghiệm đã được thực hiện với bệnh nhân được phân ngẫu nhiên để nhận thông khí bình thường (PaCO\u003Cjats:sub>2\u003C\u002Fjats:sub> 35 ± 2 mm Hg (trung bình ± độ lệch chuẩn): nhóm kiểm soát), thông khí quá mức (PaCO\u003Cjats:sub>2\u003C\u002Fjats:sub> 25 ± 2 mm Hg: nhóm HV), hoặc thông khí quá mức cộng với THAM (PaCO\u003Cjats:sub>2\u003C\u002Fjats:sub> 25 ± 2 mm Hg: nhóm HV + THAM). Phân loại theo các nhóm bệnh nhân có điểm số vận động từ 1–3 và 4–5 đã được thực hiện. Kết quả được đánh giá theo Thang điểm Kết quả Glasgow vào 3, 6 và 12 tháng. Có 41 bệnh nhân trong nhóm kiểm soát, 36 trong nhóm HV, và 36 trong nhóm HV + THAM. Điểm số Thang điểm Coma Glasgow trung bình cho mỗi nhóm lần lượt là 5.7 ± 1.7, 5.6 ± 1.7 và 5.9 ± 1.7; điểm số này và các chỉ số nghiêm trọng khác của chấn thương không khác biệt một cách có ý nghĩa. Đã đạt được một cuộc kiểm tra theo dõi 100%. Tại 3 và 6 tháng sau chấn thương, số lượng bệnh nhân có kết quả thuận lợi (khỏi nhẹ hoặc khuyết tật vừa phải) thấp hơn một cách có ý nghĩa (p \u003C 0.05) ở các bệnh nhân thông khí quá mức so với nhóm kiểm soát và nhóm HV + THAM. Điều này chỉ xảy ra ở những bệnh nhân có điểm số vận động từ 4–5. Tại 12 tháng sau chấn thương, sự khác biệt này không có ý nghĩa (p = 0.13). Dữ liệu sinh hóa cho thấy rằng thông khí quá mức không thể duy trì được độ kiềm trong CSF, mặc dù THAM có thể. Do đó, lưu lượng máu não (CBF) ở nhóm HV + THAM thấp hơn so với nhóm kiểm soát và nhóm HV, nhưng cả CBF và sự chênh lệch động tĩnh của dữ liệu oxy không cho thấy sự xuất hiện của thiếu máu não ở bất kỳ nhóm nào trong ba nhóm. Mặc dù ICP trung bình có thể duy trì ở mức dưới 25 mm Hg ở cả ba nhóm, quá trình của ICP ổn định nhất ở nhóm HV + THAM. Kết luận được đưa ra là thông khí quá mức phòng ngừa là có hại ở bệnh nhân chấn thương đầu có điểm số vận động từ 4–5. Khi thông khí quá mức kéo dài trở nên cần thiết cho việc kiểm soát ICP, tác động có hại của nó có thể được khắc phục bằng cách thêm THAM.\u003C\u002Fjats:p>",{"EN":1509,"VI":1510},"Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial","Tác động bất lợi của thông khí kéo dài ở bệnh nhân chấn thương đầu nặng: một thử nghiệm lâm sàng ngẫu nhiên",{"VOID":1512},"1919695",{"VOID":1514},"10.3171\u002Fjns.1991.75.5.0731",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F75\u002F5\u002Farticle-p731.xml",[1519,1536,1551,1566,1581,1598,1615,1630],{"id":1520,"sortIndex":25,"researcher":24,"roles":1521,"affiliations":1522,"properties":1531},"d4e3ab10-a84e-442e-87af-de0b7a6ca0e6",[],[1523],{"id":1524,"sortIndex":25,"affiliation":1525,"properties":24},"c6c19e09-e1cf-40ba-8dcf-c10b12a38f9a",{"id":1524,"createTime":24,"updateTime":24,"relativeEntities":1526,"slug":24,"properties":1527,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1530,"statistic":24},[],{"title":1528},{"EN":1529},"Division of Neurological Surgery, Medical College of Virginia, Richmond.",[],{"title":1532,"openalex":1534},{"EN":1533},"J. 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1976, The effect of THAM on acute intracranial hypertension. An experimental and clinical study, 219",{},{"id":24,"text":1713,"url":24,"identifiers":1714},"Becker, 1985, Intensive management of head injury, 2, 1593",{},{"id":24,"text":1716,"url":24,"identifiers":1717},"Bruce, 1983, Clinical care of the severely head injured child, 31",{},{"id":24,"text":1719,"url":24,"identifiers":1720},"Choi, 1991, Prediction tree for severely head-injured patients., 75, 251",{},{"id":24,"text":1722,"url":24,"identifiers":1723},"Christensen, 1976, Prolonged artificial hyperventilation in cerebral apoplexy., 62, 7",{},{"id":24,"text":1725,"url":24,"identifiers":1726},"Cold, 1975, Ventricular fluid lactate, pyruvate, bicarbonate, and pH in unconscious brain-injured patients subjected to controlled ventilation., 52, 187",{},{"id":24,"text":1728,"url":24,"identifiers":1729},"DeSalles, 1986, Prognostic significance of ventricular CSF lactic acidosis in severe head injury., 65, 615",{},{"id":24,"text":1731,"url":24,"identifiers":1732},"DeSalles, 1987, Hyperglycemia, cerebrospinal fluid lactic acidosis and cerebral blood flow in severely head-injured patients., 21, 45",{},{"id":24,"text":1734,"url":24,"identifiers":1735},"Gaab, 1980, Effect of THAM on ICP, EEG, and tissue edema parameters in experimental and clinical brain edema, 664",{},{"id":24,"text":1737,"url":24,"identifiers":1738},"Gordon, 1979, Non-operative treatment of acute head injuries: the Karolinska experience., 17, 181",{},{"id":24,"text":1740,"url":24,"identifiers":1741},"Gordon, 1970, Further studies on cerebrospinal fluid acid-base status in patients with brain lesions., 14, 97",{},{"id":24,"text":1743,"url":24,"identifiers":1744},"Harrell, 1984, Regression modelling strategies for improved prognostic prediction., 3, 143",{},{"id":24,"text":1746,"url":24,"identifiers":1747},"Hinds, 1987, 284",{},{"id":24,"text":1109,"url":24,"identifiers":1749},{},{"id":24,"text":1751,"url":24,"identifiers":1752},"Jennett, 1981, 255",{},{"id":24,"text":1754,"url":24,"identifiers":1755},"Levasseur, 1979, Responses of pial arterioles after prolonged hypercapnia and hypoxia in the awake rabbit., 46, 89",{},{"id":24,"text":1757,"url":24,"identifiers":1758},"Marmarou, 1989, The Traumatic Coma Data Bank: monitoring of ICP, 549",{},{"id":24,"text":1760,"url":24,"identifiers":1761},"Marmarou, 1978, A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics., 48, 332",{},{"id":24,"text":1763,"url":24,"identifiers":1764},"Marshall, 1987, Medical management of intracranial pressure, 177",{},{"id":24,"text":1766,"url":24,"identifiers":1767},"Maset, 1987, Pressure-volume index in head injury., 67, 832",{},{"id":24,"text":1769,"url":24,"identifiers":1770},"Muizelaar, 1985, Cerebral blood flow and blood metabolism with brain injury, 123",{},{"id":24,"text":1772,"url":24,"identifiers":1773},"Muizelaar, 1988, Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit., 69, 923",{},{"id":24,"text":1775,"url":24,"identifiers":1776},"Obrist, 1984, Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension., 61, 241",{},{"id":24,"text":1778,"url":24,"identifiers":1779},"Rosner, 1984, Experimental brain injury: successful therapy with the weak base, tromethamine. With an overview of CNS acidosis., 60, 961",{},{"id":24,"text":1781,"url":24,"identifiers":1782},"Rossanda, 1973, Role of automatic ventilation in treatment of severe head injuries., 17, 265",{},{"id":24,"text":1784,"url":24,"identifiers":1785},"Saul, 1987, Acute head injuries in adults, 776",{},{"id":24,"text":1787,"url":24,"identifiers":1788},"Schindler, 1971, Cortical metabolites during constant high CO2 concentrations and changes during pH variation., 6, 83",{},{"id":24,"text":1790,"url":24,"identifiers":1791},"Schwartz, 1967, Explanatory and pragmatic attitudes in therapeutic trials., 20, 637",{},{"id":24,"text":1793,"url":24,"identifiers":1794},"Teasdale, 1974, Assessment of coma and impaired consciousness. A practical scale., 2, 81",{},{"id":24,"text":1796,"url":24,"identifiers":1797},"Toutant, 1984, Absent or compressed basal cisterns on first CT scan: ominous predictors of outcome in severe head injury., 61, 691",{},{"id":24,"text":1799,"url":24,"identifiers":1800},"Yoshida, 1991, Effects of tromethamine and hyperventilation on brain injury in the cat., 74, 87",{},{"id":1802,"createTime":1803,"updateTime":1804,"relativeEntities":1805,"slug":1806,"properties":1807,"entityType":261,"verifyStatus":262,"verifyTime":1803,"verifyNote":263,"languages":1823,"translateLanguages":1824,"viewCount":25,"primaryUrl":1825,"fullTextUrl":24,"authors":1826,"publicationType":353,"publisherRelationship":1844,"citationCount":1898,"citationInfo":1899,"publishDate":1903,"publishYear":1900,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1904,"openAccess":24,"references":1905,"isForceReanalyzing":572},"73bdcee8-e4ea-4fc2-8442-bc3e168ee28f","2024-12-18T12:41:44.537+00:00","2025-02-23T01:37:30.318+00:00",[],"Pathophysiology-and-treatment-of-focal-cerebral-ischemia",{"mag":1808,"keywords":1810,"openalex":1811,"abstract":1813,"title":1816,"pm":1819,"doi":1821},{"VOID":1809},"2031702150",{"VI":882},{"VOID":1812},"W2031702150",{"EN":1814,"VI":1815},"\u003Cjats:p content-type=\"fine-print\">✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk.” