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Clinicopathological study of intracranial fusiform and dolichoectatic aneurysms : Insight on the mechanism of growth
Intracranial fusiform aneurysms can be divided into 2 clinically different subtypes: acute dissecting aneurysms and chronic fusiform or dolichoectatic aneurysms. Of these 2, the natural history and growth mechanism of chronic fusiform aneurysms remains unknown. A consecutive series of 16 patients wi...
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Published in: | Stroke (1970) 2000-04, Vol.31 (4), p.896-900 |
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container_title | Stroke (1970) |
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creator | NAKATOMI, H SEGAWA, H KURATA, A SHIOKAWA, Y NAGATA, K KAMIYAMA, H UEKI, K KIRINO, T |
description | Intracranial fusiform aneurysms can be divided into 2 clinically different subtypes: acute dissecting aneurysms and chronic fusiform or dolichoectatic aneurysms. Of these 2, the natural history and growth mechanism of chronic fusiform aneurysms remains unknown.
A consecutive series of 16 patients with chronic fusiform aneurysms was studied retrospectively to clarify patient clinical and neuroradiological features. Aneurysm tissues were obtained from 8 cases and were examined to identify histological features that could correspond to the radiological findings.
Four histological features were found: (1) fragmentation of internal elastic lamina (IEL), (2) neoangiogenesis within the thickened intima, (3) intramural hemorrhage (IMH) and thrombus formation, and (4) repetitive intramural hemorrhages from the newly formed vessels within thrombus. IEL fragmentation was found in all cases, which suggests that this change may be one of the earliest processes of aneurysm formation. MRI or CT detected IMH, and marked contrast enhancement of the inside of the aneurysm wall (CEI) on MRI corresponded well with intimal thickening. Eight of 9 symptomatic cases but none of 7 asymptomatic cases presented with both radiological features.
Data suggest that chronic fusiform aneurysms are progressive lesions that start with IEL fragmentation. Formation of IMH seems to be a critical event necessary for lesions to become symptomatic and progress, and this can be monitored on MRI. Knowledge of this possible mechanism of progression and corresponding MRI characteristics could help determine timing of surgical intervention. |
doi_str_mv | 10.1161/01.STR.31.4.896 |
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A consecutive series of 16 patients with chronic fusiform aneurysms was studied retrospectively to clarify patient clinical and neuroradiological features. Aneurysm tissues were obtained from 8 cases and were examined to identify histological features that could correspond to the radiological findings.
Four histological features were found: (1) fragmentation of internal elastic lamina (IEL), (2) neoangiogenesis within the thickened intima, (3) intramural hemorrhage (IMH) and thrombus formation, and (4) repetitive intramural hemorrhages from the newly formed vessels within thrombus. IEL fragmentation was found in all cases, which suggests that this change may be one of the earliest processes of aneurysm formation. MRI or CT detected IMH, and marked contrast enhancement of the inside of the aneurysm wall (CEI) on MRI corresponded well with intimal thickening. Eight of 9 symptomatic cases but none of 7 asymptomatic cases presented with both radiological features.
Data suggest that chronic fusiform aneurysms are progressive lesions that start with IEL fragmentation. Formation of IMH seems to be a critical event necessary for lesions to become symptomatic and progress, and this can be monitored on MRI. Knowledge of this possible mechanism of progression and corresponding MRI characteristics could help determine timing of surgical intervention.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.31.4.896</identifier><identifier>PMID: 10753995</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Cerebral Angiography ; Cerebral Hemorrhage - etiology ; Disease Progression ; Female ; Humans ; Intracranial Aneurysm - classification ; Intracranial Aneurysm - diagnosis ; Intracranial Aneurysm - pathology ; Intracranial Aneurysm - surgery ; Intracranial Thrombosis - etiology ; Magnetic Resonance Imaging ; Male ; Medical sciences ; Middle Aged ; Neovascularization, Pathologic - etiology ; Neurology ; Postoperative Complications - mortality ; Treatment Outcome ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2000-04, Vol.31 (4), p.896-900</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Apr 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c384t-390fee555702dd4109fe01a3e2cec9b68b89fd543484f6aa65365f2e93fc80c03</citedby><cites>FETCH-LOGICAL-c384t-390fee555702dd4109fe01a3e2cec9b68b89fd543484f6aa65365f2e93fc80c03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1327347$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10753995$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NAKATOMI, H</creatorcontrib><creatorcontrib>SEGAWA, H</creatorcontrib><creatorcontrib>KURATA, A</creatorcontrib><creatorcontrib>SHIOKAWA, Y</creatorcontrib><creatorcontrib>NAGATA, K</creatorcontrib><creatorcontrib>KAMIYAMA, H</creatorcontrib><creatorcontrib>UEKI, K</creatorcontrib><creatorcontrib>KIRINO, T</creatorcontrib><title>Clinicopathological study of intracranial fusiform and dolichoectatic aneurysms : Insight on the mechanism of growth</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Intracranial fusiform aneurysms can be divided into 2 clinically different subtypes: acute dissecting aneurysms and chronic fusiform or dolichoectatic aneurysms. Of these 2, the natural history and growth mechanism of chronic fusiform aneurysms remains unknown.
