Early Magnesium Treatment After Aneurysmal Subarachnoid Hemorrhage: Individual Patient Data Meta-Analysis.

BACKGROUND AND PURPOSE: Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Trials of magnesium treatment starting <4 days after symptom onset found no effect on poor outcome or DCI in SAH. Earlier installment of treatment might be more effective, but individual trials had not enough power for such a subanalysis. We performed an individual patient data meta-analysis to study whether magnesium is effective when given within different time frames within 24 hours after the SAH. METHODS: Patients were divided into categories according to the delay between symptom onset and start of the study medication: <6, 6 to 12, 12 to 24, and >24 hours. We calculated adjusted risk ratios with corresponding 95% confidence intervals for magnesium versus placebo treatment for poor outcome and DCI. RESULTS: We included 5 trials totaling 1981 patients; 83 patients started treatment<6 hours. For poor outcome, the adjusted risk ratios of magnesium treatment for start <6 hours were 1.44 (95% confidence interval, 0.83-2.51); for 6 to 12 hours 1.03 (0.65-1.63), for 12 to 24 hours 0.84 (0.65-1.09), and for >24 hours 1.06 (0.87-1.31), and for DCI, <6 hours 1.76 (0.68-4.58), for 6 to 12 hours 2.09 (0.99-4.39), for 12 to 24 hours 0.80 (0.56-1.16), and for >24 hours 1.08 (0.88-1.32). CONCLUSIONS: This meta-analysis suggests no beneficial effect of magnesium treatment on poor outcome or DCI when started early after SAH onset. Although the number of patients was small and a beneficial effect cannot be definitively excluded, we found no justification for a new trial with early magnesium treatment after SAH.

Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2.

The gene for spinocerebellar ataxia type 2 (SCA2) has been mapped to 12q24.1. A 1.1-megabase contig in the candidate region was assembled in P1 artificial chromosome and bacterial artificial chromosome clones. Using this contig, we identified a CAG trinucleotide repeat with CAA interruptions that was expanded in patients with SCA2. In contrast to other unstable trinucleotide repeats, this CAG repeat was not highly polymorphic in normal individuals. In SCA2 patients, the repeat was perfect and expanded to 36-52 repeats. The most common disease allele contained (CAG)37, one of the shortest expansions seen in a CAG expansion syndrome. The repeat occurs in the 5'-coding region of SCA2 which is a member of a novel gene family.

Impact of collateral flow on tissue fate in acute ischaemic stroke.

BACKGROUND: Collaterals may sustain penumbra prior to recanalisation yet the influence of baseline collateral flow on infarct growth following endovascular therapy remains unknown. METHODS: Consecutive patients underwent serial diffusion and perfusion MRI before and after endovascular therapy for acute cerebral ischaemia. We assessed the relationship between MRI diffusion and perfusion lesion indices, angiographic collateral grade and infarct growth. Tmax perfusion lesion maps were generated and diffusion-perfusion mismatch regions were divided into Tmax >or=4 s (severe delay) and Tmax >or=2 but <4 s (mild delay). RESULTS: Among 44 patients, collateral grade was poor in 7 (15.9%), intermediate in 20 (45.5%) and good in 17 (38.6%) patients. Although diffusion-perfusion mismatch volume was not different depending on the collateral grade, patients with good collaterals had larger areas of milder perfusion delay than those with poor collaterals (p = 0.005). Among 32 patients who underwent day 3-5 post-treatment MRIs, the degree of pretreatment collateral circulation (r = -0.476, p = 0.006) and volume of diffusion-perfusion mismatch (r = 0.371, p = 0.037) were correlated with infarct growth. Greatest infarct growth occurred in patients with both non-recanalisation and poor collaterals. Multiple regression analysis revealed that pretreatment collateral grade was independently associated with infarct growth. CONCLUSION: Our data suggest that angiographic collateral grade and penumbral volume interactively shape tissue fate in patients undergoing endovascular recanalisation therapy. These angiographic and MRI parameters provide complementary information about residual blood flow that may help guide treatment decision making in acute cerebral ischaemia.

Intra-arterial thrombolysis for acute stroke in patients 80 and older: a comparison of results in patients younger than 80 years.

