Concepedia

TLDR

Hyperactive stretch reflexes in upper‑motor‑neuron syndrome are often cited as hindering volitional movement, presumed to result from neural or mechanical activity of hyperactive antagonists interfering with agonists. The study examined whether this assumption holds by assessing quantitative and qualitative relationships between stretch reflexes and voluntary movement. Sixteen chronic UMN patients and eight controls underwent joint‑position and EMG recording of primary flexors and extensors, with reflex responses to passive motion, maximal isometric contraction, and time for ten rapid repetitive elbow movements measured, and EMG ratios during stretch, shortening, and isometric activity were used as spasticity indices compared to RRM time. Passive movement produced tonic reflexes dominating stretch in patients and shortening in controls; elbow flexor spasticity positively correlated with RRM time, yet qualitative EMG analysis revealed that movement impairment stems from limited, prolonged agonist recruitment and delayed cessation rather than antagonist stretch reflexes.

Abstract

Abstract Hyperactive strethch reflexes in the upper motor neuron (UMN) syndrome are frequently cited as an impediment to volitional movement. The assumption is that neural or mechanical activity of the hyperactive antagonist interferes with agonist function. The validity of this assumption was examined by evaluating quantitative and qualitative relationships between stretch reflexes and voluntary movement. Sixteen patients with chronic UMN symptoms and 8 normal volunteers were tested. Joint position and integrated electromyograms from primary flexors and extensors were recorded. Quantitated values of (1) reflex response to controlled passive motion by an automated system, (2) a maximal voluntary isometric contraction, and (3) the time required for ten voluntary rapid repetitive movements (RRM) of alternating elbow flexion and extension were obtained. Passive movement elicited tonic reflexes, which predominated during muscle stretch in patients and during muscle shortening in the volunteers. Ratios of the EMG activity elicited during stretch, shortening, and isometric activity were used as measures of spasticity and were compared with the time for RRM. A positive correlation between elbow flexor spasticity and the time for RRM was shown. Qualitative analysis of the EMG activity during voluntary isotonic movement, however, showed that primary impairment of movement is not due to antagonist stretch reflexes, but rather to limited and prolonged recruitment of agonist contraction and delayed cessation of agonist contraction at the termination of movement.

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