@article{oai:nagasaki-u.repo.nii.ac.jp:00015752,
 author = {柴田, 尚武 and 堤, 健二 and 森, 和夫 and 安永, 暁生},
 issue = {4},
 journal = {Neurologia medico-chirurgica},
 month = {Apr},
 note = {Experimental cerebral infarction was induced in 33 dogs by injecting a silicone rubber cylinder through the cervical internal carotid artery. The embolus was found to have obstructed the osseous portion of the internal carotid artery in 15 dogs, trifurcation of the internal carotid artery into the posterior communicating, anterior cerebral, and middle cerebral arteries in ten dogs, and the proximal portion of the middle cerebral artery in eight dogs. The non-perfused areas in seven standard coronal sections of each brain were shown by carbon perfusion 24 hours after embolization. The following four different patterns of cerebral infarction were established: (1) Large sized infarction of the cerebral hemisphere showing a large carbon perfusion defect in the cerebral cortex, the subcortical and deep white matter, and in the basal ganglia. Area of the perfusion defect was larger than fifty percent of the total area of the hemisphere in each of three serial slices. One of six infarcts was hemorrhagic. (2) Small sized infarction of the cerebral hemisphere showing an area of perfusion defect smaller than fifty percent of the total area of the hemisphere. All of seven infarcts were ischemic. (3) Watershed infarction demonstrating multiple carbon perfusion defects in the arterial borderline and terminal zone of the cortex and white matter or in the basal ganglia. Eight of 17infarcts were hemorrhagic. (4) Thalamic infarction showing a carbon perfusion defect in a wide area of the thalamus. Two of three infarcts were hemorrhagic. This classification of infarction in the dog may play an important role in evaluating the computed tomographic findings of cerebral infarction in clinical cases., Neurologia medico-chirurgica, 22(4), pp.262-266; 1982},
 pages = {262--266},
 title = {脳梗塞に関する実験的研究(第5報) : 梗塞巣分類について},
 volume = {22},
 year = {1982}
}