Background and Purpose— This study’s objective is to determine if nonstenotic carotid plaque of <50% luminal narrowing predominantly develops ipsilateral rather than contralateral to the stroke site. Methods— This was a cross-sectional observational study. We identified consecutive patients with anterior circulation embolic stroke of undetermined source (ESUS), excluding stroke in multiple vascular territories. Using ultrasonography, we measured the internal carotid plaque size and stenosis for each patient. We dichotomized the plaque size at several predefined thresholds and calculated the frequency of the plaque size and morphology above each threshold ipsilateral versus contralateral to the stroke site. Results— We included 53 patients with unilateral anterior circulation ESUS. Initially, we found that plaque with a thickness ≥1.5 mm was present ipsilateral to the stroke site in 59% of the patients, and present contralateral to the stroke site in 42% of the patients (31/53 versus 22/53 patients; P =0.049). Plaque with low echo likewise had a similar prevalence when present ipsilateral (9%) and contralateral (4%) to the stroke site (5/53 versus 2/53; P =0.25). Conclusions— Internal carotid artery plaque with a thickness ≥1.5 mm but that is nonstenotic (<50%) is considerably more common when ipsilateral to the ESUS site than when contralateral to the ESUS site, especially in plaque with a thickness ≥2.6 mm. Large but nonstenotic carotid artery plaque is associated with anterior circulation ESUS.

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T he goal of hyperacute stroke therapy is to recanalize the occlusive artery as soon as possible. Once a cerebral artery is occluded, blood and oxygen supply rapidly decrease and the neuron, glia cell, and vascular elements are immediately impaired, which leads to permanent damage.1 Early spontaneous recanalization occurs and rescues the brain tissue from ischemia, which is the underlying cause of most transient ischemic attacks. Over the past 2 decades, intravenous Background and Purpose-We investigated whether administration of edaravone, a free radical scavenger, before or during tissue-type plasminogen activator (tPA) can enhance early recanalization in a major arterial occlusion. Methods-The YAMATO study (Tissue-Type Plasminogen Activator and Edaravone Combination Therapy) is an investigator-initiated, multicenter (17 hospitals in Japan), prospective, randomized, and open-label study. Patients with stroke secondary to occlusion of the M1 or M2 portion of the middle cerebral artery and within 4.5 hours of the onset were studied. The subjects were randomly allocated to the early group (intravenous edaravone [30 mg] was started before or during tPA) and the late group (edaravone was started after tPA and the assessment of early recanalization). Results-One-hundred sixty-five patients (96 men; median age [interquartile range], of 78 [69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85] years) were randomized 1:1 to either the early group (82 patients) or the late group (83 patients). Primary outcome, defined as an early recanalization 1.5 hour after tPA, was observed in 53% of the early group and in 53% of the late group (P=1.000). About secondary outcomes, the rate of significant recanalization of ≥50% was not different between the 2 groups (28% versus 34%; P=0.393). The symptomatic intracerebral hemorrhage has occurred in 4 patients (5%) in the early group and in 2 patients (2%) in the late group (P=0.443). The favorable outcome (modified Rankin Scale score of 0-2) at 3 months was also similar between the groups (53% versus 57%; P=0.738). thrombolysis using tissue-type plasminogen activator (tPA) therapy was the only established therapy and the first-line treatment to recanalize an occluded artery. 2 In addition, for the past 2 years, an increasing number of endovascular therapy (EVT) studies have introduced a new era in recanalization therapy. Conclusions-The3 However, there are still many patients who do not achieve recanalization. Thus, every therapy that can increase the rate of early recanalization is truly needed.A large number of neuroprotective agents have reduced ischemic damage in experimental studies. One of the most expected agents to improve the outcome of stroke patients was NXY-059. 4 However, it failed to show clinical benefit in its second trial. In Japan, edaravone, a free radical scavenger and neuroprotectant, was approved by the Japanese Ministry of Health, Labour and Welfare in 2001 for the treatment of ischemic stroke, within 24 hours of onset.5 Edaravone suppresses free ...