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Objective Recent randomized trials have demonstrated that endovascular therapy improves outcomes in patients with an acute ischemic stroke from a large vessel occlusion. Subgroup analysis of the Multicenter Randomized CLinical trial of Endovascular treatment for Acute ischemic stroke in the Netherlands (MR CLEAN) study found that patients undergoing general anesthesia (GA) for the procedure did worse than those with nongeneral anesthesia (non-GA). Current guidelines now suggest that we consider non-GA over GA, without large, randomized trials specifically designed to address this issue. We sought to review our experience and outcomes in a program where we routinely use GA in patients undergoing mechanical thrombectomy with similar techniques. Methods Patients with anterior circulation strokes who received intravenous tissue plasminogen activator (IV-tPA) and endovascular stroke therapy were included in the analysis. The National Institutes of Health Stroke Scale (NIHSS) on admission and discharge and modified Rankin scale scores at discharge were recorded and compared with the outcome measurements of MR CLEAN. Results Sixty patients were identified: 39 males and 21 females with a mean age of 62 (range of 29–88). Forty-seven patients were transferred from outside primary stroke centers, while 13 patients presented directly to our institution. Median NIHSS on admission was 15. The median time of symptom onset to endovascular therapy was 265 minutes, with an interquartile range of 81 minutes. Using the thrombolysis in cerebral infarction (TICI) scale, recanalization of TICI 2b–3 was achieved in 76.4% of recorded patients (42/55 recorded). At discharge, mortality was 16.7% (10/60), median NIHSS was 5, and 38.3% (23/60) of patients had a modified Rankin Scale score of 0–2. Conclusions General anesthesia does not worsen outcome in patients undergoing mechanical thrombectomy when compared to historical subgroups. Despite a longer time from symptom onset to treatment, our outcomes for patients receiving GA compare favorably to the GA and non-GA groups in MR CLEAN.

PRELIMINARY REMARKSGuideline LimitationsPractice guidelines should be used in the context of individual patient characteristics and may be superseded by clinical judgment or patient preference. The use of practice guidelines does not guarantee specific outcome benefit but rather should serve as an e

Introduction: The timing of administering tissue-type plasminogen activator (tPA) in patients with an ischemic stroke is directly related to clinical outcomes. The use of a mobile stroke unit (MSU) is a strategy to provide acute ischemic stroke assessment and treatment in a more rapid fashion compared to standard stroke transport and management. Our program initiated the use of a MSU in 2017 as a part of a phased implementation program. We sought to determine the impact of the MSU on the timing of stroke care in the region as it related to proximity to the hospital. Methods: We collected data during the first 9 months of 2017 on patients who were transported to the hospital as pre-hospital stroke alerts (PHSA) via conventional ambulance or via the MSU. Using a retrospective case-controlled design we compared process metrics associated with the phased implementation of the MSU with conventional pre-hospital stroke alerts as standard of care (SOC). Results: There was a total of 178 stroke alert patients; 72 in the MSU group and 106 in the PHSA group. 35 patients received tPA, 16 in the MSU, 19 in SOC. There was no significant difference in age, body weight, race, gender, and length of stay in the hospital in the two groups. The time from 911 call to arrival on scene was 12.06 min versus 20.4 min in the PHSA and MSU groups, respectively. Despite a longer time for arrival TPA administration for patients within a 5 miles radius of the hospital was 89 ± 25 mins in the SOC group and 78±12 mins in the MSU group (p=0.11). For 911 calls originating 10-20 miles from the hospital, the time for 911 call to tPA was 106 ± 23 mins in the PHSA group (n = 4) and 86 ± 2 mins in the MSU group (n = 4). Conclusion: Our initial results are comparable with previously reported data . Our data suggests the MSU may have a greater impact on reducing time to tPA for those further from the hospital or where transport time is delayed. The role of the MSU for non tPA patients such as mechanical thrombectomy, intracerebral hemorrhage and subarachnoid hemorrhage warrants further investigation.

The use of antithrombotic agents, including anticoagulants, antiplatelet agents, and thrombolytics has increased over the last decade and is expected to continue to rise. Although antithrombotic-associated intracranial hemorrhage can be devastating, rapid reversal of coagulopathy may help limit hematoma expansion and improve outcomes. The Neurocritical Care Society, in conjunction with the Society of Critical Care Medicine, organized an international, multi-institutional committee with expertise in neurocritical care, neurology, neurosurgery, stroke, hematology, hemato-pathology, emergency medicine, pharmacy, nursing, and guideline development to evaluate the literature and develop an evidence-based practice guideline. Formalized literature searches were conducted, and studies meeting the criteria established by the committee were evaluated. Utilizing the GRADE methodology, the committee developed recommendations for reversal of vitamin K antagonists, direct factor Xa antagonists, direct thrombin inhibitors, unfractionated heparin, low-molecular weight heparin, heparinoids, pentasaccharides, thrombolytics, and antiplatelet agents in the setting of intracranial hemorrhage. This guideline provides timely, evidence-based reversal strategies to assist practitioners in the care of patients with antithrombotic-associated intracranial hemorrhage.

Cerebral vasospasm after aneurysmal subarachnoid hemorrhage typically occurs 3–14 days after aneurysm rupture. We describe a series of patients who developed vasospasm within minutes of aneurysm rupture. This phenomenon, which we term, “hyperacute vasospasm,” has been reported in animal models of SAH, but hitherto has been poorly described in humans. Eleven patients were identified from an institutional registry who had aneurysmal rupture during catheter cerebral angiography between 1997 and 2009. We quantified the degree of vasoconstriction using vascular diameter index (VDI). The change in VDI (delta VDI or DVDI) was calculated by determining the difference in VDI before and after the procedure. We also examined the relationship between hyperacute vasospasm and delayed cerebral ischemia. Ten of eleven (91 %) patients with intraoperative aneurysm rupture had cerebral vasoconstriction within minutes of intra-procedural aneurysmal rupture. Six of eleven patients (55 %) with hyperacute vasospasm developed delayed cerebral infarction. Hyperacute vasospasm is likely common in patients with intraoperative aneurysm rupture and may be an unrecognized element of the natural history of aneurysmal subarachnoid hemorrhage. In this limited series, there was an association between hyperacute vasospasm and delayed cerebral infarction.

