Abstract
In humans both cerebral hemispheres play an essential role in controlling the upper limb. However, the neurophysiological effects of noninvasive brain stimulation (NBS) of primary motor cortex (M1) have been investigated primarily from motor evoked potentials (MEPs) recorded in contralateral distal hand muscles alone. This may present an incomplete picture. For example, the idea of using NBS after stroke to suppress excitability of the contralesional hemisphere (cM1), or “re-balance” excitability, may be too simplistic, and may lead to undesirable outcomes for some patients. The purpose of this presentation is to show how NBS alters excitability of projections to contralateral and ipsilateral motoneurons (MNs) controlling the proximal upper limb, and in particular, the cortico-reticulo-propriospinal pathway (CRPP). This has implications for the use of NBS as adjuvants to upper limb rehabilitation after stroke. Experiments involved TMS to elicit MEPs in distal and proximal upper limb muscles, M1 cathodal t-DCS (c-tDCS), and sham control. Effects of M1 c-tDCS and sham were compared in healthy participants and patients with upper limb weakness after sub-cortical stroke. M1 c-tDCS modulated ipsilateral and contralateral MEPs in proximal upper limb muscles in a task-dependent manner, at least in part via the CRPP. In stroke patients, cM1 c-tDCS modified selectivity of paretic biceps brachii (BB). Mildly impaired patients showed improved selectivity, whereas moderate-severely impaired patients showed worsened selectivity, and modulation of ipsilateral BB MEPs after cM1 c-tDCS correlated with clinical, neurophysiological and neuroimaging measures. In patients with upper limb weakness after stroke, the role of the cM1 for upper limb control can vary between individuals, depending on extent of damage to the corticospinal pathway. We present a neurophysiological model that explains how the cM1 may gain control of the paretic arm via the CRPP and why suppression of cM1 with NBS can be beneficial for some patients, but detrimental for others. Finally we describe ways to predict whether cM1 suppression may be indicated or contraindicated for an individual patient after stroke.
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