BACKGROUND AND PURPOSE: Intra-arterial fibrinolytic therapy is a promising treatment for acute ischemic stroke. Few data are available on its use in elderly patients. The purpose of this study was to compare the baseline characteristics, complications, and outcomes between intra-arterially treated ischemic stroke patients aged > or = 80 years and their younger counterparts. METHODS: Patients aged > or = 80 years (n = 33) were compared retrospectively with contemporaneous patients aged < 80 years (n = 81) from a registry of consecutive patients treated with intra-arterial thrombolysis over a 9-year period. RESULTS: The very elderly and younger cohorts were very similar in baseline characteristics, including pretreatment stroke severity (National Institutes of Health Stroke Scale [NIHSS] 17 versus 16), differing only in history of stroke/transient ischemic attack (42% versus 22%, P = .01) and weight (66.8 versus 75.8 kg; P = .02). Significant differences in recanalization (TIMI 2-3) rates could not be detected between the very elderly and younger patients (79% versus 68%, P = .10). Rates of major symptomatic hemorrhage (7% versus 8%) and any intracerebral hemorrhage (39% versus 37%) did not differ. Outcomes at 90 days showed lower rates of excellent functional outcome (mRS < or = 1, 26% versus 40%, P = .02) and survival (57% versus 80%, P = .01) among the very elderly. CONCLUSIONS: Intra-arterial fibrinolysis in the elderly can be accomplished with recanalization rates and hemorrhage rates equal to that in younger patients. Although mortality rates are higher and good functional outcomes are lower than in younger persons, nondisabling outcomes may be achieved in a quarter of patients. These findings suggest that the investigation and use of intra-arterial thrombolytic treatment in very elderly patients should not be avoided but pursued judiciously.

Magnesium sulfate neither potentiates nor inhibits tissue plasminogen activator-induced thrombolysis.

BACKGROUND: Increasing circulating magnesium concentrations to 2-fold over normal baseline may afford a neuroprotective effect in patients with acute cerebral ischemia. OBJECTIVES: As patients receiving magnesium sulfate (MgSO(4)) in human clinical trials may also be candidates for subsequent thrombolytic therapy with tissue plasminogen activator (t-PA), preclinical assessment of possible inhibition or potentiation of fibrinolytic activity by MgSO(4) has important clinical relevance. METHODS: We utilized an in vitro system, in which D-dimer release served as a reflection of t-PA-induced clot lysis, to measure the effect of magnesium at the target concentration being tested in human stroke clinical trials, and at 2- and 3-fold higher levels. Clots from normal volunteers were exposed to t-PA at concentrations that correspond to therapeutic or endogenous plasma t-PA levels. RESULTS: MgSO(4) had no effect on t-PA-induced clot lysis at up to 3-fold target magnesium concentration (6x normal serum concentration). CONCLUSIONS: MgSO(4) concentrations well above the targeted level in therapeutic stroke trials does not affect t-PA-induced fibrinolytic activity, and therefore is a suitable agent for trials of combined neuroprotective and thrombolytic therapy in patients with acute ischemic stroke.

Endovascular mechanical clot retrieval in a broad ischemic stroke cohort.

BACKGROUND AND PURPOSE: Our aim was to describe an expanded experience with endovascular mechanical embolectomy in a broad group of patients, including those not meeting entry criteria for the MERCI multicenter trials. METHODS: We performed an analysis of all patients with ischemic stroke treated with the Merci Clot Retrieval Device at a single academic center outside of the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trials. RESULTS: Twenty-four patients were treated with the device. Nine were MERCI trial ineligible: 4 received intravenous (IV) tissue plasminogen activator (tPA), 1 received IV tPA and was younger than 18 years of age, and 4 had time-to-treatment of longer than 8 hours. Mean age was 64 years (range, 14-89 years; 42% women). Median National Institutes of Health Stroke Scale (NIHSS) score was 21 (range, 11-30). Median symptoms-to-procedure-start time was 303 minutes (range, 85-2385 minutes). Recanalization (Thrombolysis in Myocardial Infarction, 2-3) was achieved in 15/24 (63%). In device-only patients, recanalization occurred in 10/16. In patients who failed IV tPA undergoing rescue embolectomy, recanalization was achieved in 4/5. Three patients unresponsive to device therapy received rescue intra-arterial tPA/abciximab; recanalization was achieved in 2/3. Recanalization was achieved in 3/4 patients in whom treatment was started longer than 8 hours after symptom onset. Asymptomatic hemorrhage occurred in 38%; symptomatic hemorrhage, in 8%. Three device fractures occurred; none worsened clinical outcome. In-hospital mortality was 17%; 90-day mortality, 29%. Good 90-day functional outcome (modified Rankin Scale,

Trends in acute ischemic stroke trials through the 20th century.

