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Objective: Embolization is the most common treatment for dural arteriovenous fistulas (dAVFs). A retrospective, multicenter observational study was conducted in Japan to clarify the nature, frequency, and risk factors for complications of dAVF embolization., Methods: Patient data were derived from the Japanese Registry of Neuroendovascular Therapy 3 (JR-NET3). A total of 40,169 procedures were registered in JR-NET3, including 2121 procedures (5.28%) in which dAVFs were treated with embolization. After data extraction, the authors analyzed complication details and risk factors in 1940 procedures performed in 1458 patients with cranial dAVFs treated with successful or attempted embolization., Results: Transarterial embolization (TAE) alone was performed in 858 cases (44%), and transvenous embolization (TVE) alone was performed in 910 cases (47%). Both TAE and TVE were performed in one session in 172 cases (9%). Complications occurred in 149 cases (7.7%). Thirty-day morbidity and mortality occurred in 55 cases (2.8%) and 16 cases (0.8%), respectively. Non-sinus-type locations, radical embolization as the strategy, procedure done at a hospital that performed dAVF embolization in fewer than 10 cases during the study period, and emergency procedures were independent risk factors for overall complications., Conclusions: Complication rates of dAVF embolization in Japan were acceptable. For better results, the risk factors identified in this study should be considered in treatment decisions.

Objective: Cerebral hyperperfusion syndrome (CHS) is a serious complication after carotid artery stenting (CAS). Staged angioplasty (SAP)-i.e., angioplasty followed by delayed CAS-has been reported as a potential CHS-avoiding procedure. The purpose of this study was to clarify the effectiveness of SAP in avoiding CHS after carotid revascularization for patients at high risk for this complication., Methods: The authors retrospectively studied cases involving patients at high risk for CHS from 44 Japanese centers who were scheduled for SAP, regular CAS, angioplasty, or staged procedures other than SAP between October 2007 and March 2014. They investigated the rate of CHS in the population scheduled for SAP or regular CAS, and for safety analysis, the composite rate of transient ischemic attack (TIA) and ischemic stroke in the population eventually receiving SAP or regular CAS., Results: Data from a total of 525 patients (532 lesions, mean age 72.5 ± 7.5 years, 74 women ) were analyzed. Scheduled procedures included SAP for 113 lesions and regular CAS for 419 lesions. The rate of CHS was lower in the SAP group than in the regular CAS group (4.4% vs 10.5%, p = 0.047). Multivariate analysis showed that SAP was negatively related to CHS (OR 0.315; 95% CI 0.120-0.828). In the population eventually receiving SAP (102 lesions) or regular CAS (428 lesions), the composite rate of TIA and ischemic stroke was comparable between the SAP group and the regular CAS group (9.8% vs 9.3%)., Conclusions: SAP may be an effective and safe carotid revascularization procedure to avoid CHS.

