Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm

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.

Intraventricular hemorrhage after dural fistula embolization

“…This fact argues against the main principle underlying the NPPB theory of the CHS. 9,18 After reviewing the case with the radiology team, it seems more likely that the hemorrhage was provoked by one of two causes: iatrogeny related to a microperforation while retrieving the microcatheter used for arterial cannulation or hyperpressure inside the DAVF after occlusion of its venous drainage, maybe secondary to an arterial branch that may have inadvertently persisted open.…”

Importance of the Venous Outflow Pattern in Predicting Hyperemic Complications After Treatment of Cerebral Arteriovenous Malformations

“…Whether hyperemia occurs due to reperfusion of previously hypoperfused areas due to poor arterial autoregulation (normal perfusion pressure breakthrough or active hyperemia 2,8 ) or due to occlusion of venous outflow (occlusive or passive hyperemia 1 ), its effect significantly impacts the morbidity and mortality of these patients. As previously shown by several studies, larger and more complex AVMs are associated with higher rates of hyperemic complications 7 , but the pathophysiology of these events remains unclear and a predictive tool to identify patients with higher risks of hyperemic complications could modify postoperative care and improve patient outcomes.…”

Cerebral Arteriovenous Malformations

“…According to the theory of edema surrounding the surgical bed of excised AVM, arteries supplying cerebral AVMs become dilated and lose their capacity to dilate or constrict according to autoregulation. Acutely after removal of a cerebral AVM, excessive blood pressure in these arterial feeders can cause normal brain tissue to bleed (1) .…”