BACKGROUND AND PURPOSE: The advent of controlled clinical trials revolutionized clinical medicine over the course of the 20th century. The objective of this study was to quantitatively characterize developments in clinical trial methodology over time in the field of acute ischemic stroke. METHODS: All controlled trials targeting acute ischemic stroke with a final report in English were identified through MEDLINE and international trial registries. Data regarding trial design, implementation, and results were extracted. A formal 100-point scale was used to rate trial quality. RESULTS: A total of 178 controlled acute stroke trials were identified, encompassing 73 949 patients. Eighty-eight trials involved neuroprotective agents, 59 rheological/antithrombotic agents, 26 agents with both neuroprotective and rheological/antithrombotic effects, and 5 a nonpharmacological intervention. Only 3 trials met conventional criteria for a positive outcome. Between the 1950s and 1990s, the number of trials per decade increased from 3 to 99, and mean trial sample size increased from 38 (median, 26) to 661 (median, 113). During 1980-1999, median time window allowed for enrollment decreased per half decade from 48 to 12 hours. Reported pharmaceutical sponsorship increased substantially over time, from 38% before 1970 to 68% in the 1990s. Trial quality improved substantially from a median score of 12 in the 1950s to 72 in the 1990s. CONCLUSIONS: Accelerating trends in acute stroke controlled trials include growth in number, sample size, and quality, and reduction in entry time window. These changes reflect an increased understanding of the pathophysiology of acute stroke, the imperative for treatment initiation within a critical time window, and more sophisticated trial design.

Clinical and molecular analysis of a pedigree of southern Italian ancestry with spinocerebellar ataxia type 2.

We describe patients from five generations of a pedigree with mutations in the spinocerebellar ataxia type 2 gene (SCA2). The predominant clinical features observed included both appendicular and truncal ataxia, dysarthria, slowness of saccades, and impaired optokinetic responses. Successive generations demonstrated both earlier ages of onset as well as increasing numbers of trinucleotide repeat sequences. The signs found in this family are compared with the description of other families with SCA2 as well as with other types of dominantly inherited spinocerebellar ataxias.

Genetic mapping of the spinocerebellar ataxia type 2 gene on human chromosome 12.

The dominant spinocerebellar ataxias are a genetically heterogeneous group of diseases leading to premature death of neurons in the cerebellum and other parts of the nervous system. The mutation causing SCA1 is on human chromosome (CHR) 6p and SCA3 is on CHR 14q. To refine the location of the SCA2 gene on CHR 12q, we performed genetic linkage analysis between the SCA2 locus and nine Ioci (D12S58, D12S78, D12S317, D12S330, D12S353, D12S84, D12S105, D12S79, and PLA2) in three SCA2 families. The highest pairwise lod scores were obtained between SCA2 and D12S84/D12S105 and D12S79. We determined the best order and genetic distances among these loci in ten multigenerational families by multipoint linkage analysis and established the following order: D12S101-D12S58/IGF1- D12S78-D12S317-D12S330/D12S353-D12S84/D 12S105-D12S79-PLA2. Using this genetic map, multipoint linkage analysis placed SCA2 between D12S84/D12S105 and D12S79.

Diffusion-perfusion MR evaluation of perihematomal injury in hyperacute intracerebral hemorrhage.

BACKGROUND: It has been suggested that a zone of perihematomal ischemia analogous to an ischemic penumbra exists in patients with primary intracerebral hemorrhage (ICH). Diffusion-perfusion MRI provides a novel means of assessing injury in perihematomal regions in patients with ICH. OBJECTIVE: To characterize diffusion-perfusion MRI changes in the perihematomal region in patients with hyperacute intracerebral hemorrhage. METHOD: Twelve patients presenting with hyperacute, primary ICH undergoing CT scanning and diffusion-perfusion MRI within 6 hours of symptom onset were reviewed. An automated thresholding technique was used to identify decreased apparent diffusion coefficient (ADC) values in the perihematomal regions. Perfusion maps were examined for regions of relative hypo- or hyperperfusion. RESULTS: Median baseline NIH Stroke Scale score was 17 (range, 6 to 28). Median hematoma volume was 13.3 mL (range, 3.0 to 74.8 mL). MRI detected the hematoma in all patients on echo-planar susceptibility-weighted imaging and in all seven patients imaged with gradient echo sequences. In six patients who underwent perfusion imaging, no focal defects were visualized on perfusion maps in tissues adjacent to the hematoma; however, five of six patients demonstrated diffuse ipsilateral hemispheric hypoperfusion. On diffusion imaging, perihematomal regions of decreased ADC values were identified in three of 12 patients. All three subsequently showed clinical and radiologic deterioration. CONCLUSIONS: A rim of perihematomal decreased ADC values was visualized in the hyperacute period in a subset of patients with ICH. The presence of a rim of decreased ADC outside the hematoma correlated with poor clinical outcome. Although perfusion maps did not demonstrate a focal zone of perihematomal decreased blood flow in any patient, most patients had ipsilateral hemispheric hypoperfusion.

