title: Selective neuronal damage and borderzone infarction in carotid artery occlusive disease: a 11C-flumazenil PET study.
abstract: The pathogenesis of selective neuronal damage in internal carotid artery (ICA) occlusive disease is unclear. Imaging of the central-type benzodiazepine receptor (BZR), which is expressed by most cortical neurons, provides information on the neuronal alterations induced by ischemia in vivo. Hemodynamic ischemia due to ICA occlusive disease may cause not only borderzone infarction but also selective neuronal damage beyond the regions of infarcts, which may be detected by a decrease in BZR in the normal-appearing cerebral cortex. The purpose of this study was to determine whether selective neuronal damage is associated with borderzone infarction in ICA occlusive disease.
  
  
  METHODS
  We measured BZR using PET and 11C-flumazenil in 62 nondisabled patients with ICA steno-occlusive lesions in the chronic stage. Flumazenil binding potential (BP) was calculated using the dynamic data and the reference tissue model. The infarcts on MRI-which were categorized as territorial, borderzone (external or internal), striatocapsular, lacunar, and other white matter infarcts-were correlated with the mean cerebral/cerebellar cortical BP ratio in the hemisphere with ICA occlusive disease.
  
  
  RESULTS
  Patients with borderzone infarction (n=18) had a significantly decreased flumazenil BP ratio in the hemisphere with ICA occlusive disease compared with patients without borderzone infarction (n=44) and healthy control subjects (n=10). Multivariate analysis showed that external borderzone infarction was an independent predictor of the decreased flumazenil BP ratio.
  
  
  CONCLUSIONS
  In ICA occlusive disease, selective neuronal damage demonstrated as decreased BZR is associated with borderzone infarction, suggesting that hemodynamic ischemia leading to borderzone infarction may cause selective neuronal damage beyond the regions of infarcts in the chronic stage.
authors.affiliation: Research Institute, Shiga Medical Center, Moriyama, Japan. yamauchi@shigamed.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yamauchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Kudoh
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Kishibe
authors.forename: Jinei
authors.initials: J
authors.lastname: Iwasaki
authors.forename: Shinya
authors.initials: S
authors.lastname: Kagawa
mesh_terms: D001157:Arterial Occlusive Diseases / Q000000981:diagnostic imaging* / Q000473:pathology*; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging* / Q000473:pathology*; D002531:Cerebellum / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D005442:Flumazenil / Q000494:pharmacology*; D018757:GABA Modulators / Q000494:pharmacology*; D006439:Hemodynamics; D006801:Humans; D002546:Ischemic Attack, Transient / Q000000981:diagnostic imaging / Q000473:pathology; D008279:Magnetic Resonance Imaging / Q000379:methods; D015233:Models, Statistical; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D049268:Positron-Emission Tomography / Q000379:methods*; D019275:Radiopharmaceuticals / Q000494:pharmacology*; D020521:Stroke / Q000000981:diagnostic imaging / Q000473:pathology; D013997:Time Factors; D014055:Tomography, Emission-Computed
chemical_list: D018757:GABA Modulators; D019275:Radiopharmaceuticals; D005442:Flumazenil