Loading…
Collateralization and ischemia in hemodynamic cerebrovascular insufficiency
Background Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the...
Saved in:
| Published in: | Acta neurochirurgica 2014-11, Vol.156 (11), p.2051-2058 |
|---|---|
| Main Authors: | , , , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943 |
| container_end_page | 2058 |
| container_issue | 11 |
| container_start_page | 2051 |
| container_title | Acta neurochirurgica |
| container_volume | 156 |
| creator | Czabanka, Marcus Acker, Gueliz Jussen, Daniel Finger, Tobias Pena-Tapia, Pablo Schubert, Gerrit A. Scharf, Johann Martus, Peter Schmiedek, Peter Vajkoczy, Peter |
| description | Background
Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the development of hemodynamic ischemia remain unknown. The aim was to characterize collateralization and ischemia patterns in patients with chronic hemodynamic compromise.
Methods
Hemodynamic compromise was verified using acetazolamide-stimulated xenon-CT or SPECT in 54 patients [30 moyamoya and 24 atherosclerotic cerebrovascular disease (ACVD)]. All patients received MRI to differentiate hemodynamic ischemia into anterior/posterior cortical border zone infarction (CBI), inferior border zone infarction (IBI) or territorial infarction (TI). Digital subtraction angiography was applied to evaluate collateralization. Collateralization was compared and correlated with the localization of ischemia and number of vascular territories with impaired cerebrovascular reserve capacity (CVRC).
Results
MM patients showed collateralization significantly more often via pericallosal anastomosis and the posterior communicating artery (flow in the anterior-posterior direction; MM: 95 %/95 % vs. ACVD: 23 %/12 %,
p
|
| doi_str_mv | 10.1007/s00701-014-2227-1 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1627985181</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3460909461</sourcerecordid><originalsourceid>FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943</originalsourceid><addsrcrecordid>eNqNkUtLxDAUhYMozjj6A9xIwY2bam6aR7OUwRcKbnQd0jTVDH2MSSuMv96UjiKC4ObmhvPl5F4OQseAzwFjcRFiwZBioCkhRKSwg-ZYUpLGgndjj6PKCc9n6CCEVbwRQbN9NCOMsIwTOUf3y66udW-9rt2H7l3XJrotExfMq22cTlybxKYrN61unEmM9bbw3bsOZqi1j3IYqsoZZ1uzOUR7la6DPdqeC_R8ffW0vE0fHm_ulpcPqaGC9ankFkDgnOJSQk4ko4ZrkFoYXggoJCkgLwSzQmubUVpmBTaCc8osK7WWNFugs8l37bu3wYZeNXFeG_dobTcEBZwImTPI4R8oECkkkTiip7_QVTf4Ni4yUsAxphmLFEyU8V0I3lZq7V2j_UYBVmMoagpFxVDUGIoahzjZOg9FY8vvF18pRIBMQIhS-2L9j6__dP0E5HmV0g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1611600435</pqid></control><display><type>article</type><title>Collateralization and ischemia in hemodynamic cerebrovascular insufficiency</title><source>Springer Nature</source><creator>Czabanka, Marcus ; Acker, Gueliz ; Jussen, Daniel ; Finger, Tobias ; Pena-Tapia, Pablo ; Schubert, Gerrit A. ; Scharf, Johann ; Martus, Peter ; Schmiedek, Peter ; Vajkoczy, Peter</creator><creatorcontrib>Czabanka, Marcus ; Acker, Gueliz ; Jussen, Daniel ; Finger, Tobias ; Pena-Tapia, Pablo ; Schubert, Gerrit A. ; Scharf, Johann ; Martus, Peter ; Schmiedek, Peter ; Vajkoczy, Peter</creatorcontrib><description>Background
Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the development of hemodynamic ischemia remain unknown. The aim was to characterize collateralization and ischemia patterns in patients with chronic hemodynamic compromise.
Methods
Hemodynamic compromise was verified using acetazolamide-stimulated xenon-CT or SPECT in 54 patients [30 moyamoya and 24 atherosclerotic cerebrovascular disease (ACVD)]. All patients received MRI to differentiate hemodynamic ischemia into anterior/posterior cortical border zone infarction (CBI), inferior border zone infarction (IBI) or territorial infarction (TI). Digital subtraction angiography was applied to evaluate collateralization. Collateralization was compared and correlated with the localization of ischemia and number of vascular territories with impaired cerebrovascular reserve capacity (CVRC).
