Spastic hypertonia has been defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome. Heightened muscle tone may be the result of changes intrinsic to the muscle or to altered reflex properties. Increased motoneuronal excitability and/or enhanced stretch-evoked synaptic excitation of motoneurons are mechanisms that might enhance stretch reflexes. Two distinct parameters may be altered in the pathologic stretch reflex--the "set point," or angular threshold of the stretch reflex, and the reflex "gain," or the amount of force required to extend the limb in proportion to the increasing joint angle. Earlier studies fail to dissociate the contributions of reflex threshold and reflex gain. Recent investigations suggest that spastic hypertonia may be the result of a decrease in stretch reflex threshold without significant increase in reflex gain, as was previously believed. Various clinical scales, biomechanical paradigms, pendulum models, and electrophysiologic studies have been used to quantify spastic hypertonia. Biomechanical methods seem to correlate most closely with the clinical state. Spastic hypertonia is but one component of the upper motor neuron syndrome, whose features also include loss of dexterity, weakness, fatigability, and various reflex release phenomena. These other features of the upper motor neuron syndrome may well be more disabling to the patient than changes in muscle tone.