Stroke; a journal of cerebral circulation
-
Clinical Trial
Timing of recanalization after microbubble-enhanced intravenous thrombolysis in basilar artery occlusion.
Information about early recanalization of basilar artery occlusion after systemic tissue plasminogen activator remains unknown. We aimed to determine the timing of recanalization in basilar artery occlusion treated with systemic thrombolysis, microbubbles, and continuous transcranial Doppler monitoring. ⋯ In acute basilar artery occlusion, endovenous tissue plasminogen activator, microbubbles, and continuous ultrasound leads to early recanalization in a significant number of patients and this is associated with favorable outcome. Immediate intravenous tissue plasminogen activator treatment should be the first therapeutic option in these patients.
-
Acute-onset dysphagia after stroke is frequently associated with an increased risk of aspiration pneumonia. Because most screening tools are complex and biased toward fluid swallowing, we developed a simple, stepwise bedside screen that allows a graded rating with separate evaluations for nonfluid and fluid nutrition starting with nonfluid textures. The Gugging Swallowing Screen (GUSS) aims at reducing the risk of aspiration during the test to a minimum; it assesses the severity of aspiration risk and recommends a special diet accordingly. ⋯ The GUSS offers a quick and reliable method to identify stroke patients with dysphagia and aspiration risk. Such a graded assessment considers the pathophysiology of voluntary swallowing in a more differentiated fashion and provides less discomfort for those patients who can continue with their oral feeding routine for semisolid food while refraining from drinking fluids.
-
5' adenosine monophosphate-dependent protein kinase (AMPK) acts as a metabolic sensor. AMPK is elevated under ischemic conditions, but the role of AMPK in ischemic brain remains controversial. In this study, we examined the effects of AMPK inhibition using both pharmacological and genetic approaches in an in vivo stroke model. ⋯ AMPK activation is detrimental in a model of focal stroke. The AMPK catalytic isoform alpha-2 contributes to the deleterious effects of AMPK activation. AMPK inhibition leads to neuroprotection even when these agents are administered poststroke.