Diffusion-perfusion MRI characterization of post-recanalization hyperperfusion in humans.

BACKGROUND: Animal and human studies have demonstrated that postischemic hyperperfusion may occur both early and late timepoints following acute cerebral ischemia. OBJECTIVE: To use diffusion-perfusion MRI to characterize hyperperfusion in humans following intra-arterial thrombolysis. METHODS: MRI were performed before treatment, several hours following vessel recanalization, and at day 7 in patients successfully recanalized with intra-arterial thrombolytics. RESULTS: Hyperperfusion was visualized in 5 of 12 patients within several hours after recanalization (mean volume, 18 mL; range, 7 to 40 mL), and in 6 of 11 patients at day 7 (mean volume, 28 mL; range, 4 to 45 mL). Within the core region of hyperperfusion, mean cerebral blood flow was 2.1 times greater than in the contralateral homologous region at the early time point, and 3.1 times greater at day 7. Seventy-nine percent of voxels with hyperperfusion at day 7 demonstrated infarction at day 7, whereas only 36% of voxels (within the initial hypoperfusion region) not showing hyperperfusion at day 7 demonstrated infarction at day 7. Mean pretreatment apparent diffusion coefficient (ADC) and perfusion values were more impaired in voxels that subsequently developed hyperperfusion compared with other at-risk voxels (all p values < 0.0001). There were no significant differences in the degree of clinical improvement in patients with regions of hyperperfusion versus those without, although sample size limited power to detect group differences. CONCLUSIONS: Postischemic hyperperfusion, visualized with perfusion MRI in humans following recanalization by intra-arterial thrombolytic therapy, occurred in about 40% of patients within hours and in about 50% of patients at day 7. Hyperperfusion developed mainly in regions that went on to infarction. Compared with other abnormal regions, tissues that developed postischemic hyperperfusion had greater bioenergetic compromise in pretreatment apparent diffusion coefficient values and greater impairment in pretreatment blood flow measures.

Intraarterial thrombolysis for treatment of acute stroke: experience in 26 patients with long-term follow-up.

BACKGROUND AND PURPOSE: Since the approval of intravenous tissue plasminogen activator for acute ischemic stroke, great interest has been generated in cerebral fibrinolysis. Our purpose was to assess long-term outcome and hemorrhagic risk in patients with anterior circulation ischemic stroke treated with intraarterial urokinase. METHODS: Twenty-six patients were treated within 6 hours of ictus; of these, 21 were followed up for an average of 23 months. Angiographic reperfusion was classified according to thrombolysis in myocardial infarction (TIMI) grades. The Rankin Scale (RS) and the modified Barthel Index (mod BI) were used as outcome measures (good outcome: RS = 0-2, mod BI = 16-20; poor outcome: RS = 3-5, mod BI < or = 15). RESULTS: Ten of the 21 patients (average age, 48 years) had a good outcome; three (average age, 71 years) had a poor outcome; eight patients (average age, 78 years) died. Partial/complete (successful) recanalization was observed in 11 of 26 patients and minimal or no (unsuccessful) recanalization in 15. Recanalization favored a better outcome: nine of 21 had successful recanalization, with a good outcome in seven; 12 of 21 had unsuccessful reperfusion, with poor outcome/death in nine. Poor outcome was noted in five patients with internal carotid artery (ICA) bifurcation occlusions, four of whom had unsuccessful recanalization and poor outcome or death. Hemorrhage occurred in 10 of the 26 patients, with clinical deterioration in three. The average dose of urokinase was higher in the hemorrhage group, and mortality was higher in patients who hemorrhaged. CONCLUSION: Intraarterial thrombolysis is feasible in the setting of acute stroke. Successful reperfusion is associated with a better outcome, and the prevalence of hemorrhage does not exceed that which occurs in the natural history of embolic stroke. Poor outcome or death is associated with nonrecanalization, older age, hemorrhage, and ICA bifurcation occlusions.

