ABSTRACT
In recent years, part of the muscle resistance in spastic patients has been explained by changes in the elastic properties of muscles. However, the adaptive spinal mechanisms responsible for the exaggeration of stretch reflex activity also contribute to muscle stiffness. The available data suggest that no single spinal mechanism is responsible for the development of spasticity but that failure of different spinal inhibitory mechanisms (reciprocal IA inhibition, presynaptic inhibition, IB inhibition, recurrent inhibition) are involved in different patients depending on the site of lesion and the etiology of the spastic symptoms. A recent finding also shows no sign of exaggerated stretch reflexes in muscles voluntarily activated by the spastic patient in general. This is easily explained by the control of stretch reflex activity in healthy subjects. In healthy subjects, the stretch reflex activity is increased during voluntary muscle contraction in part because of depression of the inhibitory mechanisms that are affected in spasticity. In spastic patients, these inhibitory mechanisms are already depressed at rest and cannot be depressed further in connection with a contraction. In relation to most normal movements, antagonist muscles should remain silent and maximally relaxed. This is ensured by increasing transmission in several spinal inhibitory pathways. In spastic patients, this control is inadequate, and therefore stretch reflexes in antagonist muscles are easily evoked at the beginning of voluntary movements or in the transition from flexor to extensor muscle activity. This problem is contradicted by the fact that antispastic therapy to improve voluntary movements should be directed.
