1/7. Occlusive hyperemia: a radiosurgical phenomenon?OBJECTIVE: Causes of neurological deficits after arteriovenous malformation (AVM) radiosurgery, including hemorrhage, radiation injury, and delayed cyst formation, are described. CONCEPT: Occlusive hyperemia has been described as a reason for neurological deterioration after AVM resection. thrombosis of draining veins or dural sinuses is thought to cause postoperative bleeding or neurological deficits secondary to venous hypertension. In a similar manner, local hemodynamic changes can occur in the brain adjacent to an AVM after radiosurgery if venous outflow is obstructed. Two patients are presented whose cases demonstrate this phenomenon. CONCLUSION: patients can experience clinical worsening after AVM radiosurgery from premature thrombosis of draining veins. Local hemodynamic changes could explain why imaging changes thought to be radiation related occur more frequently after radiosurgery of AVMs than of tumors.- - - - - - - - - - ranking = 1keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |
2/7. Cerebral blood flow imaging in arteriovenous malformation complicated by normal perfusion pressure breakthrough.BACKGROUND: A patient with normal perfusion pressure breakthrough (NPPB) after surgical removal of an arteriovenous malformation (AVM) was evaluated using single photon emission computed tomography cerebral blood flow (CBF) imaging. CASE DESCRIPTION: A 48-year-old man suffered consciousness disturbance because of an intraventricular hemorrhage and underwent ventricular drainage. cerebral angiography showed a medium-sized AVM in the left parietal lobe. Three months after the ictus, a left parietal craniotomy was performed and total removal of the AVM was achieved. A brain region adjacent to the AVM with preoperative decreased vasoreactivity to acetazolamide showed marked hyperperfusion after AVM excision. hemorrhage subsequently occurred in this area. CONCLUSION: CBF mapping seems to offer a noninvasive method for the preoperative identification of AVM patients at risk for NPPB, and to allow for early postoperative diagnosis of NPPB.- - - - - - - - - - ranking = 5keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |
3/7. The relationship between occlusive hyperemia and complications associated with the radiosurgical treatment of arteriovenous malformations: report of two cases.OBJECTIVE AND IMPORTANCE: It has been suggested that impaired venous drainage of normal brain after surgical removal of an arteriovenous malformation (AVM) may cause perinidal edema and hemorrhage. The term occlusive hyperemia has been proposed for this phenomenon. There is evidence that occlusive hyperemia also may occur after radiosurgical treatment of AVMs. The purpose of this article is to lend further support to the concept that venous occlusion may be responsible for some complications observed after AVM radiosurgery. CLINICAL PRESENTATION: We report two patients with unusual radiosurgery-associated complications, and we examine the evidence for venous occlusion as the mechanism underlying the observed clinical sequelae in each patient. INTERVENTION: Patient 1 had a large parietal venous infarct remote from her frontal AVM site 11 months after radiosurgery. At that time, the AVM was confirmed by angiography to have been obliterated. During the next 4 years, the patient experienced persistent posterior hemispheric edema with recurrent focal hemorrhages until the patient's death from massive swelling and uncal herniation. During this period, radiographic studies, including repeat angiography, demonstrated sequential cortical venous occlusions and findings most consistent with venous insufficiency. Postmortem examination revealed no evidence of radionecrosis. Patient 2 exhibited a biphasic pattern of neurological deterioration at 3 and 6 years after radiosurgery. Associated with this unusual phenomenon, there was radiographic evidence of venous outflow obstruction of her thalamic AVM with prominent perinidal edema and progressive occlusion of the nidus. CONCLUSION: We conclude that occlusive hyperemia is responsible for some cases of neurological deterioration after AVM radiosurgery, especially in a setting for which the time course or other clinical features are not as might be expected from a radiobiological perspective. The two patients we describe in this report suggest that manifestations may vary.- - - - - - - - - - ranking = 5keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |
4/7. The case against staged operative resection of cerebral arteriovenous malformations.Three cases of large cerebral arteriovenous fistulae are presented in which surgical ablation was complicated by brain swelling from hyperperfusion breakthrough believed to be caused by acute intraoperative hypoperfusion superimposed on chronic preoperative hypoperfusion. On the basis of these cases, experimental data, and theoretical considerations, we seriously question the wisdom of using staged surgical resection of cerebral arteriovenous malformation to prevent complications related to alterations in cerebral hemodynamics. The reasons for this concern are: the repeated occurrence of acute-on-chronic hypoperfusion during staged resection; a lack of understanding of the time course for the correction of a disordered autoregulation; risk of hemorrhage between the initial and final resection; difficulty in assessing and substantiating flow reduction after subtotal resection; the rapidity of collateralization; the divergence of flow from large, readily accessible feeding arteries to deep penetrating vessels; and attenuation of the wall thickness in collateral vessels as a consequence of increased flow.- - - - - - - - - - ranking = 5keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |
5/7. Subacute diencephalic necrosis and dural arteriovenous malformation.We report a case of congestive venous necrosis involving the diencephalon symmetrically, presumably precipitated by a dural arteriovenous malformation (AVM). The patient presented with a 1-month history of intermittent confusion and gait ataxia. The initial radiological work-up revealed a dural AVM. The patient's subsequent deterioration was accompanied by computed tomographic findings of diencephalic congestion. Pathological examination showed subacute necrosis of the diencephalon. We discuss the pathogenesis of this case of subacute diencephalic necorsis and its possible relationship to the entity of subacute diencephalic angioencephalopathy.- - - - - - - - - - ranking = 5keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |
6/7. Hyperemic and ischemic problems of surgical treatment of arteriovenous malformations.Three patients with arteriovenous malformations are described who showed signs of massive hyperemia in the vascular territory of the normal brain proximal to arterial ligation. One additional patient had evidence of ischemia of the brain in the territory distal to ligation (steal), and in another both mechanisms were considered as operative hazards.- - - - - - - - - - ranking = 5keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |
7/7. Occlusive hyperemia: a theory for the hemodynamic complications following resection of intracerebral arteriovenous malformations.An alternative theory is proposed to explain the brain edema and hemorrhage that may occur after resection of high-flow intracerebral arteriovenous malformations (AVM's). This theory, termed "occlusive hyperemia," is based on a retrospective analysis of operative dictations along with postoperative imaging studies (191 angiograms and 273 computerized tomography scans) in 295 cases of intracerebral AVM's operated on at the Mayo Clinic between 1970 and 1990. In this series, 34 cases (12%) of postoperative deterioration were documented, of which 15 were due to incomplete resection of the AVM. Of the remaining 19 cases, six had brain edema alone and 13 had hemorrhage with edema, despite complete excision of the AVM. In these 19 cases, the AVM's were greater than 6 cm in diameter in 10 patients, between 3 and 6 cm in six, and less than 3 cm in three. Obstruction of the venous drainage system was observed in 14 (74%) of the 19 cases. Ten of these 14 were due to obstruction of the primary venous drainage of the brain parenchyma immediately surrounding the lesions, while four were due to obstruction of other venous structures. In no case was a rapid circulation identified on postoperative angiograms. The flow pattern was slow or stagnant in former AVM feeders and their parenchymal branches. It is proposed that postoperative intracranial hemorrhage and/or brain edema in AVM patients may be due to: 1) obstruction of the venous outflow system of brain adjacent to the AVM, with subsequent passive hyperemia and engorgement; and 2) stagnant arterial flow in former AVM feeders and their parenchymal branches, with subsequent worsening of the existing hypoperfusion, ischemia, and hemorrhage or edema into these areas. Supportive hemodynamic evidence for this theory was derived from the literature.- - - - - - - - - - ranking = 5keywords = arteriovenous malformation, malformation (Clic here for more details about this article) |