Normal perfusion pressure breakthrough syndrome in giant arteriovenous malformations

1997 ◽  
Vol 19 (2) ◽  
pp. 117-123 ◽  
Author(s):  
Yoko Kato ◽  
Hirotoshi Sano ◽  
Kazuhiko Nonomura ◽  
Tetsuo Kanno ◽  
Kazuhiro Katada ◽  
...  
Neurosurgery ◽  
1989 ◽  
Vol 24 (3) ◽  
pp. 406-410 ◽  
Author(s):  
Michael K. Morgan ◽  
Ian H. Johnston ◽  
Thoralf M. Sundt

Abstract Three cases are described of infants who developed malignant brain swelling (and in one case hemorrhage) after surgery for vein of Galen malformations. The cause for the brain swelling was felt to be due to hyperperfusion, or the “normal perfusion pressure breakthrough” syndrome. Although well-described for cerebral parenchymal arteriovenous malformations, cases of this complication occurring in vein of Galen malformations have not previously been reported. It is concluded from these cases that infants with large arteriovenous shunts, as attested by cardiac failure and cerebral atrophy, have an increased risk of developing this complication.


Neurosurgery ◽  
1990 ◽  
Vol 26 (2) ◽  
pp. 190-200 ◽  
Author(s):  
Karin Muraszko ◽  
Hsueh Hwa Wang ◽  
Gregory Pelton ◽  
Bennett M. Stein

Abstract Isolated segments from the feeding arteries to arteriovenous malformations (AVMs) from 24 patients were studied in vitro. In a perfusion chamber, isometric contraction of these arterial rings to various vasoactive substances was recorded and correlated with the following: spontaneous activity, spasm as seen in the operating room; radiographic evidence of ectasia preoperatively and postoperatively; and postoperative course. Of the 24 patients studied, four patients had nonreactive AVM nutrient vessels upon in vitro testing. In addition, these vessel segments displayed no spontaneous activity although all of the other vessels tested developed spontaneous activity while in the perfusion chamber. The patients with “unreactive vessels” had an increased incidence of postoperative edema and hemorrhage in the surrounding brain, consistent with the symptoms of normal perfusion pressure breakthrough. Thus, our study utilizes an in vitro technique to evaluate a specific segment of the AVM complex, the feeding vessel, which permitted us to assess abnormalities of reactivity in these vessel segments. This method may be useful for future evaluations of the pathophysiology of AVMs.


Neurosurgery ◽  
1988 ◽  
Vol 23 (4) ◽  
pp. 484-490 ◽  
Author(s):  
Daniel L. Barrow

Abstract Two cases of unruptured pial arteriovenous malformations (AVMs) presenting with intracranial hypertension and papilledema are reported. In the absence of previous hemorrhage or associated hydrocephalus, such a manifestation of pial AVMs is quite unusual. Both patients experienced prompt and sustained resolution of papilledema after surgical removal of the malformation. One case was complicated by the normal perfusion pressure breakthrough phenomenon postoperatively. The pathophysiology of intracranial hypertension associated with unruptured pial AVMs and the relationship to pseudotumor cerebri are discussed.


Neurosurgery ◽  
1987 ◽  
Vol 21 (3) ◽  
pp. 314-323 ◽  
Author(s):  
Brian T. Andrews ◽  
Charles B. Wilson

Abstract Twenty-eight patients treated for arteriovenous malformations (AVMs) of the brain had staged therapy consisting of multiple surgical procedures or endovascular embolization followed by surgical treatment. There were 10 men and 18 women, aged 15 to 60 years (mean, 34 years). The clinical symptoms were those associated with intracranial hemorrhage in 13 patients, progressive neurological deficit not due to hemorrhage in 6, intractable headache in 5, and seizures in 4. Four groups were identified based upon the reason for staging therapy. Thirteen patients with large high flow AVMs (Group A) had staged treatment because of the risk of normal perfusion pressure breakthrough. The initial afferent artery occlusion was accomplished surgically in 9 patients and by endovascular embolization in 4. Postoperatively, no patient in this group had malignant cerebral edema or intracranial hemorrhage suggestive of normal perfusion pressure breakthrough, but 1 patient had an intraventricular hemorrhage after initial embolization. In 9 patients (Group B), the AVM had a complex multiple arterial supply that precluded resection from a single operative exposure. Seven had supratentorial AVMs, and 2 had AVMs of the posterior fossa. In 6 of these cases, the AVM was located in the midline and received bilateral arterial input. Six patients had staged surgical procedures, and 3 had an initial endovascular embolization followed by operation. Two patients had intracerebral hemorrhages, one after an initial surgical procedure and another after initial embolization. In 4 patients (Group C), the AVM had a major dural component that was treated separately from the parenchymal component. In 3 of these patients, embolization through the external carotid artery satisfactorily obliterated the dural component; in the remaining patient, a persistent internal carotid supply necessitated resection of the dural malformation. The parenchymal component was excised surgically in 2 patients. Two patients (Group D) had separate surgical procedures to treat an aneurysm associated with a parenchymal AVM. Overall, 19 of 28 patients had complete excision and 9 had partial obliteration of their AVMs. Late follow-up of 27 patients at a mean of 18.6 months showed that 16 patients were in excellent condition and 8 were in good condition. Three patients were in poor condition with debilitating neurological deficits. One patient had a delayed intracranial hemorrhage 22 months after incomplete obliteration of her AVM. Staged treatment of selected AVMs of the brain may avoid the occurrence of normal perfusion pressure breakthrough. This approach also allows satisfactory obliteration of selected malformations that have multiple complex arterial supplies or a dural component and those associated with an aneurysm.


