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.

Monday, December 20, 2021

Atypical cortical drive during activation of the paretic and nonparetic tibialis anterior is related to gait deficits in chronic stroke

 So WHOM is going to put together all this gait and walking analysis research into something useful, like a rehab protocol? Specific names only since we have NO STROKE LEADERSHIP to contact or strategy to update. The answers are out there, just read all the research available. DAMN IT ALL, THIS IS SO FUCKING SIMPLE EVEN STROKE SURVIVORS KNOW WHAT NEEDS TO BE DONE. JUST DO IT!

Absolutely nothing here is going to help the 85% of survivors with gait abnormalities until this is all put together into a coherent whole stroke protocol.

 

The latest here:

Atypical cortical drive during activation of the paretic and nonparetic tibialis anterior is related to gait deficits in chronic stroke

 
 
Atypical cortical drive during activation of the paretic and nonparetictibialis anterior is related to gait deficits in chronic stroke
 Jacqueline A. Palmer
a,b,

, Alan R. Needle
c
, Ryan T. Pohlig
d
, Stuart A. Binder-Macleod
a,b
a
Department of Physical Therapy, University of Delaware, Newark, DE 19713, USA
b
Graduate Program in Biomechanics and Movement Science, University of Delaware, Newark, DE 19713, USA
c
Department of Health and Exercise Science, Appalachian State University, Boone, NC 28608, USA
d
Biostatistics Core Facility, University of Delaware, Newark, DE 19713, USA
a r t i c l e i n f o
 Article history:
Accepted 12 June 2015Available online xxxx
Keywords:
StrokeGaitTranscranial magnetic stimulationAsymmetryLower extremity
h i g h l i g h t s

 Walking recovery is associated with alterations in cortical drive during nonparetic muscle activation.

 The ability to differentially enhance cortical drive between legs may underlie post-stroke gait impairments.

 Rehabilitation strategies that promote corticomotor balance may improve walking recovery.

a b s t r a c t

Objective:
 The role of cortical drive in stroke recovery for the lower extremity remains ambiguous. The purpose of this study was to investigate the relationship between cortical drive and gait speed in a group of stroke survivors.
Methods:
 Eighteen individuals with stroke were dichotomized into fast or slow walking groups.Transcranial magnetic stimulation (TMS) was used to collect motor evoked potentials (MEPs) from thetibialis anterior of each lower extremity during rest, paretic muscle contractions, and nonparetic muscle contractions. An asymmetry-index (AI) was calculated using motor thresholds and compared between groups. The average MEP of the paretic leg during TMS at maximal intensity (MEP100) for each conditionwas compared within and between groups.
Results:
 A significant positive correlation was found between AI and walking speed. Slow-walkers had greater MEP100s during the nonparetic contraction than during the paretic contraction or rest conditions.In contrast, fast-walkers had greatest MEP100s during the paretic contraction.
Conclusions:
 Alterations in the balance of corticomotor excitability occur in the lower extremity of individuals with poor motor recovery post-stroke. This atypical cortical drive is dependent on activation of the unaffected hemisphere and contraction of the nonparetic leg.
Significance:
 Understanding mechanisms underlying motor function can help to identify specific patient deficits that impair function.(What good does this do if you don't tell us how to correct those deficits?)

 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rightsreserved.

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