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K\u003Cjats:sup>+\u003C\u002Fjats:sup>\u002FCa\u003Cjats:sup>++\u003C\u002Fjats:sup>transients, and inhibition of protein synthesis.\u003C\u002Fjats:p>\u003Cjats:p content-type=\"fine-print\">Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>, Na\u003Cjats:sup>+\u003C\u002Fjats:sup>, and Cl\u003Cjats:sup>−\u003C\u002Fjats:sup>, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH.\u003C\u002Fjats:p>\u003Cjats:p content-type=\"fine-print\">In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>.\u003C\u002Fjats:p>\u003Cjats:p content-type=\"fine-print\">A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Bài báo này nghiên cứu sinh lý bệnh của tổn thương do thiếu máu não khu trú. Thiếu máu do tắc mạch động mạch não giữa bao gồm một vùng thiếu máu dày đặc và một vùng bìa thiếu máu ít dày đặc hơn. Các tế bào trong vùng dày đặc thường không thể phục hồi trừ khi được tái tưới máu nhanh chóng. Ngược lại, mặc dù vùng bìa chứa các tế bào “có nguy cơ”, nhưng chúng có thể vẫn sống sót ít nhất từ 4 đến 8 giờ. Các tế bào trong vùng bìa có thể được cứu sống bằng cách tái tưới máu hoặc bằng các loại thuốc ngăn chặn sự mở rộng của nhồi máu vào vùng bìa. Các yếu tố chịu trách nhiệm cho sự mở rộng này có thể bao gồm tình trạng toan hóa, phù nề, sự dao động nồng độ K\u003Cjats:sup>+\u003C\u002Fjats:sup>\u002FCa\u003Cjats:sup>++\u003C\u002Fjats:sup> và sự ức chế tổng hợp protein.\u003C\u002Fjats:p>\u003Cjats:p content-type=\"fine-print\">Trung tâm của bất kỳ cuộc thảo luận nào về sinh lý bệnh của tổn thương thiếu máu là sự cạn kiệt năng lượng. Điều này xảy ra bởi vì sự không duy trì được mức adenosine triphosphate (ATP) trong tế bào dẫn đến việc phân hủy các đại phân tử có tầm quan trọng đặc biệt với tính toàn vẹn của màng và bộ khung tế bào, với sự mất cân bằng ion, bao gồm việc tích lũy Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>, Na\u003Cjats:sup>+\u003C\u002Fjats:sup>, và Cl\u003Cjats:sup>−\u003C\u002Fjats:sup> trong tế bào, cùng với nước bị bắt buộc theo áp suất thẩm thấu, và sự sản xuất các axit chuyển hóa dẫn đến sự giảm pH nội bào và ngoại bào.\u003C\u002Fjats:p>\u003Cjats:p content-type=\"fine-print\">Có khả năng cao rằng sự mất cân bằng canxi trong tế bào đóng vai trò quan trọng trong cơ chế bệnh sinh của tổn thương tế bào thiếu máu. Sự gia tăng nồng độ canxi nội bào tự do (Ca\u003Cjats:sup>++\u003C\u002Fjats:sup>) phụ thuộc vào cả sự mất chức năng của bơm canxi (do cạn kiệt ATP) và sự gia tăng tính thấm màng đối với canxi. Trong tình trạng thiếu máu, sự xâm nhập của canxi xảy ra qua nhiều con đường khác nhau. Một số con đường quan trọng nhất phụ thuộc vào sự kích hoạt các thụ thể bởi glutamate và các axit amin kích thích liên quan được phóng thích từ các điểm tận cùng trước synap bị khử cực. Tuy nhiên, thiếu máu cũng can thiệp vào việc cô lập và gắn kết canxi trong tế bào, từ đó góp phần làm gia tăng Ca\u003Cjats:sup>++\u003C\u002Fjats:sup> trong tế bào.",{"EN":1817,"VI":1818},"Pathophysiology and treatment of focal cerebral ischemia","Sinh lý bệnh và điều trị thiếu máu não khu trú",{"VOID":1820},"18312115",{"VOID":1822},"10.3171\u002Fjns.1992.77.2.0169",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F77\u002F2\u002Farticle-p169.xml",[1827],{"id":1828,"sortIndex":25,"researcher":24,"roles":1829,"affiliations":1830,"properties":1839},"110008e6-9e38-45f6-ad64-86df50e62adb",[],[1831],{"id":1832,"sortIndex":25,"affiliation":1833,"properties":24},"c91a27c3-b13b-45d9-8ac6-9102c748ed46",{"id":1832,"createTime":24,"updateTime":24,"relativeEntities":1834,"slug":24,"properties":1835,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1838,"statistic":24},[],{"title":1836},{"EN":1837},"Laboratory for Experimental Brain Research, Lund University Hospital, Sweden",[],{"title":1840,"openalex":1842},{"EN":1841},"Bo K. 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content-type=\"fine-print\">✓ The localization of cortical sites essential for language was assessed by stimulation mapping in the left, dominant hemispheres of 117 patients. Sites were related to language when stimulation at a current below the threshold for afterdischarge evoked repeated statistically significant errors in object naming. The language center was highly localized in many patients to form several mosaics of 1 to 2 sq cm, usually one in the frontal and one or more in the temporoparietal lobe. The area of individual mosaics, and the total area related to language was usually much smaller than the traditional Broca-Wernicke areas. There was substantial individual variability in the exact location of language function, some of which correlated with the patient's sex and verbal intelligence. These features were present for patients as young as 4 years and as old as 80 years, and for those with lesions acquired in early life or adulthood. These findings indicate a need for revision of the classical model of language localization. The combination of discrete localization in individual patients but substantial individual variability between patients also has major clinical implications for cortical resections of the dominant hemisphere, for it means that language cannot be reliably localized on anatomic criteria alone. A maximal resection with minimal risk of postoperative aphasia requires individual localization of language with a technique like stimulation mapping.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Việc định vị các địa điểm vỏ não cần thiết cho ngôn ngữ đã được đánh giá thông qua bản đồ kích thích ở bán cầu trái, bán cầu ưu thế của 117 bệnh nhân. Các địa điểm này liên quan đến ngôn ngữ khi kích thích với dòng điện thấp hơn ngưỡng kích hoạt đã gây ra những lỗi có ý nghĩa thống kê trong việc đặt tên đối tượng. Trung tâm ngôn ngữ được định vị rất rõ trong nhiều bệnh nhân, tạo thành một số ô ghép kích thước từ 1 đến 2 cm vuông, thường là một ở vùng trán và một hoặc nhiều ở thùy thái dương - đỉnh. Diện tích của các ô ghép cá nhân và tổng diện tích liên quan đến ngôn ngữ thường nhỏ hơn nhiều so với các khu vực truyền thống của Broca và Wernicke. Có sự biến đổi lớn giữa các cá nhân về vị trí chính xác của chức năng ngôn ngữ, một phần trong số đó tương quan với giới tính và trí thông minh ngôn ngữ của bệnh nhân. Những đặc điểm này hiện diện ở bệnh nhân từ 4 đến 80 tuổi, cũng như những người có tổn thương từ khi còn nhỏ hoặc trong độ tuổi trưởng thành. Những phát hiện này chỉ ra rằng cần phải xem xét lại mô hình cổ điển về định vị ngôn ngữ. Sự kết hợp giữa định vị riêng biệt ở từng bệnh nhân nhưng có sự biến đổi lớn giữa các bệnh nhân cũng có những tác động lâm sàng quan trọng đối với các phẫu thuật cắt bỏ vỏ não của bán cầu ưu thế, bởi vì điều này có nghĩa là không thể định vị ngôn ngữ một cách đáng tin cậy chỉ dựa trên tiêu chí giải phẫu. Một ca phẫu thuật cắt bỏ tối đa với rủi ro hậu phẫu về tình trạng mất ngôn ngữ tối thiểu cần phải có sự định vị ngôn ngữ cá nhân bằng một kỹ thuật như bản đồ kích thích.