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Updated: Jun 22, 2026

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI
Published on: April 18, 2011
Modulation of stretch reflexes of the finger flexors by sensory feedback from the proximal upper limb poststroke
Gilles Hoffmann1, Derek G Kamper, Jennifer H Kahn
1Sensory Motor Performance Program, Rehabilitation Institute of Chicago, 345 E. Superior St., Suite 1406, Chicago, IL 60611, USA. g-hoffmann@northwestern.edu
Abstract:
Neural coupling of proximal and distal upper limb segments may have functional implications in the recovery of hemiparesis after stroke. The goal of the present study was to investigate whether the stretch reflex response magnitude of spastic finger flexor muscles poststroke is influenced by sensory input from the shoulder and the elbow and whether reflex coupling of muscles throughout the upper limb is altered in spastic stroke survivors. Through imposed extension of the metacarpophalangeal (MCP) joints, stretch of the relaxed finger flexors of the four fingers was imposed in 10 relaxed stroke subjects under different conditions of proximal sensory input, namely static arm posture (3 different shoulder/elbow postures) and electrical stimulation (surface stimulation of biceps brachii or triceps brachii, or none). Fast (300 degrees/s) imposed stretch elicited stretch reflex flexion torque at the MCP joints and reflex electromyographic (EMG) activity in flexor digitorum superficialis. Both measures were greatest in an arm posture of 90 degrees of elbow flexion and neutral shoulder position. Biceps stimulation resulted in greater MCP stretch reflex flexion torque. Fast imposed stretch also elicited reflex EMG activity in nonstretched heteronymous upper limb muscles, both proximal and distal. These results suggest that in the spastic hemiparetic upper limb poststroke, sensorimotor coupling of proximal and distal upper limb segments is involved in both the increased stretch reflex response of the finger flexors and an increased reflex coupling of heteronymous muscles. Both phenomena may be mediated through changes poststroke in the spinal reflex circuits and/or in the descending influence of supraspinal pathways.
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