Monday, October 7, 2019

Contralesional Hemisphere Control of the Proximal Paretic Upper Limb following Stroke

So you found something interesting. WHAT THE HELL are you doing about it? 

  1. Nothing

  2. Wrote a protocol on it and distributed it worldwide. 

    Your choice how you want to be perceived, a success or a do nothing person.

Contralesional Hemisphere Control of the Proximal Paretic Upper Limb following Stroke

 Lynley V. Bradnam
1,2
, Cathy M. Stinear
2,3
, P. Alan Barber
2,3
and Winston D. Byblow
1,21
Movement Neuroscience Laboratory, Department of Sport & Exercise Science, and
 2
Centre for Brain Research and
 3
Neurology Research Group, Department of Medicine, The University of Auckland, Auckland, New Zealand 1142.
 Address correspondence to Winston D. Byblow, Movement Neuroscience Laboratory, Department of Sport & Exercise Science, The University of  Auckland, Auckland, New Zealand 1142. Email: w.byblow@auckland.ac.nz.
Cathodal transcranial direct current stimulation (c-tDCS) canreduce excitability of neurons in primary motor cortex (M1) and may facilitate motor recovery after stroke. However, little is known about the neurophysiological effects of tDCS on proximal upper limb function. We hypothesized that suppression of contralesionalM1 (cM1) excitability would produce neurophysiological effects that depended on the severity of upper limb impairment. Twelve patients with varying upper limb impairment after subcortical stroke were assessed on clinical scales of upper limb spasticity, impairment, and function. Magnetic resonance imaging was used to determine lesion size and fractional anisotropy (FA) within the posterior limbs of the internal capsules indicative of corticospinaltract integrity. Excitability within paretic M1 biceps brachii representation was determined from motor-evoked potentials during selective isometric tasks, after cM1 sham stimulation andafter c-tDCS. These neurophysiological data indicate that c-tDCSimproved selective proximal upper limb control for mildly impairedpatients and worsened it for moderate to severely impairedpatients. The direction of the neurophysiological after effects ofc-tDCS was strongly related to upper limb spasticity, impairment, function, and FA asymmetry between the posterior limbs of the internal capsules. These results indicate systematic variation ofcM1 for proximal upper limb control after stroke and that suppression of cM1 excitability is not a ‘‘one size fits all’’ approach. (Oh god, weasel words to justify doing nothing.)

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