\u003C\u002Fjats:p>",{"EN":2520,"VI":2521},"Cortical language localization in left, dominant hemisphere","Định vị ngôn ngữ vỏ não ở bán cầu trái, bán cầu ưu thế",{"VOID":2523},"2769383",{"VOID":2525},"10.3171\u002Fjns.1989.71.3.0316",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F71\u002F3\u002Farticle-p316.xml",[2530,2547,2558,2567],{"id":2531,"sortIndex":25,"researcher":24,"roles":2532,"affiliations":2533,"properties":2542},"fea0a833-5a16-450c-85eb-fddb8de3d4a2",[],[2534],{"id":2535,"sortIndex":25,"affiliation":2536,"properties":24},"2d38c85e-f2f0-45a3-a5c8-a381e41641f7",{"id":2535,"createTime":24,"updateTime":24,"relativeEntities":2537,"slug":24,"properties":2538,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2541,"statistic":24},[],{"title":2539},{"VI":2540},"Department of Neurological Surgery, University of Washington, Seattle",[],{"title":2543,"openalex":2545},{"EN":2544},"George A. Ojemann",{"VOID":2546},"A5017533406",{"id":2548,"sortIndex":109,"researcher":24,"roles":2549,"affiliations":2550,"properties":2551},"0c2a96f8-ed29-476a-b27f-a78181ce5c8b",[],[],{"orcid":2552,"title":2554,"openalex":2556},{"VOID":2553},"https:\u002F\u002Forcid.org\u002F0000-0001-7580-8934",{"EN":2555},"Jeffrey G. Ojemann",{"VOID":2557},"A5063843377",{"id":2559,"sortIndex":108,"researcher":24,"roles":2560,"affiliations":2561,"properties":2562},"0ea71180-8827-40ca-8f9b-a3a914e42641",[],[],{"title":2563,"openalex":2565},{"EN":2564},"Ettore Lettich",{"VOID":2566},"A5037154349",{"id":2568,"sortIndex":110,"researcher":24,"roles":2569,"affiliations":2570,"properties":2571},"49931b0c-6151-4861-94e4-d5c830fba194",[],[],{"orcid":2572,"title":2574,"openalex":2576},{"VOID":2573},"https:\u002F\u002Forcid.org\u002F0000-0003-1983-4892",{"EN":2575},"Mitchel S. Berger",{"VOID":2577},"A5006262715",{"url":24,"publisher":2579,"properties":2626},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2580,"slug":10,"properties":2581,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":2586,"manageAffiliations":2595,"indexDatabases":2606,"url":91,"thumbnailPath":24,"statistic":2621,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":2582,"eissn":2583,"issn":2584,"title":2585},{"VOID":13},{"VOID":15},{"VOID":17},{"EN":19},[2587,2591],{"id":28,"createTime":24,"updateTime":24,"relativeEntities":2588,"label":2589,"description":2590,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":31},{},{"id":34,"createTime":24,"updateTime":24,"relativeEntities":2592,"label":2593,"description":2594,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":37},{},[2596,2601],{"id":41,"createTime":24,"updateTime":24,"relativeEntities":2597,"slug":24,"properties":2598,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2600,"statistic":24},[],{"title":2599},{"EN":45},[],{"id":48,"createTime":24,"updateTime":24,"relativeEntities":2602,"slug":24,"properties":2603,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2605,"statistic":24},[],{"title":2604},{"EN":52},[],[2607,2614],{"id":56,"indexDatabase":2608,"url":69,"indexYears":24,"academicFieldIds":2613,"indexDatabaseRanking":24},{"id":58,"createTime":24,"updateTime":24,"relativeEntities":2609,"label":2610,"description":2611,"key":65,"publicationTags":2612,"standard":24},[],{"EN":61,"VI":61},{"EN":63,"VI":64},[67,68],[71,72],{"id":74,"indexDatabase":2615,"url":85,"indexYears":86,"academicFieldIds":2620,"indexDatabaseRanking":90},{"id":76,"createTime":24,"updateTime":24,"relativeEntities":2616,"label":2617,"description":2618,"key":82,"publicationTags":2619,"standard":24},[],{"EN":79,"VI":79},{"EN":79,"VI":81},[84],[88,89],{"impactFactor":25,"impactFactorByYear":2622,"i10Index":105,"i10IndexLast5Year":101,"totalPublication":106,"totalPublicationByYear":2623,"totalCitation":117,"totalCitationByYear":2624,"totalCitationPerPublication":180,"totalCitationPerPublicationByYear":2625,"hindexLast5Year":235,"hindex":235},{"2012":94,"2013":95,"2014":96,"2015":97,"2016":98,"2017":99,"2018":100,"2019":101,"2020":102,"2021":103,"2022":102,"2023":104},{"1944":108,"1945":109,"1946":109,"1950":109,"1953":109,"1958":110,"1960":109,"1962":110,"1964":111,"1965":110,"1966":108,"1967":109,"1968":110,"1969":101,"1972":112,"1973":109,"1974":108,"1975":110,"1976":110,"1977":112,"1978":108,"1979":108,"1980":111,"1981":111,"1982":111,"1983":110,"1984":112,"1985":111,"1986":110,"1987":110,"1988":111,"1989":104,"1990":101,"1991":113,"1992":101,"1993":104,"1994":112,"1995":110,"1996":104,"1997":114,"1998":115,"1999":101,"2000":115,"2001":104,"2002":114,"2003":116,"2004":113,"2005":111,"2006":112,"2007":113,"2008":101,"2009":101,"2010":112,"2011":111,"2012":101,"2013":101,"2014":111,"2015":112,"2016":101,"2018":109,"2019":109,"2020":111,"2022":109},{"1944":119,"1945":120,"1946":121,"1950":122,"1953":123,"1958":124,"1960":125,"1962":126,"1964":127,"1965":128,"1966":129,"1967":130,"1968":131,"1969":132,"1972":133,"1973":134,"1974":135,"1975":136,"1976":137,"1977":138,"1978":139,"1979":140,"1980":141,"1981":142,"1982":143,"1983":144,"1984":145,"1985":146,"1986":147,"1987":148,"1988":149,"1989":150,"1990":151,"1991":152,"1992":153,"1993":154,"1994":155,"1995":156,"1996":157,"1997":158,"1998":159,"1999":160,"2000":161,"2001":162,"2002":163,"2003":164,"2004":165,"2005":166,"2006":167,"2007":168,"2008":169,"2009":170,"2010":171,"2011":172,"2012":173,"2013":174,"2014":175,"2015":146,"2016":176,"2018":125,"2019":177,"2020":178,"2022":179},{"1944":182,"1945":120,"1946":121,"1950":122,"1953":123,"1958":183,"1960":125,"1962":184,"1964":185,"1965":186,"1966":187,"1967":130,"1968":188,"1969":189,"1972":190,"1973":134,"1974":191,"1975":192,"1976":193,"1977":194,"1978":195,"1979":196,"1980":197,"1981":198,"1982":199,"1983":200,"1984":201,"1985":202,"1986":203,"1987":204,"1988":205,"1989":206,"1990":207,"1991":208,"1992":209,"1993":210,"1994":211,"1995":212,"1996":213,"1997":214,"1998":215,"1999":216,"2000":217,"2001":218,"2002":219,"2003":220,"2004":221,"2005":222,"2006":223,"2007":224,"2008":225,"2009":226,"2010":227,"2011":228,"2012":229,"2013":230,"2014":231,"2015":232,"2016":233,"2018":125,"2019":177,"2020":234,"2022":179},{"issue":2627,"pages":2628,"volume":2630},{"VOID":779},{"VOID":2629},"316-326",{"VOID":2631},"71",1463,{"total":2632,"publishYear":2634,"statisticByYear":2635},1989,{"2012":2636,"2013":2636,"2014":1388,"2015":2637,"2016":231,"2017":1382,"2018":2638,"2019":1385,"2020":1384,"2021":2639,"2022":1019,"2023":2640,"2024":2641},73,66,47,62,32,23,"1989-09-01",[67,90],[2645,2648,2651,2654,2657,2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1988, Cortical mapping techniques used to maximize tumor resection and safety in children with brain tumors., 24, 361",{},{"id":24,"text":2649,"url":24,"identifiers":2650},"Bogen, 1975, Wernicke's region — where is it?, 280, 834",{},{"id":24,"text":2652,"url":24,"identifiers":2653},"Broca, 1861, Remarques sur le siège de la faculté du language articulé, suivies d'une observation d'aphémie (perte de la parole)., 36, 330",{},{"id":24,"text":2655,"url":24,"identifiers":2656},"Burchiel, 1989, Use of stimulation mapping and corticography in the excision of arteriovenous malformations in sensorimotor and language-related neocortex., 24, 323",{},{"id":24,"text":2658,"url":24,"identifiers":2659},"Cawthon, 1987, Human temporal lobe neuronal activity: inhibition during naming in only one of two languages., 13, 839",{},{"id":24,"text":2661,"url":24,"identifiers":2662},"Damasio, 1988, Concluding remarks: neuroscience and cognitive science in the study of language and the brain, 275",{},{"id":24,"text":2664,"url":24,"identifiers":2665},"Fried, 1981, Language-related potentials specific to human language cortex., 212, 353, 10.1126\u002Fscience.7209537",{"doi":2666},"10.1126\u002Fscience.7209537",{"id":24,"text":2668,"url":24,"identifiers":2669},"Galaburda, 1978, Human brain. Cytoarchitectonic left-right asymmetries in the temporal speech region., 35, 812, 10.1001\u002Farchneur.1978.00500360036007",{"doi":2670},"10.1001\u002Farchneur.1978.00500360036007",{"id":24,"text":2672,"url":24,"identifiers":2673},"Goldman-Rakic, 1988, Topography of cognition: parallel distributed networks in primate association cortex., 11, 137, 10.1146\u002Fannurev.ne.11.030188.001033",{"doi":2674},"10.1146\u002Fannurev.ne.11.030188.001033",{"id":24,"text":2676,"url":24,"identifiers":2677},"Heilman, 1972, Anomic aphasia following anterior temporal lobectomy., 97, 291",{},{"id":24,"text":2679,"url":24,"identifiers":2680},"Jasper, 1960, Unspecific thalamocortical relations, 2, 1307",{},{"id":24,"text":2682,"url":24,"identifiers":2683},"Kimura, 1982, Left-hemisphere control of oral and brachial movements and their