OBJECTIVE The aim of this retrospective multicenter cohort study was to assess the details of the angioarchitecture of arteriovenous fistulas (AVFs) at the craniocervical junction (CCJ) and to determine the associations between the angiographic characteristics and the clinical presentations and outcomes. METHODS The authors analyzed angiographic and clinical data for patients with CCJ AVFs from 20 participating centers that are members of the Japanese Society for Neuroendovascular Therapy (JSNET). Angiographic findings (feeding artery, location of AV shunt, draining vein) and patient data (age, sex, presentation, treatment modality, outcome) were tabulated and stratified based on the angiographic types of the lesions, as diagnosed by a member of the CCJ AVF study group, which consisted of a panel of 6 neurointerventionalists and 1 spine neurosurgeon. RESULTS The study included 54 patients (median age 65 years, interquartile range 61-75 years) with a total of 59 lesions. Five angiographic types were found among the 59 lesions: Type 1, dural AVF (22 [37%] of 59); Type 2, radicular AVF (17 [29%] of 59); Type 3, epidural AVF (EDAVF) with pial feeders (8 [14%] of 59); Type 4, EDAVF (6 [10%] of 59); and Type 5, perimedullary AVF (6 [10%] of 59). In almost all lesions (98%), AV shunts were fed by radiculomeningeal arteries from the vertebral artery that drained into intradural or epidural veins through AV shunts on the dura mater, on the spinal nerves, in the epidural space, or on the spinal cord. In more than half of the lesions (63%), the AV shunts were also fed by a spinal pial artery from the anterior spinal artery (ASA) and/or the lateral spinal artery. The data also showed that the angiographic characteristics associated with hemorrhagic presentations-the most common presentation of the lesions (73%)-were the inclusion of the ASA as a feeder, the presence of aneurysmal dilatation on the feeder, and CCJ AVF Type 2 (radicular AVF). Treatment outcomes differed among the angiographic types of the lesions. CONCLUSIONS Craniocervical junction AVFs commonly present with hemorrhage and are frequently fed by both radiculomeningeal and spinal pial arteries. The AV shunt develops along the C-1 or C-2 nerve roots and can be located on the spinal cord, on the spinal nerves, and/or on the inner or outer surface of the dura mater.

OBJECTIVE Although cortical spreading depolarization (CSD) has been observed during the early phase of subarachnoid hemorrhage (SAH) in clinical settings, the pathogenicity of CSD is unclear. The aim of this study is to elucidate the effects of loss of membrane potential on neuronal damage during the acute phase of SAH. METHODS Twenty-four rats were subjected to SAH by the perforation method. The propagation of depolarization in the brain cortex was examined by using electrodes to monitor 2 direct-current (DC) potentials and obtaining NADH (reduced nicotinamide adenine dinucleotide) fluorescence images while exposing the parietal-temporal cortex to ultraviolet light. Cerebral blood flow (CBF) was monitored in the vicinity of the lateral electrode. Twenty-four hours after onset of SAH, histological damage was evaluated at the DC potential recording sites. RESULTS Changes in DC potentials (n = 48 in total) were sorted into 3 types according to the appearance of ischemic depolarization in the entire hemisphere following induction of SAH. In Type 1 changes (n = 21), ischemic depolarization was not observed during a 1-hour observation period. In Type 2 changes (n = 13), the DC potential demonstrated ischemic depolarization on initiation of SAH and recovered 80% from the maximal DC deflection during a 1-hour observation period (33.3 ± 15.8 minutes). In Type 3 changes (n = 14), the DC potential displayed ischemic depolarization and did not recover during a 1-hour observation period. Histological evaluations at DC potential recording sites showed intact tissue at all sites in the Type 1 group, whereas in the Type 2 and Type 3 groups neuronal damage of varying severity was observed depending on the duration of ischemic depolarization. The duration of depolarization that causes injury to 50% of neurons (P 50 ) was estimated to be 22.4 minutes (95% confidence intervals 17.0-30.3 minutes). CSD was observed in 3 rats at 6 sites in the Type 1 group 5.1 ± 2.2 minutes after initiation of SAH. On NADH fluorescence images CSD was initially observed in the anterior cortex; it propagated through the entire hemisphere in the direction of the occipital cortex at a rate of 3 mm/minute, with repolarization in 2.3 ± 1.2 minutes. DC potential recording sites that had undergone CSD were found to have intact tissue 24 hours later. Compared with depolarization that caused 50% neuronal damage, the duration of CSD was too short to cause histological damage. CONCLUSIONS CSD was successfully visualized using NADH fluorescence. It propagated from the anterior to the posterior cortex along with an increase in CBF. The duration of depolarization in CSD (2.3 ± 1.2 minutes) was far shorter than that causing 50% neuronal damage (22.4 minutes) and was not associated with histological damage in the current experimental setting.

