Ipsilateral Motor Pathways after Stroke: Implications for Non-Invasive Brain Stimulation

I'm sure your doctor can figure out how to use this in your stroke rehabilitation protocols. Way beyond my pay grade.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647244/

Lynley V. Bradnam,^1,2,† Cathy M. Stinear,^3,4 and Winston D. Byblow^4,5,*†

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Abstract

In humans the two cerebral hemispheres have essential roles in controlling the upper limb. The purpose of this article is to draw attention to the potential importance of ipsilateral descending pathways for functional recovery after stroke, and the use of non-invasive brain stimulation (NBS) protocols of the contralesional primary motor cortex (M1). Conventionally NBS is used to suppress contralesional M1, and to attenuate transcallosal inhibition onto the ipsilesional M1. There has been little consideration of the fact that contralesional M1 suppression may also reduce excitability of ipsilateral descending pathways that may be important for paretic upper limb control for some patients. One such ipsilateral pathway is the cortico-reticulo-propriospinal pathway (CRPP). In this review we outline a neurophysiological model to explain how contralesional M1 may gain control of the paretic arm via the CRPP. We conclude that the relative importance of the CRPP for motor control in individual patients must be considered before using NBS to suppress contralesional M1. Neurophysiological, neuroimaging, and clinical assessments can assist this decision making and facilitate the translation of NBS into the clinical setting.

Keywords: stroke, rehabilitation, upper limb, propriospinal, transcranial direct current stimulation

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Introduction

Reaching forward with the arm to manipulate objects with the hand is a quintessential function for higher order primates. Upper limb movements involve a fine balance between proximal stability and distal dexterity, presenting a unique motor control challenge to the central nervous system. There is a growing body of evidence that skilled upper limb function is under the control of both contralateral (cM1) and ipsilateral (iM1) motor cortices (Chen et al., 1997; Gerloff et al., 1998; Muellbacher et al., 2000; Hummel et al., 2003; Sohn et al., 2003; Verstynen et al., 2005; Davare et al., 2007; Duque et al., 2008; Perez and Cohen, 2008, 2009; Lee et al., 2010). Exactly how iM1 contributes to ipsilateral upper limb control is unclear, and is likely to involve both interhemispheric and descending projections. Neurophysiological studies have shown that iM1 assists cM1 to shape motor output by modulating the degree of transcallosal inhibition between homologous muscle representations in the two hemispheres (Sohn et al., 2003; Davare et al., 2007; Perez and Cohen, 2008). The potential importance of descending pathways from iM1 to spinal cord for upper limb control has largely been ignored. In this paper we present a novel hypothesis to account for how iM1 contributes to skilled upper limb motor control. We propose that the pathway involves a robust ipsilateral projection called the cortico-reticulo-propriospinal pathway (CRPP), based on findings in the cat and non-human primate (Illert et al., 1981; Alstermark et al., 1984; Isa et al., 2006). The CRPP descends from iM1 via the reticulospinal tract and terminates on propriospinal neurons (PNs) located at C3/4 in the spinal cord (Alstermark et al., 2007). PNs project to alpha motoneurons (αMNs) innervating muscles involved in specific tasks so movements can be rapidly generated and modified as necessary (Pierrot-Deseilligny and Burke, 2005). Our hypothesis is that neural inputs from the CRPP are integrated by PNs with those from the disynaptic (indirect) portion of the contralateral corticospinal tract. As a result, descending inputs from both hemispheres shape the final motor command reaching αMNs innervating upper limb musculature for optimal movement control.

Up-regulation of contralesional motor cortex excitability and the CRPP pathway may be important for paretic arm function after stroke (Turton et al., 1996; Netz et al., 1997; Alagona et al., 2001; Lewis et al., 2004; Misawa et al., 2008), particularly in poorly recovered patients (Turton et al., 1996; Netz et al., 1997; Gerloff et al., 1998; Caramia et al., 2000; Trompetto et al., 2000; Lewis and Perreault, 2007; Misawa et al., 2008). The degree of reorganization toward contralesional hemisphere control may depend on the residual integrity of white matter tracts from the ipsilesional hemisphere (Ward et al., 2006, 2007; Stinear et al., 2008; Grefkes and Fink, 2011). The neurophysiological model proposed here explains how increased excitability of the CRPP disrupts the normal cM1-iM1 balance of descending inputs reaching C3/4 PNs. In patients with a relatively intact ipsilesional corticospinal tract, up-regulation of the CRPP pathway would interfere with descending commands to PNs from the ipsilesional cortex. The model also accounts for why the CRPP is integral to residual function when the ipsilesional corticospinal tract is severely compromised. In these patients the CRPP may be the only intact descending pathway from cortex to spinal cord, and therefore of particular importance for their motor recovery.

Finally, a contribution by contralesional M1 to upper limb motor control via the CRPP has implications for NBS protocols aimed at improving rehabilitation of the paretic upper limb after stroke. The proposed model shows that contralesional M1 suppression after NBS may affect stroke patients differently depending on the severity of damage to the ipsilesional corticospinal tract and the degree of up-regulation of the contralesional CRPP. Studies that have included more severely impaired patients seem to indicate paretic upper limb motor performance is degraded by contralesional M1 NBS (Ackerley et al., 2010; Theilig et al., 2011; Bradnam et al., 2012). We propose that NBS protocols that aim to suppress contralesional M1 may be contraindicated for some patients. We argue that NBS is not a “one size fits all” solution for recovery after stroke, but that it can be tailored to individual patients based on neurophysiological and clinical biomarkers that are relative easy to obtain (Stinear et al., 2007, 2012; Jang et al., 2010; Kwon et al., 2011; Riley et al., 2011).

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