Results
MM patients showed collateralization significantly more often via pericallosal anastomosis and the posterior communicating artery (flow in the anterior-posterior direction; MM: 95 %/95 % vs. ACVD: 23 %/12 %,
p
< 0.05). ACVD patients demonstrated collateralization via the anterior and posterior communicating arteries (flow in the posterior-anterior direction, MM: 6 %/5 % vs. ACVD: 62 %/88 %,
p
< 0.05). Patterns of infarction were comparable (aCBI: MM: 36 % vs. ACVD: 35 %; pCBI: MM: 10 % vs. ACVD: 20 %; IBI: MM: 35 % vs. ACVD: 41 %; TI: MM: 13 % vs. ACVD: 18 %). The number and localization of vascular territories with impaired CVRC were comparable.
Conclusions
Despite significant differences in collateralization, the infarct patterns and severity of CVRC impairment do not differ between MMV and ACVD patients. Cerebral collateralization does not allow reaching conclusions about the localization of cerebral ischemia or severity of impaired CVRC in chronic hemodynamic impairment.</description><identifier>ISSN: 0001-6268</identifier><identifier>EISSN: 0942-0940</identifier><identifier>DOI: 10.1007/s00701-014-2227-1</identifier><identifier>PMID: 25253629</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>Adult ; Angiography, Digital Subtraction ; Cerebral Angiography ; Cerebral Infarction - etiology ; Cerebral Infarction - physiopathology ; Cerebrovascular Circulation ; Cerebrovascular Disorders - etiology ; Cerebrovascular Disorders - physiopathology ; Clinical Article - Vascular ; Collateral Circulation ; Female ; Hemodynamics - physiology ; Humans ; Interventional Radiology ; Intracranial Arteriosclerosis - complications ; Intracranial Arteriosclerosis - physiopathology ; Magnetic Resonance Imaging ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Minimally Invasive Surgery ; Moyamoya Disease - complications ; Moyamoya Disease - physiopathology ; Neurology ; Neuroradiology ; Neurosurgery ; Surgical Orthopedics ; Tomography, Emission-Computed, Single-Photon</subject><ispartof>Acta neurochirurgica, 2014-11, Vol.156 (11), p.2051-2058</ispartof><rights>Springer-Verlag Wien 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943</citedby><cites>FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25253629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Czabanka, Marcus</creatorcontrib><creatorcontrib>Acker, Gueliz</creatorcontrib><creatorcontrib>Jussen, Daniel</creatorcontrib><creatorcontrib>Finger, Tobias</creatorcontrib><creatorcontrib>Pena-Tapia, Pablo</creatorcontrib><creatorcontrib>Schubert, Gerrit A.</creatorcontrib><creatorcontrib>Scharf, Johann</creatorcontrib><creatorcontrib>Martus, Peter</creatorcontrib><creatorcontrib>Schmiedek, Peter</creatorcontrib><creatorcontrib>Vajkoczy, Peter</creatorcontrib><title>Collateralization and ischemia in hemodynamic cerebrovascular insufficiency</title><title>Acta neurochirurgica</title><addtitle>Acta Neurochir</addtitle><addtitle>Acta Neurochir (Wien)</addtitle><description>Background
Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the development of hemodynamic ischemia remain unknown. The aim was to characterize collateralization and ischemia patterns in patients with chronic hemodynamic compromise.
Methods
Hemodynamic compromise was verified using acetazolamide-stimulated xenon-CT or SPECT in 54 patients [30 moyamoya and 24 atherosclerotic cerebrovascular disease (ACVD)]. All patients received MRI to differentiate hemodynamic ischemia into anterior/posterior cortical border zone infarction (CBI), inferior border zone infarction (IBI) or territorial infarction (TI). Digital subtraction angiography was applied to evaluate collateralization. Collateralization was compared and correlated with the localization of ischemia and number of vascular territories with impaired cerebrovascular reserve capacity (CVRC).
Results
MM patients showed collateralization significantly more often via pericallosal anastomosis and the posterior communicating artery (flow in the anterior-posterior direction; MM: 95 %/95 % vs. ACVD: 23 %/12 %,
p
< 0.05). ACVD patients demonstrated collateralization via the anterior and posterior communicating arteries (flow in the posterior-anterior direction, MM: 6 %/5 % vs. ACVD: 62 %/88 %,
p
< 0.05). Patterns of infarction were comparable (aCBI: MM: 36 % vs. ACVD: 35 %; pCBI: MM: 10 % vs. ACVD: 20 %; IBI: MM: 35 % vs. ACVD: 41 %; TI: MM: 13 % vs. ACVD: 18 %). The number and localization of vascular territories with impaired CVRC were comparable.
