Results of direct and indirect revascularisation for adult European patients with Moyamoya angiopathy.

There is little information concerning clinical data and revascularization procedures in adult European patients with Moyamoya disease. More data are available on juvenile European Moyamoya angiopathy and its microsurgical therapies. This analysis summarizes our clinical experience in European adult patients with Moyamoya angiopathy. Nine adult European patients underwent surgical revascularization for Moyamoya angiopathy between 1997 and 2005. Direct intracranial-extracranial (EC-IC) bypass was considered the primary surgical modality. In case of unsuitable donor or recipient arteries, encephalo-myo-synangiosis (EMS) was chosen as an indirect modality. The current analysis confirms that direct EC-IC-bypass is a feasible option for most cases of adult European Moyamoya disease. Exact definition of long-term benefits would require a multicentric study. EMS appears to be of questionable value in the adult European population.

Perfusion MRI before and after acetazolamide administration for assessment of cerebrovascular reserve capacity in patients with symptomatic internal carotid artery (ICA) occlusion: comparison with 99mTc-ECD SPECT.

INTRODUCTION: Impaired cerebral vascular reserve (CVR) in patients with symptomatic internal carotid artery (ICA) occlusion is regarded as a possible indication for performing extra-/intracranial (EC/IC) bypass surgery. As perfusion MR imaging (MRI) can demonstrate cerebral haemodynamics at capillary level, our hypothesis was that perfusion MRI could be used in these patients for the evaluation of CVR following acetazolamide challenge in a similar way to single photon emission CT (SPECT) and might provide additional information. METHODS: Enrolled in the study were 12 patients (mean age 61.3 years; 11 male, 1 female) with symptomatic unilateral ICA occlusion proven by angiography. Both perfusion MRI and 99m-technetium-ethyl-cysteinate dimer ((99m)Tc-ECD) SPECT were performed before and after injection of acetazolamide (Diamox ,1000 mg i.v.). CVR parameters including regional cerebral blood flow (rCBF) and volume (rCBV), and mean transit times (MTT) were measured by perfusion MRI. RESULTS: The patients with impaired CVR proven by SPECT (n = 9) had a negative mean rCBF increment (-46.52%), negative rCBV increment (-13.5%) and delayed MTT (mean +2.98 s), respectively, on the occluded side (Student's t-test all P < 0.05). The patients with sufficient CVR (n = 3) had a mean rCBF increment of 1.2%, a decrement of rCBV of 10.46%, and a mean MTT shortening of 0.27 s following the acetazolamide injection. CONCLUSIONS: Perfusion MRI before and after acetazolamide administration compares favourably with (99m)Tc-ECD SPECT for the detection of impaired CVR. The impact that perfusion MRI studies (before and after acetazolamide administration) might have on the treatment decision in patients with ICA occlusion has yet to be determined by a prospective study.

Intraprocedural thrombus formation during coil placement in ruptured intracranial aneurysms: treatment with systemic application of the glycoprotein IIb/IIIa antagonist tirofiban.

BACKGROUND AND PURPOSE: When using detachable coils to treat intracranial aneurysms, thromboembolism is the most feared and frequently reported complication during or after endovascular therapy. The purpose of this study was to document the therapeutic effect of tirofiban on patency of the parent vessel, rate of rebleedings, and outcome of the patients in the setting of acute subarachnoidal hemorrhage. METHODS: A patient data base was retrospectively reviewed to identify patients in whom thrombus occurred during endovascular treatment of ruptured cerebral aneurysms within a 34-month period and who were treated with tirofiban. All patients underwent anticoagulation with heparin during endovascular treatment procedures. Sixteen patients (age range, 52.9 +/- 10.7 years; 10 women, 6 men) were identified with intraprocedural thrombus formation. The patency of the parent vessel was assessed in a retrospective analysis blinded to outcome. Eight patients received ventriculostomy and had a follow-up CT. RESULTS: Local nonocclusive thrombus at the coil surface was detected in 5 patients, in all of whom the thrombus was dissolved. In 10 patients, partial or total occlusion of the parent vessel occurred during the intervention; in 8 of these, the vessel was recanalized completely and in 2 drug administration was assisted by mechanical means. In 1 patient, however, the occlusion persisted. No periprocedural rebleedings of the ruptured aneurysm occurred; 3 of 8 ventriculostomies had clinically silent small local bleedings. CONCLUSION: The use of tirofiban in the setting of endovascular treatment of ruptured intracranial aneurysms to dissolve platelet aggregation seems relatively safe and effective.