Literature on the endovascular treatment of occlusive acute ischemic stroke (AIS) in the pediatric population remains nebulous. Clinical trials evaluating the role of systemic and intra-arterial thrombolysis, and mechanical thrombectomy have been strictly isolated to the adult population and largely unknown in their safety and efficacy in the pediatric group.The authors present a review of the literature and their own two cases of occlusive acute ischemic stroke in children younger than the age of 10 years who were treated with modern endovascular devices, specifically with stent retrievers, and discuss their clinical and technical considerations as well as their limitations.In both pediatric patients, a combination of stent retriever and Penumbra aspiration were used to achieve Thrombolysis In Cerebral Infarction (TICI) 2a or greater with reduction of overall stroke burden. A reduction of National Institutes of Health Stroke Scale (NIHSS) of 8 or greater was achieved at discharge. At 3-month follow-up, the patients had a NIHSS of 6 and 2, respectively. One patient continued to improve from NIHSS of 6 to 3 at 6 months.In carefully, selected pediatric patients, modern endovascular techniques may be used to treat occlusive pediatric AIS. However, larger clinical trials are needed to evaluate the overall safety and effectiveness.

Brain oxygen (PbtO2) monitoring can help guide care of poor-grade aneurysmal subarachnoid hemorrhage (aSAH) patients. The relationship between PbtO2-directed therapy and long-term outcome is unclear. We hypothesized that responsiveness to PbtO2-directed interventions is associated with outcome. Seventy-six aSAH patients who underwent PbtO2 monitoring were included. Long-term outcome [Glasgow Outcome Score-Extended (GOS-E) and modified Rankin Scale (mRS)] was ascertained using the social security death database and structured telephone interviews. Univariate and multivariate regression were used to identify variables that correlated with outcome. Data from 64 patients were analyzed (12 were lost to follow-up). There were 530 episodes of compromised PbtO2 (

Background Placement of an external ventricular drain (EVD) is a commonly performed and often lifesaving procedure. Although hemorrhage is one of the commonest complications associated with the procedure, ventricular catheter-induced vascular injury is rarely reported. Objective To describe 9 cases of EVD-related vascular trauma: 7 arteriovenous fistulas and 2 traumatic aneurysms. Methods During a 3-year period, 299 patients had EVDs placed. Eight patients (2.75%), 3 male and 5 female (mean age, 48 ± 20 years), developed vascular lesions associated with EVDs. Six patients developed arteriovenous fistulas and 2 patients developed a traumatic aneurysm. The arterial feeders of 5 superficial draining fistulas arose from the middle meningeal artery, and the arterial feeder of a deep-draining fistula originated from a lenticulostriate artery. One traumatic aneurysm arose from a distal branch of the anterior cerebral artery, and the second from a branch of the superficial temporal artery. Four of the superficial fistulas were treated with transarterial embolization. Results Two superficial fistulas and the deep-draining fistula resolved spontaneously after EVD removal. The intracranial aneurysm was embolized with Onyx18, and the superficial temporal artery aneurysm was managed conservatively. There were no hemorrhages associated with any of these vascular lesions and no complications after treatment. Conclusion Our data suggest that iatrogenic vascular trauma associated with EVD insertions (2.75%) may be more common than is currently appreciated. Endovascular treatment is effective and may be necessary when these lesions do not resolve spontaneously.

Background Limited data exists on the durability and occlusion rate of treating extracranial cervical internal carotid artery pseudoaneurysms using the pipeline embolization device (PED) flow-diverting stent. Methods Three patients presenting with dissecting cervical internal carotid artery pseudoaneurysms were treated with the PED as the sole treatment modality. Results In all three patients, successful aneurysmal occlusion and parent vessel reconstruction occurred on immediate angiography and continued on 6-month follow-up. No immediate or delayed complications were seen, and all patients remained neurologically intact. Conclusion Complete aneurysmal occlusion and long-term angiographic occlusion can occur after PED treatment of cervical carotid pseudoaneurysms. In select patients, the PED can be a suitable primary treatment modality with good neurological outcome for cervical carotid pseudoaneurysms.

Optimal management of extracranial carotid artery dissections (eCAD) in pediatric patients is not well documented, and endovascular interventions are rarely reported. A 10-year-old girl sustained multiple systemic injuries in a motor vehicle accident, including an eCAD with pseudoaneurysm. She initially failed both aspirin and endovascular stenting with progressive enlargement of a traumatic cervical carotid pseudoaneurysm and stenosis. Second-stage endovascular stent placement with coiling resulted in successful occlusion of the pseudoaneurysm. At 30-month imaging follow-up, the parent vessel remained patent with no evidence of the pseudoaneurysm. In the setting of poly-trauma, management of eCAD can be complex especially in the pediatric population. There is little data on the endovascular treatment of eCAD in children. Failed endovascular therapies are extremely rare. Our report supports surveillance imaging as repeat endovascular treatment may be necessary.

Purpose A novel endovascular therapy to treat a pseudoaneurysm as a complication of molar tooth extraction is described. Patients and Methods A 20-year-old man presented 2 weeks after third molar tooth extraction with an enlarging pulsatile jaw mass, identified as a facial artery pseudoaneurysm. Endovascular embolization with microcoils and a liquid embolic agent, Onyx, was performed. The use of Onyx in this manner is an off-label use. Results Immediately after treatment, the pulsatile mass resolved and remained obliterated at 2 months of follow-up. Conclusions Onyx embolization of facial artery vascular lesions can be safely accomplished while avoiding microvascular complications and provides a satisfactory and durable result.

IntroductionThe development of new revascularization devices has significantly improved recanalization rates and time to reperfusion. A direct aspiration first-pass (ADAPT) technique for stroke thrombectomy was recently shown to be an effective and rapid way to achieve revascularization. The technique focuses on engaging and removing a clot without the use of a separator or retriever by relying on the force and aspiration generated by the catheter. We sought to compare the physical and fluid dynamic properties (force and aspiration) of commercially available catheters to determine the most effective catheter for the ADAPT technique.MethodsBenchtop models were employed to compare aspiration for each catheter by submersing the catheter into a graduated cylinder and aspirating water. The volume of fluid aspirated and flow rates were calculated. Force of aspiration at the tip of each catheter was measured using a vacuum pressure gauge while the catheter was attached to a standard aspiration pump. Force was then calculated.ResultsThe Penumbra 5MAX ACE catheter had the greatest aspiration rate of all the catheters at 245 mL/min. The Penumbra 5 MAX catheter aspirated 212 mL/min, followed by the Navien 058 and DAC 057 with 198 mL/min and 197 mL/min, respectively. The Penumbra 5MAX ACE generated the greatest tip force (18.25 g) and the 5MAX had the least amount of force (14.77 g).ConclusionsThe physical and fluid dynamic properties of currently available catheters suggest that the 5MAX ACE is the optimal catheter to use in direct aspiration for stroke therapy.