relation to communication., 298, 135",{},{"id":24,"text":2685,"url":24,"identifiers":2686},"Kimura, 1983, Sex differences in cerebral organization for speech and praxic functions., 37, 19, 10.1037\u002Fh0080696",{"doi":2687},"10.1037\u002Fh0080696",{"id":24,"text":2689,"url":24,"identifiers":2690},"Kohn, 1985, Picture-naming in aphasia., 24, 266, 10.1016\u002F0093-934X(85)90135-X",{"doi":2691},"10.1016\u002F0093-934X(85)90135-X",{"id":24,"text":2693,"url":24,"identifiers":2694},"Lesser, 1984, The location of speech and writing functions in the frontal language area. Results of extraoperative cortical stimulation., 107, 275, 10.1093\u002Fbrain\u002F107.1.275",{"doi":2695},"10.1093\u002Fbrain\u002F107.1.275",{"id":24,"text":2697,"url":24,"identifiers":2698},"Liberman, 1967, Perception of the speech code., 74, 431, 10.1037\u002Fh0020279",{"doi":2699},"10.1037\u002Fh0020279",{"id":24,"text":2701,"url":24,"identifiers":2702},"Lueders, 1983, Inhibition of motor activity by elicited electrical stimulation of the human cortex., 24, 519",{},{"id":24,"text":2704,"url":24,"identifiers":2705},"Lueders, 1986, Basal temporal language area demonstrated by electrical stimulation., 36, 505, 10.1212\u002FWNL.36.4.505",{"doi":2706},"10.1212\u002FWNL.36.4.505",{"id":24,"text":2708,"url":24,"identifiers":2709},"Merzenich, 1987, Variability in hand surface representations in areas 3b and 1 in adult owl and squirrel monkeys., 258, 281, 10.1002\u002Fcne.902580208",{"doi":2710},"10.1002\u002Fcne.902580208",{"id":24,"text":2712,"url":24,"identifiers":2713},"Mohr, 1976, Broca's area and Broca's aphasia, 1, 201",{},{"id":24,"text":2715,"url":24,"identifiers":2716},"Ojemann, 1983, Brain organization for language from the perspective of electrical stimulation mapping., 6, 189, 10.1017\u002FS0140525X00015491",{"doi":2717},"10.1017\u002FS0140525X00015491",{"id":24,"text":2719,"url":24,"identifiers":2720},"Ojemann, 1988, Effect of cortical and subcortical stimulation in human language and verbal memory, 101",{},{"id":24,"text":2722,"url":24,"identifiers":2723},"Ojemann, 1983, Electrical stimulation and the neurobiology of language., 6, 221, 10.1017\u002FS0140525X0001565X",{"doi":2724},"10.1017\u002FS0140525X0001565X",{"id":24,"text":2726,"url":24,"identifiers":2727},"Ojemann, 1979, Individual variability in cortical localization of language., 50, 164, 10.3171\u002Fjns.1979.50.2.0164",{"doi":2728},"10.3171\u002Fjns.1979.50.2.0164",{"id":24,"text":2730,"url":24,"identifiers":2731},"Ojemann, 1975, Language and the thalamus: object naming and recall during and after thalamic stimulation., 2, 101, 10.1016\u002FS0093-934X(75)80057-5",{"doi":2732},"10.1016\u002FS0093-934X(75)80057-5",{"id":24,"text":2734,"url":24,"identifiers":2735},"Ojemann, 1989, Some brain mechanisms for reading, 47",{},{"id":24,"text":2737,"url":24,"identifiers":2738},"Ojemann, 1988, Neuronal activity in human lateral temporal cortex related to shortterm verbal memory, naming and reading., 111, 1383, 10.1093\u002Fbrain\u002F111.6.1383",{"doi":2739},"10.1093\u002Fbrain\u002F111.6.1383",{"id":24,"text":2741,"url":24,"identifiers":2742},"Ojemann, 1985, Verbal memory deficits after left temporal lobectomy for epilepsy. Mechanism and intraoperative prediction., 62, 101, 10.3171\u002Fjns.1985.62.1.0101",{"doi":2743},"10.3171\u002Fjns.1985.62.1.0101",{"id":24,"text":2745,"url":24,"identifiers":2746},"Ojemann, Electrocorticographic (ECoG) correlates of language: I. Desynchronization in temporal language cortex during object naming.",{},{"id":24,"text":2748,"url":24,"identifiers":2749},"Ojemann, 1978, The bilingual brain., 35, 409, 10.1001\u002Farchneur.1978.00500310011002",{"doi":2750},"10.1001\u002Farchneur.1978.00500310011002",{"id":24,"text":2752,"url":24,"identifiers":2753},"Ojemann, 1978, Language localization and variability., 6, 239, 10.1016\u002F0093-934X(78)90061-5",{"doi":2754},"10.1016\u002F0093-934X(78)90061-5",{"id":24,"text":2756,"url":24,"identifiers":2757},"Penfield, 1954",{},{"id":24,"text":2759,"url":24,"identifiers":2760},"Penfield, 1959",{},{"id":24,"text":2762,"url":24,"identifiers":2763},"Ranck, 1975, Which elements are excited in electrical stimulation of mammalian central nervous system: a review., 98, 417, 10.1016\u002F0006-8993(75)90364-9",{"doi":2764},"10.1016\u002F0006-8993(75)90364-9",{"id":24,"text":2766,"url":24,"identifiers":2767},"Rubens, 1976, Asymmetry of the lateral (sylvian) fissures in man., 26, 620, 10.1212\u002FWNL.26.7.620",{"doi":2768},"10.1212\u002FWNL.26.7.620",{"id":24,"text":2770,"url":24,"identifiers":2771},"Siegel, 1956",{},{"id":24,"text":2773,"url":24,"identifiers":2774},"Skinner, 1977, Central grating mechanisms that regulate event-related potentials and behavior: a neural model for attention., 1, 30",{},{"id":24,"text":2776,"url":24,"identifiers":2777},"Van Buren, 1978, Mechanism and localization of speech in the parietotemporal cortex., 2, 233, 10.1227\u002F00006123-197805000-00009",{"doi":2778},"10.1227\u002F00006123-197805000-00009",{"id":24,"text":2780,"url":24,"identifiers":2781},"Van Buren, 1978, Fluorometric monitoring of NADH levels in cerebral cortex: preliminary observations in human epilepsy., 2, 114, 10.1227\u002F00006123-197803000-00007",{"doi":2782},"10.1227\u002F00006123-197803000-00007",{"id":24,"text":2784,"url":24,"identifiers":2785},"Wada, 1960, Intracarotid injections of sodium amytal for the lateralization of cerebral speech dominance., 17, 266, 10.3171\u002Fjns.1960.17.2.0266",{"doi":2786},"10.3171\u002Fjns.1960.17.2.0266",{"id":24,"text":2788,"url":24,"identifiers":2789},"Wernicke, 1874",{},{"id":24,"text":2791,"url":24,"identifiers":2792},"Whitaker, 1975, Anatomic variations in the cortex: individual differences and the problem of the localization of language functions., 280, 844",{},{"id":24,"text":2794,"url":24,"identifiers":2795},"Whitaker, 1978, Graded localisation of naming from electrical stimulation mapping of left cerebral cortex., 270, 50",{},{"id":24,"text":2797,"url":24,"identifiers":2798},"Woods, 1988, Brain injury, handedness, and speech lateralization in a series of amobarbital studies., 23, 510, 10.1002\u002Fana.410230514",{"doi":2799},"10.1002\u002Fana.410230514",{"id":2801,"createTime":2802,"updateTime":2803,"relativeEntities":2804,"slug":2805,"properties":2806,"entityType":261,"verifyStatus":23,"verifyTime":2802,"verifyNote":895,"languages":2822,"translateLanguages":2823,"viewCount":25,"primaryUrl":2824,"fullTextUrl":24,"authors":2825,"publicationType":353,"publisherRelationship":2938,"citationCount":2992,"citationInfo":2993,"publishDate":3000,"publishYear":2994,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":3001,"openAccess":24,"references":3002,"isForceReanalyzing":572},"43cbb2b1-2508-48aa-a247-e0604021c8b7","2024-10-04T07:32:13.742+00:00","2025-02-23T01:35:36.749+00:00",[],"Evaluation-of-BCNU-and-or-radiotherapy-in-the-treatment-of-anaplastic-gliomas",{"mag":2807,"keywords":2809,"openalex":2810,"abstract":2812,"title":2815,"pm":2818,"doi":2820},{"VOID":2808},"2113012900",{"VI":882},{"VOID":2811},"W2113012900",{"EN":2813,"VI":2814},"\u003Cjats:p content-type=\"fine-print\">✓ A controlled, prospective, randomized study evaluated the use of 1,3-bis(2-chloroethyl)-l-nitrosourea (BCNU) and\u002For radiotherapy in the treatment of patients who were operated on and had histological confirmation of anaplastic glioma. A total of 303 patients were randomized into this study, of whom 222 (73%) were within the Valid Study Group (VSG), having met the protocol criteria of neuropathology, corticosteroid control, and therapeutic approach. Patients were divided into four random groups, and received BCNU (80 mg\u002Fsq m\u002Fday on 3 successive days every 6 to 8 weeks), and\u002For radiotherapy (5000 to 6000 rads to the whole brain through bilateral opposing ports), or best conventional care but no chemotherapy or radiotherapy. Analysis was performed on all patients who received any amount of therapy (VSG) and on the Adequately Treated Group (ATG), who had received 5000 or more rads radiotherapy, two or more courses of chemotherapy, and had a minimum survival of 8 or more weeks (the interval that would have been required to have received either the radiotherapy or chemotherapy). Median survival of patients in the VSG was, best conventional care: 14 weeks (ATG: 17.0 weeks); BCNU: 18.5 weeks (ATG: 25.0 weeks); radiotherapy: 35 weeks (ATG: 37.5 weeks); and BCNU plus radiotherapy: 34.5 weeks (ATG: 40.5 weeks). All therapeutic modalities showed some statistical superiority compared to best conventional care. There was no significant difference between the four groups in relation to age distribution, sex, location of tumor, diagnosis, tumor characteristics, signs or symptoms, or the amount of corticosteroid used. An analysis of prognostic factors indicates that the initial performance status (Karnofsky rating), age, the use of only a surgical biopsy, parietal location, the presence of seizures, or the involvement of cranial nerves II, III, IV, and VI are all of significance. Toxicity included acceptable, reversible thrombocytopenia and leukopenia.