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.

Thursday, April 25, 2019

Influence of Sex on Stroke Prognosis: A Demographic, Clinical, and Molecular Analysis

But they don't mention frequency of sex and how the doctor is ensuring that patients get sex.  We don't want prognosis, we want to know the exact number of sexual encounters needed and their duration. Damn it all, do your research properly.

Influence of Sex on Stroke Prognosis: A Demographic, Clinical, and Molecular Analysis

Emilio Rodríguez-Castro1,2, Manuel Rodríguez-Yáñez1,2, Susana Arias1,2, María Santamaría1,2, Iria López-Dequidt1,2, Ignacio López-Loureiro1, Manuel Rodríguez-Pérez1, Pablo Hervella1, Tomás Sobrino1, Francisco Campos1, José Castillo1* and Ramón Iglesias-Rey1*
  • 1Clinical Neurosciences Research Laboratory, Department of Neurology, Clinical University Hospital, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain
  • 2Stroke Unit, Department of Neurology, Hospital Clínico Universitario, Santiago de Compostela, Spain
Identifying the complexities of the effect of sex on stroke risk, etiology, and lesion progression may lead to advances in the treatment and care of ischemic stroke (IS) and non-traumatic intracerebral hemorrhage patients (ICH). We studied the sex-related discrepancies on the clinical course of patients with IS and ICH, and we also evaluated possible molecular mechanisms involved. The study's main variable was the patient's functional outcome at 3-months. Logistic regression models were used in order to study the influence of sex on different inflammatory, endothelial and atrial dysfunction markers. We recruited 5,021 patients; 4,060 IS (54.8% male, 45.2% female) and 961 ICH (57.1% male, 42.9% female). Women were on average 5.7 years older than men (6.4 years in IS, 5.1 years in ICH), and more likely to have previous poor functional status, to suffer atrial fibrillation and to be on anticoagulants. IS patients showed sex-related differences at 3-months regarding poorer outcome (55.6% women, 43.6% men, p < 0.0001), but this relationship was not found in ICH (56.8% vs. 61.9%, p = 0.127). In IS, women had higher levels of NT-proBNP and 3-months worse outcome in both cardioembolic and non-cardioembolic stroke patients. Stroke patients showed sex-related differences in pre-hospital data, clinical variables and molecular markers, but only IS patients presented independent sex-related differences in 3-months poor outcome and mortality. There was a relationship between the molecular marker of atrial dysfunction NT-proBNP and worse functional outcome in women, resulting in a possible indicator of increased dysfunction.

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