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.
This study unravels H2 S as an astroglial mediator of motor neuron damage possibly involved in the cellular death characterizing ALS.
Background and Purpose-The pathogenesis of cervical artery dissection (CAD) remains unknown in most cases.Hyperhomocyst(e)inemia [hyperH(e)], an independent risk factor for cerebrovascular disease, induces damage in endothelial cells in animal cell culture. Consecutive patients with CAD and age-matched control subjects have been studied by serum levels of homocyst(e)ine and the genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR). Methods-Twenty-six patients with CAD, admitted to our Stroke Unit (15 men and 11 women; 16 vertebral arteries, 10 internal carotid arteries), were compared with age-matched control subjects. All patients underwent duplex ultrasound, MR angiography, and/or conventional angiography. Results-Mean plasma homocyst(e)ine level was 17.88 mol/L (range 5.95 to 40.0 mol/L) for patients with CAD and 6.0Ϯ0.99 mol/L for controls (PϽ0.001). The genetic analysis for the thermolabile form of MTHFR in CAD patients showed heterozygosity in 54% and homozygosity in 27%; comparable figures for controls were 40% (Pϭ0.4) and 10% (Pϭ0.1), respectively. Conclusions-Mild hyperH(e) might represent a risk factor for cervical artery dissection. The MTHFR mutation is not significantly associated with CAD. An interaction between different genetic and environmental factors probably takes place in the cascade of pathogenetic events leading to arterial wall damage.
The heterogeneity of published data regarding post-stroke depression (PSD) prompted an Italian multicenter observational study (DESTRO), which took place in 2000-2003. The investigation involved 53 Italian neurology centers: of these, 50 treat acute patients and 3 provide rehabilitation care; 21 centres are in Northern Italy, 20 are in Central Italy, and 12 are in Southern Italy. The time schedule was articulated into three phases: registration of 6289 stroke patients; selection of 1817 cases and enrollment of 1074 patients; and follow-up for two years (1064 patients). Mood assessment was performed by evaluating depressive symptoms according to DSM IV and the Beck depression inventory (visual analog mood scale for aphasic patients). Depressed patients were also administered the Montgomery-Asberg depression rating scale. Scores were related to function (Barthel index, modified Rankin scale), cognition (MMSE), quality of life (SF-36), and clinical data. Data analysis will provide information on PSD prevalence, onset and evolution, correlation with ischemic clinical syndrome, impact on activities of daily living, cognitive level and quality of life. The few data available at the present time concern PSD prevalence in the first six months after stroke (33.6%). DESTRO is a longitudinal investigation of a large patient sample and is expected to provide insights into the relationship of PDS with the functional and clinical consequences of stroke.
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