Conclusions
Despite significant differences in collateralization, the infarct patterns and severity of CVRC impairment do not differ between MMV and ACVD patients. Cerebral collateralization does not allow reaching conclusions about the localization of cerebral ischemia or severity of impaired CVRC in chronic hemodynamic impairment.</description><subject>Adult</subject><subject>Angiography, Digital Subtraction</subject><subject>Cerebral Angiography</subject><subject>Cerebral Infarction - etiology</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Cerebrovascular Circulation</subject><subject>Cerebrovascular Disorders - etiology</subject><subject>Cerebrovascular Disorders - physiopathology</subject><subject>Clinical Article - Vascular</subject><subject>Collateral Circulation</subject><subject>Female</subject><subject>Hemodynamics - physiology</subject><subject>Humans</subject><subject>Interventional Radiology</subject><subject>Intracranial Arteriosclerosis - complications</subject><subject>Intracranial Arteriosclerosis - physiopathology</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Minimally Invasive Surgery</subject><subject>Moyamoya Disease - complications</subject><subject>Moyamoya Disease - physiopathology</subject><subject>Neurology</subject><subject>Neuroradiology</subject><subject>Neurosurgery</subject><subject>Surgical Orthopedics</subject><subject>Tomography, Emission-Computed, Single-Photon</subject><issn>0001-6268</issn><issn>0942-0940</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqNkUtLxDAUhYMozjj6A9xIwY2bam6aR7OUwRcKbnQd0jTVDH2MSSuMv96UjiKC4ObmhvPl5F4OQseAzwFjcRFiwZBioCkhRKSwg-ZYUpLGgndjj6PKCc9n6CCEVbwRQbN9NCOMsIwTOUf3y66udW-9rt2H7l3XJrotExfMq22cTlybxKYrN61unEmM9bbw3bsOZqi1j3IYqsoZZ1uzOUR7la6DPdqeC_R8ffW0vE0fHm_ulpcPqaGC9ankFkDgnOJSQk4ko4ZrkFoYXggoJCkgLwSzQmubUVpmBTaCc8osK7WWNFugs8l37bu3wYZeNXFeG_dobTcEBZwImTPI4R8oECkkkTiip7_QVTf4Ni4yUsAxphmLFEyU8V0I3lZq7V2j_UYBVmMoagpFxVDUGIoahzjZOg9FY8vvF18pRIBMQIhS-2L9j6__dP0E5HmV0g</recordid><startdate>20141101</startdate><enddate>20141101</enddate><creator>Czabanka, Marcus</creator><creator>Acker, Gueliz</creator><creator>Jussen, Daniel</creator><creator>Finger, Tobias</creator><creator>Pena-Tapia, Pablo</creator><creator>Schubert, Gerrit A.</creator><creator>Scharf, Johann</creator><creator>Martus, Peter</creator><creator>Schmiedek, Peter</creator><creator>Vajkoczy, Peter</creator><general>Springer Vienna</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20141101</creationdate><title>Collateralization and ischemia in hemodynamic cerebrovascular insufficiency</title><author>Czabanka, Marcus ; Acker, Gueliz ; Jussen, Daniel ; Finger, Tobias ; Pena-Tapia, Pablo ; Schubert, Gerrit A. ; Scharf, Johann ; Martus, Peter ; Schmiedek, Peter ; Vajkoczy, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Angiography, Digital Subtraction</topic><topic>Cerebral Angiography</topic><topic>Cerebral Infarction - etiology</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Cerebrovascular Circulation</topic><topic>Cerebrovascular Disorders - etiology</topic><topic>Cerebrovascular Disorders - physiopathology</topic><topic>Clinical Article - Vascular</topic><topic>Collateral Circulation</topic><topic>Female</topic><topic>Hemodynamics - physiology</topic><topic>Humans</topic><topic>Interventional Radiology</topic><topic>Intracranial Arteriosclerosis - complications</topic><topic>Intracranial Arteriosclerosis - physiopathology</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Minimally Invasive Surgery</topic><topic>Moyamoya Disease - complications</topic><topic>Moyamoya Disease - physiopathology</topic><topic>Neurology</topic><topic>Neuroradiology</topic><topic>Neurosurgery</topic><topic>Surgical Orthopedics</topic><topic>Tomography, Emission-Computed, Single-Photon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Czabanka, Marcus</creatorcontrib><creatorcontrib>Acker, Gueliz</creatorcontrib><creatorcontrib>Jussen, Daniel</creatorcontrib><creatorcontrib>Finger, Tobias</creatorcontrib><creatorcontrib>Pena-Tapia, Pablo</creatorcontrib><creatorcontrib>Schubert, Gerrit A.</creatorcontrib><creatorcontrib>Scharf, Johann</creatorcontrib><creatorcontrib>Martus, Peter</creatorcontrib><creatorcontrib>Schmiedek, Peter</creatorcontrib><creatorcontrib>Vajkoczy, Peter</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Acta neurochirurgica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Czabanka, Marcus</au><au>Acker, Gueliz</au><au>Jussen, Daniel</au><au>Finger, Tobias</au><au>Pena-Tapia, Pablo</au><au>Schubert, Gerrit A.</au><au>Scharf, Johann</au><au>Martus, Peter</au><au>Schmiedek, Peter</au><au>Vajkoczy, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Collateralization and ischemia in hemodynamic cerebrovascular insufficiency</atitle><jtitle>Acta neurochirurgica</jtitle><stitle>Acta Neurochir</stitle><addtitle>Acta Neurochir (Wien)</addtitle><date>2014-11-01</date><risdate>2014</risdate><volume>156</volume><issue>11</issue><spage>2051</spage><epage>2058</epage><pages>2051-2058</pages><issn>0001-6268</issn><eissn>0942-0940</eissn><abstract>Background
Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the development of hemodynamic ischemia remain unknown. The aim was to characterize collateralization and ischemia patterns in patients with chronic hemodynamic compromise.
