Hemodynamic compromise as a cause of internal border-zone infarction and cortical neuronal damage in atherosclerotic middle cerebral artery disease.
OBJECTIVE
Hemodynamic compromise due to atherosclerotic middle cerebral artery (MCA) disease may induce internal border-zone infarction and cortical neuronal damage. This study aimed to determine whether internal border-zone infarction is associated with increased oxygen extraction fraction (OEF) and a decrease in central benzodiazepine receptors (BZRs) in the overlying cerebral cortex in atherosclerotic MCA disease.


METHODS
We measured the OEF by using positron emission tomography and (15)O gas in 100 nondisabled patients with atherosclerotic MCA disease in the chronic stage. On MRI, the infarcts were categorized as territorial, border-zone (external or internal), deep perforator, and superior perforator infarcts. In 62 patients, BZRs were measured using (11)C-flumazenil. By using 3-dimensional stereotactic surface projections, the abnormally decreased BZR index ("BZR index") [(the extent of the pixels with Z score more than 2 compared with controls)x(average Z score in those pixels)] was calculated. In the hemisphere affected by MCA disease, the type of infarcts was correlated with the value of OEF or BZR index in the cerebral cortex of the MCA distribution.


RESULTS
Compared with patients without internal border-zone infarcts, those with these infarcts (n=18) had significantly increased OEF and significantly high BZR index. Multivariate analysis revealed that internal border-zone infarction was independently associated with increased OEF and high BZR index.


CONCLUSIONS
In atherosclerotic MCA disease, internal border-zone infarction is associated with increased OEF and a decrease in BZRs in the overlying cerebral cortex, suggesting that hemodynamic compromise may induce internal border-zone infarction and cortical neuronal damage.
Yamauchi
Hiroshi
H
Human Brain Research Center, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8507, Japan. yamauchi@kuhp.kyoto-u.ac.jp
Nishii
Ryuichi
R
Higashi
Tatsuya
T
Kagawa
Shinya
S
Fukuyama
Hidenao
H
D000368:Aged; D002250:Carbon Radioisotopes; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000098:blood supply / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D018450:Disease Progression; D005260:Female; D005442:Flumazenil; D018757:GABA Modulators; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007091:Image Processing, Computer-Assisted; D020244:Infarction, Middle Cerebral Artery / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D002537:Intracranial Arteriosclerosis / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009410:Nerve Degeneration / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D010101:Oxygen Consumption / Q000502:physiology; D010104:Oxygen Radioisotopes; D049268:Positron-Emission Tomography; D011237:Predictive Value of Tests; D011963:Receptors, GABA-A / Q000378:metabolism; D012680:Sensitivity and Specificity
D002250:Carbon Radioisotopes; D018757:GABA Modulators; D010104:Oxygen Radioisotopes; D011963:Receptors, GABA-A; D005442:Flumazenil