Stroke; a journal of cerebral circulation
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Randomized Controlled Trial
Blood-brain barrier compromise does not predict perihematoma edema growth in intracerebral hemorrhage.
There are limited data on the extent of blood-brain barrier (BBB) compromise in acute intracerebral hemorrhage patients. We tested the hypotheses that BBB compromise measured with permeability-surface area product (PS) is increased in the perihematoma region and predicts perihematoma edema growth in acute intracerebral hemorrhage patients. ⋯ URL: http://www.clinicaltrials.gov. Unique identifier: NCT00963976.
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Randomized Controlled Trial
Atrial premature beats predict atrial fibrillation in cryptogenic stroke: results from the EMBRACE trial.
Many ischemic strokes or transient ischemic attacks are labeled cryptogenic but may have undetected atrial fibrillation (AF). We sought to identify those most likely to have subclinical AF. ⋯ URL: http://www.clinicaltrials.gov. Unique identifier: NCT00846924.
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The study aims to determine whether volume transfer constant (K(trans)) maps calculated from first-pass perfusion computed tomographic data are a biomarker of cerebral collateral circulation and predict the clinical outcome in acute ischemic stroke caused by proximal arterial occlusion. ⋯ K(trans) maps extracted from standard first-pass perfusion computed tomography are correlated with collateral circulation status after acute proximal arterial occlusion and predictive of outcome.
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Motor recovery after stroke has been shown to be correlated with both the fractional anisotropy (FA) of the affected corticospinal tract (CST) and the interhemispheric resting-state functional connectivity (rsFC) of the primary motor cortex (M1). However, the role of the restoration or enhancement of the M1-M1 rsFC in motor recovery remains largely unknown. We aimed to clarify this issue by investigating the correlations between the M1-M1 rsFC and the integrity of the M1-M1 anatomic connection and the affected CST in chronic subcortical stroke patients with good motor outcomes. ⋯ Our findings suggest that the M1-M1 anatomic connection impairment is secondary to CST damage, and the M1-M1 rsFC enhancement may reflect compensatory or reactive neural plasticity in stroke patients with CST impairment.