Introduction

Even today, although there are a number of validated techniques for the measurement of associated disability, the measurement of spasticity at the level of impairment is probably in its infancy. Because of the relative lack of treatment or therapy to reduce spasticity, there has been limited development of methods for its measurement. However, with the relatively recent advent of treatments for spasticity, such as botulinum toxin, there is now a considerable incentive to develop new methods.

One particular barrier to valid measurement relates to the need for a precise definition. The measurement of any physical phenomenon is impossible in the absence of a definition, and this is equally true in the case of spasticity. At the clinical level, there is almost certainly a wide variety of assumed definitions concerning stiffness and the lack or difficulty of movement. A relatively precise statement has been provided by Lance (1980), as follows: Spasticity, which is directly equated with spastic hypertonia, is a motor disorder that is ‘characterised by a velocity dependent increase in the tonic stretch reflex (muscle tone) with exaggerated tendon reflexes, resulting from the hyper excitability of the stretch reflex, as one component of the upper motor neurone syndrome’ following a lesion at any level of the corticofugal pathways – cortex, internal capsule, brainstem or spinal cord (Burke, 1988). Furthermore, spastic hypertonia has also been described as the exaggeration of the spinal proprioceptive reflexes resulting from a loss of descending inhibitory control (Burke, 1988).