Observational clinical studies demonstrate that brain hypoxia is associated with poor outcome after severe traumatic brain injury (TBI). In this study, available medical literature was reviewed to examine whether brain tissue oxygen (PbtO2)-based therapy is associated with improved patient outcome after severe TBI. Clinical studies published between 1993 and 2010 that compared PbtO2-based therapy combined with intracranial and cerebral perfusion pressure (ICP/CPP)-based therapy to ICP/CPP-based therapy alone were identified from electronic databases, Index Medicus, bibliographies of pertinent articles, and expert consultation. For analysis, each selected paper had to have adequate data to determine odds ratios (ORs) and confidence intervals (CIs) of outcome described by the Glasgow outcome score (GOS). Seven studies that compared ICP/CPP and PbtO2- to ICP/CPP-based therapy were identified. There were no randomized studies and no comparison studies in children. Four studies, published in 2003, 2009, and 2010 that included 491 evaluable patients were used in the final analysis. Among patients who received PbtO2-based therapy, 121(38.8%) had unfavorable and 191 (61.2%) had a favorable outcome. Among the patients who received ICP/CPP-based therapy 104 (58.1%) had unfavorable and 75 (41.9%) had a favorable outcome. Overall PbtO2-based therapy was associated with favorable outcome (OR 2.1; 95% CI 1.4-3.1). Summary results suggest that combined ICP/CPP- and PbtO2-based therapy is associated with better outcome after severe TBI than ICP/CPP-based therapy alone. Cross-organizational practice variances cannot be controlled for in this type of review and so we cannot answer whether PbtO2-based therapy improves outcome. However, the potentially large incremental value of PbtO2-based therapy provides justification for a randomized clinical trial.

BACKGROUND AND IMPORTANCE Endovascular management of dural arteriovenous fistulas (DAVFs) has become an accepted primary and often definitive therapy. We present the first documented case of Onyx pulmonary embolism after embolization of a low-flow DAVF. CLINICAL PRESENTATION A 63-year-old man presented with subarachnoid hemorrhage secondary to a DAVF. Computed tomographic angiography, magnetic resonance imaging, and initial conventional angiogram were negative. A repeat angiogram demonstrated a DAVF, which was cured with Onyx embolization. A routine chest computed tomography after intervention revealed an asymptomatic Onyx embolization cast in a subsegmental pulmonary artery. CONCLUSION Endovascular treatment options include transarterial embolization with microcoils, polyvinyl alcohol particles, n-butyl-2cyanoacrylate, and Onyx (ev3 Neurovascular, Irvine, California). Complications associated with the use of Onyx are low but include embolizate pulmonary embolism. Patients often remain asymptomatic, but for symptomatic patients, conservative treatment options usually result in resolution of symptoms.

Brain tissue oxygen (PbtO(2)) monitoring is used in severe traumatic brain injury (TBI) patients. How brain reduced PbtO(2) should be treated and its response to treatment is not clearly defined. We examined which medical therapies restore normal PbtO(2) in TBI patients.Forty-nine (mean age 40 ± 19 years) patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to a University-affiliated, Level I trauma center who had at least one episode of compromised brain oxygen (PbtO(2)25 mmHg for10 min), were retrospectively identified from a prospective observational cohort study. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and PbtO(2) were monitored continuously. Episodes of compromised PbtO(2) and brain hypoxia (PbtO(2)15 mmHg for10 min) and the medical interventions that improved PbtO(2) were identified.Five hundred and sixty-four episodes of compromised PbtO2 were identified from 260 days of PbtO2 monitoring. Medical management used in a "cause-directed" manner successfully reversed 72% of the episodes of compromised PbtO(2), defined as restoration of a "normal" PbtO(2) (i.e. ≥ 25 mmHg). Ventilator manipulation, CPP augmentation, and sedation were the most frequent interventions. Increasing FiO(2) restored PbtO(2) 80% of the time. CPP augmentation and sedation were effective in 73 and 66% of episodes of compromised brain oxygen, respectively. ICP reduction using mannitol was effective in 73% of treated episodes, though was used only when PbtO(2) was compromised in the setting of elevated ICP. Successful medical treatment of brain hypoxia was associated with decreased mortality. Survivors (n = 38) had a 71% rate of response to treatment and non-survivors (n = 11) had a 44% rate of response (P = 0.01).Reduced PbtO(2) may occur in TBI patients despite efforts to maintain CPP. Medical interventions other than those to treat ICP and CPP can improve PbtO(2). This may increase the number of therapies for severe TBI in the ICU.

Brain tissue oxygenation (PbtO2)-guided management facilitates treatment of reduced PbtO2 episodes potentially conferring survival and outcome advantages in severe traumatic brain injury (TBI). To date, the nature and effectiveness of commonly used interventions in correcting compromised PbtO2 in TBI remains unclear. We sought to identify the most common interventions used in episodes of compromised PbtO2 and to analyze which were effective.A retrospective 7-year review of consecutive severe TBI patients with a PbtO2 monitor was conducted in a Level I trauma center's intensive care unit or neurosurgical registry. Episodes of compromised PbtO2 (defined as20 mm Hg for 0.25-4 hours) were identified, and clinical interventions conducted during these episodes were analyzed. Response to treatment was gauged on how rapidly (ΔT) PbtO2 normalized (20 mm Hg) and how great the PbtO2 increase was (ΔPbtO2). Intracranial pressure (ΔICP) and cerebral perfusion pressure (ΔCPP) also were examined for these episodes.Six hundred twenty-five episodes of reduced PbtO2 were identified in 92 patients. Patient characteristics were: age 41.2 years, 77.2% men, and Injury Severity Score and head or neck Abbreviated Injury Scale score of 34.0 ± 9.2 and 4.9 ± 0.4, respectively. Five interventions: narcotics or sedation, pressors, repositioning, FIO2/PEEP increases, and combined sedation or narcotics + pressors were the most commonly used strategies. Increasing the number of interventions resulted in worsening the time to PbtO2 correction. Triple combinations resulted in the lowest ΔICP and dual combinations in the highest ΔCPP (p0.05).Clinicians use a limited number of interventions when correcting compromised PbtO2. Using strategies employing many interventions administered closely together may be less effective in correcting PbO2, ICP, and CPP deficits. Some PbtO2 deficits may be self-limited.

Object The object of this study was to determine whether brain tissue oxygen (PbtO2)–based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)–based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI). Methods Seventy patients with severe TBI (postresuscitation GCS score ≤ 8), admitted to a neurosurgical intensive care unit at a university-based Level I trauma center and tertiary care hospital and managed with an ICP and PbtO2 monitor (mean age 40 ± 19 years [SD]) were compared with 53 historical controls who received only an ICP monitor (mean age 43 ± 18 years). Therapy for both patient groups was aimed to maintain ICP < 20 mm Hg and CPP > 60 mm Hg. Patients with PbtO2 monitors also had therapy to maintain PbtO2 > 20 mm Hg. Results Data were obtained from 12,148 hours of continuous ICP monitoring and 6,816 hours of continuous PbtO2 monitoring. The mean daily ICP and CPP and the frequency of elevated ICP (> 20 mm Hg) or suboptimal CPP (< 60 mm Hg) episodes were similar in each group. The mortality rate was significantly lower in patients who received PbtO2-directed care (25.7%) than in those who received conventional ICP and CPP–based therapy (45.3%, p < 0.05). Overall, 40% of patients receiving ICP/CPP–guided management and 64.3% of those receiving PbtO2–guided management had a favorable short-term outcome (p = 0.01). Among patients who received PbtO2-directed therapy, mortality was associated with lower mean daily PbtO2 (p < 0.05), longer durations of compromised brain oxygen (PbtO2 < 20 mm Hg, p = 0.013) and brain hypoxia (PbtO2 < 15 mm Hg, p = 0.001), more episodes and a longer cumulative duration of compromised PbtO2 (p < 0.001), and less successful treatment of compromised PbtO2 (p = 0.03). Conclusions These results suggest that PbtO2-based therapy, particularly when compromised PbtO2 can be corrected, may be associated with reduced patient mortality and improved patient outcome after severe TBI.

