Edaravone, a novel free radical scavenger, demonstrates neuroprotective effects by inhibiting vascular endothelial cell injury and ameliorating neuronal damage in ischemic brain models. The present study was undertaken to verify its therapeutic efficacy following acute ischemic stroke. We performed a multicenter, randomized, placebo-controlled, double-blind study on acute ischemic stroke patients commencing within 72 h of onset. Edaravone was infused at a dose of 30 mg, twice a day, for 14 days. At discharge within 3 months or at 3 months after onset, the functional outcome was evaluated using the modified Rankin Scale. Two hundred and fifty-two patients were initially enrolled. Of these, 125 were allocated to the edaravone group and 125 to the placebo group for analysis. Two patients were excluded because of subarachnoid hemorrhage and disseminated intravascular coagulation. A significant improvement in functional outcome was observed in the edaravone group as evaluated by the modified Rankin Scale (p = 0.0382). Edaravone represents a neuroprotective agent which is potentially useful for treating acute ischemic stroke, since it can exert significant effects on functional outcome as compared with placebo.

Background and Purpose-We investigated whether lacunar infarct (LI) patients with Ͼ1 lacune have different vascular risk factors, a different prognosis, and poorer functional outcome than those with a single lacune. Methods-The study included 175 first-ever LI patients. The group was divided according to the presence of multiple (nϭ136)

Young patients with cryptogenic ischemic stroke with and without patent foramen ovale have a low recurrence rate in a long-term follow-up and most present a favorable outcome. Patent foramen ovale with or without atrial septal aneurysm did not increase the risk of recurrence.

Background and Purpose: Phenylpropanolamine (PPA) has been associated with an increased risk of intracranial hemorrhage (ICH). The aim of this study was to assess the association between PPA intake and ICH in a Mexican population. Methods: We included all patients with ICH aged 18 to 51 years, with no known structural etiology, diagnosed from January 1991 to December 2000. Three to 4 controls per patient matched by sex, age (within 5 years) and place of residence were included. Patients and controls were asked about use of cold medication or appetite suppressant medications within the previous year before the interview. We considered a PPA related hemorrhage when there was a temporal relationship between the use of medication and the development of the hemorrhage, and when other causes could be ruled out. Associated risks for PPA use and other possibly related variables were estimated. Results: 177 patients (mean age 39 ± 12 years) were included; 58 (33%) were diagnosed with subarachnoid hemorrhage (SAH) and 119 (67%) with ICH. 41.2% (73 of 177) of patients had documented use of PPA within the past year and 10 (5.7%) of them had a temporal relationship between ingestion of PPA and ICH. In control subjects 42.4% (422 of 996) had been exposed to PPA and none of them developed hemorrhage. The time from PPA exposure to the onset of ICH varied from 30 minutes to 24 hours. The risk of PPA exposure for hemorrhage was not significant in cases or controls, OR 0.95 (95% CI, 0.68 to 1.34; p = 0.77). No subjects (cases or controls) reported use of PPA as an appetite suppressant. Conclusions: We found no association between ingestion of PPA and cerebral hemorrhage with respect to ingestion of PPA in the previous year. When recent use was looked at an apparent risk was evident.

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