Estimate of the Incidence and Importance of Circulatory Breakthrough in the Surgery of Cerebral Arteriovenous Malformations

Luessenhop, Alfred J.; Ferraz, Francisco; Rosa, Louis

doi:10.1080/01616412.1982.11739622

Cited by 26 publications

(6 citation statements)

References 9 publications

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“…This theory has yet to be substantiated on a pathophysiological basis 26,28,29 and remains controversial. 1,21,34,47,48 Despite this, many authors have reported the onset of brain edema with or without hemorrhage in the normal brain parenchyma surrounding the bed of a totally excised AVM 3,5,6,8,9,17,18,20,27,28,30,32,[35][36][37][38]40,48,49,51,52 and it is quite possible that normal perfusion pressure breakthrough was responsible for this recognized complication. However, Batjer and colleagues 4,5,7 and Young, et al, 50 have provided evidence that vasoreactivity is intact and may be enhanced in patients developing a normal perfusion pressure breakthrough syndrome.…”

Section: Discussionmentioning

confidence: 99%

Normal perfusion pressure breakthrough: the role of capillaries

Sekhon¹,

Morgan²,

Spence³

1997

Journal of Neurosurgery

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Excision of human cerebral arteriovenous malformations (AVMs) can be complicated by postoperative edema and hemorrhage in adjacent brain tissue, despite the complete excision of the malformation. Various theories have purported to explain the hemodynamic basis for this predisposition, including disordered autoregulation causing "normal perfusion pressure breakthrough" and obstruction of venous drainage leading to "occlusive hyperemia." This study did not evaluate the arterial or venous circulations in this scenario, but rather examined the capillaries in adjacent brain parenchyma for any structural deficiencies that would predispose the brain to the postoperative formation of edema and hemorrhage. Arteriovenous fistulas (AVFs) were created surgically in the necks of 10 male Sprague-Dawley rats, which caused chronic cerebral hypoperfusion with a reduction in cerebral blood flow of between 25% and 50%. Ten age-matched animals were used as controls. Twenty-six weeks after AVF formation the animals were killed and perfusion fixed. Their brain tissue was prepared for light microscopic studies by staining for glial fibrillary acidic protein or for transmission electron microscopy. In the CA1 pyramidal cell region of the hippocampus, it was found that in the animals with AVFs there was increased capillary density and absent astrocytic foot processes in some of these vessels. It was concluded that these vessels had developed as a result of neovascularization in response to chronic cerebral ischemia and that their anatomical configuration made them prone to mechanical weakness and instability following the increase in perfusion pressure that occurs in adjacent brain parenchyma after AVM excision. The authors believe that this study pinpoints a structural accompaniment to the hemodynamic changes that occur in brain tissue in the vicinity of cerebral AVMs that predispose these areas to the formation of edema and hemorrhage after AVM excision.

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Section: Discussionmentioning

confidence: 99%

Normal perfusion pressure breakthrough: the role of capillaries

Sekhon¹,

Morgan²,

Spence³

1997

Journal of Neurosurgery

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“…Several studies using various methodologies have supported the claims of NPPB [2][3][4][5][6][7][8][9] . However, more recent investigations contradict many aspects of the theory, casting doubt on the link between impaired vasoreactivity and postoperative complications.…”

Section: Discussionmentioning

confidence: 99%

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

Alexander

Connolly²,

Meyers³

2010

WJR

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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.

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“…Alternative explanations for the phenomena cited in the literature as examples of "breakthrough" have not been rigorously excluded. 4,5,8,9,16,19,21,25,26 Moreover, the conclusions drawn from the limited early studies of this phenomenon 25 may not be applicable to the clinical situation. Furthermore, the theoretical basis for a "resetting" of autoregulation (the cornerstone of the hypothesis) remains in doubt.…”

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confidence: 99%

Cerebral arteriovenous malformations, steal, and the hypertensive breakthrough threshold

Morgan¹,

Johnston²,

Besser³

et al. 1987

Journal of Neurosurgery

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An experiment was designed to investigate the effects of arteriovenous (AV) fistula occlusion on cerebral autoregulation. A right carotid-jugular fistula was created in 63 rats in such a way as to produce an intracranial AV fistula with a loop extension into the neck. The fistula was occluded after an 8-week interval with the rats under both normotension and metaraminol-induced hypertension, and evidence of blood-brain barrier disruption was investigated with an Evans blue dye technique. The results indicate that an intracranial AV fistula may cause cerebral steal which is responsible for a reduction in the threshold for hypertensive breakthrough following fistula occlusion.

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Estimate of the Incidence and Importance of Circulatory Breakthrough in the Surgery of Cerebral Arteriovenous Malformations

Cited by 26 publications

References 9 publications

Normal perfusion pressure breakthrough: the role of capillaries

Normal perfusion pressure breakthrough: the role of capillaries

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

Cerebral arteriovenous malformations, steal, and the hypertensive breakthrough threshold

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