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Cerebral MicroembolizationI. Pathophysiological Studies
W. Michael Vise, MD;
Franz Schuier, MD;
Konstantin-A. Hossmann, MD;
Suguru Takagi, MD;
Klaus J. Zülch, MD
Arch Neurol. 1977;34(11):660-665.
Abstract
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Unilateral embolization of the brain was performed in cats by intracarotid injection of 10.5 million carbonized microspheres (15 ± 5 µ). Intracranial pressure increased from 6.1 ±1.5 to 14 ± 2.3 mm Hg within two minutes and continued to rise more slowly to 24 ± 18.3 mm Hg within four hours. Embolization caused a nonhomogenous distribution of microflow, but initially had no effect on global cerebral blood flow, nor on cortical oxygen tension. Yet, a functional suppression of cortical electrical and metabolic activity occurred. The ipsilateral EEG flattened irreversibly after 15 seconds; the contralateral EEG was transiently suppressed shortly thereafter. Arteriovenous difference of oxygen fell from 10.5 ± 0.7 to 5.3 ± 0.6 vol%, and the arteriovenous difference of glucose fell from 11.7 ± 3.9 to 2.6 ± 2.1 mg/100 ml as a consequence of reduced oxygen and glucose extraction. Subsequently, severe vasogenic brain edema, secondary ischemia, and severe functional suppression developed between two and four hours.
Author Affiliations
From the Max-Plancke-Institut für Hirnforschung, West Germany. Dr Vise is presently with the Mississippi Methodist Rehabilitation Center, University of Mississippi Medical Center, Jackson. Dr Schuier is presently with the Neurological Clinic, University of Dusseldorf, West Germany. Dr Takagi is presently with the Neurosurgical Department, Juntendo University, Tokyo.
Footnotes
Accepted for publication June 9, 1977.
Reprint requests to Max-Planck-Institut für Hirnforschung, Ostmerheimerstrasse 200, 5000 Köln 91, West Germany (Dr Hossmann).
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