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BackgroundThe purpose of this guideline is to summarize the data available for performing mechanical thrombectomy (MT) for emergent large vessel occlusion (ELVO) stroke in special populations not typically included in large randomized controlled clinical trials, including children, the elderly, pregnant women, patients who have recently undergone surgery, and patients with thrombocytopenia, collagen vascular disorders, and endocarditis.MethodsWe performed a literature review for studies examining the indications, efficacy, and outcomes for patients undergoing MT for ischemic stroke aged 80 years, pregnant patients, patients who have recently undergone surgery, and those with thrombocytopenia, collagen vascular diseases, or endocarditis. We graded the quality of the evidence.ResultsMT can be effective for the treatment of ELVO in ischemic stroke for patients over age 80 years and under age 18 years, thrombocytopenic patients, pregnant patients, and patients with endocarditis. While outcomes are worse compared to younger patients and those with normal platelet counts (respectively), there is still a benefit in the elderly (in both mRS and mortality). Data are very limited for patients with collagen vascular diseases; although diagnostic cerebral angiography carries increased risks, MT may be appropriate in carefully selected patients in whom untreated ELVO would likely result in disabling or fatal outcome.

Background Aneurysmal ruptures typically cause subarachnoid bleeding with intraparenchymal and intraventricular extension. However, rare instances of acute aneurysmal ruptures present with concomitant, non-traumatic subdural hemorrhage (SDH). We explored the incidence and difference in outcomes of SDH with aneurysmal subarachnoid hemorrhage (aSAH) as compared with aSAH alone. Methods Retrospective cohort study from 2012 to 2015 from the National (Nationwide) Inpatient Sample (NIS) (20% stratified sample of all hospitals in the United States). NIS database (2012 to September 2015) queried to identify all patients presenting with aSAH. From this population, the patients with concomitant SDH were identified. Results A total of 10 075 patients with both cerebral aneurysms and aSAH were included. Of these, 335 cases of concomitant SDH and aSAH were identified. There was no significant change in the rate of SDH in aSAH over time. SDH with aSAH patients had a mortality of 24% compared with 12% (p=0.003) in the SAH only group, and only 16% were discharged home vs 37% (p=0.003) in the SAH group. Conclusions There is a 3.5% incidence of acute SDH in patients presenting with non-traumatic aSAH. Patients with SDH and aSAH have nearly double the mortality, higher rate of discharge to nursing home and rehabilitation, and a significantly lower rate of discharge to home and return to routine functioning. This information is useful in counseling and prognostication of patients with concomitant SDH and aSAH.

