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Culley, Deborah J. MD; Crosby, Gregory MD
Department of Anesthesiology, Perioperative, and Pain Medicine
Brigham & Women’s Hospital
Harvard Medical School
To the Editor:
We enjoyed the editorial by Butterworth and Hammon (1) on lidocaine protection against postcardiopulmonary bypass cognitive dysfunction. We disagree, however, with their assertion that it is a “reasonable assumption that strokes and neurobehavioral deficits result from similar brain injury mechanisms.” There is now ample evidence that a substantial percentage of patients undergoing even routine general surgical procedures experience cognitive impairment for weeks or months thereafter (2,3). The etiology of this neurobehavioral impairment is unknown, but there is little reason to think it is due to subclinical structural neurologic injury, since, with the exception of cardiac, neurological, and a few orthopedic surgical procedures, stroke-promoting events such as emboli are unusual. Moreover, efforts to link worrisome systemic physiologic events associated with anesthesia such as hypotension and hypoxemia with postoperative cognitive dysfunction have been unsuccessful (2,3). Finally, although we do not expect the authors to be aware of soon-to-be-published data, we have laboratory evidence that isoflurane–nitrous oxide anesthesia impairs learning for several weeks in young and old rats (4,5), suggesting general anesthesia itself may affect neurochemical cascades mediating memory for longer than previously realized. Therefore, while stroke can produce cognitive impairment, there is almost certainly more to postoperative cognitive impairment than clinical or subclinical stroke.
Deborah J. Culley, MD
Gregory Crosby, MD
© 2003 International Anesthesia Research Society
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