OBJECTIVE The aim of this study was to evaluate whether combined gene therapy with vascular endothelial growth factor (VEGF) plus apelin during indirect vasoreconstructive surgery enhances brain angiogenesis in a chronic cerebral hypoperfusion model in rats. METHODS A chronic cerebral hypoperfusion model induced by the permanent ligation of bilateral common carotid arteries (CCAs; a procedure herein referred to as "CCA occlusion" [CCAO]) in rats was employed in this study. Seven days after the CCAO procedure, the authors performed encephalo-myo-synangiosis (EMS) and injected plasmid(s) into each rat's temporal muscle. Rats were divided into 4 groups based on which plasmid was received (i.e., LacZ group, VEGF group, apelin group, and VEGF+apelin group). Protein levels in the cortex and attached muscle were assessed with enzyme-linked immunosorbent assay (ELISA) on Day 7 after EMS, while immunofluorescent analysis of cortical vessels was performed on Day 14 after EMS. RESULTS The total number of blood vessels in the cortex on Day 14 after EMS was significantly larger in the VEGF group and the VEGF+apelin group than in the LacZ group (p < 0.05, respectively). Larger vessels appeared in the VEGF+apelin group than in the other groups (p < 0.05, respectively). Apelin protein on Day 7 after EMS was not detected in the cortex for any of the groups. In the attached muscle, apelin protein was detected only in the apelin group and the VEGF+apelin group. Immunofluorescent analysis revealed that apelin and its receptor, APJ, were expressed on endothelial cells (ECs) 7 days after the CCAO. CONCLUSIONS Combined gene therapy (VEGF plus apelin) during EMS in a chronic cerebral hypoperfusion model can enhance angiogenesis in rats. This treatment has the potential to be a feasible option in a clinical setting for patients with moyamoya disease.

Object: There is no description of the change in the posterior cerebral artery (PCA) in the diagnostic criteria of moyamoya disease (MMD). However, PCAs are often involved in the clinical setting, and an understanding of the significance of PCA lesions is therefore of great importance when evaluating the disease progression and predicting prognosis. The aim of this study was to assess the difference in posterior circulation involvement in pediatric and adult patients with MMD., Methods: The records of 120 consecutive patients with MMD were reviewed. The clinical manifestations at diagnosis were evaluated on the basis of symptoms and CT and MRI findings. The degree of steno-occlusive internal carotid artery (ICA) lesions and the existence of steno-occlusive PCA lesions were evaluated by observing a total of 240 ICAs and PCAs on angiography. Angiographic correlation between anterior and posterior circulation was assessed in pediatric and adult patients with MMD., Results: Seventeen (26%) of 66 pediatric patients and 18 (33%) of 54 adult patients exhibited steno-occlusive PCA lesions. There was no significant difference in the prevalence of PCA lesions between pediatric and adult patients with MMD (p = 0.36). The prevalence of infarction in pediatric and adult patients with PCA involvement was significantly higher than that in pediatric and adult patients without PCA involvement (p = 0.0003 and p = 0.003, respectively). There was no significant difference in the distribution of infarction areas between pediatric and adult patients with PCA involvement (p = 0.62). On the basis of the staging system used, steno-occlusive lesions in ICAs ipsilateral to PCAs with lesions were in significantly advanced stages compared with lesions in ICAs ipsilateral to PCAs without lesions in both pediatric and adult cases (p < 0.0001 and p = 0.0008, respectively). Pediatric patients had less advanced steno-occlusive lesions in ICAs ipsilateral to PCAs with lesions compared with adults (p < 0.05)., Conclusions: The clinical significance of posterior circulation involvement in MMD was similar between pediatric and adult patients. The only significant difference was that less advanced ICA lesions could complicate posterior circulation involvement in pediatric patients.

