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Reported frequency of post-stroke dysphagia in the literature is highly variable. In view of progress in stroke management, we aimed to assess the current burden of dysphagia in acute ischemic stroke. We studied 570 consecutive patients treated in a tertiary stroke center. Dysphagia was evaluated by using the Gugging Swallowing Screen (GUSS). We investigated the relationship of dysphagia with pneumonia, length of hospital stay and discharge destination and compared rates of favourable clinical outcome and mortality at 3 months between dysphagic patients and those without dysphagia. Dysphagia was diagnosed in 118 of 570 (20.7%) patients and persisted in 60 (50.9%) at hospital discharge. Thirty-six (30.5%) patients needed nasogastric tube because of severe dysphagia. Stroke severity rather than infarct location was associated with dysphagia. Dysphagic patients suffered more frequently from pneumonia (23.1% vs. 1.1%, p<0.001), stayed longer at monitored stroke unit beds (4.4±2.8 vs. 2.7±2.4 days; p<0.001) and were less often discharged to home (19.5% vs. 63.7%, p = 0.001) as compared to those without dysphagia. At 3 months, dysphagic patients less often had a favourable outcome (35.7% vs. 69.7%; p<0.001), less often lived at home (38.8% vs. 76.5%; p<0.001), and more often had died (13.6% vs. 1.6%; p<0.001). Multivariate analyses identified dysphagia to be an independent predictor of discharge destination and institutionalization at 3 months, while severe dysphagia requiring tube placement was strongly associated with mortality. Dysphagia still affects a substantial portion of stroke patients and may have a large impact on clinical outcome, mortality and institutionalization.

Symptomatic intracerebral hemorrhage (sICH) after bridging thrombolysis for acute ischemic stroke is a devastating complication. We aimed to assess whether the additional administration of aspirin during endovascular intervention increases bleeding rates. We retrospectively compared bleeding complications and outcome in stroke patients who received bridging thrombolysis with (tPA+ASA) and without (tPA-ASA) aspirin during endovascular intervention between November 2008 and March 2014. Furthermore, we analyzed bleeding complications and outcome in antiplatelet naïve patients with those with prior or acute antiplatelet therapy. Baseline characteristics, previous medication, and dosage of rtPA did not differ between 50 tPA+ASA (39 aspirin naïve, 11 preloaded) and 181 tPA-ASA patients (p>0.05). tPA+ASA patients had more often internal carotid artery (ICA) occlusion (p<0.001), large artery disease (p<0.001) and received more often acute stenting of the ICA (p<0.001). 10/180 (5.6%) tPA-ASA patients and 3/49 (6.1%) tPA+ASA patients suffered a sICH (p = 1.0). Rates of asymptomatic intracerebral hemorrhage, systemic bleeding complications and outcome did not differ between both groups (p>0.1). There were no differences in bleeding complications and mortality among 112 bridging patients with antiplatelet therapy (62 preloaded, 39 acute administration, 11 both) and 117 antiplatelet naïve patients. In a logistic regression analysis, aspirin administration during endovascular procedure was not a predictor of sICH. Antiplatelet therapy before or during bridging thrombolysis in patients with acute ischemic stroke did not increase the risk of bleeding complications and had no impact on outcome. This finding has to be confirmed in larger studies.

Differential diagnosis of elevated high sensitive Troponin T (hsTnT) in acute ischemic stroke includes myocardial infarction (MI) and neurogenic stunned myocardium (NSM). The aim of this study was to identify factors associated with baseline hsTnT levels and MI or NSM in acute ischemic stroke. We studied 204 consecutive patients of the prospective acquired Bern Stroke Database with acute ischemic stroke diagnosed by brain MR. All patient histories and cardiac examinations were reviewed retrospectively. Volumetry of lesions on diffusion and perfusion weighted brain imaging (circular singular value decomposition, Tmax >6sec) was performed. Voxel based analysis was performed to identify brain areas associated with hsTnT elevation. Linear regression analysis was used to identify predictors of baseline hsTnT levels and myocardial infarction. Elevated hsTnT was observed in 58 of the 204 patients (28.4%). The mean age was 68.3 years in the normal hsTnT group and 69.7 years in the elevated hsTnT group. Creatinine (p<0.001, OR 6.735, 95% CI 58.734-107.423), baseline NIHSS score (p = 0.029, OR 2.207, 95% CI 0.675-12.096), ST segment depression (p = 0.025, OR 2.259, 95% CI 2.419-35.838), and negative T waves in baseline ECG (p = 0.002, OR 3.209, 95% CI 13.007-54.564) were associated with hsTnT elevation, while infarct location and size were not. Coronary angiography was performed in 30 of the 204 patients (14.7%) and myocardial infarction was diagnosed in 7 of them (23.3%). Predictive factors for myocardial infarction could not be identified. Elevated baseline baseline hsTnT was associated with NIHSS, creatinine, ST segment depression and inverted T waves, but not with stroke location or size. None of the factors was helpful to differentiate MI and NSM. Therefore, ancillary investigations such as coronary angiography, cardiac MRI or both may be needed to solve the differential diagnosis.