Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-3-1
pubmed:abstractText
In atherosclerotic internal carotid artery (ICA) or middle cerebral artery (MCA) disease, hemodynamic compromise may cause selective neuronal damage manifested as loss of central benzodiazepine receptors (BZRs) in the normal-appearing cerebral cortex, without overt episode of stroke. To investigate the association of decreases in cortical BZRs with hemodynamic compromise and the effect of angiotensin receptor blockers (ARBs) on these receptors in patients whose atherosclerotic ICA or MCA disease is asymptomatic, we measured BZRs using positron emission tomography and (11)C-flumazenil in 79 patients with asymptomatic atherosclerotic ICA or MCA disease and no cortical infarction. Three-dimensional stereotactic surface projections were used to calculate the BZR index, a measure of abnormally decreased BZRs in the cerebral cortex within the MCA distribution. Multiple regression analysis showed this index to be positively correlated with the value of oxygen extraction fraction, with the presence of silent subcortical infarcts, and with the presence of ischemic heart disease, whereas it was negatively correlated with the treatment of hypertension with ARBs. In asymptomatic atherosclerotic ICA or MCA disease, hemodynamic compromise is associated with selective neuronal damage manifested as decreases in cortical BZRs in the noninfarcted cerebral cortex, whereas ARBs are associated with preservation of cortical BZRs.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-10563635, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-10616876, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-10690980, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-10782772, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-10791504, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-11435791, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-12932111, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-15100552, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-16330559, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-16385090, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-16545753, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-17380523, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-18287271, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-18458865, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-1852179, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-18678564, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-18705984, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-19074482, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-19223148, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-19307539, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-19727113, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-19797182, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-20035502, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-2042939, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-20508190, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-2219203, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-3532434, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-6971299, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-7790950, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-8248987, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-8614945, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-8676151, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-8784228, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-8996500, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-9472889, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-9550507, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-9757852, http://linkedlifedata.com/resource/pubmed/commentcorrection/20877388-9823834
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1559-7016
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
953-61
pubmed:dateRevised
2011-7-28
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Silent cortical neuronal damage in atherosclerotic disease of the major cerebral arteries.
pubmed:affiliation
Department of Functional Neuroimaging, Human Brain Research Center, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan. yamauchi@kuhp.kyoto-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't