1993 ◽  
Vol 78 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Michael K. Morgan ◽  
Ian H. Johnston ◽  
John M. Hallinan ◽  
Neville C. Weber

✓ A series of 112 patients undergoing complete surgical resection of arteriovenous malformations (AVM's) of the brain between 1974 and 1990 were analyzed for complications and 12-month outcomes. The cohort consisted of 44 patients with small AVM's (< 2 cm in diameter), 43 patients with medium-sized AVM's (2 to 4 cm in diameter), and 25 patients with large AVM's (> 4 cm in diameter). There was a 3.6% series mortality rate and an 18% morbidity rate. One of the four deaths was caused by normal perfusion pressure breakthrough. Analysis of logistic regression found that the most important factor influencing the occurrence of complications in this series was AVM size (p = 0.005) and that the occurrence of complications (p < 0.001) and the neurological grade at the time of surgery (p < 0.004) both significantly contributed to the outcome at 12 months. This study stresses the importance of defining complications in terms of rigid criteria when analyzing AVM series in order to allow for a correct evaluation of the risk:benefit ratio of surgery. Furthermore, it emphasizes the need for a separate analysis of the importance of complications upon outcome.


Neurocirugía ◽  
2020 ◽  
Vol 31 (5) ◽  
pp. 209-215
Author(s):  
Juan Manuel Revuelta ◽  
Álvaro Zamarrón ◽  
José Fortes ◽  
Gregorio Rodríguez-Boto ◽  
Jesús Vaquero ◽  
...  

2002 ◽  
Vol 97 (5) ◽  
pp. 1198-1202 ◽  
Author(s):  
Jian Hai ◽  
Meixiu Ding ◽  
Zhilin Guo ◽  
Bingyu Wang

Object. A new experimental model of chronic cerebral hypoperfusion was developed to study the effects of systemic arterial shunting and obstruction of the primary vessel that drains intracranial venous blood on cerebral perfusion pressure (CPP), as well as cerebral pathological changes during restoration of normal perfusion pressure. Methods. Twenty-four Sprague—Dawley rats were randomly assigned to either a sham-operated group, an arteriovenous fistula (AVF) group, or a model group (eight rats each). The animal model was readied by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein (EJV) and the ispilateral common carotid artery (CCA), followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Systemic mean arterial pressure (MAP), draining vein pressure (DVP), and CPP were monitored and compared among the three groups preoperatively, immediately postoperatively, and again 90 days later. Following occlusion of the fistula after a 90-day interval, blood—brain barrier (BBB) disruption and water content in the right cortical tissues of the middle cerebral artery territory were confirmed and also quantified with transmission electron microscopy. Formation of a fistula resulted in significant decreases in MAP and CPP, and a significant increase in DVP in the AVF and model groups. Ninety days later, there were still significant increases in DVP and decreases in CPP in the model group compared with the other groups (p < 0.05). Damage to the BBB and brain edema were noted in animals in the model group during restoration of normal perfusion pressure by occlusion of the fistula. Electron microscopy studies revealed cerebral vasogenic edema and/or hemorrhage in various amounts, which correlated with absent astrocytic foot processes surrounding some cerebral capillaries. Conclusions. The results demonstrated that an end-to-side anastomosis between the distal EJV and CCA can induce a decrease in CPP, whereas a further chronic state of cerebral hypoperfusion may be caused by venous outflow restriction, which is associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.


1995 ◽  
Vol 82 (2) ◽  
pp. 296-299 ◽  
Author(s):  
Michael K. Morgan ◽  
Maurice J. Day ◽  
Nicholas Little ◽  
Verity Grinnell ◽  
William Sorby

✓ The authors report two cases of treatment by intraarterial papaverine of cerebral vasospasm complicating the resection of an arteriovenous malformation (AVM). Both cases had successful reversal of vasospasm documented on angiography. In the first case sustained neurological improvement occurred, resulting in a normal outcome by the time of discharge. In the second case, neurological deterioration occurred with the development of cerebral edema. This complication was thought to be due to normal perfusion pressure breakthrough, on the basis of angiographic arterial vasodilation and increased cerebral blood flow. These two cases illustrate an unusual complication of surgery for AVMs and demonstrate that vasospasm (along with intracranial hemorrhage, venous occlusion, and normal perfusion pressure breakthrough) should be considered in the differential diagnosis of delayed neurological deterioration following resection of these lesions. Although intraarterial papaverine may be successful in dilating spastic arteries, it may also result in pathologically high flows following AVM resection. However, this complication has not been seen in our experience of treating aneurysmal subarachnoid hemorrhage by this technique.


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