STRETCH-INDUCED ELECTROMYOGRAPHIC ACTIVITY AND TORQUE IN SPASTIC ELBOW MUSCLES - DIFFERENTIAL MODULATION OF REFLEX ACTIVITY IN PASSIVE AND ACTIVE MOTOR-TASKS

Stretch-evoked electromyographic (EMG) activity and torque signals hav e been studied in elbow joint muscles of both sides of patients with s pastic hemiparesis and healthy subjects. In order to reveal difference s in the generation of muscle tone between clinical assessment and fun ctional movement, stretches of different velocities and amplitudes wer e applied during passive and quasi-functional active motor tasks. In s pastic patients the strength and duration of the EMG responses followi ng stretching of flexor and extensor muscles during both passive and a ctive tasks were dependent on the stretch velocity and duration, respe ctively. 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 unaffe cted limbs of the patients, but was strong in affected muscles. Under active conditions, the amplitude of the early (M1) component of the EM G signal was larger, while the later components (M2 and M3) were small er. 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, modul ation of stretch-induced EMG activity in the spastic limb becomes rest ricted to a smaller range with a poor ability to switch off under pass ive conditions. Furthermore, the reflex EMG activity suffers a reduced facilitation under active conditions. In comparison with unaffected l imbs the stretch-evoked torque on the affected side was increased unde r passive conditions (due to the extra EMG activity) and decreased und er active conditions (due to a reduced EMG activity). An increased tor que to EMG ratio was found in spastic flexor and extensor muscles duri ng active tasks. This is thought to be due to changes in mechanical mu scle fibre properties suffered as a consequence of defective muscle ac tivation following cerebral lesions. The consequences for clinical ass essment of muscle tone and therapy of spastic movement disorder are di scussed.