The Mechanism of Spastic Muscle Hypertonusvariation in Reflex Gain Over the Time Course of Spasticity

The electromyographic (EMG) response of the initially passive biceps brachii muscle to imposed extension applied at the elbow was studied in 19 hemiparetic and 12 normal subjects. In relaxed normal subjects, the biceps muscle was found to respond only at displacement velocities above 175 deg/s, with a single early burst of activity in the biceps EMG. In contrast, the hemiparetic subjects, in addition to the early EMG activity, also showed considerable late activity, which persisted even with stretch velocities as low as 35 deg/s. This late activity is a stretch reflex, present in fully plegic arms. It was seen in all spastic subjects in whom the tone of the biceps had been clinically assessed to be raised, but was never observed in subjects with normal muscle tone. The mean level of this EMG response was highly correlated with displacement velocity and its duration to the duration of the applied displacement. It is suggested that this reflex EMG activity is the major factor in the genesis of spastic hypertonus in the arm and that it arises not from a reduction in the threshold of the stretch reflexes of the muscle, but from a pathological increase in stretch reflex gain. It is further shown that this activity is at a high level between the first and third months after the onset of spasticity and that the reflex gain is significantly reduced when spasticity is established for a year or more. It is concluded that, while changes in passive mechanical properties may play a role when spasticity has been established for more than a year, the major cause of spastic muscle hypertonus is a pathological increase in stretch reflex activity.