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FRED PLUM, MD; JEROME B. POSNER, MD; ELLSWORTH C. ALVORD, JR, MD

Arch Neurol. 1963;9(6):563-570.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Some cerebral edema always accompanies ischemic infarction and contributes to symptoms in a substantial number of human cases.¹ Although the edema usually is greater with large than with small infarcts,² morphologic correlation sometimes is poor. This raises the question in ischemic lesions whether there is a stage of prenecrotic swelling or of swelling independent of necrosis; the corollary question is whether swelling itself contributes to the eventual size of the brain infarct. To investigate this we attempted to induce in rats graded anoxicischemic cerebral lesions; small animals were chosen in order to have sufficient numbers to analyze results. Because of the well-known narrow margin in rats between producing no brain lesion at all and producing death by anoxia, a modification of Levine's³ technique combining carotid ligation with anoxic exposure was employed. Whereas Levine (and Spector⁴) exposed animals to severe hypoxia for variable periods of time . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK; SEATTLE

From the divisions of Neurology and Neuropathology, University of Washington School of Medicine, Seattle, and the Department of Neurology, Cornell-New York Hospital Medical Center, New York.

Footnotes
Submitted for publication Sept 13, 1963; accepted Sept 14.

This study was assisted by grant NB 01034 from the US Public Health Service.

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