Object: Inflammation in the subarachnoid space and apoptosis of arterial endothelial cells have been implicated in the development of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). The authors investigated mechanisms of possible antivasospastic effects of N-benzyl-oxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK), a caspase inhibitor that can inhibit both inflammatory and apoptotic systems, in animal models of SAH., Methods: Rabbits were assigned to three groups of eight animals each and were subjected to SAH by injection of blood into the cisterna magna. The experiments were performed in the following groups: SA only, SAH + vehicle, and SAH + Z-VAD-FMK. The Z-VAD-FMK (1 mg) or vehicle (5% dimethyl sulfoxide) was intrathecally administered before SAH induction. Diameters of the basilar artery (BA) were measured on angiograms obtained before and 2 days after SAH. The BA diameter on Day 2 was expressed as a percentage of that before SAH. Interleukin (IL)-1 in the cerebrospinal fluid (CSF) was examined using Western blotting, and brains were immunohistochemically examined for caspase-1 and IL-1beta. In a separate experiment, 20 rats were subjected to SAH and their brains were immunohistochemically assessed for caspase-1, IL-1beta, and macrophages. RESULTS. In rabbits, Z-VAD-FMK significantly attenuated cerebral vasospasm (the BA diameter on Day 2 in SAH-only, SAH + vehicle, and SAH + Z-VAD-FMK groups was 66.6 +/- 3.2%, 66.3 +/- 3.7%, and 82.6 +/- 4.9% of baseline, respectively), and suppressed IL-1beta release into the CSF and also suppressed immunoreactivities of caspase-1 and IL-1P in macrophages infiltrating into the subarachnoid space. Immunoreactivities for caspase-1 and IL-1P were observed in immunohistochemically proven infiltrating macrophages in rats., Conclusions: These results indicate that caspase activation may be involved in the development of SAH-induced vasospasm through inflammatory reaction.

Object: Vascular endothelial growth factor (VEGF) is a secreted mitogen associated with angiogenesis. The conceptual basis for therapeutic angiogenesis after plasmid human VEGF gene (phVEGF) transfer has been established in patients presenting with limb ischemia and myocardial infarction. The authors hypothesized that overexpression of VEGF using a gene transfer method combined with indirect vasoreconstruction might induce effective brain angiogenesis in chronic cerebral hypoperfusion, leading to prevention of ischemic attacks., Methods: A chronic cerebral hypoperfusion model induced by permanent ligation of both common carotid arteries in rats was used in this investigation. Seven days after induction of cerebral hypoperfusion, encephalomyosynangiosis (EMS) and phVEGF administration in the temporal muscle were performed. Fourteen days after treatment, the VEGF gene therapy group displayed numbers and areas of capillary vessels in temporal muscles that were 2.2 and 2.5 times greater, respectively, in comparison with the control group. In the brain, the number and area of capillary vessels in the group treated with the VEGF gene were 1.5 and 1.8 times greater, respectively, relative to the control group., Conclusions: In rat models of chronic cerebral hypoperfusion, administration of phVEGF combined with indirect vasoreconstructive surgery significantly increased capillary density in the brain. The authors' results indicate that administration of phVEGF may be an effective therapy in patients with chronic cerebral hypoperfusion, such as those with moyamoya disease.

Intracerebral hemorrhage occurred in this 61-year-old woman with preexisting diplopia and proptosis. Results of angiography demonstrated a persistent primitive trigeminal artery (PPTA)-cavernous sinus fistula with cortical venous reflux. Two microcatheters were introduced transarterially through the PPTA into the two draining pathways in the cavernous sinus. Coils were delivered in both pathways simultaneously to prevent further venous overload on either path. The fistula was successfully occluded without complication while the PPTA was preserved. The authors describe this double-catheter technique for coil embolization of a fistula and review the literature concerning PPTA-cavernous sinus fistulas.

The authors describe a case of de novo formation and rupture of an aneurysm located at the junction of the left internal carotid artery and the superior hypophyseal artery in a middle-aged woman 2 months after another aneurysm, located on the anterior communicating artery, had been clipped. This case is rare because of the short interval between the last angiographic study performed at the first operation and the diagnosis of the de novo aneurysm; in this case the interval was only 47 days, compared with other cases in the literature in which the intervals were 3 to 34 years. Aneurysms can enlarge considerably in 2 to 4 weeks and can rupture at or soon after their formation. This case provides insight into aneurysm formation and rupture.

