Contralesional Hemisphere Control of the Proximal Paretic Upper Limb following Stroke

Words like 'may' and associated mean that nothing concrete is known about this. Thus useless. 

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) 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 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 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 theinternal 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.Keywords:
 corticospinal tract, ipsilateral pathways, magnetic resonanceimaging, stroke prediction, transcranial direct current stimulation
Introduction
Six months after stroke, up to two-thirds of patients are unable to incorporate a weak hand into activities of daily living(Dobkin 2005). Following stroke there is often an imbalance in primary motor cortex (M1) excitability, with relative under-excitability in the stroke affected ipsilesional hemisphere and relative ove rexcitability in the contralesional hemisphere, and worse outcomes for patients with greater imbalance ( Traversa et al. 1998). Rebalancing of cortical excitability in patients with stroke has been associated with improvement of upper limbfunction ( Traversa et al
.
 1998; Shimizu et al. 2002; Murase et al.2004; Stinear et al. 2008; Swayne et al. 2008) and can be promoted with noninvasive brain stimulation (Hummel andCohen 2006). Transcranial direct current stimulation (tDCS) is a form of noninvasive brain stimulation that suppresses or facilitates M1 depending on the electrode polarity (Nitsche and Paulus 2000, 2001; Nitsche et al. 2003; Nitsche et al. 2005). Cathodal tDCS (c-tDCS) hyperpolarizes neurons and can be used to reduce the relative overexcitability of the contrale-sional hemisphere (Nowak et al. 2009).Proximal upper limb muscles are innervated by projectionsfrom contralateral and ipsilateral motor cortex, and this bilateral pattern of organization has functional implicationsfor adjuvants such as tDCS (Kuypers and Brinkman 1970; Turton et al. 1996; Lemon 2008). There is recent evidence in healthy adults that suppression of M1 can influence control of the ipsilateral proximal upper limb by reducing or increasing excitability of ipsilateral descending projections from non-invasive brain stimulation (Bradnam, Stinear, and Byblow 2010;McCambridge et al. 2011). However, upregulation of ipsilateral projections from contralesional M1 (cM1) may be an important functional adaptation in patients severely affected by stroke( Ward et al. 2006; Ward et al. 2007). Therefore, contralesional c-tDCS might not benefit this subgroup of patients. This might explain why cM1 suppression has had mixed effects onmeasures of paretic upper limb function in stroke patients to date. While some studies have shown positive effects on upper limb function (Fregni et al. 2005; Boggio et al. 2007; Grefkes et al. 2010; Kim et al. 2010), others have reported deleterious(Johansen-Berg et al. 2002; Murase et al. 2004; Lotze et al. 2006; Ackerley et al. 2010; Bestmann et al. 2010) or no effects (Talelliet al. 2007). These mixed findings indicate it is unlikely that there will be a ‘‘one size fits all’’ strategy for promoting upper limb function after stroke with noninvasive brain stimulation and that the extent to which the cM1 contributes to control of the paretic upper limb needs to be taken into account whenselecting protocols for an individual patient. Therefore, the efficacy of contralesional c-tDCS may depend on whether patients are mildly or severely impaired (Schlaug et al. 2008). This study examined the effects of c-tDCS of cM1 on paretic proximal upper limb muscle activation in patients withsubcortical stroke. We hypothesized that because contrale-sional c-tDCS may suppress ipsilateral descending projections to proximal upper limb, after effects would depend on ther elative contribution of cM1 to control of paretic proximalmuscles. We predicted that for mildly impaired patients cM1might interfere with control from the ipsilesional M1 at thelevel of the spinal cord. Therefore, suppressive tDCS of cM1 was expected to improve the control of the paretic proximal upper limb. Conversely, we predicted that for moderate to severely impaired patients control would be degraded because suppressing cM1 would downregulate ipsilateral compensatory  pathways for proximal paretic upper limb control for these patients.