A consecutive series of 16 patients with chronic fusiform aneurysms was studied retrospectively to clarify patient clinical and neuroradiological features. Aneurysm tissues were obtained from 8 cases and were examined to identify histological features that could correspond to the radiological findings.
Four histological features were found: (1) fragmentation of internal elastic lamina (IEL), (2) neoangiogenesis within the thickened intima, (3) intramural hemorrhage (IMH) and thrombus formation, and (4) repetitive intramural hemorrhages from the newly formed vessels within thrombus. IEL fragmentation was found in all cases, which suggests that this change may be one of the earliest processes of aneurysm formation. MRI or CT detected IMH, and marked contrast enhancement of the inside of the aneurysm wall (CEI) on MRI corresponded well with intimal thickening. Eight of 9 symptomatic cases but none of 7 asymptomatic cases presented with both radiological features.
Data suggest that chronic fusiform aneurysms are progressive lesions that start with IEL fragmentation. Formation of IMH seems to be a critical event necessary for lesions to become symptomatic and progress, and this can be monitored on MRI. Knowledge of this possible mechanism of progression and corresponding MRI characteristics could help determine timing of surgical intervention.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cerebral Angiography</subject><subject>Cerebral Hemorrhage - etiology</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Humans</subject><subject>Intracranial Aneurysm - classification</subject><subject>Intracranial Aneurysm - diagnosis</subject><subject>Intracranial Aneurysm - pathology</subject><subject>Intracranial Aneurysm - surgery</subject><subject>Intracranial Thrombosis - etiology</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neovascularization, Pathologic - etiology</subject><subject>Neurology</subject><subject>Postoperative Complications - mortality</subject><subject>Treatment Outcome</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNpdkd1rFDEUxYNY7Fp99k2CiG8zvfmaSXyTRW2hILT1OWQzyU7KzGRNMsj-96bsguLThcPvHg7nIPSOQEtIR66BtA-P9y0jLW-l6l6gDRGUN7yj8iXaADDVUK7UJXqd8xMAUCbFK3RJoBdMKbFBZTuFJdh4MGWMU9wHayacyzoccfQ4LCUZm8wSqurXHHxMMzbLgIc4BTtGZ4spwVbJremY54w_49slh_1YcFxwGR2enR2rQZ6fDfcp_i7jG3ThzZTd2_O9Qj-_fX3c3jR3P77fbr_cNZZJXhqmwDsnhOiBDgMnoLwDYpij1lm16-ROKj8IzrjkvjOmE6wTnjrFvJVggV2hTyffQ4q_VpeLnkO2bppq3Lhm3ROgCgiv4If_wKe4pqVm00T1kktBZIWuT5BNMefkvD6kMJt01AT08xoaiK5raEY013WN-vH-bLvuZjf8w5_qr8DHM2ByLd7Xpm3IfzlGe8Z79gfN9pPG</recordid><startdate>20000401</startdate><enddate>20000401</enddate><creator>NAKATOMI, H</creator><creator>SEGAWA, H</creator><creator>KURATA, A</creator><creator>SHIOKAWA, Y</creator><creator>NAGATA, K</creator><creator>KAMIYAMA, H</creator><creator>UEKI, K</creator><creator>KIRINO, T</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20000401</creationdate><title>Clinicopathological study of intracranial fusiform and dolichoectatic aneurysms : Insight on the mechanism of growth</title><author>NAKATOMI, H ; SEGAWA, H ; KURATA, A ; SHIOKAWA, Y ; NAGATA, K ; KAMIYAMA, H ; UEKI, K ; KIRINO, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c384t-390fee555702dd4109fe01a3e2cec9b68b89fd543484f6aa65365f2e93fc80c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Cerebral Angiography</topic><topic>Cerebral Hemorrhage - etiology</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Humans</topic><topic>Intracranial Aneurysm - classification</topic><topic>Intracranial Aneurysm - diagnosis</topic><topic>Intracranial Aneurysm - pathology</topic><topic>Intracranial Aneurysm - surgery</topic><topic>Intracranial Thrombosis - etiology</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neovascularization, Pathologic - etiology</topic><topic>Neurology</topic><topic>Postoperative Complications - mortality</topic><topic>Treatment Outcome</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAKATOMI, H</creatorcontrib><creatorcontrib>SEGAWA, H</creatorcontrib><creatorcontrib>KURATA, A</creatorcontrib><creatorcontrib>SHIOKAWA, Y</creatorcontrib><creatorcontrib>NAGATA, K</creatorcontrib><creatorcontrib>KAMIYAMA, H</creatorcontrib><creatorcontrib>UEKI, K</creatorcontrib><creatorcontrib>KIRINO, T</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAKATOMI, H</au><au>SEGAWA, H</au><au>KURATA, A</au><au>SHIOKAWA, Y</au><au>NAGATA, K</au><au>KAMIYAMA, H</au><au>UEKI, K</au><au>KIRINO, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinicopathological study of intracranial fusiform and dolichoectatic aneurysms : Insight on the mechanism of growth</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2000-04-01</date><risdate>2000</risdate><volume>31</volume><issue>4</issue><spage>896</spage><epage>900</epage><pages>896-900</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Intracranial fusiform aneurysms can be divided into 2 clinically different subtypes: acute dissecting aneurysms and chronic fusiform or dolichoectatic aneurysms. Of these 2, the natural history and growth mechanism of chronic fusiform aneurysms remains unknown.
A consecutive series of 16 patients with chronic fusiform aneurysms was studied retrospectively to clarify patient clinical and neuroradiological features. Aneurysm tissues were obtained from 8 cases and were examined to identify histological features that could correspond to the radiological findings.
Four histological features were found: (1) fragmentation of internal elastic lamina (IEL), (2) neoangiogenesis within the thickened intima, (3) intramural hemorrhage (IMH) and thrombus formation, and (4) repetitive intramural hemorrhages from the newly formed vessels within thrombus. IEL fragmentation was found in all cases, which suggests that this change may be one of the earliest processes of aneurysm formation. MRI or CT detected IMH, and marked contrast enhancement of the inside of the aneurysm wall (CEI) on MRI corresponded well with intimal thickening. Eight of 9 symptomatic cases but none of 7 asymptomatic cases presented with both radiological features.
Data suggest that chronic fusiform aneurysms are progressive lesions that start with IEL fragmentation. Formation of IMH seems to be a critical event necessary for lesions to become symptomatic and progress, and this can be monitored on MRI. Knowledge of this possible mechanism of progression and corresponding MRI characteristics could help determine timing of surgical intervention.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10753995</pmid><doi>10.1161/01.STR.31.4.896</doi><tpages>5</tpages></addata></record> |
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subjects | Adult Aged Biological and medical sciences Cerebral Angiography Cerebral Hemorrhage - etiology Disease Progression Female Humans Intracranial Aneurysm - classification Intracranial Aneurysm - diagnosis Intracranial Aneurysm - pathology Intracranial Aneurysm - surgery Intracranial Thrombosis - etiology Magnetic Resonance Imaging Male Medical sciences Middle Aged Neovascularization, Pathologic - etiology Neurology Postoperative Complications - mortality Treatment Outcome Vascular diseases and vascular malformations of the nervous system |
title | Clinicopathological study of intracranial fusiform and dolichoectatic aneurysms : Insight on the mechanism of growth |
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