Cortical overlap of joint representations contributes to the loss of independent joint control following stroke

Yao, Jun; Chen, Albert; Carmona, Carolina; Dewald, Julius P. A.

doi:10.1016/j.neuroimage.2008.12.002

Cited by 66 publications

(59 citation statements)

References 56 publications

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“…In the experiment of Gerachshenko et al (2008), ERs correlated negatively with Fugl-Meyer upper limb scores highlighting the potential utility of ER as a neurophysiological correlate of abnormal upper synergy after stroke. The results of this study in healthy humans indicate a role for ipsilateral M1 in abnormal synergy formation consistent with current ideas that the origin of abnormal muscle synergies after stroke is the contralesional hemisphere (Schwerin et al 2008;Yao et al 2009). Although stroke is a chronic condition and effects on M1 evoked by cTBS in this study were acute, our results may provide additional evidence that contralesional M1 contributes to abnormal muscle synergies in the paretic upper limb.…”

Section: Discussionsupporting

confidence: 90%

Theta Burst Stimulation of Human Primary Motor Cortex Degrades Selective Muscle Activation in the Ipsilateral Arm

Bradnam

Stinear

Byblow³

2010

Journal of Neurophysiology

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Bradnam LV, Stinear CM, Byblow WD. Theta burst stimulation of human primary motor cortex degrades selective muscle activation in the ipsilateral arm. J Neurophysiol 104: 2594 -2602, 2010. First published September 15, 2010 doi:10.1152/jn.00365.2010. This study investigated whether repetitive transcranial magnetic stimulation (TMS) delivered as continuous theta burst stimulation (cTBS) to left M1 degraded selective muscle activation in the contralateral and ipsilateral upper limb in healthy participants. Contralateral motorevoked potentials (cMEPs) were elicited in left and right biceps brachii (BB) before either elbow flexion or forearm pronation. A neurophysiological index, the excitability ratio (ER), was computed from the relative size of BB cMEPs before each type of movement. Short interval intracortical inhibition (SICI) was assessed in cMEPs of right BB with paired-pulse TMS of left M1. Ipsilateral MEPs (iMEPs) and silent periods (iSPs) were measured in left BB with single-pulse TMS of left M1. Low-intensity cTBS was expected to suppress corticospinal output from left M1. A sham condition was also included. Real but not sham cTBS caused increases in BB ER bilaterally. In the right arm, ER increased because BB cMEPs before flexion were less facilitated, whereas cMEPs in the pronation task were unaffected. This was accompanied by an increase in left M1 SICI. In the left arm, ER increased because BB cMEPs before pronation were facilitated but were unaffected in the flexion task. There was also facilitation of left BB iMEPs. These changes in the left arm are consistent with inappropriate facilitation of left BB ␣-motoneurons (␣MNs) before pronation. This is the first demonstration that cTBS of M1 can alter excitability of neurons controlling ipsilateral proximal musculature and degrade ipsilateral upper limb motor control, providing evidence that ipsilateral and contralateral M1 shape the spatial and temporal characteristics of proximal muscle activation appropriate for the task at hand.

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Section: Discussionsupporting

confidence: 90%

Theta Burst Stimulation of Human Primary Motor Cortex Degrades Selective Muscle Activation in the Ipsilateral Arm

Bradnam

Stinear

Byblow³

2010

Journal of Neurophysiology

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“…The means by which selective increased reliance on ipsilateral reticular formation occurs is unclear since corticoreticular projections are bilateral in both the cat and monkey Kuypers 1984, 1989). However, a predominant ipsilateral corticobulbospinal circuit has been demonstrated in humans following stroke (Schwerin et al 2008(Schwerin et al , 2011Yao et al 2009) and in controls (Ziemann et al 1999), further supporting a selective increased reliance on ipsilateral reticular formation.…”

Section: Brain Stem Projections and Implications Of Current Resultsmentioning

confidence: 90%

Neck rotation modulates flexion synergy torques, indicating an ipsilateral reticulospinal source for impairment in stroke