BackgroundAntiplatelet and antithrombotic medication management before, during, and after neurointerventional procedures has significant practice variation. This document updates and builds upon the 2014 Society of NeuroInterventional Surgery (SNIS) Guideline ‘Platelet function inhibitor and platelet function testing in neurointerventional procedures’, providing updates based on the treatment of specific pathologies and for patients with specific comorbidities.MethodsWe performed a structured literature review of studies that have become available since the 2014 SNIS Guideline. We graded the quality of the evidence. Recommendations were arrived at through a consensus conference of the authors, then with additional input from the full SNIS Standards and Guidelines Committee and the SNIS Board of Directors.ResultsThe management of antiplatelet and antithrombotic agents before, during, and after endovascular neurointerventional procedures continues to evolve. The following recommendations were agreed on. (1) It is reasonable to resume anticoagulation after a neurointerventional procedure or major bleeding episode as soon as the thrombotic risk exceeds the bleeding risk in an individual patient (Class I, Level C-EO). (2) Platelet testing can be useful to guide local practice, and specific approaches to using the numbers demonstrate marked local variability (Class IIa, Level B-NR). (3) For patients without comorbidities undergoing brain aneurysm treatment, there are no additional considerations for medication choice beyond the thrombotic risks of the catheterization procedure and aneurysm treatment devices (Class IIa, Level B-NR). (4) For patients undergoing neurointerventional brain aneurysm treatment who have had cardiac stents placed within the last 6–12 months, dual antiplatelet therapy (DAPT) is recommended (Class I, Level B-NR). (5) For patients being evaluated for neurointeventional brain aneurysm treatment who had venous thrombosis more than 3 months prior, discontinuation of oral anticoagulation (OAC) or vitamin K antagonists should be considered as weighed against the risk of delaying aneurysm treatment. For venous thrombosis less than 3 months in the past, delay of the neurointerventional procedure should be considered. If this is not possible, see atrial fibrillation recommendations (Class IIb, Level C-LD). (6) For patients with atrial fibrillation receiving OAC and in need of a neurointerventional procedure, the duration of TAT (triple antiplatelet/anticoagulation therapy=OAC plus DAPT) should be kept as short as possible or avoided in favor of OAC plus single antiplatelet therapy (SAPT) based on the individual’s ischemic and bleeding risk profile (Class IIa, Level B-NR). (7) For patients with unruptured brain arteriovenous malformations there is no indication to change antiplatelet or anticoagulant management instituted for management of another disease (Class IIb, Level C-LD). (8) Patients with symptomatic intracranial atherosclerotic disease (ICAD) should continue DAPT following neurointerventional treatment for secondary stroke prevention (Class IIa, Level B-NR). (9) Following neurointerventional treatment for ICAD, DAPT should be continued for at least 3 months. In the absence of new stroke or transient ischemic attack symptoms, reversion to SAPT can be considered based on an individual patient’s risk of hemorrhage versus ischemia (Class IIb, Level C-LD). (10) Patients undergoing carotid artery stenting (CAS) should receive DAPT before and for at least 3 months following their procedure (Class IIa, Level B-R). (11) In patients undergoing CAS during emergent large vessel occlusion ischemic stroke treatment, it may be reasonable to administer a loading dose of intravenous or oral glycoprotein IIb/IIIa or P2Y12 inhibitor followed by maintenance intravenous infusion or oral dosing to prevent stent thrombosis whether or not the patient has received thrombolytic therapy (Class IIb, C-LD). (12) For patients with cerebral venous sinus thrombosis, anticoagulation with heparin is front-line therapy; endovascular therapy may be considered particularly in cases of clinical deterioration despite medical therapy (Class IIa, Level B-R).ConclusionsAlthough the quality of evidence is lower than for coronary interventions due to a lower number of patients and procedures, neurointerventional antiplatelet and antithrombotic management shares several themes. Prospective and randomized studies are needed to strengthen the data supporting these recommendations.

The purpose of this publication is to provide a comprehensive review on the techniques and tools used for vascular access in neurointerventional procedures. Using published literature, we reviewed data on access methods, sites, tools, and techniques for neurointerventions. Recommendations are provided based on quality of data/levels of evidence and, where appropriate, expert consensus. While tools and techniques continue to be developed, current literature and experience supports certain principles regarding vascular access for neurointerventional procedures.

IntroductionAtraumatic convexity subarachnoid hemorrhage is a subtype of spontaneous subarachnoid hemorrhage that often presents a diagnostic challenge. Common etiologies include cerebral amyloid angiopathy, vasculopathies, and coagulopathy; however, aneurysm is rare. Given the broad differential of causes of convexity subarachnoid hemorrhage, we assessed the diagnostic yield of common tests and propose a testing strategy.MethodsWe performed a single-center retrospective study on consecutive patients with atraumatic convexity subarachnoid hemorrhage over a 2-year period. We obtained and reviewed each patient’s imaging and characterized the frequency with which each test ultimately diagnosed the cause. Additionally, we discuss clinical features of patients with convexity subarachnoid hemorrhage with respect to the mechanism of hemorrhage.ResultsWe identified 70 patients over the study period (mean (SD) age 64.70 (16.9) years, 35.7% men), of whom 58 patients (82%) had a brain MRI, 57 (81%) had non-invasive vessel imaging, and 27 (38.5%) underwent catheter-based angiography. Diagnoses were made using only non-invasive imaging modalities in 40 patients (57%), while catheter-based angiography confirmed the diagnosis in nine patients (13%). Further clinical history and laboratory testing yielded a diagnosis in an additional 17 patients (24%), while the cause remained unknown in four patients (6%).ConclusionThe etiology of convexity subarachnoid hemorrhage may be diagnosed in most cases via non-invasive imaging and a thorough clinical history. However, catheter angiography should be strongly considered when non-invasive imaging fails to reveal the diagnosis or to better characterize a vascular malformation. Larger prospective studies are needed to validate this algorithm.

BackgroundDelayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) has a multifactorial pathophysiology, with immune dysregulation being an important component. The neutrophil–lymphocyte ratio (NLR) is an established prognostic marker in patients with cancer, cardiac disease, and sepsis.ObjectiveTo determine whether there is a relationship between NLR and DCI in patients with aSAH.MethodsWe evaluated 1067 patients with aSAH between 2006 and 2015 enrolled in a single-center, prospective, observational cohort study. Admission white blood cell differentials (NLR) were analyzed using a cut-off point of ≥5.9. DCI from cerebral vasospasm was defined as the occurrence of focal neurological impairment, or a decrease in at least two points on the Glasgow Coma Scale, which was not apparent immediately after aneurysm occlusion, and could not be attributed to other causes. Cerebral infarct was defined as a new infarct on CT that was not visible on the admission or immediate postoperative scan, when the cause was thought to be vasospasm by the research team. Logistic regression models were generated.ResultsWe found that 768 (72%) patients had an admission NLR ≥5.9. In a multivariable model, elevated NLR was associated with poor admission Hunt-Hess grade (OR=1.6, 95% CI 1.2 to 2.6, p=0.005), Caucasian ethnicity (OR=2.6, 95% CI 1.9 to 3.7, pConclusionsThis study provides further evidence of the association between inflammation and DCI. Admission NLR is a readily available and convenient biomarker that may be a clinically useful tool for prognostication when evaluating aSAH.

IntroductionCerebral collateral circulation has been studied extensively in ischemic stroke where it has been shown to be a predictor of reperfusion, final infarct size, and outcome. Little is known about the significance of the collaterals in the setting of aneurysmal subarachnoid hemorrhage (aSAH). We sought to evaluate the effect of cerebral vasospasm on the development of cerebral collaterals following aneurysmal subarachnoid hemorrhage and the effects of the latter on delayed cerebral ischemia (DCI).MethodsWe retrospectively evaluated 64 aSAH patients with evidence of DCI between day 5 and 7, enrolled in a prospectively maintained observational cohort study. Angiograms were evaluated by four blinded neurointerventionalists. We compared good collateral grades to poor collateral grades, additionally we compared enrolled individuals with any collaterals versus patients who had no collaterals.ResultsInter-rater reliability for collateral grades was substantial (weighted kappa 0.632). Mild vasospasm was more frequent in patients with poor collateral grades compared with patients with good collateral grades (32% vs 4% P=0.012). There was no difference between the collateral groups with regards to DCI, functional, or cognitive outcome. Patients adjudicated to have any collaterals were more likely to have severe vasospasm (62% vs 33% P=0.023) and less likely to have mild vasospasm (37% vs 9% P=0.007). In a multivariable model, vasospasm severity remained associated with collateral status, while aneurysm location was not.ConclusionsThe severity of vasospasm following aSAH was associated with the development of collaterals. There was no difference between collateral grades with regards to DCI or outcome.