Background Vertebral origin angioplasty and stenting (VOAS) with bare metal stents is associated with a high rate of in-stent restenosis (ISR). Objective We evaluated the rate of ISR after VOAS with drug-eluting stents. Methods Twenty patients (15 men, 5 women; age range, 36-88 years; mean, 63.7 years) were treated for VOAS with a paclitaxel-eluting stent (Taxus Express2, Boston Scientific, Natick, Massachusetts). Stenosis at follow-up was quantified as insignificant (0%-24%), mild (25%-49%), moderate (50%-74%), and severe (75%-100%). ISR was defined using a binary criteria of >50% stenosis at follow-up angiography. Results All procedures were technically successful with no periprocedural complications. Follow-up angiography (range, 4-48 months; mean, 14.7 months) showed insignificant stenosis in 9 patients, mild in 6, moderate in 4, and severe in 1. In 1 patient with "moderate" stenosis, the stent migrated distally; therefore, the lesion restenosis was not within the stent. Thus, 4 of 19 patients (21%) exhibited binary moderate or severe ISR, and 5 of 20 showed restenosis at the lesion (25%). The patient with severe stenosis developed stent thrombosis>3 years after VOAS. Conclusion VOAS with drug-eluting stents was associated with a low incidence of periprocedural complications. Although the rate of restenosis was half that seen with the use of bare metallic stents, 21% of patients still developed moderate or severe ISR. These patients may require>or=1 revascularization procedures. The risk of delayed stent thrombosis may necessitate lifelong dual antiplatelet medications.

True fast imaging with steady-state precession–based spin tagging with alternating radiofrequency is a promising unenhanced four-dimensional dynamic MR angiography technique for clinical evaluation of cerebrovascular disorders such as arteriovenous malformation, steno-occlusive disease, and aneurysm.

Introduction Occlusion of the basilar artery (BA) has a poor prognosis. We evaluated technical considerations and complications associated with reopening subacute to chronically occluded BAs. Methods Duration of BA occlusion before revascularization, symptoms and medical management before treatment, and postprocedural antiplatelet regimen and anticoagulation protocols of 9 patients were analyzed. All patients underwent endovascular low-volume balloon angioplasty followed by Wingspan stenting. Results The median time between onset of symptoms and treatment was 5 days (range, 2 days to 3.5 years). The median time between documentation of BA occlusion by cerebral angiography or computed tomography angiography and treatment was 3 days (range, 1 day to 8 months). Recanalization was successful in 8 of the 9 patients. Immediately after the procedure, 4 patients were stable, 3 patients improved, and 2 patients were worse. Four patients had periprocedural complications. Four of the 9 patients died, 2 from periprocedural complications. The mean clinical duration of follow-up was 11 months. At latest follow-up, the modified Rankin Scale scores for the 5 surviving patients were 0, 0, 2, 2, and 3, respectively. During the follow-up period, 4 patients improved, 1 patient remained stable, and 1 patient died. The mean angiographic follow-up was 8.6 months. Two patients developed significant in-stent stenosis during this period. Conclusion With current endovascular techniques, recanalization of chronically occluded BAs is feasible. The procedure carries substantial risks and should be reserved for patients with medically refractory symptoms. Careful postprocedural medical management and radiographic follow-up are warranted to prevent in-stent restenosis.

OBJECTIVE: An endovascular approach is often the first-line treatment of dural arteriovenous fistulae (DAVFs). Information on the use of Onyx (ev3 Neurovascular, Irvine, CA) for treating DAVFs, however, is limited. Therefore, we present our early experience, technical considerations, and complications associated with the use of Onyx for DAVF embolization. METHODS: Twenty-eight patients with 29 DAVFs treated with Onyx embolization were included in this analysis. Hospital records, operative reports, and angiograms were reviewed and analyzed. RESULTS: Forty Onyx procedures, including 39 transarterial and 1 transvenous approaches, were performed. Fifty-one external carotid artery branches, 8 posterior meningeal artery branches, and 3 internal carotid artery branches were used for Onyx embolization. Branches of the middle meningeal artery were embolized 32 times, and the occipital artery was embolized 15 times. Twenty-one fistulae (72%) were cured angiographically with endovascular therapy. Transarterial embolization via the middle meningeal artery cured 12 DAVFs (41%). Four complications (9.7%) were recorded, including 3 transient (7.3%) and 1 permanent neurological deficits (2.4%). Follow-up imaging, which was available for 8 fistulae with angiographic cures, showed no evidence of recurrence. CONCLUSION: Transarterial Onyx embolization of external carotid artery branches, particularly the middle meningeal artery, offers a high likelihood of cure. This technique provides a safe and effective method of embolization with few side effects and complications. However, long-term follow-up is needed to establish its efficacy.

Object Poor outcome is common after aneurysmal subarachnoid hemorrhage (SAH). Clinical studies suggest that cerebral hypoxia after traumatic brain injury is associated with poor outcome. In this study we examined the relationship between brain oxygen tension (PbtO2) and death after aneurysmal SAH. Methods Forty-six patients, including 34 women and 12 men (Glasgow Coma Scale Score ≤ 8 and median age 58.5 years) who underwent PbtO2 monitoring were studied prospectively during a 2-year period in a neurosurgical intensive care unit at a University Level I Trauma Center. Brain oxygen tension, intracranial pressure (ICP), mean arterial pressure, cerebral perfusion pressure (CPP), and brain temperature were continuously monitored, and treatment was directed toward ICP, CPP, and PbtO2 targets. The relationship between PbtO2 and 1-month survival was examined. Results Data were available from 5424 hours of PbtO2 monitoring. For the entire cohort the mean ICP, CPP, and PbtO2 were 13.85 ± 2.40, 84.05 ± 3.41, and 30.79 ± 1.91 mm Hg, respectively. Twenty-five patients died (54%). The mean daily PbtO2 was higher in survivors than nonsurvivors (33.94 ± 2.74 vs 28.14 ± 2.59 mm Hg; p = 0.05). In addition, survivors had significantly shorter episodes of compromised PbtO2 (defined as 15–25 mm Hg) than nonsurvivors (125.85 ± 15.44 vs 271.14 ± 55.23 minutes; p < 0.01). Intracranial pressure was similar in survivors and nonsurvivors. In contrast, the average CPP was significantly lower in nonsurvivors than survivors (76.96 ± 5.50 vs 92.49 ± 2.75 mm Hg; p = 0.01). When PbtO2 was stratified according to CPP level, survivors had higher PbtO2 levels. Following logistic regression, the number of episodes of compromised PbtO2 (odds ratio 1.1, 95% confidence interval 1.003–1.2) and number of episodes of cerebral hypoxia (< 15 mm Hg; odds ratio 1.3, 95% confidence interval 1.0–1.7) were more frequent in those who died. Conclusions Patient deaths after SAH may be associated with a lower mean PbtO2 and longer periods of compromised cerebral oxygenation than in survivors. This knowledge may be used to help direct therapy.

