Alexander MD, Connolly ES, Meyers PM. Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm. World J Radiol 2010; 2(6): 230-232 [PMID: 21160635 DOI: 10.4329/wjr.v2.i6.230]
Corresponding Author of This Article
Matthew D Alexander, MD, Department of Diagnostic Imaging, Santa Clara Valley Medical Center, San Jose, CA, United States. matthew.alexander@caa.columbia.edu
Article-Type of This Article
Case Report
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World J Radiol. Jun 28, 2010; 2(6): 230-232 Published online Jun 28, 2010. doi: 10.4329/wjr.v2.i6.230
Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm
Matthew D Alexander, E Sander Connolly, Philip M Meyers
Matthew D Alexander, Department of Diagnostic Imaging, Santa Clara Valley Medical Center, San Jose, CA 95128, United States
E Sander Connolly, Department of Neurological Surgery, Columbia University, College of Physicians and Surgeons, New York, NY 10032, United States
Philip M Meyers, Department of Radiology, Columbia University, College of Physicians and Surgeons, New York, NY 10032, United States
Author contributions: Alexander MD performed the literature and chart reviews and wrote the manuscript; Connolly ES participated in patient care and edited the manuscript; Meyers PM was the primary clinician caring for the patient throughout her course and edited the manuscript.
Correspondence to: Matthew D Alexander, MD, Department of Diagnostic Imaging, Santa Clara Valley Medical Center, San Jose, CA, United States. matthew.alexander@caa.columbia.edu
Telephone: +1-408-8856370 Fax: +1-408-8856360
Received: April 19, 2010 Revised: June 2, 2010 Accepted: June 28, 2010 Published online: June 28, 2010
Abstract
Cerebral arteriovenous malformations (AVMs) have abnormally enlarged arteries and veins prone to spontaneous hemorrhage. Immediately following surgical excision of a cerebral AVM, even normal brain tissue surrounding the lesion is subject to hemorrhage, a phenomenon termed normal perfusion pressure breakthrough (NPPB) syndrome. According to this theory, arteries supplying cerebral AVMs become dilated and lose their capacity to dilate or constrict to autoregulate pressure. Acutely after removal of a cerebral AVM, excessive blood pressure in these arterial feeders can cause normal brain tissue to bleed. However, this theory remains controversial. We present a patient with a cerebral AVM that demonstrated cerebrovascular reactivity and argues against an assumption underlying the theory of NPPB syndrome.