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Một nghiên cứu kiểm soát, tiềm năng, ngẫu nhiên đã đánh giá việc sử dụng 1,3-bis(2-chloroethyl)-l-nitrosourea (BCNU) và\u002Fhoặc xạ trị trong điều trị bệnh nhân đã được phẫu thuật và có xác nhận mô bệnh học của glioma anaplastik. Tổng cộng có 303 bệnh nhân đã được ngẫu nhiên vào nghiên cứu này, trong đó 222 (73%) nằm trong Nhóm Nghiên Cứu Hợp Lệ (VSG), đáp ứng các tiêu chí của giao thức về bệnh lý thần kinh, kiểm soát corticosteroid, và phương pháp điều trị. Bệnh nhân được chia thành bốn nhóm ngẫu nhiên và nhận BCNU (80 mg\u002Fm2\u002Fngày trong 3 ngày liên tiếp mỗi 6 đến 8 tuần), và\u002Fhoặc xạ trị (5000 đến 6000 rads cho toàn bộ não qua các cổng đối diện hai bên), hoặc chăm sóc truyền thống tốt nhất nhưng không có hóa trị hoặc xạ trị. Phân tích được thực hiện trên tất cả bệnh nhân đã nhận bất kỳ liệu pháp nào (VSG) và trên Nhóm Được Điều Trị Đầy Đủ (ATG), những người đã nhận 5000 rads xạ trị trở lên, hai đợt hóa trị trở lên, và đã có thời gian sống tối thiểu là 8 tuần hoặc lâu hơn (thời gian cần thiết để nhận xạ trị hoặc hóa trị). Thời gian sống trung bình của bệnh nhân trong VSG là, chăm sóc truyền thống tốt nhất: 14 tuần (ATG: 17,0 tuần); BCNU: 18,5 tuần (ATG: 25,0 tuần); xạ trị: 35 tuần (ATG: 37,5 tuần); và BCNU cộng xạ trị: 34,5 tuần (ATG: 40,5 tuần). Tất cả các phương thức điều trị đều cho thấy một số độ ưu việt thống kê so với chăm sóc truyền thống tốt nhất. Không có sự khác biệt đáng kể giữa bốn nhóm liên quan đến phân bố tuổi tác, giới tính, vị trí khối u, chẩn đoán, đặc điểm khối u, dấu hiệu hoặc triệu chứng, hoặc lượng corticosteroid đã sử dụng. Phân tích các yếu tố dự đoán cho thấy rằng tình trạng hoạt động ban đầu (đánh giá Karnofsky), tuổi tác, việc chỉ sử dụng sinh thiết phẫu thuật, vị trí thái dương, sự hiện diện của các cơn động kinh, hoặc sự tham gia của các dây thần kinh sọ II, III, IV và VI đều có ý nghĩa. Độc tính bao gồm giảm tiểu cầu và giảm bạch cầu có thể chấp nhận, có thể hồi phục.",{"EN":2816,"VI":2817},"Evaluation of BCNU and\u002For radiotherapy in the treatment of anaplastic gliomas","Đánh giá BCNU và\u002Fhoặc xạ trị trong điều trị glioma anaplastik",{"VOID":2819},"355604",{"VOID":2821},"10.3171\u002Fjns.1978.49.3.0333",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F49\u002F3\u002Farticle-p333.xml",[2826,2837,2846,2855,2864,2873,2882,2891,2900,2909,2920,2929],{"id":2827,"sortIndex":25,"researcher":24,"roles":2828,"affiliations":2829,"properties":2830},"0e608bbf-5f4c-41da-b4ca-bd5697fbb7bf",[],[],{"orcid":2831,"title":2833,"openalex":2835},{"VOID":2832},"https:\u002F\u002Forcid.org\u002F0000-0002-7389-9518",{"EN":2834},"Michael Walker",{"VOID":2836},"A5046007240",{"id":2838,"sortIndex":109,"researcher":24,"roles":2839,"affiliations":2840,"properties":2841},"20979e17-eb02-4aa3-aff0-dff88a537f7e",[],[],{"title":2842,"openalex":2844},{"EN":2843},"Eben Alexander",{"VOID":2845},"A5070824167",{"id":2847,"sortIndex":108,"researcher":24,"roles":2848,"affiliations":2849,"properties":2850},"35136d3d-0547-4a8b-93ad-5bc2c1c18057",[],[],{"title":2851,"openalex":2853},{"EN":2852},"William E. Hunt",{"VOID":2854},"A5009256943",{"id":2856,"sortIndex":110,"researcher":24,"roles":2857,"affiliations":2858,"properties":2859},"1d1d95e8-e9dc-4024-b9af-b582ca53ae76",[],[],{"title":2860,"openalex":2862},{"EN":2861},"Collin S. MacCarty",{"VOID":2863},"A5058266329",{"id":2865,"sortIndex":111,"researcher":24,"roles":2866,"affiliations":2867,"properties":2868},"af94a7fd-592a-42a7-91fc-0056792db44f",[],[],{"title":2869,"openalex":2871},{"EN":2870},"M. S. Mahaley",{"VOID":2872},"A5054571881",{"id":2874,"sortIndex":112,"researcher":24,"roles":2875,"affiliations":2876,"properties":2877},"96c8aa85-e0e3-4d66-acf5-fd8f2bfc685c",[],[],{"title":2878,"openalex":2880},{"EN":2879},"John Mealey",{"VOID":2881},"A5068650516",{"id":2883,"sortIndex":101,"researcher":24,"roles":2884,"affiliations":2885,"properties":2886},"5e7b9fef-a35f-4ca0-904c-483eba2d18d7",[],[],{"title":2887,"openalex":2889},{"EN":2888},"Horace Norrell",{"VOID":2890},"A5002673806",{"id":2892,"sortIndex":104,"researcher":24,"roles":2893,"affiliations":2894,"properties":2895},"1ac81258-33f4-4a42-8cda-d599c0a927e1",[],[],{"title":2896,"openalex":2898},{"EN":2897},"Guy Owens",{"VOID":2899},"A5071075304",{"id":2901,"sortIndex":113,"researcher":24,"roles":2902,"affiliations":2903,"properties":2904},"960e5ada-f296-40de-b2d6-718e3722de8d",[],[],{"title":2905,"openalex":2907},{"EN":2906},"Joseph Ransohoff",{"VOID":2908},"A5059680008",{"id":2910,"sortIndex":114,"researcher":24,"roles":2911,"affiliations":2912,"properties":2913},"9975b65d-c1ff-4808-8b5c-e95374b75ad5",[],[],{"orcid":2914,"title":2916,"openalex":2918},{"VOID":2915},"https:\u002F\u002Forcid.org\u002F0000-0002-2597-5694",{"EN":2917},"Charles B. Wilson",{"VOID":2919},"A5103119939",{"id":2921,"sortIndex":115,"researcher":24,"roles":2922,"affiliations":2923,"properties":2924},"5e374985-6af6-4840-90a0-0d16a679815c",[],[],{"title":2925,"openalex":2927},{"EN":2926},"Edmund A. Gehan",{"VOID":2928},"A5031020853",{"id":2930,"sortIndex":116,"researcher":24,"roles":2931,"affiliations":2932,"properties":2933},"89b5eec4-4e99-4304-8b6a-16a613c4eda6",[],[],{"title":2934,"openalex":2936},{"EN":2935},"Thomas A. 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1958, Glioblastoma multiforme. Review of 219 cases with regard to natural history, pathology, diagnostic methods and treatment., 15, 489, 10.3171\u002Fjns.1958.15.5.0489",{"doi":3006},"10.3171\u002Fjns.1958.15.5.0489",{"id":24,"text":3008,"url":24,"identifiers":3009},"Gehan, 1965, A generalized Wilcoxon test for comparing arbitrarily singly-censored samples., 52, 203, 10.1093\u002Fbiomet\u002F52.1-2.203",{"doi":3010},"10.1093\u002Fbiomet\u002F52.1-2.203",{"id":24,"text":3012,"url":24,"identifiers":3013},"Gehan, Prognostic factors for patients with brain tumors.",{},{"id":24,"text":3015,"url":24,"identifiers":3016},"Goldsmith, 1974, Glioblastoma multiforme — a review of therapy., 1, 153, 10.1016\u002FS0305-7372(74)80016-2",{"doi":3017},"10.1016\u002FS0305-7372(74)80016-2",{"id":24,"text":3019,"url":24,"identifiers":3020},"Jelsma, 1967, The treatment of glioblastoma multiforme of the brain., 27, 388, 10.3171\u002Fjns.1967.27.5.0388",{"doi":3021},"10.3171\u002Fjns.1967.27.5.0388",{"id":24,"text":3023,"url":24,"identifiers":3024},"Kaplan, 1958, Nonparametric estimation from incomplete observations., 53, 457, 10.1080\u002F01621459.1958.10501452",{"doi":3025},"10.1080\u002F01621459.1958.10501452",{"id":24,"text":3027,"url":24,"identifiers":3028},"Karnofsky, 1951, Triethylene melamine in the treatment of neoplastic disease., 87, 477, 10.1001\u002Farchinte.1951.03810040002001",{"doi":3029},"10.1001\u002Farchinte.1951.03810040002001",{"id":24,"text":3031,"url":24,"identifiers":3032},"Levin, 