Objective Pediatric cerebral aneurysms are rare. There are very few recent studies that focus on the multidisciplinary treatment of ruptured aneurysms. We reviewed our pediatric endovascular and surgical experience with ruptured cerebral aneurysms. Methods Pediatric patients aged 16 years and younger who were admitted with a diagnosis of aneurysmal subarachnoid hemorrhage and treated at the Children's Hospital of Philadelphia were included in this analysis. Results Twelve patients with 13 aneurysms (4 male patients and 8 female patients; age range, 4 months-16 years; mean age, 5.1 years), were admitted with subarachnoid hemorrhage during the past 12 years. The majority of patients were admitted in good clinical condition; 31% were in Hunt and Hess Grade II, and 31% were in Hunt and Hess Grade III. The remaining patients were in poor clinical condition and were in Hunt and Hess Grade IV (23%) or Grade V (15%). Computed tomography revealed that 15% of the patients were in Fisher Grade 2, 23% were in Fisher Grade 3, and 62% were in Fisher Grade 4. Endovascular techniques were used in the treatment of 5 aneurysms, and microsurgery was used in the treatment of 8 aneurysms. In the endovascular group, aneurysm sizes ranged from 2 to 35 mm (mean, 12.6 mm); 3 aneurysms were in the anterior circulation, and 2 were in the posterior circulation. In the microsurgery group, 6 aneurysms were in the anterior circulation, and 2 were in the posterior circulation; sizes ranged from 3 to 15 mm (mean, 6.8 mm). Sixty-nine percent of the patients were independent at follow-up. Conclusion Contemporary endovascular and microsurgical techniques can be used effectively to treat ruptured cerebral aneurysms in pediatric patients. In the time period studied, the techniques were equally effective when used in the appropriate patients.

✓The authors report the case of an 18-month-old girl who presented with a ruptured anterior communicating artery aneurysm, and who was later diagnosed with Takayasu arteritis. Her initial aneurysm was successfully treated with clip application. However, over a 6-month period she had multiple ruptures from new and rapidly recurring aneurysms adjacent to the clips. These aneurysms were treated with repeated craniotomy and clip application and then with endovascular coil placement. Aneurysmal subarachnoid hemorrhage is a rare presentation of Takayasu arteritis. To the authors' knowledge, this is the youngest reported patient with Takayasu arteritis to present with a ruptured cerebral aneurysm.

✓Spinal ependymomas are a common type of primary spinal cord neoplasm that frequently occurs in the lumbar spine. The authors report on two patients who presented with acute neurological decline after hemorrhage into ependymomas of the filum terminale. Both were transferred to the authors' institution because of diagnostic uncertainty and a concern about possible intradural vascular abnormalities. Both patients underwent lumbar laminectomies for tumor resection. The pathological finding in each case was myxopapillary ependymoma. Both patients made a significant recovery and were ambulatory and continent at follow-up review. These cases illustrate the rare but clinically significant incidence of acute neurological decline caused by hemorrhagic cauda equina ependymomas, including the potential for delayed diagnosis and treatment.

Brain death is a clinical diagnosis often confirmed with supplementary tests. In this study, we examined the relationship between brain death and the partial pressure of brain tissue oxygen (PbtO(2)). We hypothesized that a sustained PbtO(2) of 0 is associated with brain death.One hundred and twenty-six patients (Glasgow coma scaleor = 8, median age: 50 years) who underwent PbtO(2) monitoring were studied prospectively during a 2 year period in the neurointensive care unit at a university-based level I trauma center. PbtO(2), intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and brain temperature (BT) were compared before and after the diagnosis of brain death.Six patients (median age: 52 years) experienced brain death. In these patients, PbtO(2) decreased toward 0 mmHg as ICP increased and CPP decreased. PbtO(2) reached 0 only when there was clinical evidence for brain death. During the subsequent 12 hours until the second brain death examination, PbtO(2) remained 0 mmHg and did not respond to oxygen challenge. In addition, TCD examination demonstrated a 'to and fro' pattern consistent with brain death and cerebral circulatory arrest. PbtO(2) of 0 mmHg was observed in five non-brain dead patients. These episodes were transient (30 minutes) and responded to an oxygen challenge, directed treatment or catheter replacement.A sustained (30 minutes) brain PbtO(2) of 0 is consistent with brain death. We suggest that a sustained 'zero' PbtO(2) may be used to determine when a brain death examination is appropriate in the pharmacologically suppressed patient.

BackgroundMany authors have reported that general anesthesia (GA), as a generic and uncharacterized therapy, is contraindicated for patients undergoing endovascular management of acute ischemic stroke (EMAIS). The recent American Heart Association update cautiously suggests that it might be reasonable to favor conscious sedation over GA during EMAIS. We are concerned that such recommendations will result in patients undergoing endovascular treatment without consideration of the effects of specific anesthetic agents and anesthetic dose, and without appropriate critical consideration of the individual patient's issues. We hypothesized that significant variation in anesthetic practice comprises GA, and that outcome differences among types of GA would arise.MethodsWith IRB approval, we examined the records of patients who underwent anterior circulation EMAIS at the University of Pennsylvania from 2010 to 2015. Patients were managed by different anesthesiologists with no specific protocol. We analyzed American Society of Anesthesiologists status, NIH Stroke Scale, type of stroke, procedure, different types of anesthetic, blood pressure control, and outcome metrics. Modified Rankin Scale (mRS) scores were determined from medical records.ResultsGA was used in 91% of patients. Several types of GA were employed: intravenous, volatile, and intravenous/volatile combined. mRS scores ≤2 at discharge were observed in 42.8% of patients receiving volatile anesthesia and were better in patients receiving only volatile agents after induction of anesthesia (pConclusionsOur data support the notion that anesthetic techniques and associated physiology used in EMAIS are not homogeneous, making any statements about the effects of generic GA in stroke ambiguous. Moreover, our data suggest that the type of GA may affect the outcome after EMAIS.