Neuroprotective effects of a postischemic treatment with a bradykinin B2 receptor antagonist in a rat model of temporary focal cerebral ischemia.

Bradykinin, an endogenous nonapeptide produced by activation of the kallikrein-kinin system, promotes neuronal tissue damage as well as disturbances in blood-brain barrier function through activation of B2 receptors. In a rat model of focal cerebral ischemia, blockade of B2 receptors before initiation of ischemia with the B2 receptor antagonist, LF 16-0687 Ms, afforded substantial neuroprotection. In order to assess the potential clinical value of this approach, we evaluated the effect of LF 16-0687 Ms given at reperfusion following focal cerebral ischemia on local cerebral blood flow (LCBF), neurological outcome, and infarct size. Sprague-Dawley rats were subjected to MCA occlusion for 90 min by an intraluminal filament. Animals were assigned to one of four treatment arms (n = 7 each): (1) vehicle, (2) LF 16-0687 Ms (1.0 mg/kg/day), (3) LF 16-0687 Ms (3.0 mg/kg/day), or (4) LF 16-0687 Ms (10.0 mg/kg/day) given at reperfusion and repetitively over 2 days. Neurological recovery was examined daily, and infarct volume was assessed histologically on day 7 after ischemia. Physiological parameters and local CBF were not influenced by the treatment. Significant improvement of neurological outcome was observed on postischemic day 3 in animals receiving 1.0 and 3.0 mg/kg/day of LF 16-0687 Ms (P < 0.05). Inhibition of B2 receptors significantly reduced infarct volume in all treated animals predominantly in the cortex. B2 receptor blockade with LF 16-0687 Ms showed neuroprotective effectiveness even when therapy was initiated upon reperfusion, i.e. 90 min after induction of ischemia. Therefore, blockade of B2 receptors seems to be a promising therapeutic approach after focal cerebral ischemia, which deserves further experimental and clinical evaluation.

Cranial and spinal dural arteriovenous malformations and fistulas: an update.

Awareness of a potential arteriovenous fistula is critical for diagnosis of cranial as well as spinal fistulas. The natural history of cranial and spinal dural arteriovenous fistulas has been clarified during the last decade and interdisciplinary therapies have experienced a substantial development recently. The classification of Cognard & Merland is now the most widely accepted one for cranial dural AVF. It is based on the degree of flow reversal in the sinuses and cortical veins and reflects well the natural history of the different lesions and serves as basis for therapeutic indications. Several studies have defined the annual bleeding risk of cranial dural fistulas between 1.8 and 15%, depending on the pattern of venous drainage and initial symptomatology. Surgical, endovascular and radiosurgical methods must be selectively chosen for the treatment. The risk associated with surgical or endovascular treatment of benign fistulas is higher than the risk of eliminating fistulas that have already led to cortical venous reflux. Transvenous endovascular occlusion or surgical disconnection of draining veins is the treatment of first choice for cranial and spinal dAVF with venous flow reversal. Benign cranial dural arteriovenous fistulas are a developing indication for radiosurgery.

Dose finding study of intravenous magnesium sulphate in transient focal cerebral ischemia in rats.

BACKGROUND: During many neurovascular procedures temporary occlusion of cerebral arteries is inevitable. Neuroprotective drugs may reduce the risk of cerebral infarction in this situation. Increasing evidence indicates neuroprotective properties of magnesium in cerebral ischemia. Previous experimental studies on the neuroprotective efficacy of magnesium-treatment in transient focal ischemia provide widely differing results using different magnesium doses and treatment-regimens. The present study was conducted to find the maximum protective dose of intravenous magnesium sulphate in a rat model of transient focal ischemia. METHODS: 45 male Sprague-Dawley rats were subjected to 90 minutes of middle cerebral artery occlusion (MCAO) by an intraluminal thread. Animals were randomly assigned to one of 4 treatment arms: (1) vehicle (2) MgSO(4) 1x0.75 mmol/kg (3) MgSO(4) 2x1 mmol/kg (4) MgSO(4) 1 mmol/kg+0.5 mmol/kg/h. Local cortical blood flow (LCBF) was continuously measured by laser-Doppler flowmetry. Functional deficits were quantified daily, infarct volumes were assessed histologically after 7 days. RESULTS: Magnesium serum levels below 3 mmol/l were well tolerated by the animals. Above 3 mmol/l cardiodepressive effects limited neuroprotection. Total infarct volumes in groups 3 and 4 were significantly reduced by 32% and 42%, respectively, compared to controls. Postoperative neurological recovery was significantly improved in magnesium-treated groups. CONCLUSION: Continuous magnesium-administration with stable serum concentrations between 2 and 3 mmol/l offered the best protection and was well tolerated. Serum concentrations above 3 mmol/l should not be exceeded. An elevation of magnesium serum levels could be useful for brain tissue protection during procedures which are prone to the risk of temporary vessel occlusion.

