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, June 1, 2020

Inhibition versus facilitation of contralesional motor cortices in stroke: Deriving a model to tailor brain stimulation

I don't understand. 

Inhibition versus facilitation of contralesional motor cortices in stroke: Deriving a model to tailor brain stimulation

 Vishwanath Sankarasubramanian a, 
Andre G. Machado b, 
Adriana B. Conforto c,d, 
Kelsey A. Potter-Baker a,
David A. Cunningham a,e, 
Nicole M. Varnerin a, 
Xiaofeng Wang f, 
Ken Sakaie g, 
Ela B. Plow a,b,h,

a Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
b Center for Neurological Restoration, Neurological Institute, Cleveland Clinic, Cleveland, OH 44195, USA
c Neurology Clinical Division, Neurology Department, Hospital das Clinicas, São Paulo University, 05508-090 São Paulo, SP, Brazil
d Hospital Israelita Albert Einstein, 05652-900 São Paulo, SP, Brazil
e School of Biomedical Sciences, Kent State University, Kent, OH 44242, USA
f  Department of Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
g Department of Diagnostic Radiology, Imaging Institute, Cleveland Clinic, Cleveland, OH 44195, USA
h Department of Physical Medicine and Rehabilitation, Neurological Institute, Cleveland Clinic, Cleveland, OH 44195, USA
a r t i c l e i n f o
 Article history:
Accepted 14 March 2017Available online 21 March 2017
Keywords:
Diffusion tensor imagingMotor cortexPremotor cortexNeuronal plasticityRehabilitationStrokeTranscranial magnetic stimulation
h i g h l i g h t s

 Mildly affected chronic stroke patients improved upon paretic upper limb reaching with standardinhibitory 1Hz rTMS of contralesional motor cortex.

 Severely affected patients improved with a new method involving facilitatory 5Hz rTMS of contrale-sional dorsal premotor cortex.

 A preliminary cut-off level of damage/impairment separated responders to each form of stimulation.

a b s t r a c t

Objective:
 The standard approach to brain stimulation in stroke is based on the premise that ipsilesionalM1(iM1)is important for motor function of the paretic upper limb, while contralesional cortices compete with iM1. Therefore, the approach typically advocates facilitating iM1 and/or inhibiting contralesionalM1 (cM1). But, this approach fails to elicit much improvement in severely affected patients, who on account of extensive damage to ipsilesional pathways, cannot rely on iM1. These patients are believed to instead rely on the undamaged cortices, especially the contralesional dorsal premotor cortex(cPMd), for support of function of the paretic limb. Here, we tested for the first time whether facilitation of cPMd could improve paretic limb function in severely affected patients, and if a cut-off could be identified to separate responders to cPMd from responders to the standard approach to stimulation.
Methods:
 In a randomized, sham-controlled crossover study, fifteen patients received the standard approach of stimulation involving inhibition of cM1 and a new approach involving facilitation of cPMdusing repetitive transcranial magnetic stimulation (rTMS). Patients also received rTMS to control areas.At baseline, impairment [Upper Extremity Fugl-Meyer (UEFM PROXIMAL, max=36)] and damage to path-ways [fractional anisotropy (FA)] was measured. We measured changes in time to perform proximal paretic limb reaching, and neurophysiology using TMS.
Results:
 Facilitation of cPMd generated more improvement in severely affected patients, who had expe-rienced greater damage and impairment than a cut-off value of FA (0.5) and UEFM PROXIMAL
 (26–28). The standard approach instead generated more improvement in mildly affected patients. Responders to cPMd showed alleviation of interhemispheric competition imposed on iM1, while responders to the standard approach showed gains in ipsilesional excitability in association with improvement.
Conclusions:
A preliminary cut-off level of severity separated responders for standard approach vs. facilitation of cPMd

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