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Fred Plum, MD

Arch Neurol. 1973;29(6):359-360.

	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 has been the conventional wisdom among seasoned neurological clinicians that the brain is almost uniquely vulnerable to anoxia or ischemia. It has been well-documented that the greater part of brain function is temporarily lost after a circulatory interruption of as little as six seconds, and bedside experience would indicate that the organ becomes permanently damaged within a very few minutes after exposure to either nitrogen breathing, such as sometimes happens in the operating room, or an interrupted cardiac output, such as happens with cardiac arrhythmias or reversible cardiac arrest. Crises of these kinds are all too frequent in clinical work, and the physician usually gives his attention to the patient rather than to his stopwatch. Nevertheless, most of us share the nagging belief that we have had patients in whom a reasonably well-documented period of not more than two or three minutes of pulselessness was followed by permanent brain . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Neurology, New York Hospital —Cornell Medical Center, New York.

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 Department of Neurology, New York Hospital —Cornell Medical Center, 1300 York Ave, New York 10021 (Dr. Plum).

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