Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, December 18, 2022

Global Cortical Atrophy Is Associated with an Unfavorable Outcome in Stroke Patients on Oral Anticoagulation

Since you did nothing to prevent this problem from happening it was totally useless research. You're all fired.

Global Cortical Atrophy Is Associated with an Unfavorable Outcome in Stroke Patients on Oral Anticoagulation


Marta Kubacka a, b 
 Annaelle Zietz c 
 Sabine Schaedelin d  
Alexandros A. Polymeris c 
 Lisa Hert c, e
Johanna Lieb f  
Benjamin Wagner c  
David Seiffge c, g 
 Christopher Traenka c, h
Valerian L. Altersberger c, h  
Tolga Dittrich c  
Joachim Fladt c  
Urs Fisch c 
 Sebastian Thilemann c
Gian Marco De Marchis c  
Henrik Gensicke c, h  
Leo H. Bonati c  
Philippe Lyrer c
Stefan T. Engelter c, h  
Nils Peters a, c, h
a Stroke Center, Klinik Hirslanden, Zürich, Switzerland;  
b University of Basel, Basel, Switzerland; 
 c Department of Neurology and Stroke Center, University Hospital Basel and University of Basel, Basel, Switzerland; 
 d Clinical Trial Unit, Department of Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland;
e Department of Intensive Care Medicine, University Hospital Basel, Basel, Switzerland;  
f Department of
Neuroradiology, University Hospital Basel, Basel, Switzerland;  
g Department of Neurology and Stroke Center,
Inselspital, Bern, Switzerland;  
h Neurology and Neurorehabilitation, University Department of Geriatric Medicine
Felix Platter, University of Basel, Basel, Switzerland

Abstract

Introduction:  
 
Measures of cerebral small vessel disease (cSVD), such as white matter hyperintensities (WMH) and cerebral microbleeds (CMB), are associated with an unfavorable clinical course in stroke patients on oral anticoagulation (OAC) for atrial fibrillation (AF). Here, we investigated whether similar findings can be observed for global cortical atrophy (GCA).  
 
Methods:  
 
Registry-based prospective observational study of 320 patients treated with OAC following AF stroke. Patients underwent magnetic resonance imaging (MRI) allowing assessment of GCA. Using the simplified visual Pasquier scale, the severity of GCA was categorized as
follows: 0: no atrophy, 1: mild atrophy; 2: moderate atrophy, and 3: severe atrophy. Using adjusted logistic and Cox regression analysis, we investigated the association of GCA us-
ing a composite outcome measure, comprising: (i) recurrent acute ischemic stroke (IS); (ii) intracranial hemorrhage (ICH);
and (iii) death.  
 
Results:  
 
In our time to event analysis after adjusting for potential confounders (i.e., WMH, CMB, age, sex, diabetes, arterial hypertension, coronary heart disease, hyperlipidemia, and antiplatelet use), GCA was associated with an increased risk for the composite outcome in all three degrees of atrophy (grade 1: aHR 3.95, 95% CI 1.34–11.63, p = 0.013; grade 2: aHR 3.89, 95% CI 1.23–12.30, p = 0.021; grade 3: aHR 4.16, 95% CI 1.17–14.84, p = 0.028).  
Conclusion:  
 
GCA was associated with our composite outcome also after adjusting for other cSVD markers (i.e., CMB, WMH) and age, indicating that GCA may potentially serve as a prognosti marker for stroke patients with atrial fibrillation on oral anticoagulation.

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