Object Control of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is the foundation of traumatic brain injury (TBI) management. In this study, the authors examined whether conventional ICP- and CPP-guided neurocritical care ensures adequate brain tissue O2 in the first 6 hours after resuscitation. Methods Resuscitated patients with severe TBI (Glasgow Coma Scale score ≤ 8 and Injury Severity Scale score ≥ 16) who were admitted to a Level I trauma center and who underwent brain tissue O2 monitoring within 6 hours of injury were evaluated as part of a prospective observational database. Therapy was directed to maintain an ICP of 25 mm Hg or less and a CPP of 60 mm Hg or higher. Data from a group of 25 patients that included 19 men and six women (mean age 39 ± 20 years) were examined. After resuscitation, ICP was 25 mm Hg or less in 84% and CPP was 60 mm Hg or greater in 88% of the patients. Brain O2 probes were allowed to stabilize; the initial brain tissue O2 level was 25 mm Hg or less in 68% of the patients, 20 mm Hg or less in 56%, and 10 mm Hg or less in 36%. Nearly one third (29%) of patients with ICP readings of 25 mm Hg or less and 27% with CPP levels of 60 mm Hg or greater had severe cerebral hypoxia (brain tissue O2 ≤10 mm Hg). Nineteen patients had both optimal ICP (≤25 mm Hg) and CPP (> 60 mm Hg); brain tissue O2 was 20 mm Hg or less in 47% and 10 mm Hg or less in 21% of these patients. The mortality rate was higher in patients with reduced brain tissue O2. Conclusions Brain resuscitation based on current neurocritical care standards (that is, control of ICP and CPP) does not prevent cerebral hypoxia in some patients. This finding may help explain why secondary neuronal injury occurs in some patients with adequate CPP and suggests that the definition of adequate brain resuscitation after TBI may need to be reconsidered.

Intra-arterial papaverine (IAP) is used to treat symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). IAP, however, can increase intracranial pressure (ICP). In this study we examined whether IAP alters brain oxygen (BtO2). Poor clinical grade (Hunt & Hess IV or V) SAH patients who underwent continuous ICP and BtO2 monitoring during IAP infusion for symptomatic cerebral vasospasm were evaluated as part of a prospective observational study. Data are available for five patients (median age 58) who received IAP for cerebral vasospasm 4 to 7 days after SAH. In each patient, angiographic vasospasm was improved on postinfusion angiogram. Mean ICP before IAP was 23.04±1.18 mmHg; it increased immediately after IAP infusion and remained elevated (29.89±1.18 mmHg; p

Object. An intracranial pressure (ICP) monitor, from which cerebral perfusion pressure (CPP) is estimated, is recommended in the care of severe traumatic brain injury (TBI). Nevertheless, optimal ICP and CPP management may not always prevent cerebral ischemia, which adversely influences patient outcome. The authors therefore determined whether the addition of a brain tissue oxygen tension (PO2) monitor in the treatment of TBI was associated with an improved patient outcome. Methods. Patients with severe TBI (Glasgow Coma Scale [GCS] score < 8) who had been admitted to a Level I trauma center were evaluated as part of a prospective observational database. Patients treated with ICP and brain tissue PO2 monitoring were compared with historical controls matched for age, pathological features, admission GCS score, and Injury Severity Score who had undergone ICP monitoring alone. Therapy in both patient groups was aimed at maintaining an ICP less than 20 mm Hg and a CPP greater than 60 mm Hg. Among patients whose brain tissue PO2 was monitored, oxygenation was maintained at levels greater than 25 mm Hg. Twenty-five patients with a mean age of 44 ± 14 years were treated using an ICP monitor alone. Twenty-eight patients with a mean age of 38 ± 18 years underwent brain tissue PO2-directed care. The mean daily ICP and CPP levels were similar in each group. The mortality rate in patients treated using conventional ICP and CPP management was 44%. Patients who also underwent brain tissue PO2 monitoring had a significantly reduced mortality rate of 25% (p < 0.05). Conclusions. The use of both ICP and brain tissue PO2 monitors and therapy directed at brain tissue PO2 is associated with reduced patient death following severe TBI.

Object. It is well established that posttraumatic secondary ischemia contributes to poor outcome. Ion dysfunction leading to cytotoxic edema is a primary force in the formation of ischemic brain edema and is a principal component of traumatic brain swelling. Because cell swelling is the result of net ion and water movement, it is crucial to have a thorough understanding of these transient phenomena. The purpose of this study was to characterize the effects of secondary ischemia following traumatic brain injury (TBI) on the ability to restore ion homeostasis. Methods. Twenty-four Sprague—Dawley rats were divided into four groups of six animals each. The rats underwent transient forebrain ischemia via bilateral carotid artery occlusion combined with hypotension: 15 minutes of forebrain ischemia (Group 1); 60 minutes of forebrain ischemia (Group 2); impact acceleration/TBI (Group 3); and impact acceleration/TBI followed by 15 minutes of ischemia (Group 4). Ischemia resulted in a rapid accumulation of [K+]e: 41.94 ± 13.65 and 66.33 ± 6.63 mM, respectively, in Groups 1 and 2, with a concomitant decrease of [Na+]e: 64 ± 18 mM and 72 ± 11 mM in Groups 1 and 2. Traumatic brain injury resulted in a less severe although identical trend in ion dysfunction ([K+]e 30.42 ± 11.67 mM and [Na+]e 63 ± 33 mM). Secondary ischemia resulted in prolonged and sustained ion dysfunction with a concomitant elevation of intracranial pressure (ICP). Conclusions. Analysis of these results indicates that ischemia and TBI are sublethal in isolation; however, when TBI is associated with secondary ischemia, ion dysfunction is sustained and is associated with elevated ICP.

When a new technology is introduced it is important to empower the bedside practitioner with a resource tool that outlines the purpose, placement procedure, technology application guidelines, and interventions associated with that new technology. This promotes product and patient safety and successful implementation of the new technology. Continued evaluation of bedside clinical practice and the technology used in the care and treatment of the severe brain injured patient can lead to improvements in management and in technology design. Future clinical research initiatives exploring the impact of new technology will enable us to discover cost-effective treatments and interventions that will improve the outcome for a person with traumatic brain injury, a condition that devastates hundreds of thousands of Americans each year.

