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Emergency Brain Resuscitation

A Working Group on Emergency Brain Resuscitation.
[+] Article and Author Information

Requests for Reprints: Mark J. Alberts, MD, P.O. Box 3392, Duke University Medical Center, Durham, NC 27710. Acknowledgment: The authors thank Dr. Linda Gray for providing the image used in Figure 1 and Ms. Tina Brantley for excellent secretarial support in the preparation of this manuscript.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1995;122(8):622-627. doi:10.7326/0003-4819-122-8-199504150-00013
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Past efforts to reverse or limit the effects of acute stroke have been largely unsuccessful, in part because of the inability to evaluate and treat most patients soon after stroke onset.One important factor in the delay of treatment has been the nihilistic attitude of medical personnel, including physicians, toward the need to rapidly evaluate and treat patients with stroke. This is important for non-neurologists because most patients with stroke are cared for by internists, family physicians, and emergency physicians. We present the concept of emergency brain resuscitation as one method of galvanizing and motivating health professionals to take a more proactive and aggressive approach to treating the patient with acute stroke. Laboratory and clinical data support the potential efficacy of emergency brain resuscitation teams, which will use standard and experimental techniques to treat patients with stroke. A cost–benefit analysis suggests that emergency brain resuscitation may lower the costs associated with stroke by reducing length of hospital stay, disability, and lost wages. The formation of pilot programs is a logical first step toward evaluating and refining this concept.

*For a listing of members of A Working Group on Emergency Brain Resuscitation, see the Appendix.

Figures

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Figure 1.
Magnetic resonance spectroscopy image obtained from a patient with stroke approximately 12 hours after onset of symptoms.N

This image combines results of lactate and -acetyl-aspartate (NAA) spectroscopy. The bright white area (curved arrow) represents a region that has high levels of lactate and no NAA, which indicate the absence of viable neurons. The gray area (straight arrows) contains both lactate and NAA, indicating the presence of anaerobic metabolism and viable neurons. This image may represent an ischemic penumbra (gray area) surrounding a region of infarcted neurons (white area).

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Figure 2.
Relation between neurologic injury and duration of cerebral ischemia.

A brief period of ischemia followed by restoration of blood flow results in complete neurologic recovery (point CR), as seen in transient ischemic attacks. Episodes of increased ischemia lead to progressively more damage until injury is complete. At this point, further ischemia cannot produce any measurable increase in damage. Point NR defines the extent of ischemia after which no recovery is possible and the maximum window of opportunity for a therapy for an acute stroke. There are no scale markings on the x-axis because these times are now uncertain. Data suggest that the duration of ischemia associated with CR is several minutes and that several hours will produce NR. The time points will be altered (prolonged) in cases of incomplete ischemia. The shape of the curve will differ for some individual brain regions.

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