ABSTRACT
Spasticity produces numerous physical signs. These have little relationship to the patient’s disability, which is caused by impairment by a movement disorder. On the basis of the clinical signs, a widely accepted conclusion was drawn for the pathophysiology and treatment of spasticity: exaggerated reflexes are responsible for muscle hypertonia and, consequently, the movement disorder. Drug therapy is therefore usually directed at reducing the activity of stretch reflexes. The function of these reflexes during natural movements and the connection between exaggerated reflexes and movement disorder is frequently not considered. This chapter focuses on the pathophysiological basis of spastic movement disorder in children and adults with the therapeutic consequences and current drug therapy. The physiological changes during the transition from spinal shock to spasticity after an acute spinal cord injury will be discussed first.