Congested residual nidus after preoperative intranidal embolization in midsize cerebral arteriovenous malformations of 3-6 cm in diameter.

BACKGROUND: Modern delicate microcatheters allow intranidal embolization of cerebral arteriovenous malformations (AVM). The aim of the current analysis was to assess effects of preoperative intranidal deployment of embolic material on surgical time and blood loss in cerebral arteriovenous malformations of 3-6 cm in diameter. METHODS: The case records of 38 cerebral AVM between 3 and 6 cm in maximum diameter were reviewed, that had been embolized intranidally with N-butyl 2-cyanoacrylate (Histacryl) and subsequently operated on. Surgical time and blood loss as well as particular intraoperative findings such as a congested nidus and thrombosis of draining veins were registered and correlated with the extent of embolization and the time interval between embolization and surgery. FINDINGS: Preoperative embolization occluded an estimated range of 10 to 90% of the nidus. Minor embolization related bleeding without clinical relevance occurred in 5 patients. Significant embolization related bleeding resulting in earlier than planned surgery occurred in another 5 patients. All embolization related haemorrhages occurred within 24 hours. Average total operating time was 343+/-106 min and average blood loss was 684+/-858 ml. Unequivocal bleeding difficulty from the nidus and a total blood loss of more than 1000 ml were encountered in 7 instances and dissection was tedious due to a bleeding AVM core in 5 other cases. A congested AVM core was the source of bleeding in 11 patients and paraventricular neovascularization in one. 6 of the 11 cases with a congested AVM core had suffered minor or substantial haemorrhage after a preoperative endovascular procedure. Intraoperative nidus congestion was noted in this series after an interval as long as 2 weeks after the last embolization. Combined management resulted in permanent morbidity in 6 of the 38 cases. In 4 of them the neurological deficit was associated with an intraoperative bleeding problem, in all due to congested nidus. Morbidity had to be correlated with major haemorrhage resulting from preoperative embolization in 2 instances. CONCLUSIONS: Intranidal embolization prior to surgical removal of AVM can lead to a congested residual nidus and intraoperative bleeding. Minor leakage after preoperative embolization is an inconsistent warning sign of nidus congestion. Nidus outflow after intranidal embolization appears to require a few weeks for normalization. Delay of surgery after embolization should be considered in cases of suspected congested residual nidus. The danger of major haemorrhage or arterial revascularization during this waiting period appears small.

Ruptured intracranial dissecting aneurysms: management considerations with a focus on surgical and endovascular techniques to preserve arterial continuity.

BACKGROUND: The present retrospective analysis was undertaken to review an institutional experience with 13 intracranial dissecting aneurysms as source of subarachnoid haemorrhage (SAH) among a total of 585 ruptured intracranial aneurysms. METHODS AND RESULTS: In 6 patients the vertebral artery (VA) was affected, in 2 patients the basilar artery (BA), in 3 the internal carotid (ICA), in 1 the middle cerebral (MCA) and in 1 the postcommunicating (A2) segment of the anterior cerebral artery (ACA). Maintaining arterial patency was aimed at in all patients. Tangential clipping or circumferential wrapping were used as surgical methods. Endovascular stenting and/or coiling was applied in 2 instances. Four of the 6 VA dissecting aneurysms underwent surgical exploration between 1 and 22 days after haemorrhage. Two patients were in WFNS grade V and died subsequently with the aneurysms untreated, one after rehaemorrhage. In the patients with secured VA aneurysms the postoperative course was uncomplicated with the exception of additional caudal cranial nerve injury in 1 instance. Both BA aneurysms were initially treated by endovascular methods. In the first patient incomplete packing with Gugliemi detachable (GDC) coils was achieved. Follow-up angiography 6 months later showed growth and coil compaction and subsequent wrapping with Teflon fibres resulting in angiographic stabilization. The other BA aneurysm was treated by a combination of a coronary stent and GDC coils. The 3 dissecting ICA aneurysms were all explored surgically. In only 1 instance ICA continuity could be preserved by wrapping, in the other 2 cases a major portion of the vessel wall disintegrated upon removal of the surrounding clot. The only ACA dissecting aneurysm, on A2, was successfully treated with a Dacron cuff. In the single patient with a MCA aneurysm, a decision for conservative management was taken, because neither a surgical nor an endovascular solution was seen as a possibility that did not risk occlusion of lenticulostriate branches. The patient suffered a fatal rehaemorrhage 4 weeks later at her home. CONCLUSIONS: The reported experience suggests that in Western countries also dissecting aneurysms are an occasional source of SAH. The outcome in our conservatively managed patients confirms the poor prognosis of conservative management. Wrapping and endovascular stent based methods can achieve stabilization of the dissected artery without sacrificing the artery. Results of treatment appear to depend largely on the location of the dissecting aneurysm.

