In spastic paresis, factors limiting active movement include antagonist contracture, agonist paresis, and spastic cocontraction. We studied agonist and antagonist muscle activation around the elbow to determine the role of the degree of muscle stretch in modifying paresis and cocontraction.

Eighteen healthy (age 47±10) and 15hemiparetic (age 42±16) subjects performed maximal isometric elbow flexion and extension 5-second efforts, with elbow flexed and extended. Using biceps and triceps brachii surface electromyography, we determined for each muscle: (i) the Mean Rectified Voltage (MRV) during the 500ms peak voluntary agonist recruitment elbow flexed (MRV_ago500F) and elbow extended (MRV_ago500E); (ii) the coefficient of stretch-sensitivity (CSS) of agonist recruitment, calculated as (MRV_ago500F-MRV_ago500E)/MRV_ago500F; (iii) the cocontraction index (CCI) in each elbow position, ratio of the MRV from each muscle during an opposite movement, MRV_antago5 to MRV_ago500. We compared the dominant arm in healthy subjects with the non-paretic and paretic arms in hemiparetic subjects.

X_V1 was 175±11° in the elbow flexors (maximal passive elbow extension; coefficient of shortening, 2.7%) and 163±7° in the elbow extensors (no shortening). CSS was not significantly different from 0 in the healthy and non-paretic arm; however, CSS in the paretic arm was −21±10% in the paretic elbow extensors vs −4±7% in the non-paretic arm (P vs extended, P=0.013). Triceps brachii CCI with the elbow flexed was 0.10±0.05 [95%CI, 0.03–0.17], 0.15±0.10 [0.07–0.23] and 0.26±0.24 [0.18–0.34], in the healthy, non-paretic and paretic arm respectively (between-group difference P=0.011), and 0.12±0.06 [95%CI, 0.03–0.21], 0.15±0.08 [0.06–0.25], and 0.38±0.32 [0.28–0.48] with the elbow extended (between-group difference P vs extended, NS).

In hemiparesis, elbow extended position deteriorates active command at both agonist and antagonist levels: decreasing voluntary recruitment of agonist MNs–a phenomenon defined as stretch-sensitive paresis–and increasing antagonist co-contraction. This may occur through physiological effects of high-threshold afferent fiber recruitment in contractured elbow flexors.