Outcome of stroke patients without angiographically revealed arterial occlusion within four hours of symptom onset.

BACKGROUND AND PURPOSE: Follow-up imaging data from stroke patients without angiographically apparent arterial occlusions at symptom onset are lacking. We reviewed our Emergency Management of Stroke (EMS) trial experience to determine the clinical and imaging outcomes of patients with ischemic stroke who showed no arterial occlusion on angiograms obtained within 4 hours of symptom onset. METHODS: All patients in this report were participants in the EMS trial that was designed to address the safety and potential efficacy of combined IV and intraarterial thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) in patients with acute ischemic stroke. RESULTS: Thirty-five patients were randomized to receive either IV rt-PA (n = 17) or placebo (n = 18), followed by cerebral angiography. No symptomatic arterial occlusion was evident in 10 (29%) of the 34 patients. Eight (80%) of 10 patients without angiographically apparent clot within 4 hours of symptom onset had a new cerebral infarction confirmed on follow-up brain imaging. The median 72-hour infarction volume was 2.4 cc (range, 1-30 cc). Four of the 10 "no-clot" patients had a favorable 3-month outcome as assessed by Barthel Index (score, 95 or 100) and modified Rankin Scale (score, 0 or 1). The six remaining patients had 3-month Rankin Scale scores of 1 (Barthel of 90), 2, 3, 4, or 5. CONCLUSION: Acute ischemic stroke patients with a neurologic deficit but a negative angiogram during the first 4 hours after symptom onset usually develop image-documented cerebral infarction, and approximately half suffer from long-term functional disability. The two most likely explanations for negative angiograms are very early irreversible ischemic damage despite recanalization or ongoing ischemia secondary to clot in non-visible penetrating arterioles or in the microvasculature.

Overview of seizures.

Epilepsy is a chronic disorder characterized by recurrent unprovoked epileptic seizures. Not all epileptic seizures indicate the existence of an epileptic disorder; many represent a natural response of the normal brain to transient noxious insults that are not likely to be repeated (reactive seizures). Not only is it important to distinguish conditions associated with these relatively benign epileptic events from epilepsy, but also it is important to recognize the many types of epileptic seizures and many types of epilepsy, reflecting different underlying anatomic and pathophysiologic substrates, which determine therapy and prognosis. Acute care for an epileptic seizure, therefore, includes search for an underlying treatable cause and protection against recurrence, if necessary. Neurologic consultation in the emergency department can help avoid unnecessary diagnostic procedures and treatments, particularly in patients with reactive seizures and established epileptic disorders. Communication with the patient's continuing care physician is an essential part of the emergency department management plan.

[Cineangiocardiographic evaluation of mitral valve lesions. Validity of the method according to 100 angio-surgical correlations]. / Bilan des lésions valvulaires mitrales par la cinéangiocardiographie. Validité de la méthode d'après 100 confrontations angio-chirurgicales

In order to assess their validity, the findings on left bidirectional cineventriculography have been compared with the operative findings in 100 patients with mitral valve disease. This method of investigation has been shown to be a reliable one for the precise and complete evaluation of mitral valve lesions. The information which it provides about the morphology and kinetics of the valve, the site of any calcification, the state of the suspensory apparatus, and the degree and cause of any mitral incompetence often has a decisive influence on the indications for surgery and the choice of operation.

[Development of heterografts stenosis in the aortic or mitral position. Apropos of 2 cases]. / Evolution sténosante des hétérogreffes en position aortique oud mitrale. a propos de deux cas

From a series of 10 patients undergoing surgery with a homograft, two cases are reported in which stenosis of the graft occurred, one in the mitral and the other in the aortic position. The macroscopical appearances of the lesions showed sclerosis and calcification. In the case where histological material was available, there were marked changes in the collagen and elastin, disseminated calcified deposits in the valve, and inflammatory cellular changes over the surface, with a tendency to penetrations into the substance of the valve. One of the factors leading to these graft disorders is the type of chemical treatment which the valve undergoes; a combination of glutaraldehyde solution and oxidation using sodium metaperiodate would appear to be unsuitable in this respect. Emphasis is laid on the very particular clinical features of these two cases (stenosis and valvular incompetence), and on the difficulties in diagnosis of this condition.

Safety and feasibility of NeuroFlo use in eight- to 24-hour ischemic stroke patients.

