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BRAIN

Topographic Distribution of Misery Perfusion in Relation to Internal and Superficial Borderzones

Shuji Arakawaa, Kazuo Minematsua, Teruyuki Hiranoa, Yutaka Tanakaa, Yasuhiro Hasegawaa, Kohei Hayashidab and Takenori Yamaguchia

a Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan
b Department of Diagnostic Radiology, National Cardiovascular Center, Osaka, Japan

Address reprint requests to: Kazuo Minematsu, MD, Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, 5–7–1 Fujishirodai, Suita, Osaka 565-8565, Japan

BACKGROUND AND PURPOSE: Whether misery perfusion (MP) commonly accompanies brain borderzones (BZs) in patients with major cerebral artery occlusion remains unclear. We elucidated topographic patterns of chronic hemodynamic failure in such patients.

METHODS: Twenty-four patients with unilateral occlusion or severe stenosis (>75% in diameter) of the internal carotid artery (ICA) or middle cerebral arterial (MCA) trunk with minimal or no infarct underwent PET with 15O-labeled gas inhalation. Mean cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral metabolic rate of oxygen, oxygen extraction fraction (OEF), and CBV/CBF ratio were determined in the superficial BZs, internal BZ, and MCA territory excluding BZs. Values in BZs were standardized and compared with those in controls. Topographic distributions of regions with OEF greater than that in controls were determined.

RESULTS: Values in patients and controls were not significantly different. Topographic distributions included matched perfusion in 10 patients, MP in only the ipsilateral internal BZ in four, MP in both ipsilateral internal and superficial BZs in two, MP in the ipsilateral MCA territory including BZs in one, MP in the ipsilateral MCA territory including BZs and contralateral BZs in two, and MP in the ipsilateral MCA territories including BZs in five.

CONCLUSION: Only 25% of the patients had MP localized in affected BZs Although localized MP more frequently accompanied the internal BZ than other regions, no patient had elevated OEF in the superficial BZ alone. These results are inconsistent with clinical observations that 80% of BZ infarctions develop superficially. Thus, hemodynamic mechanisms may not cause most superficial BZ infarctions.




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