Contralesional Hemisphere Control of the Proximal Paretic Upper Limb following Stroke

'Can' and 'may' are not good enough. There is nothing here that I can take to any doctor and therapists to get any survivor recovered. Useless. 

Contralesional Hemisphere Control of the Proximal Paretic Upper Limb following Stroke

Lynley V. Bradnam1,2, Cathy M. Stinear2,3, P. Alan Barber2,3 and Winston D. Byblow 1,21Movement Neuroscience Laboratory, Department of Sport & Exercise Science, and 2Centre for Brain Research and 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) can reduce 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 contralesional M1 (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  (FA) within the posterior limbs of the internal capsules indicative of corticospinal tract integrity. Excitability within paretic M1 biceps brachii representation was determined from motor-evoked potentials during selective isometric tasks, after cM1 sham stimulation and after c-tDCS. These neurophysiological data indicate that c-tDCS improved selective proximal upper limb control for mildly impaired patients and worsened it for moderate to severely impaired patients. The direction of the neurophysiological after effects of c-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 of cM1 for proximal upper limb control after stroke and that suppression of cM1 excitability is not a ‘‘one size fits all’’ approach.(But you don't tell us EXACTLY which patients it does fit. What damage diagnosis would this work for? Useless. )