In this article the authors describe a rescue balloon procedure for coil implantation in three cases. In each patient, the coil seemed likely to unravel. The coils stretched when attempts were made to remove the partially implanted but trapped device. The inflation of a nondetachable microballoon in front of the aneurysm orifice allowed the surgeons to complete implantation of the coil and to avoid a more forceful and potentially harmful retrieval. This rescue balloon method may be useful for emergency situations, such as coil stretching with or without migration.

Experimental aneurysms were created using a microsurgical technique to produce anastomosed venous pouches in the bilateral common carotid arteries of 12 dogs. The 24 aneurysms were then thrombosed via an endovascular approach with injection of a cellulose acetate polymer (CAP) solution that the authors have developed for use as a liquid thrombotic material. Angiography performed 1 to 4 weeks after CAP injection revealed complete thrombosis of the aneurysm with patency of the parent artery in 16 aneurysms. Histological analysis disclosed that the aneurysmal orifice in these cases was completely covered with newly formed endothelial cells 2 weeks after CAP thrombosis. Three other aneurysms exhibited parent artery occlusion caused by protrusion of the CAP mass through the aneurysmal orifice into the parent artery; this was thought to be caused by over-injection of the CAP solution. Histological analysis of the remaining five aneurysms, initially shown to have incomplete occlusion, revealed that they each possessed a residual neck that was partially covered with endothelial cells. No rupture of the aneurysms or migration of CAP into the distal arteries was observed. These results suggest that using an endovascular approach, direct thrombosis of cerebral aneurysms with CAP is safe and effective. This technique may prove to be an alternative treatment for such aneurysms. However, there is a potential risk of regrowth or rupture of aneurysms that retain a residual neck and long-term follow-up studies will be required to evaluate this issue.

Twelve patients with Hunt and Hess neurological Grades III to V underwent thrombosis of aneurysms using cellulose acetate polymer within 23 hours of aneurysm rupture. On computerized tomography (CT), nine of these patients had difuse or localized thick subarachnoid blood clots, two had diffuse thin clots and one had intraventricular clots. Immediately after thrombosis, all patients were administered tissue plasminogen activator (TPA) through spinal or ventricular catheters. The pressure of the lumbar cerebrospinal fluid was maintained at 100 to 150 mm H2O. The TPA was given as multiple injections of 2 mg on Day 0 and 1 to 2 mg on the following 1 to 2 days. In two patients the second injection of TPA was not given because of severe brain damage resulting from the initial subarachnoid hemorrhage. Ten patients showed complete clearance of the cisternal clot on CT within 72 hours after thrombosis. Seven partially thrombosed aneurysms and five multiple aneurysms were clipped during delayed surgery. Only one patient experienced mild vasospasm as shown on the follow-up angiogram. Eight patients improved clinically and had a good recovery, two had severe disability, and two died. Urgent thrombosis of a ruptured aneurysm followed by immediate postthrombotic administration of TPA may be a safe and reasonable means of preventing vasospasm and improving patient outcome.

The authors report the treatment of seven intracranial aneurysms in six patients with direct infusion of cellulose acetate polymer solution, a new liquid thrombotic material. These aneurysms were considered inoperable because of their size or location, or because of the patient's neurological condition. This material avoids the difficulties associated with balloon occlusion, and completely fills even irregularly shaped aneurysms. Cellulose acetate polymer solution hardens in about 5 minutes and remains solid once inside the aneurysm. Because this technique is less invasive than surgery, it can be used for high-risk patients in the acute stage of subarachnoid hemorrhage. Transient motor aphasia occurred in one patient. A small residual neck, which caused rebleeding 3 months after the treatment, remained in another patient. This article describes the new material, the procedure for direct thrombosis, and preliminary clinical results.