The Impact of Shoulder Abduction Loading on Volitional Hand Opening and Grasping in Chronic Hemiparetic Stroke

Abstract

Background Up to 60% of individuals with moderate to severe chronic hemiparetic stroke experience excessive involuntary wrist/finger flexion that constrains functional hand movements including hand opening. It’s not known how stroke-induced brain injury impacts volitional hand opening and grasping forces as a result of the expression of abnormal coupling between shoulder abduction and wrist/finger flexion or the flexion synergy. Objective The goal of this study is to understand how shoulder abduction loading affects volitional hand opening and grasping forces in individuals with moderate to severe chronic hemiparetic stroke. Methods 36 individuals (stroke: 26, control: 10) were recruited for this study. Each participant was instructed to perform maximal hand opening and grasping forces while the arm was either fully supported or lifted with a weight equal to 25% or 50% of the participant’s maximum shoulder abduction torque. Hand pentagon area, defined as the area formed by the tips of thumb and fingers, was calculated during hand opening. Forces were recorded during grasping. Results In individuals with moderate stroke, increasing shoulder abduction loading reduced the ability to maximally open the hand. In individuals with severe stroke, who were not able to open the hand, grasping forces were generated and increased with shoulder abduction loading. Stroke individuals also showed a reduced ability to control volitional grasping forces due to the enhanced expression of flexion synergy. Conclusions Shoulder abduction loading reduced the ability to volitionally open the hand and control grasp forces after stroke. Neural mechanisms and clinical implications of these findings are discussed.

Intervention-Induced Changes in Cortical Connectivity and Activity in Severe Chronic Hemiparetic Stroke

“…In healthy controls, the temporal-spatial feature of motor preparation related to non-visually guided hand/finger movements is characterized by a flow of information from secondary motor areas to contralateral primary motor cortex [6][7][8] . In addition, previous results reported decreased power (i.e., desynchronization) in beta (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) and mu (8)(9)(10)(11)(12) Hz) during motor preparation, and an association between such desynchronization and the release of the motor command 12,13 .…”

“…The spectrogram from 4 to 48 Hz at each source was computed using a Morlet wavelet transform (wavelet number: 7). This range includes theta(4)(5)(6)(7) Hz), alpha(8)(9)(10)(11)(12), beta(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), and gamma (31-48 Hz) frequencies. The spectrogram was…”

Limited Capacity for Ipsilateral Secondary Motor Areas to Support Hand Function Post-Stroke

“…One of the main points of evidence for the compensatory use of these uncrossed cortico-bulbospinal pathways following stroke in humans is the presence of abnormal coupling between the shoulder abduction and the rest of the arm and hand. Lifting the arm at the shoulder leads to an abnormal coupling between shoulder abductors and elbow/forearm and finger flexor muscles that reduces reaching distance and hand opening ability, termed the flexion synergy (Dewald et al 1995;Sukal et al 2007;Miller & Dewald, 2012;Lan et al 2017). Indeed, lifting at the shoulder can lead to involuntary closing during attempted opening in individuals with more severe impairments (Lan et al 2017).…”

“…Lifting the arm at the shoulder leads to an abnormal coupling between shoulder abductors and elbow/forearm and finger flexor muscles that reduces reaching distance and hand opening ability, termed the flexion synergy (Dewald et al 1995;Sukal et al 2007;Miller & Dewald, 2012;Lan et al 2017). Indeed, lifting at the shoulder can lead to involuntary closing during attempted opening in individuals with more severe impairments (Lan et al 2017). Although the damage to CST accounts for the weakness, or inability to fully activate muscles (Thickbroom et al 2002;Schulz et al 2012), it does not affect the presence of this abnormal coupling.…”

“…Additionally, these pathways innervate a greater proportion of flexor muscles compared to extensors, and stimulation of these pathways preferentially elicits EMG activity in ipsilateral flexor muscles in the monkey (Davidson & Buford, 2006;Hirschauer & Buford, 2015). Therefore, attempting to drive movement of the arm via these compensatory ipsilateral pathways originating from secondary motor areas may allow individuals to generate greater activity at the more proximal portions of the arm, although at the detriment of individual joint control and distal hand function, especially hand opening (Lan et al 2017), as well as elbow extension and shoulder flexion (Sukal et al 2007).…”