Methods
Hemodynamic compromise was verified using acetazolamide-stimulated xenon-CT or SPECT in 54 patients [30 moyamoya and 24 atherosclerotic cerebrovascular disease (ACVD)]. All patients received MRI to differentiate hemodynamic ischemia into anterior/posterior cortical border zone infarction (CBI), inferior border zone infarction (IBI) or territorial infarction (TI). Digital subtraction angiography was applied to evaluate collateralization. Collateralization was compared and correlated with the localization of ischemia and number of vascular territories with impaired cerebrovascular reserve capacity (CVRC).
Results
MM patients showed collateralization significantly more often via pericallosal anastomosis and the posterior communicating artery (flow in the anterior-posterior direction; MM: 95 %/95 % vs. ACVD: 23 %/12 %,
p
< 0.05). ACVD patients demonstrated collateralization via the anterior and posterior communicating arteries (flow in the posterior-anterior direction, MM: 6 %/5 % vs. ACVD: 62 %/88 %,
p
< 0.05). Patterns of infarction were comparable (aCBI: MM: 36 % vs. ACVD: 35 %; pCBI: MM: 10 % vs. ACVD: 20 %; IBI: MM: 35 % vs. ACVD: 41 %; TI: MM: 13 % vs. ACVD: 18 %). The number and localization of vascular territories with impaired CVRC were comparable.
Conclusions
Despite significant differences in collateralization, the infarct patterns and severity of CVRC impairment do not differ between MMV and ACVD patients. Cerebral collateralization does not allow reaching conclusions about the localization of cerebral ischemia or severity of impaired CVRC in chronic hemodynamic impairment.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>25253629</pmid><doi>10.1007/s00701-014-2227-1</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0001-6268 |
| ispartof | Acta neurochirurgica, 2014-11, Vol.156 (11), p.2051-2058 |
| issn | 0001-6268 0942-0940 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1627985181 |
| source | Springer Nature |
| subjects | Adult Angiography, Digital Subtraction Cerebral Angiography Cerebral Infarction - etiology Cerebral Infarction - physiopathology Cerebrovascular Circulation Cerebrovascular Disorders - etiology Cerebrovascular Disorders - physiopathology Clinical Article - Vascular Collateral Circulation Female Hemodynamics - physiology Humans Interventional Radiology Intracranial Arteriosclerosis - complications Intracranial Arteriosclerosis - physiopathology Magnetic Resonance Imaging Male Medicine Medicine & Public Health Middle Aged Minimally Invasive Surgery Moyamoya Disease - complications Moyamoya Disease - physiopathology Neurology Neuroradiology Neurosurgery Surgical Orthopedics Tomography, Emission-Computed, Single-Photon |
| title | Collateralization and ischemia in hemodynamic cerebrovascular insufficiency |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T04%3A51%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Collateralization%20and%20ischemia%20in%20hemodynamic%20cerebrovascular%20insufficiency&rft.jtitle=Acta%20neurochirurgica&rft.au=Czabanka,%20Marcus&rft.date=2014-11-01&rft.volume=156&rft.issue=11&rft.spage=2051&rft.epage=2058&rft.pages=2051-2058&rft.issn=0001-6268&rft.eissn=0942-0940&rft_id=info:doi/10.1007/s00701-014-2227-1&rft_dat=%3Cproquest_cross%3E3460909461%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c475t-96e1170840d9182954c6a19a7c6b71b92b18b75e7aae344d3b0c76645e5daa943%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1611600435&rft_id=info:pmid/25253629&rfr_iscdi=true |