Isolated intraventricular hemorrhage due to dural arteriovenous fistula (dAVF) is extremely rare and has been reported only a few times in the literature. The pathophysiological cause of isolated intraventricular hemorrhage in these cases was hypothetically attributed to retrograde venous flow into subependymal vessels, although none of these cases demonstrated radiographic evidence of such reflux. We present the first case of a dAVF with radiographic evidence of severe cortical venous reflux into the subependymal venous network causing isolated intraventricular hemorrhage, thus lending proof for the underlying pathophysiology. Furthermore, ours is the first case of dAVF with isolated intraventricular hemorrhage that was successfully treated using multimodality transvenous and transarterial embolization techniques. In cases of high-grade dAVF, multimodality treatment may offer the greatest chance for success, and should be strongly considered for management.

Isolated intraventricular hemorrhage due to dural arteriovenous fistula (dAVF) is extremely rare and has been reported only a few times in the literature. The pathophysiological cause of isolated intraventricular hemorrhage in these cases was hypothetically attributed to retrograde venous flow into subependymal vessels, although none of these cases demonstrated radiographic evidence of such reflux. We present the first case of a dAVF with radiographic evidence of severe cortical venous reflux into the subependymal venous network causing isolated intraventricular hemorrhage, thus lending proof for the underlying pathophysiology. Furthermore, ours is the first case of dAVF with isolated intraventricular hemorrhage that was successfully treated using multimodality transvenous and transarterial embolization techniques. In cases of high-grade dAVF, multimodality treatment may offer the greatest chance for success, and should be strongly considered for management.

Objective Vasospasm and resultant clinical deterioration caused by delayed cerebral ischemia (DCI) are well known sources of morbidity after aneurysmal subarachnoid hemorrhage. Cerebral arteriovenous malformation (AVM) rupture is a relatively common cause of spontaneous parenchymal hemorrhage, as well as subarachnoid and intraventricular hemorrhage. However, ensuing vasospasm associated with AVM rupture is rare, with only 20 cases documented in the literature. We report a series of patients with ruptured AVMs in order to evaluate the prevalence of vasospasm and resultant DCI. Methods We retrospectively reviewed our own series of 854 patients presenting to our institution with an ICD-9 code for intracranial hemorrhage between September 2005 and May 2014. Thirty-six of these patients were found to have acute intracranial hemorrhage secondary to a ruptured cerebral AVM. Diagnostic cerebral angiograms were reviewed by two blinded neurointerventionalists. Electronic medical records, laboratory data, all related noninvasive imaging and angiographic data of the patients were reviewed. Results The mean age of the patients was 43 years; there was a 1.25:1 male to female predominance. Twenty-six patients had an intraparenchymal hemorrhagic component (72%), while 10 patients (28%) had pure extra-axial hemorrhage. Fifteen patients had subarachnoid component (42%) and 24 patients had intraventricular component (67%). Three patients (8.3%) had pure intraventricular hemorrhage. All patients had AVMs diagnosed on CT angiography or digital subtraction angiography as part of their workup for the intracranial hemorrhage. All patients had digital subtraction angiography within 7 days of hemorrhage. Twenty-seven patients had supratentorial AVM nidus. Five patients demonstrated angiographic vasospasm (13.9%), 4 of whom went on to develop DCI (11.1%). The mean time from ictus to demonstration of vasospasm was 6.6 days. All of the 5 patients who developed vasospasm had intraventricular hemorrhage. Of the 3 patients with pure intraventricular hemorrhage, all developed DCI. Conclusions Although typically associated with aneurysmal subarachnoid hemorrhage, angiographic vasospasm after AVM rupture is possible. AVM rupture classically produces parenchymal hemorrhage, but may also present with subarachnoid and/or intraventricular hemorrhage, both of which are associated with vasospasm and DCI. In cases with AVM rupture causing extra-axial hemorrhage, arterial vasospasm may be a rare, however under-reported, consequence. Specifically, in cases with pure intraventricular hemorrhage, arterial vasospasm does remain a possibility and may be a factor in patients who develop DCI. Disclosures K. Amuluru: None. F. Al-Mufti: None. C. Prestigiacomo: None. C. Gandhi: None.