Pathophysiology of lengthening contractions in human spasticity: a study of the hamstring muscles during locomotion

Abstract The pathophysiological mechanisms underlying disturbed activation of spastic muscles during functional movements were investigated with focus on the lengthening contractions (LCs) occurring while walking. In particular, the LC which takes place in the hamstrings group during the swing phase of the stride was analysed in terms of muscle kinematics (estimated muscle–tendon length and lengthening velocity), electromyographic (EMG) activity and associated changes in knee joint mechanics, in able-bodied and spastic (cerebral palsy) subjects. In healthy controls, during the last third of the stride cycle, the hamstring muscles underwent monotonic lengthening, according to a bell-shaped velocity profile. EMG activity started halfway during muscle lengthening and grew higher in parallel with muscle length. The amplitude and degree of synchronization of the above LC, as well as the lengthening velocity threshold for its initiation, proved to be progressively augmented as walking became faster. Similarly, the mechanical resistance to knee joint extension (as judged by the slope of the moment–angle relationship during muscle activation) was found to be positively correlated with the speed of progression. In spastic subjects, the late-swing LC of the hamstring muscles revealed the following abnormalities: (a) reduced muscle–tendon excursion; (b) uneven increase of muscle–tendon length with smooth or unsymmetrical velocity profile; (c) increased maximum EMG amplitude; (d) hyper-synchronous or clonic pattern of EMG recruitment; (e) reduction of the lengthening velocity thresholds for muscle activation; (f) loss of the positive correlation between lengthening velocity threshold and walking speed, with appearance of abnormal constant-threshold trends, or even negative trends with relative threshold decrease at the highest walking speeds; (g) concurrent enhancement of mechanical resistance to knee joint extension, with maximum increment in spastic patients exhibiting the lowest thresholds for EMG recruitment. It is concluded that the physiological braking action of LCs can be severely disturbed in spastic subjects, in the presence of abnormal coupling between muscle kinematics and motor output. Altered setting and/or modulation of the lengthening velocity threshold for muscle activation appear to be among the mechanically-effective underlying mechanisms.