1975, A pharmacologic basis for brain tumor chemotherapy., 2, 57",{},{"id":24,"text":3034,"url":24,"identifiers":3035},"Mahaley, Neuropathology observations on tissues from patients treated by the Brain Tumor Study Group (BTSG).",{},{"id":24,"text":3037,"url":24,"identifiers":3038},"Rubinstein, 1972",{},{"id":24,"text":3040,"url":24,"identifiers":3041},"Russell, 1970",{},{"id":24,"text":3043,"url":24,"identifiers":3044},"Schabel, 1963, Experimental evaluation of potential anticancer agents. VIII. Effects of certain nitrosoureas on intracerebral L1210 leukemia., 23, 725",{},{"id":24,"text":3046,"url":24,"identifiers":3047},"Snedecor, 1967, 215",{},{"id":24,"text":3049,"url":24,"identifiers":3050},"Vendetti, 1964, Evaluation of antileukemic agents employing advanced leukemia L1210 in mice. VIII., 24, 827",{},{"id":24,"text":3052,"url":24,"identifiers":3053},"Walker, 1973, Brain and peripheral nervous system tumors, 1385",{},{"id":24,"text":3055,"url":24,"identifiers":3056},"Walker, 1976, The evaluation of mithramycin in the treatment of anaplastic gliomas., 44, 655, 10.3171\u002Fjns.1976.44.6.0655",{"doi":3057},"10.3171\u002Fjns.1976.44.6.0655",{"id":24,"text":3059,"url":24,"identifiers":3060},"Walker, 1970, BCNU 1,3-bis(2-chloroethyl)-1-nitrosourea; (NSC-409962) in the treatment of malignant brain tumor — a preliminary report., 54, 263",{},{"id":24,"text":3062,"url":24,"identifiers":3063},"Walker, 1976, An evaluation of Methyl-CCNU, BCNU and radiotherapy in the treatment of malignant glioma., 17, 163",{},{"id":24,"text":3065,"url":24,"identifiers":3066},"Wilson, 1970, 1,bis(2-chloroethyl)-1-nitrosourea (NSC-409962) in the treatment of brain tumors., 54, 273",{},{"id":3068,"createTime":3069,"updateTime":3070,"relativeEntities":3071,"slug":3072,"properties":3073,"entityType":261,"verifyStatus":23,"verifyTime":3069,"verifyNote":895,"languages":3089,"translateLanguages":3090,"viewCount":25,"primaryUrl":3091,"fullTextUrl":24,"authors":3092,"publicationType":353,"publisherRelationship":3148,"citationCount":3201,"citationInfo":3202,"publishDate":1024,"publishYear":1015,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":3206,"openAccess":24,"references":3207,"isForceReanalyzing":572},"42a708c2-9bb4-48f7-b4dc-e2d930af2e8a","2024-10-13T02:02:20.583+00:00","2025-02-23T01:34:40.027+00:00",[],"The-International-Cooperative-Studyon-the-Timing-of-Aneurysm-Surgery",{"mag":3074,"keywords":3076,"openalex":3077,"abstract":3079,"title":3082,"pm":3085,"doi":3087},{"VOID":3075},"2079405518",{"VI":882},{"VOID":3078},"W2079405518",{"EN":3080,"VI":3081},"\u003Cjats:p content-type=\"fine-print\">✓ The International Cooperative Study on the Timing of Aneurysm Surgery evaluated the results of surgical and medical management in 3521 patients between December, 1980, and July, 1983. At admission, 75% of patients were in good neurological condition and surgery was performed in 83%. At the 6-month evaluation, 26% of the patients had died and 58% exhibited a complete recovery. Vasospasm and rebleeding were the leading causes of morbidity and mortality in addition to the initial bleed. Predictors for mortality included the patient's decreased level of consciousness and increased age, thickness of the subarachnoid hemorrhage clot on computerized tomography, elevated blood pressure, preexisting medical illnesses, and basilar aneurysms. The results presented here document the status of management in the 1980's.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Nghiên cứu Hợp tác Quốc tế về Thời điểm Phẫu thuật Phình mạch đã đánh giá kết quả của quản lý phẫu thuật và y tế trên 3521 bệnh nhân trong khoảng thời gian từ tháng 12 năm 1980 đến tháng 7 năm 1983. Tại thời điểm nhập viện, 75% bệnh nhân được đánh giá có tình trạng thần kinh tốt và 83% đã thực hiện phẫu thuật. Tại lần đánh giá 6 tháng, 26% bệnh nhân đã tử vong và 58% có sự hồi phục hoàn toàn. Co thắt mạch và tái xuất huyết là những nguyên nhân chính gây ra bệnh tật và tử vong, bên cạnh xuất huyết ban đầu. Các yếu tố dự đoán tỷ lệ tử vong bao gồm mức độ ý thức của bệnh nhân giảm, tuổi cao, độ dày của cục máu đông xuất huyết dưới nhện trên CT scanner, huyết áp cao, bệnh lý nền trước đó và phình mạch nền. Kết quả được trình bày ở đây ghi lại trạng thái quản lý trong những năm 1980.\u003C\u002Fjats:p>",{"EN":3083,"VI":3084},"The International Cooperative Studyon the Timing of Aneurysm Surgery","Nghiên cứu Hợp tác Quốc tế về Thời điểm Phẫu thuật Phình mạch",{"VOID":3086},"2191090",{"VOID":3088},"10.3171\u002Fjns.1990.73.1.0018",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F73\u002F1\u002Farticle-p18.xml",[3093,3108,3117,3124,3132,3139],{"id":3094,"sortIndex":25,"researcher":24,"roles":3095,"affiliations":3096,"properties":3103},"d546e7f6-f1fc-41d5-b8cb-0f140022fe50",[],[3097],{"id":906,"sortIndex":25,"affiliation":3098,"properties":24},{"id":906,"createTime":24,"updateTime":24,"relativeEntities":3099,"slug":24,"properties":3100,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3102,"statistic":24},[],{"title":3101},{"VI":911},[],{"title":3104,"openalex":3106},{"EN":3105},"N F Kassell",{"VOID":3107},"A5063237656",{"id":3109,"sortIndex":109,"researcher":24,"roles":3110,"affiliations":3111,"properties":3112},"cef57f86-e4b5-44d5-8f6c-88348c74b5f9",[],[],{"title":3113,"openalex":3115},{"EN":3114},"J C Torner",{"VOID":3116},"A5074119950",{"id":3118,"sortIndex":108,"researcher":24,"roles":3119,"affiliations":3120,"properties":3121},"7b7db97e-43e6-422c-b111-e5f0964050be",[],[],{"title":3122,"openalex":3123},{"EN":946},{"VOID":948},{"id":3125,"sortIndex":110,"researcher":24,"roles":3126,"affiliations":3127,"properties":3128},"ee54dafe-541c-46d3-8f24-ac81f6c80be3",[],[],{"orcid":3129,"title":3130,"openalex":3131},{"VOID":935},{"EN":937},{"VOID":939},{"id":3133,"sortIndex":111,"researcher":24,"roles":3134,"affiliations":3135,"properties":3136},"2e20215e-0221-4f8b-a6f9-b1f13994f998",[],[],{"title":3137,"openalex":3138},{"EN":955},{"VOID":957},{"id":3140,"sortIndex":112,"researcher":24,"roles":3141,"affiliations":3142,"properties":3143},"5487ed59-4de8-4394-86d9-d2810c429425",[],[],{"title":3144,"openalex":3146},{"EN":3145},"Gail L. 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1980, Epidemiology of cerebrovascular disease: some unanswered questions, 88",{},{"id":24,"text":1028,"url":24,"identifiers":3212},{"doi":1030},{"id":24,"text":3214,"url":24,"identifiers":3215},"Adams, 1985, Usefulness of computerized tomography in predicting outcome after aneurysmal subarachnoid hemorrhage: a preliminary report of the Cooperative Aneurysm Study., 35, 1263, 10.1212\u002FWNL.35.9.1263",{"doi":3216},"10.1212\u002FWNL.35.9.1263",{"id":24,"text":3218,"url":24,"identifiers":3219},"Adams, 1980, Early management of aneurysmal subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study, 84",{},{"id":24,"text":3221,"url":24,"identifiers":3222},"Andrews, 1979, Intracranial aneurysms. Age, sex, blood pressure, and multiplicity in an unselected series of patients., 51, 27, 10.3171\u002Fjns.1979.51.1.0027",{"doi":3223},"10.3171\u002Fjns.1979.51.1.0027",{"id":24,"text":3225,"url":24,"identifiers":3226},"1982, Symposium Graz, July 19–21., 63, 1",{},{"id":24,"text":3228,"url":24,"identifiers":3229},"Bahuleyan, 1980, Surgical treatment of intracranial aneurysms: changing pattern in mortality and morbidity rates., 80, 1698",{},{"id":24,"text":3231,"url":24,"identifiers":3232},"Bonita, 1983, Subarachnoid hemorrhage in New Zealand: an epidemiological study., 14, 342, 10.1161\u002F01.STR.14.3.342",{"doi":3233},"10.1161\u002F01.STR.14.3.342",{"id":24,"text":1058,"url":24,"identifiers":3235},{"doi":1060},{"id":24,"text":3237,"url":24,"identifiers":3238},"Fisher, 1980, Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomography scanning., 6, 1, 10.1227\u002F00006123-198001000-00001",{"doi":1064},{"id":24,"text":1066,"url":24,"identifiers":3240},{"doi":1068},{"id":24,"text":3242,"url":24,"identifiers":3243},"Fogelholm, 1981, Subarachnoid