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.

Saturday, September 23, 2017

The Role of the BDNF Val66Met Polymorphism in Recovery of Aphasia After Stroke

I understood nothing in this, can't even begin to figure out how this is going to help you recover from aphasia.
http://journals.sagepub.com/doi/abs/10.1177/1545968317723752
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Riemke G. A. de Boer, MD*, Kerstin Spielmann, MSc*, Majanka H. Heijenbrok-Kal, PhD, ...
First Published August 17, 2017 Research Article


Abstract

Background. Brain-derived neurotrophic factor (BDNF) is assumed to play a role in mediating neuroplasticity after stroke. Carriers of the function-limiting Val66Met (rs6265) single nucleotide polymorphism (SNP) may have a downregulation in BDNF secretion, which may lead to a poorer prognosis after stroke compared to noncarriers in motor learning and motor function recovery. The present study investigates whether this polymorphism may also affect the recovery of poststroke aphasia (ie, language impairment).  
Objective. To study the influence of the BDNF Val66Met polymorphism on the recovery of poststroke aphasia.  
Methods. We included 53 patients with poststroke aphasia, all participating in an inpatient rehabilitation program with speech and language therapy. All patients were genotyped for the Val66Met SNP and subdivided into carriers (at least one Met allele) and noncarriers (no Met allele). Primary outcome measures included the improvement over rehabilitation time on the Amsterdam-Nijmegen Everyday Language Test (ANELT) and the Boston Naming Test (BNT).  
Results. The outcome measures showed a large variability in the improvement scores on both the ANELT and BNT. There was no significant difference between noncarriers and carriers in the primary outcome measures.  
Conclusion. This study investigated the effect of the BDNF Val66Met polymorphism on clinical recovery of poststroke aphasia. In contrast to earlier studies describing a reducing effect of this polymorphism on motor function recovery after stroke, the present study does not support a reduction in language recovery for carriers compared to noncarriers with poststroke aphasia.
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