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Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation

BACKGROUND: Our purpose was to study the association between the intracranial atherosclerosis as measured by cavernous carotid artery calcification (ICAC) observed on head CT and atrophic changes of supra-tentorial brain demonstrated by MRI. METHODS: Institutional review board approval was obtained...

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Autores principales: Erbay, S, Han, R, Aftab, M, Zou, Kelly H, Polak, JF, Bhadelia, Rafeeque A
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630977/
https://www.ncbi.nlm.nih.gov/pubmed/19102733
http://dx.doi.org/10.1186/1471-2377-8-51
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author Erbay, S
Han, R
Aftab, M
Zou, Kelly H
Polak, JF
Bhadelia, Rafeeque A
author_facet Erbay, S
Han, R
Aftab, M
Zou, Kelly H
Polak, JF
Bhadelia, Rafeeque A
author_sort Erbay, S
collection PubMed
description BACKGROUND: Our purpose was to study the association between the intracranial atherosclerosis as measured by cavernous carotid artery calcification (ICAC) observed on head CT and atrophic changes of supra-tentorial brain demonstrated by MRI. METHODS: Institutional review board approval was obtained for this retrospective study incorporating 65 consecutive patients presenting acutely who had both head CT and MRI. Arterial calcifications of the intracranial cavernous carotids (ICAC) were assigned a number (1 to 4) in the bone window images from CT scans. These 4 groups were then combined into high (grades 3 and 4) and low calcium (grades 1 and 2) subgroups. Brain MRI was independently evaluated to identify cortical and central atrophy. Demographics and cardiovascular risk factors were evaluated in subjects with high and low ICAC. Relationship between CT demonstrated ICAC and brain atrophy patterns were evaluated both without and with adjustment for cerebral ischemic scores and cardiovascular risk factors. RESULTS: Forty-six of the 65 (71%) patients had high ICAC on head CT. Subjects with high ICAC were older, and had higher prevalence of hypertension, diabetes, coronary artery disease (CAD), atrial fibrillation and history of previous stroke (CVA) compared to those with low ICAC. Age demonstrated strong correlation with both supratentorial atrophy patterns. There was no correlation between ICAC and cortical atrophy. There was correlation however between central atrophy and ICAC. This persisted even after adjustment for age. CONCLUSION: Age is the most important determinant of atrophic cerebral changes. However, high ICAC demonstrated age independent association with central atrophy.
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spelling pubmed-26309772009-01-27 Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation Erbay, S Han, R Aftab, M Zou, Kelly H Polak, JF Bhadelia, Rafeeque A BMC Neurol Research Article BACKGROUND: Our purpose was to study the association between the intracranial atherosclerosis as measured by cavernous carotid artery calcification (ICAC) observed on head CT and atrophic changes of supra-tentorial brain demonstrated by MRI. METHODS: Institutional review board approval was obtained for this retrospective study incorporating 65 consecutive patients presenting acutely who had both head CT and MRI. Arterial calcifications of the intracranial cavernous carotids (ICAC) were assigned a number (1 to 4) in the bone window images from CT scans. These 4 groups were then combined into high (grades 3 and 4) and low calcium (grades 1 and 2) subgroups. Brain MRI was independently evaluated to identify cortical and central atrophy. Demographics and cardiovascular risk factors were evaluated in subjects with high and low ICAC. Relationship between CT demonstrated ICAC and brain atrophy patterns were evaluated both without and with adjustment for cerebral ischemic scores and cardiovascular risk factors. RESULTS: Forty-six of the 65 (71%) patients had high ICAC on head CT. Subjects with high ICAC were older, and had higher prevalence of hypertension, diabetes, coronary artery disease (CAD), atrial fibrillation and history of previous stroke (CVA) compared to those with low ICAC. Age demonstrated strong correlation with both supratentorial atrophy patterns. There was no correlation between ICAC and cortical atrophy. There was correlation however between central atrophy and ICAC. This persisted even after adjustment for age. CONCLUSION: Age is the most important determinant of atrophic cerebral changes. However, high ICAC demonstrated age independent association with central atrophy. BioMed Central 2008-12-22 /pmc/articles/PMC2630977/ /pubmed/19102733 http://dx.doi.org/10.1186/1471-2377-8-51 Text en Copyright © 2008 Erbay et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Erbay, S
Han, R
Aftab, M
Zou, Kelly H
Polak, JF
Bhadelia, Rafeeque A
Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation
title Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation
title_full Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation
title_fullStr Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation
title_full_unstemmed Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation
title_short Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation
title_sort is intracranial atherosclerosis an independent risk factor for cerebral atrophy? a retrospective evaluation
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630977/
https://www.ncbi.nlm.nih.gov/pubmed/19102733
http://dx.doi.org/10.1186/1471-2377-8-51
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