hemorrhage in Middle-Finland: incidence, early prognosis and indications for neurosurgical treatment., 12, 296, 10.1161\u002F01.STR.12.3.296",{"doi":3244},"10.1161\u002F01.STR.12.3.296",{"id":24,"text":1078,"url":24,"identifiers":3246},{},{"id":24,"text":3248,"url":24,"identifiers":3249},"Hori, 1979, Early intracranial operation for ruptured aneurysm, 571",{},{"id":24,"text":3251,"url":24,"identifiers":3252},"Hotta, 1982, Surgical results of intracranial ruptured aneurysms in the acute stage., 63, 193, 10.1007\u002FBF01728872",{"doi":3253},"10.1007\u002FBF01728872",{"id":24,"text":1101,"url":24,"identifiers":3255},{"doi":1103},{"id":24,"text":1105,"url":24,"identifiers":3257},{"doi":1107},{"id":24,"text":1109,"url":24,"identifiers":3259},{},{"id":24,"text":3261,"url":24,"identifiers":3262},"Kacker, 1983, Operative complications and postoperative care, II, 846",{},{"id":24,"text":1112,"url":24,"identifiers":3264},{"doi":1114},{"id":24,"text":3266,"url":24,"identifiers":3267},"Kassell, 1983, Review of the management of saccular aneurysms., 1, 73, 10.1016\u002FS0733-8619(18)31172-1",{"doi":3268},"10.1016\u002FS0733-8619(18)31172-1",{"id":24,"text":1116,"url":24,"identifiers":3270},{"doi":1118},{"id":24,"text":3272,"url":24,"identifiers":3273},"Kassell, 1985, Delay in referral of patients with ruptured aneurysms to neurosurgical attention., 16, 587, 10.1161\u002F01.STR.16.4.587",{"doi":3274},"10.1161\u002F01.STR.16.4.587",{"id":24,"text":3276,"url":24,"identifiers":3277},"Kassell, 1983, Size of intracranial aneurysms., 12, 291, 10.1227\u002F00006123-198303000-00007",{"doi":3278},"10.1227\u002F00006123-198303000-00007",{"id":24,"text":3280,"url":24,"identifiers":3281},"Kassell, 1984, Antifibrinolytic therapy in the acute period following aneurysmal subarachnoid hemorrhage. Preliminary observations from the Cooperative Aneurysm Study., 61, 225, 10.3171\u002Fjns.1984.61.2.0225",{"doi":3282},"10.3171\u002Fjns.1984.61.2.0225",{"id":24,"text":1123,"url":24,"identifiers":3284},{"doi":1125},{"id":24,"text":3286,"url":24,"identifiers":3287},"Kurtzke, 1969, 47",{},{"id":24,"text":3289,"url":24,"identifiers":3290},"Kwak, 1979, The correlation between hypertension in past history and the incidence of cerebral aneurysms, 20",{},{"id":24,"text":1127,"url":24,"identifiers":3292},{"doi":1129},{"id":24,"text":3294,"url":24,"identifiers":3295},"Ljunggren, 1982, Early management of aneurysmal subarachnoid hemorrhage., 11, 412, 10.1227\u002F00006123-198209000-00013",{"doi":3296},"10.1227\u002F00006123-198209000-00013",{"id":24,"text":1131,"url":24,"identifiers":3298},{"doi":1133},{"id":24,"text":3300,"url":24,"identifiers":3301},"Locksley, 1969, Natural history of subarachnoid hemorrhage, intracranial aneurysm and arteriovenous malformations: based on 6368 cases in the Cooperative Study, 37",{},{"id":24,"text":3303,"url":24,"identifiers":3304},"McCormick, 1970, The size of intracranial saccular aneurysms. An autopsy study., 33, 422, 10.3171\u002Fjns.1970.33.4.0422",{"doi":3305},"10.3171\u002Fjns.1970.33.4.0422",{"id":24,"text":3307,"url":24,"identifiers":3308},"McCormick, 1977, The relationship of arterial hypertension to intracranial aneurysms., 34, 285, 10.1001\u002Farchneur.1977.00500170039006",{"doi":3309},"10.1001\u002Farchneur.1977.00500170039006",{"id":24,"text":3311,"url":24,"identifiers":3312},"McDonald, 1939, Intracranial aneurysms., 42, 298, 10.1001\u002Farchneurpsyc.1939.02270200118011",{"doi":3313},"10.1001\u002Farchneurpsyc.1939.02270200118011",{"id":24,"text":3315,"url":24,"identifiers":3316},"Mizukami, 1980, Value of computed tomography in the prediction of cerebral vasospasm after aneurysm rupture., 7, 583, 10.1227\u002F00006123-198012000-00008",{"doi":3317},"10.1227\u002F00006123-198012000-00008",{"id":24,"text":3319,"url":24,"identifiers":3320},"Morley, 1968, Giant intracranial aneurysms: diagnosis, course, and management., 16, 73",{},{"id":24,"text":3322,"url":24,"identifiers":3323},"Norlén, 1965, Some aspects of the surgical treatment of intracranial aneurysms., 7, 14, 10.2176\u002Fnmc.7.14",{"doi":3324},"10.2176\u002Fnmc.7.14",{"id":24,"text":3326,"url":24,"identifiers":3327},"Ohta, 1982, Extensive evacuation of subarachnoid clot for prevention of vasospasm — effective or not?, 63, 111, 10.1007\u002FBF01728862",{"doi":3328},"10.1007\u002FBF01728862",{"id":24,"text":3330,"url":24,"identifiers":3331},"Pakarinen, 1967, Incidence, aetiology, and prognosis of primary subarachnoid haemorrhage. A study based on 589 cases diagnosed in a defined urban population during a defined period., 43, 1",{},{"id":24,"text":3333,"url":24,"identifiers":3334},"Phillips, 1980, The unchanging pattern of subarachnoid hemorrhage in a community., 30, 1034, 10.1212\u002FWNL.30.10.1034",{"doi":3335},"10.1212\u002FWNL.30.10.1034",{"id":24,"text":1155,"url":24,"identifiers":3337},{"doi":1157},{"id":24,"text":3339,"url":24,"identifiers":3340},"Ropper, 1984, Outcome 1 year after SAH from cerebral aneurysm. Management morbidity, mortality, and functional status in 112 consecutive good-risk patients., 60, 909, 10.3171\u002Fjns.1984.60.5.0909",{"doi":3341},"10.3171\u002Fjns.1984.60.5.0909",{"id":24,"text":3343,"url":24,"identifiers":3344},"Sacco, 1984, Subarachnoid and intracerebral hemorrhage: natural history, prognosis, and precursive factors in the Framingham Study., 34, 847, 10.1212\u002FWNL.34.7.847",{"doi":3345},"10.1212\u002FWNL.34.7.847",{"id":24,"text":1174,"url":24,"identifiers":3347},{"doi":1176},{"id":24,"text":1178,"url":24,"identifiers":3349},{"doi":1180},{"id":24,"text":3351,"url":24,"identifiers":3352},"Sonntag, 1977, Giant intracranial aneurysms: a review of 13 cases., 8, 81",{},{"id":24,"text":1194,"url":24,"identifiers":3354},{"doi":1196},{"id":24,"text":3356,"url":24,"identifiers":3357},"Suzuki, 1971, Intracranial aneurysms in the neurosurgical clinics in Japan., 35, 34, 10.3171\u002Fjns.1971.35.1.0034",{"doi":3358},"10.3171\u002Fjns.1971.35.1.0034",{"id":24,"text":3360,"url":24,"identifiers":3361},"Sypert, 1978, Intracranial aneurysms: natural history and surgical management., 4, 64",{},{"id":24,"text":3363,"url":24,"identifiers":3364},"Takahashi, 1981, Early operations for ruptured intracranial aneurysms. Comparative study with computed tomography., 57, 23, 10.1007\u002FBF01665109",{"doi":3365},"10.1007\u002FBF01665109",{"id":24,"text":3367,"url":24,"identifiers":3368},"Taneda, 1982, The significance of early operation in the management of ruptured intracranial aneurysms. An analysis of 251 cases hospitalized within 24 hours after subarachnoid hemorrhage., 63, 201, 10.1007\u002FBF01728873",{"doi":3369},"10.1007\u002FBF01728873",{"id":24,"text":1793,"url":24,"identifiers":3371},{},{"id":24,"text":3373,"url":24,"identifiers":3374},"Tomasello, 1982, Relation of cerebral vasospasm to operative findings of subarachnoid blood around ruptured aneurysms., 60, 55, 10.1007\u002FBF01401750",{"doi":3375},"10.1007\u002FBF01401750",{"id":24,"text":3377,"url":24,"identifiers":3378},"Torner, 1984, Epidemiology of subarachnoid hemorrhage., 4, 354, 10.1055\u002Fs-2008-1041565",{"doi":3379},"10.1055\u002Fs-2008-1041565",{"id":24,"text":3381,"url":24,"identifiers":3382},"Torner, 1981, Preoperative prognostic factors for rebleeding and survival in aneurysm patients receiving antifibrinolytic therapy: report of the Cooperative Aneurysm Study., 9, 506",{},{"id":24,"text":1216,"url":24,"identifiers":3384},{"doi":1218},{"id":24,"text":3386,"url":24,"identifiers":3387},"Weir, 1978, Time course of vasospasm in man., 48, 173, 10.3171\u002Fjns.1978.48.2.0173",{"doi":3388},"10.3171\u002Fjns.1978.48.2.0173",{"id":24,"text":3390,"url":24,"identifiers":3391},"Wiebers, 1981, The natural history of unruptured intracranial aneurysms., 304, 696, 10.1056\u002FNEJM198103193041203",{"doi":3392},"10.1056\u002FNEJM198103193041203",{"id":24,"text":3394,"url":24,"identifiers":3395},"Wilkins, 1968, Intracranial arterial spasm: a clinical analysis., 29, 121, 