To determine a) whether packed red blood cell transfusion (RBCT) increases local brain tissue oxygen partial pressure (Pbto2) in a neurocritical care population; and b) what (if any) demographic, clinical, or physiologic variables mediate the assumed change.Prospective observational study.A neurosurgical intensive care unit at a university-based level I trauma center and tertiary care hospital.Thirty-five consecutive volume-resuscitated patients with subarachnoid hemorrhage or traumatic brain injury, without cardiac disease, requiring Pbto2 monitoring and receiving RBCT were studied between October 2001 and December 2003.None.The following physiologic variables were measured and compared 1 hr before and after RBCT: Pbto2, intracranial pressure, cerebral perfusion pressure, hemoglobin oxygen saturation (Sao2), Fio2, hemoglobin, and hematocrit. An increase in Pbto2 was observed in 26 of the 35 patients (74%). In nine patients, Pbto2 decreased after RBCT. The mean (+/-sd) increase in Pbto2 for all patients was 3.2 +/- 8.8 mm Hg (p = .02), a 15% change from baseline (1 hr before RCBT). This Pbto2 increase was associated with a significant mean increase in hemoglobin and hematocrit after RBCT (1.4 +/- 1.1 g/dL and 4.2% +/- 3.3%, respectively; both p.001). Cerebral perfusion pressure, Sao2, and Fio2 were similar before and after RBCT. Among the 26 patients whose Pbto2 increased, the mean increase in Pbto2 was 5.1 +/- 9.4 mm Hg or a 49% mean increase (p.01).RBCT is associated with an increase in Pbto2 in most patients with subarachnoid hemorrhage or traumatic brain injury. This mean increase appears to be independent of cerebral perfusion pressure, Sao2, and Fio2. Further study is required to determine why Pbto2 decreases in some patients after RBCT.

Object. Disruption of ionic homeostasis during ischemia is a well-characterized event and is identified by a rise in the concentration of extracellular potassium [K+]e, with a concomitant reduction in the concentration of extracellular sodium [Na+]e. Results of clinical studies in which microdialysis has been used, however, have shown only modest changes in the levels of extracellular ions. The object of this study was to measure [K+]e and [Na+]e by using ion-selective electrodes (ISEs) and to compare these measurements with those obtained using the well-established method of microdialysis. Methods. Fifteen Sprague—Dawley rats were separated into three groups. Five animals were subjected to a 15-minute period of ischemia, and another five animals to a 60-minute period of ischemia; animals in both of these groups received K+-free microdialysis perfusate. The third group of five rats underwent a 60-minute period of ischemia and received a reduced-Na+ microdialysis perfusate. Transient forebrain ischemia was produced by bilateral carotid artery occlusion combined with hypotension. A custom-fabricated glass Na+ electrode and a flexible plastic K+ and reference electrodes were used to monitor extracellular ion transients. Microdialysis samples were obtained with the aid of a 2-mm microdialysis probe that was perfused with K+-free mock cerebrospinal fluid at a rate of 2 µl/minute. Baseline measurements of [K+]e and [Na+]e, obtained using ISEs, were 3.41 ± 0.09 mM and 145 ± 7.75 mM, respectively. Ischemia resulted in a rapid accumulation of [K+]e (in animals subjected to 15 minutes of ischemia, the concentration was 41.9 ± 13.7 mM; and in animals subjected to 60 minutes of ischemia, the concentration was 66.9 ± 11.5 mM), with a concomitant decrease in [Na+]e (in animals subjected to 15 minutes of ischemia, the concentration was 71.7 ± 2.9 mM; and in animals subjected to 60 minutes of ischemia, the concentration was 74.7 ± 1.9 mM). A comparison of microdialysis and ISE methods revealed that microdialysis underestimated the [K+]e changes and was insensitive to concomitant [Na+]e alterations that occur during ischemia. Conclusions. Our results indicate that the flexible ISE is a reliable and accurate tool for monitoring ionic dysfunction that accompanies brain injury.

Multimodality monitoring and goal-directed therapy may not prevent blood flow and brain oxygen (Flow/BrOx) crisis. We sought to determine the impact of these events on outcome in patients with severe traumatic brain injury (sTBI).Twenty-four patients with sTBI were treated to maintain intracranial pressure (ICP) less than or equal to 20 mm Hg, cerebral perfusion pressure (CPP) greater than or equal to 60 mm Hg, brain oxygen greater than or equal to 20 mm Hg, and near infrared spectroscopy greater than or equal to 60%. Flow/BrOx crisis events were recorded. The 14-day predicted mortality was compared with actual mortality.Nonsurvivors had a significantly higher number of crisis events nonresponsive to treatment (P.05). Mortality was 87.5% in patients with greater than or equal to 20 events versus 6.3% in patients with less than 20 events. The predicted mortality was 58%, whereas actual mortality was 33.3% (8/24), yielding a 42% reduction in mortality.A multimodality monitoring and goal-directed therapy may decrease mortality in sTBI. However, Flow/BrOx crisis events still occur and predict a poor outcome.

Coil migration is a rare but potentially serious complication of endovascular procedures. Occasionally coils can be retrieved via endovascular techniques. The authors describe the microsurgical management of a case in which endovascular techniques failed. A 2-year-old girl with pulmonary atresia and a Blalock-Taussig shunt underwent attempted endovascular closure of the shunt with Gianturco steel coils. During deployment, a coil was lost in the aorta and an angiogram showed that it had lodged in the proximal M1 segment of the middle cerebral artery. The coil could not be retrieved by endovascular techniques, and the patient was taken to the operating room to undergo a craniotomy. After the sylvian fissure was split, the coil was visible through the vessel wall. Temporary clips were placed on the proximal M1 and the proximal M2 segments, trapping the coil. A small arteriotomy was performed, the coil was removed, and the arteriotomy was closed. A cerebral angiogram showed excellent perfusion with no dissections. The patient's motor examination demonstrated a mild hemiparesis on the left with no tremulousness. Coil migration can be treated by microsurgical techniques in pediatric patients with a good clinical outcome.

Background Data on the timing, durability and occlusion rate of treating ruptured blister cerebral aneurysms using the Pipeline Embolization Device (PED) are limited. Clinical presentation Three patients who presented with subarachnoid hemorrhages from ruptured blister aneurysms of the internal carotid arteries were treated with the PED. Results Aneurysmal occlusion with reconstruction of the parent vessels occurred angiographically using the PED as a primary treatment modality. All three patients were treated successfully without immediate or delayed complications and remained neurologically intact during the 6-month follow-up period. Conclusions Complete occlusion of a ruptured blister aneurysm can occur immediately after PED placement. In ruptured blister aneurysms with contrast stagnation after PED treatment, early angiographic occlusion was confirmed as early as 6 weeks and continued with medium-term durability.

