Electroencephalograms and regional cerebral blood flow in cases of brain infarction.
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In four hypertensive patients, acute lowering of blood pressure by therapeutic or diagnostic procedures caused visual disturbances ranging from transient visual hallucinations to severe, long-lasting visual impairment. These symptoms were associated with occipital lobe cerebral infarcts that tended to occur in the border zones between the major cerebral arteries. The infarcts may be seen as the combined result of a "watershed" effect during acute hypotension and the presence of structural hypertensive vascular adaptation. When a hypertensive patient complains of visual disturbances during acute blood pressure lowering, the pressure should be allowed to settle at a level somewhat above normal.
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Ten cases were treated with systematic administration of mannitol followed by the blood substitute, perfluorochemicals, in the acute period of cerebral infarction in order to suppress the development of infarction and progressive deterioration. This chemotherapy was followed by reconstructive vascular surgery. There were 8 cases of cerebral infarction and 2 other cases in which cerebral vascular occlusion occurred during surgery. Due to this treatment, there were no cases of aggravated condition or death and at the time of follow-up examination after 2 months, and 8 of the ten patients returned to productive lives. We consequently believe that this therapeutic method may prove to be the effective means for treating cerebral infarction in the acute period. It is also thought that this method is applicable in surgical cases where long-term vascular occlusion is required.
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The etiology of lacunar CCT lesions is controversial. We report a patient with recurrent ischemia in the territory of the right internal carotid artery. CCT initially showed a fresh non-lacunar lesion in the area of the basal ganglia and internal capsule. Subsequently, repeat CCT revealed a singular lacunar defect in the internal capsule. The Doppler sonographic investigations showed an internal carotid artery occlusion. This case supports the hypothesis that an embolic or hemodynamic etiology of the lacunae is possible.