Ellis

Drogos

Carmona

et al. 2012

Journal of Neurophysiology

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Ellis MD, Drogos J, Carmona C, Keller T, Dewald JP. Neck rotation modulates flexion synergy torques, indicating an ipsilateral reticulospinal source for impairment in stroke. J Neurophysiol 108: 3096 -3104, 2012. First published September 5, 2012 doi:10.1152/jn.01030.2011.-The effect of reticular formation excitability on maximum voluntary torque (MVT) generation and associated muscle activation at the shoulder and elbow was investigated through natural elicitation (active head rotation) of the asymmetric tonic neck reflex (ATNR) in 26 individuals with stroke and 9 agerange-matched controls. Isometric MVT generation at the shoulder and elbow was quantified with the head rotated (face pointing) contralateral and ipsilateral to the paretic (stroke) and dominant (control) arm. Given the dominance of abnormal torque coupling of elbow flexion with shoulder abduction (flexion synergy) in stroke and welldeveloped animal models demonstrating a linkage between reticular formation and ipsilateral elbow flexors and shoulder abductors, we hypothesized that constituent torques of flexion synergy, specifically elbow flexion and shoulder abduction, would increase with contralateral head rotation. The findings of this investigation support this hypothesis. Increases in MVT for three of four flexion synergy constituents (elbow flexion, shoulder abduction, and shoulder external rotation) were observed during contralateral head rotation only in individuals with stroke. Electromyographic data of the associated muscle coactivations were nonsignificant but are presented for consideration in light of a likely underpowered statistical design for this specific variable. This study not only provides evidence for the reemergence of ATNR following stroke but also indicates a common neuroanatomical link, namely, an increased reliance on ipsilateral reticulospinal pathways, as the likely mechanism underlying the expression of both ATNR and flexion synergy that results in the loss of independent joint control. flexion synergy; strength; tonic neck reflex; asymmetric tonic neck reflex REACHING FUNCTION FOLLOWING STROKE can be profoundly impaired and has been historically described as being constrained, at least in part, to stereotypic multijoint movement patterns or synergies (Brunnstrom 1970;Foerster 1936;Twitchell 1951). Initial quantitative investigations thoroughly described the phenomena under isometric conditions highlighting the abnormal coactivation of brachialis, biceps brachii, and brachioradialis with deltoid (Dewald et al. 1995). The coactivation manifests as a "flexion synergy" and is significant for abnormal joint torque coupling of elbow flexion during shoulder abduc-

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“…The motor system is a complex, integrated system with ascending and descending pathways working in ways that defy simple hierarchical descriptions. Even though the lesions are cortical, the merging and fractionation might be dependent on either neural changes at the cortical level (23) or other processes at the brainstem or spinal cord levels unmasked by the cortical lesions (17). Although it is premature to advance any concrete hypothesis on the origin of these three patterns of muscle synergy, we believe a description of these patterns is nonetheless important because the patterns provide physiological markers that can be used for shedding light on the complex processes that follow accidents involving the cortical motor system.…”

Section: −4mentioning

confidence: 99%

Muscle synergy patterns as physiological markers of motor cortical damage

Cheung

Turolla

Agostini

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

534

594

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The experimental findings herein reported are aimed at gaining a perspective on the complex neural events that follow lesions of the motor cortical areas. Cortical damage, whether by trauma or stroke, interferes with the flow of descending signals to the modular interneuronal structures of the spinal cord. These spinal modules subserve normal motor behaviors by activating groups of muscles as individual units (muscle synergies). Damage to the motor cortical areas disrupts the orchestration of the modules, resulting in abnormal movements. To gain insights into this complex process, we recorded myoelectric signals from multiple upper-limb muscles in subjects with cortical lesions. We used a factorization algorithm to identify the muscle synergies. Our factorization analysis revealed, in a quantitative way, three distinct patterns of muscle coordination-including preservation, merging, and fractionation of muscle synergies-that reflect the multiple neural responses that occur after cortical damage. These patterns varied as a function of both the severity of functional impairment and the temporal distance from stroke onset. We think these muscle-synergy patterns can be used as physiological markers of the status of any patient with stroke or trauma, thereby guiding the development of different rehabilitation approaches, as well as future physiological experiments for a further understanding of postinjury mechanisms of motor control and recovery.motor primitive | electromyography | neurorehabilitation | nonnegative matrix factorization | Virtual Reality Rehabilitation System

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Cortical overlap of joint representations contributes to the loss of independent joint control following stroke

Cited by 66 publications

References 56 publications

Theta Burst Stimulation of Human Primary Motor Cortex Degrades Selective Muscle Activation in the Ipsilateral Arm

Theta Burst Stimulation of Human Primary Motor Cortex Degrades Selective Muscle Activation in the Ipsilateral Arm

Neck rotation modulates flexion synergy torques, indicating an ipsilateral reticulospinal source for impairment in stroke

Muscle synergy patterns as physiological markers of motor cortical damage

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