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James B. Brierley, MD; Brian S. Meldrum, MB, PhD; Alwyn W. Brown, BSc

Arch Neurol. 1973;29(6):367-374.

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

It is essential to emphasize at the outset that "anoxic-ischemic" cell change is not, as the term suggests, a neuronal alteration due to anoxiaischemia alone. The term anoxia-is-chemia was introduced by Levine¹ to characterize the stress to which one cerebral hemisphere of his preparation in the rat was exposed. The whole brain endured hypoxemia because the animal was exposed intermittently to nitrogen or nitrous oxide. One cerebral hemisphere endured an additional ischemia because the common carotid artery had been ligated on that side. Within that hemisphere (and sometimes in the other) the neuronal alteration was ischemic cell change as described by Spielmeyer.² It is equally important to emphasize that ischemic cell change is the neuropathologic common denominator in all types of "hypoxia." Thus, it is seen after (1) circulatory arrest; (2) profound hypotension without hypoxemia (oligemia); (3) hypotension with hypoxemia; (4) primary hypoxemia with secondary myocardial . . . [Full Text PDF of this Article]

Author Affiliations
Carshalton, Surrey, England; London; Carshalton

From the Medical Research Council Neuropsychiatry Unit, Carshalton, Surrey, England (Drs. Brierley and Brown), and the Department of Neurology, Institute of Psychiatry, London (Dr. Meldrum).

Footnotes
Read before the symposium held at New York Hospital—Cornell Medical Center: The Threshold and Mechanisms of Anoxic-Ischemic Brain Injury, New York, June 10,1973.

Reprint requests to Medical Research Council Neuropsychiatry Unit, Carshalton, Surrey, England (Dr. Brierley).

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