Since the studies of Sherrington(1947) on decerebrate rigidity in the cat, evidence has shown that spasticity is the result of modification of the sensitivity of the central reflex pathways. Lance defined spasticity in 1980 as a velocity-dependent increase in muscle tone in response to muscle stretch. This resistance to muscle stretch may also result in soft tissue modifications and eventually muscle and soft tissue contractures (Goldspink and Williams, 1990). In this way, it may limit movement and be a significant cause of disability and handicap. Usually spasticity is simply one part of the upper motor neuron syndrome and the other elements of the syndrome are responsible for further disability (Table 12.1).
Spasticity is a dynamic feature that can vary with the position of the limb or trunk, with time, with medication, and with a variety of other factors. Consequently, it is often difficult to evaluate the real impact of spasticity as an independent factor in its own right. The treatment must take into account all the features of the upper motor neuron syndrome, only some of which are responsive to clinical management. The main goal, as always in rehabilitation practice, is to identify the function limited by spasticity and introduce appropriate measures to improve that function. Sometimes a secondary goal can be simply to avoid unnecessary future complications associated with spasticity, such as contractures.
The aim of the first part of this chapter is to discuss the overall context of spasticity in terms of treatment decisions and outcome measures. The general management of spasticity will then be discussed both in terms of physical therapy and orthotic management as well as in terms of oral antispastic medication, focal treatments, and surgery. We will then discuss the management of various types of post-stroke pain, including hemiplegic shoulder pain.
Lance (1980) defined spasticity as “a motor disorder characterised by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting fromhyperexcitability of the stretch reflex, as one component of the upper motor neurone syndrome.” There are three main mechanisms that induce spasticity: modification of the muscle, new nerve collaterals at the spinal level, and exaggeration of the spinal reflexes, which are not appropriatelymodulated by the supraspinal pathways (Brown, 1994; Young, 1994). It is likely that the perturbations of several of these mechanisms are necessary to produce clinical spasticity.