Stretch-induced electromyographic activity and torque in spastic elbow muscles. Differential modulation of reflex...

Stretch-evoked electromyographic (EMG) activity and torque signals have been studied in elbow joint muscles of both sides of patients with spastic hemiparesis and healthy subjects. In order to reveal differences in the generation of muscle tone between clinical assessment and functional movement, stretches of different velocities and amplitudes were applied during passive and quasi-functional active motor tasks. In spastic patients the strength and duration of the EMG responses following stretching of flexor and extensor muscles during both passive and active tasks were dependent on the stretch velocity and duration, respectively. This effect was seen on both the spastic and unaffected side. Under passive conditions EMG activity after stretching was negligible in the limb muscles of healthy subjects, of small amplitude in unaffected limbs of the patients, but was strong in affected muscles. Under active conditions, the amplitude of the early (M1) component of the EMG signal was larger, while the later components (M2 and M3) were smaller. These differences were due more to a change in reflex gain than to a change in reflex threshold when the stretch velocity signal was the basis for calculation. It is suggested that in spastic paresis, modulation of stretch-induced EMG activity in the spastic limb becomes restricted to a smaller range with a poor ability to switch off under passive conditions. Furthermore, the reflex EMG activity suffers a reduced facilitation under active conditions. In comparison with unaffected limbs the stretch-evoked torque on the affected side was increased under passive conditions (due to the extra EMG activity) and decreased under active conditions (due to a reduced EMG activity). An increased torque to EMG ratio was found in spastic flexor and extensor muscles during active tasks. This is thought to be due to changes in mechanical muscle fibre properties suffered as a consequence of defective muscle activation following cerebral lesions. The consequences for clinical assessment of muscle tone and therapy of spastic movement disorder are discussed.