Background: The DRAGON score, which includes clinical and computed tomographic (CT) scan parameters, predicts functional outcomes in ischemic stroke patients treated with intravenous tissue plasminogen activator (IV tPA). We assessed the utility of the DRAGON score in predicting functional outcome in stroke patients receiving both IV tPA and endovascular therapy. Methods: A retrospective chart review of patients treated at our institution from February 2009 to October 2015 was conducted. All patients with computed tomography angiography (CTA) proven large vessel occlusions (LVO) who underwent intravenous thrombolysis and endovascular therapy were included. Baseline DRAGON scores and modified Rankin Score (mRS) at the time of hospital discharge was calculated. Good outcome was defined as mRS ≤3. Results: Fifty-eight patients with LVO of the anterior circulation were studied. The mean DRAGON score of patients on admission was 5.3 (range, 3–8). All patients received IV tPA and endovascular therapy. Multivariate analysis demonstrated that DRAGON scores ≥7 was associated with higher mRS (P < 0.006) and higher mortality (P < 0.0001) compared with DRAGON scores ≤6. Patients with DRAGON scores of 7 and 8 on admission had a mortality rate of 3.8% and 40%, respectively. Conclusions: The DRAGON score can help predict better functional outcomes in ischemic stroke patients receiving both IV tPA and endovascular therapy. This data supports the use of the DRAGON score in selecting patients who could potentially benefit from more invasive therapies such as endovascular treatment. Larger prospective studies are warranted to further validate these results.

Ibrutinib is a novel targeted therapy for B-cell malignancies. Hemorrhagic events were reported in the original trials, however the mechanism of bleeding is just being elucidated. Recent studies have demonstrated platelet dysfunction as a mechanism of bleeding. Currently we report two patients who developed life-threatening central nervous system hemorrhage while receiving ibrutinib for chronic lymphoid leukemia (CLL) and mantle cell lymphoma, respectively. Both patients improved rapidly after platelet transfusions even though their platelet counts were normal or only mildly reduced at the time of hemorrhage. We suggest that platelet transfusions can ameliorate the platelet dysfunction defect of ibrutinib and can support the patient through the critical period until new platelet production occurs.

There are numerous clinical scenarios wherein a critically ill patient may present with neurologic dysfunction. In a general sense these scenarios often involve ischemia, trauma, or neuroexcitation. Each of these may include a period of decreased cerebral perfusion pressure, usually due to elevated intracranial pressure (ICP), eventually compromising cerebral blood flow sufficiently to produce permanent neuronal loss, infarction, and possibly brain death. Elevated ICP is thus a common pathway for neural demise and it may arise from a variety of causes, many of which may result in a neurosurgical procedure intended to ameliorate the impact or etiology of elevated ICP.

Objective We described our endovascular techniques for the recanalization of chronic occlusions of the brachiocephalic and subclavian arteries. Given their large caliber, origins from the aorta, and proximity to the carotid and vertebral arteries, various complex endovascular techniques are required to achieve revascularization. Navigation of distal embolic protection devices into the carotid and vertebral arteries mandates varied catheter approaches. Methods Four women harboring chronic occlusions of the brachiocephalic and subclavian arteries were evaluated for their presenting symptoms, neurologic status, endovascular treatment, complications, and radiographic and clinical follow-up. We reviewed three specific treatment scenarios and analyzed predictive factors associated with treatment failure. Results Three chronic occlusions of the subclavian artery and 1 chronic occlusion of the brachiocephalic artery were identified in the four patients. All patients previously had experienced a stroke in the affected vascular territory or transient ischemic attacks from steal syndromes. Three target vessels were reopened successfully with angioplasty and stenting. In all cases, distal embolic protection devices were used, and multiple access points, including radial, brachial, and femoral catheterization, were required. Angiographic follow-up (range, 6-18 months) demonstrated stable patency of the stents in the three successfully treated patients. There were no transient or permanent complications. Conclusions Endovascular recanalization of the great vessels with the use of distal embolic protection devices requires multiple catheters and complex endovascular techniques but is feasible and safe. A significant percentage of these occlusions can likely be reopened through endovascular techniques.

Introduction The management of unruptured intracranial aneurysms in the elderly remains controversial. Treatment risks are thought to be higher in this group. Large series assessing endovascular treatment of unruptured intracranial aneurysms in the elderly are lacking. Our single center endovascular experience in treating unruptured intracranial aneurysms in the elderly is presented. Methods 77 patients, 70 years or older, were referred to the endovascular neurosurgery service for treatment of an unruptured intracranial aneurysm between February 2000 and May 2008. Hospital records, operative reports, angiograms and radiology reports were reviewed and analyzed retrospectively. Results 99 aneurysms were treated in 77 patients in 102 procedures. Mean patient age was 75±4 years, and the average aneurysm size was 11±7 mm. Adjuvant techniques were used in 66% of cases. Endovascular procedures included coiling alone (32%), balloon assisted coiling (19%), stent assisted coiling (37%), balloon assisted stent and coiling (8%), stent only (1%) and glue (2%). The permanent morbidity and mortality rates were 1% and 3%, respectively. Four adverse events were attributed to the patient9s age. Posterior circulation aneurysms were associated with more adverse events (41%) than anterior circulation aneurysms (14%). Endovascular treatments using adjuvant techniques were associated with a higher complication rate than coiling alone. Conclusions With only a 4% permanent rate of neurological morbidity and mortality, endovascular treatment of unruptured aneurysms can be performed safely in the elderly. Age should not be the limiting factor when considering endovascular therapy.

Delayed cerebral ischemia (DCI) is a significant cause of morbidity and mortality for patients surviving the rupture of an intracranial aneurysm. Despite an association between vasospasm and DCI, thrombosis and thromboembolism may also contribute to DCI. In this study we investigate the time course of intravascular microclot formation after experimental subarachnoid hemorrhage (SAH) and assess the effects of the following two drugs on microclot burden: mutant thrombin-activated urokinase-type plasminogen activator (scFv/uPA-T), which is bound to red blood cells for use as a thromboprophylactic agent, and clazosentan, an endothelin antagonist. In the first study, adult male C57BL/6 mice were sacrificed at 24 (n=5), 48 (n=6), 72 (n=8), and 96 (n=3) hours after SAH induced by filament perforation of the anterior cerebral artery. Sham animals (n=5) underwent filament insertion without puncture. In the second study, animals received scFv/uPA-T (n=5) 3 hours after hemorrhage, clazosentan (n=5) by bolus and subcutaneous pump after SAH just prior to skin closure, or a combination of scFv/uPA-T and clazosentan (n=4). Control (n=6) and sham (n=5) animals received saline alone. All animals were sacrificed at 48 hours and underwent intra-cardiac perfusion with 4% paraformaldehyde. The brains were then extracted and sliced coronally on a cryostat and processed for immunohistochemistry. An antibody recognizing thrombin-anti-thrombin complexes was used to detect microclots on coronal slices. Microclot burden was calculated for each animal and compared among groups. Following SAH, positive anti-thrombin staining was detected bilaterally in the following brain regions, in order of decreasing frequency: cortex; hippocampus; hypothalamus; basal ganglia. Few microclots were found in the shams. Microclot burden peaked at 48 hours and then decreased gradually. Animals receiving scFv/uPA-T and scFv/uPA-T+clazosentan had a lower microclot burden than controls, whereas animals receiving clazosentan alone had a higher microclot burden (p