BACKGROUND: Acute treatment of ischemic stroke patients presenting more than eight-hours after symptom onset remains limited and largely unproven. Partial aortic occlusion using the NeuroFlo catheter can augment cerebral perfusion in animals. We investigated the safety and feasibility of employing this novel catheter to treat ischemic stroke patients eight-hours to 24 h following symptom onset. METHODS: A multicenter, single-arm trial enrolled ischemic stroke patients at nine international academic medical centers. Eligibility included age 18-85 years old, National Institutes of Health stroke scale (NIHSS) score between four and 20, within eight-hours to 24 h after symptom onset, and perfusion-diffusion mismatch confirmed by magnetic resonance imaging. The primary outcome was all adverse events occurring from baseline to 30 days posttreatment. Secondary outcomes included stroke severity on neurological indices through 90 days. This study is registered with ClinicalTrials.gov, number NCT00436592. RESULTS: A total of 26 patients were enrolled. Of these, 25 received treatment (one excluded due to aortic morphology); five (20%) died. Favorable neurological outcome at 90 days (modified Rankin score 0-2 vs. 3-6) was associated with lower baseline NIHSS (P < 0·001) and with longer duration from symptom discovery to treatment. There were no symptomatic intracranial hemorrhages or parenchymal hematomas. Asymptomatic intracranial hemorrhage was visible on computed tomography in 32% and only on microbleed in another 20%. CONCLUSIONS: Partial aortic occlusion using the NeuroFlo catheter, a novel collateral therapeutic strategy, appears safe and feasible in stroke patients eight-hours to 24 h after symptom onset.

Partial recanalization of concomitant internal carotid-middle cerebral arterial occlusions promotes distal recanalization of residual thrombus within 24 h.

OBJECTIVES: Acute, simultaneous, concomitant internal carotid artery (ICA) and middle cerebral arteries (MCA) occlusions almost invariably lead to significant neurological disability if left untreated. Endovascular therapy is frequently the method of treatment in such situations but there remains a chance of incomplete recanalization. Successful recanalization of the proximal aspect of the occlusion may allow for endogenous thrombolysis and facilitate further endogenous recanalization of any residual MCA occlusion. METHODS: Consecutive patients with acute ischemic stroke undergoing endovascular therapy for tandem extracranial ICA-MCA or contiguous intracranial ICA-MCA occlusions were retrospectively analyzed. Rates of facilitated endogenous recanalization at 24 h (FER(24)) were compared by imaging within the immediate post-intervention 5-24 h period in those with proximal recanalization and in those without. RESULTS: 17 patients were included in the analysis. 12 patients had good initial proximal recanalization but a residual partial or total occlusion of the MCA while five patients failed any recanalization. Seven patients (58.3%) in the first group and none in the second had FER(24) on interval imaging after intervention (p=0.04). The probability of death and disability at discharge was less in patients with FER(24) than those without (p=0.05). CONCLUSIONS: More than half of all patients who present with both ICA and MCA occlusions who are only partially recanalized will undergo facilitated endogenous recanalization within the subsequent 24 h following intervention.

The risk of acute radiocontrast-mediated kidney injury following endovascular therapy for acute ischemic stroke is low.

BACKGROUND AND PURPOSE: Endovascular therapy is an alternative for the treatment of AIS resulting from large intracranial arterial occlusions that depends on the use of iodinated RCM. The risk of RCM-mediated AKI following endovascular therapy for AIS may be different from that following coronary interventions because patients may not have identical risk factors. MATERIALS AND METHODS: All consecutive patients with large-vessel AIS undergoing endovascular therapy were prospectively recorded. We recorded the baseline kidney function, and RCM-AKI was assessed according to the AKIN criteria at 48 hours after RCM administration. We compared the rate of RCM-AKI 48 hours after the procedure and sought to determine whether any preexisting factors increased the risk of RCM-AKI. RESULTS: We identified 99 patients meeting inclusion criteria. The average volume of contrast was 189 ± 71 mL, and the average creatinine change was -4.6% at 48 hours postangiography. There were 3 patients with RCM-AKI. Although all 3 patients died as a result of their strokes, return to baseline creatinine levels occurred before death. There was a trend toward higher rates of premorbid diabetes mellitus, chronic renal insufficiency, preadmission statin and NSAID use, and a higher serum creatinine level on admission for the RCM-AKI group. The volume of procedural contrast was similar between groups (those with and those without RCM-AKI) (P = .5). CONCLUSIONS: In this small study, the rate of RCM-AKI following endovascular intervention for AIS was very low. A much larger study is required to determine its true incidence.