2016
DOI: 10.1179/1945511915y.0000000023
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Contributions of voluntary activation deficits to hand weakness after stroke

Abstract: Although extrinsic finger muscles could be successfully recruited electrically, voluntary excitation of these muscles was substantially limited in stroke survivors. Thus, finger weakness after stroke results predominantly from the inability to fully activate the muscle voluntarily.

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Cited by 38 publications
(34 citation statements)
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“…Though various studies have reported positive outcomes following multiple types of interventions in more mildly impaired individuals ( 5 , 6 ), regaining hand function in individuals with moderate-to-severe impairments still remains a challenge. This is largely due to impairments, such as the loss of volitional finger extension ( 7 , 8 ), muscle coactivation ( 7 ), involuntary coupling of wrist and finger flexion with certain shoulder and elbow movements ( 9 ), and somatosensory deficits ( 10 ).…”
Section: Introductionmentioning
confidence: 99%
“…Though various studies have reported positive outcomes following multiple types of interventions in more mildly impaired individuals ( 5 , 6 ), regaining hand function in individuals with moderate-to-severe impairments still remains a challenge. This is largely due to impairments, such as the loss of volitional finger extension ( 7 , 8 ), muscle coactivation ( 7 ), involuntary coupling of wrist and finger flexion with certain shoulder and elbow movements ( 9 ), and somatosensory deficits ( 10 ).…”
Section: Introductionmentioning
confidence: 99%
“…This muscle weakness post-stroke has been attributed to alterations in the descending voluntary command, and to anatomical and physiological changes within the muscle ( McComas et al, 1971 ; Bourbonnais and Noven, 1989 ; Dattola et al, 1993 ). Previous studies have identified impairments in voluntary muscle activation ( Riley and Bilodeau, 2002 ; Knorr et al, 2011 ; Bowden et al, 2014 ; Hoffmann et al, 2016 ), altered motor unit (MU) firing rates ( Rosenfalck and Andreassen, 1980 ; McNulty et al, 2014 ), a reduced ability to modulate MU firing ( Gemperline et al, 1995 ; Mottram et al, 2014 ; Li et al, 2015 ) and abnormal MU recruitment patterns ( Tang and Rymer, 1981 ; Hu et al, 2015 , 2016 ), all of which may contribute to muscle weakness post-stroke.…”
Section: Introductionmentioning
confidence: 99%
“…In healthy individuals, differences in strength between people and groups is highly correlated with muscle mass [ 28 ] with minimal differences between men and women in their ability to activate the available muscle [ 24 , 29 ]. Following stroke, impaired neural activation of the muscle by the cortex [ 15 , 30 , 31 ] plays a larger role in decrements in strength than for healthy controls. Coupled with muscle atrophy, both neural and muscular mechanisms contribute to sarcopenia [ 32 ] and the associated weakness.…”
Section: Discussionmentioning
confidence: 99%
“…Individuals who could contract and relax their muscles faster also could walk faster. Damage to the motor cortex following stroke not only interferes with the ability to fully activate the muscle [ 31 , 30 ], but also likely impairs the speed with which muscles are fully activated due to stroke-related changes in rate modulation and recruitment. In addition, there was positive correlation between baseline resting twitch amplitudes and walking speed.…”
Section: Discussionmentioning
confidence: 99%