10.3171\u002Fjns.1968.29.2.0121",{"doi":3396},"10.3171\u002Fjns.1968.29.2.0121",{"id":24,"text":3398,"url":24,"identifiers":3399},"Winn, 1981, Long-term evaluation of patients with multiple cerebral aneurysm., 10, 106",{},{"id":24,"text":3401,"url":24,"identifiers":3402},"Winn, 1978, The long-term prognosis in untreated cerebral aneurysms. II: Morbidity and mortality., 4, 418, 10.1002\u002Fana.410040506",{"doi":3403},"10.1002\u002Fana.410040506",{"id":24,"text":1227,"url":24,"identifiers":3405},{"doi":1229},{"id":3407,"createTime":3408,"updateTime":3409,"relativeEntities":3410,"slug":3411,"properties":3412,"entityType":261,"verifyStatus":23,"verifyTime":3408,"verifyNote":895,"languages":3428,"translateLanguages":3429,"viewCount":25,"primaryUrl":3430,"fullTextUrl":24,"authors":3431,"publicationType":353,"publisherRelationship":3460,"citationCount":3515,"citationInfo":3516,"publishDate":3529,"publishYear":3517,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":3530,"openAccess":24,"references":3531,"isForceReanalyzing":572},"6b35944e-63e3-4d29-beb7-066266c3e798","2024-07-18T07:47:00.845+00:00","2025-02-23T01:33:44.512+00:00",[],"A-proposed-grading-system-for-arteriovenous-malformations",{"mag":3413,"keywords":3415,"openalex":3416,"abstract":3418,"title":3421,"pm":3424,"doi":3426},{"VOID":3414},"1973470461",{"VI":882},{"VOID":3417},"W1973470461",{"EN":3419,"VI":3420},"\u003Cjats:p content-type=\"fine-print\">✓ An important factor in making a recommendation for treatment of a patient with arteriovenous malformation (AVM) is to estimate the risk of surgery for that patient. A simple, broadly applicable grading system that is designed to predict the risk of morbidity and mortality attending the operative treatment of specific AVM's is proposed. The lesion is graded on the basis of size, pattern of venous drainage, and neurological eloquence of adjacent brain. All AVM's fall into one of six grades. Grade I malformations are small, superficial, and located in non-eloquent cortex; Grade V lesions are large, deep, and situated in neurologically critical areas; and Grade VI lesions are essentially inoperable AVM's.\u003C\u002Fjats:p>\n\u003Cjats:p content-type=\"fine-print\">Retrospective application of this grading scheme to a series of surgically excised AVM's has demonstrated its correlation with the incidence of postoperative neurological complications. The application of a standardized grading scheme will enable a comparison of results between various clinical series and between different treatment techniques, and will assist in the process of management decision-making.\u003C\u002Fjats:p>","\u003Cjats:p content-type=\"fine-print\">✓ Một yếu tố quan trọng trong việc đưa ra khuyến nghị điều trị cho bệnh nhân có dị dạng động tĩnh mạch (AVM) là ước lượng nguy cơ phẫu thuật cho bệnh nhân đó. Một hệ thống phân loại đơn giản, có thể áp dụng rộng rãi được thiết kế để dự đoán nguy cơ morbid và tử vong liên quan đến việc điều trị phẫu thuật các AVM cụ thể đã được đề xuất. Dị dạng được phân loại dựa trên kích thước, kiểu thoát huyết quản, và độ nhạy ứng thần kinh của não lân cận. Tất cả các AVM đều rơi vào một trong sáu cấp độ. Dị dạng cấp I là nhỏ, nông và nằm ở vỏ não không nhạy cảm; tổn thương cấp V là lớn, sâu, và nằm ở các khu vực có vai trò quan trọng về thần kinh; và tổn thương cấp VI hầu như không thể phẫu thuật AVM.\u003C\u002Fjats:p>\n\u003Cjats:p content-type=\"fine-print\">Việc áp dụng hồi tưởng hệ thống phân loại này cho một loạt AVM đã được cắt bỏ phẫu thuật đã chứng minh mối tương quan của nó với tỷ lệ biến chứng thần kinh sau phẫu thuật. Việc áp dụng một hệ thống phân loại chuẩn hóa sẽ cho phép so sánh kết quả giữa các loạt bệnh lý lâm sàng khác nhau và giữa các kỹ thuật điều trị khác nhau, đồng thời sẽ hỗ trợ trong quá trình ra quyết định quản lý.\u003C\u002Fjats:p>",{"EN":3422,"VI":3423},"A proposed grading system for arteriovenous malformations","Một hệ thống phân loại đề xuất cho dị dạng động tĩnh mạch",{"VOID":3425},"3760956",{"VOID":3427},"10.3171\u002Fjns.1986.65.4.0476",[265],[898],"https:\u002F\u002Fthejns.org\u002Fview\u002Fjournals\u002Fj-neurosurg\u002F65\u002F4\u002Farticle-p476.xml",[3432,3449],{"id":3433,"sortIndex":25,"researcher":24,"roles":3434,"affiliations":3435,"properties":3444},"53524e12-2cd7-465d-9582-dfe8421b9b8a",[],[3436],{"id":3437,"sortIndex":25,"affiliation":3438,"properties":24},"781fbaa1-fbdb-49be-89d7-a30bfd64384f",{"id":3437,"createTime":24,"updateTime":24,"relativeEntities":3439,"slug":24,"properties":3440,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3443,"statistic":24},[],{"title":3441},{"VI":3442},"Division of Neurological Surgery, Barrow Neurological Institute, Phoenix, Arizona, USA",[],{"title":3445,"openalex":3447},{"EN":3446},"Robert F. 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1984, Cerebral arteriovenous malformations in children. Clinical features and outcome of treatment in children and in adults., 22, 43, 10.1016\u002F0090-3019(84)90227-1",{"doi":3535},"10.1016\u002F0090-3019(84)90227-1",{"id":24,"text":3537,"url":24,"identifiers":3538},"Drake, 1979, Cerebral arteriovenous malformations: considerations for and experience with surgical treatment in 166 cases., 26, 145, 10.1093\u002Fneurosurgery\u002F26.CN_suppl_1.145",{"doi":3539},"10.1093\u002Fneurosurgery\u002F26.CN_suppl_1.145",{"id":24,"text":3541,"url":24,"identifiers":3542},"Forster, 1972, Arteriovenous malformations of the brain. A long-term clinical study., 37, 562, 10.3171\u002Fjns.1972.37.5.0562",{"doi":3543},"10.3171\u002Fjns.1972.37.5.0562",{"id":24,"text":3545,"url":24,"identifiers":3546},"Fults, 1984, Natural history of arteriovenous malformations of the brain: a clinical study., 15, 658, 10.1227\u002F00006123-198411000-00003",{"doi":3547},"10.1227\u002F00006123-198411000-00003",{"id":24,"text":3549,"url":24,"identifiers":3550},"Graf, 1983, Bleeding from cerebral arteriovenous malformations as part of their natural history., 58, 331, 10.3171\u002Fjns.1983.58.3.0331",{"doi":3551},"10.3171\u002Fjns.1983.58.3.0331",{"id":24,"text":3553,"url":24,"identifiers":3554},"Kjellberg, 1983, Bragg-peak proton-beam therapy for arteriovenous malformations of the brain., 309, 269, 10.1056\u002FNEJM198308043090503",{"doi":3555},"10.1056\u002FNEJM198308043090503",{"id":24,"text":3557,"url":24,"identifiers":3558},"Luessenhop, 1984, Natural history of cerebral arteriovenous malformations, 12",{},{"id":24,"text":3560,"url":24,"identifiers":3561},"Luessenhop, 1977, Anatomical grading of supratentorial arteriovenous malformations for determining operability., 1, 30, 10.1227\u002F00006123-197707000-00007",{"doi":3562},"10.1227\u002F00006123-197707000-00007",{"id":24,"text":3564,"url":24,"identifiers":3565},"Luessenhop, 1975, Surgical embolization of cerebral arteriovenous malformations through internal carotid and vertebral arteries. 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An analysis of 545 cases of cranio-cerebral arteriovenous malformations and fistulae reported to the Cooperative Study., 25, 467, 10.3171\u002Fjns.1966.25.4.0467",{"doi":3577},"10.3171\u002Fjns.1966.25.4.0467",{"id":24,"text":3579,"url":24,"identifiers":3580},"Spetzler, 1978, Normal perfusion pressure breakthrough theory., 25, 651, 10.1093\u002Fneurosurgery\u002F25.CN_suppl_1.651",{"doi":3581},"10.1093\u002Fneurosurgery\u002F25.CN_suppl_1.651",{"id":24,"text":3583,"url":24,"identifiers":3584},"Stein, 1980, Arteriovenous malformations of the brain. I. Current concepts and treatment., 37, 1, 10.1001\u002Farchneur.1980.00500500031002",{"doi":3585},"10.1001\u002Farchneur.1980.00500500031002",{"id":24,"text":3587,"url":24,"identifiers":3588},"Steiner, 1984, Treatment of arteriovenous malformations by radiosurgery, 295",{},{"id":24,"text":3590,"url":24,"identifiers":3591},"Wilkins, 1985, Natural history of intracranial vascular malformations: a review., 16, 421, 10.1227\u002F00006123-198503000-00026",{"doi":3592},"10.1227\u002F00006123-198503000-00026"]