Neuronavigation based on CT angiography for surgery of intracranial aneurysms: primary experience with unruptured aneurysms.

Several reports have demonstrated the use of three-dimensional (3D) computed tomographic angiography (CTA) for preoperative planning in patients with intracranial aneurysms. Until now, there are no reports on the potential role of navigation systems in combination with CTA in aneurysm surgery. In the present study we report our experience with neuronavigation based on CTA in 16 patients with unruptured anterior circulation aneurysms for 1) planning craniotomy; 2) guided approach to the aneurysm; and 3) 3D presentation of the aneurysm and adjacent arteries in correct orientation. The reconstructed CTA images were analyzed preoperatively with regard to diameter of aneurysm neck and dome as well as projection and possible daughter aneurysms, and these parameters were compared with the intraoperative findings. In addition the accuracy of the navigator to locate the aneurysm neck was measured intraoperatively. Navigated approach planning resulted in variable keyhole craniotomies for the 7 middle cerebral artery aneurysms, but did not result in deviation from small standard craniotomies for the internal carotid and anterior communicating artery aneurysms. Precision of the indication of the navigator with regard to the aneurysm neck ranged from < 1 mm to 4 mm. Intraoperative assessment confirmed the CTA data with regard to aneurysm size and projection in all, and definition of daughter aneurysms and adjacent arteries in most cases. The computer assisted approach allowed a smaller, exactly placed craniotomy primarily in MCA aneurysms. 3D presentation of the aneurysms and the adjacent arteries in correct orientation facilitated identification and dissection the aneurysms. Current navigation systems are not precise enough to allow "blind" aneurysm clipping by placing a real clip on the virtual aneurysm neck.

Neuroprotective efficacy of intra-arterial and intravenous magnesium sulfate in a rat model of transient focal cerebral ischemia.

BACKGROUND: Many neurovascular procedures necessitate temporary occlusion of cerebral arteries. In this situation neuroprotective drugs may increase the safety of the procedures. Magnesium may inhibit ischemic damage by anti-excitotoxic, calcium channel blocking and vasodilatory action. Some evidence suggests that intra-arterial administration might provide a much higher degree of protection than intravenous treatment. In this study the neuroprotective efficacy of intra-arterial and intravenous magnesium administration was examined in a rat model of transient focal ischemia. METHODS: 34 male Sprague-Dawley rats were subjected to 90 minutes of middle cerebral artery occlusion (MCAO) by an intraluminal thread. Before ischemia, animals received an infusion of either (1) vehicle (0.9% NaCl) (2) MgSO4 intra-arterially or (3) MgSO4 intravenously. Local cortical blood flow (LCBF) was continuously measured by laser-Doppler flowmetry. Functional deficits were quantified daily, infarct volumes were assessed histologically after 7 days. FINDINGS: There was no difference between the treatment groups concerning LCBF. Magnesium serum levels increased from approximately 1 mmol/l to approximately 1.8 mmol/l by either route of administration. Both intra-arterial and intravenous treatment improved neurological recovery and equally reduced total infarct volume by approximately 25%. INTERPRETATION: The results indicate that there is no advantage of intra-arterial over intravenous magnesium administration. A comparison with previous studies suggests that even within the normal range of serum magnesium concentrations, low-normal levels may be hazardous and high-normal levels may be protective in transient focal ischemia.