Background and Purpose-Acute rates of recanalization after intravenous (IV) recombinant tissue plasminogen activator (rt-PA) in proximal vessel occlusion have been estimated sparingly, typically using transcranial Doppler (TCD). We aimed to study acute recanalization rates of IV rt-PA in CT angiogram-proven proximal (internal carotid artery [ICA], M1 middle cerebral artery [MCA], M2-MCA, and basilar artery) occlusions and their effects on outcome. Materials and Methods-The CT angiogram database of the Calgary stroke program was reviewed for the period 2002 to 2009. All patients with proximal vessel occlusions receiving IV rt-PA who were assessed for recanalization by TCD or angiogram (for acute endovascular treatment) were included for analysis. Rates of acute recanalization as observed on TCD/first run of angiogram and postendovascular therapy recanalization rates were noted. Modified Rankin Scale score Յ2 at 3 months was used as a good outcome. Results-Among 1341 patients in the CT angiogram database, 388 patients with proximal occlusion were identified. Of these, 216 patients had received IV rt-PA; 127 patients underwent further imaging to assess recanalization. Among the patients undergoing TCD (nϭ46) and cerebral angiogram (nϭ103), only 27 (21.25%) patients had acute recanalization. By occlusion subtype, the rates of recanalization were: distal ICA (with or without ICA neck occlusion or stenotic disease) 1 of 24 (4.4%); M1-MCA (with or without ICA neck occlusion or stenotic disease) 21 of 65 (32.3%); M2-MCA 4 of 13 (30.8%); and basilar artery 1 of 25 (4%). Onset to rt-PA time was comparable in patients with and without recanalization. Recanalization (PϽ0.0001; risk ratio, 2.7; 95% confidence interval, 1.5-4.6) was the strongest predictor of outcome (adjusted for age and National Institutes of Health Stroke Scale score). Key Words: intracranial occlusion Ⅲ ischemic stroke Ⅲ recanalization Ⅲ thrombolysis I ntravenous (IV) recombinant tissue plasminogen activator (rt-PA) treatment for acute ischemic stroke 1,2 works by achieving recanalization of intracranial occlusion resulting in restoration of flow and prevention of infarct expansion. 3 Data on recanalization after IV thrombolysis are limited to small angiographic and transcranial Doppler (TCD) monitoring studies. 4 None of the major IV thrombolysis trials has assessed the baseline occlusion status or recanalization rates after treatment. In an era when there is increasing use of endovascular therapies for recanalization, in the absence of robust evidence from randomized controlled trials, there is a desperate need for clear data on the rates of recanalization with IV rt-PA. 5 The present study reports the rates of acute recanalization of proximal intracranial vessel occlusions identified by baseline CT angiography (CTA) among acute ischemic stroke patients treated with IV rt-PA. Conclusions- Patients and MethodsWe identified patients presenting with acute ischemic stroke secondary to major vessel occlusion from the CT Angiography database of the Calgary St...

Background-There are few validated models for prediction of in-hospital mortality after ischemic stroke. We used GetWith the Guidelines-Stroke Program data to derive and validate prediction models for a patient's risk of in-hospital ischemic stroke mortality. Methods and Results-Between October 2001 and December 2007, there were 1036 hospitals that contributed 274 988 ischemic stroke patients to this study. The sample was randomly divided into a derivation (60%) and validation (40%) sample. Logistic regression was used to determine the independent predictors of mortality and to assign point scores for a prediction model. We also separately derived and validated a model in the 109 187 patients (39.7%) with a National Institutes of Health Stroke Scale (NIHSS) score recorded. Model discrimination was quantified by calculating the C statistic from the validation sample. In-hospital mortality was 5.5% overall and 5.2% in the subset in which NIHSS score was recorded. Characteristics associated with in-hospital mortality were age, arrival mode (eg, via ambulance versus other mode), history of atrial fibrillation, previous stroke, previous myocardial infarction, carotid stenosis, diabetes mellitus, peripheral vascular disease, hypertension, history of dyslipidemia, current smoking, and weekend or night admission. The C statistic was 0.72 in the overall validation sample and 0.85 in the model that included NIHSS score. A model with NIHSS score alone provided nearly as good discrimination (C statistic 0.83). Plots of observed versus predicted mortality showed excellent model calibration in the validation sample. Conclusions-The Get With the Guidelines-Stroke risk model provides clinicians with a well-validated, practical bedside tool for mortality risk stratification. The NIHSS score provides substantial incremental information on a patient's short-term mortality risk and is the strongest predictor of mortality. (Circulation. 2010;122:1496-1504.)

Objectives: We used functional MRI (fMRI), transcranial Doppler ultrasound, and visual evoked potentials (VEPs) to determine the nature of blood flow responses to functional brain activity and carbon dioxide (CO 2 ) inhalation in patients with cerebral amyloid angiopathy (CAA), and their association with markers of CAA severity.Methods: In a cross-sectional prospective cohort study, fMRI, transcranial Doppler ultrasound CO 2 reactivity, and VEP data were compared between 18 patients with probable CAA (by Boston criteria) and 18 healthy controls, matched by sex and age. Functional MRI consisted of a visual task (viewing an alternating checkerboard pattern) and a motor task (tapping the fingers of the dominant hand).Results: Patients with CAA had lower amplitude of the fMRI response in visual cortex compared with controls (p 5 0.01), but not in motor cortex (p 5 0.22). In patients with CAA, lower visual cortex fMRI amplitude correlated with higher white matter lesion volume (r 5 20.66, p 5 0.003) and more microbleeds (r 5 20.78, p , 0.001). VEP P100 amplitudes, however, did not differ between CAA and controls (p 5 0.45). There were trends toward reduced CO 2 reactivity in the middle cerebral artery (p 5 0.10) and posterior cerebral artery (p 5 0.08).Conclusions: Impaired blood flow responses in CAA are more evident using a task to activate the occipital lobe than the frontal lobe, consistent with the gradient of increasing vascular amyloid severity from frontal to occipital lobe seen in pathologic studies. Reduced fMRI responses in CAA are caused, at least partly, by impaired vascular reactivity, and are strongly correlated with other neuroimaging markers of CAA severity. Neurology ® 2013;81:1659-1665 GLOSSARY BOLD 5 blood oxygen level-dependent; CAA 5 cerebral amyloid angiopathy; CO 2 5 carbon dioxide; DEF 5 dynamic end-tidal forcing; DSM-IV 5 Diagnostic and Statistical Manual of Mental Disorders, 4th edition; fMRI 5 functional MRI; ICH 5 intracerebral hemorrhage; PETCO 2 5 partial pressure of end-tidal carbon dioxide; VEP 5 visual evoked potential; WMH 5 white matter hyperintensity.Cerebral amyloid angiopathy (CAA) is best recognized clinically as a cause of frequent recurrent intracerebral hemorrhages (ICHs) and microbleeds, reflecting loss of vascular integrity due to b-amyloid deposition.1 However, accumulating evidence suggests that impaired vascular reactivity is another feature of CAA. In a mouse model of severe CAA, there was decreased vasodilation in response to whisker barrel stimulation and to carbon dioxide (CO 2 ) inhalation, a vasodilatory stimulus.2 In a small study of patients with probable CAA, posterior cerebral artery flow velocity responses were lower than controls when viewing a visual stimulus, but middle cerebral artery flow velocity responses to CO 2 inhalation were relatively preserved.3 It was not clear whether the differential responses observed in the visual and CO 2 experiments were due to the different arteries tested, the different types of vasodilatory stimulus used, or wer...